The impact of COVID-19 pandemic can be felt across the Healthcare Industry The growing inability in the production and manufacturing processes, in the light of the self-quarantined workforce has caused a major disruption in the supply chain across the sector. Restrictions encouraged by this pandemic are obstructing the production of essentials such as life-saving drugs.

The nature of operation in Pharmaceuticals plants that cannot be easily stopped and started, makes the operational restrictions in these plants a serious concern for the industry leaders. Restricted and delayed shipments from China have created a price hike in the raw materials, affecting the core of the Healthcare Industry

The slacking demand from different impacted industries such as automotive is negatively influencing the growth of the Healthcare Industry. In light of the current crisis, the market leaders are focused to become self-reliant which is expected to benefit the economic growth of different economies in the longer term. Companies are triggering events to restructure and recover from the losses incurred during the COVID-19 pandemic.

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Myeloproliferative disorders are disease of blood and bone marrow which have unknown cause and there are wide range of symptoms. The treatment of myeloproliferative disorders generally depends on the type and presence of symptoms. Myeloproliferative disorders is generally considered as clonal disorder which begins with one or more change in the DNA of a single stem cells in the bone marrow. The changes to the hematopoietic stem cell cause the cell to reproduce repeatedly, creating more abnormal stem cells and these abnormal cells become one or more types of blood cells. Myeloproliferative disorders gets worst with time as the number of extra blood cells build up in the bone marrow and bloodstream.

Emergence of new treatment for the myeloproliferative disorders and availability of novel drug drive the market for myeloproliferative disorders drugs market in the near future. Rising incidence of myeloproliferative disorders and presence of strong product pipeline spur the myeloproliferative disorders drugs market. Growing geriatric population, change in lifestyle and growing awareness among general population is expected to drive the market of myeloproliferative disorders in the forecast period. Advancement in the treatment for oncology further expand the treatment option for myeloproliferative disorders. Various clinical trial undergoing for the treatment of myeloproliferative disorders which further drive the growth of the myeloproliferative disorders drugs market. However, high cost of drug and treatment along with the lack of awareness among the population in developing and under developed nations hinder the growth of myeloproliferative disorders drugs market.

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The global myeloproliferative disorders drugs market is segmented on basis of Type, Drug Type, Distribution Channel, End User and Geography.

Improvement in the symptoms and reduction of in splenomegaly among patients receiving available therapy is expected to boost the market of myeloproliferative disorders. Development in new therapeutic drug and target therapy further drive the market growth of myeloproliferative disorders. Increased research and development and increased funding by the government towards the development of novel therapy spur the market growth. With the discovery of specific gene mutations in myeloproliferative disorders the market is expected to grow in the forecast period owing to increased adoption of new drugs and increased awareness along with the favorable reimbursement scenarios for the treatment of myeloproliferative disorders.

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The North America market holds the largest revenue share for myeloproliferative disorders drugs, due to presence of major pharmaceutical players undergoing various clinical innovation, government initiative and increase research and development funding for the Myeloproliferative disorders. Europe is expected to contribute for the second largest revenue share after North America in the global myeloproliferative disorders drugs market, owing to merging treatment option and development of oncology drug discovery and rising prevalence of myeloproliferative disorders. Asia Pacific is expected to show rapid growth, due to increasing number of vascular surgeons and low cost of peripheral interventions.

China is expected to register fast growth, due to significant increase in the number of innovative firm and research organization and increasing importance of pharmaceutical research & development activities and investments in research for developing new drugs. Latin America and Middle East & Africa are projected to exhibit sluggish growth in myeloproliferative disorders Drugs market, due to proper healthcare systems and adoption of new drug and therapy.

Examples of some of the key manufacturer present in the global myeloproliferative disorders drugs market are ,

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Throat Lozenges MarketThe growth of the market for throat lozenges will be driven by aging population since elderly people often suffer from throat infection that increase the uptake of throat lozenges. It has been projected by the World Health Organization (WHO) that by 2050 nearly 2 billion populations will belong to geriatric population and it also estimated that global elderly population was 524 million in 2010.For More Information.

Trigeminal Neuralgia Therapeutics MarketThere are various types of surgical procedures available for trigeminal neuralgia such as rhizotomy, stereotactic radiosurgery, microvascular decompression, transcutaneous electrical nerve stimulation and acupuncture.For More Information.

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Global Myeloproliferative Disorders Drugs Market to Witness Significant Revenue Growth on Back of Augmenting Demand and Forecast 2018 2028 -...

Bone Marrow Stem Cells Comments Off on Global Myeloproliferative Disorders Drugs Market to Witness Significant Revenue Growth on Back of Augmenting Demand and Forecast 2018 2028 -… | May 31st, 2020

Most people are seeking the secret to anti-ageing, but did you ever wonder how the skin actually ages or how you could slow the process down?

Ageing is a natural process accompanied by a continuous alteration of the body. Your body produces visible changes in its structure, function and vulnerability to environmental stress and disease. Genetics, as well as the lifestyle we lead, play a big role in the ageing process.

Your skin is an organ, and its function is to regulate the excretion of metabolic waste products, regulate the bodies temperature as well as containing receptors for pain, tactile sensation, and pressure. Therefore, the health and appearance of your skin, like the health of your other organs correspond with your lifestyle and dietary habits, as well as with age-related factors such as the imbalance of hormones.

Ageing of the skin can be influenced by many factors including ultraviolet radiation, excess alcohol consumption, tobacco abuse, and environmental pollution.

What a lot of people dont realise is that as their body weight increases and their blood sugar levels rise, biochemical reactions interrupt the structural framework of their skin. With all these factors combined they lead to cumulative deterioration in the appearance of the skin as well as the function of the skin.

Within the skin ageing is associated with a loss of fibrous tissue, a slower rate of cellular renewal, and a reduced vascular and glandular network. The barrier function that maintains cellular hydration also becomes impaired. The subcutaneous tissue (known as the hypodermis or the third layer of the skin) flattens.

The rate at which these functions decline can be more than 50% by middle age depending upon ones genetic makeup, lifestyle and normal physiological functions within the skin. If we dont take action to support our skins intrinsic defence systems, the youthful qualities of our skin will deteriorate rapidly. Luckily for us, we can harness insights gathered through the latest scientific innovations and slow or potentially reverse the signs and symptoms of accelerated skin ageing.

Intrinsic skin ageing is primarily determined by genetic factors, hormonal imbalances and metabolic reactions like oxidative stress. Signs of intrinsic ageing include skin sagging, thinning and cracking, and the appearance of fine lines and wrinkles.

There are numerous external factors that affect the skin and cause signs and symptoms of premature ageing. Generally, most premature ageing is caused by over-exposure to the suns UV rays. However, there are other contributing factors, for example, atmospheric factors such as air pollution, visible light and infrared radiation. Lifestyle choices such as smoking, chronic stress and excessive alcohol consumption can lead to older-looking skin.

The most common signs of extrinsic ageing are thinning of the skin, laxity, fragility and the increased appearance of wrinkles.

As the skin is a visual organ, the beauty industrys main objective is to improve the appearance of skin with extensive topical treatments and products. However, often overlooked is the need to support the health and beauty of the skin from within.

Ideally one should centre their diet upon fruits, vegetables, whole grains, legumes, monounsaturated fats (like those found in olive oil), and a healthy ratio of omega-3 to omega-6 polyunsaturated fatty acids. Generally, consumption of shellfish, fish rich in omega 3 fatty acids, regular tea drinking, and greater consumption of fruits and vegetables have been known to be associated with improved skin health.

Gut health is crucial to healthy skin. The human skin hosts a variety of microorganisms, collectively known as the skin microbiota. Within the skin, there is a complex network of interactions between the microbes and cells. Friendly bacteria, such as Lactobacillus and Bifidobacteria are well researched for effectively treating infections, promoting healthy immunity, and reducing inflammation in the skin. Oral pre- and probiotics help to rebalance the skin microbiota and optimise the skin barrier function.

In addition, oral probiotics boost cellular antioxidant capacity and combat inflammation in general. Probiotics also help to neutralise toxic byproducts, defend the lining of the intestine, increase the bioavailability of some nutrients and reinforce the intestinal barrier against infectious microbes that may harm healthy skin.

Cosmeceuticals are topical products that exert both cosmetic and therapeutic benefits which have continued to evolve in order to ward off the signs of skin ageing. Some of the most popular topicals include exfoliating and depigmenting agents, antioxidants and regenerating products, such as peptides and stem cells.

Sunscreens (with dual protection against UVA and UVB in a photostable complex) are the most important topical as they protect us from the UV damage caused by the sun. Sun exposure is definitely one of the biggest contributing factors to premature ageing and is actually known as photo-ageing.

Another phenomenal topical is retinoids which have proven their safety and efficacy in reducing photo-damaged skin and are a popular treatment for anti-ageing. Retinoids help combat and reverse the visual effects of ageing, such as wrinkles, laxity, and discolouration. Retinoids accelerate cell turnover and can also improve blemishes and the appearance of pores.

The use of alpha-hydroxy acids (AHAs) has also been known to improve skin texture and reduce the signs of ageing by promoting the shedding of our superficial dead skin cells which in turn helps to restore hydration and a smoother texture. Whats nice about alpha-hydroxy acids is that they can pretty much treat any skin condition or concern because there are so many different types of acids. Theres literally something for everything. The most common ingredients used in product formulations and peels include citric acid, glycolic acid, lactic acid, malic acid, pyruvic acid as well as tartaric acid.

Antioxidants are being increasingly used in anti-ageing skincare. Topical antioxidants are effective in fending off damaging free radicals and reducing inflammation within the skin. A few popular ones used are ascorbic acid (vitamin C,) tocopherols (vitamin E,) alpha-lipoic acid and coenzyme Q10. Emerging natural antioxidants proving effective include EGCG (from green tea), resveratrol, Centella Asiatica (Gotu Kola,) proanthocyanidins (grapeseed,) curcumin, pomegranate, silymarin/silibinin (milk thistle), coffeeberry, melatonin, and marine-based ingredients.

Within the skin, the deterioration of collagen results in the formation of protein fragments, called peptides. These peptides are then recognised by collagen-producing cells, which respond by increasing collagen production in order to repair the damaged skin. However, as we age this positive feedback between skin breakdown and the initiation of new collagen formation becomes inefficient. Therefore by applying specialised peptides to your skin topically you can effectively trick collagen-producing cells into boosting collagen production. There are many other active ingredients used in topical products that are focused on anti-ageing among other things.

So basically all we need to do is protect the skin from the inside by consuming nutrient-packed foods as well as reducing our exposure to extrinsic factors that cause premature ageing along with using topical skincare products. Not as difficult as we may have thought, hey?

This content has been created as part of our freelancer relief programme. We are supporting journalists and freelance writers impacted by the economic slowdown caused by #lockdownlife.

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Ageing: An expos on what really causes us to show our age - The South African

Skin Stem Cells Comments Off on Ageing: An expos on what really causes us to show our age – The South African | May 31st, 2020

In the UK 50,000 people have a spinal cord injury (SCI)[1]

Every year there are 2,500 new cases of SCI in the UK[1]

20-30% of people with SCI show clinically significant signs of depression[2]

People with spinal cord injury are two to five times more likely to die prematurely[2]

50kpeople in the UKhave spinal cord injury

A traumatic injury to the spine can cause a bruise, partial or complete tear in the spinal cord, leading to partial or total loss of feeling/movement in various body parts. The most common sites of injury are the cervical and thoracic areas.

Generally, spinal cord injuries (SCI) affect areas lower than the point of damage, so the higher the damage, the more movement and sensation will be lost. Spinal cord injury can even result in paraplegia and tetraplegia[3], although severity and recovery rate varies widely depending on the location and extent of the injury.

To aid recovery and lessen the risk of developing associated conditions, its essential that each patient receives appropriate rehabilitation and health maintenance support.

Stem cell therapy is rapidly evolving and offering treatment for spinal-cord injuries (SCI). Although there is no current treatment available to restore injury-induced loss of function, evidence is building that stem cell infusions into the spine may support spinal cord repair.

Positive results have been observed in phase I/II clinical trials at Puerta de Hierro Hospital in Madrid[4]. 12 patients were given doses of the new drug NC1 made from autologous mesenchymal stromal cells (MSCs) and autologous plasma. All 12 patients experienced improvements in sensitivity and 50% showed greater motor activity, decreased spasms and improved sexual function.

Since this clinical trial took place, the NC1 drug has been approved by the Spanish Agency of Medicines. However, there is still more research to be done for stem cell therapy to be widely administered for repairing spinal cord injury.

1. https://www.backuptrust.org.uk/spinal-cord-injury/what-is-spinal-cord-injury

2. https://www.who.int/news-room/fact-sheets/detail/spinal-cord-injury

3. https://www.spinal.co.uk/learn/understanding-sci/

4. https://www.sciencedirect.com/science/article/pii/S1465324916303772

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Stem cell therapy and spinal cord injury (SCI) | Future ...

Spinal Cord Stem Cells Comments Off on Stem cell therapy and spinal cord injury (SCI) | Future … | May 31st, 2020

The spinal cord is a long, fragile, tube-like nervous structure that connects the brain with peripheral nerves. Damage to the spinal cord, by trauma or other means, consequently results in severe motor- and sensory deficits that usually lead to the inability to move and feel. Accidents are the most common cause of Spinal Cord Injury with catastrophic consequences for the life of the patient and their relatives. While conservative therapies aim to stabilize the patient, functional recovery in most cases is minimal.

Both preclinical and clinical studies have shown improved recovery of spinal cord injury patients when the therapy was combined with a suitable stem cell therapy. Our clinic provides access to the most advanced clinically available combination of stem cell therapies.

Spinal trauma can disrupt ascending and descending axonal pathways that lead to: inflammation, demyelination and loss of neural cells (neurons). Depending on the site of injury, functional disorders induced by cellular damage usually result in the inability to move, sensory loss and/or lack of autonomous nervous system control.

Fully regenerative therapies for spinal trauma do not exist yet. However, very promising results have been obtained with stem cell transplantation in patients with spinal trauma. The use ofMesenchymal Stem Cells (MSCs) in Spinal Cord Injury has been extensively reviewed. Experiments with MSCs have shown that their abilities to stimulate repair processes in spinal cord injury are due to the paracrine secretion of the stem cells. After 21 days of observations, even though the MSCs had not been incorporated into the regenerated host tissue, there was a significant improvement in functional recovery, from as early as one week after the treatment with MSCs.

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Spinal Cord Stem Cell Treatments London | Regenerative ...

Spinal Cord Stem Cells Comments Off on Spinal Cord Stem Cell Treatments London | Regenerative … | May 31st, 2020

Content

C. Thomas Caskey, M.D. - FACP, FRSC Schizophrenia disease genes

Katarzyna Cieslik, Ph.D. - Cardiac mesenchymal progenitors

Austin Cooney, Ph.D. - Nuclear receptor regulation of embryonic stem cell function

Thomas Cooper, M.D. - Alternative splicing in cardiac development and disease

Mary Dickinson, Ph.D. - Role of fluid-derived mechanical forces in vascular remodeling and heart morphogenesis

Mark Entman, M.D. - Molecular mechanisms of cardiac injury and repair, inflammatory signaling

Charles Fraser, M.D. - Congenital heart surgery outcomes, bioengineering and assist devices

Peggy Goodell, M.D. - Hematopoietic stem cells, epigenetic modifications

Jeffrey Jacot, Ph.D. - Regenerative therapies for congenital heart disease

Sandra Haudek, Ph.D. - Circulating monocytic fibroblast precursors, cardiac hypertrophy

George Noon, M.D. - Transplant and assist devices

JoAnn Trial, Ph.D. - Origins of fibroblasts in cardiac injury healing

Peter Tsai, M.D., FACS - Custom-fenestrated endovascular stents to repair aortic transections or aneurysms

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Cardiac Regeneration, Stem Cells

Cardiac Stem Cells Comments Off on Cardiac Regeneration, Stem Cells | May 31st, 2020

-- Peer-reviewed publication in Alzheimer's & Dementia: Translational Research & Clinical Interventions validates potential of drug discovery platform and ability to study early stages of disease pathology --

Hesperos Inc., pioneers of the Human-on-a-Chip in vitro system, today announced a new peer-reviewed publication that describes how the companys functional Human-on-a-Chip system can be used as a drug discovery platform to identify therapeutic interventions targeting the preclinical stages of Alzheimers disease (AD) and mild cognitive impairment (MCI). The manuscript, titled "A human induced pluripotent stem cell-derived cortical neuron human-on-a-chip system to study A42 and tau-induced pathophysiological effects on long-term potentiation," was published this week in Alzheimer's & Dementia: Translational Research & Clinical Interventions. The work was conducted in collaboration with the University of Central Florida and with David G. Morgan, Ph.D., Professor of Translational Neuroscience at Michigan State University, and expert in AD pathology.

To date, more than 100 potential therapeutics in development for AD have been abandoned or failed during clinical trials. These therapeutics relied on research conducted in preclinical animal studies, which often are unable to accurately capture the full spectrum of the human disease phenotype, including differences in drug metabolism and excretion between humans and animals. Therefore, there is a need for human models, especially those that accurately recapitulate the functional impairments during the preclinical phases of AD and MCI.

"Hesperos offers a breakthrough technology that provides a human cell-based assay based on cognitive function metrics to evaluate drugs designed to restore cognition at early stages of the Alzheimers continuum," said Dr. Morgan. "This system can serve as a novel drug discovery platform to identify compounds that rescue or alleviate the initial neuronal deficits caused by A1-42 and/or tau oligomers, which is a main focus of clinical trials."

In 2018, Hesperos received a Phase I Small Business Innovation Research (SBIR) grant from the National Institute on Aging (NIA) division within the US National Institutes of Health (NIH) to help create a new multi-organ human-on-a-chip model for testing AD drugs. Research conducted under this grant included a study to assess therapeutic interventions based on functional changes in neurons, not neuronal death.

In the recent Alzheimer's & Dementia publication, Hesperos describes its in vitro human induced pluripotent stem cell (iPSC)-derived cortical neuron human-on-a-chip system for the evaluation of neuron morphology and function after exposure to toxic A and tau oligomers as well as brain extracts from AD transgenic mouse models.

"Researchers are now focusing on biomarker development and therapeutic intervention before symptoms arise in AD and MCI," said James Hickman, Ph.D., Chief Scientist at Hesperos and Professor at the University of Central Florida. "By studying functional disruption without extensive cell loss, we now have a screening methodology for drugs that could potentially evaluate therapeutic efficacy even before the neurodegeneration in MCI and AD occurs."

The researchers found that compared to controls, treatment with toxic A and tau oligomers or brain extracts on the iPSC cortical neurons significantly impaired information processing as demonstrated by reduction in high-frequency stimulation-induced long-term potentiation (LTP), a process that is thought to underlie memory formation and learning. Additionally, oligomer and brain extract exposure led to dysfunction in iPSC cortical neuron electrophysiological activity, including decreases in ion current and action potential firing.

While exposure to the toxic oligomers and brain extracts caused morphological defects in the iPSC cortical neurons, there was no significant loss in cell viability.

"Clinical success for AD therapies has been challenging since preclinical animal studies often do not translate to humans," said Michael L. Shuler, Ph.D., Chief Executive Officer of Hesperos. "With our recent study, we are now one step closer in developing an AD multi-organ model to better evaluate drug metabolism in the liver, penetration through the blood-brain barrier and the effects on neuronal cells."

Story continues

About Alzheimers Disease/Preclinical Stage AD

AD is a progressive disease that is characterized by memory loss and deterioration of cognitive function. Preclinical AD is the first stage of the disease, and it begins long before any symptoms become apparent. It is thought that symptoms do not manifest until there is a significant death of neuronal cells, which is caused by the aggregation of toxic amyloid beta (A) and tau oligomers, typically during the earliest stages of the disease. Unfortunately, treatment after the diagnosis of MCI may be too late to reverse or modify disease progression.

To read the full manuscript, please visit https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/trc2.12029.

About Hesperos

Hesperos, Inc. is a leading provider of Human-on-a-Chip microfluidic systems to characterize an individuals biology. Founders Michael L. Shuler and James J. Hickman have been at the forefront of every major scientific discovery in this realm, from individual organ-on-a-chip constructs to fully functional, interconnected multi-organ systems. With a mission to revolutionize toxicology testing as well as efficacy evaluation for drug discovery, the company has created pumpless platforms with serum-free cellular mediums that allow multi-organ system communication and integrated computational PKPD modeling of live physiological responses utilizing functional readouts from neurons, cardiac, muscle, barrier tissues and neuromuscular junctions as well as responses from liver, pancreas and barrier tissues. Created from human stem cells, the fully human systems are the first in vitro solutions to accurately predict in vivo functions without the use of animal models. More information is available at http://www.hesperosinc.com.

Hesperos and Human-on-a-Chip are trademarks of Hesperos Inc. All other brands may be trademarks of their respective holders.

View source version on businesswire.com: https://www.businesswire.com/news/home/20200529005128/en/

Contacts

Michelle LinnBioscribe774-696-3803michelle@bioscribe.com

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Hesperos Human-on-a-Chip System Used to Model Preclinical Stages of Alzheimers Disease and Mild Cognitive Impairment - Yahoo Finance

Cardiac Stem Cells Comments Off on Hesperos Human-on-a-Chip System Used to Model Preclinical Stages of Alzheimers Disease and Mild Cognitive Impairment – Yahoo Finance | May 31st, 2020

Central nervous system comprises brain and spinal cord, and is responsible for integration of sensory information. Brain is the largest and one of the most complex organs in the human body. It is made up of 100 billion nerves that communicate with 100 trillion synapses. It is responsible for the thought and movement produced by the body. Spinal cord is connected to a section of brain known as brain stem and runs through the spinal canal. The brain processes and interprets sensory information sent from the spinal cord. Brain and spinal cord serve as the primary processing centers for the entire nervous system, and control the working of the body. Neuroprosthetics improves or replaces the function of the central nervous system.

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Neuroprosthetics, also known as neural prosthetics, are devices implanted in the body that stimulate the function of an organ or organ system that has failed due to disease or injury. It is a brain-computer interface device used to detect and translate neural activity into command sequences for prostheses. Its primary aim is to restore functionality in patients suffering from loss of motor control such as spinal cord injury, multiple sclerosis, amyotrophic lateral sclerosis, and stroke. The major types of neuroprosthetics include sensory implants, motor prosthetics, and cognitive prosthetics. Motor prosthetics support the autonomous system and assist in the regulation or stimulation of affected motor functions.

Similarly, cognitive prosthetics restore the function of brain tissue loss in conditions such as paralysis, Parkinsons disease, traumatic brain injury, and speech deficit. Sensory implants pass information into the bodys sensory areas such as sight or hearing, and it is further classified as auditory (cochlear implant), visual, and spinal cord stimulator. Some key functions of neuroprosthetics include providing hearing, seeing, feeling abilities, pain relief, and restoring damaged brain cells. Cochlear implant is among the most popular neuroprosthetics. In addition, auditory brain stem implant is also a neuroprosthetic meant to improve hearing damage.

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North America dominates the global market for neuroprosthetics due to the rising incidence of neurological diseases and growth in geriatric population in the region. Asia is expected to display a high growth rate in the next five years in the global neuroprosthetics market, with China and India being the fastest growing markets in the Asia-Pacific region. Among the key driving forces for the neuroprosthetics market in developing countries are the large pool of patients, increasing awareness about the disease, improving healthcare infrastructure, and rising government funding in the region.

Increasing prevalence of neurological diseases such as traumatic brain injury, stroke and Parkinsons disease, rise in geriatric population, increase in healthcare expenditure, growing awareness about healthcare, rapid progression of technology, and increasing number of initiatives by various governments and government associations are some key factors driving growth of the global neuroprosthetics market. However, factors such as high cost of devices, reimbursement issues, and adverse effects pose a major restraint to the growth of the global neuroprosthetics market.

Innovative self-charging neural implants that eliminate the need for high risk and costly surgery to replace the discharge battery and controlling machinery with thoughts would help to develop opportunities for the growth of the global neuroprosthetics market.

The major companies operating in the global neuroprosthetics market are,

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Key geographies evaluated in this report are:

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Neuroprosthetics Market Scope and Opportunities Analysis Through 2021 - 3rd Watch News

Spinal Cord Stem Cells Comments Off on Neuroprosthetics Market Scope and Opportunities Analysis Through 2021 – 3rd Watch News | May 30th, 2020

SUZHOU, China and SHANGHAI, May 29, 2020 /PRNewswire/ -- Gracell Biotechnologies Co., Ltd. ("Gracell"), a clinical-stage immune cell and gene therapy company, today announced that two presentations were accepted at the 2020 American Society of Clinical Oncology (ASCO) Virtual Scientific Program.

Both presentations can be found in the Development Therapeutics Immunotherapy session, central on Gracell's TruUCAR GC027 in relapsed or refractory T-cell acute lymphoblastic leukemia (r/r T-ALL) patients and EnhancedCAR GC008t in patients with advanced mesothelin-positive solid tumors.

"We are delighted to report on both TruUCAR GC027 in T-ALL and EnhancedCAR GC008t in solid tumors" said Dr. Martina Sersch, CMO of Gracell. "and glad to share safety and preliminary efficacy data on two of our exciting new CAR-T platform therapies with the scientific community at the ASCO annual meeting." Dr. William CAO, CEO of Gracell, added "Thanks to our highly efficient gene editing capability, CAR-T cells with PD-1 gene edited are generated to have enhanced capability of tumor control in inhibitory tumor microenvironment. We believe this strategy will improve CAR-T/TCR-T's potency against solid tumors.Gracell carried out this strategy as early as 2017, upon our foundation. With two years' preclinical and clinical investigations, we are very glad to see it showing first encouraging results in an effort to enhance CAR-T cells to combat solid tumors".

Session type: poster discussionAbstract Title: Safety and efficacy results of GC027: The first-in-human, universal CAR-T cell therapy for adult relapsed/refractory T-cell acute lymphoblastic leukemia (r/r T-ALL)Abstract ID: 3013Link: https://meetinglibrary.asco.org/record/185068/poster

Session type: posterAbstract Title: Phase I study of CRISPR-engineered CAR-T cells with PD-1 inactivation in treating mesothelin-positive solid tumorsAbstract ID: 3038Link:https://meetinglibrary.asco.org/record/189057/poster

About TruUCAR

TruUCAR is Gracell's proprietary and patented platform technology, with selected genes being edited to avoid GvHD and immune rejection without using strong immunosuppressive drugs. In addition to T-ALL antigen, the platform technology can also be implemented for other targets of hematological malignancies.

About GC027

GC027is an investigational, off-the-shelf CAR-T cell therapy, redirected to CD7 for the treatment of T cell malignancies. GC027 was manufactured from T cells of human leukocyte antigen (HLA) unmatched healthy donors using TruUCAR technology, which is expected to improve efficacy and reduce production time, available for off-the-shelf use in a timely manner.

About EnhancedCAR

EnhancedCAR is Gracell's proprietary and patented platform technology, with selected genes edited to enhance immune cell performance in terms of killing efficiency, in vivo persistence, including selected PD-1 and TCR mediations. The technology can be implemented to many other targets with high editing precision and efficiency.

About GC008t

GC008t is an investigational, autologous CAR-T cell therapy, redirected to mesothelin with PD-1 disruption for the treatment of mesothelin-positive solid tumors. With PD-1 knocking out, GC008t is expected improve persistence and clinical efficacy.

About T-ALL

T - Lymphoblastic Leukemia (T-ALL) is an aggressive form of acute lymphoblastic leukemia, with a diffuse invasion of bone marrow and peripheral blood. In 2015, T-ALL affected around 876,000 people globally and resulted in 110,000 deaths worldwide. T-ALL compromises about 15%-20% of all children and adult acute lymphoblastic leukemia[1].Current standard of care therapies for T-ALL are chemotherapy and stem cell transplantation. 40-50% of patients will experience relapse within two years following front line therapy with limited treatment options available[2][3]. Treatment of relapsed and refractory T-ALL remains a high unmet medical need.

About Mesothelin-positive Solid Tumors

Mesothelin, a cell surface antigen, has high expression to a broad spectrum of solid tumors while express low levels on normal cells. Mesothelin is believed as a good target for multiple solid tumors. The GC008t study enrolled patients with advanced solid tumors, including pancreatic cancer, ovarian cancer, and colorectal cancer, of which clinical outcome of standard of care remains poor.

About Gracell

Gracell Biotechnologies Co., Ltd. ("Gracell") is a clinical-stage biotech company, committed to developing highly reliable and affordable cell gene therapies for cancer. Gracell is dedicated to resolving the remaining challenges in CAR-T, such as high production costs, lengthy manufacturing process, lack of off-the-shelf products, and inefficacy against solid tumors. Led by a group of world-class scientists, Gracell is advancing FasTCAR, TruUCAR (off-the-shelf CAR), DualCAR and EnhancedCAR-T cell therapies for leukemia, lymphoma, myeloma, and solid tumors.

[1]Pediatric hematologic Malignancies: T-cell acute lymphoblastic Leukemia, Hematology 2016

[2]Progress and innovations in the management JAMA Oncol 2018

[3]Defining the course and prognosis of adults with acute lymphoblastic leukemia, Cancer 2010

SOURCE Gracell

http://www.gracellbio.com

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Gracell Announces Two Presentations at the Annual Meeting of American Society of Clinical Oncology (ASCO) - PRNewswire

Bone Marrow Stem Cells Comments Off on Gracell Announces Two Presentations at the Annual Meeting of American Society of Clinical Oncology (ASCO) – PRNewswire | May 30th, 2020

Acute lung injury (ALI) is a devastating disease process involving pulmonary edema and atelectasis caused by capillary membrane injury [1]. The main clinical manifestation is the acute onset of hypoxic respiratory failure, which can subsequently trigger a cascade of serious complications and even death [2]. Thus, ALI causes a considerable financial burden for health care systems throughout the world. ALI can result from various causes, including multiple traumas, large-volume blood transfusions, and bacterial and viral infections [2, 3]. A variety of viruses, including influenza virus, coronavirus (CoV), adenovirus, cytomegalovirus (CMV), and respiratory syncytial virus (RSV), are associated with ALI [4]. Importantly, most viruses, whose hosts are various animal species, can cause severe and rapidly spreading human infections. In the early 2000s, several outbreaks of influenza virus and CoV emerged, causing human respiratory and intestinal diseases worldwide, including the more recent SARS-CoV-2 infection [5,6,7]. To date, SARS-CoV-2 has affected more than 80,000 people, causing nearly 3300 deaths in China and more than 1,800,000 people, causing nearly 110,000 deaths all over the world (http://2019ncov.chinacdc.cn/2019-nCoV/).

Infectious respiratory diseases caused by different viruses are associated with similar respiratory symptoms ranging from the common cold to severe acute respiratory syndrome [8]. This makes the clinical distinction between different agents involved in infection very difficult [8, 9]. Currently, the clinical experience mainly includes antibacterial and antiviral drug treatment derived from handling several outbreaks of influenza virus and human CoVs. Numerous agents have been identified to inhibit the entry and/or replication of these viruses in cell culture or animal models [10]. Although these antiviral drugs can effectively prevent and eliminate the virus, the full recovery from pneumonia and ALI depends on the resistance of the patient. Recently, stem cell-based therapy has become a potential approved tool for the treatment of virus-induced lung injury [11,12,13]. Here, we will give a brief overview of influenza virus and CoVs and then present the cell-based therapeutic options for lung injury caused by different kinds of viruses.

Influenza virus and human CoV are the two most threatening viruses for infectious lung injury [14]. These pathogens can be transmitted through direct or indirect physical contact, droplets, or aerosols, with increasing evidence suggesting that airborne transmission, including via droplets or aerosols, enhances the efficiency of viral transmission among humans and causes uncontrolled infectious disease [15]. Throughout human history, outbreaks and occasional pandemics caused by influenza virus and CoV have led to approximately hundreds of millions of deaths worldwide [16].

Influenza virus is a well-known human pathogen that has a negative-sense RNA genome [17]. According to its distinct antigenic properties, the influenza virus can be divided into 4 subtypes, types A, B, C, and D. Influenza A virus (IAV) lineages in animal populations cause economically important respiratory disease. Little is known about the other human influenza virus types B, C, and D [18]. Further subtypes are characterized by the genetic and antigenic properties of the hemagglutinin (HA) and neuraminidase (NA) glycoproteins [19]. Sporadic and seasonal infections in swine with avian influenza viruses of various subtypes have been reported. The most recent human pandemic virusesH1N1 from swine and H5N1 from aviancause severe respiratory tract disease and lung injury in humans [20, 21].

CoVs, a large family of single-stranded RNA viruses, typically affect the respiratory tract of mammals, including humans. CoVs are further divided into four genera: alpha-, beta-, gamma-, and delta-CoVs. Alpha- and beta-CoVs can infect mammals, and gamma- and delta-CoVs tend to infect birds, but some of these viruses can also be transmitted to mammals [22]. Human CoVs were considered relatively harmless respiratory pathogens in the past. Infections with the human CoV strains 229E, OC43, NL63, and HKU1 usually result in mild respiratory illness, such as the common cold [23]. In contrast, the CoV responsible for the 2002 severe acute respiratory syndrome (SARS-CoV), the 2012 Middle East respiratory syndrome CoV (MERS-CoV), and, more recently, the SARS-CoV-2 have received global attention owing to their genetic variation and rapid spread in human populations [5,6,7].

Usually, the influenza virus can enter the columnar epithelial cells of the respiratory tract, such as the trachea, bronchi, and bronchioles. Subsequently, the influenza virus begins to replicate for an asymptomatic period of time and then migrate to the lung tissue to cause acute lung and respiratory injury [24]. Similar to those with influenza virus infection, patients with SARS, MERS, or SARS-CoV-2 present with various clinical features, ranging from asymptomatic or mild respiratory illness to severe ALI, even with multiple organ failure [5,6,7]. The pathogenesis of ALI caused by influenza virus and human CoV is often associated with rapid viral replication, marked inflammatory cell infiltration, and elevated proinflammatory cytokine/chemokine responses [25]. Interestingly, in IAV- and human CoV-infected individuals, the pulmonary pathology always involves diffuse alveolar damage, but viral RNA is present in only a subset of patients [26]. Some studies suggest that an overly exaggerated immune response, rather than uncontrolled viral spread, is the primary cause in fatal cases caused by virus infection [27]. Several immune cell types have been found to contribute to damaging host responses, providing novel approaches for therapeutic intervention [28].

IAV infection, the most common cause of viral pneumonia, causes substantial seasonal and pandemic morbidity and mortality [29]. Currently, antiviral drugs are the primary treatment strategy for influenza-induced pneumonia. However, antiviral drugs cannot repair damaged lung cells. Here, we summarize the present studies of stem cell therapy for influenza virus-induced lung injury.

Mesenchymal stem/stromal cells (MSCs) constitute a heterogeneous subset of stromal regenerative cells that can be harvested from several adult tissue types, including bone marrow, umbilical cord, adipose, and endometrium [30]. They retain the expression of the markers CD29, CD73, CD90, and CD105 and have a rapid proliferation rate, low immunogenicity, and low tumorigenicity [30]. MSCs also have self-renewal and multidifferentiation capabilities and exert immunomodulatory and tissue repair effects by secreting trophic factors, cytokines, and chemokines [31]. Due to these beneficial biological properties, MSCs and their derivatives are attractive as cellular therapies for various inflammatory diseases, including virus-induced lung injury.

Several studies on IAV-infected animal models have shown the beneficial effects of the administration of different tissue-derived MSCs [32,33,34,35]. H5N1 virus infection reduces alveolar fluid clearance (AFC) and enhances alveolar protein permeability (APP) in human alveolar epithelial cells, which can be inhibited by coculture with human bone marrow-derived MSCs (BMSCs) [32]. Mechanistically, this process can be mediated by human BMSC secreted angiopoietin-1 (Ang1) and keratinocyte growth factor (KGF) [32]. Moreover, in vivo experiments have shown that human BMSCs have a significant anti-inflammatory effect by increasing the number of M2 macrophages and releasing various cytokines and chemokines, such as interleukin (IL)-1, IL-4, IL-6, IL-8, and IL-17 [32]. Similar anti-inflammatory effects have been achieved in another virus-induced lung injury model. The intravenous injection of mouse BMSCs into H9N2 virus-infected mice significantly attenuates H9N2 virus-induced pulmonary inflammation by reducing chemokine (GM-CSF, MCP-1, KC, MIP-1, and MIG) and proinflammatory cytokine (IL-1, IL-6, TNF-, and IFN-) levels, as well as reducing inflammatory cell recruitment into the lungs [33]. Another study on human BMSCs cocultured with CD8+ T cells showed that MSCs inhibit the proliferation of virus-specific CD8+ T cells and the release of IFN- by specific CD8+ T cells [36].

In addition, human umbilical cord-derived MSCs (UC-MSCs) were found to have a similar effect as BMSCs on AFC, APP, and inflammation by secreting growth factors, including Ang1 and hepatocyte growth factor (HGF), in an in vitro lung injury model induced by H5N1 virus [34]. UC-MSCs also promote lung injury mouse survival, increase the body weight, and decreased the APP levels and inflammation in vivo [34]. Unlike Ang1, KGF, and HGF mentioned above, basic fibroblast growth factor 2 (FGF2) plays an important role in lung injury therapy via immunoregulation. The administration of the recombinant FGF2 protein improves H1N1-induced mouse lung injury and promotes the survival of infected mice by recruiting and activating neutrophils via the FGFR2-PI3K-AKT-NFB signaling pathway [37]. FGF2-overexpressing MSCs have an enhanced therapeutic effect on lipopolysaccharide-induced ALI, as assessed by the proinflammatory factor level, neutrophil quantity, and histopathological index of the lung [38].

MSCs secrete various soluble factors and extracellular vesicles (EVs), which carry lipids, proteins, DNA, mRNA, microRNAs, small RNAs, and organelles. These biologically active components can be transferred to recipient cells to exert anti-inflammatory, antiapoptotic, and tissue regeneration functions [39]. EVs isolated from conditioned medium of pig BMSCs have been demonstrated to have anti-apoptosis, anti-inflammation, and antiviral replication functions in H1N1-affected lung epithelial cells and alleviate H1N1-induced lung injury in pigs [35]. Moreover, the preincubation of EVs with RNase abrogates their anti-influenza activity, suggesting that the anti-influenza activity of EVs is due to the transfer of RNAs from EVs to epithelial cells [35]. Exosomes are a subset of EVs that are 50200nm in diameter and positive for CD63 and CD81 [40]. Exosomes isolated from the conditioned medium of UC-MSCs restore the impaired AFC and decreased APP in alveolar epithelial cells affected by H5N1 virus [34]. In addition, the ability of UC-MSCs to increase AFC is superior to that of exosomes, which indicates that other components secreted by UC-MSCs have synergistic effects with exosomes [34].

Despite accumulating evidence demonstrating the therapeutic effects of MSC administration in various preclinical models of lung injury, some studies have shown contrasting results. Darwish and colleagues proved that neither the prophylactic nor therapeutic administration of murine or human BMSCs could decrease pulmonary inflammation or prevent the progression of ALI in H1N1 virus-infected mice [41]. In addition, combining MSC administration with the antiviral agent oseltamivir was also found to be ineffective [41]. Similar negative results were obtained in another preclinical study. Murine or human BMSCs were administered intravenously to H1N1-induced ARDS mice [42]. Although murine BMSCs prevented influenza-induced thrombocytosis and caused a modest reduction in lung viral load, murine or human BMSCs failed to improve influenza-mediated lung injury as assessed by weight loss, the lung water content, and bronchoalveolar lavage inflammation and histology, which is consistent with Darwishs findings [42]. However, the mild reduction in viral load observed in response to murine BMSC treatment suggests that, on balance, MSCs are mildly immunostimulatory in this model [42]. Although there are some controversial incidents in preclinical research, the transplant of menstrual-blood-derived MSCs into patients with H7N9-induced ARDS was conducted at a single center through an open-label clinical trial (http://www.chictr.org.cn/). MSC transplantation significantly lowered the mortality and did not result in harmful effects in the bodies of the patients [43]. This clinic study suggests that MSCs significantly improve the survival rate of influenza virus-induced lung injury.

The effects of exogenous MSCs are exerted through their isolation and injection into test animals. There are also some stem/progenitor cells that can be activated to proliferate when various tissues are injured. Basal cells (BCs), distributed throughout the pseudostratified epithelium from the trachea to the bronchioles, are a class of multipotent tissue-specific stem cells from various organs, including the skin, esophagus, and olfactory and airway epithelia [44, 45]. Previously, TPR63+/KRT5+ BCs were shown to self-renew and divide into club cells and ciliated cells to maintain the pseudostratified epithelium of proximal airways [46]. Several studies have shown that TPR63+/KRT5+ BCs play a key role in lung repair and regeneration after influenza virus infection. When animals typically recover from H1N1 influenza infection, TPR63+/KRT5+ BCs accumulate robustly in the lung parenchyma and initiate an injury repair process to maintain normal lung function by differentiating into mature epithelium [47]. Lineage-negative epithelial stem/progenitor (LNEP) cells, present in the normal distal lung, can activate a TPR63+/KRT5+ remodeling program through Notch signaling after H1N1 influenza infection [48]. Moreover, a population of SOX2+/SCGB1A/KRT5 progenitor cells can generate nascent KRT5+ cells as an early response to airway injury upon H1N1 influenza virus infection [49]. In addition, a rare p63+Krt5 progenitor cell population also responds to H1N1 virus-induced severe injury [50]. This evidence suggests that these endogenous lung stem/progenitor cells (LSCs) play a critical role in the repopulation of damaged lung tissue following severe influenza virus infection (Table2).

Taken together, the present in vitro (Table1) and in vivo (Table2) results show that MSCs and LSCs are potential cell sources to treat influenza virus-induced lung injury.

Lung injury caused by SARS, MERS, or SARS-CoV-2 poses major clinical management challenges because there is no specific treatment that has been proven to be effective for each infection. Currently, virus- and host-based therapies are the main methods of treatment for spreading CoV infections. Virus- and host-based therapies include monoclonal antibodies and antiviral drugs that target the key proteins and pathways that mediate viral entry and replication [51].The major challenges in the clinical development of novel drugs include a limited number of suitable animal models for SARS-CoV, MERS-CoV, and SARS-CoV-2 infections and the current absence of new SARS and MERS cases [51]. Although the number of cases of SARS-CoV-2-induced pneumonia patients is continuously increasing, antibiotic and antiviral drugs are the primary methods to treat SARS-CoV-2-infected patients. Similar to that of IAV, human CoV-mediated damage to the respiratory epithelium results from both intrinsic viral pathogenicity and a robust host immune response. The excessive immune response contributes to viral clearance and can also worsen the severity of lung injury, including the demise of lung cells [52]. However, the present treatment approaches have a limited effect on lung inflammation and regeneration.

Stem cell therapy for influenza virus-induced lung injury shows promise in preclinical models. Although it is difficult to establish preclinical models of CoV-induced lung injury, we consider stem cell therapies to be effective approaches to improve human CoV-induced lung injury. Acute inflammatory responses are one of the major underlying mechanisms for virus-induced lung injury. Innate immune cells, including neutrophils and inflammatory monocytes-macrophages (IMMs), are major innate leukocyte subsets that protect against viral lung infections [53]. Both neutrophils and IMMs are rapidly recruited to the site of infection and play crucial roles in the host defense against viruses. Neutrophils and IMMs can activate Toll-like receptors (TLRs) and produce interferons (IFNs) and other cytokines/chemokines [54]. There are two functional effects produced by the recruitment of neutrophils and IMMs: the orchestration of effective adaptive T cell responses and the secretion of inflammatory cytokines/chemokines [55]. However, excessive inflammatory cytokine and chemokine secretion impairs antiviral T cell responses, leading to ineffective viral clearance and reduced survival [56].

MSCs are known to suppress both innate and adaptive immune responses. MSCs have been suggested to inhibit many kinds of immune cells, including T cells, B cells, dendritic cells (DCs), and natural killer (NK) cells in vitro and in vivo [57] (Fig.1). Several molecules, including IL-1, TNF-, and INF-, most of which are produced by inflammatory cells, are reported to be involved in MSC-mediated immunosuppression [58]. Furthermore, MSCs can produce numerous immunosuppressive molecules, such as IL-6, PGE2, IDO, and IL-10, in response to inflammatory stimuli. PGE2 has been reported to mediate the MSC-mediated suppression of T cells, NK cells, and macrophages. Moreover, PGE2 has been found to act with IDO to alter the proliferation of T cells and NK cells [59]. In contrast, MSCs have come to be recognized as one type of adult stem cell actively participating in tissue repair by closely interacting with inflammatory cells and various other cell types [60]. Numerous reports have demonstrated that MSCs can release an array of growth and inhibitory factors, such as EGF, FGF, PDGF, and VEGF, and express several leukocyte chemokines, such as CXCL9, CCL2, CXCL10, and CXCL11. These factors provide an important microenvironment to activate adaptive immunity for lung repair [61]. Thus, the dual functions of MSCs may improve lung recovery after human CoV-induced ALI. Recently, MSCs was transplanted intravenously to enrolled patients with COVID-19 pneumonia. After treatment, the pulmonary function and symptoms of these patients were significantly improved. Meanwhile, the peripheral lymphocytes were increased, the C-reactive protein decreased, the level of TNF- was significantly decreased, and the overactivated cytokine-secreting immune cells disappeared. In addition, a group of regulatory DC cell population dramatically increased. Thus, the intravenous transplantation of MSCs was effective for treatment in patients with COVID-19 pneumonia [62, 63].

Stem cell therapies for treatment of influenza virus and coronavirus-induced lung injury. CoVs, coronavirus; MSCs, mesenchymal stem/stromal cells; LSCs, lung stem/progenitor cells; NK cells, natural killer cells; DC cells, dendritic cells

In addition, endogenous LSCs also play an important role in lung cell reconstitution after virus-induced ALI. In particular, TPR63+/KRT5+ airway BCs comprise approximately equal numbers of stem cells and committed precursors and give rise to differentiated luminal cells during steady state and epithelial repair after lung injury [44, 64]. Research has shown that KRT5+ cells repopulate damaged alveolar parenchyma following influenza virus infection [47]. However, there is still little evidence for the role of altered TPR63+/KRT5+ stem cells during lung injury repair caused by human CoVs.

In summary, exogenous MSCs may modulate human CoV-induced lung injury repair and regeneration through their immunoregulatory properties. These cells are capable of interacting with various types of immune cell, including neutrophils, macrophages, T cells, B cells, NK cells, and DCs. Furthermore, viral infections can activate endogenous LSCs to produce new lung cells and maintain lung function (Fig.1). Thus, we propose that MSCs and LSCs are two potential cell sources for treating human CoV-induced lung injury.

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Stem cell therapy: a potential approach for treatment of influenza virus and coronavirus-induced acute lung injury - BMC Blogs Network

Skin Stem Cells Comments Off on Stem cell therapy: a potential approach for treatment of influenza virus and coronavirus-induced acute lung injury – BMC Blogs Network | May 30th, 2020

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We found out why people say its better to leave things to the experts. At this salon, the barber put us through an aromatic hot towel treatment to both soften our facial hair and help us relax. Swift and gentle strokes of the straight razor gave us a close shave, leaving our skin baby smooth and looking dapper fresh. We also appreciate the massage, which made us forget our worries and feel good to be alive.Available at Truefitt + Hill for $80

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This may not be as effective as a hair transplant, but it is a much less painful alternative to revive dormant hair follicles. The treatment uses the brands potent Miracle Stem Cell Solution, which contains a blend of growth factors, botanical stem cells and nutrients that nourish the scalp and encourage hair growth. DHT blockers neutralise the effects of androgen, the hormonal culprit behind hair loss.Available at PHS Hairscience for $297

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AUGUSTMAN Grooming Awards 2020 Part IV: Best Head-To-Toe Treatment Services For Gentlemen - AUGUSTMAN

Skin Stem Cells Comments Off on AUGUSTMAN Grooming Awards 2020 Part IV: Best Head-To-Toe Treatment Services For Gentlemen – AUGUSTMAN | May 30th, 2020

According to the latest research report by Global Market Insights, Inc., minoxidil market size is projected to surpass US$ 1 billion by 2024.

Frontrunners in the Minoxidil industry:

Nanz Med Science Pharma Private Limited, Bakul Group of companies, Kumar Organic Products Limited, Changzhou Tianhua Pharmaceutical Co. Ltd., Par Pharmaceuticals, Provizer Pharma, Metapharmaceutical Ind. S.L., Pharhome International Limited, LOY Pharma Lab, Inc., Maruti Futuristic Pharma Pvt. Ltd., Dr. R. Pfleger Chemical Factory GmbH, Renata Limited, McNeil Consumer Healthcare

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2% product segment is likely to provide a positive impetus to the industry forecast as it is believed to bolster effectiveness and enhance quality of hair growth. Apparently, 2% formulation triggers the hair growth via dermal papilla and epithelial cells. Given it seemingly has minimal side effects to the skin, the product is said to be apt for patients with sensitive skin.

2% solution tends to reduce baldness at the receding hairline and at the front as the product offsets hair thinning and boosts hair growth. Prominently, soaring adoption of topical supplementation to improve hair density is expected to spur demand for 2% solution.

5% product is also expected to impel minoxidil market size as demand for high dosage medicines with minimal side effects continues to rise unabated. 5% solution is said to be highly efficacious in hair growth, thereby spurring growth of adipose-derived stem cells (ASCs) and reducing hair thinning. Stakeholders are increasingly being involved in product development to negate irritation and burning sensation.

According to the American Hair Loss Association, more than 80% of men suffer from hair loss by the age of 50. Strikingly, 40% of the 21 million women who are inflicted with hair loss problems opt for active treatments. As it pans out, North America minoxidil market size is expected to expand substantially. Prevalence of oral medication and skepticism towards surgical procedures are anticipated to bolster North America minoxidil market share.

Growth Drivers:

Pitfalls & Challenges:

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Geographies covered:

U.S., Canada, Germany, UK, France, Italy, Spain, Russia, Poland, China, India, Japan, South Korea, Indonesia, Thailand, Malaysia, Australia, Brazil, Mexico, Argentina, Saudi Arabia, UAE, South Africa

Stakeholders will continue to invest in APAC minoxidil market as number of people with thin hair line problem has soared drastically in the region. According to reports from United Nations Economic & Social Commission for Asia and the Pacific (ESCAP) in North & Central Asia, population ratio aged 60 or above will rise to 24% by 2050up 8% from 2016. As regions such as APAC and Europe witness an uptick in middle-age population, minoxidil market value will rise significantly in the next half a decade.

New product roll outs and mergers & acquisitions are expected to grab headlines among leading companies such as Renata Ltd., Kumar Organic Products, McNeil PPC, Par Pharmaceuticals, and Dr. R.P Fletcher Chemical Factory, among others. For instance, Kumar Organic Products Ltd. inaugurated a new office in Switzerland in February 2018 to expand market footprints.

Browse Related News, May You Also Like:

https://www.openpr.com/news/2008806/what-s-driving-the-bitumen-market-size-leading-players-exxon

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Minoxidil Market will witness over 100 million units demand by 2024 - Cole of Duty

Skin Stem Cells Comments Off on Minoxidil Market will witness over 100 million units demand by 2024 – Cole of Duty | May 30th, 2020

KENILWORTH, N.J. & WOODCLIFF LAKE, N.J.--(BUSINESS WIRE)--Merck (NYSE: MRK), known as MSD outside the United States and Canada, and Eisai today announced new data from analyses of two trials evaluating KEYTRUDA, Mercks anti-PD-1 therapy, plus LENVIMA, an orally available multiple receptor tyrosine kinase inhibitor discovered by Eisai. In the KEYNOTE-524/Study 116 and KEYNOTE-146/Study 111 trials, the KEYTRUDA plus LENVIMA combination demonstrated clinically meaningful objective response rates (ORR) in patients with unresectable hepatocellular carcinoma (HCC) with no prior systemic therapy and in patients with metastatic clear cell renal cell carcinoma (ccRCC) who progressed following immune checkpoint inhibitor therapy, respectively.

The tumor response rates demonstrated with KEYTRUDA plus LENVIMA in these studies underscore the potential of this combination regimen in certain types of hepatocellular and renal cell carcinoma, said Dr. Jonathan Cheng, Vice President, Oncology Clinical Research, Merck Research Laboratories. KEYTRUDA plus LENVIMA is an important pillar of our broad oncology research program, and we continue to advance the study of the combination across multiple types of cancers and stages of disease.

As data from our combination trials continue to read out, our enthusiasm for and belief in the potential of KEYTRUDA plus LENVIMA are strengthened by the growing body of evidence observed in multiple advanced cancers, said Dr. Takashi Owa, Chief Medicine Creation and Chief Discovery Officer, Oncology Business Group at Eisai. Our ongoing clinical study efforts on this combination exemplify our commitment to following the science and exploring possible solutions for patients affected by difficult-to-treat cancers.

Results from KEYNOTE-524/Study 116 (Abstract #4519) are being presented in a poster discussion session, and results from KEYNOTE-146/Study 111 (Abstract #5008) are being presented in an oral abstract session of the Virtual Scientific Program of the 2020 American Society of Clinical Oncology (ASCO) Annual Meeting.

KEYNOTE-524/Study 116 Trial Design and Data (Abstract #4519)

KEYNOTE-524/Study 116 (ClinicalTrials.gov, NCT03006926) is a Phase 1b, open-label, single-arm trial evaluating the KEYTRUDA plus LENVIMA combination in 100 patients with unresectable HCC with no prior systemic therapy. Patients were treated with KEYTRUDA 200 mg intravenously every three weeks in combination with LENVIMA 8 or 12 mg (based on baseline body weight 60 kilograms or 60 kilograms, respectively) orally once daily. The primary endpoints are ORR and duration of response (DOR) by modified Response Evaluation Criteria in Solid Tumors (mRECIST) and RECIST v1.1 per independent imaging review (IIR). Secondary endpoints include progression-free survival (PFS), time to progression (TTP) and overall survival (OS). At data cutoff (Oct. 31, 2019) and a median duration of follow-up of 10.6 months (95% CI: 9.2-11.5), 37 patients were still on study treatment (KEYTRUDA plus LENVIMA: n=34; LENVIMA only: n=3), and median duration of treatment exposure to the KEYTRUDA plus LENVIMA combination was 7.9 months (range: 0.2-31.1).

The final analysis of the studys primary endpoints showed the KEYTRUDA plus LENVIMA combination demonstrated an ORR of 36% (n=36) (95% CI: 26.6-46.2), with a complete response rate of 1% (n=1) and a partial response rate of 35% (n=35), and a median DOR of 12.6 months (95% CI: 6.9-not estimable [NE]), using RECIST v1.1 criteria per IIR. As assessed using mRECIST criteria per IIR, the KEYTRUDA plus LENVIMA combination demonstrated an ORR of 46% (n=46) (95% CI: 36.0-56.3), with a complete response rate of 11% (n=11) and a partial response rate of 35% (n=35), and a median DOR of 8.6 months (95% CI: 6.9-NE).

Treatment-related adverse events (TRAEs) led to discontinuation of KEYTRUDA and LENVIMA in 6% of patients, discontinuation of KEYTRUDA in 10% of patients, and discontinuation of LENVIMA in 14% of patients. Grade 3 TRAEs occurred in 67% of patients (Grade 3: 63%; Grade 4: 1%; Grade 5: 3%). There was one Grade 4 TRAE (leukopenia/neutropenia), and there were three Grade 5 treatment-related deaths (acute respiratory failure/acute respiratory distress syndrome, intestinal perforation and abnormal hepatic function; n=1 for each). The most common TRAEs of any grade (20%) were hypertension (36%), diarrhea (35%), fatigue (30%), decreased appetite (28%), hypothyroidism (25%), palmar-plantar erythrodysesthesia syndrome (23%), decreased weight (22%), dysphonia (21%), increased aspartate aminotransferase (20%) and proteinuria (20%).

KEYNOTE-146/Study 111 Trial Design and Data from the RCC Cohort (Abstract #5008)

KEYNOTE-146/Study 111 (ClinicalTrials.gov, NCT02501096) is a Phase 1b/2, open-label, single-arm trial evaluating the KEYTRUDA plus LENVIMA combination in patients with selected solid tumors. Results from the RCC cohort of the Phase 2 part of the study are based on 104 patients with metastatic ccRCC with disease progression following PD-1/PD-L1 immune checkpoint inhibitor therapy using RECIST v1.1 criteria. Patients were treated with KEYTRUDA 200 mg intravenously every three weeks in combination with LENVIMA 20 mg orally once daily until unacceptable toxicity or disease progression. The primary endpoint is ORR at week 24 by immune-related RECIST (irRECIST) per investigator review. Secondary endpoints include ORR, PFS, OS, safety and tolerability for a maximum of 35 cycles/treatments (approximately two years).

At data cutoff (Apr. 9, 2020), results from the Phase 2 part of the study showed the KEYTRUDA plus LENVIMA combination demonstrated an ORR at week 24 of 51% (95% CI: 41-61) by irRECIST per investigator review. As assessed by irRECIST per investigator review, ORR was 55% (95% CI: 45-65), with a partial response rate of 55%, a stable disease rate of 36% and a progressive disease rate of 5% (5% were not evaluable). Median DOR was 12 months (95% CI: 9-18). Median PFS was 11.7 months (95% CI: 9.4-17.7), and the 12-month PFS rate was 45% (95% CI: 32-57). Median OS was not reached (NR) (95% CI:16.7-NR), and the 12-month OS rate was 77% (95% CI: 67-85).

As assessed by RECIST v1.1 per investigator review, ORR was 52% (95% CI: 42-62), with a partial response rate of 52%, a stable disease rate of 38% and a progressive disease rate of 6% (5% were not evaluable). Median DOR was 12 months (95% CI: 9-18). Median PFS was 11.3 months (95% CI: 7.6-17.7), and the 12-month PFS rate was 44% (95% CI: 31-55).

TRAEs led to discontinuation of KEYTRUDA and LENVIMA in 15% of patients, discontinuation of KEYTRUDA in 12% of patients, and discontinuation of LENVIMA in 12% of patients (2% due to proteinuria). The most common TRAEs that led to dose reduction of LENVIMA were fatigue (14%), diarrhea (10%) and proteinuria (9%). Grade 4 TRAEs included lipase increased, diverticulitis, large intestine perforation and myocardial infarction, and there were two Grade 5 treatment-related deaths of upper gastrointestinal hemorrhage and sudden death. The most common TRAEs of any grade (20%) were fatigue (53%), diarrhea (46%), proteinuria (39%), dysphonia (35%), hypertension (34%), nausea (32%), stomatitis (32%), arthralgia (29%), decreased appetite (28%), palmar-plantar erythrodysesthesia syndrome (25%), hypothyroidism (23%) and headache (22%).

About KEYTRUDA (pembrolizumab) Injection, 100 mg

KEYTRUDA is an anti-PD-1 therapy that works by increasing the ability of the bodys immune system to help detect and fight tumor cells. KEYTRUDA is a humanized monoclonal antibody that blocks the interaction between PD-1 and its ligands, PD-L1 and PD-L2, thereby activating T lymphocytes which may affect both tumor cells and healthy cells.

Merck has the industrys largest immuno-oncology clinical research program. There are currently more than 1,200 trials studying KEYTRUDA across a wide variety of cancers and treatment settings. The KEYTRUDA clinical program seeks to understand the role of KEYTRUDA across cancers and the factors that may predict a patient's likelihood of benefitting from treatment with KEYTRUDA, including exploring several different biomarkers.

Selected KEYTRUDA (pembrolizumab) Indications

Melanoma

KEYTRUDA is indicated for the treatment of patients with unresectable or metastatic melanoma.

KEYTRUDA is indicated for the adjuvant treatment of patients with melanoma with involvement of lymph node(s) following complete resection.

Non-Small Cell Lung Cancer

KEYTRUDA, in combination with pemetrexed and platinum chemotherapy, is indicated for the first-line treatment of patients with metastatic nonsquamous non-small cell lung cancer (NSCLC), with no EGFR or ALK genomic tumor aberrations.

KEYTRUDA, in combination with carboplatin and either paclitaxel or paclitaxel protein-bound, is indicated for the first-line treatment of patients with metastatic squamous NSCLC.

KEYTRUDA, as a single agent, is indicated for the first-line treatment of patients with NSCLC expressing PD-L1 [tumor proportion score (TPS) 1%] as determined by an FDA-approved test, with no EGFR or ALK genomic tumor aberrations, and is stage III where patients are not candidates for surgical resection or definitive chemoradiation, or metastatic.

KEYTRUDA, as a single agent, is indicated for the treatment of patients with metastatic NSCLC whose tumors express PD-L1 (TPS 1%) as determined by an FDA-approved test, with disease progression on or after platinum-containing chemotherapy. Patients with EGFR or ALK genomic tumor aberrations should have disease progression on FDA-approved therapy for these aberrations prior to receiving KEYTRUDA.

Small Cell Lung Cancer

KEYTRUDA is indicated for the treatment of patients with metastatic small cell lung cancer (SCLC) with disease progression on or after platinum-based chemotherapy and at least 1 other prior line of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.

Head and Neck Squamous Cell Cancer

KEYTRUDA, in combination with platinum and fluorouracil (FU), is indicated for the first-line treatment of patients with metastatic or with unresectable, recurrent head and neck squamous cell carcinoma (HNSCC).

KEYTRUDA, as a single agent, is indicated for the first-line treatment of patients with metastatic or with unresectable, recurrent HNSCC whose tumors express PD-L1 [combined positive score (CPS) 1] as determined by an FDA-approved test.

KEYTRUDA, as a single agent, is indicated for the treatment of patients with recurrent or metastatic head and neck squamous cell carcinoma (HNSCC) with disease progression on or after platinum-containing chemotherapy.

Classical Hodgkin Lymphoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with refractory classical Hodgkin lymphoma (cHL), or who have relapsed after 3 or more prior lines of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Primary Mediastinal Large B-Cell Lymphoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with refractory primary mediastinal large B-cell lymphoma (PMBCL), or who have relapsed after 2 or more prior lines of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials. KEYTRUDA is not recommended for treatment of patients with PMBCL who require urgent cytoreductive therapy.

Urothelial Carcinoma

KEYTRUDA is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma (mUC) who are not eligible for cisplatin-containing chemotherapy and whose tumors express PD-L1 [combined positive score (CPS) 10], as determined by an FDA-approved test, or in patients who are not eligible for any platinum-containing chemotherapy regardless of PD-L1 status. This indication is approved under accelerated approval based on tumor response rate and duration of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.

KEYTRUDA is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma (mUC) who have disease progression during or following platinum-containing chemotherapy or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.

KEYTRUDA is indicated for the treatment of patients with Bacillus Calmette-Guerin (BCG)-unresponsive, high-risk, non-muscle invasive bladder cancer (NMIBC) with carcinoma in situ (CIS) with or without papillary tumors who are ineligible for or have elected not to undergo cystectomy.

Microsatellite Instability-High (MSI-H) Cancer

KEYTRUDA is indicated for the treatment of adult and pediatric patients with unresectable or metastatic microsatellite instability-high (MSI-H) or mismatch repair deficient (dMMR)

This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials. The safety and effectiveness of KEYTRUDA in pediatric patients with MSI-H central nervous system cancers have not been established.

Gastric Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent locally advanced or metastatic gastric or gastroesophageal junction (GEJ) adenocarcinoma whose tumors express PD-L1 (CPS 1) as determined by an FDA-approved test, with disease progression on or after two or more prior lines of therapy including fluoropyrimidine- and platinum-containing chemotherapy and if appropriate, HER2/neu-targeted therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Esophageal Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent locally advanced or metastatic squamous cell carcinoma of the esophagus whose tumors express PD-L1 (CPS 10) as determined by an FDA-approved test, with disease progression after one or more prior lines of systemic therapy.

Cervical Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent or metastatic cervical cancer with disease progression on or after chemotherapy whose tumors express PD-L1 (CPS 1) as determined by an FDA-approved test. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Hepatocellular Carcinoma

KEYTRUDA is indicated for the treatment of patients with hepatocellular carcinoma (HCC) who have been previously treated with sorafenib. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Merkel Cell Carcinoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with recurrent locally advanced or metastatic Merkel cell carcinoma (MCC). This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Renal Cell Carcinoma

KEYTRUDA, in combination with axitinib, is indicated for the first-line treatment of patients with advanced renal cell carcinoma (RCC).

Endometrial Carcinoma

KEYTRUDA, in combination with LENVIMA, is indicated for the treatment of patients with advanced endometrial carcinoma that is not MSI-H or dMMR, who have disease progression following prior systemic therapy and are not candidates for curative surgery or radiation. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trial.

Selected Important Safety Information for KEYTRUDA

Immune-Mediated Pneumonitis

KEYTRUDA can cause immune-mediated pneumonitis, including fatal cases. Pneumonitis occurred in 3.4% (94/2799) of patients with various cancers receiving KEYTRUDA, including Grade 1 (0.8%), 2 (1.3%), 3 (0.9%), 4 (0.3%), and 5 (0.1%). Pneumonitis occurred in 8.2% (65/790) of NSCLC patients receiving KEYTRUDA as a single agent, including Grades 3-4 in 3.2% of patients, and occurred more frequently in patients with a history of prior thoracic radiation (17%) compared to those without (7.7%). Pneumonitis occurred in 6% (18/300) of HNSCC patients receiving KEYTRUDA as a single agent, including Grades 3-5 in 1.6% of patients, and occurred in 5.4% (15/276) of patients receiving KEYTRUDA in combination with platinum and FU as first-line therapy for advanced disease, including Grades 3-5 in 1.5% of patients.

Monitor patients for signs and symptoms of pneumonitis. Evaluate suspected pneumonitis with radiographic imaging. Administer corticosteroids for Grade 2 or greater pneumonitis. Withhold KEYTRUDA for Grade 2; permanently discontinue KEYTRUDA for Grade 3 or 4 or recurrent Grade 2 pneumonitis.

Immune-Mediated Colitis

KEYTRUDA can cause immune-mediated colitis. Colitis occurred in 1.7% (48/2799) of patients receiving KEYTRUDA, including Grade 2 (0.4%), 3 (1.1%), and 4 (<0.1%). Monitor patients for signs and symptoms of colitis. Administer corticosteroids for Grade 2 or greater colitis. Withhold KEYTRUDA for Grade 2 or 3; permanently discontinue KEYTRUDA for Grade 4 colitis.

Immune-Mediated Hepatitis (KEYTRUDA) and Hepatotoxicity (KEYTRUDA in Combination With Axitinib)

Immune-Mediated Hepatitis

KEYTRUDA can cause immune-mediated hepatitis. Hepatitis occurred in 0.7% (19/2799) of patients receiving KEYTRUDA, including Grade 2 (0.1%), 3 (0.4%), and 4 (<0.1%). Monitor patients for changes in liver function. Administer corticosteroids for Grade 2 or greater hepatitis and, based on severity of liver enzyme elevations, withhold or discontinue KEYTRUDA.

Hepatotoxicity in Combination With Axitinib

KEYTRUDA in combination with axitinib can cause hepatic toxicity with higher than expected frequencies of Grades 3 and 4 ALT and AST elevations compared to KEYTRUDA alone. With the combination of KEYTRUDA and axitinib, Grades 3 and 4 increased ALT (20%) and increased AST (13%) were seen. Monitor liver enzymes before initiation of and periodically throughout treatment. Consider more frequent monitoring of liver enzymes as compared to when the drugs are administered as single agents. For elevated liver enzymes, interrupt KEYTRUDA and axitinib, and consider administering corticosteroids as needed.

Immune-Mediated Endocrinopathies

KEYTRUDA can cause adrenal insufficiency (primary and secondary), hypophysitis, thyroid disorders, and type 1 diabetes mellitus. Adrenal insufficiency occurred in 0.8% (22/2799) of patients, including Grade 2 (0.3%), 3 (0.3%), and 4 (<0.1%). Hypophysitis occurred in 0.6% (17/2799) of patients, including Grade 2 (0.2%), 3 (0.3%), and 4 (<0.1%). Hypothyroidism occurred in 8.5% (237/2799) of patients, including Grade 2 (6.2%) and 3 (0.1%). The incidence of new or worsening hypothyroidism was higher in 1185 patients with HNSCC (16%) receiving KEYTRUDA, as a single agent or in combination with platinum and FU, including Grade 3 (0.3%) hypothyroidism. Hyperthyroidism occurred in 3.4% (96/2799) of patients, including Grade 2 (0.8%) and 3 (0.1%), and thyroiditis occurred in 0.6% (16/2799) of patients, including Grade 2 (0.3%). Type 1 diabetes mellitus, including diabetic ketoacidosis, occurred in 0.2% (6/2799) of patients.

Monitor patients for signs and symptoms of adrenal insufficiency, hypophysitis (including hypopituitarism), thyroid function (prior to and periodically during treatment), and hyperglycemia. For adrenal insufficiency or hypophysitis, administer corticosteroids and hormone replacement as clinically indicated. Withhold KEYTRUDA for Grade 2 adrenal insufficiency or hypophysitis and withhold or discontinue KEYTRUDA for Grade 3 or Grade 4 adrenal insufficiency or hypophysitis. Administer hormone replacement for hypothyroidism and manage hyperthyroidism with thionamides and beta-blockers as appropriate. Withhold or discontinue KEYTRUDA for Grade 3 or 4 hyperthyroidism. Administer insulin for type 1 diabetes, and withhold KEYTRUDA and administer antihyperglycemics in patients with severe hyperglycemia.

Immune-Mediated Nephritis and Renal Dysfunction

KEYTRUDA can cause immune-mediated nephritis. Nephritis occurred in 0.3% (9/2799) of patients receiving KEYTRUDA, including Grade 2 (0.1%), 3 (0.1%), and 4 (<0.1%) nephritis. Nephritis occurred in 1.7% (7/405) of patients receiving KEYTRUDA in combination with pemetrexed and platinum chemotherapy. Monitor patients for changes in renal function. Administer corticosteroids for Grade 2 or greater nephritis. Withhold KEYTRUDA for Grade 2; permanently discontinue for Grade 3 or 4 nephritis.

Immune-Mediated Skin Reactions

Immune-mediated rashes, including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN) (some cases with fatal outcome), exfoliative dermatitis, and bullous pemphigoid, can occur. Monitor patients for suspected severe skin reactions and based on the severity of the adverse reaction, withhold or permanently discontinue KEYTRUDA and administer corticosteroids. For signs or symptoms of SJS or TEN, withhold KEYTRUDA and refer the patient for specialized care for assessment and treatment. If SJS or TEN is confirmed, permanently discontinue KEYTRUDA.

Other Immune-Mediated Adverse Reactions

Immune-mediated adverse reactions, which may be severe or fatal, can occur in any organ system or tissue in patients receiving KEYTRUDA and may also occur after discontinuation of treatment. For suspected immune-mediated adverse reactions, ensure adequate evaluation to confirm etiology or exclude other causes. Based on the severity of the adverse reaction, withhold KEYTRUDA and administer corticosteroids. Upon improvement to Grade 1 or less, initiate corticosteroid taper and continue to taper over at least 1 month. Based on limited data from clinical studies in patients whose immune-related adverse reactions could not be controlled with corticosteroid use, administration of other systemic immunosuppressants can be considered. Resume KEYTRUDA when the adverse reaction remains at Grade 1 or less following corticosteroid taper. Permanently discontinue KEYTRUDA for any Grade 3 immune-mediated adverse reaction that recurs and for any life-threatening immune-mediated adverse reaction.

The following clinically significant immune-mediated adverse reactions occurred in less than 1% (unless otherwise indicated) of 2799 patients: arthritis (1.5%), uveitis, myositis, Guillain-Barr syndrome, myasthenia gravis, vasculitis, pancreatitis, hemolytic anemia, sarcoidosis, and encephalitis. In addition, myelitis and myocarditis were reported in other clinical trials, including classical Hodgkin lymphoma, and postmarketing use.

Treatment with KEYTRUDA may increase the risk of rejection in solid organ transplant recipients. Consider the benefit of treatment vs the risk of possible organ rejection in these patients.

Infusion-Related Reactions

KEYTRUDA can cause severe or life-threatening infusion-related reactions, including hypersensitivity and anaphylaxis, which have been reported in 0.2% (6/2799) of patients. Monitor patients for signs and symptoms of infusion-related reactions. For Grade 3 or 4 reactions, stop infusion and permanently discontinue KEYTRUDA.

Complications of Allogeneic Hematopoietic Stem Cell Transplantation (HSCT)

Immune-mediated complications, including fatal events, occurred in patients who underwent allogeneic HSCT after treatment with KEYTRUDA. Of 23 patients with cHL who proceeded to allogeneic HSCT after KEYTRUDA, 6 (26%) developed graft-versus-host disease (GVHD) (1 fatal case) and 2 (9%) developed severe hepatic veno-occlusive disease (VOD) after reduced-intensity conditioning (1 fatal case). Cases of fatal hyperacute GVHD after allogeneic HSCT have also been reported in patients with lymphoma who received a PD-1 receptorblocking antibody before transplantation. Follow patients closely for early evidence of transplant-related complications such as hyperacute graft-versus-host disease (GVHD), Grade 3 to 4 acute GVHD, steroid-requiring febrile syndrome, hepatic veno-occlusive disease (VOD), and other immune-mediated adverse reactions.

In patients with a history of allogeneic HSCT, acute GVHD (including fatal GVHD) has been reported after treatment with KEYTRUDA. Patients who experienced GVHD after their transplant procedure may be at increased risk for GVHD after KEYTRUDA. Consider the benefit of KEYTRUDA vs the risk of GVHD in these patients.

Increased Mortality in Patients With Multiple Myeloma

In trials in patients with multiple myeloma, the addition of KEYTRUDA to a thalidomide analogue plus dexamethasone resulted in increased mortality. Treatment of these patients with a PD-1 or PD-L1 blocking antibody in this combination is not recommended outside of controlled trials.

Embryofetal Toxicity

Based on its mechanism of action, KEYTRUDA can cause fetal harm when administered to a pregnant woman. Advise women of this potential risk. In females of reproductive potential, verify pregnancy status prior to initiating KEYTRUDA and advise them to use effective contraception during treatment and for 4 months after the last dose.

Adverse Reactions

In KEYNOTE-006, KEYTRUDA was discontinued due to adverse reactions in 9% of 555 patients with advanced melanoma; adverse reactions leading to permanent discontinuation in more than one patient were colitis (1.4%), autoimmune hepatitis (0.7%), allergic reaction (0.4%), polyneuropathy (0.4%), and cardiac failure (0.4%). The most common adverse reactions (20%) with KEYTRUDA were fatigue (28%), diarrhea (26%), rash (24%), and nausea (21%).

In KEYNOTE-002, KEYTRUDA was permanently discontinued due to adverse reactions in 12% of 357 patients with advanced melanoma; the most common (1%) were general physical health deterioration (1%), asthenia (1%), dyspnea (1%), pneumonitis (1%), and generalized edema (1%). The most common adverse reactions were fatigue (43%), pruritus (28%), rash (24%), constipation (22%), nausea (22%), diarrhea (20%), and decreased appetite (20%).

In KEYNOTE-054, KEYTRUDA was permanently discontinued due to adverse reactions in 14% of 509 patients; the most common (1%) were pneumonitis (1.4%), colitis (1.2%), and diarrhea (1%). Serious adverse reactions occurred in 25% of patients receiving KEYTRUDA. The most common adverse reaction (20%) with KEYTRUDA was diarrhea (28%).

In KEYNOTE-189, when KEYTRUDA was administered with pemetrexed and platinum chemotherapy in metastatic nonsquamous NSCLC, KEYTRUDA was discontinued due to adverse reactions in 20% of 405 patients. The most common adverse reactions resulting in permanent discontinuation of KEYTRUDA were pneumonitis (3%) and acute kidney injury (2%). The most common adverse reactions (20%) with KEYTRUDA were nausea (56%), fatigue (56%), constipation (35%), diarrhea (31%), decreased appetite (28%), rash (25%), vomiting (24%), cough (21%), dyspnea (21%), and pyrexia (20%).

In KEYNOTE-407, when KEYTRUDA was administered with carboplatin and either paclitaxel or paclitaxel protein-bound in metastatic squamous NSCLC, KEYTRUDA was discontinued due to adverse reactions in 15% of 101 patients. The most frequent serious adverse reactions reported in at least 2% of patients were febrile neutropenia, pneumonia, and urinary tract infection. Adverse reactions observed in KEYNOTE-407 were similar to those observed in KEYNOTE-189 with the exception that increased incidences of alopecia (47% vs 36%) and peripheral neuropathy (31% vs 25%) were observed in the KEYTRUDA and chemotherapy arm compared to the placebo and chemotherapy arm in KEYNOTE-407.

In KEYNOTE-042, KEYTRUDA was discontinued due to adverse reactions in 19% of 636 patients with advanced NSCLC; the most common were pneumonitis (3%), death due to unknown cause (1.6%), and pneumonia (1.4%). The most frequent serious adverse reactions reported in at least 2% of patients were pneumonia (7%), pneumonitis (3.9%), pulmonary embolism (2.4%), and pleural effusion (2.2%). The most common adverse reaction (20%) was fatigue (25%).

In KEYNOTE-010, KEYTRUDA monotherapy was discontinued due to adverse reactions in 8% of 682 patients with metastatic NSCLC; the most common was pneumonitis (1.8%). The most common adverse reactions (20%) were decreased appetite (25%), fatigue (25%), dyspnea (23%), and nausea (20%).

Adverse reactions occurring in patients with SCLC were similar to those occurring in patients with other solid tumors who received KEYTRUDA as a single agent.

In KEYNOTE-048, KEYTRUDA monotherapy was discontinued due to adverse events in 12% of 300 patients with HNSCC; the most common adverse reactions leading to permanent discontinuation were sepsis (1.7%) and pneumonia (1.3%). The most common adverse reactions (20%) were fatigue (33%), constipation (20%), and rash (20%).

In KEYNOTE-048, when KEYTRUDA was administered in combination with platinum (cisplatin or carboplatin) and FU chemotherapy, KEYTRUDA was discontinued due to adverse reactions in 16% of 276 patients with HNSCC. The most common adverse reactions resulting in permanent discontinuation of KEYTRUDA were pneumonia (2.5%), pneumonitis (1.8%), and septic shock (1.4%). The most common adverse reactions (20%) were nausea (51%), fatigue (49%), constipation (37%), vomiting (32%), mucosal inflammation (31%), diarrhea (29%), decreased appetite (29%), stomatitis (26%), and cough (22%).

In KEYNOTE-012, KEYTRUDA was discontinued due to adverse reactions in 17% of 192 patients with HNSCC. Serious adverse reactions occurred in 45% of patients. The most frequent serious adverse reactions reported in at least 2% of patients were pneumonia, dyspnea, confusional state, vomiting, pleural effusion, and respiratory failure. The most common adverse reactions (20%) were fatigue, decreased appetite, and dyspnea. Adverse reactions occurring in patients with HNSCC were generally similar to those occurring in patients with melanoma or NSCLC who received KEYTRUDA as a monotherapy, with the exception of increased incidences of facial edema and new or worsening hypothyroidism.

In KEYNOTE-087, KEYTRUDA was discontinued due to adverse reactions in 5% of 210 patients with cHL. Serious adverse reactions occurred in 16% of patients; those 1% included pneumonia, pneumonitis, pyrexia, dyspnea, GVHD, and herpes zoster. Two patients died from causes other than disease progression; 1 from GVHD after subsequent allogeneic HSCT and 1 from septic shock. The most common adverse reactions (20%) were fatigue (26%), pyrexia (24%), cough (24%), musculoskeletal pain (21%), diarrhea (20%), and rash (20%).

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KEYTRUDA (pembrolizumab) plus LENVIMA (lenvatinib) Combination Demonstrated Clinically Meaningful Tumor Response Rates in Unresectable Hepatocellular...

Skin Stem Cells Comments Off on KEYTRUDA (pembrolizumab) plus LENVIMA (lenvatinib) Combination Demonstrated Clinically Meaningful Tumor Response Rates in Unresectable Hepatocellular… | May 30th, 2020

ORLANDO, Fla.--(BUSINESS WIRE)--Hesperos Inc., pioneers of the Human-on-a-Chip in vitro system, today announced a new peer-reviewed publication that describes how the companys functional Human-on-a-Chip system can be used as a drug discovery platform to identify therapeutic interventions targeting the preclinical stages of Alzheimers disease (AD) and mild cognitive impairment (MCI). The manuscript, titled A human induced pluripotent stem cell-derived cortical neuron human-on-a-chip system to study A42 and tau-induced pathophysiological effects on long-term potentiation, was published this week in Alzheimer's & Dementia: Translational Research & Clinical Interventions. The work was conducted in collaboration with the University of Central Florida and with David G. Morgan, Ph.D., Professor of Translational Neuroscience at Michigan State University, and expert in AD pathology.

To date, more than 100 potential therapeutics in development for AD have been abandoned or failed during clinical trials. These therapeutics relied on research conducted in preclinical animal studies, which often are unable to accurately capture the full spectrum of the human disease phenotype, including differences in drug metabolism and excretion between humans and animals. Therefore, there is a need for human models, especially those that accurately recapitulate the functional impairments during the preclinical phases of AD and MCI.

Hesperos offers a breakthrough technology that provides a human cell-based assay based on cognitive function metrics to evaluate drugs designed to restore cognition at early stages of the Alzheimers continuum, said Dr. Morgan. This system can serve as a novel drug discovery platform to identify compounds that rescue or alleviate the initial neuronal deficits caused by A1-42 and/or tau oligomers, which is a main focus of clinical trials.

In 2018, Hesperos received a Phase I Small Business Innovation Research (SBIR) grant from the National Institute on Aging (NIA) division within the US National Institutes of Health (NIH) to help create a new multi-organ human-on-a-chip model for testing AD drugs. Research conducted under this grant included a study to assess therapeutic interventions based on functional changes in neurons, not neuronal death.

In the recent Alzheimer's & Dementia publication, Hesperos describes its in vitro human induced pluripotent stem cell (iPSC)-derived cortical neuron human-on-a-chip system for the evaluation of neuron morphology and function after exposure to toxic A and tau oligomers as well as brain extracts from AD transgenic mouse models.

Researchers are now focusing on biomarker development and therapeutic intervention before symptoms arise in AD and MCI, said James Hickman, Ph.D., Chief Scientist at Hesperos and Professor at the University of Central Florida. By studying functional disruption without extensive cell loss, we now have a screening methodology for drugs that could potentially evaluate therapeutic efficacy even before the neurodegeneration in MCI and AD occurs.

The researchers found that compared to controls, treatment with toxic A and tau oligomers or brain extracts on the iPSC cortical neurons significantly impaired information processing as demonstrated by reduction in high-frequency stimulation-induced long-term potentiation (LTP), a process that is thought to underlie memory formation and learning. Additionally, oligomer and brain extract exposure led to dysfunction in iPSC cortical neuron electrophysiological activity, including decreases in ion current and action potential firing.

While exposure to the toxic oligomers and brain extracts caused morphological defects in the iPSC cortical neurons, there was no significant loss in cell viability.

Clinical success for AD therapies has been challenging since preclinical animal studies often do not translate to humans, said Michael L. Shuler, Ph.D., Chief Executive Officer of Hesperos. With our recent study, we are now one step closer in developing an AD multi-organ model to better evaluate drug metabolism in the liver, penetration through the blood-brain barrier and the effects on neuronal cells.

About Alzheimers Disease/Preclinical Stage AD

AD is a progressive disease that is characterized by memory loss and deterioration of cognitive function. Preclinical AD is the first stage of the disease, and it begins long before any symptoms become apparent. It is thought that symptoms do not manifest until there is a significant death of neuronal cells, which is caused by the aggregation of toxic amyloid beta (A) and tau oligomers, typically during the earliest stages of the disease. Unfortunately, treatment after the diagnosis of MCI may be too late to reverse or modify disease progression.

To read the full manuscript, please visit https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/trc2.12029.

About Hesperos

Hesperos, Inc. is a leading provider of Human-on-a-Chip microfluidic systems to characterize an individuals biology. Founders Michael L. Shuler and James J. Hickman have been at the forefront of every major scientific discovery in this realm, from individual organ-on-a-chip constructs to fully functional, interconnected multi-organ systems. With a mission to revolutionize toxicology testing as well as efficacy evaluation for drug discovery, the company has created pumpless platforms with serum-free cellular mediums that allow multi-organ system communication and integrated computational PKPD modeling of live physiological responses utilizing functional readouts from neurons, cardiac, muscle, barrier tissues and neuromuscular junctions as well as responses from liver, pancreas and barrier tissues. Created from human stem cells, the fully human systems are the first in vitro solutions to accurately predict in vivo functions without the use of animal models. More information is available at http://www.hesperosinc.com.

Hesperos and Human-on-a-Chip are trademarks of Hesperos Inc. All other brands may be trademarks of their respective holders.

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Hesperos Human-on-a-Chip System Used to Model Preclinical Stages of Alzheimer's Disease and Mild Cognitive Impairment - Business Wire

Cardiac Stem Cells Comments Off on Hesperos Human-on-a-Chip System Used to Model Preclinical Stages of Alzheimer’s Disease and Mild Cognitive Impairment – Business Wire | May 30th, 2020

For many years, the standard of care for the first-line treatment of patients with MSI-H colorectal cancer has been the combination of mFOLFOX6 plus bevacizumab. This is the first time a single-agent, anti-PD-1 therapy demonstrated a superior, statistically significant and clinically meaningful improvement in progression-free survival compared to chemotherapy for these patients, said Dr. Roy Baynes, senior vice president and head of global clinical development, chief medical officer, Merck Research Laboratories. There is an unmet need for new treatment options in the first-line setting that may provide sustained, long-term improvements in outcomes for patients with MSI-H colorectal cancer. We are grateful to have the opportunity to present these practice-changing findings at the plenary session of this years ASCO.

KEYTRUDA monotherapy significantly reduced the risk of disease progression or death by 40% versus standard of care chemotherapy, with fewer treatment-related adverse events observed, in patients with MSI-H metastatic colorectal cancer. KEYTRUDA also demonstrated a long-term, durable response that lasted over two years for those who responded to treatment, said Thierry Andre, MD, professor of medical oncology, Sorbonne University, and Head of the Medical Oncology Department in St. Antoine Hospital, Assistance Publique Hpitaux de Paris. Data from KEYNOTE-177 show that KEYTRUDA monotherapy has the potential to become the new standard of care for first-line treatment of patients with MSI-H metastatic colorectal cancer.

In May 2017, KEYTRUDA became the first cancer therapy approved by the U.S. Food and Drug Administration for use based on a biomarker, regardless of tumor type, in previously treated patients with MSI-H or dMMR solid tumors.

As announced, more than 80 abstracts in nearly 20 types of solid tumors and blood cancers will be presented from Mercks broad oncology portfolio and investigational pipeline at ASCO. A compendium of presentations and posters of Merck-led studies will be posted by Merck on Friday, May 29 at 8 a.m. ET. Follow Merck on Twitter via @Merck and keep up to date with ASCO news and updates by using the hashtag #ASCO20.

KEYNOTE-177 Study Design and Additional Data (Abstract #LBA4)

KEYNOTE-177 is a randomized, open-label, Phase 3 trial evaluating KEYTRUDA monotherapy versus standard of care chemotherapy for the first-line treatment of patients with MSI-H or dMMR metastatic colorectal cancer (ClinicalTrials.gov, NCT02563002). The dual primary endpoints are PFS and OS. The study enrolled 307 patients, who were randomized to receive either KEYTRUDA (200 mg intravenously on Day 1 of each three-week cycle for up to 35 cycles) or investigators choice of one of the following chemotherapy-based regimens: mFOLFOX6; mFOLFOX6 plus bevacizumab (5 mg/kg IV on Day 1 of each two-week cycle); mFOLFOX6 plus cetuximab (400 mg/m2 IV, then 250 mg/m2 weekly in each two-week cycle); FOLFIRI; FOLFIRI plus bevacizumab (5 mg/kg IV on Day 1 of each two-week cycle); or FOLFIRI plus cetuximab (400 mg/m2 IV, then 250 mg/m2 weekly in each two-week cycle).

In this study, KEYTRUDA demonstrated a statistically significant and clinically meaningful improvement in PFS (HR=0.60 [95% CI, 0.45-0.80; p=0.0002]) and showed a median PFS of 16.5 months compared with 8.2 months for patients treated with chemotherapy. The two-year PFS rate was 48% with KEYTRUDA versus 19% with chemotherapy. The ORR was 43.8% with KEYTRUDA versus 33.1% with chemotherapy, with a complete response observed in 11.1% and 3.9% of patients, respectively; partial responses were observed in 32.7% and 29.2% of patients, respectively. Median duration of response was not reached with KEYTRUDA (range, 2.3+ to 41.4+) versus 10.6 months with chemotherapy (range, 2.8 to 37.5+). Additionally, 83% of patients had durable responses lasting at least two years with KEYTRUDA versus 35% with chemotherapy. In the study, 59% of patients in the intent-to-treat population received subsequent anti-PD-1/PD-L1 therapy after discontinuing study treatment in the chemotherapy arm.

The safety profile of KEYTRUDA demonstrated a lower incidence of Grade 3 treatment-related adverse events (AEs) versus chemotherapy (22% versus 66%, respectively), and no new toxicities were observed. Immune-mediated AEs and infusion reactions occurred in 31% of patients receiving KEYTRUDA and 13% of patients receiving chemotherapy. The most commonly reported immune-mediated AEswere hypothyroidism (12%) and colitis (7%) with KEYTRUDA, and infusion reactions (8%) with chemotherapy.

Merck Investor Event

Merck will hold a virtual investor event in conjunction with the ASCO Annual Meeting on Tuesday, June 2 at 2 p.m. ET. Details will be provided at a date closer to the event at http://investors.merck.com/home/default.aspx.

About Microsatellite Instability High (MSI-H)

Microsatellite instability (or MSI) is defined by the National Cancer Institute as a change that occurs in the DNA of certain cells (such as tumor cells) in which the number of repeats of microsatellites (short, repeated sequences of DNA) is different from the number of repeats that was in the DNA when it was inherited. The cause of MSI may be a defect in the ability to repair mistakes made when DNA is copied in the cell. This defect is also referred to as mismatch repair deficiency (dMMR). It is estimated that approximately 5-15% of colorectal cancer patients have tumors that score as either MSI-H or dMMR when testing is performed.

About Colorectal Cancer

Colorectal cancer starts in the colon or the rectum, and these cancers are referred to as colon cancer and rectal cancer depending on where the cancer starts. Colorectal cancer often begins with growths on the inner lining of the colon or rectum called polyps, which can change into cancer over time. Colorectal cancer is the third most commonly diagnosed cancer and the second most common cause of cancer-related death worldwide. It is estimated there were nearly 850,000 new cases of colorectal cancer and more than 880,000 deaths from the disease globally in 2018. In the United States, it is estimated there will be nearly 105,000 new cases of colon cancer and more than 43,000 new cases of rectal cancer, resulting in more than 53,000 deaths from colorectal cancer in 2020. The five-year survival rates for advanced/metastatic colon cancer and rectal cancer (stage IV) are estimated to be 14% and 15%, respectively.

About KEYTRUDA (pembrolizumab) Injection, 100 mg

KEYTRUDA is an anti-PD-1 therapy that works by increasing the ability of the bodys immune system to help detect and fight tumor cells. KEYTRUDA is a humanized monoclonal antibody that blocks the interaction between PD-1 and its ligands, PD-L1 and PD-L2, thereby activating T lymphocytes which may affect both tumor cells and healthy cells.

Merck has the industrys largest immuno-oncology clinical research program. There are currently more than 1,200 trials studying KEYTRUDA across a wide variety of cancers and treatment settings. The KEYTRUDA clinical program seeks to understand the role of KEYTRUDA across cancers and the factors that may predict a patient's likelihood of benefitting from treatment with KEYTRUDA, including exploring several different biomarkers.

Selected KEYTRUDA (pembrolizumab) Indications

Melanoma

KEYTRUDA is indicated for the treatment of patients with unresectable or metastatic melanoma.

KEYTRUDA is indicated for the adjuvant treatment of patients with melanoma with involvement of lymph node(s) following complete resection.

Non-Small Cell Lung Cancer

KEYTRUDA, in combination with pemetrexed and platinum chemotherapy, is indicated for the first-line treatment of patients with metastatic nonsquamous non-small cell lung cancer (NSCLC), with no EGFR or ALK genomic tumor aberrations.

KEYTRUDA, in combination with carboplatin and either paclitaxel or paclitaxel protein-bound, is indicated for the first-line treatment of patients with metastatic squamous NSCLC.

KEYTRUDA, as a single agent, is indicated for the first-line treatment of patients with NSCLC expressing PD-L1 [tumor proportion score (TPS) 1%] as determined by an FDA-approved test, with no EGFR or ALK genomic tumor aberrations, and is stage III where patients are not candidates for surgical resection or definitive chemoradiation, or metastatic.

KEYTRUDA, as a single agent, is indicated for the treatment of patients with metastatic NSCLC whose tumors express PD-L1 (TPS 1%) as determined by an FDA-approved test, with disease progression on or after platinum-containing chemotherapy. Patients with EGFR or ALK genomic tumor aberrations should have disease progression on FDA-approved therapy for these aberrations prior to receiving KEYTRUDA.

Small Cell Lung Cancer

KEYTRUDA is indicated for the treatment of patients with metastatic small cell lung cancer (SCLC) with disease progression on or after platinum-based chemotherapy and at least 1 other prior line of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.

Head and Neck Squamous Cell Cancer

KEYTRUDA, in combination with platinum and fluorouracil (FU), is indicated for the first-line treatment of patients with metastatic or with unresectable, recurrent head and neck squamous cell carcinoma (HNSCC).

KEYTRUDA, as a single agent, is indicated for the first-line treatment of patients with metastatic or with unresectable, recurrent HNSCC whose tumors express PD-L1 [combined positive score (CPS) 1] as determined by an FDA-approved test.

KEYTRUDA, as a single agent, is indicated for the treatment of patients with recurrent or metastatic head and neck squamous cell carcinoma (HNSCC) with disease progression on or after platinum-containing chemotherapy.

Classical Hodgkin Lymphoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with refractory classical Hodgkin lymphoma (cHL), or who have relapsed after 3 or more prior lines of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Primary Mediastinal Large B-Cell Lymphoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with refractory primary mediastinal large B-cell lymphoma (PMBCL), or who have relapsed after 2 or more prior lines of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials. KEYTRUDA is not recommended for treatment of patients with PMBCL who require urgent cytoreductive therapy.

Urothelial Carcinoma

KEYTRUDA is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma (mUC) who are not eligible for cisplatin-containing chemotherapy and whose tumors express PD-L1 [combined positive score (CPS) 10], as determined by an FDA-approved test, or in patients who are not eligible for any platinum-containing chemotherapy regardless of PD-L1 status. This indication is approved under accelerated approval based on tumor response rate and duration of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.

KEYTRUDA is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma (mUC) who have disease progression during or following platinum-containing chemotherapy or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.

KEYTRUDA is indicated for the treatment of patients with Bacillus Calmette-Guerin (BCG)-unresponsive, high-risk, non-muscle invasive bladder cancer (NMIBC) with carcinoma in situ (CIS) with or without papillary tumors who are ineligible for or have elected not to undergo cystectomy.

Microsatellite Instability-High (MSI-H) Cancer

KEYTRUDA is indicated for the treatment of adult and pediatric patients with unresectable or metastatic microsatellite instability-high (MSI-H) or mismatch repair deficient (dMMR)

This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials. The safety and effectiveness of KEYTRUDA in pediatric patients with MSI-H central nervous system cancers have not been established.

Gastric Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent locally advanced or metastatic gastric or gastroesophageal junction (GEJ) adenocarcinoma whose tumors express PD-L1 (CPS 1) as determined by an FDA-approved test, with disease progression on or after two or more prior lines of therapy including fluoropyrimidine- and platinum-containing chemotherapy and if appropriate, HER2/neu-targeted therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Esophageal Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent locally advanced or metastatic squamous cell carcinoma of the esophagus whose tumors express PD-L1 (CPS 10) as determined by an FDA-approved test, with disease progression after one or more prior lines of systemic therapy.

Cervical Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent or metastatic cervical cancer with disease progression on or after chemotherapy whose tumors express PD-L1 (CPS 1) as determined by an FDA-approved test. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Hepatocellular Carcinoma

KEYTRUDA is indicated for the treatment of patients with hepatocellular carcinoma (HCC) who have been previously treated with sorafenib. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Merkel Cell Carcinoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with recurrent locally advanced or metastatic Merkel cell carcinoma (MCC). This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Renal Cell Carcinoma

KEYTRUDA, in combination with axitinib, is indicated for the first-line treatment of patients with advanced renal cell carcinoma (RCC).

Selected Important Safety Information for KEYTRUDA

Immune-Mediated Pneumonitis

KEYTRUDA can cause immune-mediated pneumonitis, including fatal cases. Pneumonitis occurred in 3.4% (94/2799) of patients with various cancers receiving KEYTRUDA, including Grade 1 (0.8%), 2 (1.3%), 3 (0.9%), 4 (0.3%), and 5 (0.1%). Pneumonitis occurred in 8.2% (65/790) of NSCLC patients receiving KEYTRUDA as a single agent, including Grades 3-4 in 3.2% of patients, and occurred more frequently in patients with a history of prior thoracic radiation (17%) compared to those without (7.7%). Pneumonitis occurred in 6% (18/300) of HNSCC patients receiving KEYTRUDA as a single agent, including Grades 3-5 in 1.6% of patients, and occurred in 5.4% (15/276) of patients receiving KEYTRUDA in combination with platinum and FU as first-line therapy for advanced disease, including Grades 3-5 in 1.5% of patients.

Monitor patients for signs and symptoms of pneumonitis. Evaluate suspected pneumonitis with radiographic imaging. Administer corticosteroids for Grade 2 or greater pneumonitis. Withhold KEYTRUDA for Grade 2; permanently discontinue KEYTRUDA for Grade 3 or 4 or recurrent Grade 2 pneumonitis.

Immune-Mediated Colitis

KEYTRUDA can cause immune-mediated colitis. Colitis occurred in 1.7% (48/2799) of patients receiving KEYTRUDA, including Grade 2 (0.4%), 3 (1.1%), and 4 (<0.1%). Monitor patients for signs and symptoms of colitis. Administer corticosteroids for Grade 2 or greater colitis. Withhold KEYTRUDA for Grade 2 or 3; permanently discontinue KEYTRUDA for Grade 4 colitis.

Immune-Mediated Hepatitis (KEYTRUDA) and Hepatotoxicity (KEYTRUDA in Combination With Axitinib)

Immune-Mediated Hepatitis

KEYTRUDA can cause immune-mediated hepatitis. Hepatitis occurred in 0.7% (19/2799) of patients receiving KEYTRUDA, including Grade 2 (0.1%), 3 (0.4%), and 4 (<0.1%). Monitor patients for changes in liver function. Administer corticosteroids for Grade 2 or greater hepatitis and, based on severity of liver enzyme elevations, withhold or discontinue KEYTRUDA.

Hepatotoxicity in Combination With Axitinib

KEYTRUDA in combination with axitinib can cause hepatic toxicity with higher than expected frequencies of Grades 3 and 4 ALT and AST elevations compared to KEYTRUDA alone. With the combination of KEYTRUDA and axitinib, Grades 3 and 4 increased ALT (20%) and increased AST (13%) were seen. Monitor liver enzymes before initiation of and periodically throughout treatment. Consider more frequent monitoring of liver enzymes as compared to when the drugs are administered as single agents. For elevated liver enzymes, interrupt KEYTRUDA and axitinib, and consider administering corticosteroids as needed.

Immune-Mediated Endocrinopathies

KEYTRUDA can cause adrenal insufficiency (primary and secondary), hypophysitis, thyroid disorders, and type 1 diabetes mellitus. Adrenal insufficiency occurred in 0.8% (22/2799) of patients, including Grade 2 (0.3%), 3 (0.3%), and 4 (<0.1%). Hypophysitis occurred in 0.6% (17/2799) of patients, including Grade 2 (0.2%), 3 (0.3%), and 4 (<0.1%). Hypothyroidism occurred in 8.5% (237/2799) of patients, including Grade 2 (6.2%) and 3 (0.1%). The incidence of new or worsening hypothyroidism was higher in 1185 patients with HNSCC (16%) receiving KEYTRUDA, as a single agent or in combination with platinum and FU, including Grade 3 (0.3%) hypothyroidism. Hyperthyroidism occurred in 3.4% (96/2799) of patients, including Grade 2 (0.8%) and 3 (0.1%), and thyroiditis occurred in 0.6% (16/2799) of patients, including Grade 2 (0.3%). Type 1 diabetes mellitus, including diabetic ketoacidosis, occurred in 0.2% (6/2799) of patients.

Monitor patients for signs and symptoms of adrenal insufficiency, hypophysitis (including hypopituitarism), thyroid function (prior to and periodically during treatment), and hyperglycemia. For adrenal insufficiency or hypophysitis, administer corticosteroids and hormone replacement as clinically indicated. Withhold KEYTRUDA for Grade 2 adrenal insufficiency or hypophysitis and withhold or discontinue KEYTRUDA for Grade 3 or Grade 4 adrenal insufficiency or hypophysitis. Administer hormone replacement for hypothyroidism and manage hyperthyroidism with thionamides and beta-blockers as appropriate. Withhold or discontinue KEYTRUDA for Grade 3 or 4 hyperthyroidism. Administer insulin for type 1 diabetes, and withhold KEYTRUDA and administer antihyperglycemics in patients with severe hyperglycemia.

Immune-Mediated Nephritis and Renal Dysfunction

KEYTRUDA can cause immune-mediated nephritis. Nephritis occurred in 0.3% (9/2799) of patients receiving KEYTRUDA, including Grade 2 (0.1%), 3 (0.1%), and 4 (<0.1%) nephritis. Nephritis occurred in 1.7% (7/405) of patients receiving KEYTRUDA in combination with pemetrexed and platinum chemotherapy. Monitor patients for changes in renal function. Administer corticosteroids for Grade 2 or greater nephritis. Withhold KEYTRUDA for Grade 2; permanently discontinue for Grade 3 or 4 nephritis.

Immune-Mediated Skin Reactions

Immune-mediated rashes, including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN) (some cases with fatal outcome), exfoliative dermatitis, and bullous pemphigoid, can occur. Monitor patients for suspected severe skin reactions and based on the severity of the adverse reaction, withhold or permanently discontinue KEYTRUDA and administer corticosteroids. For signs or symptoms of SJS or TEN, withhold KEYTRUDA and refer the patient for specialized care for assessment and treatment. If SJS or TEN is confirmed, permanently discontinue KEYTRUDA.

Other Immune-Mediated Adverse Reactions

Immune-mediated adverse reactions, which may be severe or fatal, can occur in any organ system or tissue in patients receiving KEYTRUDA and may also occur after discontinuation of treatment. For suspected immune-mediated adverse reactions, ensure adequate evaluation to confirm etiology or exclude other causes. Based on the severity of the adverse reaction, withhold KEYTRUDA and administer corticosteroids. Upon improvement to Grade 1 or less, initiate corticosteroid taper and continue to taper over at least 1 month. Based on limited data from clinical studies in patients whose immune-related adverse reactions could not be controlled with corticosteroid use, administration of other systemic immunosuppressants can be considered. Resume KEYTRUDA when the adverse reaction remains at Grade 1 or less following corticosteroid taper. Permanently discontinue KEYTRUDA for any Grade 3 immune-mediated adverse reaction that recurs and for any life-threatening immune-mediated adverse reaction.

The following clinically significant immune-mediated adverse reactions occurred in less than 1% (unless otherwise indicated) of 2799 patients: arthritis (1.5%), uveitis, myositis, Guillain-Barr syndrome, myasthenia gravis, vasculitis, pancreatitis, hemolytic anemia, sarcoidosis, and encephalitis. In addition, myelitis and myocarditis were reported in other clinical trials, including classical Hodgkin lymphoma, and postmarketing use.

Treatment with KEYTRUDA may increase the risk of rejection in solid organ transplant recipients. Consider the benefit of treatment vs the risk of possible organ rejection in these patients.

Infusion-Related Reactions

KEYTRUDA can cause severe or life-threatening infusion-related reactions, including hypersensitivity and anaphylaxis, which have been reported in 0.2% (6/2799) of patients. Monitor patients for signs and symptoms of infusion-related reactions. For Grade 3 or 4 reactions, stop infusion and permanently discontinue KEYTRUDA.

Complications of Allogeneic Hematopoietic Stem Cell Transplantation (HSCT)

Immune-mediated complications, including fatal events, occurred in patients who underwent allogeneic HSCT after treatment with KEYTRUDA. Of 23 patients with cHL who proceeded to allogeneic HSCT after KEYTRUDA, 6 (26%) developed graft-versus-host disease (GVHD) (1 fatal case) and 2 (9%) developed severe hepatic veno-occlusive disease (VOD) after reduced-intensity conditioning (1 fatal case). Cases of fatal hyperacute GVHD after allogeneic HSCT have also been reported in patients with lymphoma who received a PD-1 receptorblocking antibody before transplantation. Follow patients closely for early evidence of transplant-related complications such as hyperacute graft-versus-host disease (GVHD), Grade 3 to 4 acute GVHD, steroid-requiring febrile syndrome, hepatic veno-occlusive disease (VOD), and other immune-mediated adverse reactions.

In patients with a history of allogeneic HSCT, acute GVHD (including fatal GVHD) has been reported after treatment with KEYTRUDA. Patients who experienced GVHD after their transplant procedure may be at increased risk for GVHD after KEYTRUDA. Consider the benefit of KEYTRUDA vs the risk of GVHD in these patients.

Increased Mortality in Patients With Multiple Myeloma

In trials in patients with multiple myeloma, the addition of KEYTRUDA to a thalidomide analogue plus dexamethasone resulted in increased mortality. Treatment of these patients with a PD-1 or PD-L1 blocking antibody in this combination is not recommended outside of controlled trials.

Embryofetal Toxicity

Based on its mechanism of action, KEYTRUDA can cause fetal harm when administered to a pregnant woman. Advise women of this potential risk. In females of reproductive potential, verify pregnancy status prior to initiating KEYTRUDA and advise them to use effective contraception during treatment and for 4 months after the last dose.

Adverse Reactions

In KEYNOTE-006, KEYTRUDA was discontinued due to adverse reactions in 9% of 555 patients with advanced melanoma; adverse reactions leading to permanent discontinuation in more than one patient were colitis (1.4%), autoimmune hepatitis (0.7%), allergic reaction (0.4%), polyneuropathy (0.4%), and cardiac failure (0.4%). The most common adverse reactions (20%) with KEYTRUDA were fatigue (28%), diarrhea (26%), rash (24%), and nausea (21%).

In KEYNOTE-002, KEYTRUDA was permanently discontinued due to adverse reactions in 12% of 357 patients with advanced melanoma; the most common (1%) were general physical health deterioration (1%), asthenia (1%), dyspnea (1%), pneumonitis (1%), and generalized edema (1%). The most common adverse reactions were fatigue (43%), pruritus (28%), rash (24%), constipation (22%), nausea (22%), diarrhea (20%), and decreased appetite (20%).

In KEYNOTE-054, KEYTRUDA was permanently discontinued due to adverse reactions in 14% of 509 patients; the most common (1%) were pneumonitis (1.4%), colitis (1.2%), and diarrhea (1%). Serious adverse reactions occurred in 25% of patients receiving KEYTRUDA. The most common adverse reaction (20%) with KEYTRUDA was diarrhea (28%).

In KEYNOTE-189, when KEYTRUDA was administered with pemetrexed and platinum chemotherapy in metastatic nonsquamous NSCLC, KEYTRUDA was discontinued due to adverse reactions in 20% of 405 patients. The most common adverse reactions resulting in permanent discontinuation of KEYTRUDA were pneumonitis (3%) and acute kidney injury (2%). The most common adverse reactions (20%) with KEYTRUDA were nausea (56%), fatigue (56%), constipation (35%), diarrhea (31%), decreased appetite (28%), rash (25%), vomiting (24%), cough (21%), dyspnea (21%), and pyrexia (20%).

In KEYNOTE-407, when KEYTRUDA was administered with carboplatin and either paclitaxel or paclitaxel protein-bound in metastatic squamous NSCLC, KEYTRUDA was discontinued due to adverse reactions in 15% of 101 patients. The most frequent serious adverse reactions reported in at least 2% of patients were febrile neutropenia, pneumonia, and urinary tract infection. Adverse reactions observed in KEYNOTE-407 were similar to those observed in KEYNOTE-189 with the exception that increased incidences of alopecia (47% vs 36%) and peripheral neuropathy (31% vs 25%) were observed in the KEYTRUDA and chemotherapy arm compared to the placebo and chemotherapy arm in KEYNOTE-407.

In KEYNOTE-042, KEYTRUDA was discontinued due to adverse reactions in 19% of 636 patients with advanced NSCLC; the most common were pneumonitis (3%), death due to unknown cause (1.6%), and pneumonia (1.4%). The most frequent serious adverse reactions reported in at least 2% of patients were pneumonia (7%), pneumonitis (3.9%), pulmonary embolism (2.4%), and pleural effusion (2.2%). The most common adverse reaction (20%) was fatigue (25%).

In KEYNOTE-010, KEYTRUDA monotherapy was discontinued due to adverse reactions in 8% of 682 patients with metastatic NSCLC; the most common was pneumonitis (1.8%). The most common adverse reactions (20%) were decreased appetite (25%), fatigue (25%), dyspnea (23%), and nausea (20%).

Adverse reactions occurring in patients with SCLC were similar to those occurring in patients with other solid tumors who received KEYTRUDA as a single agent.

In KEYNOTE-048, KEYTRUDA monotherapy was discontinued due to adverse events in 12% of 300 patients with HNSCC; the most common adverse reactions leading to permanent discontinuation were sepsis (1.7%) and pneumonia (1.3%). The most common adverse reactions (20%) were fatigue (33%), constipation (20%), and rash (20%).

In KEYNOTE-048, when KEYTRUDA was administered in combination with platinum (cisplatin or carboplatin) and FU chemotherapy, KEYTRUDA was discontinued due to adverse reactions in 16% of 276 patients with HNSCC. The most common adverse reactions resulting in permanent discontinuation of KEYTRUDA were pneumonia (2.5%), pneumonitis (1.8%), and septic shock (1.4%). The most common adverse reactions (20%) were nausea (51%), fatigue (49%), constipation (37%), vomiting (32%), mucosal inflammation (31%), diarrhea (29%), decreased appetite (29%), stomatitis (26%), and cough (22%).

In KEYNOTE-012, KEYTRUDA was discontinued due to adverse reactions in 17% of 192 patients with HNSCC. Serious adverse reactions occurred in 45% of patients. The most frequent serious adverse reactions reported in at least 2% of patients were pneumonia, dyspnea, confusional state, vomiting, pleural effusion, and respiratory failure. The most common adverse reactions (20%) were fatigue, decreased appetite, and dyspnea. Adverse reactions occurring in patients with HNSCC were generally similar to those occurring in patients with melanoma or NSCLC who received KEYTRUDA as a monotherapy, with the exception of increased incidences of facial edema and new or worsening hypothyroidism.

In KEYNOTE-087, KEYTRUDA was discontinued due to adverse reactions in 5% of 210 patients with cHL. Serious adverse reactions occurred in 16% of patients; those 1% included pneumonia, pneumonitis, pyrexia, dyspnea, GVHD, and herpes zoster. Two patients died from causes other than disease progression; 1 from GVHD after subsequent allogeneic HSCT and 1 from septic shock. The most common adverse reactions (20%) were fatigue (26%), pyrexia (24%), cough (24%), musculoskeletal pain (21%), diarrhea (20%), and rash (20%).

In KEYNOTE-170, KEYTRUDA was discontinued due to adverse reactions in 8% of 53 patients with PMBCL. Serious adverse reactions occurred in 26% of patients and included arrhythmia (4%), cardiac tamponade (2%), myocardial infarction (2%), pericardial effusion (2%), and pericarditis (2%). Six (11%) patients died within 30 days of start of treatment. The most common adverse reactions (20%) were musculoskeletal pain (30%), upper respiratory tract infection and pyrexia (28% each), cough (26%), fatigue (23%), and dyspnea (21%).

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Due to the pandemic, we have included a special section on the Impact of COVID 19 on the progenitor cell productMarket which would mention How the Covid-19 is Affecting the Industry, Market Trends and Potential Opportunities in the COVID-19 Landscape, Key Regions and Proposal for progenitor cell product Market Players to battle Covid-19 Impact.

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Top Leading players covered in the progenitor cell product market report: NeuroNova AB, StemCells, ReNeuron Limited, Asterias Biotherapeutics, Thermo Fisher Scientific, STEMCELL Technologies, Axol Bio, R&D Systems, Lonza, ATCC, Irvine Scientific, CDI and More

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On the basis of product, we research the production, revenue, price, market share and growth rate, primarily split into:Pancreatic progenitor cellsCardiac Progenitor CellsIntermediate progenitor cellsNeural progenitor cells (NPCs)Endothelial progenitor cells (EPC)OthersFor the end users/applications, this report focuses on the status and outlook for major applications/end users, consumption (sales), market share and growth rate of PROGENITOR CELL PRODUCT for each application, including:Medical careHospitalLaboratory

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progenitor cell product Market Latest trending report is booming globally by Top Leading Players NeuroNova AB, StemCells, ReNeuron Limited, Asterias...

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BAR HARBOR Research by scientists at the MDI Biological Laboratoryis opening up new approaches to promoting tissue regeneration in organs damaged by disease or injury.

In recent years, research in regenerative biology has focused on stem cell therapies that reprogram the bodys own cells to replace damaged tissue, which is a complicated process because it involves turning genes in the cells nucleus on and off.

A recent paper in the journal Genetics by MDI Biological Laboratory scientist Elisabeth Marnik, Ph.D., a postdoctoral fellow in the laboratory of Dustin Updike, Ph.D., offers insight into an alternate pathway to regeneration: by recreating the properties of germ cells.

Germ cells, which are the precursors to the sperm and egg, are considered immortal because they are the only cells in the body with the potential to create an entirely new organism. The stem cell-like ability of germ cells to turn into any type of cell is called totipotency.

By getting a handle on what makes germ cells totipotent, we can promote regeneration by unlocking the stem cell-like properties of other cell types, said Updike. Our research shows that such cells can be reprogrammed by manipulating their cytoplasmic composition and chemistry, which would seem to be safer and easier than changing the DNA within a cells nucleus.

Using the tiny, soil-dwelling nematode worm, C. elegans, as a model, the Updike lab studies organelles called germ granules that reside in the cytoplasm (the contents of the cell outside of the nucleus) of germ cells. These organelles, which are conserved from nematodes to humans, are one of the keys to the remarkable attributes of germ cells, including the ability to differentiate into other types of cells.

In their recent paper entitled Germline Maintenance Through the Multifaceted Activities of GLH/Vasa in Caenorhabditis elegans P Granules, Updike and his team describe the intriguing and elusive role of Vasa proteins within germ granules in determining whether a cell is destined to become a germ cell with totipotent capabilities or a specific type of cell, like those that comprise muscle, nerves or skin.

Because of the role of Vasa proteins in preserving totipotency, an increased understanding of how such proteins work could lead to unprecedented approaches to de-differentiating cell types to promote regeneration; or alternatively, to new methods to turn off totipotency when it is no longer desirable, as in the case of cancer.

The increase in chronic and degenerative diseases caused by the aging of the population is driving demand for new therapies, said MDI Biological Laboratory President Hermann Haller, M.D. Dustins research on germ granules offers another route to repairing damaged tissues and organs in cases where therapeutic options are limited or non-existent, as well as an increased understanding of cancer.

Because of the complexity of the cellular chemistry, research on Vasa and other proteins found in germ granules is often overlooked, but that is rapidly changing especially among pharmaceutical companies as more scientists realize the impact and potential of such research, not only for regenerative medicine but also for an understanding of tumorigenesis, or cancer development, Updike said.

Recent research has found that some cancers are accompanied by the mis-expression of germ granule proteins, which are normally found only in germ cells. The mis-expression of these germ-granule proteins seems to promote the immortal properties of germ cells, and consequently tumorigenesis, with some germ-granule proteins now serving as prognosis markers for different types of cancer, Updike said.

Updike is a former postdoctoral researcher in the laboratory of Susan Strome, Ph.D., at University of California, Santa Cruz. Strome, who was inducted into the National Academy of Sciences last year, first discovered P granules more than 30 years ago. She credits Updike, who has published several seminal papers on the subject, with great imagination, determination and excellent technical skill in the pursuit of his goal of elucidating the function and biochemistry of these tiny organelles.

The lead author of the new study from the Updike laboratory, Elisabeth A. Marnik, Ph.D., will be launching her own laboratory at Husson University in Bangor, Maine, this fall. Other contributors include J. Heath Fuqua, Catherine S. Sharp, Jesse D. Rochester, Emily L. Xu and Sarah E. Holbrook. Their research was conducted at the Kathryn W. Davis Center for Regenerative Biology and Medicine at the MDI Biological Laboratory.

Updikes research is supported by a grant (R01 GM-113933) from the National Institute of General Medical Sciences (NIGMS), an institute of the National Institutes of Health (NIH). The equipment and cores used for part of the study were supported by NIGMS-NIH Centers of Biomedical Research Excellence and IDeA Networks of Biomedical Research Excellence grants P20 GM-104318 and P20 GM-203423, respectively.

We aim to improve human health and healthspan by uncovering basic mechanisms of tissue repair, aging and regeneration, translating our discoveries for the benefit of society and developing the next generation of scientific leaders. For more information, please visitmdibl.org.

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Research at MDI Biological Laboratory explores novel pathways of regeneration and tumorigenesis - Bangor Daily News

Skin Stem Cells Comments Off on Research at MDI Biological Laboratory explores novel pathways of regeneration and tumorigenesis – Bangor Daily News | May 28th, 2020

The bones of the skeletal system serve many important functions for the body, from giving your body support to allowing you to move. They also play an important role in blood cell production and fat storage.

Bone marrow is the spongy or viscous tissue that fills the inside of your bones. There are actually two types of bone marrow:

Read on to learn more about different functions of red and yellow bone marrow as well as the conditions that affect bone marrow.

Red bone marrow is involved in hematopoiesis. This is another name for blood cell production. Hematopoietic stem cells that are found in red bone marrow can develop into a variety of different blood cells, including:

Newly produced blood cells enter your bloodstream through vessels called sinusoids.

As you age, your red bone marrow is gradually replaced with yellow bone marrow. And by adulthood, red bone marrow can be found only in a handful of bones, including the:

Yellow bone marrow is involved in the storage of fats. The fats in yellow bone marrow are stored in cells called adipocytes. This fat can be used as an energy source as needed.

Yellow bone marrow also contains mesenchymal stem cells. These are cells that can develop into bone, fat, cartilage, or muscle cells.

Remember, over time, yellow bone marrow starts to replace red bone marrow. So, most bones in an adult body contain yellow bone marrow.

Bone marrow is crucial for producing blood cells. Therefore, a range of blood-related conditions involve issues with bone marrow.

Many of these conditions affect the numbers of blood cells produced in bone marrow. This causes them to share many common symptoms, including:

Heres a look at some specific conditions involving bone marrow issues.

Leukemia is a type of cancer that can affect both your bone marrow and lymphatic system.

It happens when blood cells get mutations in their DNA. This causes them to grow and divide more rapidly than healthy blood cells. Over time, these cells start to crowd out the healthy cells in your bone marrow.

Leukemia is classified as either acute or chronic, depending on how fast it progresses. Its further broken down by the type of white blood cells it involves.

Myelogenous leukemia involves red blood cells, white blood cells, and platelets. Lymphocytic leukemia involves lymphocytes, a specific type of white blood cell.

Some of the major types of leukemia include:

Theres no clear cause of leukemia, but certain things can increase your risk, including:

Aplastic anemia occurs when bone marrow doesnt produce enough new blood cells. It occurs from damage to the stem cells of bone marrow. This makes it harder from them to grow and develop into new blood cells.

This damage can be either:

Myeloproliferative disorders happen when the stem cells in bone marrow grow abnormally. This can lead to increased numbers of a specific type of blood cell.

There are several types of myeloproliferative disorders, including:

Bone marrow is found in the bones throughout your body. There are two types of bone marrow. Red bone marrow is involved in production of blood cells, while yellow marrow is important for fat storage. As you age, yellow bone marrow replaces red bone marrow.

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SHANGHAI, May27, 2020 /PRNewswire/ -- Shanghai Cell Therapy Group (SHCell) recently entered intoa six-year research collaborative project with Professor Qi-Long Ying from the University of Southern California (USC). Through the project, sponsored by $3.6 million from the Baize Plan Fund, the Ying laboratory aims to develop conditions for the long-term ex vivo expansion of mouse and human hematopoietic stem and progenitor cells.

"Hematopoietic stem cells, or HSCs, are found in the bone marrow of adults," said Professor Qijun Qian, CEO of Shanghai Cell Therapy Group. "HSCs have the ability for long-term self-renewal and differentiation into various types of mature blood cells, and for rebuilding normal hematopoiesis and immune function in patients. They also have enormous potential to treat diseases, including tumors, autoimmune diseases, severe infectious disease, and inherited blood diseases, and to combat the effects of aging."

This research project will be conducted and supervised by Professor Qi-Long Ying, a Professor of Stem Cell Biology and Regenerative Medicine at the Keck School of Medicine of USC. Professor Ying's pioneering stem cell research has won international acclaim, including the 2016 McEwen Award for Innovation, the highest honor in the field.

"We'll develop and optimize culture conditions for the long-term ex vivo expansion of HSCs," said Professor Ying. "We'll also test combinations of basal media, small molecules, cytokines and growth factors, and characterize ex vivo expanded hematopoietic stem and progenitor cells. These cells will then be genetically modified and tested for their potential to treat different diseases, including blood disorders and cancers."

Professor Andrew P. McMahon, Director of Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research of USC, added: "Stem cell biology represents an exciting area in medicine with great therapeutic potential. I am delighted SHCell is supporting Professor Ying. A breakthrough in the ability to propagate and manipulate HSCs will have lasting clinical significance."

The project also plans to build animal models of different blood diseases and cancers and test the safety and effectiveness of genetically modified hematopoietic stem and progenitor cells before clinical translation. SHCell will actively explore clinical applications of hematopoietic stem and progenitor cells in the treatment of cancers or blood diseases.

As SHCell's first overseas collaboration, this project aims to advance the goals of the Baize Plan: to provide first-class cell treatments and cell therapies at an affordable price to cure cancer and increase life expectancy. SHCell hopes that this project will also accelerate original scientific breakthroughs in the stem cell field.

Shanghai Cell Therapy Group

Founded in 2013, Shanghai Cell Therapeutics Group Co., Ltd is located at the Shanghai Municipal Engineering and Technology Research Center, which was established by the Shanghai Science and Technology Commission. With a mission of "changing the length and abundance of life with cell therapy", SHCell has created a closed-loop industrial chain and an integrated platform for cell treatment and cell therapy. It comprises cell storage, cell drug research and cell clinical transformation with cell therapy as its core business.

The Baize Plan was proposed in 2016 by Wu Mengchao, an Academician of the Chinese Academy of Sciences (CAS) and initiated by Professor Qian, aiming to provide first-class cell treatments and cell therapies at an affordable price with the goal of curing cancers and increasing life expectancy. The Baize Plan Fund was created by the Shanghai Cell Therapy Group to realize the vision of the Baize Plan.

University of Southern California (USC)

Founded in 1880, the University of Southern California is one of the world's leading educational and research institutions, and also the oldest private research university in California. Located in the heart of Los Angeles, the University of Southern California comprises 23 schools and units, and students are encouraged to explore different fields of study. The University of Southern California ranked #22 in National Universities in the 2020 edition of Best Colleges, published by U.S. News & World Report.

For more information, visit http://www.shcell.com/

SOURCE Shanghai Cell Therapy Group

http://www.shcell.com

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She just wanted to be somewhere safe, somewhere familiar, where people looked and spoke like her and she could stand to eat the food. Midnight Robber by Nalo Hopkinson

Midnight Robber (2000) is about a woman, divided. Raised on the high-tech utopian planet of Touissant, Tan-Tan grows up on a planet populated by the descendants of a Caribbean diaspora, where all labor is performed by an all-seeing AI. But when she is exiled to Touissants parallel universe twin planet, the no-tech New Half-Way Tree, with her sexually abusive father, she becomes divided between good and evil Tan-Tans. To make herself and New Half-Way Tree whole, she adopts the persona of the legendary Robber Queen and becomes a legend herself. It is a wondrous blend of science fictional tropes and Caribbean mythology written in a Caribbean vernacular which vividly recalls the history of slavery and imperialism that shaped Touissant and its people, published at a time when diverse voices and perspectives within science fiction were blossoming.

Science fiction has long been dominated by white, Western perspectives. Vernes tech-forward adventures and Wells sociological allegories established two distinctive styles, but still centered on white imperialism and class struggle. Subsequent futures depicted in Verne-like pulp and Golden Age stories, where lone white heroes conquered evil powers or alien planets, mirrored colonialist history and the subjugation of non-white races. The civil rights era saw the incorporation of more Wellsian sociological concerns, and an increase in the number of non-white faces in the future, but they were often tokensparts of a dominant white monoculture. Important figures that presaged modern diversity included Star Treks Lieutenant Uhura, played by Nichelle Nichols. Nichols was the first black woman to play a non-servant character on TV; though her glorified secretary role frustrated Nichols, her presence was a political act, showing there was space for black people in the future.

Another key figure was the musician and poet Sun Ra, who laid the aesthetic foundation for what would become known as the Afrofuturist movement (the term coined by Mark Dery in a 1994 essay), which showed pride in black history and imagined the future through a black cultural lens. Within science fiction, the foundational work of Samuel Delany and Octavia Butler painted realistic futures in which the histories and cultural differences of people of color had a place. Finally, an important modern figure in the decentralization of the dominant Western perspective is Nalo Hopkinson.

A similarly long-standing paradigm lies at the heart of biology, extending back to Darwins theoretical and Mendels practical frameworks for the evolution of genetic traits via natural selection. Our natures werent determined by experience, as Lamarck posited, but by genes. Therefore, genes determine our reproductive fitness, and if we can understand genes, we might take our futures into our own hands to better treat disease and ease human suffering. This theory was tragically over-applied, even by Darwin, who in Descent of Man (1871) conflated culture with biology, assuming the Wests conquest of indigenous cultures meant white people were genetically superior. After the Nazis committed genocide in the name of an all-white future, ideas and practices based in eugenics declined, as biological understanding of genes matured. The Central Dogma of the 60s maintained the idea of a mechanistic meaning of life, as advances in genetic engineering and the age of genomics enabled our greatest understanding yet of how genes and disease work. The last major barrier between us and our transhumanist future therefore involved understanding how genes determine cellular identity, and as well see, key figures in answering that question are stem cells.

***

Hopkinson was born December 20, 1960 in Kingston, Jamaica. Her mother was a library technician and her father wrote, taught, and acted. Growing up, Hopkinson was immersed in the Caribbean literary scene, fed on a steady diet of theater, dance, readings, and visual arts exhibitions. She loved to readfrom folklore, to classical literature, to Kurt Vonnegutand loved science fiction, from Spock and Uhura on Star Trek, to Le Guin, James Tiptree Jr., and Delany. Despite being surrounded by a vibrant writing community, it didnt occur to her to become a writer herself. What they were writing was poetry and mimetic fiction, Hopkinson said, whereas I was reading science fiction and fantasy. It wasnt until I was 16 and stumbled upon an anthology of stories written at the Clarion Science Fiction Workshop that I realized there were places where you could be taught how to write fiction. Growing up, her family moved often, from Jamaica to Guyana to Trinidad and back, but in 1977, they moved to Toronto to get treatment for her fathers chronic kidney disease, and Hopkinson suddenly became a minority, thousands of miles from home.

Development can be described as an orderly alienation. In mammals, zygotes divide and subsets of cells become functionally specialized into, say, neurons or liver cells. Following the discovery of DNA as the genetic material in the 1950s, a question arose: did dividing cells retain all genes from the zygote, or were genes lost as it specialized? British embryologist John Gurdon addressed this question in a series of experiments in the 60s using frogs. Gurdon transplanted nuclei from varyingly differentiated cells into oocytes stripped of their genetic material to see if a new frog was made. He found the more differentiated a cell was, the lower the chance of success, but the successes confirmed that no genetic material was lost. Meanwhile, Canadian biologists Ernest McCulloch and James Till were transplanting bone marrow to treat irradiated mice when they noticed it caused lumps in the mices spleens, and the number of lumps correlated with the cellular dosage. Their lab subsequently demonstrated that each lump was a clonal colony from a single donor cell, and a subset of those cells was self-renewing and could form further colonies of any blood cell type. They had discovered hematopoietic stem cells. In 1981 the first embryonic stem cells (ESCs) from mice were successfully propagated in culture by British biologist Martin Evans, winning him the Nobel Prize in 2007. This breakthrough allowed biologists to alter genes in ESCs, then use Gurdons technique to create transgenic mice with that alteration in every cellcreating the first animal models of disease.

In 1982, one year after Evans discovery, Hopkinson graduated with honors from York University. She worked in the arts, as a library clerk, government culture research officer, and grants officer for the Toronto Arts Council, but wouldnt begin publishing her own fiction until she was 34. [I had been] politicized by feminist and Caribbean literature into valuing writing that spoke of particular cultural experiences of living under colonialism/patriarchy, and also of writing in ones own vernacular speech, Hopkinson said. In other words, I had models for strong fiction, and I knew intimately the body of work to which I would be responding. Then I discovered that Delany was a black man, which opened up a space for me in SF/F that I hadnt known I needed. She sought out more science fiction by black authors and found Butler, Charles Saunders, and Steven Barnes. Then the famous feminist science fiction author and editor Judy Merril offered an evening course in writing science fiction through a Toronto college, Hopkinson said. The course never ran, but it prompted me to write my first adult attempt at a science fiction story. Judy met once with the handful of us she would have accepted into the course and showed us how to run our own writing workshop without her. Hopkinsons dream of attending Clarion came true in 1995, with Delany as an instructor. Her early short stories channeled her love of myth and folklore, and her first book, written in Caribbean dialect, married Caribbean myth to the science fictional trappings of black market organ harvesting. Brown Girl in the Ring (1998) follows a young single mother as shes torn between her ancestral culture and modern life in a post-economic collapse Toronto. It won the Aspect and Locus Awards for Best First Novel, and Hopkinson was awarded the John W. Campbell Award for Best New Writer.

In 1996, Dolly the Sheep was created using Gurdons technique to determine if mammalian cells also could revert to more a more primitive, pluripotent state. Widespread animal cloning attempts soon followed, (something Hopkinson used as a science fictional element in Brown Girl) but it was inefficient, and often produced abnormal animals. Ideas of human cloning captured the public imagination as stem cell research exploded onto the scene. One ready source for human ESC (hESC) materials was from embryos which would otherwise be destroyed following in vitro fertilization (IVF) but the U.S. passed the Dickey-Wicker Amendment prohibited federal funding of research that destroyed such embryos. Nevertheless, in 1998 Wisconsin researcher James Thomson, using private funding, successfully isolated and cultured hESCs. Soon after, researchers around the world figured out how to nudge cells down different lineages, with ideas that transplant rejection and genetic disease would soon become things of the past, sliding neatly into the hole that the failure of genetic engineering techniques had left behind. But another blow to the stem cell research community came in 2001, when President Bushs stem cell ban limited research in the U.S. to nineteen existing cell lines.

In the late 1990s, another piece of technology capturing the public imagination was the internet, which promised to bring the world together in unprecedented ways. One such way was through private listservs, the kind used by writer and academic Alondra Nelson to create a space for students and artists to explore Afrofuturist ideas about technology, space, freedom, culture and art with science fiction at the center. It was wonderful, Hopkinson said. It gave me a place to talk and debate with like-minded people about the conjunction of blackness and science fiction without being shouted down by white men or having to teach Racism 101. Connections create communities, which in turn create movements, and in 1999, Delanys essay, Racism and Science Fiction, prompted a call for more meaningful discussions around race in the SF community. In response, Hopkinson became a co-founder of the Carl Brandon society, which works to increase awareness and representation of people of color in the community.

Hopkinsons second novel, Robber, was a breakthrough success and was nominated for Hugo, Nebula, and Tiptree Awards. She would also release Skin Folk (2001), a collection of stories in which mythical figures of West African and Afro-Caribbean culture walk among us, which would win the World Fantasy Award and was selected as one ofThe New York Times Best Books of the Year. Hopkinson also obtained masters degree in fiction writing (which helped alleviate U.S. border hassles when traveling for speaking engagements) during which she wrote The Salt Roads (2003). I knew it would take a level of research, focus and concentration I was struggling to maintain, Hopkinson said. I figured it would help to have a mentor to coach me through it. That turned out to be James Morrow, and he did so admirably. Roads is a masterful work of slipstream literary fantasy that follows the lives of women scattered through time, bound together by the salt uniting all black life. It was nominated for a Nebula and won the Gaylactic Spectrum Award. Hopkinson also edited anthologies centering around different cultures and perspectives, including Whispers from the Cotton Tree Root: Caribbean Fabulist Fiction (2000), Mojo: Conjure Stories (2003), and So Long, Been Dreaming: Postcolonial Science Fiction & Fantasy (2004). She also came out with the award-winning novelThe New Moons Arms in 2007, in which a peri-menopausal woman in a fictional Caribbean town is confronted by her past and the changes she must make to keep her family in her life.

While the stem cell ban hamstrung hESC work, Gurdons research facilitated yet another scientific breakthrough. Researchers began untangling how gene expression changed as stem cells differentiated, and in 2006, Shinya Yamanaka of Kyoto University reported the successful creation of mouse stem cells from differentiated cells. Using a list of 24 pluripotency-associated genes, Yamanaka systematically tested different gene combinations on terminally differentiated cells. He found four genesthereafter known as Yamanaka factorsthat could turn them into induced-pluripotent stem cells (iPSCs), and he and Gurdon would share a 2012 Nobel prize. In 2009, President Obama lifted restrictions on hESC research, and the first clinical trial involving products made using stem cells happened that year. The first human trials using hESCs to treat spinal injuries happened in 2014, and the first iPSC clinical trials for blindness began this past December.

Hopkinson, too, encountered complications and delays at points in her career. For years, Hopkinson suffered escalating symptoms from fibromyalgia, a chronic disease that runs in her family, which interfered with her writing, causing Hopkinson and her partner to struggle with poverty and homelessness. But in 2011, Hopkinson applied to become a professor of Creative Writing at the University of California, Riverside. It seemed in many ways tailor-made for me, Hopkinson said. They specifically wanted a science fiction writer (unheard of in North American Creative Writing departments); they wanted someone with expertise working with a diverse range of people; they were willing to hire someone without a PhD, if their publications were sufficient; they were offering the security of tenure. She got the job, and thanks to a steady paycheck and the benefits of the mild California climate, she got back to writing. Her YA novel, The Chaos (2012), coming-of-age novelSister Mine (2013), and another short story collection, Falling in Love with Hominids (2015) soon followed. Her recent work includes House of Whispers (2018-present), a series in DC Comics Sandman Universe, the final collected volume of which is due out this June. Hopkinson also received an honorary doctorate in 2016 from Anglia Ruskin University in the U.K., and was Guest of Honor at 2017 Worldcon, a year in which women and people of color dominated the historically white, male ballot.

While the Yamanaka factors meant that iPSCs became a standard lab technique, iPSCs are not identical to hESCs. Fascinatingly, two of these factors act together to maintain the silencing of large swaths of DNA. Back in the 1980s, researchers discovered that some regions of DNA are modified by small methyl groups, which can be passed down through cell division. Different cell types have different DNA methylation patterns, and their distribution is far from random; they accumulate in the promoter regions just upstream of genes where their on/off switches are, and the greater the number of methyl groups, the lesser the genes expression. Furthermore, epigenetic modifications, like methylation, can be laid down by our environments (via diet, or stress) which can also be passed down through generations. Even some diseases, like fibromyalgia, have recently been implicated as such an epigenetic disease. Turns out that the long-standing biological paradigm that rejected Lamarck also missed the bigger picture: Nature is, in fact, intimately informed by nurture and environment.

In the past 150 years, we have seen ideas of community grow and expand as the world became more connected, so that they now encompass the globe. The histories of science fiction and biology are full of stories of pioneers opening new doorsbe they doors of greater representation or greater understanding, or bothand others following. If evolution has taught us anything, its that nature abhors a monoculture, and the universe tends towards diversification; healthy communities are ones which understand that we are not apart from the world, but of it, and that diversity of types, be they cells or perspectives, is a strength.

Kelly Lagor is a scientist by day and a science fiction writer by night. Her work has appeared at Tor.com and other places, and you can find her tweeting about all kinds of nonsense @klagor

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On the Origins of Modern Biology and the Fantastic: Part 19 Nalo Hopkinson and Stem Cell Research - tor.com

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Trusted Business Insights answers what are the scenarios for growth and recovery and whether there will be any lasting structural impact from the unfolding crisis for the Cell Therapy market.

Trusted Business Insights presents an updated and Latest Study on Cell Therapy Market 2019-2026. The report contains market predictions related to market size, revenue, production, CAGR, Consumption, gross margin, price, and other substantial factors. While emphasizing the key driving and restraining forces for this market, the report also offers a complete study of the future trends and developments of the market.The report further elaborates on the micro and macroeconomic aspects including the socio-political landscape that is anticipated to shape the demand of the Cell Therapy market during the forecast period (2019-2029).It also examines the role of the leading market players involved in the industry including their corporate overview, financial summary, and SWOT analysis.

Get Sample Copy of this Report @ Cell Therapy Market Size, Share, Market Research and Industry Forecast Report, 2020-2027 (Includes Business Impact of COVID-19)

Industry Insights, Market Size, CAGR, High-Level Analysis: Cell Therapy Market

The global cell therapy market size was valued at USD 5.8 billion in 2019 and is projected to witness a CAGR of 5.4% during the forecast period. The development of precision medicine and advancements in Advanced Therapies Medicinal Products (ATMPS) in context to their efficiency and manufacturing are expected to be the major drivers for the market. In addition, automation in adult stem cell and cord blood processing and storage are the key technological advancements that have supported the growth of the market for cell therapy.The investment in technological advancements for decentralizing manufacturing of this therapy is anticipated to significantly benefit the market. Miltenyi Biotec is one of the companies that has contributed to the decentralization in manufacturing through its CliniMACS Prodigy device. The device is an all-in-one automated manufacturing system that exhibits the capability of manufacturing various cell types.

An increase in financing and investments in the space to support the launch of new companies is expected to boost the organic revenue growth in the market for cell therapy. For instance, in July 2019, Bayer invested USD 215 million for the launch of Century Therapeutics, a U.S.-based biotechnology startup that aimed at developing therapies for solid tumors and blood cancer. Funding was further increased to USD 250 billion by a USD 35 million contribution from Versant Ventures and Fujifilm Cellular Dynamics.The biomanufacturing companies are working in collaboration with customers and other stakeholders to enhance the clinical development and commercial manufacturing of these therapies. Biomanufacturers and OEMs such as GE healthcare are providing end-to-end flexible technology solutions to accelerate the rapid launch of therapies in the market for cell therapy.The expanding stem cells arena has also triggered the entry of new players in the market for cell therapy. Celularity, Century Therapeutics, Rubius Therapeutics, ViaCyte, Fate Therapeutics, ReNeuron, Magenta Therapeutics, Frequency Therapeutics, Promethera Biosciences, and Cellular Dynamics are some startups that have begun their business in this arena lately.Use-type InsightsThe clinical-use segment is expected to grow lucratively during the forecast period owing to the expanding pipeline for therapies. The number of cancer cellular therapies in the pipeline rose from 753 in 2018 to 1,011 in 2019, as per Cancer Research Institute (CRI). The major application of stem cell treatment is hematopoietic stem cell transplantation for the treatment of the immune system and blood disorders for cancer patients.In Europe, blood stem cells are used for the treatment of more than 26,000 patients each year. These factors have driven the revenue for malignancies and autoimmune disorders segment. Currently, most of the stem cells used are derived from bone marrow, blood, and umbilical cord resulting in the larger revenue share in this segment.On the other hand, cell lines, such as Induced Pluripotent Stem Cells (iPSC) and human Embryonic Stem Cells (hESC) are recognized to possess high growth potential. As a result, a several research entities and companies are making significant investments in R&D pertaining to iPSC- and hESC-derived products.TherapyType Insights of Cell Therapy Market

An inclination of physicians towards therapeutic use of autologous and allogeneic cord blood coupled with rising awareness about the use of cord cells and tissues across various therapeutic areas is driving revenue generation. Currently, the allogeneic therapies segment accounted for the largest share in 2019 in the cell therapy market. The presence of a substantial number of approved products for clinical use has led to the large revenue share of this segment.

Furthermore, the practice of autologous tissue transplantation is restricted by the limited availability of healthy tissue in the patient. Moreover, this type of tissue transplantation is not recommended for young patients wherein tissues are in the growth and development phase. Allogeneic tissue transplantation has effectively addressed the above-mentioned challenges associated with the use of autologous transplantation.However, autologous therapies are growing at the fastest growth rate owing to various advantages over allogeneic therapies, which are expected to boost adoption in this segment. Various advantages include easy availability, no need for HLA-matched donor identification, lower risk of life-threatening complications, a rare occurrence of graft failure, and low mortality rate.

Regional Insights of Cell Therapy Market

The presence of leading universities such as the Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, and Yale Stem Cell Center that support research activities in U.S. is one of the key factor driving the market for cell therapy in North America. Moreover, strong regulatory and financing support from the federal bodies for expansion of this arena in U.S. as well as Canada is driving the market.In Asia Pacific, the market is anticipated to emerge as a lucrative source of revenue owing to the availability of therapies at lower prices coupled with growing awareness among the healthcare entities and patients pertaining the potential of these therapies in chronic disease management. Japan is leading the Asian market for cell therapy, which can be attributed to its fast growth as a hub for research on regenerative medicine.Moreover, the Japan government has recognized regenerative medicine and cell therapy as a key contributor to the countrys economic growth. This has positively influenced the attention of global players towards the Asian market, thereby driving marketing operations in the region.

Market Share Insights of Cell Therapy Market

Some key companies operating in this market for cell therapy are Fibrocell Science, Inc.; JCR Pharmaceuticals Co. Ltd.; Kolon TissueGene, Inc.; PHARMICELL Co., Ltd.; Osiris Therapeutics, Inc.; MEDIPOST; Cells for Cells; NuVasive, Inc.; Stemedica Cell Technologies, Inc.; Vericel Corporation; and ANTEROGEN.CO.,LTD. These companies are collaborating with the blood centers and plasma collection centers in order to obtain cells for use in therapeutics development.Several companies have marked their presence in the market by acquiring small and emerging therapy developers. For instance, in August 2019, Bayer acquired BlueRock Therapeutics to establish its position in the market for cell therapy. BlueRock Therapeutics is a U.S. company that relies on a proprietary induced pluripotent stem cell (iPSC) platform for cell therapy development.Several companies are making an entry in the space through the Contract Development and Manufacturing Organization (CDMO) business model. For example, in April 2019, Hitachi Chemical Co. Ltd. acquired apceth Biopharma GmbH to expand its global footprint in the CDMO market for cell and gene therapy manufacturing.

Segmentations, Sub Segmentations, CAGR, & High-Level Analysis overview of Cell Therapy Market Research ReportThis report forecasts revenue growth at global, regional, and country levels and provides an analysis of the latest industry trends in each of the sub-segments from 2019 to 2030. For the purpose of this study, this market research report has segmented the global cell therapy market on the basis of use-type, therapy-type, and region:

Use-Type Outlook (Revenue, USD Million, 2019 2030)

Clinical-use

By Therapeutic Area

Malignancies

Musculoskeletal Disorders

Autoimmune Disorders

Dermatology

Others

By Cell Type

Stem Cell Therapies

BM, Blood, & Umbilical Cord-derived Stem Cells

Adipose derived cells

Others

Non-stem Cell Therapies

Research-use

Therapy Type Outlook (Revenue, USD Million, 2019 2030)

Allogeneic Therapies

Autologous Therapies

Quick Read Table of Contents of this Report @ Cell Therapy Market Size, Share, Market Research and Industry Forecast Report, 2020-2027 (Includes Business Impact of COVID-19)

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