When young athletes experiences sudden cardiac death as they run down the playing field, it's usually due to arrhythmogenic cardiomyopathy (ACM), an inherited heart disease. Now, Johns Hopkins researchers have shed new light on the role of the immune system in the progression of ACM and, in the process, discovered a new drug that might help prevent ACM disease symptoms and progression to heart failure in some patients.

"We realized that heart muscle inflammation in ACM is much more complicated than we thought, but also might provide a therapeutic strategy," saysStephen Chelko, Ph.D., assistant professor of medicine at the Johns Hopkins University School of Medicine and senior author of the new paper, inSept. inCirculation.

In ACM, patients often harbor mutations in any of the five genes that make up the cardiac desmosome -- the gluelike material that holds heart cells together and helps coordinate mechanical and electrical synchronization of heart cells. Because of this, it's often called "a disease of the cardiac desmosome." In patients with ACM, heart cells pull apart over time, and these cells are replaced with damaged and inflamed scar tissue. These scars can increase risk of instances of irregular heart rhythms and lead to sudden cardiac death if the scar tissue causes the heart wall to stiffen and renders it unable to pump.

If a person is aware they carry an ACM-causing genetic mutation, doctors help them avoid cardiac death through lifestyle changes, such as exercise restriction, and medications that keep their heart rate low. However, there are currently no drugs that treat the underlying structural defects of the desmosome. People who live for many years with ACM still accumulate scar tissue and inflammation in their hearts, leading to chronic heart disease.

"We tended in the past to view ACM as something that kills due to a sudden arrhythmic event," said Chelko. "But now we're starting to also see it as a chronic inflammatory disease that can progress more slowly over time, leading to heart failure."

Chelko and his colleagues wanted to determine the molecular cause of inflammation in the hearts of people with ACM. So they studied mice with an ACM-causing mutation, as well as heart muscle cells generated from stem cells isolated from an ACM patient. They found that the inflammation associated with the disease arose from two separate causes. First, they noticed high levels of macrophages, a type of immune cell that's normally found at sites of inflammation, such as around cuts or scrapes that are healing.

"Macrophages are usually the good guys who help heal a wound and then leave," said Chelko. "But in ACM they're permanently setting up shop in the heart, which, over time, reduces its function."

Chelko's team also found that in ACM, the heart cells themselves are triggered by a protein known as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-B) to produce chemicals called cytokines, which act as homing beacons for other inflammatory cells and molecules. When the researchers treated mice or isolated cells with a drug blocking NF-B, heart cells stopped producing many of these cytokines, leading to decreased inflammation and infiltration of inflammatory cells. In mouse models of ACM, animals treated with the NF-B-blocking drug Bay-11-7082 had a twofold increase in heart function, measured by how much blood their hearts could pump over time compared with untreated ACM animals. They also had a twofold reduction of damaged and inflammatory scar tissue in the heart.

More than one-third of patients with ACM who die of sudden cardiac death have no previous cardiac symptoms, so wouldn't ever know to seek treatment. However, for relatives of these people who discover that they carry a genetic mutation causing ACM -- or those who discover the mutation for other reasons -- a drug could help stave off long-term heart disease, Chelko said.

While the Bay-11-7082 drug is currently only used in the lab for experimental purposes, the U.S. Food and Drug Administration has approved canakinumab, a drug that targets the same inflammatory pathway, for use in juvenile arthritis and a collection of rare auto-inflammatory syndromes. Canakinumab is also being studied for use in coronary artery disease. Chelko's group is now investigating whether this drug would have the same effect as Bay-11-7082 in ACM.

"We're very excited to have found an FDA-approved drug that can reduce heart inflammation in ACM, and we're eager to do more research to ultimately help those who carry these genetic mutations," said Chelko.

Reference:Chelko, et al. (2019) Therapeutic Modulation of the Immune Response in Arrhythmogenic Cardiomyopathy. Circulation. DOI:https://doi.org/10.1161/CIRCULATIONAHA.119.040676

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

View post:
Drug Treats Inflammation Related to Genetic Heart Disease - Technology Networks

Cardiac Stem Cells Comments Off on Drug Treats Inflammation Related to Genetic Heart Disease – Technology Networks | October 18th, 2019

Mediating systemic health

Sphingosine 1-phosphate (S1P) is an important circulating lipid mediator that is derived from the metabolism of cell membranes. Its diverse homeostatic roles, particularly in immunology and vascular biology, can go awry in numerous diseases, including multiple sclerosis, cardiovascular diseases, and fibrosis. The centrality of S1P signaling has led to the development of several drugs, including two approved for treatment of multiple sclerosis. In a Review, Cartier and Hla discuss the current understanding of how one mediator can carry out so many signaling roles in different tissues, how these become dysregulated in disease, and efforts in drug development to target S1P signaling.

Science, this issue p. eaar5551

Sphingosine 1-phosphate (S1P), a product of membrane sphingolipid metabolism, is secreted and acts through G proteincoupled S1P receptors (S1PRs) in vertebrates. S1PR isoforms mediate complex cellular actions either alone or in combination in most organ systems. This stable lysolipid circulates as a complex with protein chaperones that not only enables aqueous solubility but also helps facilitate specific modes of receptor signaling. However, differential concentration gradients of S1P are normally present in various compartments and are perturbed under disease conditions. The abundance of circulatory S1P and the high expression of S1PRs in exposed cellsthat is, vascular and hematopoietic cellsposes a key question of how this signaling axis is regulated. This question is of clinical relevance because the first S1PR-targeted drug, fingolimod, has been approved for the treatment of multiple sclerosis since 2010. Recent findings from basic research as well as insights gleaned from clinical and translational studies have enriched our understanding of how this simple lysolipid evolved as a complex regulator of multiple physiological systems and, when dysregulated, contributes to numerous diseases.

Extracellular spatial gradients of S1P, demonstrated by using S1P reporters, are tightly regulated and control fundamental processes such as hematopoietic cell trafficking, immune cell fate, and vascular integrity. The gradients are formed through location-specific function of metabolic enzymes, S1P transporters, and chaperones. Such physiological S1P gradients are altered in diseases, thus contributing to conditions such as inflammation, autoimmunity, and vascular dysfunction. S1P complexed to chaperone proteinsfor example, high-density lipoproteinbound apolipoprotein Mmediate distinct modes of receptor activation, resulting in biased receptor signaling and specific biological outcomes. S1PRs are also regulated tightly through endocytic mechanisms and receptor modulators that enhance or inhibit signal strength and duration. Various signaling mechanisms of this simple lysolipid mediator has helped reveal its multiple actions in the immune system, which include adaptive immune cell localization in various compartments (egress versus retention), fate switching, survival, and activation that influences both cell-mediated and humoral immunity. In the cardiovascular system, high expression of multiple S1PR isoforms in various cell types regulate development, homeostasis, and physiology. Current S1PR-targeted drugs that aim to tame autoimmunity exhibit considerable cardiovascular-adverse events. In the central nervous system (CNS), widespread application of S1PR-targeted drugs in autoimmune neuroinflammatory diseases has stimulated research that revealed the broad but poorly understood effects of S1P signaling in neurodevelopment, the neurovascular unit, neurons, and glia. Furthermore, in addition to the involvement of pathological S1P signaling in acute ischemic conditions of various organs, chronic dysregulated S1P signaling has been implicated in fibrotic diseases of lung, heart, liver, and kidney.

Considerable challenges remain to fully harness the new knowledge in S1P pathobiology to translational utility in clinical medicine. Approaches that mimic S1P chaperones, S1P neutralizing agents, modulation of transporters, biased agonists and antagonists of S1PR isotypes, and sphingolipid metabolic enzyme modulators provide viable pathways to therapy. Focusing on the immune system, such approaches may widen the autoimmunity therapeutic landscape and provide new directions in cancer and chronic inflammatory diseases. For cardiovascular diseases, ischemic conditions as well as chronic heart failure are likely candidates for future translational efforts. Although further work is needed, S1P-targeted approaches may also be useful in regenerative therapies for the aging and diseased myocardium. The CNS-targeted efforts may cross into neurodegenerative diseases, given the success with S1PR-targeted drugs in reducing brain atrophy in multiple sclerosis. Other potential applications include approaches in pain management and neurodevelopmental disorders. Such strategies, although challenging, are greatly helped by findings from basic research on S1P pathobiology as well as pharmacological and clinical insights derived from the application of S1P-targeted therapeutics.

Extracellular S1P gradients created by transporters, chaperones (ApoM+HDL), and metabolic enzymes (LPP3) interact with S1PRs on the cell surface. Receptor activity, transmitted by means of G proteins, is regulated by multiple mechanisms, including -arrestin coupling, endocytosis, and receptor modulators. The resultant cellular changes influence multiple organ systems in physiology and disease.

Sphingosine 1-phosphate (S1P), a metabolic product of cell membrane sphingolipids, is bound to extracellular chaperones, is enriched in circulatory fluids, and binds to G proteincoupled S1P receptors (S1PRs) to regulate embryonic development, postnatal organ function, and disease. S1PRs regulate essential processes such as adaptive immune cell trafficking, vascular development, and homeostasis. Moreover, S1PR signaling is a driver of multiple diseases. The past decade has witnessed an exponential growth in this field, in part because of multidisciplinary research focused on this lipid mediator and the application of S1PR-targeted drugs in clinical medicine. This has revealed fundamental principles of lysophospholipid mediator signaling that not only clarify the complex and wide ranging actions of S1P but also guide the development of therapeutics and translational directions in immunological, cardiovascular, neurological, inflammatory, and fibrotic diseases.

Link:
Sphingosine 1-phosphate: Lipid signaling in pathology and therapy - Science Magazine

Cardiac Stem Cells Comments Off on Sphingosine 1-phosphate: Lipid signaling in pathology and therapy – Science Magazine | October 18th, 2019

Sudden Infant Death Syndrome (SIDS), sometimes known as crib death, occurs when an infant under the age of one dies inexplicably.The typically healthy child will often die while sleeping and is the leading cause of death of children between the ages of one month and one year, claiming approximately 3000 lives a year. There has been little known about the cause of SIDS but new research is now showing that some form of SIDS could be linked to a genetic inability to digest milk.

A study out of theUniversity of Washington School of Medicine focused on the "mitochondrial tri-functional protein deficiency, a potentially fatal cardiac metabolic disorder caused by a genetic mutation in the gene HADHA."

It found that newborns with had the genetic mutation are unable toproperly digest some of the fats found in breastmilk, resulting in cardiac arrest. It found that "the heart cells of affected infants do not convert fats into nutrients properly," and once these fats build up they can cause serious heart and heart health issues.

There are multiple causes for sudden infant death syndrome, said Hannele Ruohola-Baker, who is also associate director of the UW Medicine Institute for Stem Cell and Regenerative Medicine. There are some causes which are environmental. But what were studying here is really a genetic cause of SIDS. In this particular case, it involves a defect in the enzyme that breaks down fat.

Lead author on the study Dr. Jason Miklassaid that it was his experience researching heart disease that prompted him to look at the possible link with SIDS. There was one particular study that had noted a link between children who had problems processing fats and who also had cardiac disease that caused him to delve a little deeper.

Miklas andRuohola-Baker teamed up to begin their own research study.If a child has a mutation, depending on the mutation the first few months of life can be very scary as the child may die suddenly,Miklas noted. An autopsy wouldnt necessarily pick up why the child passed but we think it might be due to the infants heart-stopping to beat.

Were no longer just trying to treat the symptoms of the disease, Miklas added. Were trying to find ways to treat the root problem. Its very gratifying to see that we can make real progress in the lab toward interventions that could one day make their way to the clinic.

Ruohola-Baker says their findings are a big breakthrough in understanding SIDS. There is no cure for this, she said. But there is now hope because weve found a new aspect of this disease that will innovate generations of novel small molecules and designed proteins, which might help these patients in the future.

Read Next:Babies May Not Be 'Designed' For Sleeping, According To SIDS Expert

Tags:study,SIDS

Jill Duggar's Husband Seems To Take Aim At Josh Duggar Years After Scandal

See original here:
SIDS May Be Linked To A Genetic Inability To Digest Milk, Study Finds - Moms

Cardiac Stem Cells Comments Off on SIDS May Be Linked To A Genetic Inability To Digest Milk, Study Finds – Moms | October 18th, 2019

Every week there are numerous scientific studies published. Heres a look at some of the more interesting ones.

Mutation Found in Dark Matter of the Genome New Target for Cancer

The so-called dark matter of the genome is the non-coding regions that make up about 98% of the genome. Researchers at the Ontario Institute for Cancer Research (OICR) recently identified a novel cancer-driven mutation in this region that is linked to brain, liver and blood cancer. They published the two studies in the journal Nature.

Non-coding DNA, which makes up 98% of the genome, is notoriously difficult to study and is often overlooked since it does not code for proteins, said Lincoln Stein, co-lead of the two research studies and Head of Adaptive Oncology at OICR. By carefully analyzing these regions, we have discovered a change in one letter of the DNA code that can drive multiple types of cancer. In turn, weve found a new cancer mechanism that we can target to tackle the disease.

The mutation is dubbed U1-snRNA, and it appears to disrupt normal RNA splicing, which changes the transcription of genes that drive cancer. The mutation was identified in tumors of patients with specific subtypes of brain cancer and was found in almost all of the samples. The cancer was sonic hedgehog medulloblastoma. It was also found in samples of chronic lymphocytic leukemia (CLL) and hepatocellular carcinoma.

Our unexpected discovery uncovered an entirely new way to target these cancers that are tremendously difficult to treat and have high mortality rates, said Michael Taylor, pediatric neurosurgeon and senior scientist in Development and Stem Cell Biology and Garron Family Chair in in Childhood Cancer Research at The Hospital for Sick Children and co-lead of the studies. Weve found that with one typo in the DNA code, the resultant cancers have hundreds of mutant proteins that we might be able to target using currently available immunotherapies.

Diagnosing Lyme Disease in 15 Minutes

About 300,000 people are diagnosed with Lyme disease each year. Borrelia burgdorferi is transmitted by the bite of infected Ixodes ticks, and if untreated, can cause neurologic, cardiac, and rheumatologic complications. Current testing involves two complex tests, ELISA and western blot. Researchers have developed a rapid microfluidic test that can provide comparable results in as little as 15 minutes. It will require more refinement and testing before widespread use.

Gene Therapy for Wet Age-Related Macular Degeneration Shows Promise

Research was recently presented on six patients who received a gene therapy for wet age-related macular degeneration (AMD). The patients have gone at least six months without continued injections for the disease that were previously required every four to six weeks. The therapy, which is injected into the eye, generates a molecule much like aflibercept, a broadly used anti-VEGF drug.

How Dementia Spreads Throughout Brain Networks

Frontotemporal dementia (FDT) is similar to Alzheimers disease, but tends to hit patients earlier and affects different parts of the brain. Researchers studied how well neural network maps made from brain scans in healthy people could predict the spread of brain atrophy in FTD patients over several years. They recruited 42 patients at the UCSF Memory and Aging Center with a form of FTD and 30 with another form. They received MRI scans and then follow-up scans a year later to determine how the disease had progressed. They found that the standardized connectivity maps were able to predict the spread of the disease.

Mucus and Microbes: A Therapeutic Gold Mine.

A specific type of molecule called glycans that are found in mucus prevent bacteria from communicating with each other. Mucus also prevents the bacteria from forming infectious biofilms. It is also pointed out that more than 200 square meters of our bodies are lined with mucus. There are hundreds of different types of glycans found in mucus, and most of them are responsible for suppressing bacteria. Katharina Ribbeck, a professor at the Massachusetts Institute of Technology, says, What we have in mucus is a therapeutic gold mine.

Mechanisms that Regulate Brain Inflammation

The role of brain inflammation in diseases like Alzheimers and Parkinsons is becoming better understood. Researchers recently identified mechanisms that regulate brain inflammation, which has the potential to open new avenues for treating and preventing these diseases. The scientists found that a protein called TET2 modulates the immune response in microglia, immune cells in the brain, during inflammation. In mice engineered not to have TET2 in the microglia, neuroinflammation is reduced. Normally, TET2 with other proteins regulates the activity of genes by removing specific chemical markers from DNA, but TET2 appears to behave differently in microglia.

Pilot Study: Even Short-Term Vaping Causes Lung Inflammation

Research out of The Ohio State University Comprehensive Cancer Center found cellular inflammation was caused by e-cigarette, i.e., vaping, use in both long-term smokers and people who did not smoke. They used bronchoscopy to evaluate for inflammation and smoking-related effects and found a measurable increase in inflammation after only four weeks of vaping without nicotine or flavors. The amount of inflammation was small compared to the control group, but the data suggests that even short-term use can result in inflammatory changes at a cellular level. Inflammation in smoking is a driver of lung cancer and other respiratory diseases.

Read the original:
Research Roundup: Genomic Dark Matter Mutation and More - BioSpace

Cardiac Stem Cells Comments Off on Research Roundup: Genomic Dark Matter Mutation and More – BioSpace | October 18th, 2019

KENILWORTH, N.J.--(BUSINESS WIRE)--Merck (NYSE: MRK), known as MSD outside the United States and Canada, today announced that the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency has adopted a positive opinion recommending approval of two regimens of KEYTRUDA, Mercks anti-PD-1 therapy, for the first-line treatment of metastatic or unresectable recurrent head and neck squamous cell carcinoma (HNSCC). KEYTRUDA, as monotherapy or in combination with platinum and 5-fluorouracil (5-FU) chemotherapy, is recommended in patients whose tumors express PD-L1 (combined positive score [CPS] 1). This recommendation is based on data from the pivotal Phase 3 KEYNOTE-048 trial, in which KEYTRUDA, as monotherapy and in combination with chemotherapy, demonstrated a significant improvement in overall survival, compared with standard treatment (cetuximab with carboplatin or cisplatin plus 5-FU), in these patient populations.

Head and neck cancer remains a devastating disease with poor long-term outcomes and advances in survival have been difficult to achieve for more than 10 years said Dr. Jonathan Cheng, vice president, clinical research, Merck Research Laboratories. The positive EU CHMP opinion further validates the potential of KEYTRUDA, as monotherapy and in combination with chemotherapy, to help patients and address the high unmet need in this aggressive form of head and neck cancer.

Merck currently has the largest immuno-oncology clinical development program in HNSCC and is continuing to advance multiple registration-enabling studies investigating KEYTRUDA as monotherapy and in combination with other cancer treatmentsincluding, KEYNOTE-412 and KEYNOTE-689. The CHMPs recommendation will now be reviewed by the European Commission for marketing authorization in the EU, and a final decision is expected in the fourth quarter of 2019.

About Head and Neck CancerHead and neck cancer describes a number of different tumors that develop in or around the throat, larynx, nose, sinuses and mouth. Most head and neck cancers are squamous cell carcinomas that begin in the flat, squamous cells that make up the thin surface layer of the structures in the head and neck. Two substances that greatly increase the risk of developing head and neck cancer are tobacco and alcohol. It is estimated that there were more than 705,000 new cases of head and neck cancer diagnosed and over 358,000 deaths from the disease worldwide in 2018. In Europe, it is estimated that there were more than 146,000 newly diagnosed cases of head and neck cancer and around 66,000 deaths from the disease in 2018.

About KEYTRUDA (pembrolizumab) InjectionKEYTRUDA 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 1,000 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 patients likelihood of benefitting from treatment with KEYTRUDA, including exploring several different biomarkers.

About KEYTRUDA (pembrolizumab) InjectionKEYTRUDA 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 1,000 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 patients likelihood of benefitting from treatment with KEYTRUDA, including exploring several different biomarkers.

Selected KEYTRUDA (pembrolizumab) IndicationsMelanomaKEYTRUDA 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 CancerKEYTRUDA, 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 CancerKEYTRUDA 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 one 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 CancerKEYTRUDA, 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 HNSCC with disease progression on or after platinum-containing chemotherapy.

Classical Hodgkin LymphomaKEYTRUDA 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 LymphomaKEYTRUDA 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 the treatment of patients with PMBCL who require urgent cytoreductive therapy.

Urothelial CarcinomaKEYTRUDA 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 [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 the 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.

Microsatellite Instability-High (MSI-H) CancerKEYTRUDA 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 CancerKEYTRUDA 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 CancerKEYTRUDA 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 CancerKEYTRUDA 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 CarcinomaKEYTRUDA 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 CarcinomaKEYTRUDA is indicated for the treatment of adult and pediatric patients with recurrent locally advanced or metastatic Merkel cell carcinoma. 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 CarcinomaKEYTRUDA, 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 PneumonitisKEYTRUDA 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 Grade 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 ColitisKEYTRUDA 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 HepatitisKEYTRUDA 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 AxitinibKEYTRUDA 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 EndocrinopathiesKEYTRUDA can cause hypophysitis, thyroid disorders, and type 1 diabetes mellitus. 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 hypophysitis (including hypopituitarism and adrenal insufficiency), thyroid function (prior to and periodically during treatment), and hyperglycemia. For hypophysitis, administer corticosteroids and hormone replacement as clinically indicated. Withhold KEYTRUDA for Grade 2 and withhold or discontinue for Grade 3 or 4 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 DysfunctionKEYTRUDA 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 ReactionsImmune-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 ReactionsImmune-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 cHL, 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 ReactionsKEYTRUDA 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 MyelomaIn 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 ToxicityBased 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 ReactionsIn 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-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; 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%).

In KEYNOTE-052, KEYTRUDA was discontinued due to adverse reactions in 11% of 370 patients with locally advanced or metastatic urothelial carcinoma. Serious adverse reactions occurred in 42% of patients; those 2% were urinary tract infection, hematuria, acute kidney injury, pneumonia, and urosepsis. The most common adverse reactions (20%) were fatigue (38%), musculoskeletal pain (24%), decreased appetite (22%), constipation (21%), rash (21%), and diarrhea (20%).

In KEYNOTE-045, KEYTRUDA was discontinued due to adverse reactions in 8% of 266 patients with locally advanced or metastatic urothelial carcinoma. The most common adverse reaction resulting in permanent discontinuation of KEYTRUDA was pneumonitis (1.9%). Serious adverse reactions occurred in 39% of KEYTRUDA-treated patients; those 2% were urinary tract infection, pneumonia, anemia, and pneumonitis. The most common adverse reactions (20%) in patients who received KEYTRUDA were fatigue (38%), musculoskeletal pain (32%), pruritus (23%), decreased appetite (21%), nausea (21%), and rash (20%).

Adverse reactions occurring in patients with gastric cancer were similar to those occurring in patients with melanoma or NSCLC who received KEYTRUDA as a monotherapy.

Adverse reactions occurring in patients with esophageal cancer were similar to those occurring in patients with melanoma or NSCLC who received KEYTRUDA as a monotherapy.

In KEYNOTE-158, KEYTRUDA was discontinued due to adverse reactions in 8% of 98 patients with recurrent or metastatic cervical cancer. Serious adverse reactions occurred in 39% of patients receiving KEYTRUDA; the most frequent included anemia (7%), fistula, hemorrhage, and infections [except urinary tract infections] (4.1% each). The most common adverse reactions (20%) were fatigue (43%), musculoskeletal pain (27%), diarrhea (23%), pain and abdominal pain (22% each), and decreased appetite (21%).

Adverse reactions occurring in patients with HCC were generally similar to those in patients with melanoma or NSCLC who received KEYTRUDA as a monotherapy, with the exception of increased incidences of ascites (8% Grades 3-4) and immune-mediated hepatitis (2.9%). Laboratory abnormalities (Grades 3-4) that occurred at a higher incidence were elevated AST (20%), ALT (9%), and hyperbilirubinemia (10%).

Among the 50 patients with MCC enrolled in study KEYNOTE-017, adverse reactions occurring in patients with MCC were generally similar to those occurring in patients with melanoma or NSCLC who received KEYTRUDA as a monotherapy. Laboratory abnormalities (Grades 3-4) that occurred at a higher incidence were elevated AST (11%) and hyperglycemia (19%).

In KEYNOTE-426, when KEYTRUDA was administered in combination with axitinib, fatal adverse reactions occurred in 3.3% of 429 patients. Serious adverse reactions occurred in 40% of patients, the most frequent of which (1%) included hepatotoxicity (7%), diarrhea (4.2%), acute kidney injury (2.3%), dehydration (1%), and pneumonitis (1%). Permanent discontinuation due to an adverse reaction occurred in 31% of patients; KEYTRUDA only (13%), axitinib only (13%), and the combination (8%). The most common adverse reactions (>1%) resulting in permanent discontinuation of KEYTRUDA, axitinib or the combination were hepatotoxicity (13%), diarrhea/colitis (1.9%), acute kidney injury (1.6%), and cerebrovascular accident (1.2%). When KEYTRUDA was used in combination with axitinib, the most common adverse reactions (20%) were diarrhea (56%), fatigue/asthenia (52%), hypertension (48%), hepatotoxicity (39%), hypothyroidism (35%), decreased appetite (30%), palmar-plantar erythrodysesthesia (28%), nausea (28%), stomatitis/mucosal inflammation (27%), dysphonia (25%), rash (25%), cough (21%), and constipation (21%).

LactationBecause of the potential for serious adverse reactions in breastfed children, advise women not to breastfeed during treatment and for 4 months after the final dose.

Pediatric UseThere is limited experience in pediatric patients. In a trial, 40 pediatric patients (16 children aged 2 years to younger than 12 years and 24 adolescents aged 12 years to 18 years) with various cancers, including unapproved usages, were administered KEYTRUDA 2 mg/kg every 3 weeks. Patients received KEYTRUDA for a median of 3 doses (range 117 doses), with 34 patients (85%) receiving 2 doses or more. The safety profile in these pediatric patients was similar to that seen in adults; adverse reactions that occurred at a higher rate (15% difference) in these patients when compared to adults under 65 years of age were fatigue (45%), vomiting (38%), abdominal pain (28%), increased transaminases (28%), and hyponatremia (18%).

Mercks Focus on CancerOur goal is to translate breakthrough science into innovative oncology medicines to help people with cancer worldwide. At Merck, the potential to bring new hope to people with cancer drives our purpose and supporting accessibility to our cancer medicines is our commitment. As part of our focus on cancer, Merck is committed to exploring the potential of immuno-oncology with one of the largest development programs in the industry across more than 30 tumor types. We also continue to strengthen our portfolio through strategic acquisitions and are prioritizing the development of several promising oncology candidates with the potential to improve the treatment of advanced cancers. For more information about our oncology clinical trials, visit http://www.merck.com/clinicaltrials.

About MerckFor more than a century, Merck, a leading global biopharmaceutical company known as MSD outside of the United States and Canada, has been inventing for life, bringing forward medicines and vaccines for many of the worlds most challenging diseases. Through our prescription medicines, vaccines, biologic therapies and animal health products, we work with customers and operate in more than 140 countries to deliver innovative health solutions. We also demonstrate our commitment to increasing access to health care through far-reaching policies, programs and partnerships. Today, Merck continues to be at the forefront of research to advance the prevention and treatment of diseases that threaten people and communities around the world - including cancer, cardio-metabolic diseases, emerging animal diseases, Alzheimers disease and infectious diseases including HIV and Ebola. For more information, visit http://www.merck.com and connect with us on Twitter, Facebook, Instagram, YouTube and LinkedIn.

Forward-Looking Statement of Merck & Co., Inc., Kenilworth, N.J., USAThis news release of Merck & Co., Inc., Kenilworth, N.J., USA (the company) includes forward-looking statements within the meaning of the safe harbor provisions of the U.S. Private Securities Litigation Reform Act of 1995. These statements are based upon the current beliefs and expectations of the companys management and are subject to significant risks and uncertainties. There can be no guarantees with respect to pipeline products that the products will receive the necessary regulatory approvals or that they will prove to be commercially successful. If underlying assumptions prove inaccurate or risks or uncertainties materialize, actual results may differ materially from those set forth in the forward-looking statements.

Risks and uncertainties include but are not limited to, general industry conditions and competition; general economic factors, including interest rate and currency exchange rate fluctuations; the impact of pharmaceutical industry regulation and health care legislation in the United States and internationally; global trends toward health care cost containment; technological advances, new products and patents attained by competitors; challenges inherent in new product development, including obtaining regulatory approval; the companys ability to accurately predict future market conditions; manufacturing difficulties or delays; financial instability of international economies and sovereign risk; dependence on the effectiveness of the companys patents and other protections for innovative products; and the exposure to litigation, including patent litigation, and/or regulatory actions.

The company undertakes no obligation to publicly update any forward-looking statement, whether as a result of new information, future events or otherwise. Additional factors that could cause results to differ materially from those described in the forward-looking statements can be found in the companys 2018 Annual Report on Form 10-K and the companys other filings with the Securities and Exchange Commission (SEC) available at the SECs Internet site (www.sec.gov).

Please see Prescribing Information for KEYTRUDA at http://www.merck.com/product/usa/pi_circulars/k/keytruda/keytruda_pi.pdf andMedication Guide for KEYTRUDA at http://www.merck.com/product/usa/pi_circulars/k/keytruda/keytruda_mg.pdf.

View original post here:
Merck Receives Positive EU CHMP Opinion for Two New Regimens of KEYTRUDA (pembrolizumab) as First-Line Treatment for Metastatic or Unresectable...

Cardiac Stem Cells Comments Off on Merck Receives Positive EU CHMP Opinion for Two New Regimens of KEYTRUDA (pembrolizumab) as First-Line Treatment for Metastatic or Unresectable… | October 18th, 2019

Spontaneous recovery from disease is often painted as superstition but our body can heal itself

It may come as a surprise to some, especially those with conventional medical training, but the default state of the body is one of ceaselessregeneration. Without the flame-like process of continual cell turnover within the bodylife and death ceaselessly intertwinedthe miracle of the human body would not exist

In times of illness, however, regenerative processes are overcome by degenerative ones. This is where medicine may perform its most noble feat, nudging the body back into balance with foods, herbs, nutrients, and healing energies and intentions.

Today, however, drug-based medicine invariably uses chemicals that lackregenerative potential; to the contrary, they commonly interfere with bodily self-renewal in order to suppress the symptoms against which they are applied.

In other words, most medicines attack disease symptoms rather than support the bodys own ability to combat disease.

Over the course of the past few years of trolling MEDLINE (the National Institutes of Healths website produced by the National Library of Medicine), we have collected a series of remarkable studies on a topic considered all but heretical by the conventional medical systemspontaneous remission.

There is actually a broad range of natural compounds with proven nerve-regenerative effects. A 2010 study published in the journalRejuvenation Research, for instance, found a combination of blueberry, green tea and carnosine have neuritogenic (i.e. promoting neuronal regeneration) and stem-cell regenerative effects in an animal model ofneurodegenerative disease.Other researched neuritogenic substances include:

There is another class of nerve-healing substances, known asremyelinatingcompounds, which stimulate the repair of the protective sheath around the axon of the neurons known as myelin. Myelin is often damaged in neurological injury and/or dysfunction, especially autoimmune and vaccine-induceddemyelination disorders.

It should also be noted that evenmusicandfalling in lovehave been studied for possibly stimulating neurogenesis, regeneration and/or repair of neurons, indicating that regenerative medicine does not necessarily require the ingestion of anything; rather, a wide range oftherapeutic actionsmay be employed to improve health and well-being, as well.

[To view the first-hand biomedical citations on these neuritogenic substances, visit GreenMedinfosneuritogenicresearch page online.]

Glycyrrhizin, a compound found within licorice that is also a powerfulanti-SARS virus agent, has also been found to stimulate the regeneration of liver mass and function in the animal model of hepatectomy. Other liver regenerative substances include:

[To view the first-hand biomedical citations, visit GreenMedinfosliver regenerationresearch page on the topic online.]

The medical community has yet to harness the diabetes-reversing potential of natural compounds. Whereas expensive stem cell therapies, islet cell transplants, and an array of synthetic drugs in the developmental pipeline are the focus of billions of dollars of research, annually, our kitchen cupboards and backyards may already contain the long sought-after cure for type 1 diabetes. Nature has a way of providing the things our bodies need.

The following compounds have been demonstrated experimentally to regenerate the insulin-producing beta cells, which are destroyed in insulin-dependent diabetes, and once restored, may (at least in theory) restore the health of the patient to the point where they no longer require insulin replacement.

[To view the first-hand biomedical citations onbeta cell regeneration, visit GreenMedinfos research page on the topic online.]

Secretagogues are substances in the body that cause other substances to be secreted, like sulfonylureas, which triggers insulinrelease. Secretagogues, includingsynthetic secretagogues, can increase the endocrine glands ability to secrete more of a hormone. But even better are substances thattruly regeneratehormones which have degraded. They do this by emitting electrons into potentially carcinogenic transient hormone metabolites. One of these substances isvitamin C.

A powerful electron donor, this vitamin has the ability to contribute electrons to resurrect the form and function of estradiol (estrogen; E2), progesterone, and testosterone, for instance. In tandem withfoods that are able to support the function of glandslikethe ovaries, vitamin C may represent an excellent complement or alternative to hormone replacement therapy.

Not too long ago, it was believed that cardiac tissue was uniquely incapable of being regenerated. A new and rapidly growing body of experimental research now indicates that this is simply untrue. A class of heart-tissue regenerating compounds, known asneocardiogenicsubstances, are able to stimulate the formation of cardiac progenitor cells which can differentiate into healthy heart tissue. Neocardiogenicsubstances include the following:

Another remarkable example of cardiac cell regeneration is through what is known as the fetomaternal trafficking of stem cells through the placenta. The amazing process known as fetal microchimerism allows a fetus to contribute stem cells to the mother which are capable of regenerating her damaged heart cells, and possibly a wide range of other cell types.

Curcuminandresveratrolhave been shown to improve recovery from spinal cord injury. Over a dozen other natural compounds hold promise in this area, which can be viewed on GreenMedinfosspinal cord injurypage online. As far as degenerative joint disease, i.e. osteoarthritis, there are a broad range of potentially regenerative substances, with 50 listed on the sitesosteoarthritisresearch page.

Regenerative medicine poses a unique challenge to the current medical paradigm, which is based on costly drug trials, patents, and an economic infrastructure supported by drug-based interventions. It is a simple truth that symptom suppression is profitable. It guarantees both the perpetuation of the original underlying disease and the generation of an ever-expanding array of additional, treatment-induced symptoms known as side effects.

But cures, especially those that come from natural sources, dont have this built-in income potential. Worse perhaps, from a Big Pharma perspective, they can not be easily patented. In the current regulatory environment, that means that companies have no incentive to conduct the costly trials required to have these cures approved by the FDA and then used in clinical settings. Without patents, they cant be controlled and sold.

But suppressing symptoms with drugs that cause side effects requiring other drugs is a non-sustainable, infinite growth model. It is doomed to fail and eventually collapse.

The current approach also interferes with the bodys natural regenerative and immune capabilities. Cultivating diets, lifestyles and attitudes conducive to bodily regeneration can interrupt this pathological circuit. With true health, we can attain the bodily freedom that is a precondition for the liberation of the human spirit.

SayerJiis the founder ofGreenmedinfo.com, a reviewer at theInternational Journal of Human Nutrition and Functional Medicine, co-founder and CEO ofSystome Biomed, vice chairman of the board of theNational Health Federation, and steering committee member of theGlobal GMO Free Coalition.This article was originally published on GreenMedinfo.com

Read more:
6 Bodily Tissues That Can Be Regenerated Through Nutrition - The Epoch Times

Cardiac Stem Cells Comments Off on 6 Bodily Tissues That Can Be Regenerated Through Nutrition – The Epoch Times | October 18th, 2019

We are contrasting Cellular Biomedicine Group Inc. (NASDAQ:CBMG) and VistaGen Therapeutics Inc. (NASDAQ:VTGN) on their institutional ownership, profitability, risk, analyst recommendations, dividends, earnings and valuation. They both are Biotechnology companies, competing one another.

Valuation and Earnings

Table 1 showcases the gross revenue, earnings per share and valuation of Cellular Biomedicine Group Inc. and VistaGen Therapeutics Inc.

Profitability

Table 2 hightlights the return on equity, return on assets and net margins of the two companies.

Volatility & Risk

Cellular Biomedicine Group Inc. is 167.00% more volatile than Standard & Poors 500 because the company has a beta of 2.67. In other hand, VistaGen Therapeutics Inc. has beta of -0.48 which is 148.00% less volatile than Standard & Poors 500.

Liquidity

Cellular Biomedicine Group Inc. has a Current Ratio of 4.4 and a Quick Ratio of 4.4. Competitively, VistaGen Therapeutics Inc.s Current Ratio is 4.9 and has 4.9 Quick Ratio. VistaGen Therapeutics Inc.s better ability to pay short and long-term obligations than Cellular Biomedicine Group Inc.

Analyst Ratings

The table given features the ratings and recommendations for Cellular Biomedicine Group Inc. and VistaGen Therapeutics Inc.

Cellular Biomedicine Group Inc. has a 55.30% upside potential and an average target price of $23. Competitively VistaGen Therapeutics Inc. has an average target price of $22, with potential upside of 1,592.31%. The results from earlier shows that analysts opinion suggest that VistaGen Therapeutics Inc. seems more appealing than Cellular Biomedicine Group Inc.

Institutional & Insider Ownership

Institutional investors held 23.8% of Cellular Biomedicine Group Inc. shares and 20.4% of VistaGen Therapeutics Inc. shares. Insiders held roughly 37.14% of Cellular Biomedicine Group Inc.s shares. Competitively, insiders own roughly 0.2% of VistaGen Therapeutics Inc.s shares.

Performance

Here are the Weekly, Monthly, Quarterly, Half Yearly, Yearly and YTD Performance of both pretenders.

For the past year Cellular Biomedicine Group Inc. has stronger performance than VistaGen Therapeutics Inc.

Summary

On 6 of the 11 factors VistaGen Therapeutics Inc. beats Cellular Biomedicine Group Inc.

Cellular Biomedicine Group Inc., a biopharmaceutical company, develops treatments for cancerous and degenerative diseases in Greater China. It focuses on developing and marketing cell-based therapies to treat serious diseases, such as cancer, orthopedic, and various inflammatory diseases, as well as metabolic diseases. The company develops treatments utilizing proprietary cell based technologies, including immune cell therapy for the treatment of a range of cancers; human adipose-derived mesenchymal progenitor cells for the treatment of joint and autoimmune diseases; and tumor cell specific dendritic cell therapy. The company has a strategic research collaboration with GE Healthcare Life Sciences China to co-develop industrial control processes in Chimeric Antigen Receptor T-cell (CAR-T) and stem cell manufacturing. Cellular Biomedicine Group Inc. was incorporated in 2001 and is headquartered in Cupertino, California.

VistaGen Therapeutics, Inc., a clinical-stage biopharmaceutical company, engages in developing and commercializing medicines for depression and other central nervous system (CNS) disorders. The company's lead product candidate is AV-101, which is in Phase II development stage, an adjunctive treatment used for major depressive disorder. It also focuses on potential commercial applications of its human pluripotent stem cell (hPSC) technology platform to discover, rescue, develop, and commercialize new chemical entities (NCEs) for CNS and other diseases; and regenerative medicine involving hPSC-derived blood, cartilage, heart, and liver cells. In addition, the company develops CardioSafe 3D, an in vitro cardiac bioassay system for predicting human heart toxicity of small molecule NCEs. VistaGen Therapeutics, Inc. has licensing, sublicensing, and collaboration agreements with BlueRock Therapeutics, LP; U.S. National Institutes of Health; Cato Research Ltd.; and University Health Network. The company was founded in 1998 and is headquartered in South San Francisco, California.

Receive News & Ratings Via Email - Enter your email address below to receive a concise daily summary of the latest news and analysts' ratings with our FREE daily email newsletter.

Read more here:
Reviewing Cellular Biomedicine Group Inc. (CBMG)'s and VistaGen Therapeutics Inc. (NASDAQ:VTGN)'s results - MS Wkly

Cardiac Stem Cells Comments Off on Reviewing Cellular Biomedicine Group Inc. (CBMG)’s and VistaGen Therapeutics Inc. (NASDAQ:VTGN)’s results – MS Wkly | October 18th, 2019

Share this Article

You are free to share this article under the Attribution 4.0 International license.

New research links a genetic anomaly and some forms of SIDS, or sudden infant death syndrome, which claims the lives of more than 3,000 infants a year.

The research, published in Nature Communications, focuses on mitochondrial tri-functional protein deficiency, a potentially fatal cardiac metabolic disorder caused by a genetic mutation in the gene HADHA.

Newborns with this genetic anomaly cant metabolize the lipids found in milk, and die suddenly of cardiac arrest when they are a couple months old. Lipids are a category of molecules that include fats, cholesterol, and fatty acids.

There are multiple causes for sudden infant death syndrome, says Hannele Ruohola-Baker, professor of biochemistry at the University of Washington School of Medicine, who is also associate director of the Medicine Institute for Stem Cell and Regenerative Medicine.

There are some causes which are environmental. But what were studying here is really a genetic cause of SIDS. In this particular case, it involves defect in the enzyme that breaks down fat.

Lead author Jason Miklas, who earned his PhD at the University of Washington and is now a postdoctoral fellow at Stanford University, says he first came up with the idea while researching heart disease and noticed a small research study that had examined children who couldnt process fats and who had cardiac disease that was not readily explained.

So he and Ruohola-Baker started looking into why heart cells, grown to mimic infant cells, died in the petri dish where they were growing.

If a child has a mutation, depending on the mutation the first few months of life can be very scary as the child may die suddenly, Miklas says. An autopsy wouldnt necessarily pick up why the child passed but we think it might be due to the infants heart stopping to beat.

Were no longer just trying to treat the symptoms of the disease, Miklas says. Were trying to find ways to treat the root problem. Its very gratifying to see that we can make real progress in the lab toward interventions that could one day make their way to the clinic.

In MTP deficiency, the heart cells of affected infants dont convert fats into nutrients properly, resulting in a build-up of unprocessed fatty material that can disrupt heart functions. More technically, the breakdown occurs when enzymes fail to complete a process known as fatty acid oxidation. It is possible to screen for the genetic markers of MTP deficiency; but effective treatments remain a ways off.

Ruohola-Baker says the latest laboratory discovery is a big step towards finding ways to overcome SIDS.

There is no cure for this, she says. But there is now hope, because weve found a new aspect of this disease that will innovate generations of novel small molecules and designed proteins, which might help these patients in the future.

One drug the group is focusing on is Elamipretide, used to stimulate hearts and organs that have oxygen deficiency, but barely considered for helping infant hearts, until now. In addition, prospective parents can undergo screening to see if there is a chance that they could have a child who might carry the mutation.

Ruohola-Baker has a personal interest in the research: one of her friends in Finland, her home country, had a baby who died of SIDS.

It was absolutely devastating for that couple, she says. Since then, Ive been very interested in the causes for sudden infant death syndrome. Its very exciting to think that our work may contribute to future treatments, and help for the heartbreak for the parents who find their children have these mutations.

The National Institutes of Health, the Academy of Finland, Finnish Foundation for Cardiovascular Research. Wellstone Muscular Dystrophy Cooperative Research Center, Natural Sciences and Engineering Research of Canada, an Alexander Graham Bell Graduate Scholarship, and the National Science Foundation funded the work.

Source: University of Washington

Original Study DOI: 10.1038/s41467-019-12482-1

Read this article:
Some cases of SIDS may have this genetic cause - Futurity: Research News

Cardiac Stem Cells Comments Off on Some cases of SIDS may have this genetic cause – Futurity: Research News | October 15th, 2019

In 2006, Shinya Yamanaka shook stem cell research with his discovery that mature cells can be converted into stem cells, relieving a longstanding political-ethical blockage and throwing open medical research on everything from curbing eye degeneration to organ printing.

But that process still has pitfalls, including in risk and scalability, and some researchers are exploring another way first hinted at years ago: new technology to convert mature cells directly into other mature cells without the complex and time-consuming process of first making them into stem cells.

One of those companies, Mogrify, just raised $16 million in Series A financing to bring its overall funding to over $20 million since its February launch. Led by CEO Darrin Disley, the funding will help expand their new base in Cambridge to a 60-strong staff and push forward their direct-conversion approach to cell therapy through research and licensing. Investors include Parkwalk Advisors and Ahren Innovation Capital.

They list potential applications as treatments for musculoskeletal and auto-immune disorders, cancer immunotherapy, and therapies for ocular and respiratory diseases. For example, you could use it regenerate cartilage in arthritis patients.

If you could take a cell from one part of the body and turn it into any other cell at any other stage of development for another part of the body, you effectively have the Holy Grail of regenerative medicine, Disley told Labiotech.eu in April.

Mogrifys advantage over the Yamanaka method called induced pluripotent stem cells (iPS), is that in theory it can be more scalable and avoid the problems associated with iPS. These include instabilities arising from the induced immature state and an increased risk of cancer if any pluripotent cells remain in the body.

The concept behind Mogrify actually predates, by nearly 19 years, Yamanakas discovery, which fast won him the 2012 Nobel Prize in Medicine. A 2017 Nature study on transdifferentiation, as the process is called, of fibroblasts into cardiac tissue traced the idea to a 1987 findingthat a master gene regulator could convert mice fibroblasts into skeletal muscle.

The problem though, according to Mogrify, is that most current efforts rely on an exhausting guess-and-check process. With hundreds of cell types and an even greater number of transcription factors the program that recodes the cell finding the right factor for the right cell can be like a custodian with a jangling, unmarked key ring trying to get into a building with thousands of locks.

Mogrifys key tech is a computer model they say can predict the right combination. The scientists behind the platform published a 2016 study in Nature applying the model to 173 human cell types and 134 tissues.

Before Mogrify, Disley led the Cambridge-based gene-editing company Horizon Discovery.

Continue reading here:
Cell therapy startup raises $16 million to fund its quest for the Holy Grail in regenerative medicine - Endpoints News

Cardiac Stem Cells Comments Off on Cell therapy startup raises $16 million to fund its quest for the Holy Grail in regenerative medicine – Endpoints News | October 15th, 2019

Both Tenax Therapeutics Inc. (NASDAQ:TENX) and Neuralstem Inc. (NASDAQ:CUR) are each others competitor in the Biotechnology industry. Thus the contrast of their analyst recommendations, profitability, institutional ownership, risk, dividends, earnings and valuation.

Valuation and Earnings

Table 1 highlights Tenax Therapeutics Inc. and Neuralstem Inc.s gross revenue, earnings per share and valuation.

Profitability

Table 2 shows Tenax Therapeutics Inc. and Neuralstem Inc.s return on assets, net margins and return on equity.

Risk & Volatility

Tenax Therapeutics Inc.s 1.4 beta indicates that its volatility is 40.00% more volatile than that of S&P 500. Neuralstem Inc.s 94.00% more volatile than S&P 500 which is a result of the 1.94 beta.

Liquidity

Tenax Therapeutics Inc.s Current Ratio is 11 while its Quick Ratio is 11. On the competitive side is, Neuralstem Inc. which has a 3.8 Current Ratio and a 3.8 Quick Ratio. Tenax Therapeutics Inc. is better positioned to pay off short and long-term obligations compared to Neuralstem Inc.

Insider and Institutional Ownership

Institutional investors owned 22.2% of Tenax Therapeutics Inc. shares and 4.9% of Neuralstem Inc. shares. Tenax Therapeutics Inc.s share owned by insiders are 4.73%. On the other hand, insiders owned about 1% of Neuralstem Inc.s shares.

Performance

Here are the Weekly, Monthly, Quarterly, Half Yearly, Yearly and YTD Performance of both pretenders.

For the past year Tenax Therapeutics Inc. had bullish trend while Neuralstem Inc. had bearish trend.

Summary

Tenax Therapeutics Inc. beats Neuralstem Inc. on 5 of the 9 factors.

Tenax Therapeutics, Inc., a specialty pharmaceutical company, focused on the identification, development, and commercialization of a portfolio of products for the critical care market in the United States and Canada. It focuses on the development and commercialization of pharmaceutical products containing levosimendan, 2.5 mg/ml concentrate for solution for infusion/5ml vial for use in the reduction of morbidity and mortality in cardiac surgery patients at risk for developing Low Cardiac Output Syndrome. The company was formerly known as Oxygen Biotherapeutics, Inc. and changed its name to Tenax Therapeutics, Inc. in September 2014. Tenax Therapeutics, Inc. was founded in 1967 and is headquartered in Morrisville, North Carolina.

Neuralstem, Inc., a clinical stage biopharmaceutical company, focuses on the research and development of nervous system therapies based on its proprietary human neuronal stem cells and small molecule compounds. The companys stem cell based technology enables the isolation and expansion of human neural stem cells from various areas of the developing human brain and spinal cord enabling the generation of physiologically relevant human neurons of various types. It is developing products include NSI-189, a chemical entity, which is in Phase II clinical trial for the treatment of major depressive disorder, as well as is in preclinical programs for the MCAO stroke, type 1 and 2 diabetes related neuropathy, irradiation-induced cognition, long-term potentiation enhancement, and angelman syndrome. The company is also developing NSI-566, which has completed Phase II clinical trial for treating amyotrophic lateral sclerosis disease, as well as is in Phase I clinical trials for the treatment of chronic spinal cord injury and motor deficits due to ischemic stroke. Neuralstem, Inc. was founded in 1996 and is headquartered in Germantown, Maryland.

Receive News & Ratings Via Email - Enter your email address below to receive a concise daily summary of the latest news and analysts' ratings with our FREE daily email newsletter.

See the rest here:
Reviewing Tenax Therapeutics Inc. (TENX)'s and Neuralstem Inc. (NASDAQ:CUR)'s results - MS Wkly

Cardiac Stem Cells Comments Off on Reviewing Tenax Therapeutics Inc. (TENX)’s and Neuralstem Inc. (NASDAQ:CUR)’s results – MS Wkly | October 15th, 2019

This is a contrast between VistaGen Therapeutics Inc. (NASDAQ:VTGN) and Gamida Cell Ltd. (NASDAQ:GMDA) based on their institutional ownership, profitability, risk, analyst recommendations, dividends, earnings and valuation. The two companies are Biotechnology and they also compete with each other.

Earnings and Valuation

Table 1 shows gross revenue, earnings per share (EPS) and valuation of the two companies.

Profitability

Table 2 provides us the return on equity, net margins and return on assets of both companies.

Liquidity

The Current Ratio of VistaGen Therapeutics Inc. is 4.9 while its Quick Ratio stands at 4.9. The Current Ratio of rival Gamida Cell Ltd. is 6.5 and its Quick Ratio is has 6.5. Gamida Cell Ltd. is better equipped to clear short and long-term obligations than VistaGen Therapeutics Inc.

Analyst Recommendations

The table shown features the ratings and recommendations for VistaGen Therapeutics Inc. and Gamida Cell Ltd.

VistaGen Therapeutics Inc. has a 1,975.47% upside potential and a consensus price target of $22. Meanwhile, Gamida Cell Ltd.s consensus price target is $16, while its potential upside is 261.17%. The data provided earlier shows that VistaGen Therapeutics Inc. appears more favorable than Gamida Cell Ltd., based on analyst view.

Insider & Institutional Ownership

Roughly 20.4% of VistaGen Therapeutics Inc. shares are owned by institutional investors while 13.1% of Gamida Cell Ltd. are owned by institutional investors. Insiders owned 0.2% of VistaGen Therapeutics Inc. shares. Comparatively, 65.61% are Gamida Cell Ltd.s share owned by insiders.

Performance

Here are the Weekly, Monthly, Quarterly, Half Yearly, Yearly and YTD Performance of both pretenders.

For the past year VistaGen Therapeutics Inc. was more bearish than Gamida Cell Ltd.

Summary

On 6 of the 11 factors VistaGen Therapeutics Inc. beats Gamida Cell Ltd.

VistaGen Therapeutics, Inc., a clinical-stage biopharmaceutical company, engages in developing and commercializing medicines for depression and other central nervous system (CNS) disorders. The company's lead product candidate is AV-101, which is in Phase II development stage, an adjunctive treatment used for major depressive disorder. It also focuses on potential commercial applications of its human pluripotent stem cell (hPSC) technology platform to discover, rescue, develop, and commercialize new chemical entities (NCEs) for CNS and other diseases; and regenerative medicine involving hPSC-derived blood, cartilage, heart, and liver cells. In addition, the company develops CardioSafe 3D, an in vitro cardiac bioassay system for predicting human heart toxicity of small molecule NCEs. VistaGen Therapeutics, Inc. has licensing, sublicensing, and collaboration agreements with BlueRock Therapeutics, LP; U.S. National Institutes of Health; Cato Research Ltd.; and University Health Network. The company was founded in 1998 and is headquartered in South San Francisco, California.

Gamida Cell Ltd., a clinical stage biopharmaceutical company, focuses on developing cell therapies to cure cancer, and rare and serious hematologic diseases in the United States, the European Union, and internationally. The company's lead product candidate is NiCord, a nicotinamide (NAM)-expanded cord blood cell therapy that is in Phase 3 clinical trials for use as a curative stem cell graft for patients in hematopoietic stem cell transplant. It is also developing NAM-NK, an innate immunotherapy of expanded natural killer cells, which is in Phase 1 clinical trials for the treatment of refractory non-Hodgkin lymphoma and multiple myeloma. The company was founded in 1998 and is headquartered in Jerusalem, Israel.

Receive News & Ratings Via Email - Enter your email address below to receive a concise daily summary of the latest news and analysts' ratings with our FREE daily email newsletter.

Read the original post:
Reviewing VistaGen Therapeutics Inc. (VTGN)'s and Gamida Cell Ltd. (NASDAQ:GMDA)'s results - MS Wkly

Cardiac Stem Cells Comments Off on Reviewing VistaGen Therapeutics Inc. (VTGN)’s and Gamida Cell Ltd. (NASDAQ:GMDA)’s results – MS Wkly | October 14th, 2019

DUBLIN--(BUSINESS WIRE)--The "Cell Therapy - Technologies, Markets and Companies" report from Jain PharmaBiotech has been added to ResearchAndMarkets.com's offering.

This report describes and evaluates cell therapy technologies and methods, which have already started to play an important role in the practice of medicine. Hematopoietic stem cell transplantation is replacing the old fashioned bone marrow transplants. The role of cells in drug discovery is also described. Cell therapy is bound to become a part of medical practice.

Stem cells are discussed in detail in one chapter. Some light is thrown on the current controversy of embryonic sources of stem cells and comparison with adult sources. Other sources of stem cells such as the placenta, cord blood and fat removed by liposuction are also discussed. Stem cells can also be genetically modified prior to transplantation.

Cell therapy technologies overlap with those of gene therapy, cancer vaccines, drug delivery, tissue engineering and regenerative medicine. Pharmaceutical applications of stem cells including those in drug discovery are also described. Various types of cells used, methods of preparation and culture, encapsulation and genetic engineering of cells are discussed. Sources of cells, both human and animal (xenotransplantation) are discussed. Methods of delivery of cell therapy range from injections to surgical implantation using special devices.

Cell therapy has applications in a large number of disorders. The most important are diseases of the nervous system and cancer which are the topics for separate chapters. Other applications include cardiac disorders (myocardial infarction and heart failure), diabetes mellitus, diseases of bones and joints, genetic disorders, and wounds of the skin and soft tissues.

Regulatory and ethical issues involving cell therapy are important and are discussed. The current political debate on the use of stem cells from embryonic sources (hESCs) is also presented. Safety is an essential consideration of any new therapy and regulations for cell therapy are those for biological preparations.

The cell-based markets was analyzed for 2018 and projected to 2028. The markets are analyzed according to therapeutic categories, technologies, and geographical areas. The largest expansion will be in diseases of the central nervous system, cancer, and cardiovascular disorders. Skin and soft tissue repair, as well as diabetes mellitus, will be other major markets.

The report contains information on the following:

Key Topics Covered:

Part I: Technologies, Ethics & Regulations

Executive Summary

1. Introduction to Cell Therapy

2. Cell Therapy Technologies

3. Stem Cells

4. Clinical Applications of Cell Therapy

5. Cell Therapy for Cardiovascular Disorders

6. Cell Therapy for Cancer.

7. Cell Therapy for Neurological Disorders

8. Ethical, Legal and Political Aspects of Cell therapy

9. Safety and Regulatory Aspects of Cell Therapy

Part II: Markets, Companies & Academic Institutions

10. Markets and Future Prospects for Cell Therapy

11. Companies Involved in Cell Therapy

12. Academic Institutions

13. References

For more information about this report visit https://www.researchandmarkets.com/r/9q5tz1

Go here to read the rest:
Global Cell Therapy Technologies, Companies & Markets During the Forecast Period, 2018-2028 - ResearchAndMarkets.com - Business Wire

Cardiac Stem Cells Comments Off on Global Cell Therapy Technologies, Companies & Markets During the Forecast Period, 2018-2028 – ResearchAndMarkets.com – Business Wire | October 9th, 2019

Mesenchymal Stem CellDerived Extracellular Vesicles as Therapeutics and as a Drug Delivery PlatformGyuhyeon Baek, et al., STEM CELLS Translational Medicine

The future of exosome therapeutics has great potential, but several challenges, as discussed in the present study, must be overcome before exosomebased therapy will become an important option as a nextgeneration drug delivery system.

Bmi1 Overexpression in Mesenchymal Stem Cells Exerts Antiaging and Antiosteoporosis Effects by Inactivating p16/p19 Signaling and Inhibiting Oxidative StressGuangpei Chen, et al., STEM CELLS

his study demonstrates that mesenchymal stem cell (MSC) overexpressing Bmi1 exerts antiaging and antiosteoporosis effects. These findings might provide a strategy to enhance the functionality of MSCs for use in therapeutic applications. The results suggest a clinical relevance of Bmi1 in MSCs, for example, upregulation of BMI1 expression in human MSCs by hypoxiccultures or treatment with sonic hedgehog activators, then using them for bone marrow concentrate therapy to enhance MSC potency in antiaging and antiosteoporosis.

Read the original:
Stem Cells Portal

Cardiac Stem Cells Comments Off on Stem Cells Portal | October 6th, 2019

JavaScript is disabled on your browser. Please enable JavaScript to use all the features on this page.Abstract

Stem cells have the potential to differentiate into cardiovascular cell lineages and to stimulate tissue regeneration in a paracrine/autocrine manner; thus, they have been extensively studied as candidate cell sources for cardiovascular regeneration. Several preclinical and clinical studies addressing the therapeutic potential of endothelial progenitor cells (EPCs) and cardiac progenitor cells (CPCs) in cardiovascular diseases have been performed. For instance, autologous EPC transplantation and EPC mobilization through pharmacological agents contributed to vascular repair and neovascularization in different animal models of limb ischemia and myocardial infarction. Also, CPC administration and in situ stimulation of resident CPCs have been shown to improve myocardial survival and function in experimental models of ischemic heart disease. However, clinical studies using EPC- and CPC-based therapeutic approaches have produced mixed results. In this regard, intracoronary, intra-myocardial or intramuscular injection of either bone marrow-derived or peripheral blood progenitor cells has improved pathological features of tissue ischemia in humans, despite modest or no clinical benefit has been observed in most cases. Also, the intriguing scientific background surrounding the potential clinical applications of EPC capture stenting is still waiting for a confirmatory proof. Moreover, clinical findings on the efficacy of CPC-based cell therapy in heart diseases are still very preliminary and based on small-size studies.

Despite promising evidence, widespread clinical application of both EPCs and CPCs remains delayed due to several unresolved issues. The present review provides a summary of the different applications of EPCs and CPCs for cardiovascular cell therapy and underlies their advantages and limitations.

bone marrow-derived cells

cardiac progenitor cells

C-X-C chemokine receptor type 4

1,1-dioctadecyl-3,3,3,3-tetramethylindocarbocyanine-acetylated low density lipoprotein

endothelial colony forming cells

endothelial progenitor cells

granulocyte colony-stimulating factor

individual patient data

induced pluripotent stem cells

platelet-derived growth factor receptor

stromal cell derived factor-1

stage specific embryonic antigen-1

ST-segment elevation myocardial infarction

vascular endothelial growth factor

Ulex europaeus agglutinin-1

Endothelial progenitor cells

Stem cells

EPC

CPC

Myocardial infarction

Regenerative medicine

Recommended articlesCiting articles (0)

2017 Elsevier Inc. All rights reserved.

Here is the original post:
Endothelial and cardiac progenitor cells for ...

Cardiac Stem Cells Comments Off on Endothelial and cardiac progenitor cells for … | June 6th, 2019

Overview of current stem cell-based approaches to treat heart disease

Since heart failure after heart attacks results from death of heart muscle cells, researchers have been developing strategies to remuscularize the damaged heart wall in efforts to improve its function. Researchers are transplanting different types of stem cell and progenitor cells (see above) into patients to repair the damaged heart muscle. These strategies have mainly used either adult stem cells (found in bone marrow, fat, or the heart itself) or pluripotent (ES or iPS) cells.

Preliminary results from experiments with adult stem cells showed that they appeared to improve cardiac function even though they died shortly after transplantation. This led to the idea that these cells can release signals that can improve function without replacing the lost muscle. Clinical trials began in the early 2000s transplanting adult stem cells from the bone marrow and then from the heart. These trials demonstrated that transplanting cells into damaged hearts is feasible and generally safe for patients. However, larger trials that were randomized, blinded, and placebo-controlled, showed fewer indications of improved function. The consensus now is that adult stem cells have modest, if any, benefit to cardiac function.

Research shows that pluripotent stem cell-derived cardiomyocytes can form beating human heart muscle cells that both release the necessary signals and replace muscle lost to heart attack. Transplantation of pluripotent stem cell-derived cardiac cells have demonstrated substantial benefits to cardiac function in animal models of heart disease, from mice to monkeys. Recently, pluripotent stem cell-derived interventions were used in clinical trials for the first time. Patches of human heart muscle cells derived from the stem cells were transplanted onto the surface of failing hearts. Early results suggest that this approach is feasible and safe, but it is too early to know whether there are functional benefits.Research is ongoing to test cellular therapies to treat heart attacks by combining different types of stem cells, repeating transplantations, or improving stem cell patches. Clinical trials using these improved methods are currently targeted to begin around 2020.Unfortunately, many unscrupulous clinics are making unsubstantiated claims about the efficacy of stem cell therapies for heart failure, creating confusion about the current state of cellular approaches for heart failure. To learn more about warning signs of these unproven interventions, please visit Nine Things to Know About Stem Cell Treatments.

See the original post here:
Heart Disease A Closer Look at Stem Cells

Cardiac Stem Cells Comments Off on Heart Disease A Closer Look at Stem Cells | June 1st, 2019

How do Stem Cellsfunction?Stem cells have the capacity to migrate to injured tissues, a phenomenon calledhoming. This occurs by injury or disease signals that are released from the distressed cells and tissue. Once stem cells arrive,they dock on adjacent cells to commence performing their job to repair the problem.

Stem cells serve as a cell replacementwhere they change into the required cell type such as a muscle cell, bone orcartilage. This is ideal for traumaticinjuries and many orthopedic indications.

They do not express specific human leukocyte antigens (HLAs) which helpthem avoid the immune system. Stemcells dock on adjacent cells and release proteins called growth factors, cytokines and chemokines. These factors help control many aspects of the healing and repairprocess systemically.

Stem cells control the immune system and regulate inflammation which is a keymediator of disease, aging, and is ahallmark of autoimmune diseases such as rheumatoid arthritis and multiple sclerosis.

They help to increase new blood vesselformation so that tissues receive proper blood flow and the correct nutrients needed to heal as in stroke, peripheral arterydisease and heart disease.

Stem cells provide trophic support forsurrounding tissues and help hostendogenous repair. This works wellwhen used for orthopedics. In case ofdiabetes, it may help the remaining beta cells in the pancreas to reproduce orfunction optimally.

As CSN research evolves, the field ofregenerative medicine and stem cells offers the greatest hope for those suffering from degenerative diseases, conditions for which there is currently no effective treatment or conditions that have failed conventional medical therapy.

Stem cell treatment is a complex process allowing us to harvest the bodys own repair mechanism to fight against degeneration, inflammation and general tissue damage. Stem cells are cells that can differentiate into other types of tissue to restore function and reduce pain.

Adult stem cells are found in abundance in adipose (fat) tissue, where more than 5million stem cells reside in every gram. These stem cells are called adult mesenchymal stem cells.

Our medical doctors extract stromal vascular fraction (SVF) from your own body to provide treatment using your very own cells. This process is calledautologous mesenchymal stem celltherapy. Our multi-specialty team deploys SVF under an institutional review board (IRB). This is an approved protocol that governs investigational work and the focus is to maintain safety of autologous use of SVF for various degenerative conditions.

How do we perform the stem cell treatment?Our procedure is very safe and completed in a single visit to our clinic. On the day of treatment, our physicians inject a localanaesthetic and harvest approximately 60 cc (2 oz.) of stromalvascular fraction (SVF) from under the skin of your flanks or abdomen. The extracted SVF is then refined in a closed system using strictCSN protocols to produce pure stromalvascular fraction (SVF). SVF containsregenerative cells including mesenchymal and hematopoietic stem cells, macrophages, endothelial cells, immune regulatory cells, and important growth factors that facilitate your stem cell activity. CSN technology allows us to isolate high numbers of viable stem cells that we can immediately deploy directly into a joint, trigger point, and/or byintravascular infusion. Specific deployment methods have been developed that are unique for each condition being treated.

During the refinement process, thesubcutaneous harvested cells andtheir connecting collagen matrix willbe separated, leaving purified free stem cells. About half of the SVF will be pure stem cells, while the remainder will be acombination of other regenerative cellsand growth factors. Before the SVF isre-injected into your body during the final part of the process we perform a qualityand quantity test which will examine the cell count and viability.

Perfecting the stem cell treatmentOur team records cell numbers and viability so that we can gain a better understanding of what constitutes a successful treatment. Although it is not yet possible to predict what number of cells that will be recovered in a harvest, it is very important that we know the total cell count and cell viability. It is only with this data that we will beginto understand why treatments are verysuccessful, only slightly successful orunsuccessful.

While vigilant about patient safety, we are also learning and sharing with the CSN data bank about which diseases respond best and which deployment methods are most effective with over 80 other clinics.

This data collection from all over the world makes the Cell Surgical Network the worlds largest regenerative medicineclinical research organization.

Network physicians have the opportunity to share their data, as well as their clinical experiences, thus helping one anotherto achieve higher levels of scientificunderstanding and optimizing medical protocols.

Injecting into thevascular system and/ora jointWe will administer the stem cell treatment with two methods:

The belief is that for many degenerative joint conditions IV and intra-articulardeployment is superior because each of these conditions have a local pathology and a central pathology. The local resident stem cell population has been working very hard to repair the damage and over the course of time these stem cells have become worn out, depleted and slowly die. This essentially causes a state of stem cell depletion. When we inject our mix of stem cells, cytokines and growth factors (known as SVF)inflammation is decreased and theregenerative process improved.

The stem cells that we have injected will then bring the level of stem cells closer to the normal level, thus restoring the natural balance and allow the body to heal itself.

Caplan et al, The MSC: An Injury Drugstore, DOI 10.1016/j .stem.2011.06.008

How long does it last?Many studies have shown the healing and regenerative ability of stem cells. Forexample, a study in World Journal of Plastic Surgery (Volume 5[2]; May 2016) followed a woman with knee arthritis. Before and after analysis of MRI images confirmed new growth of cartilage tissue. Unlike steroids, lubricants, and other injectable treatments, stem cells actually repair damaged tissue.

As published in Experimental andTherapeutic Medicine (Volume 12[2]; August 2016), numerous studies with hundreds of patients showed continuous improvement of arthritis for two years. Patients showed improvement three months after a single treatment and they continued to show improvement for two full years. This is why stem cells are often referred to as regenerative medicine.

No one can guarantee results for this or any other treatment. Outcomes will vary from patient to patient. Each potential patient must be assessed individually to determine the potential for optimum results from this regenerative therapy. To learn more about stem cell therapy, please contact us by clicking here or calling our clinic at 604-708-CELL (604-708-2355).

Like Loading...

Continue reading here:
Vancouver Stem Cell Treatment Centre | Stem Cells

Cardiac Stem Cells Comments Off on Vancouver Stem Cell Treatment Centre | Stem Cells | May 1st, 2019

By: Ian Murnaghan BSc (hons), MSc - Updated: 12 Sep 2015| *Discuss

One of the biggest hurdles in stem cell research involves the use of embryonic stem cells. While these stem cells have the greatest potential in terms of their ability to differentiate into many different kinds of cells in the human body, they also bring with them enormous ethical controversies. The extraction of embryonic stem cells involves the destruction of an embryo, which upsets and outrages some policy makers and researchers as well as a number of public members. Not only that, but actually obtaining them is a challenge in itself and one that has become more difficult in places such as the United States, where policies have limited the availability of embryonic stem cells for use.

Although researchers have focused on harnessing the power of adult stem cells, there have still been many difficulties in the practical aspects of these potential therapies. In an ideal world, we would be able to use embryonic stem cells without destroying an embyro. Now, however, this ideal hope may actually have some realistic basis. In recent medical news, there has been important progress in the use of embryonic stem cells.

There are still many more tests and research that must be conducted to verify the safety and reliability of the procedure but it is indeed hopeful that funding can now increase for stem cell research. If you are an avid reader of health articles, you will probably be able to stay up-to-date on the latest developments related to this medical news. This newest research into embryonic stem cells holds promise and hope for appeasing the controversy around embryonic stem cell use and allowing for research to finally move forward with fewer challenges and controversies. For those who suffer from one of the many debilitating diseases and conditions that stem cell treatments may help or perhaps cure one day, this is welcome news.

You might also like...

Share Your Story, Join the Discussion or Seek Advice..

Time for Change - 12-Sep-15 @ 12:54 PM

Ellie - 25-Apr-14 @ 6:02 PM

Title:

(never shown)

View post:
Creating Embryonic Stem Cells Without Embryo Destruction

Cardiac Stem Cells Comments Off on Creating Embryonic Stem Cells Without Embryo Destruction | April 22nd, 2019

There are many ways in which human stem cells can be used in research and the clinic. Studies of human embryonic stem cells will yield information about the complex events that occur during human development. A primary goal of this work is to identify how undifferentiated stem cells become the differentiated cells that form the tissues and organs. Scientists know that turning genes on and off is central to this process. Some of the most serious medical conditions, such as cancer and birth defects, are due to abnormal cell division and differentiation. A more complete understanding of the genetic and molecular controls of these processes may yield information about how such diseases arise and suggest new strategies for therapy. Predictably controlling cell proliferation and differentiation requires additional basic research on the molecular and genetic signals that regulate cell division and specialization. While recent developments with iPS cells suggest some of the specific factors that may be involved, techniques must be devised to introduce these factors safely into the cells and control the processes that are induced by these factors.

Human stem cells are currently being used to test new drugs. New medications are tested for safety on differentiated cells generated from human pluripotent cell lines. Other kinds of cell lines have a long history of being used in this way. Cancer cell lines, for example, are used to screen potential anti-tumor drugs. The availability of pluripotent stem cells would allow drug testing in a wider range of cell types. However, to screen drugs effectively, the conditions must be identical when comparing different drugs. Therefore, scientists must be able to precisely control the differentiation of stem cells into the specific cell type on which drugs will be tested. For some cell types and tissues, current knowledge of the signals controlling differentiation falls short of being able to mimic these conditions precisely to generate pure populations of differentiated cells for each drug being tested.

Perhaps the most important potential application of human stem cells is the generation of cells and tissues that could be used for cell-based therapies. Today, donated organs and tissues are often used to replace ailing or destroyed tissue, but the need for transplantable tissues and organs far outweighs the available supply. Stem cells, directed to differentiate into specific cell types, offer the possibility of a renewable source of replacement cells and tissues to treat diseases including maculardegeneration, spinal cord injury, stroke, burns, heart disease, diabetes, osteoarthritis, and rheumatoid arthritis.

Figure 3. Strategies to repair heart muscle with adult stem cells. Click here for larger image.

2008 Terese Winslow

For example, it may become possible to generate healthy heart muscle cells in the laboratory and then transplant those cells into patients with chronic heart disease. Preliminary research in mice and other animals indicates that bone marrow stromal cells, transplanted into a damaged heart, can have beneficial effects. Whether these cells can generate heart muscle cells or stimulate the growth of new blood vessels that repopulate the heart tissue, or help via some other mechanism is actively under investigation. For example, injected cells may accomplish repair by secreting growth factors, rather than actually incorporating into the heart. Promising results from animal studies have served as the basis for a small number of exploratory studies in humans (for discussion, see call-out box, "Can Stem Cells Mend a Broken Heart?"). Other recent studies in cell culture systems indicate that it may be possible to direct the differentiation of embryonic stem cells or adult bone marrow cells into heart muscle cells (Figure 3).

Cardiovascular disease (CVD), which includes hypertension, coronary heart disease, stroke, and congestive heart failure, has ranked as the number one cause of death in the United States every year since 1900 except 1918, when the nation struggled with an influenza epidemic. Nearly 2,600 Americans die of CVD each day, roughly one person every 34 seconds. Given the aging of the population and the relatively dramatic recent increases in the prevalence of cardiovascular risk factors such as obesity and type 2 diabetes, CVD will be a significant health concern well into the 21st century.

Cardiovascular disease can deprive heart tissue of oxygen, thereby killing cardiac muscle cells (cardiomyocytes). This loss triggers a cascade of detrimental events, including formation of scar tissue, an overload of blood flow and pressure capacity, the overstretching of viable cardiac cells attempting to sustain cardiac output, leading to heart failure, and eventual death. Restoring damaged heart muscle tissue, through repair or regeneration, is therefore a potentially new strategy to treat heart failure.

The use of embryonic and adult-derived stem cells for cardiac repair is an active area of research. A number of stem cell types, including embryonic stem (ES) cells, cardiac stem cells that naturally reside within the heart, myoblasts (muscle stem cells), adult bone marrow-derived cells including mesenchymal cells (bone marrow-derived cells that give rise to tissues such as muscle, bone, tendons, ligaments, and adipose tissue), endothelial progenitor cells (cells that give rise to the endothelium, the interior lining of blood vessels), and umbilical cord blood cells, have been investigated as possible sources for regenerating damaged heart tissue. All have been explored in mouse or rat models, and some have been tested in larger animal models, such as pigs.

A few small studies have also been carried out in humans, usually in patients who are undergoing open-heart surgery. Several of these have demonstrated that stem cells that are injected into the circulation or directly into the injured heart tissue appear to improve cardiac function and/or induce the formation of new capillaries. The mechanism for this repair remains controversial, and the stem cells likely regenerate heart tissue through several pathways. However, the stem cell populations that have been tested in these experiments vary widely, as do the conditions of their purification and application. Although much more research is needed to assess the safety and improve the efficacy of this approach, these preliminary clinical experiments show how stem cells may one day be used to repair damaged heart tissue, thereby reducing the burden of cardiovascular disease.

In people who suffer from type1 diabetes, the cells of the pancreas that normally produce insulin are destroyed by the patient's own immune system. New studies indicate that it may be possible to direct the differentiation of human embryonic stem cells in cell culture to form insulin-producing cells that eventually could be used in transplantation therapy for persons with diabetes.

To realize the promise of novel cell-based therapies for such pervasive and debilitating diseases, scientists must be able to manipulate stem cells so that they possess the necessary characteristics for successful differentiation, transplantation, and engraftment. The following is a list of steps in successful cell-based treatments that scientists will have to learn to control to bring such treatments to the clinic. To be useful for transplant purposes, stem cells must be reproducibly made to:

Also, to avoid the problem of immune rejection, scientists are experimenting with different research strategies to generate tissues that will not be rejected.

To summarize, stem cells offer exciting promise for future therapies, but significant technical hurdles remain that will only be overcome through years of intensive research.

Previous|VII. What are the potential uses of human stem cells and the obstacles that must be overcome before these potential uses will be realized?|Next

Here is the original post:
Stem Cell Basics VII. | stemcells.nih.gov

Cardiac Stem Cells Comments Off on Stem Cell Basics VII. | stemcells.nih.gov | April 20th, 2019

Adult stem cells are the bodys toolbox, called into action by normal wear and tear on the body, and when serious damage or disease attack. Researchers believe that adult stem cells also have the potential, as yet untapped, to be tools in medicine. Scientists and physicians are working towards being able to treat patients with their own stem cells, or with banked donor stem cells that match them genetically.

Grown in large enough numbers in the lab, then transplanted into the patient, these cells could repair an injury or counter a diseaseproviding more insulin-producing cells for people with type 1 diabetes, for example, or cardiac muscle cells to help people recover from a heart attack. This approach is called regenerative medicine.

A number of challenges must be overcome before the full therapeutic potential of adult stem cells can be realized. Scientists are exploring practical ways of harvesting and maintaining most types of adult stem cells. Right now, scientists do not have the ability to grow the cells in the amounts needed for treatment. More work is also needed to find practical ways to direct the different kinds of cells to where theyre needed in the body, preferably without the need for surgery or other invasive methods.

Research in all aspects of adult stem cells and their potential is underway at Childrens Hospital Boston. Realizing that potential will require years of research, but promising strides are being made.

More:
Why are Adult Stem Cells Important? Boston Children's ...

Cardiac Stem Cells Comments Off on Why are Adult Stem Cells Important? Boston Children’s … | April 20th, 2019

Stem cells in menstrual blood have similar regenerative capabilities as thestem cells in umbilical cord blood and bone marrow. Cryo-Cell's patent-pendingmenstrual stem cell service offers women in their reproductive years the ability to store and preserve these cells for potential use by herself or a family memberfree from ethical or political controversy.

Cryo-Cell is the only stem cell bank in the world that can offer womenthe reassurance and peace of mind that comes with this opportunity.

What are menstrual stem cells?Stem cells in menstrual blood are highly proliferativeandpossess the unique ability to develop into various other types of healthy cells. During a womans menstrual cycle, these valuable stem cells are discarded.

Cryo-Cell'smenstrual stem cell bankingservice captures those self-renewing stem cells, processes and cryopreserves them for emerging cellular therapies that hold the promise of potentially treatinglife-threatening diseases.

How are menstrual stem cells collected, processed and stored?The menstrual blood is collected in a physicians officeusing a medical-grade silicone cup in place of a tampon orsanitary napkin. The sample is shipped to Cryo-Cell via a medical courier and processed in our state-of-the-art ISO Class 7 clean room.

The menstrual stem cells are stored in two cryovials that are overwrapped to safeguard them during storage. The overwrapped vials are cryogenically preserved in a facility that isclosely monitored at all times to ensure that your menstrual stem cells are safe and ready for future use.

What are the benefits of banking menstrual stem cells?Cryo-Cell's innovative menstrual stem cell banking service provides women with the exclusive opportunity to build their own personal healthcare portfolio with stem cells that will be a 100% match for the donor. Menstrual stem cells have demonstrated the capability of differentiating into many other types of stem cells such as cardiac, neural, bone, fat and cartilage.

Bankingmenstrual stem cells now is an investment in your future medical needs. Currently, they are being studied to treat stroke, heart disease, diabetes, neurodegenerative disease, and ischemic wounds in pre-clinical and clinical models.

Cryo-Cells activities for New York State residents are limited to collection, processing, and long-term storage ofmenstrual stem cells. Cryo-Cells possession of a New York State license for such collection, processing, and long-term storage does not indicate approval or endorsement of possible future uses or future suitability of these cells.

More:
Banking Menstrual Stem Cells | What are Menstrual Stem ...

Cardiac Stem Cells Comments Off on Banking Menstrual Stem Cells | What are Menstrual Stem … | April 14th, 2019