A new standard in pluripotent stem cell characterization -- TaqMan hPSC Scorecard trade; Panel
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A new standard in pluripotent stem cell characterization -- TaqMan® hPSC Scorecard™ Panel - Video
London, Jun 17:
Scientists have made a stem cell breakthrough that could make it possible to treat diabetics with an annual insulin jab, eliminating the need for painful daily injections.
The new technique involves engineering blood stem cells into insulin-secreting cells.
Experts at Londons Imperial College, led by Professor Nagy Habib, and scientists at Hammersmith Hospital are now planning human trials of the new treatment after success in laboratory studies, the Daily Express reported.
This is a fantastic breakthrough that we hope will end the burden of daily jabs for diabetics, said Dr Paul Mintz, a leading stem cell researcher at Imperial College, who is part of the team pioneering the research.
The beauty of this treatment is that we manipulate the patients own stem cells, avoiding the complication of giving them something foreign which their body will reject, he said.
In diabetes the pancreas fails to make any insulin which crucially controls blood sugar levels or it doesnt make enough.
In laboratory studies, the researchers were able to get 35 per cent of engineered cells to make insulin.
They are now planning to nurture and grow these cells so they have a colony of 100 per cent insulin-making cells that can be injected into a patients body.
The team is working to develop stem cells that could release insulin for up to a year by coating the cells in a special biodegradable matrix.
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Stem cell breakthrough can lead to one diabetes jab a year
Public release date: 17-Jun-2013 [ | E-mail | Share ]
Contact: David McKeon dmckeon@nyscf.org 212-365-7440 New York Stem Cell Foundation
NEW YORK, NY (June 17, 2013) A team from the New York Stem Cell Foundation (NYSCF) Research Institute and the Naomi Berrie Diabetes Center of Columbia University has generated patient-specific beta cells, or insulin-producing cells, that accurately reflect the features of maturity-onset diabetes of the young (MODY).
The researchers used skin cells of MODY patients to produce induced pluripotent stem (iPS) cells, from which they then made beta cells. Transplanted into a mouse, the stem cell-derived beta cells secreted insulin in a manner similar to that of the beta cells of MODY patients. Repair of the gene mutation restored insulin secretion to levels seen in cells obtained from healthy subjects. The findings were reported today in the Journal of Clinical Investigation.
Previous studies have demonstrated the ability of human embryonic stem cells and iPS cells to become beta cells that secrete insulin in response to glucose or other molecules. But the question remained as to whether stem cell-derived beta cells could accurately model genetic forms of diabetes and be used to develop and test potential therapies.
"We focused on MODY, a form of diabetes that affects approximately one in 10,000 people. While patients and other models have yielded important clinical insights into this disease, we were particularly interested in its molecular aspectshow specific genes can affect responses to glucose by the beta cell," said co-senior author Dieter Egli, PhD, Senior Research Fellow at NYSCF, who was named a NYSCFRobertson Stem Cell Investigator in 2012.
MODY is a genetically inherited form of diabetes. The most common form of MODY, type 2, results in a loss-of-function mutation in one copy of the gene that codes for the sugar-processing enzyme glucokinase (GCK). With type 2 MODY, higher glucose levels are required for GCK to metabolize glucose, leading to chronic, mildly elevated blood sugar levels and increased risk of vascular complications.
MODY patients are frequently misdiagnosed with type 1 or 2 diabetes. Proper diagnosis can not only change the patient's course of treatment but affect family members, who were previously unaware that they, too, might have this genetic disorder.
NYSCF scientists took skin cells from two Berrie Center type 2 MODY patients and "reprogrammed"or revertedthem to an embryonic-like state to become iPS cells. To examine the effect of the GCK genetic mutation, they also created two genetically manipulated iPS cell lines for comparison: one fully functional (two correct copies of the GCK gene) and one with complete loss of function (two faulty copies of the GCK gene). They then generated beta cell precursors from the fully functional and loss-of-function iPS cell lines and transplanted the cells for further maturation into immune-compromised mice.
"Our ability to create insulin-producing cells from skin cells, and then to manipulate the GCK gene in these cells using recently developed molecular methods, made it possible to definitively test several critical aspects of the utility of stem cells for the study of human disease," said Haiqing Hua, PhD, lead author on the paper, a postdoctoral fellow in the Division of Molecular Genetics, Department of Pediatrics and Naomi Berrie Diabetes Center at Columbia University and the New York Stem Cell Foundation Research Institute.
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NYSCF and Columbia researchers demonstrate use of stem cells to analyze causes, treatment of diabetes
LUGANO, Switzerland--(BUSINESS WIRE)--
Takeda Pharmaceutical Company Limited (TSE:4502) and Seattle Genetics, Inc. (SGEN) today announced data from a post-hoc analysis examining progression-free survival (PFS) following treatment with ADCETRIS (brentuximab vedotin) versus last prior therapy in patients diagnosed with relapsed or refractory Hodgkin lymphoma (HL) post-autologous stem cell transplant (ASCT) or relapsed or refractory systemic anaplastic large cell lymphoma (sALCL). The data were highlighted during a presentation at the 12th International Conference on Malignant Lymphoma (ICML) being held June 1922, 2013 in Lugano, Switzerland.
ADCETRIS is an antibody-drug conjugate (ADC) directed to CD30, a defining marker of classical HL and sALCL.
The post-hoc analysis compared investigator assessed PFS following ADCETRIS single-agent treatment to the last prior systemic therapy in patients taking part in two pivotal Phase 2 studies. The post-hoc analysis was conducted in patients with relapsed or refractory HL post-ASCT or relapsed or refractory sALCL in the intent-to-treat (ITT) population. It also included prior systemic treatment histories and post-ADCETRIS stem cell transplant experience for each patient in the ITT populations.
These encouraging data suggest that ADCETRIS may delay disease progression compared to prior therapies used in this heavily pretreated patient population, said John Radford, M.D., Professor of Medical Oncology, University of Manchester, Manchester, UK. ADCETRIS is a CD30-targeted treatment option for patients with relapsed or refractory HL or relapsed or refractory sALCL that has shown a high overall response rate, including durable complete responses in both of its approved indications.
Progression-free survival analyses of two pivotal phase 2 studies of brentuximab vedotin in patients with relapsed or refractory Hodgkin lymphoma or systemic anaplastic large-cell lymphoma (Poster #303)
The analysis, presented by Dr. Radford, included:
Relapsed or Refractory HL post-ASCT
Relapsed or Refractory sALCL
Details of the poster presentation are as follows:
Original post:
Takeda and Seattle Genetics Highlight Post-Hoc Analysis Examining Progression-free Survival with ADCETRIS® ...
A team from the New York Stem Cell Foundation (NYSCF) Research Institute and the Naomi Berrie Diabetes Center of Columbia University has generated patient-specific beta cells, or insulin-producing cells, that accurately reflect the features of maturity-onset diabetes of the young (MODY).
The researchers used skin cells of MODY patients to produce induced pluripotent stem (iPS) cells, from which they then made beta cells. Transplanted into a mouse, the stem cell-derived beta cells secreted insulin in a manner similar to that of the beta cells of MODY patients. Repair of the gene mutation restored insulin secretion to levels seen in cells obtained from healthy subjects. The findings were reported today in the Journal of Clinical Investigation.
Previous studies have demonstrated the ability of human embryonic stem cells and iPS cells to become beta cells that secrete insulin in response to glucose or other molecules. But the question remained as to whether stem cell-derived beta cells could accurately model genetic forms of diabetes and be used to develop and test potential therapies.
We focused on MODY, a form of diabetes that affects approximately one in 10,000 people. While patients and other models have yielded important clinical insights into this disease, we were particularly interested in its molecular aspects-how specific genes can affect responses to glucose by the beta cell, said co-senior author Dieter Egli, PhD, Senior Research Fellow at NYSCF, who was named a NYSCF-Robertson Stem Cell Investigator in 2012.
MODY is a genetically inherited form of diabetes. The most common form of MODY, type 2, results in a loss-of-function mutation in one copy of the gene that codes for the sugar-processing enzyme glucokinase (GCK). With type 2 MODY, higher glucose levels are required for GCK to metabolize glucose, leading to chronic, mildly elevated blood sugar levels and increased risk of vascular complications.
MODY patients are frequently misdiagnosed with type 1 or 2 diabetes. Proper diagnosis can not only change the patients course of treatment but affect family members, who were previously unaware that they, too, might have this genetic disorder.
NYSCF scientists took skin cells from two Berrie Center type 2 MODY patients and reprogrammed-or reverted-them to an embryonic-like state to become iPS cells. To examine the effect of the GCK genetic mutation, they also created two genetically manipulated iPS cell lines for comparison: one fully functional (two correct copies of the GCK gene) and one with complete loss of function (two faulty copies of the GCK gene). They then generated beta cell precursors from the fully functional and loss-of-function iPS cell lines and transplanted the cells for further maturation into immune-compromised mice.
Our ability to create insulin-producing cells from skin cells, and then to manipulate the GCK gene in these cells using recently developed molecular methods, made it possible to definitively test several critical aspects of the utility of stem cells for the study of human disease, said Haiqing Hua, PhD, lead author on the paper, a postdoctoral fellow in the Division of Molecular Genetics, Department of Pediatrics and Naomi Berrie Diabetes Center at Columbia University and the New York Stem Cell Foundation Research Institute.
Read the original: Researchers use patient-specific stem cells to correct deficient insulin-producing cells
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Researchers use patient-specific stem cells to correct deficient ...
BOSTON, June 12, 2013 /PRNewswire/ --Scotland's standing as Europe's largest and most highly regarded stem cell research community has been reaffirmed recently by announcements of funding from the UK Medical Research Council (MRC) and the British Heart Foundation to the MRC Centre for Regenerative Medicine (CRM) based at the Edinburgh BioQuarter. As part of a major $25m boost for UK regenerative medicine, the Edinburgh center will play a key role in the development of new therapies.
This and other recent news exemplify Scotland's strength and depth of expertise in this field. Developments at an academic level describing increased understanding of the mechanism of cellular reprogramming were recently reported by Dr. Keisuke Kaje from the MRC-CRM in Nature, whilst Scottish company Roslin Cells and the MRC-CRM have been actively collaborating on iPS cell line production ensuring a more quality-oriented perspective and generating more commercial opportunities.
Elsewhere, exciting research at Heriot-Watt University has seen the use of 3D printing techniques to produce clusters of viable stem cells that could speed up progress towards creating artificial organs. In the immediate future, Professor Will Shu and his team hope the technique can be used to generate biopsy-like tissue samples for drug testing.
At a clinical level also, Scotland has seen some major developments. ReNeuron has announced the successful conclusion of its Phase 1 stem cell clinical trial (PISCES) using its ReN001 therapy for treatment of stroke. This trial has been conducted at the Southern General Hospital, Greater Glasgow & Clyde, by Professor Keith Muir. The company is currently seeking final regulatory and ethical approvals for a Phase II studyscheduled to begin this summer. In a separate announcement ReNeuron has selected Dundee as the location of choice for another Phase 1 stem cell-based clinical trial, this time focused on critical limb ischemia.
Also underway is a 20-patient Phase 1 clinical trial using limbal cells to repair corneal blindness. This is being led by Professor Bal Dhillon in Edinburgh and is funded jointly by the UK Stem Cell Foundation and Scottish Enterprise in partnership with Scotland's Chief Scientist's Office.
Finally, a significant boost to Scotland's capabilities for supporting clinical trials was received with news that the new GMP Manufacturing Facility within the MRC-CRM, and managed by Roslin Cells along with the Scottish National Blood Transfusion Service (SNBTS), has been awarded a license by the Medicines and Healthcare products Regulatory Authority (MHRA), which permits the manufacture and release of Advanced Therapy Medicinal Products (ATMPs) for use in clinical trials.
"Scotland is once again demonstrating its expertise in academic, translational and clinical applications in stem cells and regenerative medicine" says Dr. Ed Hutchinson, spokesperson for life sciences at Scottish Enterprise. "These advances have been made possible through a collaborative approach whereby Scotland's universities, companies and health boards all actively participate in developments in this exciting area. With a supportive supply chain in place, Scotland can be seen as the place to go to undertake stem cell clinical trials and as a base for the European market."
This week, a Scottish delegation including the MRC Center for Regenerative Medicine, Roslin Cells and Universities of Edinburgh and Glasgow, in addition to stem-cell focused companies such as Biogelx and Sistemic, will attend the International Society for Stem Cell Research (ISSCR) conference in Boston. Further information on Scotland's stem cell industry can be found at the Scottish Development International booth, number 331, at the ISSCR conference or visit http://www.sdi.co.uk.
Media Contact: Rebecca Gehman Development Counsellors International rgehman@aboutdci.com; 212-725-0707
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Scotland Continues to Forge Ahead in Stem Cell Research
June 17, 2013 A team from the New York Stem Cell Foundation (NYSCF) Research Institute and the Naomi Berrie Diabetes Center of Columbia University has generated patient-specific beta cells, or insulin-producing cells, that accurately reflect the features of maturity-onset diabetes of the young (MODY).
The researchers used skin cells of MODY patients to produce induced pluripotent stem (iPS) cells, from which they then made beta cells. Transplanted into a mouse, the stem cell-derived beta cells secreted insulin in a manner similar to that of the beta cells of MODY patients. Repair of the gene mutation restored insulin secretion to levels seen in cells obtained from healthy subjects. The findings were reported today in the Journal of Clinical Investigation.
Previous studies have demonstrated the ability of human embryonic stem cells and iPS cells to become beta cells that secrete insulin in response to glucose or other molecules. But the question remained as to whether stem cell-derived beta cells could accurately model genetic forms of diabetes and be used to develop and test potential therapies.
"We focused on MODY, a form of diabetes that affects approximately one in 10,000 people. While patients and other models have yielded important clinical insights into this disease, we were particularly interested in its molecular aspects -- how specific genes can affect responses to glucose by the beta cell," said co-senior author Dieter Egli, PhD, Senior Research Fellow at NYSCF, who was named a NYSCF-Robertson Stem Cell Investigator in 2012.
MODY is a genetically inherited form of diabetes. The most common form of MODY, type 2, results in a loss-of-function mutation in one copy of the gene that codes for the sugar-processing enzyme glucokinase (GCK). With type 2 MODY, higher glucose levels are required for GCK to metabolize glucose, leading to chronic, mildly elevated blood sugar levels and increased risk of vascular complications.
MODY patients are frequently misdiagnosed with type 1 or 2 diabetes. Proper diagnosis can not only change the patient's course of treatment but affect family members, who were previously unaware that they, too, might have this genetic disorder.
NYSCF scientists took skin cells from two Berrie Center type 2 MODY patients and "reprogrammed" -- or reverted -- them to an embryonic-like state to become iPS cells. To examine the effect of the GCK genetic mutation, they also created two genetically manipulated iPS cell lines for comparison: one fully functional (two correct copies of the GCK gene) and one with complete loss of function (two faulty copies of the GCK gene). They then generated beta cell precursors from the fully functional and loss-of-function iPS cell lines and transplanted the cells for further maturation into immune-compromised mice.
"Our ability to create insulin-producing cells from skin cells, and then to manipulate the GCK gene in these cells using recently developed molecular methods, made it possible to definitively test several critical aspects of the utility of stem cells for the study of human disease," said Haiqing Hua, PhD, lead author on the paper, a postdoctoral fellow in the Division of Molecular Genetics, Department of Pediatrics and Naomi Berrie Diabetes Center at Columbia University and the New York Stem Cell Foundation Research Institute.
When given a glucose tolerance test three months later, mice with MODY beta cells had decreased sensitivity to glucose but a normal response to other molecules that stimulate insulin secretion. This is the hallmark of MODY. Mice with two faulty copies of the GCK gene secreted no additional insulin in response to glucose. When the researchers repaired the GCK mutation using molecular techniques, cells with two restored copies of GCK responded normally to the glucose stress test. Unlike other reported techniques, the researchers' approach efficiently repaired the GCK mutation without introducing any potentially harmful additional DNA.
"Generation of patient-derived beta cells with gene correction could ultimately prove to be a useful cell-replacement therapy by restoring patients' ability to regulate their own glucose. This result is truly exciting," said Susan L. Solomon, Chief Executive Officer of The New York Stem Cell Foundation.
See original here:
Researchers demonstrate use of stem cells to analyze causes, treatment of diabetes
NYSCF AND COLUMBIA RESEARCHERS DEMONSTRATE USE OF STEM CELLS TO ANALYZE CAUSES AND TREATMENT OF DIABETES
Using patient-specific stem cells to correct deficient insulin-producing cells
Newswise NEW YORK, NY (June 17, 2013) A team from the New York Stem Cell Foundation (NYSCF) Research Institute and the Naomi Berrie Diabetes Center of Columbia University has generated patient-specific beta cells, or insulin-producing cells, that accurately reflect the features of maturity-onset diabetes of the young (MODY).
The researchers used skin cells of MODY patients to produce induced pluripotent stem (iPS) cells, from which they then made beta cells. Transplanted into a mouse, the stem cell-derived beta cells secreted insulin in a manner similar to that of the beta cells of MODY patients. Repair of the gene mutation restored insulin secretion to levels seen in cells obtained from healthy subjects. The findings were reported today in the Journal of Clinical Investigation.
Previous studies have demonstrated the ability of human embryonic stem cells and iPS cells to become beta cells that secrete insulin in response to glucose or other molecules. But the question remained as to whether stem cell-derived beta cells could accurately model genetic forms of diabetes and be used to develop and test potential therapies.
We focused on MODY, a form of diabetes that affects approximately one in 10,000 people. While patients and other models have yielded important clinical insights into this disease, we were particularly interested in its molecular aspectshow specific genes can affect responses to glucose by the beta cell, said co-senior author Dieter Egli, PhD, Senior Research Fellow at NYSCF, who was named a NYSCFRobertson Stem Cell Investigator in 2012.
MODY is a genetically inherited form of diabetes. The most common form of MODY, type 2, results in a loss-of-function mutation in one copy of the gene that codes for the sugar-processing enzyme glucokinase (GCK). With type 2 MODY, higher glucose levels are required for GCK to metabolize glucose, leading to chronic, mildly elevated blood sugar levels and increased risk of vascular complications.
MODY patients are frequently misdiagnosed with type 1 or 2 diabetes. Proper diagnosis can not only change the patients course of treatment but affect family members, who were previously unaware that they, too, might have this genetic disorder.
NYSCF scientists took skin cells from two Berrie Center type 2 MODY patients and reprogrammedor revertedthem to an embryonic-like state to become iPS cells. To examine the effect of the GCK genetic mutation, they also created two genetically manipulated iPS cell lines for comparison: one fully functional (two correct copies of the GCK gene) and one with complete loss of function (two faulty copies of the GCK gene). They then generated beta cell precursors from the fully functional and loss-of-function iPS cell lines and transplanted the cells for further maturation into immune-compromised mice.
Our ability to create insulin-producing cells from skin cells, and then to manipulate the GCK gene in these cells using recently developed molecular methods, made it possible to definitively test several critical aspects of the utility of stem cells for the study of human disease, said Haiqing Hua, PhD, lead author on the paper, a postdoctoral fellow in the Division of Molecular Genetics, Department of Pediatrics and Naomi Berrie Diabetes Center at Columbia University and the New York Stem Cell Foundation Research Institute.
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Researchers Demonstrate Use of Stem Cells to Analyze Causes ...
June 17, 2013 Harvard Stem Cell Institute (HSCI) researchers have identified in the most aggressive forms of cancer a gene known to regulate embryonic stem cell self-renewal, beginning a creative search for a drug that can block its activity.
The gene, SALL4, gives stem cells their ability to continue dividing as stem cells rather than becoming mature cells. Typically, cells only express SALL4 during embryonic development, but the gene is re-expressed in nearly all cases of acute myeloid leukemia and 10 to 30 percent of liver, lung, gastric, ovarian, endometrial, and breast cancers, strongly suggesting it plays a role in tumor formation.
In work published in the New England Journal of Medicine, two HSCI-affiliated labs -- one in Singapore and the other in Boston -- show that knocking out the SALL4 gene in mouse liver tumors, or interfering with the activity of its protein product with a small inhibitor, treats the cancer.
"Our paper is about liver cancer, but it is likely true about lung cancer, breast cancer, ovarian cancer, many, many cancers," said HSCI Blood Diseases Program leader Daniel Tenen, who also heads a laboratory at the Cancer Science Institute of Singapore (CSI Singapore). "SALL4 is a marker, so if we had a small molecule drug blocking SALL4 function, we could also predict which patients would be responsive."
Studying the therapeutic potential of a transcription factor is unusual in the field of cancer research. Transcription factors are typically avoided because of the difficulty of developing drugs that safely interfere with genetic targets. Most cancer researchers focus their attention on kinases.
The HSCI researchers' inquiry into the basic biology of the SALL4 gene, however, revealed another way to interfere with its activity in cancer cells. The gene's protein product is responsible for turning off a tumor-suppressor gene, causing the cell to divide uncontrollably. Using this knowledge, the researchers demonstrated that targeting the SALL4 protein with druglike molecules could halt tumor growth. "The pharmaceutical companies decided that if it is not a kinase and it is not a cell surface molecule, then it is 'undruggable,' " Tenen said. "To me, if you say anything is 'undoable,' you are limiting yourself as a biomedical scientist."
Earlier this year, Tenen's co-author, HSCI-affiliated faculty member Li Chai, a Harvard Medical School assistant professor of pathology at Brigham and Women's Hospital, published a paper in the journal Blood, reporting that a SALL4 inhibitor has similar treatment potential in leukemia cells.
Chai took blood samples from patients with acute myeloid leukemia, treated the leukemic cells with the inhibitor that interferes with SALL4 protein activity, and then transplanted the blood into mice. The result was a gradual regression of the same cancer in mice.
"I am excited about being on the front line of this new drug development," Chai said. "As a physician-scientist, if I can find a new class of drug that has very low toxicity to normal tissues, my patients can have a better quality of life."
Chai and Tenen are now working with HSCI Executive Committee member Lee Rubin, the Harvard Institute of Chemistry and Cell Biology, and James Bradner of Dana-Farber Cancer Institute, another HSCI-affiliated faculty member, to overcome the technical challenges of drug development and demonstrate the potential of SALL4 interference to treat other forms of cancer.
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'Undruggable' cancer may be druggable after all: New target identified
SOUTH SAN FRANCISCO, CA--(Marketwired - Jun 17, 2013) - VistaGen Therapeutics, Inc. (OTCQB: VSTA), a biotechnology company applying stem cell technology for drug rescue, predictive toxicology and drug metabolism assays, presented key developments involving its CardioSafe 3D and LiverSafe 3D bioassay systems in poster presentations at the 11th Annual Meeting of the International Society of Stem Cell Research(ISSCR), the largest forum for stem cell and regenerative medicine professionals from around the world, held June 12 to 15, 2013, in Boston, Massachusetts.
Dr. Hai-Qing Xian, Senior Scientist, presented VistaGen's poster entitled "Cardiotoxicity Assessment of Anti-Cancer Kinase Inhibitors using Human Pluripotent Stem Cell-Derived Cardiomyocyte Based Assays," which detailed important developments demonstrating that CardioSafe 3D, VistaGen's high throughput, human heart cell-based bioassay, is a clinically predictive system for preclinical cardiac safety screening of anti-cancer drug candidates, including small molecule kinase inhibitors (KIs), a new category of drugs that have revolutionized cancer therapy due to decreased systemic toxicity and increased target cell efficacy compared to classic cancer drugs, as well as other therapeutic compounds. VistaGen demonstrated the utility of CardioSafe 3D to detect cardiac toxicities of well-known anti-cancer KIs, including imatinib, dasatinib, sunitinib, erlotinib and temsirolimus, which have been associated with adverse clinical cardiac events that were not detected during the drug development process. As demonstrated in the poster presentation, CardioSafe 3D successfully detected cardiotoxicity induced by representative compounds from different KI categories.Additionally, the bioassay system provided clues to the major mechanisms of cardiac cytotoxicity induced by each compound, thus enabling not only the identification of toxicities early in the drug development process, but also discovery of potential mechanisms of action.
Dr. Kristina Bonham, Senior Scientist, Hepatocyte Biology Project Leader, presented VistaGen's poster entitled "Semi-quantitative assay of CYP3A4 allows the identification and selection of mature human stem cell derived hepatocytes," which detailed developments indicating that LiverSafe 3D, VistaGen's human liver cell-based bioassay, can monitor the induction of the key metabolic enzyme, CYP3A4, and its expression level over time. Using an optimized protocol for the differentiation of hepatocyte-like cells, VistaGen demonstrated levels of CYP3A4 mRNA approaching that in human adult liver on a per cell basis. The reported data suggest that VistaGen's liver cells have many of the functional properties of mature adult liver cells, enabling multiple functional analyses and providing a powerful system to evaluate the effects of drug candidates on CYP3A4 expression and liver function, offering a valuable aid for assessing potential drug candidates for toxicity and adverse drug-drug interactions.
H. Ralph Snodgrass, PhD, VistaGen's President and Chief Scientific Officer, stated, "For the first time, our technology has caught up with the dreams and visions we had 15 years ago when we founded VistaGen.We now have the type and quality of human cell-based biological assay systems that provide real insight into both the therapeutic and toxic effects of new drug candidates long before they are ever tested in humans. Next-generation biological assays can now provide important preclinical human data that will increase the probability of selecting safer and effective therapeutics for clinical development."
"It is evident from the mood, tone and scientific discussions throughout the ISSCR conference that this is the most exciting time in the history of stem cell research," continued Dr. Snodgrass. "We anticipate that we will see an explosion over the next ten years in the contribution of human pluripotent stem cell-based biological assays to drug development, in parallel with phenomenal advancements in the therapeutic uses of mature cells and tissues derived from human pluripotent stem cells to treat some of the most intractable human diseases and conditions. Our team is truly fortunate and excited about being a part of this transformational process."
About VistaGen Therapeutics
VistaGen is a biotechnology company applying human pluripotent stem cell technology for drug rescue, predictive toxicology and drug metabolism screening. VistaGen's drug rescue activities combine its human pluripotent stem cell technology platform, Human Clinical Trials in a Test Tube, with modern medicinal chemistry to generate novel, safer chemical variants (Drug Rescue Variants) of once-promising small molecule drug candidates. These are drug candidates discontinued by pharmaceutical companies, the U.S. National Institutes of Health (NIH) or university laboratories, after substantial investment in discovery and development, due to heart or liver toxicity or metabolism issues. VistaGen uses its pluripotent stem cell technology to generate early indications, or predictions, of how humans will ultimately respond to new drug candidates before they are ever tested in humans, bringing human biology to the front end of the drug development process.
VistaGen's small molecule prodrug candidate, AV-101, has completed Phase 1 development for treatment of neuropathic pain. Neuropathic pain, a serious and chronic condition causing pain after an injury or disease of the peripheral or central nervous system, affects millions of people worldwide.
Visit VistaGen at http://www.VistaGen.com, follow VistaGen at http://www.twitter.com/VistaGen or view VistaGen's Facebook page at http://www.facebook.com/VistaGen.
Cautionary Statement Regarding Forward Looking Statements
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VistaGen Therapeutics Presents CardioSafe 3D(TM) and LiverSafe 3D(TM) Developments at International Society of Stem ...