Company Overview of Capricor Therapeutics, Inc.
Capricor Therapeutics, Inc., a biotechnology company, is focused on the development of novel therapeutics to prevent and treat cardiovascular diseases. Its lead product candidates include CAP-1002 and Cenderitide. The company was founded in 2005 and is based in Beverly Hills, California.
8840 Wilshire Boulevard
Beverly Hills, CA 90211
Founded in 2005
Key Executives for Capricor Therapeutics, Inc.
Total Annual Compensation: $232.3K
Executive Vice President
Total Annual Compensation: $189.4K
Compensation as of Fiscal Year 2013.
Capricor Therapeutics, Inc. Key Developments
Capricor Therapeutics, Inc. Presents at 26th Annual Piper Jaffray Healthcare Conference, Dec-02-2014 09:00 AM
Dec 2 14
Capricor Therapeutics, Inc. Presents at 26th Annual Piper Jaffray Healthcare Conference, Dec-02-2014 09:00 AM. Venue: The New York Palace Hotel, 455 Madison Ave, New York, NY 10022, United States. Speakers: Linda Marbán, Co-Founder, Chief Executive Officer, President and Director.
Capricor Therapeutics Announces Favorable ALLSTAR Phase I Safety Results
Nov 18 14
Capricor Therapeutics, Inc. announced at the American Heart Association's Annual Scientific Sessions 2014, the one-year results of the Phase I ALLSTAR (Allogeneic Heart Stem Cells to Achieve Myocardial Regeneration) clinical trial, which indicate that intracoronary injection of allogeneic cardiosphere-derived stem cells (CAP-1002) to achieve myocardial regeneration in patients with left-ventricular dysfunction who have had an anterior myocardial infarction appears to be safe, with no deaths, no acute myocarditis and no major adverse cardiac events. The safety endpoints of the trial, including no acute myocarditis attributable to CAP-1002, no deaths due to ventricular tachycardia or ventricular fibrillation, no sudden death and no major adverse cardiac events, were achieved with no endpoint events in the 14 enrolled subjects at 1 month and at 12 months. The results showed that none of the pre-specified safety endpoints occurred. In addition, exploratory efficacy data in this Phase I trial have shown improvements in ejection fraction and reduction in scar size, most notably in the Phase II equivalent population. This study prospectively enrolled 14 adults from 40 to 66 years old with a recent (within 28 to 90 days) or chronic (within 91 to 365 days) anterior myocardial infarction, left-ventricular dysfunction and an infarct size >15% of left-ventricular mass and infused them with CAP-1002 at a dose of either 12.5M or 25M using stop-flow intracoronary infusion. At baseline, the participants had left-ventricular function impairment with a mean ejection fraction of 42% with a range of 26.7% to 55.1%. Phase I was funded in large part by a grant received from the NIH. In addition, exploratory efficacy data in this Phase I trial have shown improvements in ejection fraction and reduction in scar size, most notably in those participants who would be included in the Phase II clinical study by virtue of dose and tissue type compatibility. With respect to those participants, the data showed a relative reduction at one year of 15% of infarct scar size and a nearly 4% absolute improvement in ejection fraction. The company suggests that these data be interpreted with caution as the sample size was small and there was no contemporaneous control group. The Phase II portion of the trial, currently underway, began enrollment in January 2014, and is expected to enroll approximately 300 patients who have had an anterior myocardial infarction within 30 days to one year prior to enrollment, left-ventricular function and an infarct size >15% of left-ventricular mass. The participants will be randomized to receive either CAP-1002 or placebo in a 2:1 ratio favoring CAP-1002. In addition, the Phase II portion of the ALLSTAR trial will aim to further establish the safety and determine the efficacy of this therapy in reducing the scar size and improving the ejection fraction in these subjects with moderate to large anterior myocardial infarction who are at significant risk of deterioration into heart failure and early death. Phase II of the ALLSTAR trial has been funded with the support of the California Institute for Regenerative Medicine.
Capricor Therapeutics, Inc. Announces Positive Pre-Clinical Data for Cardiosphere-Derived Cells on Duchenne Muscular Dystrophy Cardiomyopathy
Nov 18 14
Capricor Therapeutics, Inc. announced positive data from the laboratory of Eduardo Marbán, M.D., Ph.D., Capricor's Scientific Advisory Board Chairman and the Director of the Cedars-Sinai Heart Institute. The abstract was presented at the Late Breaking Basic Science Posters and Reception at the American Heart Association's Scientific Sessions 2014 on November 17, 2014. Capricor's Cardiosphere-derived cells (CDCs), also known as CAP-1002, promote cardiomyogenesis and angiogenesis, while inhibiting oxidative stress, inflammation and fibrosis. Dr. Marbán tested the hypothesis that CDC transplantation may be beneficial in mice with muscular dystrophy (mdx mice), which progressively develop cardiomyopathy due to dystrophin deficiency and the resultant intense oxidative stress, inflammation and apoptosis. A total of 56 mice were studied at a point when global cardiac dysfunction was already evident by echocardiography. Wild-type syngeneic mouse CDCs (10(5) cells total) or control were injected intra-myocardium in 5 left ventricular (LV) sites in 10-month old mdx mice. LV ejection fraction markedly improved 3 weeks after treatment in CDC-treated mice compared to vehicle-treated mice (60.4+/-1.6 against 48.1+/-2.2; p<0.005), CDC-treated mdx mice exhibited higher maximal exercise capacity compared to vehicle-treated mice over 3 months of follow up (p<0.05), the functional improvement was associated with enhanced Nrf2 activation, up-regulation of Nrf2 downstream gene products, increased expression of mitochondrial transcription factor A and cellular mitochondrial content, restored expression of mitochondrial respiratory complex proteins, reduced collagen I and III deposition, and attenuated infiltration of inflammatory cells [CD68+ macrophages and CD3+ T cells] in the CDC-treated mouse hearts. The data demonstrated that cardiac function and exercise capacity improved in CDC-treated mdx mice, accompanied by enhanced activation of the antioxidative Nrf2 pathway, attenuation of inflammation, reduction in collagen content and fibrosis, and augmented cardiomyogenesis in CDC-treated mdx hearts. The findings raise the possibility that CDCs may be useful therapeutically to treat heart failure in patients with Duchenne muscular dystrophy.
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