CODA Biotherapeutics Receives Grant from the National Institute of Neurological Disorders and Stroke (NINDS) of the National Institutes of Health (NIH) to Help Advance its Next-Generation Gene Therapy-Mediated Chemogenetic Platform
SOUTH SAN FRANCISCO, Calif., Nov. 10, 2020 /PRNewswire/ -- CODA Biotherapeutics, Inc., a preclinical-stage biopharmaceutical company developing a gene therapy-mediated chemogenetic platform to treat neurological disorders and diseases with an initial focus on neuropathic pain and epilepsy, today announced it has been awarded a Small Business Innovation Research (SBIR) grant from the National Institute of Neurological Disorders and Stroke (NINDS) of the National Institutes of Health (NIH). As part of the NIH Helping to End Addiction Long-term InitiativeSM, or NIH HEAL InitiativeSM, the funding of $670,000 over two years will be used to support CODA's plans to evaluate and advance the Company's unique receptor-ligand pairs toward the clinic for the treatment of neuropathic pain. Orion P. Keifer, Jr. M.D., Ph.D., Vice President, Discovery and Translation at CODA, will serve as the program's principal investigator.
"We are unwavering in our commitment to developing novel chemogenetic therapies for the treatment of neurological disorders and diseases like neuropathic pain for which current treatment options have significant limitations," said Michael Narachi, President and Chief Executive Officer, CODA. "We are honored to receive this grant from NINDS, as this funding will help advance our chemogenetic platform toward human clinical trials where we hope to demonstrate transformative results for patients."
CODA Biotherapeutics is developing a paradigm-shifting gene therapy approach for neuropathic pain by deploying a chemogenetic strategy for treating neuropathic pain sensations at their origin. The Company's innovative treatment aims to modulate specific neuronal circuits where pain arises via adeno-associated virus-mediated delivery of an engineered inhibitory receptor. The receptor is designed to be quiescent in the transduced cells but will specifically and dose-dependently inhibit neurons when exposed to a novel, orally bioavailable small-molecule agonist. CODA expects this treatment will produce substantially improved and durable pain relief while potentially avoiding off-target/adverse effects of currently available treatments.
The NINDS SBIR/Small Business Technology Transfer (STTR) program funds small business concerns to conduct innovative neuroscience research and/or development that has both the potential for commercialization and public health benefit.
In addition, CODA was recently selected to collaborate with NIH's National Center for Advancing Translational Science (NCATS), also as part of the NIH HEAL initiative. CODA will partner with the Stem Cell Translation Laboratory led by Ilyas Singec, M.D., Ph.D., in the NCATS Division of Preclinical Innovation (DPI) in developing induced pluripotent stem cell (iPSC)-derived human Ab sensory neurons for the identification and characterization of novel neuropathic pain therapies. The joint NCATS/CODA collaboration will leverage expertise and technologies available at Dr. Singec's lab to jointly develop protocols for generating iPSC-derived Aβ primary sensory neurons, which CODA will then use for the identification and evaluation of inhibitory chemogenetic receptors for the treatment of neuropathic pain. G. Steven Dodson, Ph.D., Vice President of Pharmacology and Early Development at CODA will serve as lead collaborator.
"Ab neurons are a key cell type for the evaluation of our receptor-ligand combinations and their development should advance the translational understanding of how our approach may impact pain states in patients. Through this partnership, CODA will collaborate with and gain access to the scientific capabilities, expertise, state-of-the-art technologies, and resources of the NCATS DPI to develop iPSC-derived human Ab sensory neurons, which will help us progress our neuropathic pain therapies toward the clinic," added Mr. Narachi.
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