Dr. Grossman will succeed Dr. Adrian Hepner in this role, effective July 17th, 2023, and will leverage his over two decades of clinical development expertise to guide and oversee all of Coya's development programs, including its lead asset, COYA 302, for the treatment of Amyotrophic Lateral Sclerosis.
Prior to joining Coya, Dr. Grossman held executive positions at Eli Lilly, Johnson & Johnson, Bristol Myers Squibb, and Sunovion. He also served as president and chief medical officer at Glenmark Pharmaceuticals, (BSE: 532296), a USD 1.5 bn per annum global pharmaceutical company based in India, overseeing development of the entire pipeline including generics, complex generics including 505(b) (2) candidates, and next-generation biologics (including bi-specific antibodies).
He also previously served as Chief Medical officer at Mesoblast, Inc. (NASDAQ: MESO), developing allogeneic cellular therapies for inflammatory diseases.
Headquartered in Houston, TX, Coya Therapeutics, Inc. (NASDAQ: COYA) is a clinical-stage biotechnology company developing proprietary treatments focused on the biology and potential therapeutic advantages of regulatory T cells to target systemic inflammation and neuroinflammation.
Dysfunctional Tregs underlie numerous conditions including neurodegenerative, metabolic, and autoimmune diseases, and this cellular dysfunction may lead to a sustained inflammation and oxidative stress resulting in lack of homeostasis of the immune system.
Coya's investigational product candidate pipeline leverages multiple therapeutic modalities aimed at restoring the anti-inflammatory and immunomodulatory functions of Tregs.
Coya's lead therapeutic programs includes Treg-enhancing biologics (COYA 300 Series product candidates) COYA 301 and COYA 302, which are intended to enhance Treg function and expand Treg numbers. COYA 301 is a cytokine biologic for subcutaneous administration intended to enhance Treg function and expand Treg numbers in vivo, and COYA 302 is a biologic combination for subcutaneous and/or intravenous administration intended to enhance Treg function while depleting T effector function and activated macrophages.
These two mechanisms may be additive or synergistic in suppressing inflammation.
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