Company Overview of Kadmon Holdings, LLC
Kadmon Holdings, LLC, a biopharmaceutical company, discovers, develops, and commercializes small molecules and biologics to address unmet medical needs. The company markets and distributes a portfolio of branded generic ribavirin products for chronic hepatitis C virus infection; co-promotes a product for chronic weight management; distributes products for chorea, cytomegalovirus retinitis, and for the prevention of CMV disease. It is also developing product candidates in autoimmune and fibrotic diseases, oncology, and genetic diseases. The company is headquartered in New York, New York.
450 East 29th Street
New York, NY 10016
Key Executives for Kadmon Holdings, LLC
Chief Executive Officer, President and Director
Total Annual Compensation: $1.0M
Chief Financial Officer and Executive Vice President
Total Annual Compensation: $515.4K
Chief Administrative, Compliance & Legal Officer, Executive Vice President and General Counsel
Total Annual Compensation: $500.0K
Compensation as of Fiscal Year 2015.
Kadmon Holdings, LLC Key Developments
Kadmon Corporation, LLC Initiates Phase 2 Clinical Trial Evaluating KD025 in Idiopathic Pulmonary Fibrosis
Jun 3 16
Kadmon Corporation, LLC announced that the first patient has been dosed in a Phase 2 clinical trial of KD025, the Company's rho-associated coiled-coil kinase 2 (ROCK2) inhibitor, for the treatment of idiopathic pulmonary fibrosis (IPF), a chronic and ultimately fatal disease characterized by the scarring of lung tissue. The randomized, open-label, 24-week study examines the safety, tolerability and activity of KD025 in IPF patients in the United States who have received or been offered pirfenidone and/or nintedanib. Thirty-six patients will be randomized into two cohorts: one cohort of 24 patients treated with KD025 at 400 mg QD, versus another cohort of 12 patients treated with standard of care. In fibrotic diseases like IPF, ROCK2 signaling is up-regulated in fibrotic tissues, effecting macrophage infiltration, endothelial cell activation and myofibroblast differentiation. These processes result in excess collagen deposition, scar tissue formation, organ malfunction and death. Preclinical research conducted by Kadmon has demonstrated that ROCK2 inhibition has the potential to halt and reverse these fibrotic processes. ROCK2 inhibition with KD025 significantly reduced established lung fibrosis and inflammation and improved pulmonary function in a dose-dependent manner in a bleomycin-induced mouse IPF model.
Kadmon Corporation, LLC Presents at NewYork BIO Annual Conference 2016, May-12-2016 10:45 AM
May 4 16
Kadmon Corporation, LLC Presents at NewYork BIO Annual Conference 2016, May-12-2016 10:45 AM. Venue: New York, United States. Speakers: Thomas Gallagher, Senior VP, Licensing and Intellectual Property.
Kadmon Corporation, LLC to Present Preclinical Data Demonstrating ROCK2 Signaling as Key Regulator of T Follicular Helper Cell Function in Autoimmune Conditions
Feb 25 16
Kadmon Corporation, LLC announced preclinical data demonstrating that selective inhibition of rho-associated coiled-coil kinase 2 (ROCK2), a signaling pathway implicated in the pathogenesis of autoimmunity, significantly decreased the development and function of cells involved in the inflammatory response while preserving normal immune system function, supporting the potential of targeted ROCK2 inhibition to treat autoimmune disease. The data will be reported in a poster presentation at the 2016 Keystone Symposia Conference taking place February 26 - March 1, 2016 in Monterey, California. The immune response is regulated in part by T follicular helper (Tfh) cells, which help generate antibodies to foreign antigens. In autoimmune disease, uncontrolled Tfh cell activity leads to the development of high levels of auto-antibodies, causing organ dysfunction. Recent Kadmon research has demonstrated that treatment with KD025, the company's selective ROCK2 inhibitor currently in Phase 2 clinical development, blocks specific signaling pathways that regulate Tfh cell development and function while leaving normal immune responses intact. New preclinical data demonstrated that ROCK2 inhibition with KD025 reduced the percentage of Th17 type Tfh cells and also diminished the ability of Tfh cells to promote antibody production. Importantly, treatment with KD025 had no effect on Th1 type Tfh cells, helping to preserve normal humoral immune response. The role of ROCK2 signaling in regulating Tfh production was further demonstrated in a mouse model of lupus, in which KD025-treated animals showed a reduction in the percentage of Tfh cells in spleens, mirrored by substantial improvements in both clinical and histological scoring.
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