SOURCE: Kadmon Corporation

Kadmon Corporation

February 25, 2016 08:30 ET

Kadmon to Present Preclinical Data Demonstrating ROCK2 Signaling as a Key Regulator of T Follicular Helper Cell Function in Autoimmune Conditions

Data Suggest the Potential of Targeting ROCK2 to Attenuate Autoimmune Disease

NEW YORK, NY--(Marketwired - Feb 25, 2016) - Kadmon Corporation, LLC today 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. 

"These data demonstrate that selective ROCK2 inhibition with KD025 reduced the number and function of Tfh cells, a key driver of dysregulated antibody production during systemic autoimmunity," said Jonathan Weiss, Ph.D., Senior Scientist I, Immunology Research Group at Kadmon and first author of the abstract. "Oral administration of KD025 also prevented disease progression in a lupus mouse model in a manner consistent with our in vitro human cell data, further supporting the defined molecular mechanism of ROCK2 in the modulating immune response." 

"Research conducted by Kadmon and others has demonstrated time and again that ROCK2 signaling plays a critical role across multiple facets of the immune response," said Harlan W. Waksal, M.D., President and CEO at Kadmon. "We continue to learn more about the role of selective ROCK2 inhibition through our preclinical work as well as in our ongoing and planned clinical studies of KD025 in autoimmunity." 

About Kadmon Corporation
Kadmon Corporation, LLC is a fully integrated biopharmaceutical company engaged in the discovery, development and commercialization of small molecules and biologics to address disease areas of significant unmet medical need. We have a diversified product pipeline in autoimmune and fibrotic diseases, oncology, and genetic and metabolic diseases. 

This press release contains forward-looking statements. These forward-looking statements are based on management's expectations and are subject to certain factors, risks and uncertainties that may cause actual results, outcome of events, timing and performance to differ materially from those expressed or implied by such statements. The information contained in this press release is believed to be current as of the date of original issue. Kadmon expressly disclaims any obligation or undertaking to release publicly any updates or revisions to any forward-looking statements contained herein to reflect any change in our expectations with regard thereto or any change in events, conditions or circumstances on which any such statements are based.

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