Kadmon Corporation Presents Data on Role of ROCK2 Inhibition at AAI Annual Meeting
-- Data Presented in Two Oral Presentations --
NEW YORK, May 6, 2015 – Kadmon Corporation, LLC, today announced preclinical data defining the role of ROCK2 (Rho-associated coiled-coiled kinase 2) in regulating immune response at the cellular level. The data will be presented in two oral presentations at the American Association of Immunologists (AAI) Annual Meeting, taking place May 8-12 in New Orleans.
Recent research conducted by Kadmon and others has demonstrated the involvement of the ROCK2 signaling pathway in modulation of T-cell mediated immune responses, including regulating the secretion of pro-inflammatory cytokines such as IL-21 and IL-17. New preclinical data presented suggest that ROCK2 also controls the development and function of T follicular helper (Tfh) cells that are essential for generating high-affinity antibodies and B cell memory, further supporting the mechanism of ROCK2 inhibition to rebalance the immune response in autoimmune conditions. Specifically, KD025, Kadmon’s Phase 2 selective ROCK2 inhibitor, reduced the number of human IL-21-producing Tfh cells and the expression of Tfh cell-specific transcription factors in vitro in a dose-dependent manner. Additionally, oral treatment with KD025 reduced the percentage of Tfh and plasma B cells by more than two-fold and blocked disease progression in an Mrl/lpr murine model of systemic lupus erythematosus through defined molecular mechanisms of concurrent regulation of STAT3/STAT5 phosphorylation. Furthermore, in data previously presented at the 56th American Society of Hematology (ASH) Annual Meeting, KD025 effectively reversed chronic graft-versus-host disease in an IL-21-driven aggressive multi-organ system rodent model through reduction in the number of germinal centers, Tfh cells and antibody deposition in the lungs. Together, the data underscore the importance of ROCK2 signaling in controlling auto-aggressive immune responses.
“These data demonstrate the cellular mechanism by which selective ROCK2 inhibition regulates the balance between pro- and anti-inflammatory immune cell responses,” said Alexandra Zanin-Zhorov, Ph.D., Senior Director of Immunology at Kadmon. “ROCK2 contributes to regulation of Tfh cells in the disease state, supporting the therapeutic potential of selective ROCK2 inhibition for the treatment of autoimmunity.”
“Kadmon has demonstrated in several disease models that the ROCK2 signaling pathway controls inflammatory responses,” said Harlan W. Waksal, M.D., President and CEO of Kadmon. “These data provide further support for our study of KD025 in several autoimmune and fibrotic disease indications.”
The abstract titled, “ROCK2 signaling is required for development and function of T follicular helper cells” (Abstract #2203431) will be presented on Sunday, May 10 at 12:45 p.m. CT by Jonathan Weiss, Ph.D., Senior Scientist, Immunology at Kadmon. The abstract titled, “Selective ROCK2 inhibitor reverses experimental chronic graft-versus-host disease (cGVHD) via concurrent regulation of STAT3/STAT5 phosphorylation” (Abstract #2203439) will be presented by Dr. Zanin-Zhorov on Monday, May 11 at 4:30 p.m. CT.
About Kadmon Corporation
Kadmon Corporation, LLC, is a vertically integrated biopharmaceutical company focused on developing innovative products for significant unmet medical needs. We have a diversified product pipeline in autoimmune and fibrotic diseases, oncology, monogenic diseases and metabolic disease. For more information, visit www.kadmon.com.
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.