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Aclaris Therapeutics Announces Publication of Preclinical Research of Zunsemetinib in Pancreatic Cancer in Science Translational Medicine
WAYNE, Pa., Dec. 03, 2021 (GLOBE NEWSWIRE) -- Aclaris Therapeutics, Inc. (NASDAQ: ACRS), a clinical-stage biopharmaceutical company focused on developing
About this update from Aclaris Therapeutics, Inc.
[{"type":"text","content":"WAYNE, Pa., Dec. 03, 2021 (GLOBE NEWSWIRE) -- Aclaris Therapeutics, Inc. (NASDAQ: ACRS), a clinical-stage biopharmaceutical company focused on developing novel drug candidates for immuno-inflammatory diseases, today announced the publication of preclinical research of zunsemetinib in pancreatic cancer in the peer-reviewed journal Science Translational Medicine, on December 1, 2021. The article, entitled “The MK2/Hsp27 axis is a major survival mechanism for pancreatic ductal adenocarcinoma under genotoxic stress,” presents the results from a preclinical study using patient-derived cell lines and an autochthonous pancreatic ductal adenocarcinoma mouse model that evaluated the role of MK2, as well as the impact of zunsemetinib (ATI-450), Aclaris’ investigational oral MK2 inhibitor, in pancreatic cancer. This study was a multi-year collaboration between Aclaris and Washington University School of Medicine, led by the laboratory of Dr. Kian-Huat Lim, MD, PhD, Associate Professor in Oncology and Dr. Patrick Grierson, MD, PhD, Assistant Professor in Oncology. In the study, Dr. Lim and his team identified the MK2/HSP27 axis as an important resistance mechanism resulting in pancreatic tumor cell survival following exposure to components of FOLFIRINOX chemotherapy - the current standard-of-care treatment for pancreatic cancer. His team also demonstrated that DNA damage induced by FOLFIRINOX chemotherapy components upregulated tumor necrosis factor alpha (TNFa) in pancreatic cancer cells, which had the dual effect of impacting cell death and cell survival, and that the selective inhibition of MK2 downstream of TNFa signaling abrogated survival through blocking HSP27 activation and beclin1 mediated autophagy, which allowed TNFa to execute its pro-death mechanism. With this understanding, his team then showed that mouse survival in an autochthonous KPPC model of pancreatic cancer was statistically significantly (p","length":2315,"tagName":"div"}]