Chemomab announces poster presentation at AASLD’s The Liver Meeting 2021

New preclinical data further supports ability of CM-101 to break the vicious cycle of inflammation and fibrosis in primary sclerosing cholangitis

16 Nov 2021
Dora Wells
Clinical Content Editor

Chemomab Therapeutics, Ltd. (Chemomab), a clinical-stage biotech company focused on the discovery and development of innovative therapeutics for fibrotic and inflammatory diseases with high unmet need, announced a poster presentation at The Liver Meeting® 2021, hosted by the American Association for the Study of Liver Diseases (AASLD), which took place November 12-15, 2021.

The preclinical poster, entitled: “CCL24 Overexpression Resulting From Bile Duct Injury Induces an Inflammatory-Fibrotic Vicious Cycle in Primary Sclerosing Cholangitis,” highlights the role of the soluble protein CCL24 in Primary Sclerosing Cholangitis (PSC) pathophysiology. CCL24 is the target for Chemomab’s first-in-class monoclonal antibody CM-101, which is in a Phase 2 clinical trial for the treatment of PSC.

CCL24, which is expressed by both bile duct epithelial cells and inflammatory cells, was shown to play an important role in promoting inflammation and fibrosis in the livers of PSC patients. The studies reported in the Chemomab poster were designed to provide additional insight into these mechanisms. In these studies, Chemomab researchers focused on the injured areas in the bile duct that initiate and promote the development of PSC inflammatory-fibrotic liver damage in a vicious cycle.

The study results confirmed that human PSC liver biopsies show high CCL24 expression in both bile duct epithelial cells and recruited inflammatory cells. Importantly, CCR3, the receptor for CCL24, was found to be expressed on both immune cells and activated myofibroblasts, reflecting CCL24’s ability to induce the activity of these cells. The studies also demonstrated that inhibiting CCL24 function with CM-101 led to improvement of PSC liver injury in mouse models of the disease.

“These results further strengthen our previously published data showing that CCL24 induces liver inflammation and fibrosis,” said Adi Mor, PhD, co-founder and CSO of Chemomab. “Furthermore, we show that treating knockout mice that spontaneously develop PSC-like disease with our anti-CCL24 antibody reduced liver inflammation, liver fibrosis and proliferation of the epithelial cells that line the bile ducts. The ability of CM-101 in these preclinical studies to interfere with the core mechanisms that drive PSC pathophysiology are encouraging, providing further evidence that it has the potential to be an effective treatment for PSC, as well as for other fibrotic and inflammatory diseases.”

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