Leading Researcher: Fibrosis Improved in Systemic Sclerosis and IPF Models With Monoclonal Antibody

Leading Researcher: Fibrosis Improved in Systemic Sclerosis and IPF Models With Monoclonal Antibody

Researchers at ChemomAb and Meir Medical Center in Tel Aviv, Israel, and the University of Florence, Italy, recently presented a study investigating the therapeutic effect of the monoclonal antibody CM-101 in animal models of systemic sclerosis (SSc) and idiopathic pulmonary fibrosis (IPF). The data was presented last week in a talk titled “CM-101, a Novel Monoclonal Antibody Blocking CCL24 Ameliorates Experimental Systemic Sclerosis (SSc) and Idiopathic Pulmonary Fibrosis (IPF)” at the 4th Systemic Sclerosis World Congress in Lisbon, Portugal.

Systemic sclerosis and IPF are two conditions that involve the development and accumulation of fibrotic tissue and progressive decline of the patient’s health status. This shared pathology also involves the expression of chemokines: small proteins with an important role in the immune system. Previous research has shown that the pathway involving the chemokine CCL24 and its receptor CCR3 is significantly expressed in SSc skin tissues and in the lungs of IPF patients.

ChemomAb, an Israeli biotech company specialized in the development of monoclonal antibodies for the treatment of immune mediated disorders and orphan indications, developed a monoclonal antibody, called CM-101, capable of targeting CCL24. CM-101 was shown to reduce fibroblast and inflammatory cell migration in lab experiments.

Researchers aimed to investigate the effect of CM-101 in two mice models of SSc and IPF, induced by either subcutaneous or intratracheal injections of bleomycin (BLM), an anticancer medication with pulmonary toxicity effects. Each group consisted of nine to 12 animals with induced IPF or SSc that were treated with CM-101. Despite the fact that CM-101 was developed against the human CCL24, it also has reactivity to murine CCL24.

As compared to controls injected with antibody immunoglobulin G (IgG), CM-101 significantly reduced collagen deposition and dermal thickness in the SSc model. In the IPF model, CM-101 was found to significantly reduce inflammatory cell counts, lung collagen content, and fibrotic tissue in several lung sections, compared to controls. When CM-101 was administered seven days after IPF induction, it was still able to attenuate lung fibrosis when compared to the controls.

The research team concluded in their presentation’s abstract that: “CM-101, a novel mAb [monoclonal antibody] blocking CCL24 is effective in reducing skin thickness and lung fibrosis in two murine models of experimental SSc and IPF, respectively. These findings may merit further investigation and potential application of this new monoclonal antibody in the clinic.”

At the Congress, Scleroderma News Today correspondent Ana de Barros, PhD, had the opportunity to interview Dr. Adi Mor, founder and CEO of ChemomAb, concerning their findings and future plans for CM-101.

Mor emphasized the results obtained in SSc and IPF mouse models where the animals “treated with CM-101 actually reversed completely back into being … healthy mice.” She also said the team is “going to begin a Phase 1a/1b in systemic sclerosis patients during 2017” to test the therapeutic effects of CM-101, first in a small cohort of patients, and then move into a multicenter Phase 2 trial.

The complete Scleroderma News Today interview with Mor is available below, or can be accessed through this link.

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