Chemomab Therapeutics Ltd. announced that clinical data presented showed that CM-101 was safe and well-tolerated and achieved reductions in biomarkers associated with lung inflammation and fibrogenesis in a clinical study in patients hospitalized with COVID-19-derived lung injury. CM-101 is a first-in-class monoclonal antibody that neutralizes CCL24, a soluble protein with pro-fibrotic and pro-inflammatory effects. It is in development for the treatment of fibro-inflammatory disorders, including primary sclerosingcholangitis (PSC) and systemic sclerosis (SSc).

The presentation, Treatment with CM-101 Reduced Inflammatory & Fibrotic Biomarkers in Patients with COVID-19-Derived Lung Damage, was discussed by Chemomab co-founder and Chief Scientific Officer Dr. Adi Mor at the Union World Conference on Lung Health 2022. Some of the mechanisms underlying lung inflammation resulting from COVID-19 infection are similar to those seen in chronic diseases involving lung inflammation and fibrosis, and this study was initiated by a physician/researcher who treats patients with systemic sclerosis and other rheumatological diseases. The objective of the study was to evaluate the drug's safety and activity in hospitalized COVID-19 patients with severe pneumonia, including its impact on biomarkers related to lung inflammation that are also relevant in systemic sclerosis.

The open label, single arm trial enrolled 16 adult COVID-19 patients with severe respiratory involvement. All patients were hospitalized and were receiving standard of care therapy. All were treated with a single 10mg/kg intravenous dose of CM-101 on the first day of the study and followed for 30 days.

Clinical parameters were tested daily during hospitalization and serum biomarkers were tested at baseline and on days 1, 3, 7 and 30 following drug administration. Administration of CM-101 to this acutely ill patient population was found to be safe and well tolerated. CM-101 exposures and target engagement profiles were similar to what Chemomab researchers have seen in previous clinical studies of CM-101.

Importantly, rapid reductions in serum biomarkers of lung inflammation, fibrogenesis and neutrophil activity were observed post-treatment with CM-101, consistent with the effects seen in previous preclinical and early clinical data. Reductions in the serum levels of biomarkers seen in the study included the cytokines CXCL9 and CXCL10, two biomarkers that are highly associated with lung inflammation and are known to be strongly correlated with respiratory severity. For example, CXCL10 was reduced by a median change of 65% from baseline as soon as 24-hours post treatment with CM-101 and further reduced by almost 80% at day 3. The effect was sustained through the end of the follow-up period.

It was noteworthy too that patients receiving CM-101 demonstrated a rapid and robust median reduction of 50% in c-reactive protein, or CRP, a well-known general marker of inflammation, as soon as 48 hours post-administration. CRP levels were further decreased by more than 90% at day 6 after CM-101 administration and remained stable until the end of the follow-up period. CM-101 also demonstrated larger and more rapid CRP reductions compared to a retrospective Covid-19 control group who had similar clinical characteristics and also received standard of care therapy.

Lastly, treatment with CM-101 impacted biomarkers that are associated with the formation and degradation of the extracellular matrix, such as Procollagen 4 and C3M, which were highly elevated in these patients at baseline and were significantly reduced by a median change of 25% as soon as 72 hours post-treatment, a reduction that remained stable until the end of the follow-up period.