About CCL24
Over the last 15 years, our scientific team discovered the role of the soluble protein CCL24 as a key regulator in fibro-inflammatory processes, specifically, its pivotal pro-fibrotic and pro-inflammatory effects in fibrotic diseases.
Chemomab researchers have documented CCL24 up-regulation and its correlation with disease severity in fibrotic disease tissues, including liver, skin and lung fibrosis-related pathologies. Based on these discoveries, Chemomab established a comprehensive preclinical package to support the therapeutic effects of blockading CCL24.
We have demonstrated that CCL24 works through a dual biological pathway directly activating fibroblasts while recruiting immune cells and thereby maintaining the inflammatory environment that supports fibrogenesis. Chemomab has shown that inhibiting these pathways by blocking CCL24 prevents and potentially reverses fibrotic tissue growth within the liver, skin and lung.
Based on patient data and a variety of relevant disease models, Chemomab developed nebokitug, a first-in-class monoclonal antibody that targets and neutralizes CCL24, ameliorating its overexpression and blocking its harmful effects.
About Nebokitug Therapeutic Platform
Nebokitug is a novel therapy that addresses the high unmet need for effective treatments for fibrotic diseases. In preclinical studies, treatment with nebokitug demonstrated strong anti-fibrotic effects, reduced inflammatory injury and significantly improved organ damage. Numerous in-vivo, in-vitro and ex-vivo studies showed that nebokitug demonstrated potent anti-CCL24 effects in disease models of primary sclerosing cholangitis (PSC), systemic sclerosis (SSc), metabolic-associated steatohepatitis (MASH) and idiopathic pulmonary fibrosis (IPF). In 5 clinical trials to date, nebokitug appeared safe and well tolerated in healthy subjects and in patients with metabolic-associated fatty liver disease (MALFD), with MASH, with acute lung injury and with PSC.
Based on CM-101’s broad, robust biological effects, favorable tolerability profile, unique mechanism of action and extensive preclinical and clinical data. Chemomab believes nebokitug may have the potential to interrupt the deleterious pathological processes that drive fibrosis, with the potential to become a first-in-class, effective anti-fibrotic therapeutic agent.
Nebokitug Reduces Both Inflammation and Fibrosis by Neutralizing CCL24
CCL24 Dual Role in Promoting Fibrosis & Inflammation
- Directly activates fibroblasts
- Enhances local immune cell recruitment
- Drives self-reinforcing vicious cycle
Neutralizing CCL24 Has Advantages Over Blocking the Receptor
- Avoids context dependence of CCR3 receptor
- Potential efficacy of direct approach
- Favorable tolerability profile; retains normal repair functions; reduced risk of off-target effects