Anti-CCL24 Therapeutic Platform


Chemomab's R&D talent, infrastructure and capabilities are paving the way for successful drug introduction from early-stage discovery through clinical development. Our R&D team is investigating the underlying fibrosis biology via various in-vitro and in-vivo models, which are propelling our development of transformative patient therapeutics forward.

Our science-driven approach explores novel pharmacodynamic parameters from our clinical trials to equip us with powerful biological insights. Using patients' tissues and serum samples, as well as primary cell cultures, we are developing deeper understanding of CCL24 expression and its specific roles in primary sclerosing cholangaitis (PSC) and systemic sclerosis (SSc) pathologies.

Chemomab leverages collaborations with leading investigators from prestigious research centers around the world to both obtain further evidence on CCL24’s unique role in fibrosis and demonstrate CM-101’s potential therapeutic effects on fibrosis.

The Roles of CCL24 and CM-101

CCL24 Recruits Immune Cells

CCL24 promotes inflammation by recruiting immune cells from circulation to the injured tissue

CCL24 Activates Fibroblasts

CCL24 stimulates the transition of fibroblasts to myofibroblasts and elevates production and secretion of the extracellular matrix

CM-101 Attenuates Fibrosis and Inflammation

CM-101 binds to CCL24, attenuating its pro-inflammatory and pro-fibrotic activities, which improves the injured tissues’ inflammatory-fibrotic damage

  • Immune cell

  • CCL24

  • Fibroblast

  • Activated fibroblast

  • CM-101

About CCL24

Over the last decade, our scientific team discovered the role of CCL24 as a key regulator in fibrotic-inflammatory processes, specifically, the pivotal pro-fibrotic and pro-inflammatory effects of CCL24 in fibrotic diseases.

Chemomab observed CCL24 up-regulation and its correlation with disease severity in fibrotic disease tissues, including liver, skin and lung fibrosis related pathologies (e.g. PSC, SSc).

Based on these revelations, Chemomab established a comprehensive preclinical package to support the therapeutic effects of blockading CCL24.

We revealed that CCL24 works through a dual biological pathway directly activating fibroblasts while recruiting immune cells and maintaining the inflammatory environment that is required to enhance fibrosis.

Chemomab proved that inhibiting these pathways by blocking CCL24 prevents and reverses fibrotic tissue growth within the liver, skin and lung.

Based on strong human data and relevant disease models, Chemomab developed CM-101, a monoclonal antibody that targets CCL24 and blocks its downstream pathways.

About CM-101 Therapeutic Platform

CM-101 is a novel, safe and potentially effective therapy that fills the huge gap in fibrotic disease care. Treatment with CM-101 revealed strong anti-fibrotic effects, reduced inflammatory injury and significantly improved organ damage. Numerous in-vivo, in-vitro and ex-vivo studies verified that using CM-101 in fibrotic disease models including PSC, SSc, idiopathic pulmonary fibrosis (IPF) and NASH demonstrated potent therapeutic CCL24 blockade effects.

CM-101 is safe and well tolerated up to the highest tested dose in healthy subjects and in fatty liver disease patients with both intravenous and subcutaneous administrations. Both routes of administration support long dosing intervals – once every 2-4 weeks – and provide evidence of target engagement and biological activity in humans.

Based on CM-101’s broad, robust biological effects, favorable tolerability profile and unique mechanism of action, Chemomab believes CM-101 will counteract deleterious pathological processes that drive fibrosis, having the potential to become a leading anti-fibrotic therapeutic agent.

CM-101 phase II trials in patients with PSC and NASH are currently underway.


  1. A blocking monoclonal antibody to CCL24 alleviates liver fibrosis and inflammation in experimental models of liver damage

    Segal-Salto et al. JHEP Rep. 2020 Jan 2;2(1):100064
  2. Blockade of CCL24 with a monoclonal antibody ameliorates experimental dermal and pulmonary fibrosis

    Mor et al. Ann Rheum Dis 2019;78:1260–1268
  3. Protective effect of eotaxin-2 inhibition in adjuvant-induced arthritis

    Ablin et al. Clinical and Experimental Immunology. 2010; V161(2):276–83
  4. Eotaxin-2 blockade ameliorates experimental autoimmune encephalomyelitis

    Mausner-Fainberg et al. World J. Immunol. 2013 Mar; 3(1):7-14.
  5. Anti eotaxin-2 antibodies attenuate the initiation and progression of experimental atherosclerosis

    Mor et al. World J. Cardiovascular Dis. 2013; 3:339-46


  1. EASL 2022-Combination of Whole Liver Single Cell RNA Sequencing and Spatial Transcriptomics Reveals Specific Cell Sub-Populations and Pathways Regulated by CCL24

  2. ECM Congress 2022-CCL Inhibition by CM-101 Attenuates Extracellular Matrix and Fibrotic Biomarkers in Both Patients and Experimental Murine Models

  3. CCL24 overexpression resulting from bile duct injury induces an inflammatory-fibrotic vicious cycle in primary sclerosing cholangitis - AASLD 2021

  4. The peri-ductular CCL24 rich niche promotes bile duct fibrosis related liver damage in primary sclerosing cholangitis - EASL 2021

  5. CM-101 Demonstrates Reduction in Serum Fibrotic Biomarkers in a Phase 1b Clinical Trial - AASLD 2020

  6. CM-101 a Novel CCL24 Blocking Monoclonal Antibody Demonstrates Safety, Target Engagement and Long Half- Life in a Phase 1 Clinical Trial - AASLD 2020

  7. CCL24 modulates fibrosis development in Primary Sclerosing Cholangitis - EASL 2020

  8. CCL24 Blocking Monoclonal Antibody Reduces Cholangiocites Proliferation in Cholestasis Models – EASL 2019

  9. CCL24 Blocking Monoclonal Antibody Reduces Cholangiocites Proliferation in Cholestasis Models – AASLD 2019

  10. CCL24 -A novel target playing a significant role in Systemic Sclerosis (SSc)

  11. CCL24 Blocking Monoclonal Antibody Ameliorates Liver Injury in Models of Cholestasis – EASL 2018

  12. CM-101, CCL24 Blocking Antibody, Suppresses Hepatic Injury and Fibrosis in Models of NASH and Liver Fibrosis – AASLD 2018

  13. Expression of CCL24 and its Receptor CCR3 in Patients with Non-Alcoholic Fatty Liver Disease – EASL 2018