Namodenoson at the Crossroad of Metabolic Dysfunction-Associated Steatohepatitis and Hepatocellular Carcinoma

Ohad Etzion, Avital Bareket-Samish, David Yardeni, Pnina Fishman

Research output: Contribution to journalReview articlepeer-review

1 Scopus citations

Abstract

Namodenoson (CF102) is a small, orally available, anti-inflammatory, and anti-cancer drug candidate currently in phase 2B trial for the treatment of metabolic dysfunction-associated steatohepatitis (MASH; formerly known as non-alcoholic steatohepatitis (NASH)) and in phase 3 pivotal clinical trial for the treatment of hepatocellular carcinoma (HCC). In both MASH and HCC, the mechanism-of-action of namodenoson involves targeting the A3 adenosine receptor (A3AR), resulting in deregulation of downstream signaling pathways and leading to inhibition of inflammatory cytokines (TNF-α, IL-1, IL-6, and IL-8) and stimulation of positive cytokines (G-CSF and adiponectin). Subsequently, inhibition of liver inflammation, steatosis, and fibrosis were documented in MASH experimental models, and inhibition of HCC growth was observed in vitro, in vivo, and in clinical studies. This review discusses the evidence related to the multifaceted mechanism of action of namodenoson, and how this mechanism is reflected in the available clinical data in MASH and HCC.

Original languageEnglish
Article number848
JournalBiomedicines
Volume12
Issue number4
DOIs
StatePublished - 1 Apr 2024

Keywords

  • A3AR
  • agonist
  • cirrhosis
  • clinical trial
  • fibrosis
  • hepatocellular carcinoma
  • liver cancer
  • metabolic dysfunction-associated steatohepatitis
  • metabolic dysfunction-associated steatotic liver disease
  • namodenoson
  • non-alcoholic fatty liver disease
  • non-alcoholic steatohepatitis

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • General Biochemistry, Genetics and Molecular Biology

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