Iqirvo (elafibranor)

P3, N=18, Not yet recruiting, Ipsen

Additionally, alcohol disrupts the gut-liver axis at several interconnected levels, contributing to a proinflammatory environment in the liver. EFN helps alleviate intestinal hyperpermeability by restoring tight junction protein expression and autophagy, inhibiting apoptosis and inflammatory responses, and enhancing intestinal barrier function through PPARδ activation.

P2, N=68, Active, not recruiting, Ipsen | Trial completion date: Dec 2024 --> Aug 2026 | Trial primary completion date: Dec 2024 --> Aug 2026

P3, N=276, Recruiting, Ipsen | Trial completion date: May 2030 --> May 2029

In this letter, we review the article "Effects of elafibranor on liver fibrosis and gut barrier function in a mouse model of alcohol-associated liver disease"...Furthermore, we summarize the clinical management of all stages of ALD and present new insights into its pathogenesis and potential therapeutic targets. Additionally, we discuss the mechanisms of action of PPARα and δ agonists, the significance of their antifibrotic effects on ALD and future research directions.

P3, N=276, Recruiting, Ipsen | Trial completion date: May 2029 --> May 2030

P=N/A, N=424, Recruiting, Ipsen | Not yet recruiting --> Recruiting | Initiation date: Jul 2024 --> Oct 2024

Agents in this group include peroxisome proliferator-activated receptor agonists (e.g., pioglitazone, elafibranor, saroglitazar), bile acid-farnesoid X receptor axis regulators (obeticholic acid), de novo lipogenesis inhibitors (aramchol, NDI-010976), and fibroblast growth factor 21/19 analogs...Agents in this group include antioxidants (vitamin E), tumor necrosis factor α pathway regulators (emricasan, pentoxifylline, ZSP1601), and immune modulators (cenicriviroc, belapectin). The final group targets the gut (IMM-124e, solithromycin). Combination therapies targeting different pathogenetic pathways may provide an alternative to MASLD treatment with higher efficacy and fewer side effects. This review aimed to provide an update on these medications.

P3, N=72, Recruiting, Ipsen | Not yet recruiting --> Recruiting | Trial primary completion date: Jun 2026 --> Oct 2026

P3, N=276, Recruiting, Ipsen | N=450 --> 276 | Trial completion date: Oct 2030 --> May 2029 | Trial primary completion date: Oct 2030 --> May 2029

P2, N=68, Active, not recruiting, Ipsen | Recruiting --> Active, not recruiting

P=N/A, N=424, Not yet recruiting, Ipsen

P3, N=72, Not yet recruiting, Ipsen

P2, N=60, Recruiting, Ipsen | Trial completion date: Dec 2025 --> Dec 2024

P2, N=60, Recruiting, Ipsen | Trial primary completion date: Feb 2024 --> Dec 2024

P3, N=161, Active, not recruiting, Ipsen | Trial primary completion date: Sep 2023 --> Jun 2023

Methionine-choline deficiency (MCD) induced C57BL/6J NASH model mice was used for the in vivo biological experiments and the compound 3d demostrated lower liver toxicity than that of GFT 505 in the body at the same dose, and it did more effectively improve hyperlipidemia, liver fat degeneration and liver inflammation as well as significantly enhance the content of the GSH which is inportant for the liver protection. This study suggested that the compound 3d is a very promising lead compound for the treatment of NASH.

This reduction in inflammatory response was NFκB-mediated. In summary, this human-relevant, in vitro system proved to be a sensitive testing tool for the investigation of novel anti-NASH compounds.

Preneoplastic lesion development was prevented to a significant extent upon ELA treatment. In addition, ELA directly reduces tumour cell proliferation. These results open new perspectives to evaluate ELA for liver cancer prevention and treatment in NAFLD patients.References:.