Alentis Announces Presentations on Claudin-1 in Fibrosis at the ERA and ATS Conferences

ERA abstract by Delbet et al. was ranked as one of the ten best abstracts

Basel, Switzerland – May 14, 2024, Alentis Therapeutics (“Alentis”), a clinical-stage biotechnology company developing treatments for Claudin-1 positive (CLDN1+) tumors and organ fibrosis, announced today two presentations at the European Renal Association (ERA) and American Thoracic Society (ATS) conferences this May.

The ERA and ATS conferences will take place May 23-26 in Stockholm, Sweden and May 17-22 in San Diego, CA, respectively.

ERA oral presentation
• Title: Novel therapeutic for crescentic glomerulonephritis through targeting CLDN1 in parietal epithelial cells (abstract 2837)
• Presenter: Dr. Jean-Daniel Delbet, Inserm, Paris Centre de Recherche Cardiovasculaire, France
• Session: FC 17 – Novel treatments of immune mediated kidney diseases
• Date and time: Saturday, May 25 at 16:12 CEST

ATS presentation
• Title: P473 – Expression of exposed CLDN1 is linked to early pathological lesions in idiopathic pulmonary fibrosis
• Presenter: Dr. Emanuela Cortesi, BREATHE lab – Department of Chronic Diseases and Metabolism, KU Leuven, Leuven, Belgium
• Session: A69 – Pathogenesis of interstitial and pleural diseases
• Date and time: Sunday, May 19 at 11:30am PDT

Dr. Geoffrey Teixeira, SVP Head of Fibrosis of Alentis said, “The outstanding work performed by the research groups at KU Leuven and Inserm show that CLDN1 plays a key role in the early pathogenesis of fibrosis. It further validates CLDN1 as a therapeutic target across fibrotic indications, in this case IPF and crescentic glomerulonephritis in ANCA-associated vasculitis.

Pr. Pierre-Louis Tharaux at Inserm highlighted, “It is important to understand the pathophysiological mechanisms driving kidney fibrosis in crescentic glomerulonephritis (CrGN) as we need a targeted therapeutic approach that considers the complex interactions within fibrotic signaling pathways. Our work suggests a functional role of CLDN1 in the pathogenesis of CrGN and a potential benefit of targeting CLDN1 in CrGN patients.

Pr. Wim Wuyts at KU Leuven added, “There is an urgent need to improve outcomes for patients with idiopathic pulmonary fibrosis (IPF). We must target the root causes of disease by developing therapies that prevent damage to the epithelial barrier and limit the production of extracellular matrix. Enrichment of exposed CLDN1 during disease progression and its association with epithelial injury and active fibrotic lesions suggest a functional role of CLDN1 in IPF early pathogenesis.

About Lixudebart (ALE.F02)
Lixudebart is a first-in-class monoclonal antibody developed for liver, lung and kidney fibrosis. The investigational antibody is designed to reverse organ fibrosis by specifically targeting a unique CLDN1 epitope exposed in fibrotic tissue. In Phase 1 single- and multiple-ascending dose studies in healthy volunteers lixudebart was observed to be well tolerated, with no serious safety concerns. Lixudebart is currently tested in clinical trials for advanced liver fibrosis (NCT05939947) and ANCA-associated vasculitis (NCT06047171).

About Alentis Therapeutics
Alentis Therapeutics, the CLDN1 company, is a clinical-stage biotech developing breakthrough treatments for CLDN1+ tumors and organ fibrosis. CLDN1 is a previously unexploited target that plays a key role in the pathology of cancer and fibrotic disease. Alentis is the leading company pioneering anti-CLDN1 antibodies and ADCs to modify and reverse the course of disease.

Alentis was founded in 2019 based on ground-breaking research in the laboratory of Prof. Thomas Baumert, MD at the University of Strasbourg and the French National Institute of Health and Medical Research (Inserm). Alentis is headquartered in pharma-biotech hub Basel, Switzerland with an R&D subsidiary in Strasbourg, France and clinical operations in the US. Visit www.alentis.ch

For more information please contact:

Alentis Therapeutics
Sariette Witte
sariette.witte@alentis.ch
+41 78 245 7310

O Public Relations GmbH
O’Patrick Wilson
o@os-pr.com
+41 78 888 4332