Acurx Pharma Says Lead Antibiotic Candidate, Ibezapolstat, Is Ready To Advance To International Pivotal Phase 3 Clinical Trials For Treatment Of Patients With C. Difficile Infection

Results are from Acurx's ongoing scientific collaboration with Leiden University Medical Center (LUMC) partially under a grant from Health Holland to further study the mechanism of action of DNA pol IIIC inhibitors

LUMC highlighted Acurx's new class of promising antimicrobials, ibezapolstat and related analogues Novel chemotype specifically targeting gram-positive bacteria through an unexploited target Ibezapolstat ready to enter pivotal Phase 3 clinical trials for C. difficile Infection (CDI), with no cross resistance reported to date

Ibezapolstat has previously been granted FDA QIDP and Fast-Track Designations and has received SME (Small and Medium-sized Enterprise) designation by the EMA

STATEN ISLAND, N.Y., June 9, 2025 /PRNewswire/ -- Acurx Pharmaceuticals, Inc. (NASDAQ:ACXP) ("Acurx" or the "Company") is a late-stage biopharmaceutical company developing a new class of small molecule antibiotics for difficult-to-treat bacterial infections. Its lead antibiotic candidate, ibezapolstat (IBZ), is ready to advance to international pivotal Phase 3 clinical trials for treatment of patients with C. difficile infection (CDI).

The Company today announced that a presentation of a poster and an oral presentation regarding Acurx's overall DNA pol IIIC inhibitor platform was presented at a scientific conference on May 21 by Mia Urem, PhD, from Leiden University Medical Center in the Netherlands entitled: "A Unique Inhibitor Conformation Selectively Targets the DNA Polymerase PolC of Gram-Positive Priority Pathogens".  This scientific conference is sponsored by the Federation of American Societies for Experimental Biology and is the premier venue for the newest research and technological trends in molecular "machines" inside the human body that ensure DNA replication and expression of genes to create proteins that make up a cell. The distinctive non-planar conformation of ACX-801 and IBZ, together with high conservation of the induced binding pocket in PolC, suggests that this is a general mechanism for this class of inhibitor and is conserved in Gram-positive bacteria.