Lisata Therapeutics announces results from pancreatic cancer cohort of CENDIFOX

Lisata Therapeutics (LSTA) announced encouraging preliminary data from the pancreatic ductal adenocarcinoma cohort of the Phase 1/2a CENDIFOX trial. The investigator-initiated trial, led by Anup Kasi, M.D., M.P.H., at The University of Kansas Cancer Center, is evaluating Lisata’s proprietary investigational iRGD cyclic peptide product candidate, certepetide, in combination with FOLFIRINOX-based therapies for the treatment of pancreatic, colon, and appendiceal cancers. The preliminary data will be presented in poster A070, titled “CENDIFOX: Phase I/II Trial of CEND-1 with Neoadjuvant mFOLFIRINOX in Resectable and Borderline Resectable PDAC,” at the American Association for Cancer Research Special Conference in Cancer Research: Advances in Pancreatic Cancer Research-Emerging Science Driving Transformative Solutions on September 29, 2025, from 4:30 p.m. – 7:00 p.m. in Boston, Massachusetts. The poster presentation will highlight findings from patients with resectable and borderline resectable PDAC, with the full abstract available on the AACR website, The abstract highlights that the combination of certepetide with FOLFIRINOX was safe and feasible in patients with resectable and borderline resectable PDAC, with no serious adverse events attributed to certepetide. Among the 35 patients enrolled in the PDAC cohort, 10 completed the protocol-prescribed pre-surgical courses of therapy and were eligible to undergo pancreatic cancer resection. Based on these 10 patients, the R0 resection rate was 50%, and 70% experienced a pathologic partial response. The results also demonstrated promising early survival data, including a 60% two-year overall survival rate and a 12-month median disease-free survival. Additionally, analysis of tumor tissue demonstrated enhanced immune cell infiltration, along with increased expression of immune markers such as CD68, PD-1, and PD-L1. These findings support the potential of certepetide to transform pancreatic tumors from “immune-cold” to “immune-hot,” which may make them more responsive to immunotherapies.