Moleculin Biotech Reports Preclinical Data Showing Annamycin Plus PD-1 Blockade Extends Survival in Pancreatic Cancer Models

Inhibition of CD8+ T cells shortens survival in Annamycin-treated mice, demonstrating the immune system is a functional contributor to Annamycin’s antitumor activity, not a bystander

Annamycin achieves substantially higher pancreatic tissue exposure than doxorubicin, offering a potential explanation for why topoisomerase II, a validated target in pancreatic cancer, has never been successfully drugged there

HOUSTON, Nov. 10, 2026 (GLOBE NEWSWIRE) -- Moleculin Biotech, Inc. (NASDAQ:MBRX) ("Moleculin" or the "Company") today announced new preclinical data showing that its lead drug candidate, Annamycin (naxtarubicin), combined with PD-1 immune checkpoint blockade, extended survival in pancreatic cancer models beyond that achieved with either agent alone. The findings will be presented today by Waldemar Priebe, PhD, of The University of Texas MD Anderson Cancer Center, in an oral presentation at the 6th Annual Marie Skłodowska-Curie Symposium on Cancer Research and Care organized by Moffitt Cancer Center, being held November 8–11, 2026 in Tampa, Florida.

The presentation, titled "Targeting pancreatic cancer with Annamycin and turning immune cold tumor into hot tumor," is scheduled for November 10th at 2:45 p.m. ET during the symposium’s gastrointestinal and urologic malignancies session.

In a syngeneic, immunocompetent KPC mouse model of advanced pancreatic ductal adenocarcinoma, treatment with liposomal Annamycin (L-ANN) in combination with PD-1 checkpoint blockade significantly increased survival compared with cohorts treated with either agent alone. The result has been reconfirmed in a second, independent experiment. Pancreatic cancer is among the tumor types least responsive to immune checkpoint inhibitors such as pembrolizumab and nivolumab, in large part because its tumor microenvironment is immunologically "cold," with few infiltrating T cells. The Company believes these data support the evaluation of Annamycin in combination with approved PD-1 inhibitors in pancreatic cancer and, potentially, in other tumors where efficacy of checkpoint inhibitors is limited by an immunologically cold microenvironment.

The combination result builds on a series of findings from Dr. Priebe’s laboratory. Topoisomerase II alpha (TOP2A) is elevated in pancreatic cancer, and its expression correlates with shorter overall survival and higher rates of metastasis; yet approved topoisomerase II -targeting agents such as doxorubicin have not proven effective in the disease. Pharmacokinetic studies show that Annamycin achieves substantially higher and more sustained exposure in pancreatic tissue than doxorubicin at the same dose, offering a potential explanation. In treated tumors, Annamycin was measured at high concentrations, accompanied by evidence of DNA damage consistent with topoisomerase II targeting and by significantly increased infiltration of both CD8+ cytotoxic T cells and CD4+ helper T cells. Inhibiting CD8+ T cells in treated animals shortened survival, demonstrating that these cells are functional contributors to Annamycin’s antitumor activity rather than bystanders. These data extend results presented at the AACR Annual Meeting in April 2026 and at the AACR Conference on Pancreatic Cancer in September 2026, which demonstrated Annamycin’s activity across human orthotopic and syngeneic pancreatic cancer models, including liver metastasis models, and first identified the contribution of CD8+ T cells to its antitumor effect.