New Findings from Academic Collaboration Examine Tumor-Cell Behavior, TGF-Β/SMAD Signaling & Stromal Responses; Australian Patent Application Filed for the Combination Approach MELBOURNE, Australia , Nov. 02, 2026 (GLOBE NEWSWIRE) -- Propanc Biopharma, Inc. (Nasdaq: PPCB) (“Propanc” or the “Company”), a biopharmaceutical company focused on developing novel treatments for chronic diseases including recurrent and metastatic cancer, today announced highlighted new preclinical findings evaluating its pancreatic proenzyme formulation (PRP) alone and in combination with galunisertib (GAL), a small-molecule inhibitor of transforming growth factor beta receptor I (TGF-βRI), in pancreatic ductal adenocarcinoma (PDAC) models. The Company has filed an Australian patent application relating to the combination approach. The research was conducted in collaboration with investigators at the University of Jaén and the University of Granada in Spain . The study compared PRP, GAL and PRP plus GAL in wild-type BxPC-3 pancreatic cancer cells, gemcitabine-resistant BxPC-3 cells, normal-associated fibroblasts (NAFs) and cancer-associated fibroblasts (CAFs). Experiments assessed cell proliferation, colony formation, migration and invasion, together with molecular readouts associated with TGF-β signaling, epithelial–mesenchymal transition (EMT), extracellular-matrix (ECM) remodeling and fibroblast activation. PDAC is characterized by complex interactions between malignant cells and the surrounding tumor microenvironment. TGF-β signaling can contribute to tumor-cell plasticity, EMT and stromal activation, although its effects depend on cellular context. The study investigated whether PRP could modulate these tumor- and stroma-associated processes and whether adding a TGF-β pathway inhibitor provided further effects. “Our academic collaboration with the Universities of Jaén and Granada in Spain continues to provide strong scientific evidence and a rationale for the administration of PRP as a stand-alone therapy, but also as a combinatorial approach with inhibitor drugs that can successfully stop tumor growth and dissemination but can be limited due to resistance mechanisms developed over time as a result of alterations to the tumor microenvironment,” said Mr. James Nathanielsz , Propanc’s Chief Executive Officer. “PRP represents a new approach addressing these resistance mechanisms by inducing biological effects that alters the behavior of these malignant cells, rather than using the inhibitory approach. Our unique intellectual property portfolio continues to grow and strengthen as a result and is positioning the Company for long-term future growth, which our shareholders understand will come to fruition as future planned R&D milestones are achieved. Management believe these milestones are near term as PRP (now called Company Candidate, PPC-001) enters the clinic. Further announcements are expected regarding current preparatory activities for our Phase 1b, First-In-Human study as we progress further.” Key preclinical findings: Anti-proliferative activity in tumor models: PRP reduced cell proliferation by approximately 50% in wild-type and gemcitabine-resistant BxPC-3 cells relative to untreated controls. PRP plus GAL reduced proliferation by 75% and 66%, respectively. The additional reduction versus PRP alone was significant in wild-type cells; in resistant cells, the further reduction was not statistically significant. Reduced long-term colony-forming capacity: PRP reduced colony formation by 59% in wild-type cells and 39% in gemcitabine-resistant cells. The combination reduced colony formation by 68% and 64%, respectively. The additional effect of the combination over PRP alone was significant in the resistant model, but not in the wild-type model. Suppression of migration and invasion: In wound-healing assays at 72 hours, wound closure was 21% with PRP in wild-type cells and 57% in resistant cells, compared with untreated controls. PRP plus GAL resulted in 19% and 30% wound closure, respectively; the combination significantly improved the result over PRP alone in resistant cells, but not in wild-type cells. In Matrigel invasion assays, PRP reduced invasion by 81% in wild-type cells and 47% in resistant cells. PRP plus GAL produced reductions of 89% and 80%, respectively. Modulation of TGF-β/SMAD pathway-associated gene expression: PRP significantly reduced SMAD2, SMAD3 and TGFBR1 transcript levels to 0.45-, 0.63- and 0.55-fold of control in wild-type cells, and to 0.42-, 0.36- and 0.23-fold in resistant cells, compared to control group. The combination produced further reductions in selected readouts, although the magnitude and statistical significance of the additional effects varied across models and markers. Changes in EMT-associated markers: PRP increased E-cadherin expression 5.29-fold in wild-type cells and 4.86-fold in resistant cells, while reducing Vimentin to 0.31- and 0.32-fold and Snail to 0.62- and 0.28-fold, respect