Peer-Reviewed Scientific Reports Data & Academic Collaboration Show Potent Anti-Tumor Activity, EMT Reversal, & Sequential Chemo-Sensitization; Phase 1b First-In-Human Study Planned for Q1 2027 MELBOURNE, Australia , Oct. 26, 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 new preclinical data supporting the potential of its lead asset, PRP (a proprietary fixed-ratio 1:6 intravenous formulation of trypsinogen and chymotrypsinogen), to address chemotherapy resistance in pancreatic cancer. In collaborative research led by Dr. Maria Belén Toledo at the Universities of Jaén and Granada , PRP was shown to remodel the resistant cellular state in pancreatic cancer models with acquired chemotherapy resistance. The study used a sequential design (chemoresistant cells → PRP pre-treatment → chemotherapy challenge) and demonstrated that PRP functions as a resistance-modulating intervention rather than a conventional cytotoxic agent. Key preclinical findings: Proliferation and survival: PRP monotherapy reduced cancer cell proliferation by ~50–54% and suppressed long-term clonogenic survival by up to 59%. Metastatic behavior: Migration limited to 21–57% wound closure (vs. 100% in untreated controls); invasive capacity reduced by 47–81%. EMT reversal: Strong epithelial differentiation with E-cadherin upregulated up to 5.29-fold and EPCAM up to 4.39-fold; mesenchymal drivers Vimentin reduced to ~0.31–0.32-fold and Snail to 0.28–0.62-fold. Pathway effects: Significant downregulation of TGF-β/SMAD signaling, induction of pro-apoptotic BAX (up to 2.74-fold), and suppression of oncogenic stemness drivers MYC and SOX2 (down to 0.11–0.22-fold in resistant cells). Combination synergy: PRP plus TGF-β inhibition further amplified responses, including 80% invasion inhibition and stronger apoptotic signaling. These results complement the Company’s recent peer-reviewed pilot study published in Scientific Reports ( Nature Publishing Group ), which reported an 85.9% reduction in mean tumor weight in an orthotopic pancreatic (Pan 02) model at the higher dose, ~50% tumor-weight inhibition in an ovarian (A2780) model, anti-angiogenic activity, near-complete blockade of invasion in select lines, and EMT reversal. The Pan 02 cancer cell line is particularly noteworthy since it is a syngeneic (genetically identical or similar) tumor model conducted in immunocompetent mice and is clinically relevant for patients where cytotoxic agents induce immunosuppression and are at risk of infection—one of the main causes of death for cancer patients. Conversely, PRP reduces chemoresistance whilst enhancing immunorecognition. In addition, earlier orthotopic and patient-derived xenograft data have also shown >90% mean tumor growth inhibition and >2.5-fold median survival extension in advanced PDAC models, with reduced metastatic burden and tumor microenvironment remodeling. In vivo anti-tumor activity of PRP (A) Images of excised tumors at study termination of orthotropic pancreatic tumors. Mean tumor weight at termination day after daily I.V. injection of PBS , T/C 27.5/165 (mg/kg) or T/C 83.3/500 (mg/kg) ( ∗ P PBS , T/C 9.1/54 (mg/kg) or T/C 27.5/165 (mg/kg) ( ∗ P PRP’s differentiation-based mechanism—targeting cancer stem cells, EMT, fibrosis, and metastatic dissemination—is distinct from and potentially complementary to emerging RAS-targeted approaches. Revolution Medicines’ daraxonrasib (RASONQUE), recently FDA-approved for metastatic pancreatic adenocarcinoma, has set a clinical benchmark with median overall survival of 13.2 months versus 6.6–6.7 months for chemotherapy in the Phase 3 RASolute 302 trial. Erasca’s pan-RAS molecular glue ERAS-0015 similarly focuses on oncogenic RAS signaling. PRP does not inhibit RAS and is not genotype-restricted; its preclinical package of deep tumor control, fewer metastases, a less fibrotic microenvironment, and chemo re-sensitization, addresses residual biology that RAS pathway blockade does not directly target. Limited prior compassionate-use experience with related proenzyme formulations has shown signals of prolonged survival in advanced solid-tumor patients with a favorable safety profile. PRP holds FDA Orphan Drug Designation for pancreatic cancer. “These findings are highly significant as we progress PRP to our world-first Phase 1b First-in-Human study for advanced solid-tumor patients planned for Q1 2027,” said Mr. James Nathanielsz , Propanc’s Chief Executive Officer. “We envision PRP as a long-term, metronomic therapy that minimizes the threat of recurrence while enabling patients to better respond to standard treatments when resistance becomes critical. The data positions PRP as a potential sequential or combination partner to RAS inhibitors from companies such as Revolution Medicines and Erasca, addressing biology