Propanc Biopharma Publishes New Data: PRP Reprograms Chemotherapy-Resistant Pancreatic Cancer Cells & Restores Therapeutic Vulnerability
Key Highlights
- ➤PRP cut chemotherapy-resistant pancreatic cancer cell proliferation approximately 50–54% in preclinical testing
- ➤PRP reduced invasive capacity 47–81% and limited migration to 21–57% wound closure
- ➤PRP plus TGF-β inhibition achieved 80% invasion inhibition in resistant pancreatic cancer models
- ➤Phase 1b study planned for Q1 2027, enrolling up to 50 advanced solid-tumor patients
- ➤Earlier models showed over 90% mean tumor growth inhibition and over 2.5-fold median survival extension
Expert Statements
Maria Belén Toledo, Research collaborator at the Universities of Jaén and Granada
“PRP functions as a resistance-modulating intervention rather than a conventional cytotoxic agent.”
James Nathanielsz, Chief Executive Officer of Propanc Biopharma
“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.”
James Nathanielsz, Chief Executive Officer of Propanc Biopharma
“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.”
James Nathanielsz, Chief Executive Officer of Propanc Biopharma
“The data positions PRP as a potential sequential or combination partner to RAS inhibitors from companies such as Revolution Medicines and Erasca, addressing biology—cancer stem cells, EMT, fibrosis, and metastatic spread—that those agents do not primarily target.”
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.
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