Propanc Biopharma Reports Preclinical Data with PRP & PRP plus TGF-β Inhibitor on TGF-β Pathway in Pancreatic Cancer
Key Highlights
- ➤PRP reduced proliferation approximately 50% in wild-type and gemcitabine-resistant BxPC-3 cells.
- ➤PRP plus GAL reduced proliferation 75% in wild-type and 66% in resistant cells.
- ➤PRP reduced CAF invasion 85%, while NAF proliferation reduction was modest and nonsignificant.
- ➤Australian patent application filed covering the PRP and galunisertib combination approach.
- ➤PRP monotherapy showed more favorable stromal selectivity than the PRP-plus-GAL combination.
Expert Statements
James Nathanielsz, Chief Executive Officer of Propanc Biopharma
“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.”
James Nathanielsz, Chief Executive Officer of Propanc Biopharma
“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.”
James Nathanielsz, Chief Executive Officer of Propanc Biopharma
“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.”
James Nathanielsz, Chief Executive Officer of Propanc Biopharma
“Management believe these milestones are near term as PRP (now called Company Candidate, PPC-001) enters the clinic.”
James Nathanielsz, Chief Executive Officer of Propanc Biopharma
“Further announcements are expected regarding current preparatory activities for our Phase 1b, First-In-Human study as we progress further.”
Dr. Maria Belén Toledo, Lead Investigator at the University of Jaén
“These preclinical findings provide a rationale for continued investigation of PRP, both as a monotherapy and in combination with TGF-β pathway inhibition, in pancreatic cancer.”
Dr. Maria Belén Toledo, Lead Investigator at the University of Jaén
“They also identify stromal selectivity as a potentially valuable consideration in treatment development and suggest that therapeutic value of targeting the tumor microenvironment should be assessed not only by the extent of pathway suppression, but also by which cellular populations are affected and how this translates into tumor control.”
Dr. Maria Belén Toledo, Lead Investigator at the University of Jaén
“Further validation in more complex models will be conducted to confirm whether these effects can be reproduced and support a clinically meaningful therapeutic strategy.”
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.
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