Propanc Biopharma Positions PRP as Complementary to RAS Inhibitors

MELBOURNE, Australia, Sept. 16, 2026 /CourierPR/ -- Propanc Biopharma, Inc., a biopharmaceutical company focused on developing novel treatments for chronic diseases, including recurrent and metastatic cancer, has positioned its lead candidate PRP as a complementary backbone to emerging RAS inhibitors from Revolution Medicines, Inc. and Erasca, Inc. The analysis, intended to clarify two distinct layers of tumor biology, highlights the potential of PRP to address residual drivers of resistance, dormancy, and metastasis that can persist after RAS pathway blockade.

RAS inhibitors, such as daraxonrasib (RASONQUE™; RMC-6236) from Revolution Medicines and ERAS-0015 from Erasca, have shown promising results in clinical trials. In the randomized Phase 3 RASolute 302 trial, daraxonrasib produced median overall survival of 13.2 months in previously treated metastatic pancreatic ductal adenocarcinoma (PDAC) patients, compared to 6.6-6.7 months with investigator’s-choice chemotherapy. The drug also demonstrated median progression-free survival of 7.3 months and an objective response rate of approximately 33%. Similarly, in a Phase 1/2 study, ERAS-0015 showed unconfirmed overall response rates of 62% in second-line or later KRAS G12X non-small cell lung cancer (NSCLC) patients and 75% in the post-checkpoint-inhibitor / platinum 2/3L NSCLC subset.

Despite these encouraging results, a critical question remains: how to convert high response rates and doubled survival into durable, metastasis-free outcomes when residual mesenchymal and stem-like cells remain. Propanc Biopharma believes that PRP, a proprietary fixed-ratio combination of the pancreatic proenzymes trypsinogen and chymotrypsinogen, can address this issue by reversing epithelial-mesenchymal transition (EMT) and depleting cancer stem cells (CSCs).

In preclinical studies, PRP demonstrated significant tumor-growth inhibition in advanced PDAC models, with greater than 90% mean tumor-growth inhibition compared to vehicle controls. The treatment also led to a marked reduction in metastatic burden in the liver and peritoneum, significant tumor microenvironment (TME) remodeling, and re-sensitization of chemo-resistant PDAC cells to gemcitabine/nab-paclitaxel. Median overall survival was extended more than 2.5-fold compared to controls.

The mechanism of action of PRP involves the activation of proenzymes and engagement of proteinase-activated receptors (PAR-1 and PAR-2), which are frequently overexpressed on tumor cells. This cascade is associated with reduced TGF-β pathway output, a master inducer of EMT in late-stage cancer. PRP also restores an epithelial phenotype, depletes cancer stem cells, remodels the TME, and sensitizes chemo-resistant PDAC cells to gemcitabine/nab-paclitaxel.

Propanc Biopharma plans to initiate a multicenter, open-label Phase 1b first-in-human study of PRP in February 2027. The study will enroll up to 50 patients with advanced solid tumors, including pancreatic, ovarian, and refractory prostate cancers, at sites in Australia. The two-part design will use Bayesian optimal interval dose escalation with backfill, followed by tumor-specific expansion. PRP is planned as a weekly intravenous infusion on Days 1, 8, 15, and 22 of each 28-day cycle.

James Nathanielsz, Propanc Biopharma’s Chief Executive Officer, stated, "RAS inhibitors have rewritten what is possible in pancreatic and RAS-mutant lung cancer. That is a genuine inflection point for patients. Our thesis is that turning RAS off is necessary but may not be sufficient. The cells that survive RAS blockade are often the mesenchymal, stem-like cells that PRP differentiates and disarms. If that biology holds in the clinic, PRP could help RAS-focused companies convert high response rates into longer, cleaner remissions."

Dr. Ralf Brandt, Propanc Biopharma’s Research & Development Director, added, "EMT is the program that lets a carcinoma leave home, hide, and return. PRP does not compete with daraxonrasib or ERAS-0015 at the GTPase. It reverses the downstream identity change those tumors used to resist almost every class of drug. That is why we see suppression of EMT markers, loss of CSC phenotypes, less fibrosis, fewer metastases, and more than a two-and-a-half-fold survival extension in PDAC models. Those are the exact liabilities a RAS inhibitor leaves on the table."

Propanc Biopharma is not announcing a partnership with Revolution Medicines or Erasca. The Company is putting the mechanistic case on record as it advances PRP into first-in-human development and as the RAS field looks beyond first-generation survival gains.