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 issued a comparative analysis of its lead candidate PRP against recently reported clinical datasets from leading RAS-targeted programs, including Revolution Medicines’ daraxonrasib (RASONQUE™; RMC-6236) and Erasca’s pan-RAS molecular glue ERAS-0015.

The analysis is intended to clarify two distinct layers of tumor biology. RAS inhibitors block oncogenic RAS signaling and have produced practice-changing clinical results in RAS-mutant pancreatic ductal adenocarcinoma (PDAC) and encouraging activity in RAS-mutant non-small cell lung cancer (NSCLC). PRP, a proprietary fixed-ratio combination of the pancreatic proenzymes, trypsinogen and chymotrypsinogen, does not inhibit RAS. Instead, it promotes differentiation of malignant cells toward a more normal phenotype, reverses epithelial-mesenchymal transition (EMT), depletes cancer stem cells (CSCs), and remodels the fibrotic tumor microenvironment (TME).

Propanc believes these mechanisms address residual drivers of resistance, dormancy, and metastasis that can persist after RAS pathway blockade – creating a scientific rationale for combination or sequential use with RAS inhibitors.

A Landmark Moment for RAS-Targeted Therapy

RAS mutations drive approximately 90% of PDAC and roughly 30% of NSCLC. For decades the target was considered undruggable. That landscape has shifted rapidly.

Revolution Medicines – daraxonrasib: In the randomized Phase 3 RASolute 302 trial in previously treated metastatic PDAC, oral once-daily daraxonrasib produced median overall survival (OS) of 13.2 months versus 6.6–6.7 months with investigator’s-choice chemotherapy (hazard ratio 0.40; p < 0.0001), median progression-free survival (PFS) of 7.3 months versus 3.5 months, and an objective response rate (ORR) of approximately 33% versus 12%. The U.S. Food and Drug Administration approved daraxonrasib in August 2026 for pretreated metastatic pancreatic adenocarcinoma. In previously treated RAS-mutant NSCLC, a Phase 1/2 study published in The New England Journal of Medicine reported ORRs of 31–37% across evaluated dose bands; in a docetaxel-naïve subgroup treated at 160–220 mg, confirmed ORR was 42%, disease-control rate 89%, median PFS 8.3 months, and median OS 16.0 months.

Erasca – ERAS-0015: Preliminary Phase 1 monotherapy data from the U.S. AURORAS-1 and China JYP0015M101 trials showed unconfirmed overall response rates (uORR) of 62% in second-line or later KRAS G12X NSCLC at pharmacologically active doses of 16–32 mg once daily, and 75% in the post-checkpoint-inhibitor / platinum 2/3L NSCLC subset. In second-line KRAS G12X PDAC, uORR was 40% at 16–32 mg and 42% at recommended expansion doses of 24–32 mg; a July 2026 update reported a 57% uORR at 8 weeks at the 32 mg recommended expansion dose in 2L+ KRAS G12X PDAC. The program has been generally well tolerated to date, with mostly low-grade treatment-related adverse events and no dose-limiting toxicities reported at disclosed cutoffs. Erasca has described ERAS-0015 as a potentially best-in-class pan-RAS molecular glue and has outlined registration-enabling plans in pancreatic and lung cancers.

These datasets validate RAS as a therapeutically tractable node. They also leave an open clinical question: how to convert high response rates and doubled survival into durable, metastasis-free outcomes when residual mesenchymal and stem-like cells remain.

PRP Preclinical Profile in Advanced PDAC

In orthotopic and patient-derived xenograft (PDX) models of advanced PDAC, three-times-weekly intravenous PRP achieved:

  • Greater than 90%, mean, tumor-growth inhibition versus vehicle controls (p < 0.001).
  • Marked reduction in metastatic burden in liver and peritoneum.
  • Significant TME remodeling, including decreased cancer-associated fibroblast (CAF) activity, reduced fibrosis, and suppression of EMT markers.
  • Re-sensitization of chemo-resistant PDAC cells to gemcitabine/nab-paclitaxel, supporting lower chemotherapy doses with improved efficacy.
  • Median overall survival extension of more than 2.5-fold versus controls.

     

These findings are built on previously reported >85% tumor-growth inhibition, peer-reviewed work on PRP’s effects on PDAC fibroblasts and CSCs, and limited prior compassionate-use experience with related proenzyme formulations that showed signals of prolonged survival and a favorable safety profile with no severe treatment-related adverse events. PRP holds FDA Orphan Drug Designation for pancreatic cancer and is not restricted to a specific RAS genotype.

Important context: PRP efficacy cited here is preclinical. Daraxonrasib and ERAS-0015 data are from human clinical trials. Cross-modality numerical comparisons are directional only and are not head-to-head results.