{"id":1003919,"date":"2026-09-16T10:50:30","date_gmt":"2026-09-16T14:50:30","guid":{"rendered":"https:\/\/www.marketnewsdesk.com\/index.php\/propanc-biopharma-positions-prps-emt-reversal-mechanism-as-a-complementary-backbone-to-emerging-ras-inhibitors-from-revolution-medicines-inc-and-erasca-inc\/"},"modified":"2026-09-16T10:50:30","modified_gmt":"2026-09-16T14:50:30","slug":"propanc-biopharma-positions-prps-emt-reversal-mechanism-as-a-complementary-backbone-to-emerging-ras-inhibitors-from-revolution-medicines-inc-and-erasca-inc","status":"publish","type":"post","link":"https:\/\/www.marketnewsdesk.com\/index.php\/propanc-biopharma-positions-prps-emt-reversal-mechanism-as-a-complementary-backbone-to-emerging-ras-inhibitors-from-revolution-medicines-inc-and-erasca-inc\/","title":{"rendered":"Propanc Biopharma Positions PRP\u2019s EMT-Reversal Mechanism as a Complementary Backbone to Emerging RAS Inhibitors from Revolution Medicines, Inc. and Erasca, Inc."},"content":{"rendered":"

\nNew Preclinical PDAC Data for PRP Show >90% Tumor-Growth Inhibition & >2.5-Fold Survival Benefit; Company Highlights How Reversing Epithelial-Mesenchymal Transition May Deepen & Extend Responses to RAS(ON) & Pan-RAS Therapies
\n<\/h2>\n
\n

MELBOURNE, Australia, Sept. 16, 2026 (GLOBE NEWSWIRE) — Propanc Biopharma, Inc. (Nasdaq: PPCB) (\u201cPropanc\u201d or the \u201cCompany\u201d), 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\u2019 daraxonrasib (RASONQUE\u2122; RMC-6236) and Erasca\u2019s pan-RAS molecular glue ERAS-0015.<\/p>\n

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).<\/p>\n

Propanc believes these mechanisms address residual drivers of resistance, dormancy, and metastasis that can persist after RAS pathway blockade \u2013 creating a scientific rationale for combination or sequential use with RAS inhibitors.<\/p>\n

\n A Landmark Moment for RAS-Targeted Therapy<\/strong>\n <\/p>\n

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

\n Revolution Medicines \u2013 daraxonrasib:<\/strong> 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\u20136.7 months with investigator\u2019s-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\u201337% across evaluated dose bands; in a docetaxel-na\u00efve subgroup treated at 160\u2013220 mg, confirmed ORR was 42%, disease-control rate 89%, median PFS 8.3 months, and median OS 16.0 months.<\/p>\n

\n Erasca \u2013 ERAS-0015:<\/strong> 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\u201332 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\u201332 mg and 42% at recommended expansion doses of 24\u201332 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.<\/p>\n

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.<\/p>\n

\n PRP Preclinical Profile in Advanced PDAC<\/strong>\n <\/p>\n

In orthotopic and patient-derived xenograft (PDX) models of advanced PDAC, three-times-weekly intravenous PRP achieved:<\/p>\n