Propanc Biopharma Highlights Differentiated PRP Pancreatic Cancer Data Versus Emerging Pan-RAS Program ERAS-0015
Propanc presents preclinical PDAC data for PRP and outlines a February 2027 start for a Phase 1b trial targeting advanced solid tumors.
Rhea-AI Summary
Propanc Biopharma (PPCB) reported new preclinical pancreatic ductal adenocarcinoma (PDAC) data for its lead candidate PRP, showing more than 90% mean tumor-growth inhibition and over 2.5-fold median overall survival extension versus controls in orthotopic and patient-derived xenograft models.
PRP, an intravenous fixed-ratio proenzyme combination, is described as non-cytotoxic and differentiation-based, targeting epithelial-mesenchymal transition, cancer stem cells, fibrosis, and the tumor microenvironment rather than RAS itself. The company contrasts this profile with Erasca’s oral pan-RAS molecular glue ERAS-0015 and daraxonrasib, positioning PRP as potentially complementary. PRP holds FDA Orphan Drug Designation for pancreatic cancer, with a multicenter Phase 1b first-in-human study in advanced solid tumors planned to start dosing in February 2027.
Positive
- >90% tumor-growth inhibition and >2.5-fold median survival extension in PDAC models
- Marked reduction in liver and peritoneal metastases and tumor fibrosis in preclinical PDAC
- Chemo-resensitization of gemcitabine/nab-paclitaxel–resistant PDAC cells in preclinical studies
- PRP has FDA Orphan Drug Designation for pancreatic cancer and is genotype-agnostic
- Planned Phase 1b multicenter study to enroll ~40–50 advanced solid tumor patients
- Differentiation-based mechanism designed to complement RAS inhibitors such as ERAS-0015 and daraxonrasib
Negative
- PRP evidence in PDAC is preclinical only, with limited compassionate-use data and no completed trials
- First-in-human Phase 1b study is not expected to start dosing until February 2027, delaying potential clinical readouts
News Explained
The release adds a stage distinction rather than a new company milestone: PRP remains preclinical, while the compared ERAS-0015 evidence comes from human Phase 1 studies; Propanc’s own Phase 1b remains planned for
Details
Market move: PPCB +3.38% in the Sep 22 session. preclinical PDAC data
On Sep 22, the day this news came out, PPCB closed 3.38% above the previous close. Argus tracked a peak move of +10.3% during that session. Our momentum scanner recorded 6 alerts for this stock that day. Relative volume reached 6.5x the daily average during tracking.
Data tracked by StockTitan Argus for the Sep 22 session.
Key Figures
- Tumor-growth inhibition
- >90%
- Advanced PDAC orthotopic and PDX models versus vehicle controls
- Statistical significance
- p < 0.001
- PRP tumor-growth inhibition results
- Median survival extension
- >2.5-fold
- Treated animals versus controls in PDAC models
- PRP formulation ratio
- 1:6
- Trypsinogen to chymotrypsinogen fixed-ratio combination
- Phase 1b enrollment
- Approximately 40 to 50 patients
- Planned advanced solid-tumor first-in-human study
- First patient dosing
- February 2027
- Target for the planned Phase 1b study
- ERAS-0015 uORR
- 57% unconfirmed 8-week ORR
- 32 mg once-daily recommended expansion dose in second-line or later KRAS G12X PDAC
Historical Context
-
PRP showed greater than 90% tumor inhibition and more than 2.5-fold survival extension
-
Company highlighted PRP's preclinical activity and planned Phase 1b development
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Company planned a February 2027 first-in-human study of PRP
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Company finalized protocol and feasibility work for a Phase 1b study
24h Move is the share-price change in the day after each event; other market factors may also have contributed.
Key Terms
pdac medical
epithelial-mesenchymal transition medical
cancer stem cells medical
tumor microenvironment medical
unconfirmed overall response rate medical
pharmacokinetics medical
AI-generated analysis. How Rhea-AI works. Not financial advice.
New Preclinical PDAC Package for PRP Shows >
MELBOURNE, Australia, Sept. 22, 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 issued a comparative analysis of lead candidate PRP against recently reported clinical datasets from Erasca, Inc.’s pan-RAS molecular glue ERAS-0015 in pancreatic ductal adenocarcinoma (PDAC).
The analysis follows FDA approval of Revolution Medicines’ daraxonrasib in pretreated metastatic PDAC in August 2026 and FDA Fast Track designation for ERAS-0015 in metastatic pancreatic adenocarcinoma on August 24, 2026. Propanc believes these advances validate RAS as a tractable driver in PDAC while simultaneously highlighting the biology RAS inhibition leaves unaddressed — epithelial-mesenchymal transition (EMT), cancer stem cells (CSCs), fibrosis, and metastatic dissemination.
PRP, a proprietary fixed-ratio combination of the pancreatic proenzymes, trypsinogen and chymotrypsinogen (1:6), does not inhibit RAS. Instead, it promotes differentiation of malignant cells toward a more normal phenotype, reverses EMT, depletes CSCs, and remodels the fibrotic tumor microenvironment (TME). The Company believes this non-cytotoxic, differentiation-based approach is complementary to — not competitive with — RAS(ON) inhibitors and pan-RAS molecular glues, including ERAS-0015.
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 the liver and peritoneum.
- Significant remodeling of the tumor microenvironment, including decreased cancer-associated fibroblast activity, reduced fibrosis, and suppression of EMT markers.
- Enhanced sensitivity of chemo-resistant PDAC cells to standard-of-care gemcitabine/nab-paclitaxel, supporting the potential for lower chemotherapy doses with improved efficacy.
- Median overall survival extension of more than 2.5-fold in treated animals compared with controls.
These results complement previously reported >
PRP holds FDA Orphan Drug Designation for pancreatic cancer and is not restricted to a specific RAS genotype, supporting potential broad applicability across solid tumors and possible use in combination or sequential settings with RAS inhibitors or standard chemotherapy.
ERAS-0015 Clinical Snapshot in PDAC
According to Erasca’s public disclosures, ERAS-0015 is an oral pan-RAS molecular glue designed to inhibit RAS signaling, including signaling driven by mutant RAS. Preliminary Phase 1 monotherapy data from the U.S. AURORAS-1 trial and the China JYP0015M101 study have shown:
- Unconfirmed overall response rates (uORR) of
40% at pharmacologically active doses of 16–32 mg once daily and42% at recommended expansion doses of 24–32 mg in second-line KRAS G12X PDAC. - A July 2026 update reporting a
57% unconfirmed 8-week ORR at the 32 mg once-daily recommended expansion dose in second-line or later KRAS G12X PDAC. Responding patients remained on treatment as of May 25, 2026, data cutoff. - Generally favorable early tolerability, with mostly low-grade treatment-related adverse events, no dose-limiting toxicities at disclosed cutoffs, and
100% median relative dose intensity at 24 mg and 32 mg once daily. - FDA Fast Track designation for metastatic pancreatic adenocarcinoma (August 24, 2026), with Erasca outlining a planned Phase 3 PDAC trial and additional registration-oriented studies in lung cancer.
Propanc congratulates Erasca on Fast Track designation and on the early clinical activity observed with ERAS-0015. High response rates in RAS-mutant PDAC are an important advance for patients. The Company’s thesis is that converting those responses into deeper, more durable remissions will require a second layer of biology — reversing the mesenchymal, stem-like, fibrotic program that enables residual disease to persist, disseminate, and resist pathway blockade.
Comparative Snapshot
Sources: Company disclosures and peer-reviewed or conference reports as of September 2026. PRP efficacy cited is preclinical. ERAS-0015 and daraxonrasib data are from human clinical trials. Cross-modality numerical comparisons are directional only and are not head-to-head results.
| Attribute | PRP (PPCB) | ERAS-0015 (ERAS) | Daraxonrasib (RVMD) |
| Modality | IV proenzyme combo (trypsinogen + chymotrypsinogen, 1:6) | Oral pan-RAS molecular glue | Oral RAS(ON) multi-selective inhibitor |
| Primary node | Differentiation / EMT reversal / CSCs / TME | Pan-RAS (KRAS G12X and related) | Oncogenic RAS(ON) signaling |
| Evidence stage | Preclinical PDAC + limited compassionate use; Phase 1b planned February 2027 | Phase 1 dose-escalation / expansion; Fast Track; registration path outlined | Phase 3 PDAC; FDA approved August 2026 for pretreated metastatic PDAC |
| PDAC activity | > | Ph1 2L KRAS G12X: uORR 40– | Ph3 2L: mOS 13.2 vs 6.6–6.7 mo; mPFS 7.3 vs 3.5 mo; ORR ~ |
| Genotype limit | Not RAS-mutation restricted; FDA Orphan Drug Designation for pancreatic cancer | RAS / KRAS G12X-enriched populations | RAS-mutant tumors (multi-selective, not G12C-only) |
| Resistance biology addressed | EMT, CSCs, CAFs, fibrosis, metastasis, chemo re-sensitization | RAS output; combinations (e.g., anti-EGFR) being explored | Oncogene-addicted proliferation; adaptive MAPK reactivation remains a known class issue |
Why PRP May Complement ERAS-0015 and Other RAS Agents
RAS mutations drive approximately
Cells that survive RAS blockade are frequently mesenchymal and stem-like. EMT is the program that allows carcinoma cells to leave the primary site, hide from therapy, and return. Fibrosis and cancer-associated fibroblasts further limit drug penetration and sustain a CSC reservoir through TGF-β signaling. None of those liabilities is the primary target of a “pan-RAS molecular glue”.
PRP is designed to act downstream of the GTPase:
- Proenzyme activation and PAR signaling. After intravenous administration, trypsinogen and chymotrypsinogen are activated and engage 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.
- Restoration of an epithelial phenotype. PRP increases epithelial adhesion proteins such as E-cadherin and β-catenin and decreases EMT transcription factors. Cells become less motile, more adherent, and more differentiated.
- Depletion of cancer stem cells. In pancreatic CSC models, PRP reduced ALDH-high cells and surface markers CD44, CD326, and CXCR4; suppressed primary and secondary sphere formation; and impaired tumor engraftment in vivo.
- TME remodeling and chemo-sensitization. Decreased CAF activity and fibrosis can improve drug delivery. By pushing cells out of a mesenchymal, drug-tolerant state, PRP resensitized chemo-resistant PDAC cells to gemcitabine/nab-paclitaxel. The same logic applies to RAS inhibitors: a smaller mesenchymal reservoir should leave fewer cells capable of adaptive resistance.
“RAS inhibitors have rewritten what is possible in pancreatic and RAS-mutant lung cancer. That is a genuine inflection point for patients,” said Mr. James Nathanielsz, Propanc’s Chief Executive Officer. “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 differentiate and disarm. If that biology holds in the clinic, PRP could help RAS-focused companies — including programs such as ERAS-0015 — convert high response rates into longer, cleaner remissions.”
“EMT is the program that lets a carcinoma leave home, hide, and return,” said Dr. Ralf Brandt, Propanc’s Research & Development Director. “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.”
“Pancreatic cancer remains one of oncology’s greatest challenges, with five-year survival rates still near
Clinical Development Path
The Company is progressing GMP manufacturing, pharmacokinetics assay validation, and clinical partnerships in support of a planned Phase 1b First-in-Human study. The multicenter, open-label study is expected to enroll approximately 40 to 50 patients with advanced solid tumors, including pancreatic, ovarian, and other refractory cancers, with first patient dosing targeted for February 2027. A clinical trial application is expected in the coming months.
Propanc intends to evaluate PRP both as a single agent and, subject to emerging clinical data and partner interest, as a potential backbone in combination or sequential regimens with RAS-targeted therapies and standard chemotherapy.
About Propanc Biopharma, Inc.
Propanc Biopharma, Inc. (Nasdaq: PPCB) is developing a novel approach to preventing cancer recurrence and metastasis by targeting and eradicating cancer stem cells through proenzyme activation. The Company’s lead product candidate, PRP, is designed to address the underlying drivers of cancer proliferation and spread.
More information: www.propanc.com
Forward-Looking Statements
All statements in this press release that are not historical are forward-looking statements, including, among other things, statements relating to the Company’s expectations regarding its market position and market opportunity, expectations and plans as to its product development, manufacturing and sales, and relations with its partners and investors, made in reliance upon the safe harbor provisions of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. These statements are not historical facts but rather are based on the Company’s current expectations, estimates, and projections regarding its business, operations and other similar or related factors. Words such as “may,” “will,” “could,” “would,” “should,” “anticipate,” “predict,” “potential,” “continue,” “expect,” “intend,” “plan,” “project,” “believe,” “estimate,” and other similar or related expressions are used to identify these forward-looking statements, although not all forward-looking statements contain these words. You should not place undue reliance on forward-looking statements because they involve known and unknown risks, uncertainties, and assumptions that are difficult or impossible to predict and, in some cases, beyond the Company’s control. Forward-looking statements are not guarantees of future actions or performance. Actual results may differ materially from those in the forward-looking statements because of several factors, including, without limitation, risks and uncertainties related to market conditions, as well as those risks described under “Risk Factors” in the prospectus related to the proposed offering and those described in the Company’s filings with the SEC. The Company undertakes no obligation to revise or update information in this release to reflect events or circumstances in the future, even if new information becomes available.
Company:
Propanc Biopharma, Inc.
James Nathanielsz
+61-3-9882-0780
info@propanc.com
Investor Contact:
irteam@propanc.com
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