Propanc Biopharma’s Lead Asset PRP Reprograms Chemotherapy-Resistant Pancreatic Cancer Cells
PRP pre-treatment suppressed 21-day colony formation by 39% in chemotherapy-resistant cells and 59% in wild-type cells.
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Rhea-AI Summary
Propanc Biopharma (Nasdaq: PPCB) announced preclinical findings showing its PRP formulation altered chemotherapy-resistant pancreatic cancer cells and their subsequent chemotherapy response. PRP alone reduced proliferation by 54% in resistant cells and 50% in wild-type cells. PRP pre-treatment followed by chemotherapy produced the study’s strongest functional response. Separate experiments combining PRP with a TGF-β inhibitor achieved 80% invasion inhibition in resistant cells.
The research, involving the Universities of Jaén and Granada, examined cell behavior and gene activity. Results showed changes in programs associated with resistance, invasion and susceptibility to cell death, with responses differing between tumor models. Propanc plans a Phase 1b first-in-human study in Q1 2027 for advanced cancer patients with solid tumors. Further validation in clinically relevant models is planned to assess whether the resistance-remodeling effect can benefit patients.
How this balance works
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Hollow bars mark forward-looking points. How the balance works
Positive
- Moderate point. Forward-looking: it has not happened yet and may not happen.Propanc plans a Phase 1b first-in-human study in Q1 2027 for advanced cancer patients with solid tumors.
- Minor pointPRP monotherapy reduced proliferation by 54% in chemoresistant cells and 50% in wild-type cells.
- Minor pointPRP pre-treatment followed by chemotherapy produced the study’s strongest functional response in cell models.
- Minor pointPRP pre-treatment suppressed 21-day colony formation by 59% in wild-type and 39% in chemoresistant cells.
- Minor pointPRP monotherapy limited 72-hour wound closure to 21% in wild-type and 57% in chemoresistant cells, versus 100% untreated.
14 minor points
- Minor pointPRP monotherapy reduced invasive capacity by 81% in wild-type and 47% in chemoresistant cells.
- Minor pointPRP increased E-cadherin, an epithelial marker, up to 5.29-fold in wild-type and 4.86-fold in chemoresistant cells.
- Minor pointPRP increased epithelial marker EPCAM up to 4.39-fold in wild-type cells.
- Minor pointPRP reduced mesenchymal markers Vimentin to approximately 0.31–0.32-fold of control and Snail to 0.28–0.62-fold.
- Minor pointPRP reduced SMAD2, SMAD3 and TGFBR1 gene expression to 0.23–0.42-fold in chemoresistant cells.
- Minor pointPRP monotherapy reduced nuclear movement of signaling proteins SMAD2/3 by 81% in wild-type and 78% in chemoresistant cells.
- Minor pointPRP increased cell-death-promoting BAX expression 2.49-fold in wild-type and 2.74-fold in chemoresistant cells.
- Minor pointPRP decreased cell-survival-associated BCL2 expression to 0.49-fold.
- Minor pointPRP increased cell-cycle and stress regulators: CDKN1A 3.90–4.10-fold, ATM 2.88–3.34-fold and TP53 3.29–3.64-fold.
- Minor pointPRP suppressed aggressiveness-associated MYC and SOX2 to 0.11-fold and 0.22-fold, respectively, in chemoresistant cells.
- Minor pointPRP plus a TGF-β inhibitor achieved 80% invasion inhibition in chemoresistant cells.
- Minor pointPRP plus a TGF-β inhibitor increased E-cadherin 8.24-fold in chemoresistant cells.
- Minor pointPRP plus a TGF-β inhibitor reduced nuclear SMAD2/3 movement by 93% in chemoresistant cells.
- Minor pointPRP plus a TGF-β inhibitor increased BAX 4.42-fold in chemoresistant cells.
Negative
- Minor pointTranslation of resistance remodeling into patient benefit requires further validation in clinically relevant models.
Details
Market Reaction – PPCB
On Oct 16, the day this news came out, the latest delayed price for PPCB is 2.49% above the previous close. Our momentum scanner has recorded 18 alerts for this stock so far that day. The latest delayed price is $0.35. Relative volume is exceptionally heavy at 41.2x the average.
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Key Figures
- Proliferation reduction
- 50% (WT); 54% (GR)
- PRP monotherapy in pancreatic cancer cells
- Clonogenic survival suppression
- 59% (WT); 39% (GR)
- After PRP pre-treatment; assessed over 21 days
- Invasion reduction
- 81% (WT); 47% (GR)
- PRP monotherapy in Matrigel invasion assays
- Invasion inhibition
- 80%
- PRP plus a TGF-β inhibitor in chemoresistant cells
- E-cadherin increase
- 8.24-fold
- PRP plus a TGF-β inhibitor
- Nuclear SMAD2/3 translocation reduction
- 93%
- PRP plus a TGF-β inhibitor
Historical Context
-
Reported PRP sensitized chemotherapy-resistant cells to gemcitabine plus nab-paclitaxel.
24h Move is the share-price change in the day after each event; other market factors may also have contributed.
Key Terms
epithelial–mesenchymal transition medical
rt-qpcr technical
clonogenic medical
apoptosis medical
AI-generated analysis. How Rhea-AI works. Not financial advice.
New Preclinical Findings Identify Potential Strategy to Remodel Resistant Tumor State & Restore Therapeutic Vulnerability
MELBOURNE, Australia, Oct. 16, 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 new preclinical research from an academic–industry collaboration from the Universities of Jaén and Granada, led by Dr. Maria Belén Toledo, has identified pancreatic proenzyme formulation, PRP, as a potential strategy for addressing chemotherapy resistance in pancreatic cancer.
Chemotherapy-resistant tumor cells can acquire adaptive cellular states that allow them to survive treatment and maintain aggressive characteristics. The study investigated whether PRP could remodel these resistant states and increase their vulnerability to subsequent chemotherapy. It combined functional cellular analyses with transcriptome-wide (i.e. RNA molecules within the cell) profiling in pancreatic cancer models with acquired chemotherapy resistance.
“These findings are highly significant as we progress PRP to a world-first, Phase 1b, First-In-Human study for advanced cancer patients with solid tumors in Q1 2027, because we envision PRP as a welcome addition to the treatment process, as a long term, metronomic therapy that minimizes threat of recurrence, whilst enabling patients to respond to standard treatment options where tumor resistance has become a critical, life threatening factor,” said Mr. James Nathanielsz, Propanc’s Chief Executive Officer. “Dr. Toledo’s findings shows that PRP’s targeted multiple effects reprograms pancreatic cancer cells through interconnected biological programs which alters chemoresistance, tumor cell plasticity and aggressive behavior. We are now in the unique position to investigate sequential combinatorial approaches that rely on inhibition of specific tumor pathways which are effective, but do not address tumor led resistance mechanisms.”
A sequential strategy to remodel resistance
A defining feature of the experimental design was the treatment sequence. Chemoresistant (GR) cells were first exposed to PRP. Chemotherapy was then added to determine whether PRP pre-treatment had altered the resistant state and changed the subsequent response to chemotherapy.
GR CELLS → PRP PRE-TREATMENT → CHEMOTHERAPY → ASSESSMENT OF RESPONSE
According to Dr. Toledo, “This distinction is central to the study: PRP was used first as a resistance-modulating intervention, while chemotherapy was subsequently used as the challenge to test whether the cells had become more responsive and sensitive.”
Reprogramming the resistant cellular state
PRP induced coordinated changes across interconnected biological processes associated with chemoresistance, tumor cell plasticity and aggressive behavior. At a high level, these included:
- Tumor-cell plasticity and epithelial–mesenchymal transition (EMT)
- Drug-response and metabolic processes
- DNA replication and repair
- Cellular stress and survival programs
- Extracellular matrix organization
- Apoptotic susceptibility
Importantly, PRP treatment alone produced changes consistent with partial restoration of features associated with chemotherapy sensitivity in resistant models. This supports the concept of PRP as a resistance-modulating intervention rather than simply a conventional cytotoxic agent.
Testing whether resistance can be overcome
Following PRP pre-treatment, chemotherapy was introduced to determine whether the resistant phenotype had been functionally weakened. The sequential PRP → chemotherapy strategy produced the strongest functional response in the study, supporting the hypothesis that remodeling the resistant state before chemotherapy can increase therapeutic vulnerability. The study evaluated complementary phenotypes including cellular growth, clonogenic capacity, migration, invasion and cell-death susceptibility.
A multimodal mechanism
Transcriptomic analyses revealed that PRP does not appear to act through a single resistance mechanism. Instead, the response involved coordinated remodeling of interconnected biological programs. The nature and magnitude of these changes differed between tumor models (WT and GR), highlighting the heterogeneity of chemotherapy resistance. Together, the data supports a systems-level interpretation in which PRP weakens adaptive programs sustaining the resistant state, creating a cellular context that is more vulnerable to subsequent chemotherapy.
Summary of Preclinical Findings
| Observations | Results |
| Restoring Chemotherapy Sensitivity & Reducing Proliferation |
|
| Suppressing Metastatic Behavior (Migration and Invasion) |
|
| Reversing Epithelial-Mesenchymal Transition (EMT) & Plasticity |
|
| Inhibiting Canonical TGF-β/SMAD Signaling |
|
| Inducing Apoptosis and Suppressing Oncogenic Stemness Drivers |
|
| Enhanced Synergistic Effect with TGF-β Inhibition (PRP + TGF-β inhibitor) |
|
Future development
These findings provide a preclinical rationale for further investigation of PRP as a resistance-modulating strategy, including its potential use as a standalone intervention to remodel resistant tumor cells and as a sequential approach preceding chemotherapy.
Validation in clinically relevant models will be undertaken to determine whether this resistance-remodeling effect can translate into a therapeutic benefit, ultimately, in patients.
CHEMORESISTANCE → RESISTANCE REMODELLING → THERAPEUTIC VULNERABILITY
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
Investor Contact:
irteam@propanc.com
A photo accompanying this announcement is available at https://www.globenewswire.com/NewsRoom/AttachmentNg/da1afeef-78de-4c02-a16a-7edcb0f4fc0d
FAQ
AI-generated questions and answers. How Rhea-AI works. Not financial advice.
What did Propanc Biopharma’s PRP study show in chemotherapy-resistant pancreatic cancer cells?
PRP monotherapy reduced proliferation by 54% in chemotherapy-resistant cells, while PRP pre-treatment followed by chemotherapy produced the study’s strongest functional response. These were preclinical cell-model findings; validation in clinically relevant models is planned to assess whether resistance remodeling can translate into patient benefit.
When does Propanc Biopharma plan to begin its PRP first-in-human study?
Propanc plans to advance PRP into a Phase 1b first-in-human study in Q1 2027 for advanced cancer patients with solid tumors.