*Doses are commonly-reported figures from public sources, not a recommendation. Educational only.
| Year | Title / venue | Source |
|---|---|---|
| 2025 | HDM-2-Targeting Peptide PNC-27 Kills Cervical Cancer Cells but not Normal Cervical Cells Annals of clinical and laboratory science · preclinical | PMID 40750238 |
| 2024 | Anti-Cancer Peptide PNC-27 Kills Cancer Cells by Unique Interactions with Plasma Membrane-Bound hdm-2 and with Mitochondrial Membranes Causing Mitochondrial Disruption Annals of clinical and laboratory science · preclinical | PMID 38802154 |
| 2022 | PNC-27, a Chimeric p53-Penetratin Peptide Binds to HDM-2 in a p53 Peptide-like Structure, Induces Selective Membrane-Pore Formation and Leads to Cancer Cell Lysis Biomedicines · preclinical | PMID 35625682 |
| 2022 | Conjugated PNC-27 peptide/PEI-superparamagnetic iron oxide nanoparticles (SPIONs) as a double targeting agent for early cancer diagnosis: In vitro study Iranian journal of basic medical sciences · preclinical | PMID 36311203 |
| 2020 | Targeting Membrane HDM-2 by PNC-27 Induces Necrosis in Leukemia Cells But Not in Normal Hematopoietic Cells Anticancer research · preclinical | PMID 32878773 |
| 2017 | Synergy between Paclitaxel and Anti-Cancer Peptide PNC-27 in the Treatment of Ovarian Cancer Annals of clinical and laboratory science · preclinical | PMID 28667027 |
| 2014 | The anti-cancer peptide, PNC-27, induces tumor cell necrosis of a poorly differentiated non-solid tissue human leukemia cell line that depends on expression of HDM-2 in the plasma membrane of these cells Annals of clinical and laboratory science · preclinical | PMID 25117093 |
| 2010 | The anti-cancer peptide, PNC-27, induces tumor cell lysis as the intact peptide Cancer chemotherapy and pharmacology · preclinical | PMID 20182728 |
PNC-27 (PNC-27 (p53-derived membrane-disrupting peptide)). Peptide containing a p53-derived domain plus a membrane-resident-peptide segment; reported preclinically to selectively form membrane pores in cancer cells expressing HDM-2 at the membrane, causing necrosis.
Commonly discussed uses: anticancer mechanism research (preclinical/in vitro). The evidence base is largely preclinical (animal/in-vitro); published randomised human clinical trials are lacking or absent. Note: most uses are not approved indications.
Mechanism: Peptide containing a p53-derived domain plus a membrane-resident-peptide segment; reported preclinically to selectively form membrane pores in cancer cells expressing HDM-2 at the membrane, causing necrosis.
Reported considerations: no human safety data, membrane-disrupting mechanism — non-trivial theoretical toxicity. The evidence base is largely preclinical (animal/in-vitro); published randomised human clinical trials are lacking or absent. Preclinical anticancer research compound. No human safety/efficacy data. Not a treatment. Not approved. This is not a safety endorsement; safety data for unapproved compounds is incomplete.
Commonly cited ranges (educational reference, not a recommendation): low research-defined, typical no established human dose, high unknown. Administration: in vitro / animal models (research). Half-life: not characterised in humans.
Australian status: Not ARTG-registered; research. Preclinical anticancer research compound. No human safety/efficacy data. Not a treatment. Not approved. General regulatory context: most active peptides are Schedule 4 and require a prescription; import via the Personal Importation Scheme requires a valid Australian prescription for prescription-only goods.
Reconstitution/storage reference: research-defined; storage: frozen aliquots.
Commonly discussed combinations (anecdotal for unapproved compounds): research compound; no human protocols. Stacking increases interaction/safety uncertainty.