Peptide Schedule
PNC-2731 residues (approx.)PQHLRVKRPQHLRVRQIKIWFQNRRMKWKKEach bubble = one amino acid. Size = residue mass. Color = chemical class.Uses closest standard amino acids for non-standard residues.

PNC-27 Dosage Calculator

ImmuneInjectionResearch~2-4 hours half-life

PNC-27 is a 32-residue synthetic anticancer peptide engineered from two functional domains: the p53 transactivation domain (residues 12-26) responsible for binding HDM-2 (the human homologue of MDM2), and a cell-penetrating peptide (CPP) leader sequence derived from Drosophila Antennapedia that enables membrane interaction.

Selectively kills cancer cells while sparing normal cells in preclinical modelsInduces rapid necrotic cell death via transmembrane pore formationActive against multiple cancer types including breast, pancreatic, melanoma, leukemia, and ovarian cancer in vitroDoes not rely on p53 function inside the cancer cell — works on p53-mutant cancers8 weeks on / 4 weeks off

100mcg · Daily

100500
4.0 units
100 units (1mL)
Concentration
2,500
mcg/mL
Draw Volume
0.040
mL
Syringe Units
4.0
units
Doses / Vial
50
doses

Summary: Add 2mL BAC water to your 5mg vial. Draw to 4.0 units on a U-100 syringe for a 100mcg dose. This vial will last 50 doses.

Cycle Planner

Subcutaneous. Typical beginner frequency: daily.

PNC-27 Pharmacokinetics

Pharmacokinetics — Active Dose Over Time

t½ = ~2-4 hours (estimated from in vitro decay; no formal human PK studies)
50%25%12.5%100%75%50%25%0%03h6h9h12h15hTime after injectionDose remaining
After 1 half-life (3h): 50% remainsAfter 2 half-lives (6h): 25% remainsAfter 3 half-lives (9h): 12.5% remains
At a 250mcg dose: 50% = 125mcg remaining after 3h. Recommended frequency: Daily.

Disclaimer: This curve is a simplified first-order exponential decay model. Actual pharmacokinetics vary based on injection site, individual metabolism, body composition, and other factors. Half-life values are approximate and based on available preclinical and clinical literature. Many research peptides lack formal human pharmacokinetic studies. This is for educational purposes only — not medical advice.

PNC-27 Dosing Protocol

LevelDose / InjectionFrequency
Beginner100mcgDaily
Moderate250mcgDaily
Aggressive500mcgDaily

Note: Experimental anticancer peptide — preclinical only with zero completed human trials. Contains residues 12-26 of p53 (the HDM-2/MDM2 binding domain) fused to a cell-penetrating leader sequence. Selectively kills cancer cells by binding to HDM-2 on their plasma membranes and forming transmembrane pores, while leaving normal cells unaffected. All dosing is theoretical and extrapolated from in vitro concentrations and a single murine MTD study. Not FDA-approved for any indication.

About PNC-27

PNC-27 is a 32-residue synthetic anticancer peptide engineered from two functional domains: the p53 transactivation domain (residues 12-26) responsible for binding HDM-2 (the human homologue of MDM2), and a cell-penetrating peptide (CPP) leader sequence derived from Drosophila Antennapedia that enables membrane interaction. The peptide was developed primarily by researchers at SUNY Downstate Medical Center and has been studied since the mid-2000s. PNC-27 exploits a key difference between cancer cells and normal cells — cancer cells express significant amounts of HDM-2 protein on their outer plasma membranes, while normal cells do not. When PNC-27 encounters a cancer cell, the p53-derived domain binds to membrane-associated HDM-2 in approximately 1:1 stoichiometric complexes. These complexes then aggregate within the membrane to form large ring-shaped transmembrane pores with interior diameters averaging 34.5 nm. The pore formation process is temperature-dependent: PNC-27 binds to HDM-2 at any temperature, but the lateral diffusion, aggregation, and pore assembly require physiological temperature (37 degrees C). Once pores form, the cancer cell membrane loses integrity, causing rapid necrotic cell death — not apoptosis — with detectable LDH release within 4 hours. Preclinical studies have demonstrated PNC-27 activity against breast cancer (MDA-MB-231), pancreatic cancer (MIA PaCa-2), melanoma (A2058), multiple leukemia cell lines (U937, OCI-AML3, HL-60), cervical cancer, and patient-derived epithelial ovarian cancer cells. In an in vivo mouse model, PNC-27 was administered daily via intraperitoneal injection with a maximum tolerated dose of 2 mg/day. It also enhanced paclitaxel activity in a mouse ovarian cancer model, producing greater tumor reduction than either agent alone. A 2024 study revealed that PNC-27 also disrupts mitochondrial membranes in cancer cells, suggesting a dual-mechanism of action. Despite these promising preclinical results, no human clinical trials have been completed, and all safety and dosing information remains speculative.

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