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IMMUNE SUPPORT

KPV Protocol

C-terminal alpha-MSH fragment studied for anti-inflammatory and gut-healing research without pigmentation effects.

Preclinical compoundInvestigational / Theoretical
Cycle
4–8 weeks

Evidence Level: Investigational / Theoretical

Primarily preclinical or very limited human data — mechanism-based reasoning more than a demonstrated clinical effect. Treat as investigational.

Human evidence: No controlled human trials.

Animal evidence: Rodent colitis and gut-inflammation models form the primary evidence base.

Introduction & Mechanism of Action

C-terminal alpha-MSH fragment studied for anti-inflammatory and gut-healing research without pigmentation effects.

Tripeptide fragment of alpha-MSH that retains anti-inflammatory activity while lacking the melanocortin-receptor pigmentation effects of the full hormone — studied particularly for gut-mucosal inflammation models.

Receptors/targets: Proposed non-melanocortin-receptor anti-inflammatory pathway (mechanism not fully established)

Areas of Research Interest

Benefits Reported in Research

Reported Research Dosing Range

The figures below are cited from published research literature and protocol references — they describe what has been studied, not a personal prescription or instruction.

Reported range: 200–500 mcg

Reported frequency: 1× daily, oral

Reported cycle duration: 4–8 weeks

Escalation & maintenance: A dedicated weekly escalation and maintenance schedule specific to this peptide has not yet been published here — follow the dose range and frequency above, titrating conservatively from the low end, and consult a physician before adjusting.

Side Effects

Contraindications

Drug interactions

Safety

Derived from alpha-MSH but studied for non-pigmentary anti-inflammatory effects; human clinical trials are limited.

Expected Results & Comparison

KPV and BPC-157 are both studied for gut-related research, but via different mechanisms — KPV as an anti-inflammatory melanocortin fragment, BPC-157 via broader tissue-repair/angiogenic signaling. Neither has strong human trial support, so choosing between them for gut research is a mechanism-fit question, not an evidence-strength one.

References

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