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GutBarrier FunctionInflammationSkin QualityGut inflammation / IBD-type support

RESEARCH REFERENCE

KPV

α-MSH C-terminal tripeptide fragment with potent anti-inflammatory effects, especially in the gut.

01

Quick Reference

Dose
Oral 500 mcg–1 mg; SC 250–500 mcg
Frequency / schedule
1–2× daily
Route
Oral (preferred for gut) or subcutaneous
Timing
Flexible (empty stomach preferred for oral)
Fasting
Oral best on empty stomach; SC flexible
Cycle
4–8 weeks
Time off
2–4 weeks off
Common vial strengths
5 mg, 10 mg
02

How this works

KPV enters cells and inhibits IκB kinase, blocking NF-κB translocation. This reduces pro-inflammatory cytokines (TNF-α, IL-6, IL-1β). It is preferentially taken up via the PepT1 transporter in inflamed intestinal tissue, making oral use particularly relevant for gut applications.

03

Benefits + side effects

Potential Benefits

  • Rapid anti-inflammatory action (hours to days)
  • Gut barrier support

Side Effects

  • Generally mild; limited human data
02

Dosing / Protocol

Reference Protocol

Phase / weekDoseFrequencyTimingNotes
Gut500 mcg1–2× dailyEmpty stomachOral preferred
Systemic250–500 mcg1–2× dailyFlexibleSC

Timing + Fasting Notes

Oral: empty stomach preferred for better PepT1 uptake. SC: any time.

03

Reconstitution

Common vial strengths5 mg, 10 mg

Approved preparation example
5 mg + 2 mL BAC → 2.5 mg/mL

04

Practical Reference

Storage
Refrigerated reconstituted
Route / injection context
Oral (preferred for gut) or subcutaneous
Bloodwork / markers
CRP, calprotectin (if gut)
Common vial strengths
5 mg, 10 mg
Cycle / time off
4–8 weeks · 2–4 weeks off
Practical notes
Often stacked with BPC-157 for gut. Research use only.
10

References

01
PepT1-mediated tripeptide KPV uptake reduces intestinal inflammationGastroenterology · 2008 · DOI 10.1053/j.gastro.2007.10.026
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