What KPV is
KPV is the three-amino-acid tail of alpha-MSH (lysine-proline-valine), which carries most of that hormone's anti-inflammatory signal without its pigmentation effects. The published work is preclinical, heaviest in gut inflammation models, which is why community use clusters around IBD-adjacent and general anti-inflammatory protocols and why it is the K in the KLOW blend.
What we do not know
- No published human trials of any kind. The evidence is animal colitis models and cell work.
- No human pharmacokinetics, so oral versus injected dosing has no established basis.
- Whether the PepT1 uptake route that makes it interesting in the gut applies to systemic administration is untested.
Reconstitution math
Concentration is everything: the same 5 mg vial gives a different draw for every amount of bacteriostatic water you add. The table uses the common 2 mL setup for each vial size, which puts every unit on a U-100 insulin syringe at 25 mcg for the default vial. Dashes mark draws too small to measure or larger than the syringe.
| Vial | BAC water | Concentration | 200 mcg | 250 mcg | 500 mcg |
|---|---|---|---|---|---|
| 5 mg | 2 mL | 2.5 mg/mL | 8 u | 10 u | 20 u |
| 10 mg | 2 mL | 5 mg/mL | 4 u | 5 u | 10 u |
Dosing and protocol
Community protocol: 200 to 500 mcg daily, subcutaneous or oral, typically in 4 to 8 week runs.
Community dosing runs 200 to 500 mcg daily, subcutaneously or orally for gut-focused use. On a 5 mg vial with 2 mL of water, 250 mcg is 10 units. When it rides in a KLOW vial with GHK-Cu, BPC-157, and TB-500, dosing is by injection volume; the blend calculator handles that math.
Pharmacokinetics
No curve is shown, on purpose.
KPV has no human pharmacokinetic data at all; the literature is cell and animal work on inflammatory models. Injection dosing is entirely community convention, so no curve is shown.
How it is thought to work
The C-terminal tripeptide of alpha-MSH. It carries the anti-inflammatory activity of the parent hormone without the pigmentation effects, and is taken up by intestinal epithelium through the PepT1 transporter, which is why most of the work on it concerns gut inflammation.
What the evidence supports
This table grades how well each outcome has been studied in humans, not how well KPV works. A strong grade means the question was asked properly, and the answer may still have been negative. Nothing here is inherited from a drug class, a close analog, or the parent molecule of a fragment.
| Outcome | Strongest published evidence |
|---|---|
| Intestinal inflammation | Animal only |
| Skin inflammation | Animal only |
| PepT1-mediated epithelial uptake | Mechanistic only |
| Any outcome in humans | No data |
Storage and handling
Lyophilized vials keep best cold, dark, and dry; refrigeration is the community default and freezing lyophilized powder is common for long holds. After reconstitution, refrigerate at 2 to 8 C, do not freeze the solution, and date the vial. Bacteriostatic water's preservative keeps multi-dose use practical for about 28 days by USP convention, though our 120-day stability study found the preservative itself outlasts that window.
Got a certificate of analysis with your vial? Run it through our COA Reader: it reads the report in plain English, checks purity and mass against the label claim, and links the testing lab’s own verification page. Our guide to reading a COA explains what the numbers do and do not tell you.
Sources
- Dalmasso et al., PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation, Am J Physiol Gastrointest Liver Physiol 2008PMID 18061177 · DOI
- Brzoska et al., Alpha-MSH and derived tripeptide KPV: anti-inflammatory mechanisms, Endocr Rev 2008