Kisspeptin-10 vs KPV
Specialty
Kisspeptin-10
C-terminal decapeptide of kisspeptin, the upstream regulator of GnRH release via the KISS1R receptor.
Specialty
KPV
C-terminal tripeptide fragment of α-MSH studied for anti-inflammatory signaling without melanocortin receptor pigmentation effects.
Side by side
| Dimension | Kisspeptin-10 | KPV |
|---|---|---|
| Molecular weight A 3.8× difference in mass — these are not comparable on a milligram-for-milligram basis. | 1302.45 g/mol | 342.44 g/mol |
| Size class | short peptide | small molecule / short peptide |
| CAS number | 374675-21-5 | 67727-97-3 |
| Research area | specialty | specialty |
| Sequence | Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2 | Lys-Pro-Val |
| Available sizes | 5mg | 10mg |
| Entry price | $39 | $49 |
| Cost per mg | $7.80 | $4.90 |
Mechanism
Kisspeptin-10
Kisspeptin-10 is the shortest fully active fragment of kisspeptin, the product of the KISS1 gene. Its discovery reframed reproductive neuroendocrinology: kisspeptin signaling through KISS1R (GPR54) sits upstream of GnRH neurons and is now understood as a gatekeeper of the reproductive axis. Loss-of-function mutations in KISS1R cause hypogonadotropic hypogonadism, which is the genetic evidence anchoring the pathway.
KPV
KPV is the C-terminal tripeptide (residues 11-13) of alpha-melanocyte-stimulating hormone. Its research interest stems from retaining anti-inflammatory activity attributed to the parent hormone while lacking the melanocortin receptor binding responsible for pigmentation effects — making it a useful tool for separating those two activities. Work has examined NF-κB pathway inhibition in intestinal epithelial models.
Evidence quality
Mechanism is not the same as evidence. Where we have assessed the literature, the verdict is stated plainly.
Kisspeptin-10
Evidence base: solid receptor pharmacology with an established genetic basis. The desensitisation result under continuous exposure is specific, published, and frequently overlooked. Non-reproductive mechanisms are emerging and less replicated.
Full research reference →KPV
Evidence base: small but mechanistically coherent in the intestinal context, where PepT1-mediated uptake gives a defined transport route. Antimicrobial findings are thinner. Search results require filtering, since the sequence occurs incidentally in unrelated proteins.
Full research reference →Research applications
Kisspeptin-10
- KISS1R (GPR54) receptor binding and activation assays
- GnRH pulse generation studies in hypothalamic models
- Reproductive axis and puberty-onset research
- Metastasis suppression studies (the original KISS1 context)
KPV
- NF-κB signaling pathway inhibition assays
- Intestinal epithelial inflammation models
- PepT1 transporter-mediated uptake studies
- Cytokine expression profiling
Common questions
What is the difference between Kisspeptin-10 and KPV?
Kisspeptin-10 is c-terminal decapeptide of kisspeptin, the upstream regulator of GnRH release via the KISS1R receptor. KPV is c-terminal tripeptide fragment of α-MSH studied for anti-inflammatory signaling without melanocortin receptor pigmentation effects. They differ in molecular weight (1302.45 vs 342.44 g/mol) and in the pathways they are studied against.
Which is more cost-effective per milligram, Kisspeptin-10 or KPV?
KPV is lower at approximately $4.90 per milligram at its best tier, against $7.80 for the other. Cost per milligram is only meaningful relative to the concentrations a given protocol requires, since these compounds are not used at comparable masses.
Can Kisspeptin-10 and KPV be studied together?
Combination designs appear in the published literature for a number of these compounds. Whether it is appropriate for a given protocol depends entirely on the model and endpoint. We supply research compounds and do not provide protocol guidance — consult the primary literature for your specific model.
How should Kisspeptin-10 and KPV be stored?
Store lyophilized at -20°C protected from light. Reconstituted at 2-8°C for up to 30 days. For KPV: Store lyophilized powder at -20°C protected from light. Reconstituted solution stable at 2-8°C for up to 30 days.
Which has the stronger evidence base?
Kisspeptin-10 — Evidence base: solid receptor pharmacology with an established genetic basis. The desensitisation result under continuous exposure is specific, published, and frequently overlooked. Non-reproductive mechanisms are emerging and less replicated. KPV — Evidence base: small but mechanistically coherent in the intestinal context, where PepT1-mediated uptake gives a defined transport route. Antimicrobial findings are thinner. Search results require filtering, since the sequence occurs incidentally in unrelated proteins.
All products sold on this website are intended for research and identification purposes only. These products are not intended for human dosing, injection, or ingestion.
Comparison generated from Lyra Vital catalog data. Every specification is reconciled against the certificate of analysis for the shipped batch.