See how research connects peptides to biological targets, signaling pathways, and biological processes.
This tool shows, for each peptide, which biological target the available research points to, how directly that relationship is supported, and how it connects to broader signaling pathways and biological processes. It describes what research suggests about biological mechanisms -- not proven health or treatment outcomes, and not medical advice. See each peptide's full research profile for complete detail, citations, and safety information.
Mechanism research for MitoCore's current product catalog.
Showing 37 of 37 peptides
Evidence legend
Relationship support
Directly supported
Supported indirectly
Inferred from related evidence
Uncertain
Evidence context
Human research
Preclinical research
Human + preclinical research
Review / established literature
Related compound/program context
Evidence context uncertain
Understanding mechanism evidence
This tool describes research into biological targets, signaling pathways, and biological processes -- not proven health or treatment outcomes, and not medical advice. Relationship-support and evidence-context labels describe the type and directness of research available, not proof of safety or effectiveness. See each peptide's full research profile for complete detail, citations, and safety information.
Mechanism profiles
KPV
1 mechanism relationship · Directly supported · Preclinical research
PathwayOther Defined PathwayPepT1/SLC15A1 mediates defined intestinal di- and tripeptide transport. The current PF01-PF21 taxonomy does not contain a dedicated nutrient/solute-transport family, so this established transport relationship is placed in PF14 rather than being misclassified under the inflammatory disease context in which KPV was studied.
Relationship details
KPV → PepT1 — Directly supportedExact KPV was directly transported by PepT1/SLC15A1 in radiolabeled uptake and substrate-competition experiments, with PepT1 dependence supported by transporter-overexpression and knockout models; this is a transporter/substrate relationship, not receptor agonism, and does not establish PepT1 as the sole mechanism of all KPV effects.
Evidence context
Preclinical research
Evidence is preclinical only, drawn from cell-culture and mouse-model transport and functional-dependence studies; no human efficacy is established. This is a transporter/substrate relationship -- exact KPV (Lys-Pro-Val) is transported by PepT1/SLC15A1 -- and does not establish or imply receptor agonism, receptor activation, or PepT1 signaling. Direct transport evidence comes from radiolabeled [3H]KPV uptake and cold-KPV competition experiments against a classic PepT1 substrate in PepT1-expressing cell systems (PMID 18061177). PepT1 functional dependence is further supported by PepT1-overexpression and PepT1-knockout mouse models. A numeric Km or other transport-affinity constant is intentionally omitted from this record unless independently re-verified from the original paper's primary figures/tables. The disease models used are primarily intestinal/inflammatory (colitis, colitis-associated cancer) and this record's findings should not be automatically generalized to other tissues or to human treatment. PepT1 dependence in these models does not establish PepT1 as the sole mechanism of all KPV biological effects. A separate p65RelA/importin-alpha3 intracellular mechanism has been reported for KPV and is outside the scope of this record. KPV's interaction with FPR2 is not established and is not part of this record. This record must not be used to transfer parent alpha-MSH melanocortin-receptor (MC1R/MC3R/MC4R/MC5R) pharmacology onto KPV. The supporting citation (PMID 27458604, PepT1-knockout colitis-associated-cancer model) demonstrates functional dependence on PepT1 but does not independently re-demonstrate direct KPV transport.
Sources
Central Citation Library reference: kpv-pept1-dalmasso-2008-transport-pmid18061177
Central Citation Library reference: kpv-pept1-viennois-2016-knockout-pmid27458604
What is established
A target (PepT1) and pathway family (Other Defined Pathway) are documented.
What remains unclear
Specific downstream signaling steps and biological-process associations are not yet documented.
Evidence is preclinical only, drawn from cell-culture and mouse-model transport and functional-dependence studies; no human efficacy is established. This is a transporter/substrate relationship -- exact KPV (Lys-Pro-Val) is transported by PepT1/SLC15A1 -- and does not establish or imply receptor agonism, receptor activation, or PepT1 signaling. Direct transport evidence comes from radiolabeled [3H]KPV uptake and cold-KPV competition experiments against a classic PepT1 substrate in PepT1-expressing cell systems (PMID 18061177). PepT1 functional dependence is further supported by PepT1-overexpression and PepT1-knockout mouse models. A numeric Km or other transport-affinity constant is intentionally omitted from this record unless independently re-verified from the original paper's primary figures/tables. The disease models used are primarily intestinal/inflammatory (colitis, colitis-associated cancer) and this record's findings should not be automatically generalized to other tissues or to human treatment. PepT1 dependence in these models does not establish PepT1 as the sole mechanism of all KPV biological effects. A separate p65RelA/importin-alpha3 intracellular mechanism has been reported for KPV and is outside the scope of this record. KPV's interaction with FPR2 is not established and is not part of this record. This record must not be used to transfer parent alpha-MSH melanocortin-receptor (MC1R/MC3R/MC4R/MC5R) pharmacology onto KPV. The supporting citation (PMID 27458604, PepT1-knockout colitis-associated-cancer model) demonstrates functional dependence on PepT1 but does not independently re-demonstrate direct KPV transport.
Key terms
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