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
Semax
1 mechanism relationship · Supported indirectly · Preclinical research
Semax → TrkB receptor — Supported indirectlySemax increases BDNF protein, trkB mRNA, and TrkB tyrosine phosphorylation in rat brain, without demonstrated direct Semax-TrkB binding or TrkB agonism.
Evidence context
Preclinical research
Semax administration increased BDNF protein, trkB mRNA, and TrkB tyrosine phosphorylation in rat brain. These data do NOT demonstrate direct Semax binding to TrkB and do NOT establish Semax as a TrkB agonist. A separate, specific, saturable Semax membrane-binding site has been reported; the molecular identity of that binding site remains unresolved and must NOT be conflated with TrkB. Evidence is preclinical, from rat models only.
Sources
Central Citation Library reference: semax-dolotov-2006-bdnf-trkb-hippocampus-pmid16996037
Central Citation Library reference: b106-semax-dolotov-bdnf-16635254
Central Citation Library reference: b106-semax-stavchansky-pgp-transcription-19633950
Central Citation Library reference: semax-agapova-2007-neurotrophin-gene-expression-pmid17353092
What is established
A target (TrkB receptor) and pathway family (Neuropeptide & CNS Signaling) are documented.
What remains unclear
Specific downstream signaling steps and biological-process associations are not yet documented.
Semax administration increased BDNF protein, trkB mRNA, and TrkB tyrosine phosphorylation in rat brain. These data do NOT demonstrate direct Semax binding to TrkB and do NOT establish Semax as a TrkB agonist. A separate, specific, saturable Semax membrane-binding site has been reported; the molecular identity of that binding site remains unresolved and must NOT be conflated with TrkB. Evidence is preclinical, from rat models only.
Key terms
Looking for research areas instead?
Peptide Explorer shows what areas a peptide is researched in. This tool shows how the underlying biology appears to work.
Educational use only. Not medical advice. MitoCore Biosciences does not diagnose, treat, cure, prevent, prescribe, sell peptides, recommend dosing, or provide instructions for human use.
