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
Selank
1 mechanism relationship · Supported indirectly · Preclinical research
Selank → GABA receptor system — Supported indirectlySelank alters [3H]GABA binding in isolated brain-cell membrane preparations in a manner described as positive allosteric modulation, while the molecular Selank binding site and GABA receptor subtype/subunit remain unresolved.
Evidence context
Preclinical research
The exact Selank molecular binding site has NOT been identified. No direct radiolabelled-Selank binding to a cloned molecular GABA receptor has been demonstrated. This record does NOT claim benzodiazepine-site binding, does NOT claim GABA-A agonism, and does NOT resolve a GABA receptor subtype or subunit. Selank's interaction patterns with diazepam and olanzapine were non-additive/different from those reference compounds and must not be simplified into a benzodiazepine-like mechanism claim. A separate IMR-32 gene-expression experiment found a null result for Selank alone on the GABAergic/neurotransmission genes tested; that counterweight is acknowledged here, not omitted. Evidence is preclinical only.
Sources
Central Citation Library reference: b106-selank-vyunova-gaba-mechanism-30255741
Central Citation Library reference: selank-volkova-2016-gaba-gene-expression-pmid26924987
Central Citation Library reference: selank-filatova-2017-imr32-gaba-gene-expression-pmid28293190
What is established
A target (GABA receptor system) and pathway family (Neuropeptide & CNS Signaling) are documented.
What remains unclear
Specific downstream signaling steps and biological-process associations are not yet documented.
The exact Selank molecular binding site has NOT been identified. No direct radiolabelled-Selank binding to a cloned molecular GABA receptor has been demonstrated. This record does NOT claim benzodiazepine-site binding, does NOT claim GABA-A agonism, and does NOT resolve a GABA receptor subtype or subunit. Selank's interaction patterns with diazepam and olanzapine were non-additive/different from those reference compounds and must not be simplified into a benzodiazepine-like mechanism claim. A separate IMR-32 gene-expression experiment found a null result for Selank alone on the GABAergic/neurotransmission genes tested; that counterweight is acknowledged here, not omitted. Evidence is preclinical only.
Key terms
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