Colivelin
Aliases: CL · Colivelin peptide
Last verified: 2026-09-24
The short version
Colivelin is scientifically beautiful and clinically dead. In the mouse brain it is impressive; the problem is that this result was obtained by injection into a brain ventricle, which is a technique, not a therapy. Gray-market sale of Colivelin vials as a 'neuroprotection nootropic' ignores the central problem of the entire peptide neurology field: peptides do not cross from blood into brain at relevant concentrations, and the intranasal route — the only real alternative — has variable, poorly mapped efficiency. This is a laboratory substance, not a vial substance.
Identity & type
- Molecular type
- hybrid peptide
- Origin
- Synthesis of Humanin-derived sequences with a poly-arginine transduction motif.
Mechanism of action
A hybrid peptide created by joining Humanin with a C8R cluster; in neuronal models it protects cells via STAT3 and JAK pathway activation and inhibition of pro-apoptotic signals — one of the most potent neuroprotective peptides described in vitro and in the mouse brain (central administration).
not confirmed in humans
Dosing & routes
Official / clinical context
No official context exists.
Regulator-approved labeling and published study designs — never a recommendation.
Community-reported practice
Practically nonexistent in the community; occasionally in the most exotic nootropic circles with intranasal attempts, without measurements.
Unverified self-reports. Not medical advice. Not endorsement.
Protocol — official vs community
Official / label
No approved protocol exists — preclinical agent. Colivelin has been dosed only intracerebroventricularly or intranasally in ng–µg ranges in rodents.
Duration: —
Its potency in neuronal models is genuine and unusually strong for a peptide, but central administration in mice tells you almost nothing usable about human dosing.
Community (anecdotal)
Structured protocol data for this entry is coming.
Human evidence
None.
Preclinical evidence
Strong in vitro and in central-administration models; the key gap — systemic bioavailability and translatability to humans.
Known risks
- Complete uncertainty of pharmacokinetics by any route of administration in humanstheoretical
Teal: characterized in clinical/labeling contexts. Amber: theoretical or reported outside controlled settings.
Unknowns & evidence gaps
- Everything — bioavailability, effect, safety in humans
Frequently asked questions
References
- Chiba T et al. — colivelin, a potent neuroprotective peptide (J Neurosci, 2004–2005)
- Colivelin in SOD1/ALS mouse models — delayed onset