Colivelin (CLN)
A lab-built hybrid of two neuroprotective peptides — far more potent than Humanin — studied against Alzheimer's and ALS in animals. A research peptide, not a drug
Colivelin (CLN) is a designed, 26-amino-acid peptide built by stitching together two natural neuroprotective peptides: activity-dependent neurotrophic factor (ADNF) and a potent derivative of Humanin, the small peptide first found in a surviving part of an Alzheimer's brain. The goal was to make a 'superagonist' — and it worked: colivelin blocks neuronal death caused by Alzheimer's-related insults (amyloid-beta and familial-Alzheimer's genes) at femtomolar concentrations in cells, roughly a hundred times lower than the Humanin derivative alone and vastly lower than Humanin itself. Its power comes from hitting two survival pathways at once: an ADNF-triggered CaMKIV pathway and a Humanin-triggered STAT3 pathway. In animals, colivelin rescues memory in Alzheimer's models — even when given into the nose or the bloodstream, so it reaches the brain — and prolongs survival in an ALS mouse model by protecting motor neurons. It is studied as a drug candidate for neurodegenerative disease; it is not an approved medicine and has not been given to people as a treatment.
No established human dose Details ↓
Recommended Dosing
No established human dose
Colivelin is a synthetic peptide that has never been given to people as a treatment. The work is in animals and cells, where it is given into the brain, by injection, or intranasally at experimental amounts that do not carry over to people.
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What is it?
Humanin is a short peptide, first identified in a surviving region of an Alzheimer's-disease brain, that protects neurons from death by activating a Jak2/STAT3 survival pathway. Researchers made it far more potent in steps: a 17-amino-acid derivative, AGA-(C8R)HNG17, is about a hundred thousand times stronger than Humanin. Colivelin took the next step — fusing activity-dependent neurotrophic factor (ADNF), another neuroprotective peptide, onto the front of that derivative to create a 26-amino-acid hybrid.
The result is a femtomolar-acting neuroprotectant. In cell models, colivelin completely suppresses death caused by overexpressed familial-Alzheimer's genes and by amyloid-beta at concentrations around 100 femtomolar, where the Humanin derivative alone needs about 10 picomolar. The reason is that colivelin engages two independent prosurvival routes simultaneously: a calcium/calmodulin-dependent protein kinase IV (CaMKIV) pathway triggered by the ADNF part, and a STAT3 pathway triggered by the Humanin part.
In live animals, colivelin rescues memory in Alzheimer's models. Given into the brain ventricles it reverses the spatial-memory impairment caused by amyloid-beta and protects neurons in the hippocampal CA1 region; given intraperitoneally or even intranasally it still works, because enough crosses into the brain — the nasal route delivering it via the olfactory bulb and boosting STAT3 signalling and cholinergic markers in the memory circuits. In rats and in APP/PS1 Alzheimer's-model mice, colivelin preserved spatial and working memory and restored hippocampal long-term potentiation while reducing amyloid deposition.
Its protective reach extends to motor-neuron disease. In the G93A-SOD1 mouse model of ALS, where ADNF alone improved motor performance without extending life, colivelin both improved motor function and dose-dependently prolonged survival, with more surviving motor neurons in the spinal cord — marking it as a promising neurotrophic peptide for ALS as well as Alzheimer's.
Colivelin is a synthetic neuroprotective peptide and a drug candidate for neurodegenerative disease. No published study has given colivelin to people as a treatment — the evidence is animal and cell work — it is approved nowhere, and material sold online under its name is an unregulated research chemical. Nothing here is a dose or a therapy; this page records what the published science says.
Mechanism of Action
Colivelin is a synthetic hybrid of ADNF and a potent Humanin derivative. It suppresses neuronal death at femtomolar concentrations by activating two prosurvival pathways at once — an ADNF-driven CaMKIV pathway and a Humanin-driven STAT3 pathway — protecting memory and motor neurons in Alzheimer's and ALS animal models.
Dual prosurvival signalling
The ADNF part triggers a Ca2+/calmodulin-dependent protein kinase IV (CaMKIV) pathway and the Humanin part a STAT3 pathway; together they give femtomolar neuroprotection (PMID 16267233).
Anti-amyloid memory rescue
Colivelin reverses amyloid-beta-induced memory loss, LTP suppression and CA1 neuron loss, and reduces amyloid deposition in Alzheimer's models (PMIDs 25332198, 28731445).
Motor-neuron protection
In ALS model mice colivelin prolongs survival and preserves spinal motor neurons, beyond what ADNF alone achieves (PMID 16564029).
Published Research
These are studies of colivelin read from their PubMed records on November 7, 2026: the discovery paper characterising its design, femtomolar potency and dual-pathway mechanism against Alzheimer's insults; an ALS mouse survival study; a review of humanin and colivelin for Alzheimer's and ALS; and animal studies of nasal and injected colivelin rescuing memory and synaptic plasticity in Alzheimer's models. Colivelin has not been given to people as a treatment; the evidence is animal and cell work.
Discovery of colivelin, a femtomolar Humanin superagonist
A hybrid peptide, colivelin, was made by fusing ADNF to the Humanin derivative AGA-(C8R)HNG17. It completely suppressed neuronal death from familial-Alzheimer's genes and amyloid-beta at 100 femtomolar (vs 10 picomolar for the derivative alone) via two pathways — ADNF-triggered CaMKIV and Humanin-triggered STAT3 — and, given into the brain or intraperitoneally in mice, reversed amyloid-beta-induced memory impairment and CA1 neuron loss (a discovery and characterisation study).
Colivelin prolongs survival of an ALS model mouse
In G93A-SOD1 transgenic ALS mice, intracerebroventricular colivelin dose-dependently improved motor performance AND prolonged survival — unlike ADNF alone, which had improved motor function without extending life — with increased motor-neuron survival in the spinal cord, marking colivelin as a promising neurotrophic peptide for ALS (a preclinical result).
Humanin and colivelin for Alzheimer's and ALS (review)
A review of the Humanin family: Humanin suppresses neuronal death via a Jak2/STAT3 pathway; its derivative AGA-(C8R)HNG17 is ~100,000-fold more potent; and colivelin, adding ADNF, gives complete neuroprotection at 100 femtomolar in vitro. Mouse Alzheimer's and ALS studies support efficacy in vivo, framing Humanin and colivelin as candidates for neuronal-death-suppression therapy.
Nasal colivelin ameliorates Alzheimer's-related memory impairment (mice)
Intranasally administered colivelin reached the central nervous system via the olfactory bulb and dose-dependently ameliorated memory impairment in mouse Alzheimer's models, correlating with increased STAT3 phosphorylation in the septohippocampal region and support of cholinergic neurotransmission (upregulated ChAT and VAChT) — showing a less-invasive delivery route works preclinically.
Colivelin rescues amyloid-beta-induced memory, LTP and calcium deficits (rats)
Intrahippocampal colivelin prevented amyloid-beta(25-35)-induced deficits in spatial learning and memory (Morris water maze), nearly completely prevented suppression of in-vivo hippocampal long-term potentiation, and inhibited amyloid-beta-induced calcium overload in cultured hippocampal neurons in rats — significant neuroprotection against amyloid-beta (a preclinical result).
Colivelin improves cognition and synaptic plasticity in APP/PS1 mice
Chronic intranasal colivelin in 9-month-old APP/PS1 Alzheimer's-model mice prevented impairments in object recognition, working memory and long-term spatial memory, reversed depression of in-vivo hippocampal long-term potentiation, and reduced amyloid-beta deposition in the hippocampus — linking behavioural improvement to less amyloid and relieved LTP suppression (a preclinical result).
No Established Human Dose
Colivelin is a synthetic peptide that has never been given to people as a treatment. The work is in animals and cells, where it is given into the brain, by injection, or intranasally at experimental amounts that do not carry over to people. No regulator has approved any dose, and no published human dose exists, so no amount is printed here.
What this rests on: PMID 16267233, PMID 16564029, PMID 17928813.
Educational information, not medical advice. The doses on this page come from approved labels, published studies and, where no study exists, amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
What a Buyer Needs to Know
What is sold, how it is mixed, stored and taken, and what is known about its safety, quality and legal status. Each part names its source. Where we have none, it says unknown.
What is sold
Unknown: we hold no label and no published test that says what forms or vial sizes Colivelin (CLN) is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
Unknown: no human dose of Colivelin (CLN) has been established (see No Established Human Dose below), so there is no amount to work out. The reconstitution calculator does the arithmetic for any vial, water and dose.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store Colivelin (CLN), before or after mixing. The mixing guide sets out the general rules, with their sources: keep a mixed vial in the fridge, and use it promptly, as the bacteriostatic water label says of any drug dissolved in it. The 28 days often quoted is the limit for an opened multiple-dose vial from a manufacturer, an outer limit set for sterility, not a time a mixed solution has been shown to keep. Nobody has published how long Colivelin (CLN) stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking Colivelin (CLN). What the human studies gave and how is set out under No Established Human Dose.
What to expect, and when
How long it stays in the body: a half-life of not established for humans; a short synthetic peptide studied by CNS and nasal delivery. After about five half-lives almost none is left.
When effects appear: unknown; no source on this page gives a time to effect for Colivelin (CLN). Results reported in the studies are under Published Research.
Source: half-life: PMID 17928813.
Side effects, and when to stop or get help
From the Side Effects section: No human adverse-event data exist: no published study has administered colivelin to people; In animal studies it was given to protect neurons and improve memory/survival without reported overt toxicity (PMIDs 16564029, 17928813) — a preclinical signal, not a human safety profile; As a potent activator of growth/survival (STAT3) signalling, long-term effects on cell proliferation would be an expected area of caution — a mechanistic inference, not human data for this peptide; Material sold online as 'colivelin' is an unregulated research chemical of unverified content. Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Colivelin (CLN). Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Colivelin is a research peptide that has not been given to people as a drug, so there is no human safety profile; the points below reflect that research status”).
Interactions
Unknown: a PubMed search for human interaction studies of Colivelin (CLN) (reviewed 2026-11-07) found none. Unknown is not the same as safe to combine.
Every peptide's record, with its source: the interaction matrix.
Checking what you bought
Unknown: no published independent test of Colivelin (CLN) products is in our lab-results database yet, so how products sold under this name measure up is not known.
To read a certificate of analysis, paste it into the COA decoder. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Research Chemical (Not a drug: Drugs@FDA and the openFDA label endpoint hold no record, and FDA GSRS and ChEMBL hold no drug record for colivelin (searched November 7, 2026)). Sport: Not on the 2026 List.
Country by country ↓ · Regulatory tracker
Source: this entry's approval status and the WADA Prohibited List, as in Legal Status below.
Side Effects & Contraindications
Reported Side Effects
Colivelin is a research peptide that has not been given to people as a drug, so there is no human safety profile; the points below reflect that research status.
Contraindications & Cautions
Colivelin has no approved use and no label. These points reflect its research status.
Legal Status
Colivelin is a synthetic neuroprotective peptide studied as a research compound; it is not a drug and is not approved in any country.
Frequently Asked Questions
?What is colivelin?
A synthetic 26-amino-acid peptide made by fusing activity-dependent neurotrophic factor (ADNF) to a potent derivative of Humanin. It is a 'superagonist' that protects neurons from death at femtomolar concentrations in cells.
?What does it do?
In animal models it rescues memory in Alzheimer's disease and prolongs survival in ALS mice (PMIDs 16564029, 28731445), acting through two survival pathways (ADNF→CaMKIV and Humanin→STAT3).
?How is it different from Humanin?
Colivelin is built from a Humanin derivative plus ADNF and is far more potent — neuroprotective at ~100 femtomolar versus much higher concentrations for Humanin — because it engages two pathways at once (PMID 16267233).
?Is it approved or available to buy?
No. Colivelin is not a medicine, has no FDA application or label, and is approved nowhere. Material sold online as colivelin is an unregulated research chemical. Grey Peptides lists no sellers and recommends no source; this page records the published science.
References
- [mechanism] Chiba T, et al. "Development of a femtomolar-acting humanin derivative named colivelin by attaching activity-dependent neurotrophic factor to its N terminus: characterization of colivelin-mediated neuroprotection against Alzheimer's disease-relevant insults in vitro and in vivo." J Neurosci, 2005;25(44):10252-61. PMID: 16267233.
- [animal] Chiba T, et al. "Colivelin prolongs survival of an ALS model mouse." Biochem Biophys Res Commun, 2006;343(3):793-8. PMID: 16564029.
- [review] Matsuoka M, et al. "Humanin and colivelin: neuronal-death-suppressing peptides for Alzheimer's disease and amyotrophic lateral sclerosis." CNS Drug Rev, 2006;12(2):113-22. PMID: 16958985.
- [animal] Yamada M, et al. "Nasal Colivelin treatment ameliorates memory impairment related to Alzheimer's disease." Neuropsychopharmacology, 2008;33(8):2020-32. PMID: 17928813.
- [animal] Wu MN, et al. "Colivelin ameliorates amyloid β peptide-induced impairments in spatial memory, synaptic plasticity, and calcium homeostasis in rats." Hippocampus, 2015;25(3):363-72. PMID: 25332198.
- [animal] Wu M, et al. "Colivelin Ameliorates Impairments in Cognitive Behaviors and Synaptic Plasticity in APP/PS1 Transgenic Mice." J Alzheimers Dis, 2017;59(3):1067-1078. PMID: 28731445.
- [other] Colivelin was created by Chiba, Matsuoka and colleagues (2005) as a hybrid neuroprotective peptide: activity-dependent neurotrophic factor (ADNF) fused to the N-terminus of AGA-(C8R)HNG17, a potent derivative of Humanin, to make a femtomolar-acting Humanin superagonist. It is a synthetic construct, not a natural gene product; its design and dual-pathway mechanism are described in the discovery paper and reviews carded on this page (read November 7, 2026).
- [other] US FDA, Drugs@FDA and the openFDA label endpoint, searched November 7, 2026: no application and no label record for colivelin. It is a synthetic neuroprotective peptide studied as a drug candidate for neurodegenerative disease, not a registered drug; FDA GSRS and ChEMBL hold no drug record for it.
Sources & Citations
The six studies carded above were read from their PubMed records on November 7, 2026. Colivelin's design (ADNF fused to the Humanin derivative AGA-(C8R)HNG17), its femtomolar potency, its dual CaMKIV/STAT3 mechanism, and its memory-rescuing and ALS-survival effects in animal models are from the discovery paper, reviews and animal studies carded here; the absence of US approval or a drug record from Drugs@FDA, openFDA, FDA GSRS and ChEMBL was checked the same day. Grey Peptides sells nothing and links to no vendor.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.