Reference

Compare peptides

Two to four compounds, field by field: identity, United States regulatory status, and what kinds of documents are on file. The table records differences. It does not rank them.

Compound 1

Compound 2

Compound 3 (optional)

Compound 4 (optional)

No winner, no score, no recommendation. Counts describe how many documents of each kind Therapept has indexed — not how well a compound works, and not how much has been published overall.

Link to this comparison: /compare?peptides=ahk-cu,ghk-cu,minoxidil

Side-by-side comparison of AHK-Cu, GHK-Cu, Minoxidil
Identity
	AHK-Cu	GHK-Cu	Minoxidil
Class	Copper(II) complex of the tripeptide L-alanyl-L-histidyl-L-lysine; a structural analogue of GHK-Cu in which glycine is replaced by alanine	Copper(II) complex of the tripeptide glycyl-L-histidyl-L-lysine. Cosmetic ingredient under the INCI name Copper Tripeptide-1	Small-molecule vasodilator and ATP-sensitive potassium-channel opener, supplied as a topical solution or foam and as oral tablets
Also listed as	Copper tripeptide-3, Ala-His-Lys copper, AHK copper complex	Copper tripeptide-1, Prezatide copper, Copper peptide	Rogaine, Loniten, U-10858
Molecular formula	Not recorded	C14H23CuN6O4+ (prezatide copper, PubChem CID 71587328)	C9H15N5O
Molecular weight	Not recorded	402.92 g/mol (as prezatide copper)	209.25 g/mol
CAS	Not recorded	89030-95-5 (copper complex) · 49557-75-7 (uncomplexed GHK)	38304-91-5
PubChem CID	Not recorded	71587328	4201
Sequence length	Described structurally, not as a residue list	Described structurally, not as a residue list	Not recorded
Data caveat	AHK-Cu is not GHK-Cu. Full caveat	PubChem holds three non-equivalent records and no neutral 1:1 complex: prezatide copper (CID 71587328, cationic), copper tripeptide (CID 139035031, anionic), and bisprezatide copper (CID 9831891, a 2:1 complex). Full caveat	None recorded
United States regulatory status
Status	No FDA-approved product	No FDA-approved product	FDA-approved drug substance
FDA application	None recorded	None recorded	None recorded
Compounding	No FDA compounding entry recorded	FDA nomination withdrawn; the published entry is scoped to injectable routes.	No FDA compounding entry recorded
WADA	Not named in this record	Not named in this record	Not named in this record
Research profile
Research purpose	Copper-peptide follicle biology	Copper-peptide skin and follicle biology	Approved topical hair-regrowth treatment
Proposed mechanism	Proposed copper-dependent effects on dermal papilla cells and follicle growth. The published evidence is ex vivo human follicle culture and cell culture, not a human trial.	Proposed to deliver copper to skin cells and modulate collagen, elastin and matrix-metalloproteinase activity. Much of the mechanistic work is in vitro or in animal models.	Opens ATP-sensitive potassium channels and dilates blood vessels; it also prolongs the growth phase of the hair cycle. The precise reason it grows hair is still debated.
Human evidence	One directly relevant published study: human hair follicles ex vivo and cultured dermal papilla cells. No human clinical trial is indexed.	Topical cosmetic studies exist, but they are small and formulation-specific. Therapept indexes no approved drug product and no large clinical trial for hair growth.	Randomised trials and decades of clinical use support topical minoxidil for androgenetic alopecia in men and women. Oral low-dose use for hair loss is off-label.
Evidence tier	No human data indexed	Preclinical models; no human efficacy trial indexed	Approved drug product in the United States
Known safety concerns	No approved product and no registered human trial identified. Copper peptide cosmetics have a topical-use history; injectable use is a different and unapproved route. Human safety for hair-growth use is uncharacterised.	FDA's withdrawn compounding nomination is scoped to injectable routes and cites immunogenicity and limited human data. Topical cosmetic use has a different risk profile from injection. No approved product; the injectable route is not a lawful consumer category.	Topical products can cause scalp irritation and unwanted facial hair growth. Oral minoxidil is a vasodilator with cardiovascular effects and is not a casual supplement. The approved label lists warnings and side effects; this is not a complete safety profile.
Evidence gaps	Any human trial with hair density or shedding endpoints. Whether the ex vivo effect survives topical delivery in vivo. A verified identity standard for commercial material.	Well-powered human trials with hair-count or pigmentation endpoints. Whether topical delivery reaches the follicle at meaningful concentrations. Any evidence that graying is reversible.	Why some people respond and others do not. Long-term maintenance after stopping. Whether low-dose oral minoxidil has an acceptable long-term risk profile for cosmetic use.
Head-to-head evidence	No controlled comparison with GHK-Cu, minoxidil or any other hair treatment has been published.	No published controlled comparison of GHK-Cu against AHK-Cu, minoxidil or finasteride for hair outcomes.	Oral minoxidil 5 mg was compared with topical 5% in a 2024 randomised trial and was not superior over 24 weeks.
Named pathways	Copper transport · Dermal papilla proliferation · Apoptosis signalling	Copper transport · Collagen synthesis · Matrix metalloproteinases · Dermal papilla biology	Potassium channels · Vasodilation · Anagen prolongation
Evidence on file
Records	1Open evidence file	4Open evidence file	1Open evidence file
Human-interventional records	0	0	0
Human-observational records	0	0	0
Animal records	0	0	0
In-vitro records	1	0	0
Reviews	0	3	0
Regulatory documents	0	1	1
Earliest indexed	2007	2008	2006
Latest indexed	2007	2026	2006

Every identity and regulatory value above is taken from the compound’s record, where its sources are listed. Evidence counts are derived from the published evidence file at build time. A missing class means no document of that kind is indexed — not that none exists.

Overlapping pathways

Named in the mechanism discussion for at least two of these compounds: Copper transport.

Shared biology is not shared evidence. No claim of synergy is made here, and overlapping pathways do not mean the compounds have been studied together.