Research center

Hair loss and pigmentation research

Hair loss is not one condition, and 'hair growth' is not one outcome. This page separates the biology, the approved treatments and the experimental compounds — and shows where each claim actually stops.

The four outcomes Types of hair loss Approved treatments Alopecia areata Topical antiandrogens Emerging research Gray hair

Most hair-loss marketing works by collapsing four different outcomes into one phrase. A product that reduces shedding is presented as if it regrows hair. A laboratory study on follicle cells is presented as if it were a human trial. A cosmetic ingredient is presented as if it were a medicine.

This center keeps them separate. Every compound named here has its own record: what it is, what has been tested in humans, what remains laboratory work, and what regulator — if any — has approved it.

Four outcomes that are not interchangeable

Hair-loss outcomes, how each is measured, and the evidence each would require
Outcome	What it means	How it is measured	What would count as evidence
Regrowth	New terminal hairs emerge from follicles that had stopped producing visible hair.	Non-vellus (terminal) hair count in a defined scalp target area, usually by phototrichogram.	A randomised comparison with a vehicle or active control, counting terminal hairs — not patient satisfaction alone.
Thickening	Existing hairs become wider or longer, so the scalp looks fuller without new follicles switching on.	Hair diameter or cross-sectional area, sometimes combined with hair weight.	Calibrated measurement at the same scalp site, because diameter varies naturally across the scalp.
Reduced shedding	Fewer hairs enter or complete the shedding phase, so density is maintained rather than restored.	Hair counts on a wash test or collection over a fixed period, with a baseline and a control.	A long enough run-in to account for seasonal and cyclical shedding, and a control group.
Repigmentation	Pigment-producing cells resume melanin production in a gray or white follicle.	Objective colour measurement or blinded photographic grading of the same clipped area.	A controlled human study with blinded assessment. Therapept identified none for any peptide.

Therapept does not score products on these outcomes. The point of the table is to make a claim checkable: which outcome, measured how, in whom.

The follicle, in one screen

The cycle

Each follicle cycles through growth (anagen), regression (catagen) and rest/shedding (telogen). Most scalp hairs are in anagen at any moment; the proportion shifts with age, hormones, illness and nutrition.

Miniaturisation

In androgenetic alopecia, susceptible follicles progressively produce thinner, shorter hairs before they stop producing visible hair. The follicle is often still present — which is why slowing miniaturisation is a plausible strategy.

Stem cells and pigment

Follicle stem cells in the bulge region and melanocyte stem cells near the bulb maintain the next cycle and its colour. Experimental treatments target these populations; approved treatments act further upstream.

Why the biology matters:a treatment that slows androgen-driven miniaturisation, a treatment that wakes dormant stem cells and a cosmetic that conditions the scalp are three different propositions. Grouping them as “hair peptides” hides the only distinction that matters.

Types of hair loss, and why the evidence does not transfer

Male-pattern hair loss (androgenetic alopecia)

A patterned, progressive reduction in terminal hair density driven by follicular sensitivity to androgens, with miniaturisation of genetically susceptible follicles.

Evidence that applies: Topical minoxidil and oral finasteride 1 mg carry FDA-approved indications in men. Dutasteride is used off-label in the United States.

Important limit: Approved treatments slow or partially reverse miniaturisation. They do not restore a hairline that has already been lost, and benefit depends on continuing treatment.

Female-pattern hair loss

Diffuse thinning over the crown and part line, usually without the receding hairline seen in men.

Evidence that applies: Topical minoxidil is FDA-approved for women. Finasteride is not indicated for women. Oral dutasteride is off-label.

Important limit: The causes overlap with iron deficiency, thyroid disease and other conditions. A hair-loss diagnosis is a clinical assessment, not a supplement decision.

Diffuse shedding / telogen effluvium

A general increase in shedding, often weeks to months after a trigger such as illness, surgery, severe stress, childbirth or rapid weight loss.

Evidence that applies: The evidence base is largely clinical observation rather than randomised trials of specific compounds. Treatment is usually trigger-directed.

Important limit: Peptide 'repair' protocols are not established treatment for telogen effluvium. The relevant question is what caused the shift into shedding.

Shedding during rapid weight reduction

Increased shedding reported by some people during or after substantial weight loss, including with incretin-based treatment.

Evidence that applies: Therapept has not identified a controlled study establishing that any incretin drug directly causes hair loss. Weight loss itself, reduced intake and other factors are plausible contributors.

Important limit: A temporal association is not causation. This is an open question, and it is not a reason to start an unapproved peptide.

Alopecia areata

An autoimmune, patchy hair loss that can progress to total scalp or body hair loss.

Evidence that applies: It has its own approved and investigational treatments. It is not androgenetic alopecia and does not respond to the same logic.

Important limit: Minoxidil, finasteride and copper peptides are not interchangeable treatments for alopecia areata. Management belongs with a clinician.

Established treatments: what is actually approved

FDA-approved hair-loss treatments and their limits
Treatment	US status	Route	Supported by	Limit
Minoxidil	FDA-approved, over the counter	Topical 2% or 5%	Randomised trials and decades of clinical use in male and female androgenetic alopecia.	Not for scarring alopecia or alopecia areata by default; regrowth is variable and maintenance depends on continued use.
Finasteride	FDA-approved, prescription	Oral 1 mg	Randomised trials in men with mild-to-moderate androgenetic alopecia.	Men only. Efficacy in bitemporal recession was not established. Label warnings apply.
Dutasteride	FDA-approved for BPH, not hair loss	Oral, off-label for hair	Trials and reviews in male androgenetic alopecia; approved for AGA in Japan and South Korea.	Off-label in the United States. Longer half-life than finasteride. Not an approved hair-loss product here.

Approved status applies to a specific product, route and indication. It is not a general endorsement of the molecule for every hair-loss pattern.

Alopecia areata: a different disease with different drugs

Alopecia areata is an autoimmune, non-scarring hair loss. It can present as coin-sized patches, as total scalp loss (alopecia totalis) or as loss of all body hair (alopecia universalis). It is not androgenetic alopecia, and the drugs that work for pattern loss are not its established treatment.

Severity is usually measured with the Severity of Alopecia Tool (SALT). In the trials supporting approval, “severe” meant at least 50% scalp hair loss. That threshold matters: the approved JAK inhibitors were studied in extensive disease, not in a few small patches.

The three approved medicines are oral JAK inhibitors. They carry serious class warnings, require monitoring, and are not a cure: benefit generally depends on continuing treatment. Limited patches may instead be managed with topical or intralesional corticosteroids. Which option fits is a specialist clinical decision, not a supplement choice.

Alopecia areata treatments, their regulatory status and the limits of their evidence
Treatment	US status	Route	What the evidence shows	Main limit
Baricitinib (Olumiant)Oral JAK1/JAK2 inhibitor	FDA-approved for severe alopecia areata in adults (June 2022); indication extended to ages 12 and older (September 2026)	Oral tablet	Two randomised, placebo-controlled Phase 3 trials in adults with at least 50% scalp hair loss. A clinically meaningful minority achieved major regrowth compared with placebo; the 2026 supplement extended the approved population to adolescents 12 and older.	The label carries serious warnings, including serious infections, mortality, malignancy, major cardiovascular events and thrombosis. It is not a cure, and benefit often depends on continuing treatment.FDA — OLUMIANT prescribing information (2026) ↗
Ritlecitinib (Litfulo)Oral JAK3/TEC kinase inhibitor	FDA-approved for severe alopecia areata in adults and adolescents 12 years and older (June 2023)	Oral capsule	A randomised Phase 2b/3 programme in adolescents and adults with at least 50% scalp hair loss reported significant improvement versus placebo at the primary 24-week endpoint.	Restricted to ages 12 and older. Class warnings apply, and long-term safety is still being characterised. Response is not universal.FDA — LITFULO approval package (2023) ↗
Deuruxolitinib (Leqselvi)Oral JAK1/JAK2 inhibitor	FDA-approved for severe alopecia areata in adults (July 2024)	Oral tablet	Two randomised, placebo-controlled Phase 3 trials enrolled 1,209 adults with at least 50% scalp hair loss. The approved strength is 8 mg twice daily; a 12 mg twice-daily regimen was studied but is not approved.	Adults only. Class warnings apply. There is no published head-to-head trial establishing superiority over the other approved JAK inhibitors.FDA — LEQSELVI prescribing information (2026) ↗
Topical corticosteroidsAnti-inflammatory steroid, prescribed off-label for alopecia areata	Not FDA-approved for alopecia areata	Topical cream, lotion or foam	The 2026 German S3 guideline gives corticosteroids the only high-level recommendation among topical alopecia areata treatments. Potency, formulation and the size of the treated area vary widely across studies.	Most useful for limited patches. Prolonged use can thin the skin, and the evidence base is heterogeneous rather than a single pivotal programme.S3 guideline for alopecia areata, part 2 — PubMed 42076948 (2026) ↗
Intralesional corticosteroidsSteroid injected into affected scalp, prescribed off-label	Not FDA-approved for alopecia areata	Injection into affected areas	FDA's review of the deuruxolitinib application describes intralesional corticosteroids as a first-line option for patchy alopecia areata, with repeated injections often needed.	Painful and impractical for extensive hair loss. Requires a clinician and carries the local risks of repeated steroid injection.FDA — NDA 217900 multidisciplinary review (2024) ↗
Contact immunotherapy (DPCP, SADBE)Topical sensitizer used in specialist clinics, off-label	Not FDA-approved for alopecia areata	Topical application under clinical supervision	Used for extensive alopecia areata, but a 2023 Cochrane network meta-analysis found confidence in the evidence for comparisons other than baricitinib to be low or very low.	Requires a trained clinician and follow-up. Contact dermatitis is an expected part of the treatment, not an adverse event that can be avoided. Not a home protocol.Cochrane — treatments for alopecia areata, network meta-analysis (2023) ↗
Oral corticosteroidsSystemic steroid, prescribed off-label for alopecia areata	Not FDA-approved for alopecia areata	Oral tablet	The 2026 S3 guideline gives systemic corticosteroids a high recommendation for selected adults, generally for short-term use rather than maintenance.	Relapse is common after stopping, and systemic steroid adverse effects are well established. This is a clinician-directed decision, not a consumer protocol.S3 guideline for alopecia areata, part 2 — PubMed 42076948 (2026) ↗

Do not merge the categories: minoxidil is sometimes used as an adjunct in alopecia areata, but it is not approved for it; finasteride and dutasteride target androgen signalling and are not alopecia areata treatments. The JAK inhibitors are systemic medicines with labelled serious risks, not “hair peptides”.

Topical antiandrogens: what is verified, and what is not

The appeal of a topical antiandrogen is straightforward: block androgen signalling in the scalp while avoiding the systemic effects of an oral drug. The appeal is not the same as a result. Four compounds have enough human research to separate — and only one of them is approved, for acne rather than hair loss.

“Topical” does not guarantee “local only”. Human pharmacokinetic data, not the route of application, decide whether a compound reaches the rest of the body. The 2026 RU58841 study is included here precisely because it measured that question.

Topical antiandrogens studied for hair loss, with verified identity and human evidence
Compound	Verified identity	Status	Human evidence	What is missing
Clascoterone (Winlevi, CB-03-01)Topical androgen-receptor inhibitor	C24H34O5 · 402.5 g/mol (FDA label)	FDA-approved as a 1% cream for acne vulgaris in patients 12 and older (2020); not approved for androgenetic alopeciaTopical cream	A Phase 3, vehicle-controlled trial in men with androgenetic alopecia (NCT05910450) completed in January 2026 after a six-month blinded phase and a six-month single-blind extension. No peer-reviewed results were indexed at this review.FDA — WINLEVI prescribing information (2022) ↗	Approval for acne does not establish a hair-loss indication. The AGA efficacy and safety results remain unpublished.
GT20029Topical androgen-receptor degrader (investigational)	No public CAS number or structure standard identified	Investigational; no approved productTopical solution	A randomised, placebo-controlled Phase 2 trial in 180 Chinese men with androgenetic alopecia reported significant improvements in target-area hair count in some dose groups versus placebo over 12 weeks. Adverse-event incidence was similar across groups and mostly mild.Hu et al., J Dermatolog Treat (2025) — GT20029 Phase 2. PubMed 41328006 ↗	One Phase 2 trial. There is no Phase 3 report, no long-term safety data and no publicly assigned chemical identity standard for the drug substance.
Pyrilutamide (KX-826)Topical nonsteroidal androgen-receptor antagonist	KX-826; no public identity standard recorded in this library	Investigational; no approved productTopical solution	Phase 2 trials in men and women and a 740-participant Phase 3 trial in Chinese men are registered. The Phase 2 studies are listed as completed; no peer-reviewed Phase 3 report was indexed at this review.ClinicalTrials.gov — NCT06126965 (Phase 3) ↗	Registry completion is not a published result. The clinical advantage over existing treatments is not established.
RU58841 (PSK-3841)Topical nonsteroidal androgen-receptor antagonist	C17H18F3N3O3 · 369.34 g/mol · CAS 154992-24-2 · PubChem CID 132981	No approved product anywhere; supplied as a research chemical, not a medicineTopical solution (investigational)	Two completed human trials were registered under the code PSK-3841: a four-week safety and tolerability study and a six-month hair-regrowth study. Neither has posted published results. A 2026 human study in six men detected five urinary metabolites and measurable parent drug in dried blood after a single 30 mg topical dose, demonstrating systemic exposure.ISRCTN — PSK-3841 hair-regrowth trial (ISRCTN71083772) ↗	No published efficacy or safety result exists, and the human study measures metabolism, not hair growth. A verified structure does not make a research chemical safe, effective or pharmaceutical-grade.

Why RU58841 is included — and what it is not

RU58841 passes two independent checks that most research chemicals fail: a primary human record exists, and its chemical identity is documented rather than inferred from a vendor label. Neither check is evidence that it works. Two human trials were completed in the early 2000s under the code PSK-3841; neither published results. The 2026 human study characterises metabolism and systemic exposure in six men, not hair growth.

Formula: C17H18F3N3O3
Molecular weight: 369.34 g/mol
CAS number: 154992-24-2
PubChem CID: 132981

4-[3-(4-hydroxybutyl)-4,4-dimethyl-2,5-dioxoimidazolidin-1-yl]-2-(trifluoromethyl)benzonitrile. Identity source: PubChem CID 132981 — RU 58841.

What follows: RU58841 has no approved product, no published efficacy result and no pharmaceutical-grade supply chain. It is supplied as a research chemical. A verified structure makes the molecule identifiable; it does not make it safe, effective or suitable for human use.

Emerging research: five compounds people ask about

“Emerging” is not a stage of approval. It means there is a registered trial, a laboratory signal, or both — and that the compound has no approved hair-loss product. The stage column is the highest tier of human evidence Therapept has indexed, not a prediction.

Investigational and cosmetic compounds studied for hair outcomes
Compound	Evidence tier	Research purpose	Principal evidence gap
PP405Small molecule	Phase 2	Follicle stem-cell reactivation	Peer-reviewed Phase 2a efficacy and safety results.
PyrilutamideSmall molecule	Phase 3	Topical androgen-receptor blockade	Peer-reviewed Phase 3 efficacy and safety results.
SM04554Small molecule	Phase 2	Wnt-pathway modulation	Peer-reviewed efficacy results from the Phase 2 programme.
GHK-CuPeptide	Preclinical	Copper-peptide skin and follicle biology	Well-powered human trials with hair-count or pigmentation endpoints.
AHK-CuPeptide	Lab only	Copper-peptide follicle biology	Any human trial with hair density or shedding endpoints.

GHK-Cu vs AHK-Cu: one letter of difference, two different files

Both are copper tripeptides. GHK-Cu is glycyl-L-histidyl-L-lysine complexed with copper; AHK-Cu replaces glycine with alanine. They are not the same molecule, and studies of one are not studies of the other.

GHK-Cu

A cosmetic ingredient with a long formulation history and laboratory evidence on collagen and extracellular-matrix markers. Therapept indexes no approved drug product and no large human hair-growth trial. The injectable route is the subject of a withdrawn FDA compounding nomination.

Open the GHK-Cu file →

AHK-Cu

A structural analogue with a much smaller literature: one published ex vivo human follicle and dermal-papilla cell study. That is a laboratory signal, not a clinical result, and Therapept identified no human trial. There is no controlled comparison between the two copper peptides.

Open the AHK-Cu file →

Compare GHK-Cu and AHK-Cu side by side →Compare the approved treatments →Compare the investigational approaches →

Gray hair: what would count as evidence

Hair colour depends on pigment-producing melanocytes associated with the follicle. Graying is not the same process as miniaturisation, and a treatment that changes hair density would not automatically change hair colour.

Therapept searched for controlled human studies reporting repigmentation after any peptide, copper peptide or over-the-counter “gray reversal” product. We identified none that met the standard used elsewhere on this site: a defined population, a control group, blinded assessment and a measured colour endpoint.

The honest position: reports of darkened or repigmented hair after a product are anecdotes. They are not nothing — they are a reason to look for a trial — but they cannot distinguish a real effect from photograph lighting, shedding of pigmented hairs, dye, or selective attention. Therapept does not present them as evidence, and does not sell a protocol.

Rapid weight loss and shedding: an open question

People report increased hair shedding during and after substantial weight loss, including while taking incretin-based medicines. It is a reasonable question and a poorly answered one.

Therapept has not identified a controlled study that establishes a direct causal link between any GLP-1 or dual agonist and hair loss. Rapid weight loss, reduced protein or micronutrient intake, illness and other stressors can all shift follicles into shedding. A temporal association is not causation, and the existence of a report is not a mechanism.

What follows from that: an unapproved peptide is not a rational response to a question that has not been characterised. The clinically useful steps are to review the weight-loss trajectory, nutrition and micronutrient status, and any other trigger with a clinician.

Semaglutide record Tirzepatide record Retatrutide record

How to read a hair-loss claim

1Does the claim name the outcome — regrowth, thickening, reduced shedding or repigmentation — or does it blur them into 'hair health'?
2Is the evidence a human study with a control group, or a cell culture, an animal model, or a before-and-after photograph?
3How many people, for how long, and in which type of hair loss? Results in one population do not transfer automatically.
4Was hair counted by a blinded assessor, or self-reported by the person paying for the product?
5Does the page distinguish an approved drug, an investigational drug, a cosmetic ingredient and a research chemical?
6Is there a primary citation that can be opened, or only a summary of a summary?

Therapept does not sell peptides, does not publish protocols and does not provide personal medical advice. If you are losing hair, the useful next step is a clinical assessment of the cause — not a research chemical.

Sources

Explore the compound files

Last reviewed 13 November 2026 · Compiled by Therapept Editorial · How these records are built