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What is known, and what isn't.
A plain account of how clascoterone works, what has actually been studied, and where the published evidence runs out.
A receptor blocker that works where you put it.
Androgens such as dihydrotestosterone act by binding the androgen receptor inside cells. In skin, those receptors sit in sebaceous glands and in the dermal papilla cells at the base of the hair follicle.
Clascoterone is an androgen receptor inhibitor. Applied topically, it competes with dihydrotestosterone for those receptors in the tissue it is applied to. It is designed to be metabolised quickly once it reaches the circulation.
That is the pharmacological rationale. A rationale is not an outcome, and the rest of this page is about the difference.
In one paragraph
Clascoterone blocks the androgen receptor locally and is broken down systemically. It is authorised in some markets as a 1% cream for acne. Higher concentrations have been studied on the scalp, and that work has not produced an authorised product for hair loss anywhere.
Where our formulations sit
Our 5% and 7.5% creams are unauthorised preparations supplied with batch analysis. They are not approved medicines and are not a substitute for clinical care.
The published record, summarised without spin.
Follow the links and read the primary sources. We link to searches rather than single papers so you can see the whole field, including results that do not suit us.
| Area | What was studied | Stage | Regulatory status |
|---|---|---|---|
| Acne vulgaris | Clascoterone cream 1%, randomised vehicle-controlled trials | Phase 3, published | Authorised in some markets at 1% |
| Androgenetic alopecia | Topical clascoterone at higher concentrations, including 5% and 7.5% | Phase 2, dose-ranging | Not authorised anywhere |
| Pharmacology | Androgen receptor binding in sebocytes and dermal papilla cells | Preclinical / in vitro | Not applicable |
| Systemic exposure | Absorption and metabolism following topical application | Clinical pharmacology | Studied at authorised strength |
Where the evidence stops.
Four limits worth holding on to, none of which are resolved by anything on this site.
No authorised hair-loss product exists
Higher-concentration topical clascoterone has been investigated for scalp use. No regulator anywhere has authorised it for that purpose.
Cream is not the studied vehicle
Scalp research has used solution formulations. A cream base is a different vehicle, and vehicle affects how much active reaches the target.
Long-term data is thin
Published follow-up at higher concentrations is short. Nobody can currently tell you what years of use looks like.
Higher is not automatically better
Concentration and effect are not the same axis. A dose-ranging study exists precisely because the relationship is not assumed.
This page is not medical advice
Nothing here is a recommendation to use these formulations, and nothing here is personalised to you. If you are considering a topical containing an active pharmaceutical ingredient, that is a conversation to have with a qualified clinician who can see your history.
Terms used on this page.
A protein inside cells that binds androgens such as testosterone and dihydrotestosterone. Binding switches on the cell’s response to those hormones.
A potent androgen derived from testosterone. It binds the androgen receptor strongly and is the androgen most often discussed in relation to scalp hair.
The clinical name for patterned hair loss associated with androgen sensitivity in genetically predisposed follicles.
A trial in which the comparison group receives the formulation base without the active ingredient, so the effect of the active can be separated from the effect of the cream itself.
Phase 2 studies explore dose and early effect in a modest number of participants. Phase 3 studies test the chosen dose in far larger groups.
A topical is applied to the surface and intended to act locally. Systemic means acting through the bloodstream on the whole body.
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