Clascoterone, pyrilutamide, and the other new topical antiandrogens: where do they stand, and when might they arrive?

The main driver of pattern, inherited hair loss is DHT (dihydrotestosterone), a potent male sex hormone. DHT binds the androgen receptor in the cells of the dermal papilla, a group of cells sitting at the base of the hair follicle; the androgen receptor is a protein that switches on genes once it binds the hormone. According to Rosette and colleagues' 2019 publication, DHT thereby triggers the transcription of genes that, in genetically predisposed people, contribute to hair loss.1

Finasteride breaks this chain earlier. It inhibits the 5-alpha reductase enzyme, which converts testosterone into DHT, and it does this throughout the whole body, so blood DHT levels fall too; I wrote about this and about the side effects of oral agents in a separate article. The antiandrogen works at the end of the chain: it doesn't touch DHT formation, it occupies the receptor or has it broken down, so the hormone can't switch it on. An agent that occupies the receptor is called an antagonist. The US drug label describes clascoterone as an androgen receptor inhibitor,2 according to its manufacturer pyrilutamide competes with DHT for the receptor,3 and according to its manufacturer's description GT20029 has the receptor protein itself broken down.4

The idea is that if the agent acts locally, on the scalp, the hormonal effect on the rest of the body may be smaller. The word "local" only means this if it's actually been measured. Finasteride sprayed on the scalp also lowered blood DHT levels in Piraccini and colleagues' 2022 phase III trial, though to a smaller extent than the tablet: by 34.5 percent from baseline, versus 55.6 percent in the tablet group.5 For clascoterone's hair-formulated solution, a peer-reviewed phase I trial found, according to the authors, a measurable blood level at a dose larger than the therapeutic one, and accumulation over the days;35 I didn't find the hormone- and blood-level results of the efficacy trials publicly, and for pyrilutamide I only found human blood-level data from the manufacturer, none independent.

Drug trials proceed in phases. According to a summary from the US drug authority (FDA), a phase I trial in 20 to 100 participants looks at safety and dosing, phase II in up to a few hundred patients looks at effect and side effects, and phase III in 300 to 3,000 patients looks at effect, while still monitoring side effects.6 The agent under study is compared against a vehicle: this is the same solution without the active substance, playing the role of a placebo. The main measure in hair trials is target area hair count (abbreviated TAHC): the hairs are counted in a small, marked scalp area at the start and end of the trial. A publication is peer-reviewed if a journal's independent experts reviewed it before publication; a manufacturer's press release or stock-exchange announcement doesn't go through this kind of review.

What to take from this: finasteride lets less DHT form, the antiandrogen blocks DHT's path at the follicle, and how much of a substance applied to the skin reaches the blood has to be measured separately for each agent.

Clascoterone is chemically cortexolone 17α-propionate, and the US drug label describes it as an androgen receptor inhibitor.2 One formulation is already on the market: a 1 percent cream called Winlevi, approved for acne; it's been available in the US since November 2021,7 and it received EU approval, on prescription, on 17 October 2025.8 For hair loss a different formulation is being developed, a 5 percent solution whose earlier development name was Breezula.9 Cassiopea started the development, and today's disclosures are issued by Cosmo Pharmaceuticals. In Rosette and colleagues' 2019 lab study, one of whose authors is, per the trial registry, a Cassiopea employee, the company developing the agent,10 clascoterone inhibited DHT-induced IL-6 production (IL-6 is an inflammatory signalling molecule) in dermal papilla cells derived from human scalp, and it outperformed another receptor inhibitor, enzalutamide, in this;1 this is a cell-culture study, no conclusion about a human effect can be drawn from it.

The phase II trial in men, per Cassiopea's 2018 disclosure, enrolled 404 men, aged 18 to 55, at six trial sites in Germany. Their hair loss was mild to moderate on the crown and temples (Norwood IIIv–V; the Norwood scale sorts male pattern hair loss into grades). Four dosing regimens were compared against the vehicle: a 2.5, 5, and 7.5 percent solution twice daily, and a 7.5 percent solution once daily. In a 6-month interim analysis of the 12-month trial, on data from 375 participants, all four groups were significantly better than the vehicle in hair count, meaning better by a margin not easily explained by chance; on the other primary endpoint, the participants' own photograph-based hair-growth rating, the company reported only a directional improvement, without significance. On the one-square-centimetre target area, the hair count grew on average by 13.0, 12.2, 20.8, and 11.5 strands, while the vehicle group barely changed (−0.1).9 The analysis counted only participants who followed the protocol as planned (a per-protocol analysis), and it was an interim result from a trial still running. The company planned a peer-reviewed publication in 2018, but I couldn't find one, nor could I find the final 12-month, per-dose figures in a primary source. The 5 percent solution carried into phase III didn't outperform the 2.5 percent one in this interim analysis.

The two phase III trials, SCALP 1 and SCALP 2, ran, per the ClinicalTrials.gov trial registry, on an identical design, with 703 and 762 men, 1,465 in total. Participants applied 1.5 ml of a 5 percent solution to the crown and temples twice daily, or the same amount of vehicle; randomisation split them two to one between the drug and the vehicle. The first part ran for 6 months, double-blind, meaning neither the participant nor the investigator knew who received what. The primary endpoint was the change in target area hair count at month 6, alongside the participant's own rating of how much their hair covered their scalp.10 Per Cosmo's December 2025 disclosure, the trials ran in the US and Europe, and both were statistically significantly better than the vehicle in hair count. The result was given as a relative improvement: 539 percent in one trial, 168 percent in the other, versus the vehicle. The participants' own rating reached significance in one trial, and was only directionally favourable in the other, with the two combined reaching significance. Per the disclosure, treatment-emergent adverse events were similar to the vehicle's in both trials, and mostly weren't linked to the agent.11 No actual hair counts were reported for the clascoterone or the vehicle group, nor a confidence interval, only that p<0.05, the usual significance threshold.

By the disclosure's own wording ("a 5.39-fold improvement versus vehicle"), the figure is relative to the vehicle group; how it was calculated wasn't described. If the baseline for comparison is the vehicle group's hair-count change, and that change is small, the ratio can grow large even if the difference between the two groups is only a few hairs. How much this matters is shown by the company's own phase II data: there, the vehicle group's hair count barely changed over six months, and a percentage measured against a number close to zero can come out as almost anything. The two phase III trials had an identical design, yet gave 539 and 168 percent; in my own reading, a gap this large shows that this figure is very sensitive to how much the groups actually changed. The actual size of the effect isn't known from the public data.

The 12-month data concerns a filtered group. Only those who, per their own rating, felt an improvement after the first 6 months could enter the second part of the trial, including some from the vehicle group. Per the registry, they were re-randomised, two to one to the drug or the vehicle, in a single-blind design, which is weaker control than double-blind.10 Cosmo's April 2026 disclosure compares two groups who started on the drug and felt an improvement: those who stayed on the drug for 12 months achieved a significant, 2.39-fold relative improvement in target area hair count compared with those who switched to vehicle from month 7, whose hair count declined.12 What this shows is that in this group, hair count fell back after stopping; here too the figure is relative, and it applies only to those who felt an improvement.

In women, clascoterone hasn't so far produced a clear result. Per Cassiopea's 2021 disclosure, in a phase II trial 293 women aged 18 to 55 received a 5 or 7.5 percent solution twice daily, or 2 percent minoxidil, or vehicle, for 6 months. The disclosure names a significant result in only one subgroup: women under 30, with the 5 percent solution, measured against baseline, meaning their own starting hair count (p=0.0391), and per the disclosure this subgroup wasn't sized for this. No significant difference versus vehicle was reported; per the company, a substantial placebo effect was expected, and it did appear, so the trial was expected to give a mixed result from the start.13 I didn't find a phase III trial done in women.

What to take from this: the manufacturer has disclosed a positive result from two large, placebo-controlled trials of clascoterone, in men; the size of the effect can't be judged until actual hair counts are published, and in women there's no convincing data so far.

The Cosmo press release from December 2025 says clascoterone blocks DHT at the hair follicle's receptor, without entering the body.11 One of the trial's investigators, Maria Hordinsky, told the trade outlet Healio that the adverse events were similar to the vehicle, no sexual side effects were reported, and the drug acts locally without measurable absorption.14 There is, however, a peer-reviewed measurement of blood levels for the solution developed for hair. Täubel and colleagues, in 2021, with a co-authorship from a staff member of the developer Cassiopea and funded by the company, studied the solution in its 7.5 percent form, at a dose the authors call higher than the therapeutic one, over four days in healthy volunteers. Clascoterone reached a measurable level in the blood, an average peak of 4.81 ng/ml on day 1 and 7.65 ng/ml on day 4, meaning it accumulated over the days. There was no effect on the QT interval, the ECG measure that flags arrhythmia risk, by the regulatory criterion; heart rate rose in the hours after dosing with the drug. There was no serious adverse event.35 I did not find the hormone and blood-level results of the phase III efficacy trials publicly.

The regulatory documents for the acne cream paint a more cautious picture. According to the US label, clascoterone reaches a measurable level in the blood alongside the Winlevi cream; according to the European summary of product characteristics, less than 1 percent of the total dose enters the body.28 In the body it breaks down into cortexolone: according to the European Medicines Agency's (EMA) assessment report, enzymes in the skin and blood convert it quickly, and cortexolone has only weak glucocorticoid activity, meaning a steroid effect of the same type as cortisol.15 The HPA axis (hypothalamus, pituitary gland, adrenal gland) is the hormonal regulatory loop that controls the adrenal gland's cortisol production; cortisol is one of the body's main stress hormones. According to the US label, in a pharmacokinetic study where acne patients applied the cream twice daily for two weeks, on day 14, 1 out of 20 adults and 2 out of 22 adolescents showed a below-threshold cortisol response on an adrenal stimulation lab test; it had recovered in everyone 4 weeks after treatment.2 According to the European summary, this appeared under maximum use conditions, with the cream applied to the whole face, shoulders, chest and upper back, which the summary calls a supratherapeutic dose, greater than the recommended one, and no clinical sign or symptom of adrenal suppression was observed.8 According to the EMA's summary, it is a theoretical risk that the drug entering the blood suppresses this axis, which could lead to disruption of growth and sexual maturation, and this is a key concern in adolescents; no report of such a consequence has come from trials or clinical practice.8 The lab deviation above appeared without clinical symptoms, and in adolescents, per the European summary, the cream may only be applied to the face.8

The rest of the regulatory data also concerns the acne cream. According to the US label, blood potassium rose from normal to high in 5 percent of those receiving clascoterone, versus 4 percent of those on the vehicle, and the cream absorbs more when used over a large area, for a long time, or under occlusive dressing.2 Tao and colleagues, in 2026, analysed data from the US adverse event reporting system (FAERS): among 1,085 reported adverse events for the acne cream, alongside common redness and dryness of the skin, the rarer but strongly flagged signals described were suppression of the HPA axis, skin striae, and abnormal hair growth.16 These are voluntary reports, without a denominator, so they do not prove cause and effect.

How far these acne data apply to the hair solution is not known: the concentration is different there (5 percent instead of 1), the formulation is different, the area is different, and use continues for months; the phase I trial above provides data on the hair solution's absorption, but I did not find a measurement of adrenal function or potassium. Cosmo's April 2026 press release says only that no significant systemic hormonal side effect was observed over 12 months.12 In pregnancy, per the European summary, the Winlevi cream must not be used; in women of childbearing potential, pregnancy must be excluded before treatment, and effective contraception is required during treatment and for at least 10 days after the last dose, while an interaction with hormonal contraceptives cannot be ruled out; use during breastfeeding is not recommended.8 In animal studies, clascoterone given subcutaneously increased developmental abnormalities in pregnant rats, and post-implantation fetal loss in rabbits, at 8 and 39 times the recommended maximum human dose respectively.2

Ask your doctor this, once the hair solution can be prescribed: what was measured in the trials about adrenal function and potassium, and what to watch for with long-term use. If you're a woman and could become pregnant, this question comes before you start.

Per Cosmo's July 2026 half-year report, the company plans to file the US regulatory submission in the first quarter of 2027, and the European one in the second quarter of 2027, and scientific publications are also expected from the programme, without a date.7 The title of the December 2025 disclosure still said the US and EU submissions were underway;11 the April disclosure, about the 12-month data, already put the US one at early 2027.12 This is a filing plan; the regulator's decision comes after that, and neither the company nor any other source I found has published an approval date.

Watch for this: first a peer-reviewed publication with the actual hair counts and the vehicle group's value, then the FDA and EMA decision. Until both of these are in, every efficacy figure on clascoterone for hair comes from the manufacturer.

Pyrilutamide (development code KX-826) is the agent of Kintor Pharmaceutical, listed on the Hong Kong stock exchange. The company has issued disclosures about its hair results since 2021, mostly from Chinese trials; I didn't find a peer-reviewed journal article on any of its human trials.

Kintor reported in 2021 that the Chinese male phase II trial, with 120 participants, hit its primary endpoint; it gave no figure, promised detailed data later, and carried the 0.5 percent concentration into phase III.17 In a 2022 Chinese phase II, in 160 women, per the manufacturer the 0.5 percent solution once daily produced 11.39 more hairs per square centimetre than placebo after 24 weeks (p=0.0087); of the four treated groups, a figure was reported only for this one.18 In the US phase II, 123 men took part in 2023; per the manufacturer, the 0.5 percent solution twice daily produced roughly a 10 hair/cm² increase from baseline after 24 weeks (p=0.0088), while versus placebo it only stated a directional improvement, without a figure or p-value.19

In November 2023 the Chinese phase III didn't beat placebo. Per Kintor's stock-exchange announcement, the 0.5 percent solution twice daily produced a significant increase in hair growth from baseline after 24 weeks (P<0.0001); versus placebo it was better at every visit, but the difference wasn't statistically significant, which the company called "a trend toward efficacy."20 The announcement called the change from baseline the trial's main endpoint; the primary endpoint recorded in the trial registry (NCT06126965), though, was the change versus placebo.20 The company switched from the earlier 0.5 percent tincture (a solution applied to the skin) to a 1 percent one.21 It explained the switch by saying that in animal testing this gave a seven-fold active-substance concentration in the skin, without the amount reaching the animals' bodies changing, and it expected the new trial to succeed because the confounding effects of the coronavirus pandemic were gone and clinical quality control and participant compliance had improved.22 The company's KX-826 product page cites, from the 2023 result, only the significance versus baseline, not the result versus placebo.3

The new trial succeeded in 2025 and 2026, according to the manufacturer. The phase II stage had 90 men: after 24 weeks, the 0.5 percent solution twice daily produced a 22.39, the 1 percent solution a 21.87, and the placebo an 8.73 hair/cm² increase from baseline; the difference versus placebo was 13.66 (P=0.002) and 13.14 hair/cm² (P=0.004) respectively.23 Per Kintor's March 2026 disclosure, in the phase III stage, in 666 Chinese men, after 24 weeks the 1 percent solution produced a 15.33, the 0.5 percent a 14.46, and the placebo a 4.68 hair/cm² increase from baseline; the difference versus placebo was 10.65 and 9.78 hair/cm² respectively (both P<0.0001), and no serious agent-related adverse event was observed.24 These are manufacturer, non-peer-reviewed figures; the final analysis was presented by the trial's lead investigators in May 2026 at the World Congress for Hair Research (WCHR), and was chosen as a top poster; I didn't find its text.25

Three things don't add up in these figures. The first is the dose: the 1 percent solution, which the company switched to because of the seven-fold skin concentration, barely outperformed the 0.5 percent one in phase III (10.65 versus 9.78 hairs versus placebo). The second is that the same 0.5 percent concentration, twice daily, didn't beat placebo in 2023, but did in 2026. The third is the placebo group: in two stages of the same trial, the placebo group's hair count rose by 8.73 in one and 4.68 per square centimetre in the other. This shows why a result "significant versus baseline" is misleading: the hair of those on placebo can grow too, versus baseline, so only the difference versus placebo says what the agent actually added.

In March 2026 the company wrote that it would soon initiate the marketing authorisation application for the 1 percent solution with the Chinese drug authority, and in June, that it was actively advancing the application.2425 Per the half-year report of 19 August 2026, the company plans the filing for the second half of 2026, and expects approval in 2027;25 I didn't find a disclosure of the actual filing. I haven't found news of a US or European phase III trial since the company's 2023 statement of intent.19

Safety comes from a 52-week trial without a control group, with the 0.5 percent solution twice daily: per the manufacturer, among the 95 men who completed it, the common (occurring in at least 5 percent), agent-related side effect was itching at the application site, mostly mild, and no agent-related sexual dysfunction was observed.21 Without a placebo group, no conclusion about efficacy can be drawn from this. Per the manufacturer, the agent works locally, and what enters the bloodstream breaks down quickly into inactive metabolites;3 I didn't find independent, human-measured absorption data.

What to take from this: for a pyrilutamide figure, first check whether it was measured versus placebo or versus baseline; the peer-reviewed publication of the 2026 result still doesn't exist.

Kintor announced in July 2024 that its cosmetics containing KX-826 as a main ingredient had launched worldwide, starting with a solution for androgenetic hair loss, and that the substance had also received a cosmetic ingredient name.3 The cosmetic ingredient name (INCI name) is part of a naming system, it isn't a regulatory approval and it isn't proof of efficacy. The manufacturer's cosmetics-brand online shop offered, in September 2026, a 0.5 and 0.9 percent KX-826 solution and foam, and also a combination product containing two other hair ingredients, copyrrol and copexil.26 The formulation to be filed as a drug is a 1 percent tincture;24 whether the cosmetics' composition matches the trial solutions, I don't know. The product page states that new hair growth appears within 4–6 weeks; among pyrilutamide's efficacy results reported with a figure, the earliest is 12 weeks, and even that is a baseline figure without a control group;21 none of them supports the 4–6-week promise. If the combination product has an effect, it isn't any single ingredient's alone.

It's also sold as a powder, as a "research chemical." One such online shop offered it in September 2026 labelled "for laboratory research only," and stated it sends lab test sheets only on request.27 This is the same situation as with RU58841: not a pharmaceutical-grade substance, its purity backed only by the seller's own paperwork, and I didn't find an independent purity test of it.

The EU's cosmetics regulation places steroid-structured antiandrogens among substances banned in cosmetics.28 Clascoterone has a steroid structure, so in my own reading it couldn't be marketed as a cosmetic in the EU. Pyrilutamide isn't steroid-structured, so this item doesn't apply to it; whether its effect would classify it as a drug in the EU, I haven't found a regulatory or legal opinion on that, and I can't judge it either.

What to take from this: the concentration of KX-826 sold as a cosmetic differs from the one to be filed as a drug, the quality of the "research chemical" is unverified, and there's no regulatory pregnancy data for pyrilutamide, because it isn't approved anywhere; if you're a woman who could become pregnant, discuss this with a doctor before starting.

GT20029 is Kintor's other agent, a PROTAC: a molecule that binds the target protein, here the androgen receptor, to the cell's own protein-degradation system, and thereby has it broken down. Per the manufacturer's description, it directs the receptor to an enzyme called an E3 ubiquitin ligase (this enzyme tags proteins for degradation), and has it broken down through that route.4 An antagonist occupies the receptor; this agent has it broken down.

In the US phase I, per the manufacturer, after 14 days of use the blood level stayed around the detection limit; the most common side effects were mild and occurred at the application site: dryness, itching, a burning sensation, and pain, and no serious adverse event was reported.29 This is short, manufacturer data.

Of the three main agents, GT20029 is the only one with a peer-reviewed clinical publication on a measured effect in hair loss. In Hu and colleagues' 2025 phase II trial, 180 Chinese men (Norwood IIIv–V) were sorted into six groups of 30: a 0.5 or 1 percent solution once daily or twice weekly, and, for the two dosing regimens, one placebo group each, for 12 weeks. Hair count grew from baseline in all four treated groups (p<0.001), but versus its own placebo it was significantly better in only two: the 0.5 percent once-daily group (p=0.032) and the 1 percent twice-weekly group (p=0.023). Hair thickness improved significantly versus placebo in the 1 percent twice-weekly group (p=0.011); the frequency of adverse events was similar across groups, and mostly mild.30 Per the manufacturer's disclosure, the 0.5 percent once-daily group grew 6.69, and the 1 percent twice-weekly group 7.36 more hairs/cm² than placebo.4

The trial was 12 weeks, with groups of 30, three of the manufacturer's own employees are among the authors, and I only had access to the abstract of the publication, not the full text. At the once-daily dose, the 0.5 percent solution was significantly better than placebo, the 1 percent wasn't, so the higher concentration carried no detectable extra benefit here. A short publication with methodological remarks about the trial also appeared in 2026, whose text I likewise couldn't access.31 For the Chinese phase III, the company recommended the 1 percent, twice-weekly dose;4 per the company's half-year report of 19 August 2026, it plans to start the phase IIb/III trial in China in the second half of 2026.25

What to take from this: there's peer-reviewed data on GT20029, but this is a 12-week, early trial, and a phase III result doesn't exist yet.

RU58841 is likewise a topical androgen receptor inhibitor, but there's no published human efficacy data on it, and it's sold as a research chemical; I wrote about it in detail in the article about DHT blockers.

Fluridil (also called topilutamide) is another topical antiandrogen, sold as a cosmetic by its distributor.32 I found only one placebo-controlled trial of it: Sovak and colleagues, in 2002, compared 2 percent fluridil to placebo in 43 men (Norwood II–Va), double-blind, for 3 months. Per the abstract, the proportion of hairs in the growth (anagen) phase didn't change in the placebo group; per the full text's table, it did rise there too, from 70 to 77 percent, but not significantly, which the authors partly attribute to the vasodilating effect of isopropanol, used as the placebo. In the fluridil group the proportion rose from 76 to 85 percent. After month 3, all participants received fluridil, so the 87 percent measured at month 9 is a figure without a control group. Neither fluridil nor its breakdown product could be detected in the blood.33 This is a small, 2002 trial: the hairs were counted, but no data on the change in hair count was reported, and the first author is the agent's developer; I didn't find a newer randomised trial. The efficacy claims on the distributor's site can't be derived from this trial.

Topical finasteride and dutasteride, which, unlike the antiandrogens, slow DHT formation, are covered in separate articles: on topical finasteride and on dutasteride mesotherapy.

What to take from this: fluridil is backed by a single small, placebo-controlled trial from 2002, with a three-month controlled phase and no reported data on the change in hair count; a topical agent's promise, sold as a cosmetic, is worth measuring against this.

Oral finasteride is approved for hair loss in men, backed by several large, placebo-controlled trials followed for years; I wrote about this here. Finasteride sprayed on the scalp is backed by one peer-reviewed phase III trial: Piraccini and colleagues, in 2022, randomised 458 men, and after 24 weeks the target area hair count changed by an average of 20.2 strands with the spray, versus 6.7 with placebo.5 Against this, here's where the new agents stand, as of September 2026:

• Clascoterone solution: two phase III trials, 1,465 men in total, known only from a manufacturer summary and as a relative percentage; there's no peer-reviewed publication on the phase III (peer-reviewed, there's one blood-level measurement of the hair solution and the acne cream's phase III trials),3536 not approved for hair loss, filing planned for 2027.
• Pyrilutamide: one Chinese phase III that failed versus placebo (2023) and one that succeeded (2026), both from manufacturer disclosures; I didn't find a peer-reviewed publication, the Chinese application is in preparation.
• GT20029: one peer-reviewed phase II, 12 weeks, 180 men; not approved.
• RU58841: no published human efficacy data, not approved anywhere.
• Fluridil: a single small, placebo-controlled trial from 2002, with a three-month controlled phase, no reported data on the change in hair count; sold as a cosmetic.

I didn't find a trial that compared any of these directly against finasteride, nor one that studied them together with finasteride or minoxidil, placebo-controlled; on pyrilutamide and minoxidil used together, Kintor in 2026 presented only an observational trial at a conference.25 The hair counts of the different trials can't be placed side by side either: the target area differs, the participant pool differs, and, as seen with pyrilutamide's two stages, the placebo group's gain varies strongly by trial. Cassiopea itself, in 2018, compared its own 6-month phase II result against finasteride tablet's 12-month approval data, and wrote that the 7.5 percent clascoterone reaches the tablet's efficacy within six months.9 These are two separate trials, with different durations and differently sized target areas, converted between them, so in my own reading this doesn't reveal which works better.

Ask your doctor this, if you're looking for a topical agent because of finasteride's side effects: whether the already-studied, scalp-sprayed finasteride could be an option for you, and what's worth monitoring alongside it.

If you're deciding now because of your hair loss, none of these can be prescribed by a doctor as a drug approved for hair loss. I wrote about finasteride, which is approved for hair loss, here, and about dutasteride in the same place, which in the EU is indicated for the symptomatic treatment of benign prostate enlargement, not hair loss.34 You can read about minoxidil here, and if your pattern isn't clear yet, this page can help you find your way. The decision is yours and your doctor's.

If you're watching the topical antiandrogens, three things are worth following. The first is a peer-reviewed publication with the actual hair counts and the placebo group's value. The second is the FDA, EMA, or Chinese authority's decision, which comes after the filing plan. The third is the hair trials' hormone and blood-level measurement, because a blood level was measurable both with clascoterone's acne cream and in one short phase I trial of the hair solution. For women, there's less data on every one of these agents. If you're pregnant, clascoterone's acne cream is contraindicated; if you could become pregnant, per the European label, pregnancy must be excluded before treatment, effective contraception is required during and for at least 10 days after, and an interaction with hormonal contraceptives can't be ruled out.8 For the other agents there isn't even regulatory pregnancy data.

What to take from this: until there's a peer-reviewed publication and a regulatory decision, the efficacy figures you read about clascoterone and pyrilutamide are the manufacturers' own disclosures.

Microneedling is a mechanical stimulus with no hormonal effect, so it can be added alongside drugs that act on DHT. The Dermastamp is a fixed 1 mm, at-home device: the needle stimulates the area around the follicle, and doesn't touch DHT through its mechanism. This is inferred from the mechanism, not measured. You don't skip oral finasteride or dutasteride on the day you stamp. With scalp-applied products, stamping day is a pause, and the exact timing differs by product: the timing of actives. For anyone who doesn't want to touch their hormones, this is a route that stays available, with one limitation: in the study measuring the combination, both groups also received minoxidil, and the study used a 1.5 mm clinical roller, not our fixed 1 mm device; there's less data on it used alone. What it can do, what it can't, and who it's not for: I've written it all on its page.

See the Dermastamp