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A Review of Pharmaceutical Interventions for Scalp Hair Loss and Implications for Transfeminine People

By Sam | First published September 8, 2025 | Last modified September 9, 2025

Abstract / TL;DR

Androgenetic alopecia is a common condition affecting a significant proportion of transfeminine people at onset of hormonal transition. Although several studies have assessed the influence of gender-affirming hormone therapy on scalp hair, there are no robust data to guide optimal dosing regimens. In the wider population, 5α-reductase inhibitors and other treatments, such as minoxidil, have been found to act dose-dependently and additively or synergistically with each other to halt and partially reverse hair loss caused by androgens. Some transfeminine people prefer to add these treatments to their regimens to try to regrow more hair or as prophylaxis against further hair loss. Dutasteride is a superior 5α-reductase inhibitor to finasteride in terms of efficacy and has similar adverse effects. For transfeminine people who wish to use minoxidil, the route of administration should be considered and determined on an individual basis. Other agents, such as spironolactone, may also provide benefit. Research into new therapies which could one day result in new pharmaceutical options for transfeminine people is currently ongoing in the general population.

Introduction

Scalp hair loss, particularly androgenetic alopecia (AGA), is a condition that affects millions of people worldwide and that carries significant psychosocial implications. Hair is a major component of human identity and is often integral to gender expression. As such, hair loss can be particularly distressing for transfeminine people (Marks & Senna, 2020; Gao et al., 2023a; Tang et al., 2023). Over the last decade, there has been a surge in interest in pharmaceutical treatments for treating AGA among both the scientific community and the general population. However, considerably less attention has been devoted to treating AGA in transfeminine people, specifically.

A few studies have evaluated the effects of feminising hormone therapy on scalp hair. A multicentre prospective study found a slight but statistically significant reduction in average Norwood–Hamilton score after 12 months in transfeminine people treated with estradiol and cyproterone acetate (Cocchetti et al., 2023). In another study, duration of estradiol use with or without spironolactone was associated with a −0.07 cm (95% CI: [−0.10, −0.04]) reduction in lateral forehead length per year in the first few years of treatment (Nguyen et al., 2025). Finally, a prospective study demonstrated statistically significant increases in follicular density and total hair count at both the midfrontal and vertex (crown) scalp after 24 weeks in transfeminine people on an unspecified regimen (Tang et al., 2025a). This was accompanied by a reduction in average hair shaft diameter, driven by increases in intermediate and vellus hair density, but with no significant change in terminal hair density. Individual case studies and series showing improvement have also been reported in the literature (Dewhurst & Underhill, 1979; Adenuga, Summers, & Bergfel, 2012; Stevenson, Wixon, & Safer, 2016). Overall, it appears that AGA progression is usually halted and partially reversed due to reduced or suppressed testosterone levels. However, there is a lack of data to inform long-term outcomes. Reversal of AGA may be incomplete in many transfeminine people, particularly in advanced stages, due to irreversible follicular miniaturisation.

The most common therapies for AGA in cisgender people include 5α-reductase inhibitors (5-ARIs) and minoxidil (Gao et al., 2023b; Devjani et al., 2023). Minoxidil use in transfeminine people has been examined by a small study (Zaminski et al., 2025). A study also found that concomitant use of finasteride, dutasteride, and/or minoxidil was associated with a lower hairline compared to treatment with estradiol alone or estradiol and spironolactone alone (Nguyen et al., 2025). However, limitations of these studies include risk of bias due to study design, possible confounding due to secondary factors, and in the case of the former study, lack of a control group. As such, there is a paucity of reliable data to show if these treatments, especially 5-ARIs, provide additional benefit over gender-affirming hormone therapy alone (T’Sjoen et al., 2019; Prince & Safer, 2020; Irwig, 2021; Coleman et al., 2022; Gao et al., 2023b). Despite this, a considerable subset of transfeminine people opt to use 5α-reductase inhibitors and minoxidil (Leinung, Feustel, & Joseph, 2018; Nguyen et al., 2025).

The purpose of this literature review is to critically summarise various pharmaceutical interventions that have been shown to have an acceptable safety profile in the general population and that may therefore be used as adjunct therapy to treat and as prophylaxis against hair loss in transfeminine people if desired. Non-pharmaceutical interventions, such as microneedling and hair transplantation, are outside the scope of this article. Specifically, this review focuses predominantly on 5-ARIs and minoxidil but also discusses androgen receptor antagonists, in addition to some further therapies that may be available in the future.

Etiology of Androgenetic Scalp Hair Loss

Androgenetic alopecia, commonly referred to as male-pattern or female-pattern hair loss, is a polygenic condition characterised by progressive miniaturisation of scalp hair follicles in a pattern-specific distribution (Anastassakis, 2022; Ovcharenko, Khobzei, & Lortkipanidze, 2025). The pathophysiology of male-pattern hair loss is fundamentally androgen-dependent. Specifically, dihydrotestosterone (DHT) binds to the androgen receptors in susceptible hair follicles, in turn initiating a cascade of transcriptional changes that alter the follicular growth cycle. This includes shortening of the anagen (growth) phase, prolongation of the telogen (resting) phase, and eventually, follicular miniaturisation (Dhurat & Daruwalla, 2021). Notably, while androgens are necessary for the development of AGA, they are not sufficient on their own; individuals with high circulating androgens may not develop AGA if their follicles lack the required sensitivity level (Khaled et al. 2020).

The genetic architecture of AGA is complex and involves multiple loci, although the AR gene on the X chromosome is generally thought to be a significant contributor (Sadasivam et al., 2024). Polymorphisms in the AR gene, particularly those affecting receptor sensitivity, have been associated with increased risk of AGA. Additionally, epigenetic factors, including methylation patterns and histone modifications, may also play a role in regulating gene expression relevant to hair follicle cycling. Large genome-wide association studies (GWAS) have identified other loci which modulate follicular response to androgens in the scalp (Pirastu et al., 2017; Chen et al., 2022; Janivara et al., 2025).

Not all scalp follicles are equally sensitive to androgens. Susceptibility is region-specific and genetically determined, with the vertex and frontal scalp being most affected (Severi et al., 2003; Fujimaki et al., 2024). The expression of 5α-reductase, the enzyme responsible for converting testosterone to DHT, is elevated in these regions, which serves to further amplify local androgenic signalling (Dhurat & Daruwalla, 2021). While androgens promote hair growth in areas such as the beard and chest, they paradoxically cause scalp hair loss in genetically predisposed individuals (Anastassakis, 2022; Ovcharenko, Khobzei, & Lortkipanidze, 2025). Miniaturised scalp hair follicles in AGA undergo a progressive transformation. There may be a critical window for intervention in which current therapeutic strategies may reverse or significantly slow progression. Ultimately, the follicles eventually enter a state of dormancy or senescence, rendering them unable to produce cosmetically significant hair. However, the follicles themselves do appear to remain in situ.

Although pattern hair loss is often divided into “male-“ or “female-“ pattern hair loss in the literature, the presentation is often similar. Studies of men with pattern hair loss have consistently shown the role of DHT (Vierhapper et al., 2001; Ryu et al., 2006; Olsen et al., 2006). There are three isoforms of 5α-reductase: type I, II, and III, all of which are thought to contribute to AGA. However, the mechanism of type III 5α-reductase is less well understood. It is notable that men with 5α-reductase type II deficiency do not experience AGA (Imperato-McGinley & Zhu, 2002). Consequently, reducing intracellular DHT concentrations can prevent AGA. However, the involvement of DHT in female AGA is less clear. A study of women with pattern hair loss found that mean average concentrations of testosterone and DHT were higher than in controls without AGA, but still within the female range (Vierhapper et al., 2003). Hence, female concentrations of testosterone and DHT appear to be associated with pattern hair loss in a certain subset of women. A case of a woman with complete androgen insensitivity syndrome (CAIS) with female pattern hair loss has been reported in the literature (Cousen & Messenger, 2010).

5α-Reductase Inhibitors

5α-Reductase inhibitors are a class of medications developed to treat conditions caused by the effects of DHT, such as benign prostatic hyperplasia and androgenetic alopecia. As implied by their name, these medications function by inhibiting 5α-reductase enzyme activity. Whilst not curative, 5-ARIs appear to halt or substantially slow hair loss in cisgender men. Globally, the two most widely used 5-ARIs include finasteride and dutasteride.

Efficacy of Finasteride Compared to Dutasteride in AGA

In the United States, finasteride prescriptions have increased exponentially in recent years, largely driven by its use in the treatment of hair loss (AHLA, 2024). Dutasteride prescriptions are far fewer, estimated in the hundreds of thousands, but also growing due to increased use for AGA. This difference is largely due to finasteride being widely licensed for this indication throughout the world, whilst dutasteride remains off-label in most countries (Altendorf et al., 2025). However, dutasteride is licensed for use in the treatment of AGA in South Korea, Japan and Mexico. Increasing interest is driving further adoption and research into its use.

Despite its use for AGA being mostly off-label, dutasteride is now widely regarded as a more efficacious and hence superior 5-ARI than finasteride. Numerous studies have established that dutasteride results in greater suppression of serum DHT concentrations (i.e., about 70% with finasteride vs 90–95% with dutasteride) (Clark et al., 2004; Olsen et al., 2006; Amory et al., 2007; Upreti et al., 2015). Another study directly comparing scalp tissue concentrations found that dutasteride reduced DHT substantially more than finasteride (mean reduction of about 65% with finasteride versus 90% with dutasteride, though with wide interindividual variation). (Hobo et al., 2023). These differences have been primarily attributed to its broader inhibition of the 5α-reductase enzyme. More specifically, finasteride is a selective inhibitor of type II and III 5α-reductase, whereas dutasteride indiscriminately acts on all three isoforms (Gisleskog et al., 1998; Keam & Scott, 2008; Yamana, Labrie, & Luu-The, 2010). Dutasteride has also been theorised to accumulate inside certain tissues, further enhancing its therapeutic effect.

In accordance with the above, two large network meta-analysis studies found that oral dutasteride is superior to oral and topical finasteride in the treatment of male AGA in terms of both total hair density and terminal hair density (Gupta et al., 2024a; Gupta et al., 2025a). These studies also found the effects of finasteride and dutasteride to be dose-dependent. On average, there was no difference between treatment groups using oral and topical finasteride. A systematic review found that dutasteride was superior to finasteride in some studies in terms of hair thickness (Almudimeegh et al., 2024). However, in contrast to the above findings in the case of male AGA, a network meta-analysis of studies investigating different interventions for female AGA found that clinical trials assessing the effectiveness of dutasteride do not yet exist (Gupta et al., 2024b). Notably, oral finasteride given at a dose of 1 mg/day was not found to be effective in treating female AGA, yet oral finasteride used at a dose of 5 mg/day outperformed all other single-agent interventions. Because of the dose-dependent effects of 5-ARIs, it could well be that dutasteride might be more efficacious than finasteride in the treatment of female AGA, as in male AGA. Hopefully, future clinical trials will shed light on this.

Adverse Effects of 5α-Reductase Inhibitors

5-ARIs are associated with certain adverse effects in a subset of individuals. These include, but are not limited to decreased libido, erectile dysfunction, reduced ejaculate volume and, possibly, fatigue and depression (Gupta, Vujcic, & Gupta, 2020; Choi et al., 2022; Zhong et al., 2025; Cilio et al., 2025). In the case of transfeminine hormone therapy, some of these effects may actually be desirable.

Currently, there are no large cohort studies or randomised controlled trials that have investigated the incidence of certain adverse effects of hormone therapy with 5-ARIs in transfeminine people. Studies of the general cisgender population may provide some limited insight. A meta-analysis of clinical trials found that the odds of hypoactive sexual desire and erectile dysfunction were each approximately 1.5-fold greater, in male users of 5-ARIs versus placebo (Corona et al., 2017). No difference was found between finasteride and dutasteride in their effects on sexual desire. This is in accordance with findings from more recent publications (Zhou et al., 2019; Zahkem et al., 2019; Estill et al., 2023; Neubauer, Ong, & Lipner, 2025). It is possible that 5-ARIs could produce further reduction in sexual function combined with other hormone therapy medications in transfeminine people, but there are no data to confirm or refute this.

Some studies have found that 5-ARIs are associated with slightly increased circulating testosterone levels (Amory et al., 2007; Stanczyk, Azen, & Pike, 2013; Maeda et al., 2018). However, a 2019 meta-analysis of studies of cisgender men concluded that finasteride and dutasteride use did not unequivocally result in statistically significant increases in serum testosterone levels (Traish et al., 2019). The relevance of marginally raised testosterone in individuals receiving gender-affirming hormone therapy is unclear because exogenous estrogen and antiandrogen therapy typically suppresses endogenous testosterone production to concentrations far below the male range. Nevertheless, a retrospective analysis of transfeminine people using oral estradiol and spironolactone did find that finasteride use appeared to have a moderately deleterious effect on testosterone suppression (Leinung, Feustel, & Joseph, 2018). Studies have generally found that spironolactone does not, by itself, actually lower testosterone concentrations in transfeminine people (Angus et al., 2021). As such, these findings might not be applicable to other antigonadotrophic antiandrogens such as GnRH agonists and progestogens including cyproterone acetate. The influence of 5-ARIs on testosterone concentrations in transfeminine people would be an interesting point for more studies to explore in the future.

The possible effect of 5-ARIs on cognitive function, mood, depression, and suicide risk is controversial. Androgen deprivation therapy, in general, results in an increased risk of psychiatric complications (Izard & Siemens, 2020; Siebert, Lapping-Carr, & Morgans, 2020). These effects have been attributed to the depletion of circulating testosterone available for conversion into estrogens and hence can be mitigated with the use of concomitant estradiol administration (Coelingh Bennink et al., 2024). However, in some studies, 5-ARIs have been associated with increased rates of depression despite testosterone levels remaining well within the male range. Several large pharmacovigilance studies have found signals for reduced cognitive function, depression, and suicidality in users of finasteride and dutasteride (Nguyen et al., 2021; Cho et al., 2024; Zhong et al., 2025; Gupta et al., 2025b; Lee at al., 2025). In some of these studies, the signals have been quite strong. These data have prompted some countries to mandate warnings about possible long-term side effects on product labels. The psychiatric effects of 5-ARIs have been hypothesised to be a consequence of this class of drugs also inhibiting the synthesis of neuroactive steroids such as allopregnanolone. These neurosteroids may have antidepressant and anxiolytic effects. In contrast to the findings of pharmacovigilance studies, a 2024 meta-analysis incorporating prospective study data from around 2 million users of 5-ARIs did not find associations for depression (aHR: 1.30, 95% CI: 0.85–2.00) or suicide (aHR 1.30, 95% CI: 0.65–2.61) (Uleri et al., 2024). Subgroup analyses for finasteride and dutasteride yielded similar findings. It should be noted that despite the extremely large sample size, the confidence intervals in the pooled risk estimates were still wide and hence could not rule out marginal risk increases. Overall, these findings may be both concerning and reassuring at the same time. Whilst the involvement of 5-ARIs in mood and depression still remains unclear, the preponderance of evidence strongly suggests that any excess risk is likely to be small.

Post-Finasteride Syndrome

“Post-finasteride syndrome” (PFS) is an even more controversial and poorly understood condition characterised by persistent sexual, neurological, and psychological symptoms that arise during or after the use of finasteride or dutasteride (Cilio et al., 2025; Leliefeld, Debruyne, & Reisman, 2025). PFS has gained increasing attention since it was popularised in the literature in 2012 following a subset of 5-ARI users reporting enduring adverse effects after discontinuation (Irwig, 2012).

Various case reports and studies have been published reporting associations between 5-ARIs and PFS symptoms (Traish et al., 2011; Irwig & Kolukula, 2011; Irwig, 2012; Irwig, 2014; Caruso et al, 2015; Ali, Heran, & Etminan, 2015; Guo et al., 2016; Kiguradze et al., 2017; Pereira & Coelho, 2020). Notably, one apparently well-designed study reported altered levels of neuroactive steroids in cerebrospinal fluid and plasma after discontinuation of finasteride in men who reported suffering from PFS symptoms (Caruso et al, 2015). A retrospective analysis also found that rates of erectile dysfunction were higher in men with cumulatively greater exposure to finasteride and dutasteride (Kiguradze et al., 2017). However, overall these data have been of low-quality, at high risk of bias, may have been confounded by secondary variables, and universally suffer from the lack of a placebo control group to establish causation (Hirshburg et al., 2016; Trüeb et al., 2019; Trüeb et al., 2024). As such, by themselves they are of limited usefulness. More recently, a pharmacovigilance study identified the existence of a signal for “post-finasteride syndrome” with finasteride in the FAERS database (Zhong et al., 2025).

A substantial nocebo effect appears to exist in users of 5-ARIs pertaining to PFS-like symptoms (Maksym, Kajdy, & Rabijewski, 2019). A study found that men who were made aware of sexual adverse effects before being treated were much more likely to report them during follow-up (43.6%), compared to men who were not (14.3%) (Mondaini et al., 2007). These data show that the power of suggestion is likely to influence the experience of many individuals using 5-ARIs. A more comprehensive pharmacovigilance study of the FAERS database performed analyses stratified by time period and 5-ARI medication (Gupta et al., 2025b). The study conducted disproportionality analyses for five adverse events related to suicide between 2006 and 2011, 2013 and 2018, and 2019 and 2023. No signals were detected for oral finasteride between 2006 and 2011, but signals emerged in later periods, with increased reporting odds for suicidal ideation between 2013 and 2018 and between 2019 and 2023. Despite oral dutasteride being more efficacious in its action as a 5-ARI, dutasteride showed no significant signals across any time period. The authors concluded that these findings were suggestive of increased awareness of PFS being the cause of heightened reporting of psychiatric adverse events to FAERS, rather than reflecting a true pharmacological effect (Gupta et al., 2025b).

Taken together, all these findings provide limited evidence for the existence of PFS in a small subset of individuals. However, the evidence for persistent long-term adverse effects stemming from finasteride and dutasteride use is tenuous at best.

Minoxidil

Minoxidil is a medication with antihypertensive and vasodilator effects which was originally developed as an oral formulation for high blood pressure. However, it was found to have the unexpected side effect of promoting hair growth, which led to its reformulation as a topical solution and adoption for AGA. Oral minoxidil is also now increasingly being used at lower doses to treat hair loss.

Mechanism of Action of Minoxidil in Hair Loss

The exact means by which minoxidil is involved in promoting hair growth is not fully understood (Gupta et al., 2023; Iyengar & Li, 2025). It is believed that minoxidil functions by improving blood flow to hair follicles, which in turn increases circulation and which may help revitalise shrunken follicles, extend the growth phase of the hair cycle, and encourage thicker, longer hair strands (Zeltzer et al., 2024; Tan et al., 2025). A sulphotransferase enzyme converts minoxidil into its active metabolite, minoxidil sulfate. Differences in sulphotransferase enzyme expression between individuals appear to augment the efficacy of minoxidil (Goren & Naccarato, 2018). Clinical effects on hair growth typically begin after 2 to 4 months of consistent use, with maximal results seen around 6 to 12 months. Clinical response with minoxidil therapy appears to be highly variable. In randomised controlled trials, minoxidil monotherapy has been effective in increasing total hair density, as well as terminal hair density in both male and female AGA compared to controls (Gupta et al., 2022a; Gupta et al., 2024a; Gupta et al., 2024b; Gupta et al., 2025a). In these studies, the efficacy of minoxidil has also been shown to be strongly dose-dependent.

Minoxidil has also been found to act synergistically with 5-ARIs and certain other therapies in the treatment of AGA. Studies have shown that users of both minoxidil and a 5-ARI experience greater improvements in hair density and thickness compared to those using monotherapy (Tanglertsampan, 2012; Hu et al., 2015; Suchonwanit et al., 2018; Suchonwanit, Iamsumang, & Rojhirunsakool, 2019; Rossi & Caro, 2024; Asad, Naseer, & Ghafoor, 2024). In some cases, the combination of minoxidil with a 5-ARI has also been associated with faster onset of visible results and improved patient satisfaction.

Minoxidil has been evaluated for its therapeutic effects on hair loss in some small studies of transfeminine and transmasculine people (Zaminski et al., 2025; Tang et al., 2025b). These studies have reported positive results, in line with data from the wider population.

Comparison of Different Minoxidil Routes of Administration

The most widely used formulations of minoxidil include oral minoxidil and topical minoxidil. The main difference is that oral minoxidil is absorbed extensively into systemic circulation, whereas topical minoxidil is designed to act locally at the site of application, at which it stimulates hair follicles directly, hence resulting in limited systemic exposure.

Oral minoxidil is metabolised rapidly into minoxidil sulfate in the gastrointestinal tract (Patel, Nessel & Kumar, 2023). Peak plasma concentrations are typically reached within 1 hour. Oral minoxidil has been used at a range of 0.25–7.5 mg/day for AGA in clinical trials. The oral route has an average bioavailability of nearly 100%, whereas the local absorption of topical minoxidil into the scalp is around 1.4%. However, there remains substantial interindividual variation for each. As such, clinical doses of topical minoxidil are much higher (typically a 2 or 5% concentration) in order to compensate. Food does not appear to influence the bioavailability of oral minoxidil (Gupta et al., 2023).

The efficacy of oral and topical minoxidil has been investigated extensively in clinical studies. Higher doses of oral minoxidil have been associated with more favourable outcomes for AGA in terms of hair diameter, total hair density, and terminal hair density, but also with increasing adverse effects (Gupta et al., 2022b). Generally, lower doses have been used in women as compared to men. Oral minoxidil has been investigated at doses of up to 7.5 mg/day in clinical trials in this indication (Sanabria et al., 2024a). Large meta-analyses have found that studies are mixed on whether oral or topical minoxidil, on average, results in better, worse, or equal efficacy (Gupta et al., 2022a; Gupta et al., 2024a; Gupta et al., 2024b; Fazal et al., 2025; Gupta et al., 2025a). However, the dose-dependent effects of oral minoxidil have similarly been found to occur with topical minoxidil (Singh et al., 2022). A possibility is that oral and topical minoxidil may not have always been used at clinically equivalent doses.

The inconsistent differences in efficacy shown between oral and topical minoxidil in clinical studies may be driven by interindividual variation in response due to sulphotransferase enzyme expression, particularly in the scalp (Patel, Nessel & Kumar, 2023). There is growing evidence that in some individuals oral minoxidil may be more efficacious than topical minoxidil and vice versa (Goren et al., 2015; Goren et al., 2016; Gupta et al., 2024b; Gupta et al., 2025a). These data suggest that a subset of individuals who may not respond to one route of administration could see benefit by changing to the other.

Sublingual minoxidil has also been investigated for treating AGA (Sinclair et al., 2020; Bokhari, Jones, & Sinclair, 2021; Sinclair et al., 2025). Another route of administration which is being considered is injectable minoxidil (Needle et al., 2025). However, these routes have received comparatively much less attention and so limited data are available to inform their usage. A randomised controlled trial comparing oral and sublingual minoxidil at a daily dosage of 5 mg found similar efficacy at 24 weeks follow-up, suggesting that sublingual minoxidil may be a useful alternative to oral minoxidil (Sanabria et al., 2024b). Whilst these initial data are promising, further and larger scale studies are likely to be needed before sublingual minoxidil could see the same level of adoption as oral and topical administration.

Safety and Tolerability of Oral and Topical Minoxidil

Minoxidil has generally been shown to be well tolerated in clinical trials. Nevertheless, usage is associated with various adverse effects in some individuals (Gupta et al., 2022b; Gupta et al., 2023; Iyengar & Li, 2025). The adverse effects of minoxidil have been shown to be dependent on the route of administration, as well as being positively dose-dependent.

A retrospective study of users of oral minoxidil investigated the frequency of adverse effects in both men and women receiving a median dose of 1.63 mg/day (Vañó-Galván et al., 2021). The following were found to occur: hypertrichosis (excessive facial/body hair) in 15.1%, lightheadedness in 1.7%, fluid retention in 1.3%, tachycardia in 0.9%, headache in 0.4%, periorbital edema (temporary swelling around the eyes) in 0.3%, and insomnia in 0.2%. The total frequency of adverse effects was 20.4%, which prompted discontinuation in 1.2% of users, overall. Another study reported an overall hypertrichosis incidence of 24%, with the highest rates being found in the sideburns (81%), temples (73%), arms (63%), and upper lip (51%) (Jimenez-Cauhe et al., 2021). By contrast, topical minoxidil is associated with much lower overall rates of hypertrichosis. Most studies have reported incidence rates of between 0 and 5% (Lucky et al., 2004; Blume-Peytavi et al., 2016; Ramos et al., 2020; Penha et al., 2024; Yang et al., 2024). These findings are consistent with a meta-analysis that reported point estimates of incidence rates for hypertrichosis of 10%, 15%, and 33% for oral minoxidil at 0.25 mg/day, 0.5 mg/day, and 1.25 mg/day, respectively, and 0% and 2% for topical minoxidil at a 2% and 5% concentration, respectively (Wiechert et al., 2025). Despite this, the discontinuation rate across all studies was 0.49%. There also seemed to be no statistically significant difference between the rate of discontinuation for oral and topical formulations, suggesting that hypertrichosis appears to be very well tolerated.

A concern associated with the use of oral minoxidil is its potential impact on cardiovascular health (Ibraheim et al., 2023). Since tachycardia can increase myocardial workload and lead to symptoms such as palpitations or chest discomfort, oral minoxidil should be approached cautiously, especially by individuals with underlying cardiovascular issues. Fortunately, the overall risk of severe cardiovascular complications from low-dose oral minoxidil seems to be very low in the general population (Randolph & Tosti, 2021; Vañó-Galván et al., 2021). Meanwhile, skin reactions appear to be relatively common in users of topical minoxidil. This often manifests as scalp eczema and itching, although rates of incidence vary by study (Lucky et al., 2004; Rossi et al., 2012; Penha et al., 2024). The culprit behind this irritating effect appears not to be minoxidil itself, but rather the ingredients in certain formulations such as propylene glycol (Suchonwanit, Thammarucha, & Leerunyakul, 2019). These solvents help deliver minoxidil into the scalp, but are known to cause skin irritation in susceptible individuals. It also appears that, for most people, long-term topical minoxidil therapy may be precluded by non-compliance (Ali Mapar & Omidian, 2007; Shadi, 2023).

The increase in overall body hair growth (i.e., hypertrichosis) is arguably the most consequential side effects for transfeminine people found to occur with minoxidil. As noted above, hypertrichosis is much more common with oral minoxidil than with topical minoxidil. This is a result of the differences in pharmacology between these routes and the extensive systemic absorption that occurs in the case of the former (Desai et al., 2024; Wiechert et al., 2025). In transmasculine people, an increase in body hair growth and diameter could be beneficial. However, these effects are usually not desired by transfeminine people. Consequently, some transfeminine people may prefer to use topical minoxidil over oral minoxidil, despite possible benefits to effectiveness from the latter in some individuals.

Steroidal and Non-Steroidal Antiandrogens

Antiandrogens such as spironolactone and cyproterone acetate are widely employed to reduce or suppress testosterone levels in transfeminine people. Some clinics have also used the non-steroidal antiandrogen bicalutamide. However, these medications have all also been investigated in the treatment of pattern hair loss in cisgender women. After gonadectomy, antiandrogen treatment is often discontinued. Nevertheless, it appears some transfeminine people continue antiandrogen treatment, particularly spironolactone, in order to suppress the effects of non-gonadal androgen production.

Spironolactone

Spironolactone has been studied at oral doses of 25 to 200 mg/day for the treatment of pattern hair loss in women (Wang et al., 2023; Rosenthal et al., 2024). Oral spironolactone has been found to be effective in halting and, in some cases, reversing female AGA (Sinclair, Wewerinke & Jolley, 2005; Burns et al., 2020). Often, it has been paired with other interventions such as minoxidil. A randomised controlled trial found that oral spironolactone at a dose of 80 to 100 mg/day had similar efficacy to minoxidil when used as a single agent therapy (Liang et al., 2022). Spironolactone has also been studied topically (Abdel‐Raouf et al., 2020; Ammar et al., 2022). In the highest quality studies, spironolactone has been found to act additively with minoxidil in improving hair density and hair diameter.

Overall, spironolactone appears to be well tolerated for treating AGA, as well as other androgen sensitive conditions in women (Barbieri et al., 2021; Wang et al., 2023; Martin et al., 2025). Likewise, it may also be useful for some transfeminine people as an adjunct therapy, especially when paired with minoxidil. However, spironolactone has been scarcely studied for male AGA. It could well be the case that other more established therapies, such as dutasteride, would be better for transfeminine people with more extensive hair loss.

Flutamide and Bicalutamide

Flutamide is a potent non-steroidal antiandrogen and antagonist of the androgen receptor which has predominantly been used to treat prostate cancer. Some clinicians have also employed the use of flutamide in treating female AGA, with positive findings (Carmina & Lobo, 2003; Yazdabadi & Sinclair, 2011; Paradisi et al., 2011; Faghihi et al., 2022). In a randomised controlled trial, 500 mg/day flutamide was found to be superior to 100 mg/day spironolactone in treating scalp hair loss (Cusan et al., 1994). However, this may have been at least partially down to the cyclic use of spironolactone, which meant that women randomised to spironolactone were not actually receiving it for the duration of the entire month. In spite of the above findings, flutamide is associated with a high risk of elevated liver enzymes, which can progress to life-threatening organ failure in a very small but clinically significant subset of cases (Ozono et al., 2000; Paradisi et al., 2011; Giorgetti et al., 2017). This appears to have precluded its widespread adoption for female AGA.

Bicalutamide is another non-steroidal antiandrogen which has been considered for female AGA (Perez, Nguyen, & Senna, 2025). Generally, bicalutamide is believed to have a lower risk of liver toxicity than flutamide, making it a much more promising candidate for large-scale adoption in otherwise healthy people (Kolvenbag & Blackledge, 1996; Devjani et al., 2023). A number of retrospective studies have reported encouraging data with 10 to 50 mg/day oral bicalutamide, both in terms of safety and efficacy (Ismali et al., 2020; Fernandez-Nieto et al., 2020; Yoong et al., 2025). Interestingly, a study also found that bicalutamide was associated with improvements in hypertrichosis induced by oral minoxidil (Moussa et al., 2022). Only one randomised controlled trial has been conducted with bicalutamide, in which minoxidil plus 25 mg/day oral bicalutamide was compared to minoxidil plus placebo (da Silva Libório et al., 2025). In this study, there was no additional benefit of bicalutamide on total hair density. This finding is surprising in light of the seemingly additive effects that occur with minoxidil and spironolactone. It is possible that differences in methodology could be responsible for this discrepancy. Another study, although also retrospective, found that 50 mg/day oral bicalutamide was associated with moderately greater improvement in scalp hair loss than was 100 mg/day oral spironolactone (Jha et al., 2024).

Concerns about safety have also historically precluded widespread adoption of bicalutamide in transgender medicine. However, increasing numbers of studies are adding to our knowledge of bicalutamide in transfeminine people (Fuqua, Shi, & Eugster, 2024; Angus et al., 2024).

Other Medications and Future Developments

Despite several decades of research, only two medications have been approved for male AGA by the FDA in the United States. These are minoxidil and finasteride. Even though the use of these agents is increasingly common in men, they remain only partially effective in reversing androgenic hair loss.

Topical Androgen Receptor Antagonists

Two novel topical androgen receptor antagonists of possible interest are clascoterone and pyrilutamide (Saceda-Corralo et al., 2023; Devjani et al., 2023). Unlike oral non-steroidal antiandrogens such as flutamide and bicalutamide, these medications are applied topically so that there is minimal systemic absorption. Clascoterone has shown some limited success in phase 3 clinical trials for treating acne in men and women and has been approved by the FDA for this indication (Hebert et al., 2020). It is hoped that clascoterone could also be effective in treating AGA. An exploratory study found that clascosterone was superior to topical cyproterone acetate and alfatradiol in improving hair shaft diameter and hair follicle density and had comparable efficacy to minoxidil (Cartwright et al., 2019). Phase 3 clinical trials of clascosterone in AGA are currently underway. Pyrilutamide had shown favourable results in phase 2 clinical trials for both male and female AGA, however it failed to outperform placebo in phase 3 clinical trials (Kintor Pharmaceuticals, 2024). Studies are now underway using a higher dose of pyrilutamide over a longer duration of follow-up in the hope that this will show improved results.

Despite the above, these findings are rather disappointing. Notably, clascoterone only marginally outperformed placebo in clinical trials for acne (reduction in symptoms by about 8 to 18% more than placebo) (Hebert et al., 2020). A systematic review and network meta-analysis found that oral spironolactone was substantially more effective for treating acne than topical clascoterone (Basendwh et al., 2024). Clascoterone and pyrilutamide may someday provide another option for treating AGA in transfeminine people. However, since their mechanism of action is not dissimilar to well-established therapies such as 5-ARIs, it seems that this class of medications is unlikely to ever be revolutionary.

Prostaglandin Analogues

Prostaglandin analogues could have some utility in treating AGA. These include latanoprost and bimatoprost. Prostaglandin analogues have mostly been used to treat glaucoma by lowering intraocular pressure but are also believed to prolong the anagen phase and hence cause hair growth in certain susceptible tissues (Valente Duarte de Sousa & Tosti, 2013).

Latanoprost has mostly been studied for alopecia areata within the context of hair loss. However, one small randomised controlled trial found that topical latanoprost outperformed placebo after 24 weeks in increasing hair density in young men with mild AGA (Blume-Peytavi et al., 2012). Bimatoprost has also been evaluated in various clinical trials. In four separate phase 2 clinical trials, bimatoprost mildly to moderately outperformed placebo (Anastassakis, 2022). However, compared to minoxidil, findings were inconsistent. Bimatoprost had similar efficacy in some measures in some studies, but inferior efficacy in others. Overall, prostaglandin analogues appear to have received little subsequent attention. These data are relatively underwhelming by themselves compared to the large amount of literature pertaining to more established AGA therapies.

Mitochondrial Pyruvate Carrier Inhibition

In perhaps one of the more interesting developments in recent years, researchers have identified a topically delivered molecule, called PP-405, that appears to be capable of reactivating dormant follicles by modulating mitochondrial pyruvate carrier (MPC) activity (Brown, 2025). Unlike current therapies that focus on hormone suppression and increased blood flow, PP-405 is a regenerative, stem-cell-focused approach to treating hair loss. The molecule is currently being investigated for male and female AGA.

Recently, a phase 2a clinical trial that randomised 78 men and women to either PP-405 or placebo concluded with positive safety findings (Meara, 2025). However, preliminary results from 4 weeks of treatment at 8 weeks follow-up also showed a rapid and statistically significant clinical response versus placebo. This was despite the study not actually being conducted to show efficacy. The researchers found that 31% of the men with advanced AGA who were treated with the active medication showed a 20% or greater increase in total hair density, compared to 0% of patients in the placebo group. This is particularly notable because current interventions for AGA, such as minoxidil, typically take at least several months of follow-up to show a statistically significant difference from placebo. Most strikingly, PP-405 apparently induced new terminal hair growth from follicles where no hair was previously present.

As of September 2025, PP-405 is in phase 2b clinical trials and is expected to enter phase 3 clinical trials early next year if subsequent clinical findings are promising. With all this said, it should be noted that these are merely early results. More rigorous studies are necessary to determine if PP-405 can be an effective intervention against AGA.

Summary and Conclusions

AGA is a common and distressing condition that has particular relevance for transfeminine people, given the role of hair in gender identity and expression. While feminising hormone therapy appears to at least partially reverse AGA, many individuals appear to experience incomplete regrowth. Limited data suggest that adjunct use of 5-ARIs and/or minoxidil, particularly in the first few years of hormonal transition, may have positive effects but more studies are necessary to confirm this.

The most established treatments for AGA in the wider population are 5-ARIs, including finasteride and dutasteride, and minoxidil. The role of 5-ARIs in women remain less clear. Nevertheless, dutasteride achieves superior outcomes in male AGA to finasteride, whilst having similar safety and tolerability. Hence, wherever possible, it seems reasonable to use the former should the use of a 5α-reductase inhibitor be desired. Minoxidil, whether oral or topical, provides dose-dependent improvements in total and terminal hair density in male and female AGA and acts synergistically with 5-ARIs. However, oral minoxidil is associated with higher rates of hypertrichosis, which may be undesirable for many transfeminine individuals.

Other agents, such as spironolactone and bicalutamide, could also offer additional benefit by antagonising the androgen receptor. Spironolactone is already widely used in transfeminine hormone therapy and shows synergy with minoxidil in studies of female AGA. Bicalutamide is of emerging interest given its relatively favourable safety profile. Novel therapies of benefit to transfeminine people may also become available in the future.

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