INTRODUCTION
Male androgenetic alopecia (AGA) and female pattern hair loss (FPHL) are common nonscarring hair loss disorders characterized by progressive scalp thinning, affecting up to 50% of men and women.1 In men, it typically begins with bitemporal recession and crown thinning, while women often present with diffuse thinning and central part widening. Variability exists, with some women also exhibiting vertex or bitemporal involvement.
AGA is driven by dihydrotestosterone (DHT), which shortens the anagen phase and causes follicular miniaturization. Current FDA-approved treatments, topical minoxidil and oral finasteride require long-term use, have a delayed onset, and can trigger initial shedding, often limiting adherence. Notably, the role of androgens is not clear in female androgenetic alopecia. Female AGA may progress more slowly, often with preserved frontal hairlines and normal androgen levels, necessitating careful differential diagnosis and tailored management approaches.2
While these agents remain first-line, a range of off-label and emerging therapies are being investigated with promising results. This review summarizes established and investigational treatments for AGA and their clinical efficacy.
AGA is driven by dihydrotestosterone (DHT), which shortens the anagen phase and causes follicular miniaturization. Current FDA-approved treatments, topical minoxidil and oral finasteride require long-term use, have a delayed onset, and can trigger initial shedding, often limiting adherence. Notably, the role of androgens is not clear in female androgenetic alopecia. Female AGA may progress more slowly, often with preserved frontal hairlines and normal androgen levels, necessitating careful differential diagnosis and tailored management approaches.2
While these agents remain first-line, a range of off-label and emerging therapies are being investigated with promising results. This review summarizes established and investigational treatments for AGA and their clinical efficacy.
DISCUSSION
Topical Therapies
Topical Minoxidil
To date, topical minoxidil is one of the most commonly used medications to treat AGA. Its therapeutic effect is believed to involve several complementary mechanisms, including vasodilation, modulation of local inflammation, indirect antiandrogenic effects, and activation of the Wnt/β-catenin signaling pathway, which plays a key role in hair follicle regeneration. Minoxidil may also alter hair cycle dynamics by extending the anagen phase and shortening telogen.3 Minoxidil 2–5% topical solution has been shown to increase hair count and density compared to placebo when applied twice daily.4,5,6 In men with androgenetic alopecia, 5% topical minoxidil demonstrated greater efficacy over 48 weeks compared to 2% minoxidil and placebo, with earlier and more substantial improvements in non-vellus hair count, scalp coverage, and perceived treatment benefit.4 Patients using the 5% formulation also reported enhanced quality of life and more favorable psychosocial perceptions of hair loss.4 Increased rates of pruritus and local irritation were observed with the higher concentration in this study.4 Despite its widespread use, response rates to topical minoxidil remain variable. Approximately 60% of male AGA patients are classified as non-responders. This variability is thought to be linked to scalp sulfotransferase activity, which is essential for converting minoxidil into its active form. The follicular sulfotransferase assay (FSA) has emerged as a promising biomarker to predict treatment response prior to initiating therapy.3
Topical Anti-androgens
Topical antiandrogens aim to locally inhibit androgen activity while minimizing systemic side effects. Topical finasteride, a type II 5α-reductase inhibitor, reduces dihydrotestosterone (DHT) at the follicular level, mitigating the miniaturization process central to androgenetic alopecia (AGA).7 Other agents, such as topical flutamide, have also shown efficacy. In a comparative study
Topical Minoxidil
To date, topical minoxidil is one of the most commonly used medications to treat AGA. Its therapeutic effect is believed to involve several complementary mechanisms, including vasodilation, modulation of local inflammation, indirect antiandrogenic effects, and activation of the Wnt/β-catenin signaling pathway, which plays a key role in hair follicle regeneration. Minoxidil may also alter hair cycle dynamics by extending the anagen phase and shortening telogen.3 Minoxidil 2–5% topical solution has been shown to increase hair count and density compared to placebo when applied twice daily.4,5,6 In men with androgenetic alopecia, 5% topical minoxidil demonstrated greater efficacy over 48 weeks compared to 2% minoxidil and placebo, with earlier and more substantial improvements in non-vellus hair count, scalp coverage, and perceived treatment benefit.4 Patients using the 5% formulation also reported enhanced quality of life and more favorable psychosocial perceptions of hair loss.4 Increased rates of pruritus and local irritation were observed with the higher concentration in this study.4 Despite its widespread use, response rates to topical minoxidil remain variable. Approximately 60% of male AGA patients are classified as non-responders. This variability is thought to be linked to scalp sulfotransferase activity, which is essential for converting minoxidil into its active form. The follicular sulfotransferase assay (FSA) has emerged as a promising biomarker to predict treatment response prior to initiating therapy.3
Topical Anti-androgens
Topical antiandrogens aim to locally inhibit androgen activity while minimizing systemic side effects. Topical finasteride, a type II 5α-reductase inhibitor, reduces dihydrotestosterone (DHT) at the follicular level, mitigating the miniaturization process central to androgenetic alopecia (AGA).7 Other agents, such as topical flutamide, have also shown efficacy. In a comparative study
