Androgenetic alopecia (AGA) is characterized by a progressive reduction in hair density, typically following a defined pattern. By the age of 70 years or older, 80% of White men and up to 40% of women show signs of AGA, with a substantial impact on mental health and quality of life, particularly among women. Currently, treatments approved by American and European regulatory agencies have demonstrated safety and efficacy in the management of this condition. However, several additional therapies have also shown effectiveness, although the absence of randomized clinical trials has limited their inclusion in the Summary of Product Characteristics (SmPC). Therefore, this review aims to summarize currently available treatments and propose a practical management algorithm to help clinicians select the most appropriate therapy for each patient according to clinical experience and disease severity.
Androgenetic alopecia (AGA) is a chronic, androgen-dependent hereditary condition characterized by progressive hair loss, typically following a defined pattern.1,2 In men, AGA is associated with androgenetic and genetic factors, whereas in women the etiology is more complex and less well understood,3 particularly in cases associated with polycystic ovary syndrome.4 Its prevalence varies according to sex and ethnicity, affecting 30–50% of the population around the age of 50 years.3,5 By the age of 70 years, approximately 80% of men and up to 40–50% of women may exhibit signs of the condition.6 Although benign, AGA can substantially impair mental health and quality of life, especially among women.7
The pathogenesis of AGA involves the binding of dihydrotestosterone (DHT) to androgen receptors located in the hair follicle. DHT is produced from testosterone through the action of 5-α-reductase type 2, an enzyme expressed in the dermal papilla of the follicle.2 Male AGA is well established as a genetically determined androgen-dependent trait.8 The main physiologic alteration is progressive follicular miniaturization, characterized by shortening of the anagen phase and prolongation of the telogen phase of the hair cycle.9 In female AGA, the role of androgens is less clear. Levels of 5α-reductase and androgen receptors in frontal follicles are lower than in men, and women frequently have normal androgen levels, suggesting the involvement of additional androgen-independent mechanisms.3
Currently, only topical minoxidil (for men and women) and oral finasteride 1mg (for men) are approved by the US Food and Drug Administration (FDA) for the treatment of androgenetic alopecia. Within the European Union, the regulatory status and availability of these agents may vary among countries because authorization is granted either nationally or through European procedures. Topical finasteride formulations have been approved only in selected countries and are not approved by the FDA.2 Nevertheless, a broad range of off-label therapies and procedures has demonstrated clinical benefit. The lack of standardization, however, complicates treatment selection.10 Management should therefore be individualized according to available evidence, patient expectations, feasibility, and adherence.11 This review aims to provide clinicians with a comprehensive overview of current therapeutic options and to propose a practical algorithm for the pharmacologic treatment of AGA.
MethodsWe conducted a narrative review of the literature using PubMed and Google Scholar without date restrictions. Searches were performed in English and Spanish and were last updated in December 2024. The search strategy combined the terms “androgenetic alopecia,” “female pattern hair loss,” “male pattern baldness,” “minoxidil,” “finasteride,” “dutasteride,” “spironolactone,” “bicalutamide,” “antiandrogens,” “mesotherapy,” “platelet-rich plasma,” “low-level light therapy,” “hair transplantation,” and “nutraceuticals,” together with additional free-text terms and Boolean operators to identify clinical trials, observational studies, narrative and systematic reviews, meta-analyses, and clinical practice guidelines.
Studies were eligible if they included human participants with androgenetic alopecia, evaluated pharmacologic or procedural treatments, and reported efficacy, safety, or therapeutic positioning data applicable to routine clinical practice. Articles had to be published in English or Spanish. Studies focusing exclusively on other types of alopecia, purely preclinical experiments without direct clinical implications, single case reports, and non-peer-reviewed material (e.g., conference abstracts or theses) were excluded. When multiple reports referred to the same study population, the most recent or most informative publication was retained.
Titles and abstracts retrieved from the searches were screened manually by one author; therefore, screening was not performed in duplicate. Full texts of potentially relevant articles were reviewed in detail, and duplicates were removed manually. Given the narrative nature of the review and the heterogeneity of the available evidence, no formal risk-of-bias assessment tool was applied. Instead, key methodological aspects such as study design, sample size, presence of a control group, objectivity of outcome measures, and duration of follow-up were considered qualitatively to assess the robustness of the evidence.
The treatment algorithms were developed by 3 specialists on the basis of their clinical expertise and routine practice. Consensus was achieved during 2 structured meetings in which therapeutic options were discussed according to evidence-based efficacy and feasibility in real-world settings. Consequently, the proposed algorithm integrates current evidence with practical applicability for patient management.
TreatmentsTopical therapiesIn recent years, the use of topical therapies as first-line or adjuvant treatment has gained increasing relevance because of their potential efficacy and safety, with markedly fewer adverse effects vs systemic therapies.2,10,12,13
Topical minoxidilMinoxidil is a prodrug converted into its active metabolite, minoxidil sulfate, through sulfotransferase activity in different tissues.10 It acts as a hair growth stimulant by prolonging the anagen phase, shortening the telogen phase, and enlarging miniaturized follicles through mechanisms that remain incompletely understood.13–16
The efficacy of topical minoxidil depends on the presence and activity of sulfotransferase, scalp absorption, and drug concentration.17 Topical minoxidil is available as 2% and 5% solutions and foam formulations with variable efficacy.10 According to European clinical practice guidelines, the 5% topical solution is more effective than the 2% solution when applied twice daily in men. In women, studies suggest that the 5% solution is superior or equivalent to the 2% solution.15 In addition, some studies have shown that 5% foam may be equivalent to 2% or 5% solutions depending on frequency of use, sulfotransferase activity, absorption, and formulation vehicle.10,17
Patients should be informed about the possibility of transient telogen shedding during the first months of treatment.1,14 With adequate adherence, hair growth may become evident within 4–8 months.10 However, discontinuation of topical minoxidil is usually followed by increased hair shedding.1,10 Gradual withdrawal is therefore recommended to minimize disruption of the hair cycle.
A 6-month prospective randomized assessor-blinded trial in men with AGA compared 0.25% topical finasteride combined with 5% minoxidil against both monotherapies. Significant improvement was observed only in the combination group at both 3 months (+56hairs/cm2; P<.05) and 6 months (+81hairs/cm2; P<.001), with comparable tolerability and safety profiles.18
Local cutaneous adverse effects, including contact dermatitis with pruritus or scaling and hypertrichosis, are more common with higher-concentration minoxidil solutions, likely because of the increased propylene glycol content.14
Topical finasterideTopical finasteride preferentially inhibits type II 5-α-reductase in the scalp.19 By blocking the conversion of testosterone into DHT, it reduces follicular DHT production while potentially limiting systemic exposure vs oral administration.15
The safety and efficacy profile of topical finasteride were first demonstrated more than 20 years ago.20 Phase I and II studies showed that topical finasteride reduced plasma DHT levels comparably to oral administration while producing substantially lower systemic drug concentrations.21 Furthermore, lower concentrations of topical finasteride (100–200μL administered once daily) produced greater inhibition of scalp DHT (52.4% and 46.8%, respectively) than serum DHT (24.4% and 26.2%, respectively).22
Piraccini et al. conducted a phase III clinical trial evaluating daily application of 0.25% topical finasteride spray in 458 patients with AGA (189 assigned to topical finasteride, 184 to placebo, and 85 to oral finasteride). After 24 weeks, a statistically significant increase in hair count vs placebo was observed (adjusted mean change, 20.2 vs 6.7 hairs; P<.001). Efficacy was similar to oral finasteride (target area hair count increase, 21.1 hairs), although systemic exposure was 100-fold lower and serum DHT suppression was less pronounced (34.5% vs 55.6%; P<.05).23
More recent studies demonstrated that inclusion of hydroxypropyl chitosan (HPCH) in topical finasteride formulations significantly improves skin penetration and bioavailability of the active ingredient, thereby enhancing therapeutic response. By contrast, compounded formulations may exhibit variability in active ingredient concentration and absorption, potentially compromising efficacy and patient satisfaction.24
Reported adverse effects are usually local and mild to moderate in severity, including itching, irritation, dryness, peeling, contact dermatitis, and erythema. Regarding sexual adverse effects, no significant complications have been reported.15,23,25 Overall, current evidence suggests that topical finasteride provides clinical benefit; however, any apparent equivalence with oral finasteride should be interpreted cautiously because the available evidence remains heterogeneous and direct comparative data are limited.
Other topical therapiesSeveral newer topical therapies have demonstrated promising efficacy results. A study comparing 5% topical spironolactone with 0.1% topical finasteride over 6 months found that topical spironolactone improved hair density and shaft diameter in both men and women to a greater extent than topical finasteride.26
A systematic review evaluating ketoconazole for AGA treatment demonstrated increased hair shaft diameter and improvement in the pilary index.27 Prostaglandin analogues such as latanoprost have also been investigated because they prolong the anagen phase of the hair cycle. Studies have reported increased hair density in treated groups, although only patients with mild AGA were included.28
Cetirizine 1% solution and combinations of adipose tissue-derived stem cells with cetirizine, together with minoxidil or finasteride, may also represent viable alternative therapies for AGA.19
A more recent therapeutic approach involves self-assembled micelle inhibitory RNAs (SAMiRNA). Two studies reported mean increases in hair growth comparable to those observed with finasteride (7.5hairs/cm2 over 16 weeks vs 9.3hairs/cm2 over 24 weeks with oral finasteride 1mg), although direct head-to-head comparisons are lacking.29
Oral therapiesAlthough oral therapies are associated with more systemic adverse effects than topical treatments, they are generally more convenient for patients and may therefore improve treatment adherence.10
Oral finasterideOral finasteride is available in 1-mg and 5-mg formulations, although only the 1-mg dose is approved for the treatment of male androgenetic alopecia and exclusively in men.30 It has demonstrated promotion of hair growth within the first year of treatment, with continued improvement observed even after 10 years of therapy.31
Although some authors reported that the maximal degree of improvement occurred after the first year of treatment, systematic reviews and long-term studies extending to 5 and 10 years showed that the efficacy of finasteride did not decline over time.32–35 In a retrospective study, 21% of patients continued to improve beyond 5 years, 65% maintained previously achieved benefits, and progressive improvement in hair growth was observed for up to 5 years.31,34
Nevertheless, among patients with frontal and vertex-pattern male androgenetic alopecia, recurrence after achieving maximal response occurred in approximately 10% and 16% of patients, respectively.34
Off-label use in female AGA has demonstrated clinical efficacy profile.36 Higher daily doses (2.5–5mg) have been associated with noticeable improvement in hair loss, whereas lower doses (1mg/d) have shown limited benefit.1,15
Reported adverse effects in men mainly involve sexual dysfunction, including decreased libido, erectile dysfunction, and reduced ejaculate volume. In women, breast enlargement and teratogenicity have been reported; therefore, finasteride is contraindicated during pregnancy.1,14,15
Oral dutasterideDutasteride is a second-generation 5-α-reductase inhibitor that suppresses both type I and type II isoenzymes.14,15,19 It is widely used off label for the treatment of AGA.37
A systematic review and meta-analysis comparing oral dutasteride with finasteride over 24 weeks demonstrated that dutasteride was more effective than finasteride in male androgenetic alopecia. Significant differences were observed in total hair count (P<.00001), investigator assessment of global photographs for both vertex (P=.02) and frontal (P=.01) regions, panel global photographic assessment for vertex (P<.00001) and frontal (P<.00001) views, and patient self-assessment (P=.003).38
A recent meta-analysis evaluating different monotherapies identified dutasteride 0.5mg once daily for 24 weeks as the most effective treatment regarding changes in total hair density and terminal hair density at 6 months (surface under the cumulative ranking curve, 87% and 98%, respectively).39
In real-world clinical practice, intermittent dosing (2–3 capsules weekly) as monotherapy resulted in slightly lower efficacy than daily administration (90% vs 66%) but was not associated with reported adverse effects. Intermittent regimens may therefore be useful in early-stage AGA or in patients concerned about adverse events.40
Although its use in women is less common, daily oral dutasteride administered for 3 years significantly increased hair thickness and prevented further progression in women with androgenetic alopecia (signed-rank test; P=.02).41
Oral minoxidilAlthough oral minoxidil represents an alternative to topical administration with potential advantages regarding convenience, cosmetic acceptability, cost, and adherence,15 it remains an off-label therapy. In oral administration, conversion to the active metabolite occurs in the liver, where sulfotransferase activity is consistently expressed, unlike in the follicle. This results in greater bioavailability and potentially enhanced efficacy profile.42
Low-dose oral minoxidil has demonstrated efficacy in both women and men with AGA. In women, doses ranging from 0.25 to 1.25mg/d have been shown to be effective and safe. Combination therapy with oral minoxidil 0.25mg and spironolactone 25mg represents an attractive option because the natriuretic effect of spironolactone may counterbalance the sodium and fluid retention associated with minoxidil.
In men, however, lower doses appear less effective, and optimal results are generally achieved with daily doses of 2.5 or 5mg.43
A dose-dependent relationship has been observed for both efficacy and adverse effects. A systematic review with meta-regression analyses demonstrated that increasing the daily dose by 1mg over 6 months was associated with significant improvements in hair diameter (P=.001), total hair density (P=.007), and terminal hair density (P=.001), but also with a higher risk of hypertrichosis (P=.006) and cardiovascular adverse events (P=.004).44
Oral minoxidil is commercially available in 10-mg tablets that can be divided into halves or quarters to achieve individualized dosing for AGA treatment.1,10 The absence of lower-dose commercial formulations often requires compounding in pharmacies, which may increase the risk of dosing errors and severe adverse events.45
Adverse effects of oral minoxidil are generally dose dependent and reversible after discontinuation.10,15 The most commonly reported events include hypertrichosis (15.1%), lightheadedness (1.7%), fluid retention (1.3%), tachycardia (0.9%), headache (0.4%), periorbital edema (0.3%), and insomnia (0.2%).46,47
Other antiandrogen therapiesAccording to current guidelines, the use of antiandrogen therapies in men with AGA is not recommended.1
SpironolactoneSpironolactone is an off-label synthetic aldosterone receptor antagonist that lowers total testosterone levels and inhibits androgen receptors in target tissues.
A systematic review analyzing 5 studies of oral spironolactone in women found that, in 4 studies, 81% of participants reported improvement in hair growth with doses ranging from 25 to 200mg, either as monotherapy or combined with topical minoxidil.48 Another recent review reported improvement in hair loss and follicular density in 49.3% of patients treated with spironolactone monotherapy, emphasizing that effective doses usually began at 100mg/d for at least 12 months.49
The best results, however, appear to occur when spironolactone is combined with topical minoxidil formulations.50
There is also evidence supporting its use in specific clinical situations, as safety has been demonstrated in women with a history of breast cancer51 and in women older than 45 years with renal disease, although close monitoring of serum electrolyte levels is recommended.52
BicalutamideBicalutamide is a nonsteroidal pure antiandrogen.53 In a retrospective study, women received daily doses of 25–50mg for 2 years. Among patients treated for longer than 6 months (n=32), the mean reduction in Sinclair scale score was 27.5%.54 Mild elevations in liver enzymes occurred in 11.4% of patients, resolved spontaneously, and did not require treatment discontinuation.
Similar findings were reported in a larger retrospective study involving 316 women treated with oral bicalutamide 10mg/d. The mean reduction in Sinclair stage was 28.9% at 2 years, and the most common adverse effect was mild elevation of liver transaminases in 2.85% of patients.53
Oral hormonal contraceptivesOral hormonal contraceptives generally contain estrogens (estradiol) and/or progestins (cyproterone, drospirenone), which exert antiandrogenic effects.55,56 However, supporting evidence for their efficacy in AGA remains limited.55,56 They may nonetheless serve as complementary therapy, particularly in women with polycystic ovary syndrome or when contraception is required because of the teratogenic potential of antiandrogen therapies.
PhototherapyLow-level light therapyLow-level light therapy (LLLT) is a noninvasive treatment option for men and women with AGA that uses wavelengths between 600 and 1100nm to stimulate hair regrowth and has been described as cost-effective.
Two meta-analyses including 1157 and 758 double-blind randomized clinical trials demonstrated significantly greater hair density in patients treated with LLLT vs controls (standardized mean difference [SMD], 1.316; 95%CI, 0.993–1.639 and SMD, 1.27; 95%CI, 0.993–1.639) in both sexes and with both comb- and helmet-type devices. However, the included studies differed substantially regarding device design, wavelength, fluence, and treatment schedules, introducing considerable heterogeneity and limiting direct comparisons.
Adverse effects are minimal, making LLLT a potential adjunctive therapy with minoxidil or finasteride.15 Although some studies reported superior outcomes with combination therapy, a large real-world study involving 1383 patients with AGA treated with 650-nm wavelength LLLT for 20min every other day did not demonstrate enhanced efficacy when LLLT was combined with minoxidil or finasteride vs LLLT alone.59 Overall, these data do not support a consistent synergistic effect of combination therapy.
Another study demonstrated that use of LLLT for longer than 1 year was associated with greater perceived efficacy, particularly in men and in patients presenting with dandruff, erythema, or scalp pruritus. These factors may therefore predict better clinical response.59
“Non-ablative” fractional laserFractional laser therapy has been proposed to act as a controlled wounding stimulus that increases blood flow, induces cytokine and growth factor expression, and stimulates dermal papilla and stem cell activity.60,61 Individual studies have reported clinical improvement in hair growth and, for some outcomes, efficacy comparable or slightly superior to topical 5% minoxidil.62
Overall, currently available evidence suggests that this is a generally safe modality for AGA treatment, although comparative studies remain limited.
In recent years, both ablative and Non-ablative lasers have also been increasingly used to create microchannels for drug delivery, thereby enhancing topical absorption and potentially producing synergistic effects between medical and physical therapies.63,64
When primary therapies fail to adequately halt disease progression, adjuvant therapies may be used to complement treatment. Some of these options are summarized in Table 1.
Complementary treatments for androgenetic alopecia.
| Other treatments | Description | Current evidence and recommendations |
|---|---|---|
| 5. Injectables | ||
| Platelet-rich plasma (PRP) | PRP contains growth factors and proteins that promote tissue repair.65–68 However, the efficacy of PRP remains controversial due to the lack of standardized protocols and preparation methods.65–67 | However, the efficacy of PRP remains controversial because of the lack of standardized protocols and preparation methods.65–67 Two recent meta-analyses reported significant increases in hair density, especially in men, although no significant differences in hair diameter were found between PRP and control groups.65,68 Combining PRP with topical minoxidil appears to enhance outcomes.69–71 Adverse effects are generally mild and transient, including scalp pain and headache.10 |
| Mesotherapy with dutasteride | Injectable dutasteride has gained popularity because of its limited systemic absorption, leading to fewer adverse effects. | Between 2009 and 2013, 3 placebo-controlled studies assessed the efficacy of a 0.05% dutasteride solution combined with vitamins compared with saline. Two studies involving male participants showed significant improvement after treatment.72,73 A third study found that more women improved in the dutasteride group than in the control group (62.8% vs 17.5%, respectively; P<.05).74 Later, Saceda-Corralo et al. tested a simplified regimen with 0.01% dutasteride mesotherapy, showing improvement in hair density and diameter in all cases.37 A 2022 multicenter retrospective study found that 80% of patients, both men and women, showed clinical improvement, with marked improvement in 38.4%.75 |
| Mesotherapy with bicalutamide | The off-label use of bicalutamide 0.5% in mesotherapy has recently been studied. | In a case report involving 6 premenopausal women with AGA and seborrhea, 3 monthly sessions resulted in subtle improvement in hair density, seborrhea, and overall patient satisfaction. However, it should be regarded as an adjuvant option within the overall management of AGA.76 |
| Microneedling (MN) | The efficacy of microneedling as monotherapy remains uncertain because clinical trials are often small, nonrandomized, or involve combination therapies.77 | A single-arm meta-analysis by Gupta et al. found that combining MN with topical minoxidil 5% significantly increased total hair count compared with either therapy alone (P<.05).77 Women appear to respond better to MN therapy than men. Combining MN with PRP also appears to improve hair growth parameters.77 |
| Other injectables | • Botulinum toxin has shown positive results in the treatment of AGA,14,15 although recent studies suggest that its overall effectiveness is low or inconsistent.78• Mesenchymal stem cell-derived exosomes have shown potential for promoting hair regrowth because of their cytokine and growth factor content; however, further research is required to confirm their efficacy and safety.14,22 | |
| 6. Surgery/hair transplantation | Hair transplantation is a surgical procedure that implants hair into areas with significant hair loss, providing a natural appearance and permanent results, with graft survival rates of up to 90%.This technique should be complemented with long-term anti-AGA therapy.15 Adverse effects include reactions to anesthesia, bleeding, postoperative pain, edema, and patient dissatisfaction.10 | |
| 7. Emerging therapies | Several novel therapeutic approaches are emerging for AGA management.Pyrilutamide and clascoterone have demonstrated safety and efficacy in phase II studies.14 GT20029, an androgen receptor antagonist, has shown a favorable safety and tolerability profile in phase I trials and is currently under investigation in phase II studies.79 | |
| 8. Nutricosmetics | Nutraceuticals are generally well tolerated in clinical trials and may be used as monotherapy or adjunctive therapy.However, clinical evidence supporting their efficacy remains limited.7,12 The most extensively studied nutraceuticals are those hypothesized to inhibit 5-α-reductase, such as Serenoa repens and pumpkin seed oil, or those that stimulate IGF-1 production, such as Pygeum africanum.15,80 | |
The expert panel reached a consensus to develop an algorithm (Fig. 1) outlining the reviewed therapeutic options in a stepwise manner across 3 main tiers and to compile a summary table (Table 2) detailing, for each intervention, its regulatory status, level of evidence, and grade of recommendation, thereby facilitating selection of the most appropriate therapeutic combination. Treatment should be individualized and agreed upon with each patient, taking into account disease severity, pattern of involvement, comorbidities such as seborrheic dermatitis, personal medical history, patient expectations, and reproductive intentions in women of childbearing potential.
Regulatory status and level of evidence for therapeutic options included in the proposed algorithm for androgenetic alopecia.
| Drug/procedure | Regimen (AGA) | Regulatory status | Level of evidence |
|---|---|---|---|
| Minoxidil | Topical 2%–5% (men) | Approved: FDA; national EU authorities (including AEMPS) | A |
| Topical 2%–5% (women) | Approved: FDA; national EU authorities (including AEMPS) | A | |
| Oral 2.5–5mg/day (men) | Off-label (no FDA/EMA/AEMPS approval for AGA) | C | |
| Oral 0.5–2.5mg/day* (women) | Off-label (no FDA/EMA/AEMPS approval for AGA) | C | |
| Finasteride | Oral 1mg/day (men) | Approved: FDA; national EU authorities (including AEMPS) | A |
| Oral 2.5–5mg/day (women) | Off-label (no FDA/EMA/AEMPS approval for AGA) | C | |
| Topical 0.25% (men) | Authorized in selected EU countries | B | |
| Topical 0.25% (women) | Off-label (no FDA/EMA/AEMPS approval for AGA) | C | |
| Dutasteride | Oral 0.5mg/day (men) | Off-label (no FDA/EMA/AEMPS approval) | B |
| Oral 0.5mg/day (women) | Off-label (no FDA/EMA/AEMPS approval) | C | |
| Spironolactone | Oral 50–200mg/day* (women) | Off-label (no FDA/EMA/AEMPS approval) | B |
| Bicalutamide | Oral 10–50mg/day* (women) | Off-label (no FDA/EMA/AEMPS approval) | C |
| Hair transplantation surgery | – | Surgical procedure (no medicinal marketing authorization for AGA) | B |
| Nutricosmetics | – | Food/cosmetic supplement (no medicinal authorization for AGA) | C |
| Mesotherapy with dutasteride±bicalutamide | – | Injection technique using off-label medicinal products; no specific indication for AGA | C |
| Platelet-rich plasma | – | Autologous procedure; devices approved as medical devices in some regions | B |
| Low-level light therapy | – | Medical device for hair growth in some regions; not a medicinal product | B |
| Microneedling | – | Medical device/procedure; no specific medicinal authorization for AGA | C |
| “Non-ablative” fractional laser | – | Medical device/procedure; no specific medicinal authorization for AGA | C |
AGA, androgenetic alopecia; AEMPS, Agencia Española de Medicamentos y Productos Sanitarios; EMA, European Medicines Agency; EU, European Union; FDA, US Food and Drug Administration; LoE, level of evidence.
Levels of evidence: LoE A: Multiple randomized clinical trials and/or meta-analyses with consistent results. LoE B: At least 1 randomized trial or several well-designed comparative/observational studies. LoE C: Mainly observational studies, small case series, or heterogeneous data. LoE D: Expert opinion or consensus with minimal empirical evidence.
The first tier consists of a foundational combination of minoxidil and antiandrogenic agents. Minoxidil may be administered topically, at concentrations ranging from 2% to 5%, or orally at off-label doses of 2.5–5mg/d in men and 0.5–2.5mg/d in women. In women, doses up to 1.25mg/d are those most consistently supported by published evidence, whereas higher doses (up to 2.5mg/d) are occasionally used by the authors in carefully selected patients who show insufficient response and tolerate lower doses without clinically relevant adverse events. The route of administration should be selected according to clinical severity, patient preference, and individual tolerability. In selected cases, gradual dose escalation under strict medical supervision may be considered, although routine use of higher doses is discouraged.
Based on expert-panel consensus and considering that oral minoxidil for AGA remains an off-label indication, routine laboratory monitoring is not considered necessary in otherwise healthy patients receiving low-dose therapy. However, a careful baseline cardiovascular history and physical examination are recommended, with particular attention to concomitant antihypertensive medications. Blood pressure and heart rate should be assessed at baseline and during follow-up, especially in patients with cardiovascular comorbidities or those receiving 2 or more antihypertensive agents. Oral minoxidil should be avoided in patients with a history of myocardial infarction and reduced left ventricular ejection fraction or severe decompensated heart failure. Relative contraindications include previous myocardial infarction with preserved ejection fraction, moderate heart failure, clinically significant arrhythmias, and prior intolerance to oral minoxidil-related adverse effects such as edema or marked hypertrichosis. In patients with impaired renal function, the dose should be adjusted according to the estimated glomerular filtration rate.
Regarding antiandrogen therapy, men may be treated with oral finasteride 1mg/d or oral dutasteride 0.5mg administered 3–7 times weekly, depending on disease severity. As a second-line option, topical finasteride 0.25% may also be used. In premenopausal women, spironolactone represents an effective option, particularly in the presence of acne, a personal or family history of breast cancer, or adolescent age, with doses ranging from 50 to 200mg/d. In cases associated with seborrhea, bicalutamide is preferred at doses of 10–50mg/d. Topical finasteride 0.25% is also considered a second-line alternative in this population. In postmenopausal women, finasteride 2.5–5mg/d or dutasteride 0.5mg administered 3–7 times weekly are recommended, again considering topical finasteride as an additional alternative.
Reproductive intentions must always be considered in women of childbearing potential. In refractory cases without future pregnancy plans, dutasteride may be considered. In addition, oral contraceptives containing dienogest or drospirenone may be used to improve hormonal balance and facilitate therapeutic control.
Several second-line adjuvant therapies may also be considered, either as monotherapy or in combination with first-line pharmacologic agents. In patients with areas unresponsive to medical treatment, hair transplantation surgery is recommended, particularly in regions with irreversible involvement or markedly reduced density. The use of nutraceutical products should be individualized because of their variable efficacy. This is particularly relevant in patients receiving oral antiandrogen therapy, since some nutricosmetics possess intrinsic antiandrogenic activity. Techniques such as mesotherapy with dutasteride or bicalutamide, LLLT, platelet-rich plasma, microneedling, and nonablative fractional lasers may also be considered as adjunctive options and combined when appropriate according to the clinical scenario and compatibility of their routes of administration. However, real-world data show highly heterogeneous outcomes and, to date, do not consistently demonstrate a synergistic effect with minoxidil or finasteride.
Lastly, the third tier includes experimental and emerging therapies currently under clinical investigation, such as topical antiandrogens (GT20029 and pyrilutamide) and regenerative approaches including mesenchymal stem cell-derived exosomes. Other investigational agents with preliminary clinical evidence include cetirizine 1%, SAMiRNA, and botulinum toxin.
The high prevalence of androgenetic alopecia and the broad age range at presentation require tailored approaches for multiple special clinical scenarios. Key considerations are summarized in Table 3. These recommendations are intended to support therapeutic decision-making in complex or sensitive settings, including adolescence, reproductive planning, cardiovascular comorbidities, and postmenopausal patients.
Special considerations for the management of androgenetic alopecia.
| Condition | Recommendation |
|---|---|
| MAGA | |
| Adolescents | With beard development: topical and oral finasteride may be considered.Without beard development: in adolescents with fully developed secondary sexual characteristics, treatment may proceed as in adults. However, in those with incomplete secondary sexual development, systemic 5-α-reductase inhibitors are not recommended. |
| Age >55 years | PSA monitoring before initiation and after 6 months of therapy with 5-α-reductase inhibitors. |
| Desire for fertility | Discuss the potential effects of 5-α-reductase inhibitors on semen parameters, including their presence in and elimination from semen. Topical and/or oral minoxidil may be continued. |
| Advanced alopecia and older patients | Balance the potential benefits of 5-α-reductase inhibitors against the risk of sexual adverse effects. Hair transplantation may be considered. |
| Past medical history of acute myocardial infarction with reduced ejection fraction | Consider alternatives to oral minoxidil. |
| Use of >2 antihypertensive agents, including doxazosin | Use oral minoxidil with caution and under close monitoring. |
| Treatment with verapamil or diltiazem | Use oral minoxidil with caution because of potential cardiovascular interactions. |
| Adverse effects with 5-α-reductase inhibitors | Consider replacing systemic therapy with mesotherapy or topical formulations. |
| FAGA | |
| Past medical history of breast cancer | Current literature supports the use of minoxidil and spironolactone; other options should be discussed with the treating oncologist. |
| Desire for fertility | Restrict treatment to minoxidil and platelet-rich plasma (PRP). Once pregnancy is achieved, PRP alone is recommended. Drug half-lives should be considered when planning treatment discontinuation before conception. |
| Lactation | Spironolactone and topical minoxidil may be considered. |
| History of acute myocardial infarction with reduced ejection fraction | Consider alternatives to oral minoxidil. |
| Use of >2 antihypertensive agents, including doxazosin | Use oral minoxidil with caution and under close monitoring. |
| Treatment with verapamil or diltiazem | Use oral minoxidil with caution because of potential cardiovascular interactions. |
| Presence of seborrhea | Bicalutamide may be preferred. |
| Acne or adolescence | Spironolactone may be preferred. |
| Hair transplantation | Avoid very extensive procedures because of the limited donor area. |
| General considerations | Oral contraceptives should always be offered, although not imposed. When prescribed, formulations containing drospirenone or dienogest are preferred. |
AGA, androgenetic alopecia; FAGA, female androgenetic alopecia; MAGA, male androgenetic alopecia; PRP, platelet-rich plasma; PSA, prostate-specific antigen.
This review is limited by its narrative design and does not constitute a systematic review of the literature. In addition, many of the analyzed studies were retrospective or presented heterogeneous methodologies, including variable assessment tools and follow-up periods. Furthermore, there are no adequately designed comparative studies to establish the superiority of one therapeutic agent over another.
ConclusionsAndrogenetic alopecia is a chronic and highly prevalent condition that represents a complex clinical challenge. The wide age range at presentation and the etiologic heterogeneity of the disease require individualized patient assessment. In addition to FDA-approved first-line treatments such as minoxidil and finasteride, a broad spectrum of therapeutic options has demonstrated efficacy and safety in the management of this condition. This therapeutic diversity allows treatment to be tailored according to patient profile and disease severity. The present review summarizes currently available therapies and their therapeutic positioning in order to provide practical evidence-based guidance for the management of androgenetic alopecia.
FundingThis article was supported by a grant from Cantabria Labs.
Conflicts of interestA. Gómez Zubiaur has served as a scientific advisor and consultant for Isdin, Olistic, Pfizer, and Cantabria Labs. G. Garnacho-Saucedo declares no conflicts of interest. S. Vañó-Galván has received honoraria for lectures or consultancy work from Pfizer, Lilly, Cantabria Labs, Pierre Fabre, and L’Oréal.
The authors thank Meisys for medical writing support.
