Abstract
Background
Dutasteride, a 5-alpha reductase inhibitor, is prescribed for male androgenetic alopecia (AGA) in Korea and Japan. Despite its efficacy, its use is limited by its long half-life, potent dihydrotestosterone suppression, and adverse effects.
Objective
To investigate the efficacy and safety of 0.2 mg dutasteride for male AGA.
Methods
Patients with male AGA were randomized to receive 0.2 mg dutasteride, placebo, or 0.5 mg dutasteride (2:2:1) once daily for 24 weeks. Safety and efficacy endpoints were assessed.
Results
Overall, 139 men were analyzed. At week 24, the change in hair count within the target area at the vertex from baseline was significantly higher in the 0.2 mg dutasteride group than in the placebo group (21.53 vs. 5.96, p=0.0072). Dutasteride (0.2 mg) treatment led to greater hair growth improvement, as assessed by investigators at week 24 (p=0.0096) and an independent panel at weeks 12 and 24 (p=0.0306, p=0.0001). For all efficacy endpoints, 0.2 mg dutasteride was as effective as 0.5 mg dutasteride. The incidence of adverse events was low and not statistically different between the 0.2 mg dutasteride and placebo groups. The limitation of this study is the limited number of participants.
Conclusion
Low-dose (0.2 mg) dutasteride for male AGA showed significant efficacy and favorable safety profile.
Trial Registration
ClinicalTrials.gov Identifier: NCT04825561
Keywords: 5-Alpha reductase inhibitor, Androgenic alopecia, Dutasteride
INTRODUCTION
Androgenetic alopecia (AGA) is a progressive hair loss disorder influenced by androgens and characterized by strong genetic predisposition1. AGA is the most common form of hair loss after puberty, and its incidence increases with age2,3. The pathophysiology of AGA involves the conversion of testosterone to the more potent androgen dihydrotestosterone (DHT) by 5-alpha reductase4,5. DHT binds to androgen receptors in hair follicles, causing miniaturization and a shortened anagen phase, leading to hair loss in the frontoparietal and vertex areas6.
Current treatments for AGA include oral finasteride (a type II 5-alpha reductase inhibitor) and topical minoxidil (a vasodilator), which are the only 2 widely used drugs approved by the US Food and Drug Administration7. Dutasteride, a more recent 5-alpha reductase inhibitor, is considerably more potent than finasteride and can reduce serum DHT levels by up to 92%8. Despite its effectiveness, its use is limited to off-label applications in several parts of the world because of its longer half-life and more potent DHT suppression, raising concerns about its adverse effects9,10. Dutasteride was approved for AGA treatment in South Korea and Japan in 2009 and 2015, respectively; however, only the 0.5-mg dose is available11,12,13.
Hair loss can cause significant psychological burden on AGA patients; some suffer from anxiety, depression, and negative body image14. This psychological distress leads to decreased quality of life15,16. Over half of patients with AGA are not satisfied with their treatment, underscoring an unmet need for effective treatment17. While dutasteride may serve an alternative treatment option to finasteride, its adverse effects limit its widespread use. This calls for diversifying the available dose, presuming that the lower the dose, the lower the rate of adverse effects.
Previous studies reported that 0.1 mg dutasteride increased the hair count in patients with AGA18. Given the dose-dependent nature of its effects, we hypothesized that a lower dose of dutasteride (0.2 mg) would be effective in promoting hair growth and slowing disease progression while maintaining a better safety profile. Therefore, we conducted this multicenter, randomized, double-blind, placebo-controlled, parallel-group phase III study to investigate the efficacy and safety of 0.2 mg dutasteride over 24 weeks in male patients with AGA.
MATERIALS AND METHODS
Study design
This multicenter, randomized, double-blind, placebo-controlled, parallel-group phase 3 clinical trial was conducted at 11 centers in Korea from June 2021 to January 2023 and was registered at ClinicalTrials.gov (NCT04825561). After an initial screening, 139 men were randomized to receive 0.2 mg dutasteride, placebo, or 0.5 mg dutasteride (2:2:1) daily for 24 weeks. For efficacy comparison, 0.5 mg dutasteride, which is approved for AGA treatment in Korea, was included as an exploratory group.
This study was conducted in accordance with the principles embodied in the Declaration of Helsinki. The study protocol and all amendments were approved by the Institutional Review Board (IRB) of Eunpyeong St. Mary’s Hospital (IRB protocol approval no. PC21MDDT0001; approval date: March 04, 2021) and all other participating institutions. Written informed consent was obtained from all patients prior to their participation.
Study participants
Male patients aged 18–50 years with AGA classified as basic type M2–3 or C2–3 and specific type V1–3 or F1–3 (excluding types M2 and M3 only) based on the BASP classification were screened. Detailed inclusion and exclusion criteria are listed in Supplementary Data 1.
Outcomes
The primary efficacy endpoint was the change in hair count within a 1 cm2 target area at the vertex at 24 weeks, with a 1-mm hair tattoo as a marker. The secondary endpoints were as follows: (i) change in the hair count at the vertex from baseline at 12 weeks; (ii) change in the average thickness of the 5 thickest hairs within the target area from baseline at 12 and 24 weeks; (iii) global photographic assessment of hair growth at 12 and 24 weeks by an independent panel and study site investigators using a 7-point rating scale (−3 to +3) to grade changes in hair growth; and (iv) participants’ self-assessment of hair growth change from baseline to 12 and 24 weeks using a questionnaire encompassing changes in hair loss (Q1), hair loss progression (Q2), overall appearance of hair thickness, texture, and volume (Q3), and hair maintenance (Q4). This was graded on a 7-point Likert scale. The full version of the questionnaire is provided in Supplementary Data 2.
Serum testosterone and DHT levels were measured at baseline, 12 weeks, and 24 weeks. Safety outcomes were the number of treatment-emergent adverse events (TEAEs) and adverse events (AEs) of special interest (sexual dysfunction and breast abnormalities). Safety assessments included a detailed history, physical examination, vital signs, electrocardiography, and laboratory tests at each visit. Patients were followed up until the last visit or resolution of AEs or when no further follow-up was deemed necessary.
Statistical analyses
For continuous variables, data were summarized as means with standard deviations or as medians with ranges (minimum, maximum). Between-group differences were analyzed using a 2-sample t-test or Wilcoxon rank-sum test, whereas intragroup changes were examined using a paired t-test or Wilcoxon signed-rank test. For categorical variables, data were presented as the number of patients and percentages. Between-group differences were analyzed using Pearson’s χ2 test or Fisher’s exact test. The full analysis set (FAS) was used as the primary population for the efficacy endpoints. Analysis of covariance was conducted on the changes in hair count, hair thickness, and serum total testosterone and DHT levels, with baseline values as covariates. AEs were coded using MedDRA version 25.1. All statistical analyses were performed using SAS statistical analysis software version 9.4 (SAS Institute Inc., Cary, NC, USA).
RESULTS
Baseline demographics
Out of 190 patients screened, 139 men from 11 centers were randomized, and 135 completed the study (Fig. 1). The median age of participants was 39.84 years, and the median disease was 79.81 months. No participant had a history of 5-alpha reductase inhibitor use prior to the study. No significant differences in participants’ demographics or baseline characteristics were observed among the treatment groups (Table 1).
Fig. 1. Patient disposition.
Table 1. Baseline characteristics.
| Characteristics | Placebo (n=55) | 0.2 mg dutasteride (n=56) | 0.5 mg dutasteride (n=28) | p-value* | |
|---|---|---|---|---|---|
| Age (yr) | 40.5 (7.5) | 39.5 (7.0) | 39.3 (7.3) | 0.3740 | |
| 18 to <30 | 5 (9.1) | 7 (12.5) | 2 (7.1) | ||
| 30 to <40 | 18 (32.7) | 13 (23.2) | 11 (39.3) | ||
| 40 to 49 | 32 (58.2) | 36 (64.3) | 15 (53.6) | ||
| Body weight (kg) | 77.65±12.3 | 80.35±14.8 | 78.1±11.4 | 0.2983 | |
| BMI (kg/m2) | 25.7±3.9 | 26.95±5.5 | 25.9±3.2 | 0.2278 | |
| Time since diagnosis (mo) | 52.9 (0.0, 245.8) | 69.4 (0.0, 270.2) | 77.7 (0.0, 245.9) | 0.9786 | |
| BASP | 0.4659 | ||||
| M2–3V1–3 | 31 (56.4) | 37 (66.1) | 19 (67.9) | ||
| M2–3F1–3 | 14 (25.5) | 14 (25.0) | 6 (21.4) | ||
| C2–3 | 2 (3.6) | 2 (3.6) | 1 (3.6) | ||
| C2–3V1–3 | 5 (9.1) | 3 (5.4) | 2 (7.1) | ||
| C2–3F1–3 | 3 (5.5) | 0 (0) | 0 (0) | ||
| Family history | 38 (71.7) | 47 (83.9) | 26 (92.9) | 0.1235 | |
| Paternal | 31 (81.6) | 36 (76.6) | 23 (88.5) | ||
| Maternal | 4 (10.5) | 7 (14.9) | 1 (3.8) | ||
| Both | 3 (7.9) | 4 (8.5) | 2 (7.7) | ||
Data are presented as number (%), mean ± standard deviation, or median (minimum, maximum).
BMI: body mass index, BASP: basic and specific.
*The p-values were calculated between the placebo and 0.2 mg dutasteride only.
Efficacy endpoints
1) Hair count
Low-dose (0.2 mg) dutasteride treatment significantly increased the hair count in male patients with AGA. At week 24, the least squares (LS) mean change in the hair count within target area from baseline was 22.38 hairs/cm2 in the 0.2 mg dutasteride group, 5.09 hairs/cm2 in the placebo group, and 15.86 hairs/cm2 in the 0.5 mg dutasteride group. The increase in hair count was significantly higher in the 0.2 mg dutasteride group than in the placebo group at week 24 (95% confidence interval [CI], 4.30, 26.83; p=0.0072) (Figs. 2 and 3A). The 0.2 mg dutasteride group showed a greater increase in the LS mean hair count from baseline, compared to the 0.5 mg dutasteride treated group. However, when the per-protocol set (PPS) was analyzed, no difference was found between the 0.2 mg and 0.5 mg dutasteride groups at week 24 (95% CI, −7.22, 20.78; p=0.3379) (Supplementary Fig. 1).
Fig. 2. Change in the hair count. Change in the LS mean hair count within the target area (1 cm2) at the vertex from baseline.
LS: least squares, ANCOVA: analysis of covariance.
*The presented LS mean (standard error) values are based on the full analysis set.
†ANCOVA test using baseline values as covariate for difference between dutasteride 0.2 mg and placebo groups.
‡ANCOVA test using baseline values as covariate for difference between dutasteride 0.2 mg and dutasteride 0.5 mg groups.
§ANCOVA test using baseline values as covariate for difference between dutasteride 0.5 mg and placebo groups.
Fig. 3. Change in the hair count and thickness. Placebo-adjusted LS mean (A) hair count change and (B) hair thickness (μm) change from baseline.
FAS: full analysis set, PPS: per-protocol set, LS: least squares, CI: confidence interval.
2) Hair thickness
Treatment with 0.2 mg and 0.5 mg dutasteride did not improve the hair thickness. The mean change in the average thickness from baseline showed no significant difference between the 0.2 mg dutasteride and placebo groups at week 12 (95% CI, −1.71, 7.05; p=0.2296) and week 24 (95% CI, −1.56, 8.66; p=0.1712) in the FAS (Fig. 3B). However, hair thickness exhibited an increasing trend.
3) Photographic assessment by the investigators and an independent expert panel
Low-dose dutasteride significantly improved the hair growth change from baseline at week 24, as photographically assessed by the investigators (p=0.0096). The mean assessment score was 1.00 for the 0.2 mg dutasteride group, which was significantly higher than the mean assessment score of 0.57 for placebo group (p=0.0096). Specifically, the proportions of positive scores (≥1) for the photographic evaluation by the investigators were greater in the 0.2 mg dutasteride group (70.9%) than in the placebo group (47.2%) (Supplementary Fig. 2). The average score of the 0.5 mg dutasteride group was 1.39, which was not significantly different from that of the 0.2 mg dutasteride group (p=0.1076). Assessment by the independent panel showed similar results. The score of the 0.2 mg dutasteride group was superior to that of the placebo group in the independent photographic assessment of hair growth change from baseline at week 24 (0.40 vs. −0.34, p<0.0001). No between-group difference was found between the 0.2 mg and 0.5 mg dutasteride groups.
4) Participants’ self-assessment
With respect to participants’ self-assessment, 0.2 mg dutasteride treatment improved the patients’ evaluation regarding the overall change (Q3) in hair thickness, texture, and volume at week 24 (1.09 vs. 0.70, p=0.0302). The 0.2 mg dutasteride and placebo groups showed no significant differences in participants’ self-assessment of the change in hair loss (Q1), hair loss progression (Q2), and hair maintenance (Q4).
5) Serum androgen levels
Low-dose (0.2 mg) dutasteride significantly decreased the serum DHT levels without altering the serum testosterone levels compared to placebo; this change was evident from week 12 and maintained over 24 weeks (p<0.0001, p=0.0001). Serum DHT levels seemed to decrease in a dose-dependent manner; compared to 0.5 mg, the DHT suppression effect by 0.2 mg was significantly lower (−115.79 vs. −186.22; 95% CI, 4.57, 136.30; p=0.0364) (Fig. 4). As a counterbalance mechanism, the increase in testosterone levels was greater in the dutasteride-treated group than in the placebo group at week 12; however, the change soon became non-significantly different from that in the placebo group at week 24 (95% CI, 0.10, 1.12; p=0.0192 and 95% CI, −0.12, 0.92; p=0.1281).
Fig. 4. Serum androgen levels. Mean serum (A) total testosterone and (B) DHT levels. The error bars denote the standard deviations.
DHT: dihydrotestosterone.
Safety
Out of 139 participants, 29 (20.86%) reported 50 TEAEs (Table 2). Most TEAEs were mild, with erectile dysfunction being the most common symptom (10/139, 7.19%), followed by ejaculation disorder (3/139, 2.16%) and increased alanine aminotransferase levels (3/139, 2.16%). There were no statistically significant differences in the incidence of AEs between treatment and placebo groups. Three serious AEs were reported: duodenal ulcer and meniscal injury (n=1) in the 0.2 mg dutasteride group and hemorrhoids (n=1) in the placebo group; none were drug-related. One patient withdrew from the study because of erectile dysfunction.
Table 2. Summary of adverse event and list of adverse drug reactions.
| Characteristics | Placebo (n=55) | 0.2 mg dutasteride (n=56) | 0.5 mg dutasteride (n=28) | |
|---|---|---|---|---|
| Any AEs | 12 (21.8) [21] | 9 (16.1) [12] | 8 (28.6) [17] | |
| Mild | [20] | [10] | [17] | |
| Moderate | [1] | [1] | - | |
| Severe | - | [1] | - | |
| Serious AEs | 1 (1.8) [1] | 2 (3.6) [2] | - | |
| ADRs | 6 (10.9) [8] | 4 (7.1) [4] | 6 (21.4) [12] | |
| Erectile dysfunction | 4 (7.3) [4] | 2 (3.6) [2] | 4 (14.3) [4] | |
| Ejaculation disorder | 1 (1.8) [1] | - | 2 (7.1) [2] | |
| Sexual dysfunction | - | - | 1 (3.6) [2] | |
| Increased alanine aminotransferase levels | - | 1 (1.8) [1] | 2 (7.1) [2] | |
| Increased aspartate aminotransferase levels | 1 (1.8) [1] | - | 1 (3.6) [1] | |
| Increased blood lactate dehydrogenase | 1 (1.8) [1] | - | - | |
| Decreased semen volume | - | 1 (1.8) [1] | - | |
| Epididymitis | - | - | 1 (3.6) [2] | |
| Decreased libido | - | - | 1 (3.6) [2] | |
| Laryngeal disorder | 1 (1.8) [1] | - | - | |
| Adverse events of special interest | 4 (7.3) [5] | 3 (5.4) [3] | 5 (17.9) [9] | |
| Decreased libido | - | - | 1 (3.6) [2] | |
| Erectile dysfunction | 4 (7.3) [4] | 2 (3.6) [2] | 4 (14.3) [4] | |
| Ejaculation disorder | 1 (1.8) [1] | - | 2 (7.1) [2] | |
| Gynecomastia | - | - | - | |
| Breast tenderness | - | - | - | |
The MedDRA terminology has been changed to American spelling. Data are presented as the number of patients who experienced adverse events (%). Numbers within square brackets represent the number of events.
AE: adverse event, ADR: adverse drug reaction.
The incidence of AEs of special interest was low in the 0.2 mg dutasteride group, as reported by 3 patients (3/56, 5.36%): erectile dysfunction (2/56, 3.57%) and ejaculation disorder (1/56, 1.79%). In the 0.5 mg dutasteride group, 5 patients (5/28, 17.86%) reported 9 AEs of special interest: decreased libido (2/28, 7.14%), erectile dysfunction (4/28, 14.29%), and ejaculation disorder (2/28, 7.14%). No significant differences were observed between the treatment and placebo groups.
DISCUSSION
Low-dose (0.2 mg) dutasteride showed significant efficacy in increasing the hair count in male patients with AGA over 24 weeks, with statistically significant improvements compared to placebo. At week 24, the change in the hair count within the target area from baseline was 22.38 hairs/cm2 in patients treated with 0.2 mg dutasteride, which was significantly higher than that in the placebo group (p=0.0072).
Patients treated with 0.2 mg dutasteride exhibited multidimensional positive outcomes, showing greater improvement in hair growth, as assessed by an independent panel at weeks 12 and 24 and by the study site investigators at week 24. Improvements in overall hair thickness, texture, and volume were also subjectively perceived.
Our FAS dataset showed that the 0.2 mg dutasteride group had a greater increase in LS mean hair count from baseline at 24 weeks than the 0.5 mg dutasteride group, although this was not statistically significant. These seemingly misleading data can be explained in 2 ways. First, the difference became negligible in the PPS analysis, likely because of the small sample size. Second, at week 12, the mean hair count for 0.5 mg dutasteride was greater than that for 0.2 mg dutasteride; nevertheless, this trend was reversed at week 24, with a decrease in hair count in the 0.5 mg dutasteride group (Supplementary Fig. 3). A similar trend was observed in previous study19. Therefore, we concluded that there was no significant difference between 0.2 mg and 0.5 mg dutasteride and that low-dose (0.2 mg) dutasteride was equally effective as 0.5 mg dutasteride.
Gubelin Harcha et al.18 reported that the change in the hair count within the target area from baseline was 63.0 and 89.6 in patients treated with 0.1 mg and 0.5 mg dutasteride, respectively, at week 24. After adjustment to a 1-cm-diameter circle, the change in the hair count was estimated to be 12.45–17.71 in patients treated with 0.2 mg dutasteride. The observed efficacy of the 0.2-mg dose in our study exceeded this estimate, indicating a potential nonlinear dose-response relationship.
Low-dose (0.2 mg) dutasteride effectively reduced the serum DHT levels without significantly affecting the testosterone levels over 24 weeks. The 0.2 mg dutasteride group showed a significant reduction in serum DHT levels from week 12, which was maintained over 24 weeks. In response, serum testosterone levels increased significantly compared to placebo at week 12 but became insignificant at week 24. Our data suggest the dose-dependent effect of DHT suppression, as the serum DHT levels decreased significantly more in the 0.5 mg dutasteride group than in the 0.2 mg dutasteride group in the FAS. The 0.2-mg dose effectively increased the hair count with less impact on serum DHT levels.
Consistent with previous reports, 0.2 mg dutasteride once daily for 24 weeks was well-tolerated8,18,20. In our study, the 0.2 mg dutasteride group did not significantly differ from the placebo group in terms of AEs. Most AEs were mild. One patient treated with 0.2 mg dutasteride developed erectile dysfunction and withdrew from the trial. Nevertheless, erectile dysfunction was frequently reported in the placebo and 0.2 mg dutasteride groups (7.3% vs. 3.6%), suggesting no strong link between AEs and the study drug.
A previous meta-analysis measuring the relative effectiveness of AGA treatments showed that 0.5 mg dutasteride once daily was the most effective option for AGA despite concerns about sexual dysfunction21,22,23,24. Our study showed that the incidence of TEAEs and AEs of special interest was low in low-dose-treated patients, with no statistical difference from the placebo group. This is consistent with a previous study reporting no statistical difference in incidence of sexual dysfunction between 0.5 mg dutasteride and 1 mg finasteride group22.
Low-dose 0.2 mg dutasteride led to positive improvements in hair count, photographic assessment, and subjective hair change without compromising safety. This supports the potential of lower-dose dutasteride as a viable treatment option with reduced side effects, providing more options for patient-specific risk-benefit assessments.
Our findings suggest that lower doses can achieve therapeutic benefits while minimizing adverse effects. However, the small sample size and restrictions on Korean male patients limit the results’ generalizability. Further research with larger, more diverse populations and longer follow-up periods is necessary to confirm these findings and assess their long-term safety and efficacy.
Low-dose (0.2 mg) dutasteride showed promise as treatment for male AGA, providing a potential alternative to higher doses with fewer side effects. Future studies should focus on expanding on these findings to explore the long-term benefits and risks of low-dose dutasteride therapy.
Footnotes
FUNDING SOURCE: This study was sponsored by Addpharma Co., Ltd., Yuhan Corporation, Daewoong Pharmaceutical Co., Ltd., KYUNG DONG Pharm. Co., Ltd., YU & Life Science Co., Ltd., HANDOK Inc.
CONFLICTS OF INTEREST: The trial was designed by the sponsor, Addpharma Co., Ltd., which collected and analyzed the data.
DATA SHARING STATEMENT: The data that support the findings of this study are available from the corresponding author upon reasonable request.
SUPPLEMENTARY MATERIALS
Full inclusion and exclusion criteria
Self-assessment of hair improvement
Change in the hair count within the target area (1 cm2) at the vertex from baseline in the FAS and PPS.
Global photographic assessment. Results of global photographic assessment by (A) the investigators and (B) the independent expert panel. (C) Results of patients’ self-assessment.
Mean number of hairs in the target area (1 cm2) at the vertex at weeks 12 and 24.
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Associated Data
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Supplementary Materials
Full inclusion and exclusion criteria
Self-assessment of hair improvement
Change in the hair count within the target area (1 cm2) at the vertex from baseline in the FAS and PPS.
Global photographic assessment. Results of global photographic assessment by (A) the investigators and (B) the independent expert panel. (C) Results of patients’ self-assessment.
Mean number of hairs in the target area (1 cm2) at the vertex at weeks 12 and 24.