Androgenetic alopecia (AGA) is the most common form of hair loss, affecting both men and women, and is primarily driven by genetic follicular sensitivity to androgens, particularly dihydrotestosterone (DHT).^[1] Testosterone is converted to DHT by 5α-reductase, with Type I expressed in hair follicles and sebaceous glands and Type II predominantly in the prostate, genitalia, and hair follicles. DHT promotes progressive follicular miniaturization, making androgen suppression a key therapeutic strategy. Finasteride, a selective Type II 5α-reductase inhibitor, is an established first-line DHT-blocking therapy with demonstrated long-term efficacy and safety, although 30–45% of patients may have a suboptimal response.^[2] Dutasteride inhibits both Type I and Type II 5α-reductase, producing greater DHT suppression, greater improvements in hair count, scalp coverage, and patient satisfaction; a 0.5-mg/day regimen is used in clinical practice.^[3] Emerging androgen-targeted approaches include clascoterone, pyrilutamide, bicalutamide, and spironolactone, although their evidence and clinical roles differ. Dutasteride’s high lipophilicity and formulation-dependent pharmacokinetic considerations further emphasize the importance of appropriate drug delivery. Overall, DHT suppression remains a central strategy for slowing miniaturization and supporting hair regrowth in AGA.