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Clascoterone (cortexolone 17-alpha-propionate) is a first-in-class topical androgen receptor inhibitor developed by Cassiopea SpA. In August 2020, the FDA approved Winlevi (clascoterone cream 1%) for the treatment of acne vulgaris in patients aged 12 and older, making it the first new mechanism of action for acne treatment in nearly four decades and the first topical anti-androgen approved for acne in the United States. Clascoterone is also under development as Breezula (clascoterone solution 7.5%) for androgenetic alopecia, where it has completed Phase 3 clinical trials. The compound works by competitively inhibiting androgen receptor activation at the site of application -- the sebaceous gland for acne and the hair follicle for androgenetic alopecia -- without producing the systemic anti-androgenic effects associated with oral anti-androgens such as spironolactone or cyproterone acetate. Its steroidal structure allows it to fit precisely into the androgen receptor binding pocket, and its rapid local metabolism to cortexolone (an inactive metabolite) limits systemic exposure. This pharmacological profile makes clascoterone suitable for use in both men and women, unlike systemic anti-androgens which carry risks of feminization in male patients.

Dutasteride is a potent dual 5-alpha reductase inhibitor that blocks both Type I and Type II isoforms of the enzyme responsible for converting testosterone to dihydrotestosterone (DHT). FDA-approved at 0.5mg daily for benign prostatic hyperplasia (BPH) under the brand name Avodart, it is widely used off-label for the treatment of androgenetic alopecia (male pattern hair loss). By inhibiting both isoforms, dutasteride achieves approximately 90% suppression of serum DHT, compared to roughly 70% with finasteride, which blocks only the Type II isoform. This greater DHT suppression translates to potentially superior hair regrowth outcomes in head-to-head comparisons, though it also carries a somewhat higher risk of DHT-related side effects. Dutasteride has an exceptionally long half-life of approximately 5 weeks, meaning it takes several months to reach steady-state levels and equally long for effects to fully wash out after discontinuation.

Finasteride is an FDA-approved 5-alpha reductase inhibitor that blocks the conversion of testosterone to dihydrotestosterone (DHT), the primary androgen responsible for androgenetic alopecia (male pattern hair loss) and benign prostatic hyperplasia (BPH). At 1mg daily, it reduces scalp DHT levels by approximately 66%, slowing or halting hair loss in roughly 90% of men and producing visible regrowth in about 48% over one to two years. Originally developed for prostate enlargement at 5mg (Proscar), the lower 1mg dose (Propecia) was approved specifically for hair loss in 1997. It remains one of only two FDA-approved oral treatments for androgenetic alopecia and has decades of long-term safety data.

Ketoconazole is an FDA-approved azole antifungal that has gained widespread use as a topical adjunct in hair loss treatment. Available as a 1-2% medicated shampoo, ketoconazole disrupts DHT binding at the hair follicle and reduces scalp inflammation driven by the fungus Malassezia, both of which contribute to follicular miniaturization. It is a core component of the widely referenced "big 3" hair loss stack alongside finasteride and minoxidil. While ketoconazole was originally developed as a systemic antifungal for conditions like fungal infections and seborrheic dermatitis, its topical anti-androgenic properties at the scalp level have made it a practical and low-risk addition to hair loss regimens. When used as a shampoo, systemic absorption is negligible, keeping the side effect profile limited to occasional local irritation.

Minoxidil is an FDA-approved vasodilator originally developed in the 1970s as an oral antihypertensive medication. Its hair growth properties were discovered as a side effect, and topical formulations (2% and 5%) were subsequently approved for the treatment of androgenetic alopecia. It remains one of only two FDA-approved treatments for pattern hair loss and is available over the counter in most countries. In recent years, off-label oral minoxidil at low doses (0.625-5mg) has gained significant traction among dermatologists and the biohacker community as a more convenient and potentially more effective alternative to topical application, particularly for individuals who find the topical formulation inconvenient or who experience scalp irritation.

PP405 is an investigational topical drug developed by Pelage Pharmaceuticals for the treatment of androgenetic alopecia. Based on research conducted at UCLA, PP405 works through a fundamentally different mechanism than existing hair loss treatments: rather than blocking androgens like finasteride or promoting blood flow like minoxidil, it targets the metabolic dormancy of hair follicle stem cells directly. By inhibiting the mitochondrial pyruvate carrier (MPC1/MPC2), PP405 causes pyruvate accumulation in hair follicle stem cells, stimulating lactate dehydrogenase activity and triggering a metabolic shift that reactivates dormant follicles. Phase 2a clinical trial results showed increased hair count and thickness with a 0.05% gel formulation applied once daily. As of 2025, the drug has completed Phase 2a trials, with Phase 3 trials planned for 2026.

RU-58841 is a non-steroidal anti-androgen originally developed by Roussel Uclaf (later Hoechst Marion Roussel) in the 1970s-80s for topical treatment of androgen-dependent conditions including acne and androgenetic alopecia. It works by competitively binding to androgen receptors at the hair follicle, blocking the effects of dihydrotestosterone (DHT) locally without significantly reducing systemic androgen levels. Development was abandoned after Phase II clinical trials, and the compound was never submitted for regulatory approval. Despite this, RU-58841 has developed a substantial following in the hair loss community, where users source it as a raw research chemical and prepare their own topical solutions. Its extremely short systemic half-life means that even if absorbed through the skin, it is rapidly metabolized, limiting systemic anti-androgenic effects. However, the lack of completed clinical trials means its long-term safety profile remains unknown.