antiandrogenic

Antiandrogenic describes a property of substances that oppose the action of androgens, the male sex hormones such as testosterone and dihydrotestosterone (DHT). Antiandrogenicity can occur by blocking androgen receptors, reducing androgen production, or inhibiting conversion of testosterone to DHT.

Mechanisms and examples vary. Androgen receptor (AR) antagonists, such as flutamide, bicalutamide, nilutamide, enzalutamide, and apalutamide, bind the AR and prevent signaling. 5-alpha-reductase inhibitors, including finasteride and dutasteride, decrease the formation of DHT and are used for conditions like benign prostatic hyperplasia and androgenic alopecia. Agents that suppress androgen synthesis include GnRH agonists or antagonists (which lower gonadotropin release and downstream androgen production) and CYP17A1 inhibitors like abiraterone, which reduce androgen synthesis in multiple tissues. Steroidal antiandrogens such as cyproterone acetate combine AR antagonism with progestogenic effects. Some drugs aim to reduce AR signaling by downregulating receptor activity or expression, contributing to their antiandrogenic profile.

Clinical use and considerations. Antiandrogenic therapies are used to treat androgen-dependent conditions, notably prostate cancer and certain hyperandrogenic states in women (such as hirsutism and severe acne). They may also be used in transgender hormone regimens as part of gender-affirming therapy. The choice of agent depends on the condition, desired degree of androgen suppression, and potential side effects.

Common adverse effects can include fatigue, hot flashes, sexual dysfunction, gynecomastia, and liver toxicity with some agents. Long-term use requires monitoring and consideration of risks versus benefits in the individual patient.