General side effects of NSAAs, including<unk> , include gynecomastia, breast pain/tenderness, hot flashes (67%), depression, fatigue, sexual dysfunction (including loss of libido and erectile dysfunction), decreased muscle mass, and decreased bone mass with an associated increase in fractures. Also, nausea (24–27%), vomiting, constipation (20%), and insomnia (16%) may occur with<unk> .<unk>  monotherapy is known to eventually induce gynecomastia in 40 to 80% of men treated with it for prostate cancer, usually within 6 to 9 months of treatment initiation. Relative to other NSAAs,<unk>  has been uniquely associated with mild and reversible visual disturbances (31–58%) including delayed ocular adaptation to darkness and impaired color vision, a disulfiram-like alcohol intolerance (19%), interstitial pneumonitis (0.77–2.4%) (which can result in dyspnea (1%) as a secondary effect and can progress to pulmonary fibrosis), and hepatitis (1%), and has a higher incidence of nausea and vomiting compared to other NSAAs. The incidence of interstitial pneumonitis with<unk>  has been found to be much higher in Japanese patients (12.6%), warranting particular caution in Asian individuals. There is a case report of simultaneous liver and lung toxicity in a<unk> -treated patient. There is also a risk of hepatoxicity with<unk> , though occurrence is very rare and the risk is significantly less than with flutamide. The incidence of abnormal liver function tests (e.g., elevated liver enzymes) has been variously reported as 2 to 33% with<unk> . For comparison, the risk of elevated liver enzymes has been reported as 4 to 62% in the case of flutamide. The risk of hepatotoxicity with<unk>  has been described as far less than with flutamide. Fulminant hepatic failure has been reported for<unk> , with fatal outcome. Between 1986 and 2003, the numbers of published cases of hepatotoxicity for antiandrogens totaled 46 for flutamide, 21 for cyproterone acetate, 4 for<unk> , and 1 for bicalutamide. Similarly to flutamide,<unk>  exhibits mitochondrial toxicity in hepatocytes by inhibiting respiratory complex I (NADH ubiquinone oxidoreductase) (though not respiratory complexes II, III, or IV) in the electron transport chain, resulting in reduced ATP and glutathione production and thus decreased hepatocyte survival. The nitro group of<unk>  has been theorized to be involved in both its hepatotoxicity and its pulmonary toxicity.
Nilutamide
Darolutamide
Acetothiolutamide
Apalutamide
Bicalutamide
Topilutamide
Flutamide
Enzalutamide