Asteroidogenesis inhibitor, also known as asteroid biosynthesis inhibitor, is a type ofdrug whichinhibits one or more of theenzymes that are involved in the process ofsteroidogenesis, thebiosynthesis ofendogenoussteroids andsteroid hormones.^[1] They may inhibit the production ofcholesterol and othersterols,sex steroids such asandrogens,estrogens, andprogestogens,corticosteroids such asglucocorticoids andmineralocorticoids, andneurosteroids.^[1][2] They are used in the treatment of a variety ofmedical conditions that depend on endogenous steroids.^[1]

Steroidogenesis inhibitors are analogous in effect and use toantigonadotropins (which specifically inhibitgonadal sex steroid production), but work via a differentmechanism of action; whereas antigonadotropins suppress gonadal production of sex steroids by effectingnegative feedback on and thereby suppressing thehypothalamic–pituitary–gonadal axis, steroidogenesis inhibitors directly inhibit the enzymatic biosynthesis of steroids.^[1]

• HMG-CoA reductase (HMGCR) inhibitors, also known as statins, prevent the conversion ofHMG-CoATooltip 3-hydroxy-3-methylglutaryl-coenzyme A intomevalonic acid, a relatively early step in the biosynthesis of cholesterol fromacetyl coenzyme A (acetyl-CoA), and thereby decrease cholesterol levels.^[3] Examples of statins includeatorvastatin,lovastatin,rosuvastatin, andsimvastatin.^[3] They are used in the treatment ofhypercholesterolemia for the purpose of lowering the risk ofatherosclerosis-relatedcardiovascular disease.^[3]

• Farnesyl pyrophosphate synthase (FPPS) inhibitors prevent the conversion ofisopentenyl pyrophosphate (IPP) intofarnesyl pyrophosphate (FPP), a mid-range step in the biosynthesis of cholesterol from acetyl-CoA, and thereby inhibit cholesterol production.^[4][5] They notably do not significantly lowercirculating levels of cholesterol however, and hence, unlike statins, are not suitable for the treatment of hypercholesterolemia.^[6] The main examples of FPPS inhibitors arenitrogenousbisphosphonates such asalendronate,ibandronate,pamidronate,risedronate, andzoledronate, which are used in the treatment ofosteoporosis.^[4][5]

• Other early-stage cholesterol synthesis inhibitors likecolestolone.^[7][8][9]

• 7-Dehydrocholesterol reductase (7-DHCR) inhibitors such asAY-9944 andBM-15766 inhibit the production of cholesterol from7-dehydrocholesterol, one of the last steps in cholesterol biosynthesis.^[10][11]Loss-of-function mutations in thegene encoding 7-DHCR result inSmith–Lemli–Opitz syndrome (SLOS) and dramatic accumulation of7-dehydrocholesterol.^[10][11] 7-DHCR inhibitors produce an acquired form of SLOS in animals, and as such, like 24-DHCR inhibitors (see below), are probably tootoxic to be used clinically.^[10][11]

• 24-Dehydrocholesterol reductase (24-DHCR) inhibitors such asazacosterol andtriparanol inhibit the production of cholesterol fromdesmosterol, one of the last steps in cholesterol biosynthesis, and were formerly used to treat hypercholesterolemia, but were withdrawn from the market due to toxicity caused by accumulation of desmosterol in tissues.^[12][13]

• Cholesterol side-chain cleavage enzyme (P450scc, CYP11A1) inhibitors such asaminoglutethimide,^[15]ketoconazole,^[16] andmitotane^[16] inhibit the production ofpregnenolone from cholesterol and thereby prevent the synthesis of all steroid hormones.^[17][15] They have been used to inhibitcorticosteroid synthesis in the treatment ofCushing's syndrome andadrenocortical carcinoma,^[18] and ketoconazole has also been used to inhibit androgen production in the treatment ofprostate cancer.^[15][19]

• 3β-Hydroxysteroid dehydrogenase (3β-HSD) inhibitors such asamphenone B,^[20]azastene,cyanoketone,epostane,mitotane,^[16] andtrilostane inhibit the conversion of Δ⁵-3β-hydroxysteroids into Δ⁴-3-ketosteroids and thereby inhibit the production of most of the steroid hormones.^[21] Due to inhibition ofprogesterone biosynthesis, they have been investigated ascontraceptives andabortifacients (though ultimately have never been marketed for this indication),^[21] and trilostane was formerly used to inhibit corticosteroid synthesis in the treatment of Cushing's syndrome.^[22]

• 17α-Hydroxylase/17,20-lyase (CYP17A1) inhibitors such asabiraterone acetate,etomidate,^[16]galeterone,ketoconazole,^[16] andorteronel inhibit the production of androgens and glucocorticoids and are used to reduce androgen levels in the treatment of prostate cancer.^[17][23] Selective 17,20-lyase inhibitors such asseviteronel inhibit only androgen production without affecting glucocorticoid synthesis and are under development for the treatment of prostate cancer.^[24]

• 21-Hydroxylase (CYP21A2) inhibitors prevent the production of corticosteroids fromprogesterone and17α-hydroxyprogesterone.^[17]

• 11β-Hydroxylase (CYP11B1) inhibitors such asamphenone B,^[20]etomidate,^[16]ketoconazole,^[16]metyrapone,^[16]mitotane,^[16] andosilodrostat^[25] inhibit the production of the potent corticosteroidscortisol,corticosterone, andaldosterone from the less potent corticosteroids11-deoxycorticosterone and11-deoxycortisol and are used in the diagnosis and treatment of Cushing's syndrome.^[17]

• Aldosterone synthase (CYP11B2) inhibitors such asmetyrapone,^[26]mitotane,^[16] andosilodrostat^[25] prevent the production of the potent mineralocorticoid aldosterone from the less potent mineralocorticoid corticosterone.^[17] Osilodrostat was investigated for the treatment ofhypertension,heart failure, andrenal disease, but development for these indications was discontinued.^[25]

• 17β-Hydroxysteroid dehydrogenase (17β-HSD) inhibitors prevent thereversible conversion of the weak androgensdehydroepiandrosterone (DHEA) and4-androstenedione into the more potent androgentestosterone and the weak estrogenestrone into the more potent estrogenestradiol.^[27]

• 5α-Reductase inhibitors (5-ARIs) such asfinasteride,dutasteride,epristeride, andalfatradiol^[28] prevent the conversion oftestosterone into the more potent androgendihydrotestosterone (DHT) and are used in the treatment ofbenign prostatic hyperplasia (BPH) andandrogenic alopecia (pattern hair loss).^[29] These drugs alsoinhibit the formation of neurosteroids such asallopregnanolone,tetrahydrodeoxycorticosterone (THDOC), and3α-androstanediol from progesterone, 11-deoxycorticosterone, and DHT, respectively, which may contribute toside effects such asdepression andsexual dysfunction.^[2]

• Aromatase inhibitors (AIs) such asaminoglutethimide,anastrozole,exemestane,letrozole, andtestolactone inhibit the production of estrogens from androgens and are used mainly in the treatment ofestrogen receptor-positivebreast cancer.^[30]

• Steroid sulfotransferase (SST) inhibitors prevent the conversion of steroid hormones such as estrone and DHEA into hormonally inactive steroidsulfates.^[31] Although hormonally inactive, some steroid sulfates, such aspregnenolone sulfate andDHEA sulfate, are importantneurosteroids.^[32][33]

• Steroid sulfatase (STS) inhibitors such asestradiol sulfamate,estrone sulfamate,irosustat, anddanazol^[34] inhibit the conversion of steroid sulfates such asestrone sulfate andDHEA sulfate into their hormonally active forms.^[35][36] They have potential applications in the treatment ofbreast cancer andendometriosis, and are currently under investigation for such indications.^[35][36]

• Lanosterol 14α-demethylase (CYP51A1) inhibitors such asclotrimazole,fluconazole,itraconazole,ketoconazole,miconazole, andvoriconazole prevent the production ofergosterol fromlanosterol.^[17][37] Ergosterol is absent in animals but is an essential component of thecell membranes of manyfungi andprotozoa, and so lanosterol 14α-demethylase inhibitors are used asantifungals andantiprotozoals in the treatment ofinfections.^[37]

• Steroidogenic enzyme
• Neurosteroidogenesis inhibitor

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• Steroidogenesis inhibitors

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