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| Clinical data | |
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| Trade names | Winlevi |
| Other names | CB-03-01; Breezula; 11-Deoxycortisol 17α-propionate; 17α-(Propionyloxy)- deoxycorticosterone; 21-Hydroxy-3,20-dioxopregn-4-en-17-yl propionate |
| AHFS/Drugs.com | Monograph |
| License data | |
| Pregnancy category | |
| Routes of administration | Topical |
| ATC code | |
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| DrugBank | |
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| CompTox Dashboard(EPA) | |
| ECHA InfoCard | 100.210.810 |
| Chemical and physical data | |
| Formula | C24H34O5 |
| Molar mass | 402.531 g·mol−1 |
| 3D model (JSmol) | |
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Clascoterone, sold under the brand nameWinlevi, is anantiandrogen medication which is usedtopically in the treatment ofacne.[5] The medication is used as acream byapplication to the skin, for instance theface andscalp.[6] Clascoterone is an antiandrogen, orantagonist of theandrogen receptor (AR), thebiological target ofandrogens such astestosterone anddihydrotestosterone.[7][8] It shows minimalsystemicabsorption when applied toskin.[6]
Clascoterone was developed by Cassiopea and was approved for medical use in the United States in August 2020.[9][10] The USFood and Drug Administration (FDA) considers it to be afirst-in-class medication.[11]
Clascoterone isindicated for thetopical treatment ofacne vulgaris in people aged twelve years of age and older.[5][12]
Two largephase IIIrandomized controlled trials evaluated the effectiveness of clascoterone for the treatment of acne over a period of 12 weeks.[5][12][13] Clascoterone decreased acne symptoms by about 8 to 18% more thanplacebo.[5][13] The defined treatment success endpoint was achieved in about 18 to 20% of individuals with clascoterone relative to about 7 to 9% of individuals with placebo.[5][12][13] The comparative effectiveness of clascoterone between males and females was not described.[5][13]
The effects of localskin reactions with clascoterone were similar toplacebo in two large phase III randomized controlled trials.[5][13] Suppression of thehypothalamic–pituitary–adrenal axis (HPA axis) may occur during clascoterone therapy in some individuals due to itscortexolonemetabolite.[5][12] HPA axis suppression as measured by thecosyntropin stimulation test was observed to occur in 3 of 42 (7%) of adolescents and adults using clascoterone for acne.[5][12] HPA axis function returned to normal within 4 weeks following discontinuation of clascoterone.[5][12]Hyperkalemia (elevated potassium levels) occurred in 5% of clascoterone-treated individuals and 4% of placebo-treated individuals.[5]
Clascoterone is asteroidal antiandrogen, orantagonist of theandrogen receptor (AR), thebiological target ofandrogens such astestosterone anddihydrotestosterone (DHT).[5][7][8] In abioassay, the topical potency of the medication was greater than that ofprogesterone,flutamide, andfinasteride and was equivalent to that ofcyproterone acetate.[14] Likewise, it is significantly moreefficacious as an antiandrogen than other AR antagonists such asenzalutamide andspironolactone inscalpdermal papillacells andsebocytesin vitro.[8]
Steady-state levels of clascoterone occur within 5 days of twice daily administration.[5] At a dosage of 6 g clascoterone cream applied twice daily,maximal circulating levels of clascoterone were 4.5 ± 2.9 ng/mL,area-under-the-curve levels over the dosing interval were 37.1 ± 22.3 h*ng/mL, andaverage circulating levels of clascoterone were 3.1 ± 1.9 ng/mL.[5] In rodents, clascoterone has been found to possess strong local antiandrogenic activity, but negligible systemic antiandrogenic activity when administered viasubcutaneous injection.[14] Along these lines, the medication is notprogonadotropic in animals.[14]
Theplasma protein binding of clascoterone is 84 to 89% regardless of concentration.[5]
Clascoterone is rapidlyhydrolyzed intocortexolone (11-deoxycortisol) and this compound is a possible primarymetabolite of clascoterone based onin-vitro studies in humanliver cells.[5][12] During treatment with clascoterone, cortexolone levels were detectable and generally below or near the low limit of quantification (0.5 ng/mL).[5] Clascoterone may also produce other metabolites, includingconjugates.[5]
Theelimination of clascoterone has not been fully characterized in humans.[5]
Clascoterone, also known as cortexolone 17α-propionate or 11-deoxycortisol 17α-propionate, as well as 17α,21-dihydroxyprogesterone 17α-propionate or 17α,21-dihydroxypregn-4-en-3,20-dione 17α-propionate, is asyntheticpregnanesteroid and aderivative ofprogesterone and11-deoxycortisol (cortexolone).[15] It is specifically the C17αpropionateester of 11-deoxycortisol.[14]
Ananalogue of clascoterone is9,11-dehydrocortexolone 17α-butyrate (CB-03-04).[16]Corticosteroids related to clascoterone, for instancecortisone acetate andprednisolone acetate, show antiandrogenic activity in animals similarly to clascoterone.[17]
C17α esters of 11-deoxycortisol were unexpectedly found to possess antiandrogenic activity.[14] Clascoterone, also known as cortexolone 17α-propionate, was selected for development based on its optimal drug profile.[14] The medication was approved by the USFood and Drug Administration (FDA) for the treatment of acne in August 2020.[10]
The FDA approved clascoterone based on evidence from two clinical trials (Trial 1/NCT02608450 and Trial 2/NCT02608476) of 1,440 participants 9 to 58 years of age with acne vulgaris.[18] The trials were conducted at 99 sites in the United States, Poland, Romania, Bulgaria, Ukraine, Georgia, and Serbia.[18] Participants applied clascoterone or vehicle (placebo) cream twice daily for 12 weeks.[18] Neither the participants nor the health care providers knew which treatment was being given until after the trial was completed.[18] The benefit of clascoterone in comparison to placebo was assessed after 12 weeks of treatment using the Investigator's Global Assessment (IGA) score that measures the severity of disease (on a scale from 0 to 4) and a decrease in the number of acne lesions.[18]
In April 2025, theEuropean Medicines Agency (EMA) recommended the refusal of a marketing authorization for Winlevi, a medicine intended for treating acne vulgaris.[19] The EMA noted that Winlevi is a new class of medicine that blocks receptors for androgens.[19] However, there is a risk of the medicine suppressing the working of three organs: the hypothalamus and pituitary glands in the brain and adrenal glands.[19] The suppression of these organs could lead to impaired growth and sexual maturation, which is a major concern in adolescents.[19] Although the company presented data to show that the risk was low, the EMA considered that these data, as well as measures the company proposed to minimize the risk, were not sufficient to approve the medicine for people from 12 years of age to less than 18 years of age.[19] In May 2025, Cassiopea requested a re-examination of the EMA's April 2025 opinion.[19]
Clascoterone is theinternational nonproprietary name and theUnited States Adopted Name.[15][20]
Clascoterone has been suggested as a possible treatment forhidradenitis suppurativa (acne inversa), an androgen-dependent skin condition.[21]
It is also under development in a higher concentration for the treatment ofandrogen-dependentscalp hair loss.[22][6]
This article incorporates text from this source, which is in thepublic domain. This article incorporates text from this source, which is in thepublic domain.