Clascoterone (CB-03-01)

Overview

Clascoterone is a non-peptide steroidal topical androgen receptor antagonist—a 17α-propionate ester of cortexolone (11-deoxycortisol). Winlevi (clascoterone 1% cream) is FDA-approved (2020) for topical treatment of acne vulgaris in patients 12 years and older. A higher-strength 5% topical solution (Breezula) has completed Phase 3 trials for male androgenetic alopecia but remains investigational for that indication. Despite established androgen-receptor binding, the FDA label states the mechanism of action for acne treatment is unknown.

Mechanism of Action

Clascoterone is a competitive androgen receptor (AR) antagonist that binds the AR in skin (sebocytes, hair-follicle tissue) and competes with dihydrotestosterone (DHT) for receptor binding, blocking DHT-driven transcription of androgen-responsive genes tied to sebum production and inflammation (in vitro human sebocyte data, Rosette et al. 2019, PMID 31141847). The FDA-approved Winlevi prescribing information states plainly, 'The mechanism of action of WINLEVI cream for the topical treatment of acne vulgaris is unknown' (FDA label, Section 12.1)—so while AR-antagonist binding is established, the clinical mechanism producing the acne benefit is formally unconfirmed per the regulator-reviewed label. Clascoterone does not inhibit skin 5α-reductase (Celasco et al. 2004, PMID 15646372).

Research Summary

Clascoterone is an FDA-approved prescription drug. Winlevi (clascoterone 1% cream) was approved in 2020 for topical treatment of acne vulgaris in patients 12 years of age and older, based on two identical Phase 3 RCTs (NCT02608450, NCT02608476; n=1421, ages 12+) showing IGA success rates of 18.8% and 20.9% for clascoterone vs. 8.7% and 6.6% for vehicle at Week 12. A separate, higher-strength 5% topical solution (Breezula) has completed a Phase 3 trial (SCALP2, NCT05914805, actual enrollment 762) for male androgenetic alopecia; this indication is investigational/unapproved. In hamster flank-organ models (topical antiandrogen bioassay), CB-03-01 showed strong local antiandrogenic activity—roughly 4× more potent than progesterone, ~3× more potent than flutamide, ~2× more potent than finasteride, and approximately equipotent with cyproterone acetate (Celasco et al., 2004, PMID 15646372). In rat subcutaneous injection and parabiotic rat models, no systemic antiandrogenic activity was observed, supporting a peripherally-selective (non-systemic) antiandrogen profile (Celasco et al., 2004). In human primary sebocyte cultures (in vitro), clascoterone dose-dependently suppressed lipid synthesis and inflammatory cytokine production, significantly outperforming spironolactone at inhibiting inflammatory cytokine synthesis (Rosette et al., 2019, PMID 31141847).

Vendors selling Clascoterone (CB-03-01)

Scored vendors carrying Clascoterone (CB-03-01), ranked by trust grade. Grades are computed from indexed Certificates of Analysis. Full $/mg pricing is on the comparison page.

Reported Side Effects

• Local skin reactions: erythema/redness, pruritus, scaling/dryness (7–12% in pivotal trials)
• Edema, stinging, burning at application site (>3%)
• HPA axis suppression (9% adolescents, 5% adults in PK sub-study; reversible)
• Hyperkalemia signal (5% clascoterone vs. 4% vehicle)
• Increased malformations and pregnancy loss in animal reproduction studies at high systemic exposures

Compare Clascoterone (CB-03-01) with Others

Research References

• WINLEVI (clascoterone) Cream, 1% — Highlights of Prescribing Information. 2022.
• Clascoterone, Compound Summary for CID 11750009 (PubChem).
• Biological profile of cortexolone 17alpha-propionate (CB-03-01), a new topical and peripherally selective androgen antagonist. 2004. PMID 15646372.
• Cortexolone 17α-propionate (Clascoterone) Is a Novel Androgen Receptor Antagonist that Inhibits Production of Lipids and Inflammatory Cytokines from Sebocytes In Vitro. 2019. PMID 31141847.

Frequently asked questions

Has Clascoterone (CB-03-01) been independently lab-tested?

Disclosed Labs has collected 2 Certificates of Analysis (COA) for Clascoterone (CB-03-01) from 2 independent testing labs. 1 vendor has submitted material for testing. Products average 98.8% tested purity across the corpus. Full testing data is available at https://www.disclosedlabs.com/peptides/clascoterone/testing.

Where can researchers source Clascoterone (CB-03-01)?

1 vendor with Disclosed Labs trust grades currently list Clascoterone (CB-03-01), including Kimera Chems. Compare live prices and lab-verified COAs at https://www.disclosedlabs.com/prices/clascoterone.

How does Clascoterone (CB-03-01) work?

Clascoterone is a competitive androgen receptor (AR) antagonist that binds the AR in skin (sebocytes, hair-follicle tissue) and competes with dihydrotestosterone (DHT) for receptor binding, blocking DHT-driven transcription of androgen-responsive genes tied to sebum production and inflammation (in vitro human sebocyte data, Rosette et al. 2019, PMID 31141847). The FDA-approved Winlevi prescribing information states plainly, 'The mechanism of action of WINLEVI cream for the topical treatment of acne vulgaris is unknown' (FDA label, Section 12.1)—so while AR-antagonist binding is established, the clinical mechanism producing the acne benefit is formally unconfirmed per the regulator-reviewed label. Clascoterone does not inhibit skin 5α-reductase (Celasco et al. 2004, PMID 15646372).

What does the research say about Clascoterone (CB-03-01)?

Clascoterone is an FDA-approved prescription drug. Winlevi (clascoterone 1% cream) was approved in 2020 for topical treatment of acne vulgaris in patients 12 years of age and older, based on two identical Phase 3 RCTs (NCT02608450, NCT02608476; n=1421, ages 12+) showing IGA success rates of 18.8% and 20.9% for clascoterone vs. 8.7% and 6.6% for vehicle at Week 12. A separate, higher-strength 5% topical solution (Breezula) has completed a Phase 3 trial (SCALP2, NCT05914805, actual enrollment 762) for male androgenetic alopecia; this indication is investigational/unapproved. In hamster flank-organ models (topical antiandrogen bioassay), CB-03-01 showed strong local antiandrogenic activity—roughly 4× more potent than progesterone, ~3× more potent than flutamide, ~2× more potent than finasteride, and approximately equipotent with cyproterone acetate (Celasco et al., 2004, PMID 15646372). In rat subcutaneous injection and parabiotic rat models, no systemic antiandrogenic activity was observed, supporting a peripherally-selective (non-systemic) antiandrogen profile (Celasco et al., 2004). In human primary sebocyte cultures (in vitro), clascoterone dose-dependently suppressed lipid synthesis and inflammatory cytokine production, significantly outperforming spironolactone at inhibiting inflammatory cytokine synthesis (Rosette et al., 2019, PMID 31141847).