Bromantane and Trenbolone Interaction: Avoid | Peptide Database

Selectively induces apoptosis in senescent cells while sparing healthy tissue. Restores tissue homeostasis and function in naturally aged animal models. Improved fitness, mobility, and physical appearance in aged mice. Restored renal function in aged and fast-aging mouse models. Improved testicular microenvironment and testosterone secretion in aged mice. Removes senescent chondrocytes, potentially benefiting joint health. Neutralizes doxorubicin-induced chemotoxicity by clearing treatment-induced senescent cells.

Join others researching Clascoterone — share findings, ask questions, and learn from real experiences Clascoterone (cortexolone 17-alpha-propionate) is a first-in-class topical androgen receptor inhibitor developed by Cassiopea SpA. In August 2020, the FDA approved Winlevi (clascoterone cream 1%) for the treatment of acne vulgaris in patients aged 12 and older, making it the first new mechanism of action for acne treatment in nearly four decades and the first topical anti-androgen approved for acne in the United States. Clascoterone is also under development as Breezula (clascoterone solution 7.5%) for androgenetic alopecia, where it has completed Phase 3 clinical trials. The compound works by competitively inhibiting androgen receptor activation at the site of application -- the sebaceous gland for acne and the hair follicle for androgenetic alopecia -- without producing the systemic anti-androgenic effects associated with oral anti-androgens such as spironolactone or cyproterone acetate. Its steroidal structure allows it to fit precisely into the androgen receptor binding pocket, and its rapid local metabolism to cortexolone (an inactive metabolite) limits systemic exposure. This pharmacological profile makes clascoterone suitable for use in both men and women, unlike systemic anti-androgens which carry risks of feminization in male patients. Clascoterone acts as a competitive antagonist of the androgen receptor (AR). When applied topically, it penetrates the skin and binds directly to androgen receptors in target tissues -- sebaceous glands (for acne) and dermal papilla cells of hair follicles (for alopecia). By occupying the AR binding site, clascoterone prevents dihydrotestosterone (DHT) and testosterone from activating the receptor and initiating the downstream signaling cascade that drives sebum overproduction and hair follicle miniaturization. Structurally, clascoterone is a synthetic derivative of cortexolone (11-deoxycortisol), modified with a 17-alpha-propionate ester. This structural design serves two purposes: the steroidal backbone provides high binding affinity for the androgen receptor, while the ester group is rapidly cleaved by local esterases in the skin, converting clascoterone to cortexolone, which has negligible androgen receptor binding. This built-in metabolic inactivation ensures that any compound reaching systemic circulation is pharmacologically inactive, confining the anti-androgenic effect to the treatment site. In clinical studies, clascoterone showed no meaningful impact on systemic hormone levels including testosterone, DHT, luteinizing hormone, or follicle-stimulating hormone at therapeutic doses, confirming its local mechanism of action.