Finasteride and RAD-140 Interaction: Avoid | Peptide Database

Join others researching Vilon — share findings, ask questions, and learn from real experiences Vilon is a Khavinson bioregulator dipeptide (KE) consisting of lysine and glutamic acid, originally isolated from thymus gland extracts. Developed by Professor Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology, it acts as a molecular signaling compound that restores normal gene expression and protein synthesis in immune and epithelial cells. Research shows Vilon increases mean lifespan by 20-40% in animal studies and suppresses tumor development. Vilon works through epigenetic modulation, restoring chromatin structure and gene expression in immune cells. It stimulates thymocyte proliferation, activates T-helper cells, and increases the proliferative index in thymus tissue (from 26% to 37% in studies). The peptide modulates tyrosine phosphorylation of mitogen-activated cytoplasmic kinases and helps rejuvenate aged immune systems by restoring proper gene expression patterns.

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.