Chlormadinone acetate

Koike H, et al. Prostate International, 2013, 1, 113-116.

Chlormadinone acetate was clinically evaluated for alleviating hot flushes in prostate cancer patients receiving long-term androgen deprivation therapy. In this prospective clinical application, 32 patients with severe hot flushes persisting for over three months were administered oral CMA at an initial dose of 100 mg/day. Symptom response was systematically categorized as disappeared, improved, or unchanged. Responsive patients underwent stepwise dose reduction to 50 mg/day and subsequently 25 mg/day, with continuous symptom monitoring and dose readjustment upon relapse. Treatment discontinuation was applied to non-responders after two months. Clinical outcomes demonstrated hot flush disappearance or improvement in 84% of patients, with a median response time of 1.16 months. Importantly, prostate-specific antigen levels remained stable throughout CMA treatment. This case highlights the dose-titration-based clinical application of CMA as an effective and well-tolerated intervention for hormone therapy-induced vasomotor symptoms.

Menshawy A, et al. Journal of Gynecology Obstetrics and Human Reproduction, 2019, 48, 763-770.

Chlormadinone acetate was evaluated as the progestin component of ethinyl estradiol-based oral contraceptives for treating hyperandrogenism in women with polycystic ovary syndrome (PCOS). This systematic review and meta-analysis integrated data from three randomized controlled trials comparing EE/CMA with EE/drospirenone regimens. Endocrinal outcomes-including Ferriman-Gallwey score, total testosterone, delta-4-androstenedione, and sex hormone-binding globulin-were quantitatively analyzed using weighted mean differences under a fixed-effect model. EE/CMA demonstrated significant antiandrogenic activity, reflected by reductions in androgen biomarkers and clinical hirsutism scores, although to a lesser extent than EE/DRSP. The study underscores the clinical experimental application of CMA as an antiandrogenic progestin, functioning through suppression of ovarian androgen production and modulation of circulating free testosterone via SHBG elevation.

Zia MK, et al. Journal of Molecular Structure, 2025, 1331, 141541.

The molecular interaction between chlormadinone acetate and human α2-macroglobulin (α2M) was systematically investigated using multi-spectroscopic techniques and isothermal titration calorimetry. UV-visible absorption spectroscopy revealed hyperchromic shifts indicative of α2M conformational changes upon CMA binding. Intrinsic fluorescence quenching analyses, interpreted via Stern-Volmer equations across multiple temperatures, identified a static quenching mechanism. Circular dichroism spectroscopy further demonstrated a reduction in β-sheet content, confirming secondary structure perturbation. Thermodynamic characterization by ITC yielded a binding constant of 3.83 × 10⁴ M⁻¹, with negative ΔH and ΔG values, confirming a spontaneous and exothermic binding process. Hydrogen bonding and hydrophobic interactions were identified as dominant forces. This case highlights the experimental application of CMA in drug-protein interaction studies, providing mechanistic insight into its plasma transport behavior.