Oral High Quality Female Anti-Estrogenic Steroid Chlormadinone Acetate CAS;302-22-7
Product Name: Chlormadinone Acetate
Suitable for: Elderly, Adult
Appearance: White Powder
Molecular Formula: C23H29ClO4
Fuction: Female Sex Hormone
Usage: Potent progesterone,Orally active progesteron with antiandrogenic activity; has been used in combinations as an oral contraceptive. Progestogen; antineoplastic (hormonal).
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Delivery Time: 3-5 Working Days Door to Door
Transport Package: Disguised package; Foil bag
Certification: ISO 9001, USP, GMP
Storage: Cool Dry Place
Payment: Western Union, Money Gram, Bank Transfer, Bitcoin
Reship Policy: Reship for Fee
HS Code: 2937290019
Chlormadinone acetate (CMA) is a derivative of progesterone (17-acetoxy-6-chloro-4,6-pregnadiene-3,20-dione), first synthesized in 1961 and is used as an orally effective progestogen in hormone replacement therapy (HRT), and in combination with ethinyl estradiol (EE) in contraception since 1999. Chlormadinone acetate has a strong progestogenic effect about one-third higher than that of progesterone and may vary depending on the previous effect of an estrogen, i.e., estrogens may promote the formation of progesterone receptors and proliferation of the endometrium. Like progesterone, it is anti-estrogenic and has no partial androgenic effect (at the doses used for contraception and HRT). In contrast to progesterone, it has a slight glucocorticoid effect, a pronounced anti-androgenic effect and no anti-mineralocorticoid effect. No pregnancy-maintaining effect of CMA has been demonstrated in humans.
The anti-androgenic effect of CMA is presumed to be the result of both its binding to androgen receptors competitively inhibiting the effect of endogenous testosterone and dihydrotestosterone and the competitive inhibition of 5-reductase. In this respect, dosing of CMA is crucial; agonistic effects are observed when doses are increased from those optimal for an antagonistic effect.
Chlormadinone acetate has a strong anti-gonadotropic effect, through negative feedback on gonadotropin secretion, and has been used for more than 20 years alone for contraception in arterial risk patients. The clinical and metabolic tolerability of CMA has been demonstrated in numerous clinical studies with duration of treatment of up to 2.5 years.
The more recent application of CMA as an oral contraceptive in combination with EE (Neo Eunomin, Belara) has proven highly successful, with studies reporting excellent contraceptive efficacy, high tolerability and adherence due to a good side effect profile and positive effects on preexisting dysmenorrhea, skin and hair conditions.
CMA acts predominantly as a potent progestogen, but also as an antiandrogen. Due to its potent actions as a progestogen, CMA also has strong antigonadotropic properties, and thus additional antiandrogen as well as antiestrogen properties.
Like other steroidal progestins with antiandrogen properties such as cyproterone acetate, medroxyprogesterone acetate, and megestrol acetate, as well as spironolactone (a steroidal antimineralocorticoid with antiandrogen and progestogen properties), but unlike non-steroidal antiandrogens such as flutamide and bicalutamide, CMA is not a silent antagonist of the androgen receptor (AR) but rather a weak partial agonist of the AR with the capacity to activate the receptor in the absence of more efficacious agonists such as testosterone.
Similarly to other 17α-hydroxyprogesterone derivatives such as cyproterone acetate, medroxyprogesterone acetate, and megestrol acetate, CMA is a weak glucocorticoid, and has the potential to cause adrenal insufficiency upon abrupt discontinuation of the drug at sufficient dosages.
Chlormadinone acetate is a competitive inhibitor of 5α-reductase.
Chlormadinone acetate (CMA) is a derivative of naturally secreted progesterone that shows high affinity and activity at the progesterone receptor. It has an anti-estrogenic effect and, in contrast to natural progesterone, shows moderate anti-androgenic properties. CMA acts by blocking androgen receptors in target organs and by reducing the activity of skin 5alpha-reductase. It suppresses gonadotropin secretion and thereby reduces ovarian and adrenal androgen production. CMA shows high contraceptive efficacy by inhibiting ovulation due to its ability to suppress or disrupt endogenous gonadotropin secretion and, by this, inhibits follicular growth and maturation. In addition, it suppresses endometrial thickness and increases the viscosity of cervical mucus.
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