Progesterone Estrogen Steroids Chlormadinone Acetate CAS 302-22-7

Progesterone Estrogen Steroids Chlormadinone Acetate CAS 302-22-7

Chlormadinone Acetate

English Synonyms: 17-(Acetyloxy)-6-chloropregna-4,6-diene-3,20-dione;
17-Acetoxy-6-chloro-6-dehydroprogesterone;17-alpha-Acetoxy-6-chloro-6,7-dehydroprogesterone;
17-alpha-acetoxy-6-chloro-6-dehydroprogesterone;17alpha-Acetoxy-6-chloro-6-dehydroprogesterone;
17-alpha-acetoxy-6-chloropregna-4,6-diene-3,20-dione;17alpha-Acetoxy-6-chloropregna-4,6-diene-3,
20-dione;20-dione,17-(acetoxy)-6-chloro-pregna-6-diene-3 
CAS NO.: 302-22-7 
Molecular Formula: C23H29ClO4 
Molecular Weight:404.93 
EINECS:206-118-0
Assay: 98%
Chemical Properties: White Crystalline Solid
Usage: Potent progesterone,Orally active progesteron with antiandrogenic activity; has been used in 

combinations as an oral contraceptive. Progestogen; antineoplastic (hormonal).
Packing:foil bag
Delivery: Express courier.

What is the Chlormadinone Acetate CAS 302-22-7?

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.

Description:

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.

Application:

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 andby 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. Inaddition, it suppresses endometrial 

thickness and increases the viscosity of cervical mucus.

Usage:

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.
 

Specifications:

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