EE2 Steroid Raw Powder Ethynyl Estradiol CAS 57-63-6
|Synonyms||Amenoron; Esteed; Estoral; Estorals; Ethinoral; Ethynylestradiol;
Ethynyloestradiol; Eticyclin; Eticyclol|
|Melting Point||182-183 ° C(lit. )|
|Boiling Point||457.2 ° C at 760 mmHg|
|Flash Point||211.2 ° C|
|Solubility||Ethanol: 50 mg/mL, clear, slightly yellow|
|Appearance||Off-White to Light-Yellow Crystalline Powder|
Ethinyl estradiol (EE2) (USP) (former brand name Estinyl), or
ethinylestradiol (INN, USAN, JAN), also spelled as ethinylœstradiol
(BAN) and also known as
17α-ethynylestra-1,3,5(10)-triene-3,17β-diol, is a synthetic,
steroidal estrogen. It is a derivative of estradiol, the
major endogenous estrogen in humans; specifically, EE2 is
17α-ethynylestradiol. EE2 is an orally active estrogen used in
almost all formulations of combined oral contraceptives (COCs),
being nearly the exclusive estrogen used for this purpose.
As Estinyl, EE2 was formerly used for hormone replacement therapy
in menopause and the treatment of female hypogonadism, loss of
menstruation, dysmenorrhea, acne, prostate cancer, and breast
However, in more recent times, EE2 is mainly used in COCs. In
contraception, due to concerns of unopposed estrogen action and the
possible increased risk of endometrial cancer that accompanies
this, EE2 is formulated in combination with progestins. EE2 is
little used in menopausal hormone replacement therapy.
EE2 has been used at very high dosages (1–2 mg/day) in the
treatment of prostate cancer.
EE2 should be avoided in women with a history of or known
susceptibility to thrombosis (blood clots), particularly venous
Due to risk of cholestatic hepatotoxicity, it is widely considered
that COCs containing EE2 should be avoided in women with a history
of cholestasis of pregnancy, hepatic tumors, active hepatitis, and
familial defects in biliary excretion.
Inducers of certain cytochrome P450 enzymes such as CYP3A4 can
decrease circulating concentrations of EE2. Examples include
anticonvulsants like phenytoin, primidone, ethosuximide,
phenobarbital, and carbamazepine, azole antifungals like
fluconazole, and rifamycin antibiotics like rifampin and
rifampicin. Conversely, inhibitors of CYP3A4 and certain other
cytochrome P450 enzymes may increase circulating levels of EE2. An
example is troleandomycin, which is a potent and highly selective
inhibitor of CYP3A4.
Paracetamol has been found to competitively inhibit the sulfation
of EE2, with pretreatment of 1 g paracetamol significantly
increasing the AUC levels of EE2 (by 22%) and decreasing the AUC
levels of EE2 sulfate in women. The same has been found for
ascorbic acid (vitamin C) and EE2, although the significance of the
interaction has been regarded as dubious.
Unlike the case of estradiol, there is probably no pharmacokinetic
interaction between smoking (which potently induces certain
cytochrome P450 enzymes and markedly increases the 2-hydroxylation
of estradiol) and EE2. This suggests that estradiol and EE2 are
metabolized by different cytochrome P450 enzymes. There is however
still an increased risk of cardiovascular complications with
smoking and EE2, similarly to the case of smoking and other
The 19-nortestosterone progestins, gestodene and, to a lesser
extent, desogestrel, have been found to inhibit cytochrome P450
enzymes and to progressively inhibit the metabolism and increase
the concentrations of EE2.
EE2 has been found to significantly increase (by 38%) the AUC of
omeprazole (which is metabolized by CYP2C19).