| Stereochemistry | ACHIRAL |
| Molecular Formula | C26H28ClNO |
| Molecular Weight | 405.96 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 1 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
CCN(CC)CCOC1=CC=C(C=C1)C(=C(/Cl)C2=CC=CC=C2)\C3=CC=CC=C3
InChI
InChIKey=GKIRPKYJQBWNGO-QPLCGJKRSA-N
InChI=1S/C26H28ClNO/c1-3-28(4-2)19-20-29-24-17-15-22(16-18-24)25(21-11-7-5-8-12-21)26(27)23-13-9-6-10-14-23/h5-18H,3-4,19-20H2,1-2H3/b26-25-
| Molecular Formula | C26H28ClNO |
| Molecular Weight | 405.96 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 1 |
| Optical Activity | NONE |
Clomiphene (CLOMID®) is a triphenyl ethylene stilbene derivative which is an estrogen agonist or antagonist depending on the target tissue. It is an orally administered, nonsteroidal, ovulatory stimulant. Clomiphene (CLOMID®) is a mixture of two geometric isomers [cis (zuclomiphene) and trans (enclomiphene)] containing between 30% and 50% of the cis-isomer. Clomiphene (CLOMID®) initiates a series of endocrine events culminating in a preovulatory gonadotropin surge and subsequent follicular rupture. The first endocrine event in response to a course of clomiphene therapy is an increase in the release of pituitary gonadotropins. This initiates steroidogenesis and folliculogenesis, resulting in growth of the ovarian follicle and an increase in the circulating level of estradiol. Following ovulation, plasma progesterone and estradiol rise and fall as they would in a normal ovulatory cycle.
CNS Activity
Originator
Approval Year
Sample Use Guides
Treatment of the selected patient should begin with a low dose, 50 mg daily (1 tablet) for 5 days. The dose should be increased only in those patients who do not ovulate in response to cyclic 50 mg CLOMID®. If ovulation does not appear to occur after the first course of therapy, a second course of 100 mg daily (two 50 mg tablets given as a single daily dose) for 5 days should be given.
Route of Administration:
Oral
Clomiphene at lower doses (10^-10 M and 10^-12 M), but not higher doses (10^-6 M and 10^-8 M) elicited estrogenic activity via estrogen receptor alpha (ER alpha). However, clomiphene at concentrations between 10^-6 M and 10^-12 M did not elicit any estrogenic activity via estrogen receptor beta (ER beta). In the presence of 17beta-estradiol (E2), clomiphene behaved either as an agonist or as an antagonist via ER alpha depending on the concentrations of E2, i.e., antagonistic when combined with the higher E2 concentrations, agonistic with the lower E2 concentrations. On the other hand, via ER beta, clomiphene acted as an estrogen antagonist regardless of the concentration of E2 added together. In conclusion, clomiphene acts as an estrogen agonist/antagonist via ER alpha in a coexisting estrogen concentration-dependent way whereas it acts as an estrogen antagonist via ER beta whether or not estrogen is present.
