Add time:09/09/2019         Source:sciencedirect.com

Azastene (cas 13074-00-5), a synthetic steroid of the androstano (2,3-d) isoxazole family, has been shown to terminate pregnancy in the rat and in the primate. Its antifertility effect in the rat is associated with a decrease of progesterone and an increase in prostaglandin F (PGF). Its mechanism of action has been explained by the ability of azastene to inhibit 3β-hydroxysteroid dehydrogenase, thereby critically decreasing progesterone production. However, azastene-induced PGF release could be directly responsible for the decreased progesterone production and hence for its antifertility effect. To test this hypothesis PGF release associated witch azastene administration was blocked by indomethacin. In indomethacin-treated rats, azastene administered at day 10 of pregnancy failed to decrease uterine blood progesterone [100.6 ± 11 (mean ± SE) ng/ml (N = 10) for azastene-indomethacin–treated rats versus 30.6 ± 4.4 (mean ± SE) ng/ml (N = 10) for azastene alone; p < 0.01] or increase uterine blood PGF metabolities [329.8 ± 41 (mean ± SE) pg/ml (N = 10) for azastene-indomethacin–treated rats versus 707 ± 45 (mean ± SE) pg/ml (N = 10) for azastene alone; p < 0.01]. Azastene treatment alone results in fetal death in all treated animals. Treatment with indomethacin and azastene at day 10 of pregnancy resulted in live fetuses at day 14 of gestation. When allowed to go to term indomethacin-azastene–treated rats gave birth to normal litters [6.8 ± 0.4 (mean ± SD) gm mean weight of 11 fetuses per rat in four azastene-indomethacin–treated animals versus 6.6 ± 2.2 (mean ± SD) gm mean weight of 11 fetuses per animal in four control rats]. When 5 mg/day progesterone was administered along with azastene, uterine blood progesterone did not change, but PGF metabolites increased when compared with control [539 ± 2.2 pg/ml (N = 5) versus 258 ± 2.4 pg/ml (N = 4) at day 10½ of pregnancy; p < 0.01]. Moreover, the fetuses in the azastene-progesterone group were unaffected. Because the antifertility effects of azastene can be reversed by indomethecin, and because in the presence of elevated blood progesterone levels azastene-induced PGF release is not sufficient to terminate pregnancy, our study suggests that the mechanism of azastene action is directly mediated by prostaglandin release but that a regulatory imbalance between progesterone and prostaglandin is required for interruption of pregnancy.

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