The ID50 for progesterone was approximately 5 mg/kg. At the lowest dose (0.25 mg/rat), NOMAC inhibited ovulation in 78.2% (5/6) of rats, indicating that the 50% inhibition dose (ID50) for NOMAC was <1.25 mg/kg. In this study, the rate of ovulation in the vehicle-treated control animals was 76.5%. After 3 consecutive, regular 4-day cycles, animals in the metestrus phase received single subcutaneous injections of NOMAC or progesterone at doses of 0.25, 1, or 4 mg (n = 5-6 per dosage group) or vehicle (n = 17). and van Diepen investigated the ability of NOMAC to inhibit ovulation in the rat. These experiments support the overall conclusion that NOMAC has a progestational profile that is similar to progesterone. In addition, NOMAC did not have antimineralocorticoid activity. None of the progestogens tested (including NOMAC) activated or antagonized hER alpha, hER beta, or hGR or were hMR agonists. NOMAC, DRSP, DNG, LNG, and progesterone were all capable of antagonizing hAR. NOMAC did not display antagonistic activity against hPRB. NOMAC and LNG were the most potent progestogens in activating hPRB in CHO cells. used established cellular assays to determine the agonistic and antagonistic profiles of NOMAC, levonorgestrel (LNG), drospirenone (DRSP), dienogest (DNG), and progesterone in Chinese hamster ovary (CHO)-K1 cells that were stably transfected with cDNAs encoding human receptors, including progesterone receptor B (hPRB), androgen receptor (hAR), mineralocorticoid receptor (hMR), glucocorticoid receptor (hGR), and estrogen receptors (ER) α and β (hER alpha and hER beta, respectively). Receptor-binding experiments, although useful, do not distinguish between agonistic and antagonistic activity.
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