Chlormadinone acetate was given orally in an aqueous vehicle to mature female rabbits, using a variety of dosage schedules, in a model ℌminipillℍ test. Two distinct mechanisms effective in preventing pregnancy were identified. At a dose level of 0.9 mg/kg/day, given for 3 or 4 days before artificial insemination and ovulation induction, fertilization of eggs was reduced to 12%. Continuation of the dosing for 8 days after ovulation did not alter the ED100. Acceleration of the rate of egg transport was observed whether progestin administration ceased before or after ovulation, indicating a direct effect of progestins upon the musculature of the reproductive tract. When similarly dosed animals were examined on the 15th day of pregnancy, complete inhibition of pregnancy was caused by 0.09 mg/kg/day. Investigation of the animals just prior to implantation revealed that the mechanism was compounded of accelerated egg transport, together with inhibition of blastocyst growth, shown by reduced egg recoveries and computation of blastocyst volumes, respectively. The results obtained are discussed as being analogous to the differing contraceptive mechanisms of high and low dose levels of chlormadinone acetate in the human. Comparisons are drawn between the ovulation-inhibiting action of high dose levels in human, and the fact that the high dose level used in this study (0.9 mg/kg/day) is above that needed for ovulation inhibition in the rabbit. Further similarities also exist between suboptimal ovulation inhibiting doses in the human (0.5 mg/kg/day) and in the rabbit (0.09 mg/kg/day), in that penetration of cervical mucus by spermatozoa is possible. It is suggested that inhibition of implantation may be implicated in the action of low doses of 17-acetoxy progestins in women.