In vitro cyclofenil [bis-(p-acetoxyphenyl)-cyclo-hexylidene methane] competitively inhibited the binding of [3H]oestradiol-17\g=b\ to the uterine cytoplasmic receptor (Kdi = 9\m=.\41 nmol/l). By 24 h after cyclofenil treatment of ovariectomized rats, cytoplasmic oestrogen receptors were altered, in a similar manner, in brain, pituitary gland and uterus. The lowest dose depleted the receptor concentration which was re-established at the intermediate dose and depleted again after the highest dose. Nuclear oestrogen receptors measured in the uterus were raised only after the highest dose of cyclofenil. Uterine cytoplasmic progesterone receptors were increased after cyclofenil, the concentration of progesterone receptor after the high dose of cyclofenil being greater than after a large dose of oestradiol-17\g=b\ or oestradiol-17\g=b\ benzoate. Cyclofenil was uterotrophic; the increase in uterine weight was apparently dose-related and at 24 and 48 h the increase was greater or similar to the increases produced by oestradiol-17\g=b\ or oestradiol-17\g=b\ benzoate. Accumulation of uterine luminal fluid was also observed but oestradiol-17\g=b\ benzoate was more active in this respect. Cyclofenil antagonized all the uterine effects of oestradiol-17\g=b\ benzoate in the immature female rat but only the changes in uterine luminal fluid in the adult ovariectomized rat. Cyclofenil decreased serum LH and increased serum FSH concentrations, effects similar to those of oestrogen except when administered as three daily doses when, unlike oestrogen, no changes in FSH were observed. Antagonism of the activity of oestrogen upon the serum gonadotrophins was not seen. Serum prolactin concentrations were increased 24 h after 0\m=.\5 and 50 mg cyclofenil/kg but not after 10 mg/kg. Cyclofenil was not active in inducing sexual receptivity in ovariectomized adult rats unless previously treated with progesterone when a high level of activity was observed. The results show that the cyclofenil molecule possesses high oestrogenicity which is probably mediated via the oestrogen receptor system. This would suggest that the mechanism by which cyclofenil induces ovulation is most probably related to its oestrogenicity rather than its antioestrogenicity.