In four experiments, different preparations and modes of prenatal administration of ACTH all failed to produce any substantial effects upon male sexual behavior in mice. In Experiment 1, CD‐1 females implanted during the third trimester of pregnancy with osmotic pumps releasing varied dosages of ACTH1−24 produced male offspring with essentially normal copulatory behavior. In Experiment 2, prenatal injections of high doses of ACTH1−24 had no effect upon male sexual activity. In Experiment 3, osmotic pumps releasing ACTH1−39 during the third trimester of pregnancy had no effect upon sexual behavior of offspring. However, aggressive behavior was significantly reduced, relative to untreated controls, in offspring of all females implanted with pumps, including those releasing only saline. In Experiment 4, third‐trimester injections of ACTH1−39 in long‐acting gel form had no effect on the sexual behavior or aggression of offspring of C57 strain females. In most of these experiments, ACTH treatment significantly reduced body weight. These results do not confirm previous suggestions that pituitary‐adrenal hormones influence the perinatal differentiation of sexually dimorphic behavior.