N,N′-4-Xylylene-bis(N-ethyldichloroacetamide), Compound I,and N,N′-bis (dichloroacetyl)-l,8-octamethylenediamine, Compound II, produced in rats marked testicular weight regression associated with complete arrest of spermatogenesis. Compound II was approximately eight times more active, per mg., than Compound I. At maximal effects the seminiferous tubules consisted merely of a ring of Sertoli cells with spermatogonia interspersed. Leydig cell morphology and androgen production were not altered by antispermatogenic doses of either agent. The weight of the adrenal glands was lowered by high doses of both compounds although the adrenals appeared normal histologically. The plasma corticosterone level of chronically medicated rats was not different from that of control animals. Also, the rise in plasma corticosterone concentration observed two hours after ACTH administration was not altered by prior medication with Compound II. Concurrent injections of 10 r.u. per rat per day of commercial pituitary gonadotrophin (predominantly FSH) tended to enhance rather than reverse the testicular effects of Compound I. Also, testosterone propionate at 25 mg./kg./day increased the antispermatogenic action of Compound II, although the androgen by itself did not alter normal spermatogenesis. The antispermatogenic activity of Compound I was not blocked by α tocopherol, corn oil, ascorbic acid, calcium pantothenate, methionine, cysteine, ergothionine, lysine, arginine, histidine or spermine tetrahydrochloride. Neither compound blocked the growth of microorganisms when folic acid, calcium pantothenate, vitamin B12, cystine or phenylalanine were limiting nutrilites. Various screening tests indicated that Compounds I and II are not myotrophic, androgenic, estrogenic, progestational, nor glycogenic.