AbstractPregnant Wistar rats were each injected once ip with various doses of 2‐amino‐l,3,4‐thiadiazole hydrochloride (ATDA) at days 1–16 of gestation (sperm day = day 0). The optimal teratogenic dose was determined to be 100 mg/kg and this dose was employed throughout the experiment. At autopsy at day 20 resorptions and malformations were found in all litters from treated females. Two periods of increased embryonic susceptibility to the lethal effects of ATDA were observed. The first at day 5 (100% resorbed) and the second at days 9 and 10 (71.5 and 92.5% resorbed). Periods of increased sensitivity to the teratogenic action of ATDA were at days 9 through 13, when the incidence of abnormal fetuses produced exceeded 90%. The major malformations were anophthalmia, microphthalmia, hydrocephalus, short tail, taillessness, ectrodactyly, syndactyly, and cleft palate. Other malformations occurred occasionally. The malformations were related to the developmental stage at the time of treatment. Supplemental treatment with nicotinamide at days 5, 11, 12, and 13 markedly diminished the teratogenic and lethal effects of ATDA, and at day 11 the administration of nicotinamide completely abolished its teratogenic activity. ATDA probably acts by interfering with NAD‐dependent enzyme