The potential of isopropyl triphenyl phosphate (ITP) to produce delayed neurotoxicity in hens was examined using several techniques. ITP contained O,O,O‐triphenyl phosphate (24%), O‐o‐isopropylphenyl O,O‐diphenyl phosphate (25%), O,O‐diisopropyl‐phenyl O‐phenyl phosphate (20%), O‐o, p‐diisopropylphenyl O,O‐diphenyl phosphate (18%) and O‐p‐isopropylphenyl O,O‐diphenyl phosphate (6%). Hens treated twice, 3 wk apart, with doses of ITP as high as 11.7 g/kg showed no clinical signs of delayed neurotoxicity and only mild signs of general toxicity. Furthermore, none showed even subtle neurohistologic changes suggestive of delayed neurotoxicity. ITP produced dose‐dependent inhibition of hen plasma cholinesterase and brain neurotoxic esterase (NTE). The study was continued because NTE inhibition has been shown to be a reliable predictor of organophosphates that produce delayed neurotoxicity. ITP was administered prior to tri‐o‐tolyl phosphate (TOCP) challenge in order to determine if it altered development of TOCP delayed neurotoxicity. ITP neither enhanced nor reduced the onset or severity of neurotoxicity produced by TOCP. The time‐course for brain and spinal cord NTE inhibition by ITP and TOCP were compared and found to be different. The maximum brain NTE inhibition produced by ITP (doses up to 11.7 g/kg) was never complete (always less than 90%), and spinal cord NTE inhibition was significantly less than that produced in the brain. In contrast, brain and spinal cord inhibition produced by 500 mg TOCP/kg were equal and greater than 90%.