Traumatic brain injury (TBI) is a major cause for fatality and disability across the world. Primary injury represents immediate mechanical damage which is non-reversible and non-treatable whereas secondary injury is the delayed consequences of primary injury and life-long disability that can be therapeutically influenced. After many efforts, little success has been achieved toward the evolution of efficacious pharmacological invention to lessen the devastating effects of TBI. The neuroprotective approaches of Kynurenic acid (an endogenous metabolite of tryptophan metabolic pathway) have been found in an experimental model of migraine, Alzheimer’s, and Huntington’s disease. Therefore, In the present study, we evaluated the potential of Kynurenic acid amide analogue (KAA) at 72 h in delayed secondary consequences of TBI in mice. Materials and methods: The injury was used swiss albino mice (25-30 g) and analyzed biochemical parameters (Oxidative stress, BBB permeability, and edema formation, mitochondrial dysfunction), and Histopathological studies. Results: Our data showed significant rise in oxidative stress, % water content and BBB permeability at 72 h of injury. Meanwhile, cortical neuronal cell death was also evident at 72 h of injury. KAA administration (100, 200, 400, mg/kg, ip) to animals (swiss albino mice; 25-30 g) administered with KAA after 30 minutes of TBI showed a significant and dose dependent neuroprotective effect on oxidative stress, edema and BBB permeability. KAA also showed improvement in neuronal survival and neurological functions significantly. Conclusion: Overall, our data shows that KAA depicted neuroprotection against TBI-induced secondary cascades and improves neurological damage in the mice model of TBI.