A traumatic brain injury (TBI) is a severe form of neurotrauma resulting from the disruption of normal brain function due to external forces such as direct impact, rapid acceleration/deceleration or a penetrating object. TBIs have been attributed to long-term deficits including physical and cognitive changes, sensory effects, and social-emotional alterations. Current therapeutic options are limited to handling the acute trauma; however, drugs preventing nerve damage and promoting healing are not available. In recent years, the therapeutic use of bioactive peptides (small chains of amino acids, 2-20 a.a.), have been explored due to their low-production cost, stabile shelf life, and high specificity. Likewise, peptides derived from the active regions of a protein may selectively block the protein’s function. For example, the inhibition of Phosphatase and tensin homolog (PTEN) has been shown to enhance regeneration of the central nervous system (CNS) after injury through the activation of the phosphoinositide-3-kinase–protein kinase B (PI3K-Akt) pathway. This project investigates the use of the PTEN antagonist peptide 2 (PAP2), which is derived from the phosphatase domain of the PTEN protein to competitively block PTEN’s function. In vitro data from primary neuronal cell culture has shown that the PAP2 peptide has led to an increase in neurite growth and neuron numbers. Presently, this project explores the use of PAP2 at the site of injury to encourage neuronal regeneration in a mouse model of TBI.