A derivative of the CRMP2 binding compound lanthionine ketimine provides neuroprotection in a mouse model of cerebral ischemia

► We have demonstrated that LKE is neuroprotective in a p-MCAO model of stroke. ► LKE's putative mechanism is in-part due to its CRMP2 mediated neurotrophic effects. ► LKE modulates the expression of apoptotic cascade-proteins, PARP1 and SIRT1. ► LKE salvaged neurons against H2O2 and t-BuOOH-mediated oxidative stress in vitro. ► LKE may be useful for therapeutic benefits in diseases such as stroke and ischemia.