Neuroprotection therapies have made limited progress in recent years. Several compounds shown to be efficacious in animals were tested in humans in cost-expensive trials. Unfortunately, none of these studies were able to demonstrate efficacy under clinical conditions in patients. In order to establish treatments that are of benefit not only in animals but also humans, new strategies and research to understand pathophysiology of stroke are clearly needed, comprising (i) The role of solute carrier OATP1a5 in the brain pharmacotherapy after stroke: By preventing access of drugs to the CNS, the bloodbrain barrier hampers developments in brain pharmacotherapy. Strong efforts are currently being made to identify drugs that accumulate more efficaciously in ischemic- brain tissue. We identified a solute carrier transporter OATP1a5, which is expressed in the CNS and playing roles in the accumulation of its substrates and their neuroprotective efficacy; (ii) The role of melatonin and circadian rhythm protein Bmal1 on the pathophysiological changes occurring after ischemic stroke: Circadian rhythm plays an important role in the regulation of almost all physiological conditions as well as pathophysiological processes such as cerebral ischemia. The role of these molecules in the brain neuroprotection will be discussed; and (iii) The role of fetal microchimerism on the brain injury and plasticity after ischemic stroke: Microchimerism is the presence of a very small population of genetically different cells in another person. Fetal microchimerism was described as the transition of stem cells of the fetus to mother during pregnancy. Here, the fetal cell transition from fetus to maternal ischemic brain tissue will be discussed. In this talk, aforementioned studies, pursued at the REMER at the Istanbul Medipol University will be presented. These projects are/were funded by TUBITAK 115S471; 118S306; 217S453, respectively.