 Adenosine may be a plausible means to transiently disrupt the BBB. Adenosine function is regulated by its four structurally related G-protein coupled receptors: A1, A2A, A2B and A3. Specifically, A1 and A2A have high expression levels within the brain. In 2011, Carman et al demonstrated, with the selective A2A receptor agonist, Regadenoson, increased BBB permeability to 70kD Dextran in both mice and rat brains. The large molecule of Dextran was seen in the brain for up to 180 minutes following a single injection in both mice and rats. Studies performed at Johns Hopkins have also demonstrated a transient disruption of the BBB from Regadenoson in rodents by measuring temozolomide concentrations. The investigators found that brainplasma concentrations in rats post Regadenoson resulted in a 1.6 fold increase of temozolomide compared to temozolomide given alone in normal rat brains. Future animal studies will evaluate varied chemotherapy agents within the brain and brain tumor with and without Regadenoson. 