Caffeine is the most widely used psychoactive drug in the world and forms a mild dependency in users who overuse the drug for an extended period of time. Other psychoactive drugs, including methamphetamine, have been shown to induce apoptosis in the brain's reward pathways, leading to lasting neuronal damage. Similarly, caffeine has been shown to activate the p53‐mediated apoptotic pathway in JB6 C141 cells derived from mice. However, other studies suggest that caffeine produces contradictory effects. Caffeine exposure has been reported to extend the lifespan of Caenorhabditis elegans through activation of the IGF‐1 signaling pathway. Additionally, caffeine has been shown to bind to ador‐1 receptors, the homolog of ADORA2A in humans, in C. elegans. We suspect that the seemingly contradictory effects of caffeine exposure are mediated by ador‐1, signifying that p53 and IGF‐1 activation occur downstream to adenosine receptors. Here we examine the role of ador‐1 in activation of the CEP‐1 apoptotic pathway, the C. elegans homolog of the p53‐apoptotic pathway in humans, and the IGF‐1 signaling pathway in C. elegans. Our current data clarifies the relationship between caffeine exposure and CEP‐1. We plan to further investigate the relationship of the CEP‐1 and IGF‐1 pathways in order to determine whether their activation is mediated by ador‐1.Support or Funding InformationThis work was supported by The Nueva School.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.