The nuclear pore complex (NPC) is the sole gateway to the nuclear interior and its function is to regulate the materials entering or leaving the nucleus. Previous data from the Soukas laboratory suggests that the NPC turns “leaky” with aging, allowing proteins to be transported with less mediation over time. As a result, protein concentrations within both the cytoplasm and nucleus are altered resulting in an increased likelihood of  physiological dysfunction. Specific structural changes in the aging NPC have not yet been identified. Here we investigate the mechanisms of recovery in the NPC following treatment with drugs known to improve “leaky” NPCs. Metformin is a commonly used type 2 diabetes drug that has been shown to restrict NPC transport by restoring the passive transport barrier. The Soukas lab previously demonstrated  that metformin exhibits lifespan-extension properties in an NPC-dependent manner. Additionally the Soukas lab demonstrated that phenformin, an analog to metformin with bioactivity in C. elegans, restores the passive transport barrier of the NPC by acting on specific NPC structural components, one of which are nucleoporins (NUPs). This family of proteins is crucial for the restoration of the passive transport barrier and is required for phenformin-mediated lifespan extension. Unbiased genetic screens corroborated the importance of a specific NUP, NUP153. Here, we measured changes in protein concentration in C. elegans following phenformin exposure using western blot analysis. We correlated protein levels with aging and drug treatment using specific antibodies against various NPC structural components. Having this transgenic mutant allows us to understand the localization of NUP153 as it relates to aging. Ongoing studies in the lab using transgenic strains of C. elegans containing labeled NUP153 will be crucial in progressing towards understanding the changes in the NPC during aging.