Abstract: Rheumatoid arthritis (RA) is a chronic autoimmune disease that often causes inflammation of the synovial joints resulting in severe pain, bone erosion, and joint deformity which affects more than 2 million Americans. Current treatments for RA are based on anti-inflammatory treatments including steroids, non-steroidial anti-inflammatory drugs (NSAIDs), disease-modifying antirheumatic drugs (DMARDs), immunosuppressants, and TNF-alpha inhibitors. Side effects of current treatments can lead to heart problems, liver and kidney damage, bone marrow suppression, and severe lung infections. Improved pharmaceutical targeting of inflammatory proteins such as phosphphatidylinositol 3-kinase (PI3K) should yield drugs with increased efficacy and decreased side effects.1-9 This research sought to understand the pharmaceutical blockade of the PI3K kinase functionality to inhibit its function in the inflammatory pathway. 16 crystal structures of the tyrosine kinase of the PI3K protein were docked using IGEMDock to FDA approved pharmaceupticals, Alkaloids, Lactams, Lactones, Flavinoids, Sulfanilamide, Cyclic Imides, and NSAIDs drugs to determine structural correlation for the most effective binders. Structural similarities were determined with IGEMDock and partition coefficient was determined using DRAGON program. This data found a cluster of approximately 10 drugs to preferentially bind to the PI3K kinase for use as targeted anti-inflammatory treatments. This work will be used in the engineering of improved PI3K kinase inhibitors.