With the combined data showing the analog 38 displayed mid-nanomolar AC1 potency with sub-20% AC8 inhibition, little modulation at other AC isoforms, and had the best overall predicted and measured physicochemical and MDCK permeability metrics it was prioritized for testing in an in vivo CFA mouse model for inflammatory pain. The analog did display modest, yet significant, anti-allodynic properties in this model at the 1-hour timepoint. The results are promising for the scaffold as we believe there are still alterations to be made for improvement of the physicochemical and pharmacokinetic properties of the molecules. For example, mice were dosed i.p. which may reduce the amount of molecule that enters circulation at the site of action. Solubility improvements should provide a means to increase testable doses.