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CpdA is a non-steroidal selective glucocorticoid receptor modulator. It is an aziridine precursor that can infiltrate cells and is translocated to the nucleus. It inhibits glucocorticoid receptor dimerization, which prevents transcription of gene targets such as NF-κB and subsequent cytokines through transrepression. Studies have shown contradictory results for binding affinity of CpdA compared with dexamethasone that were either higher (4-fold, IC50 = 6.4 nM and 25.9 nM, respectively, in L929sA cells) or lower (63-fold, Kd = 81.8 nM and 1.29 nM, respectively, in BWTG3 cells) in whole cell binding assays.

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