TMP269 has no impact on the mitochondrial activity and/or the viability of human CD4+ T cells at 10 μM, and may be used as tools to identify the endogenous substrates of the class IIa HDAC enzymes. In IEC-18 intestinal epithelial cells, TMP269 prevents cell cycle progression, DNA synthesis, and proliferation induced in response to G protein-coupled receptor/PKD1 activation.