NSC 23766 is a Rac1 GTPase inhibitor that inhibits Rac1 activation by targeting guanine nucleotide exchange factors (GEFs), while it has no inhibitory effect on the closely related targets Cdc42 and RhoA, affecting the cell cycle and inhibiting cell proliferation in a dose-dependent manner. It also regulates endothelial NO synthase expression and endothelial function, and inhibits platelet aggregation and γ-secretase activity.NSC23766 competitively inhibits M2 muscarinic acetylcholine receptor (M2 mAChR)-induced Rac1 activation in neonatal rat cardiomyocytes.

NSC 23766 (100?μM) treatment effectively inhibits polar body emission in a dose-dependent manner. NSC 23766 (200 μM) increases the percentage of morphologically abnormal spindles of oocytes. In NSC 23766-treated oocytes, the p-MAPK protein expression is significantly decreased[2]. NSC23766 (50?μM) plus 100?ng/mL Jagged1, GDF9 and BMP15, reduces the number of germLine cell cysts and increases the number of primordial follicles[3]. NSC23766 significantly inhibits GTP-Rac1 activity and phosphorylation of Rac1-PAK, ERKs and p38 MAPK in the spinal dorsal horn neurons[4].

NSC23766 (2.5 mg/kg/day, i.p.) significantly attenuates the onset of spontaneous diabetes in NOD mice, without significant effects on the growth (body weights) of the mice. NSC23766 significantly increases the expression of Rac1 and CHOP, a marker for ER-stress, in islets from NOD mice[1].