OK2, a specific inhibitor of the CCN2/EGFR interaction, effectively disrupts this interaction by binding to the CT domain of CCN2 and holds potential for research on kidney fibrosis and chronic kidney disease [1].

OK2 at concentrations ranging from 0 to 100 μM over a time course of 24 hours inhibits the activation of EGFR, phosphorylation of STAT3, and the synthesis of ECM proteins in HK-2 cells [1].

OK2 (50 μg/kg, intraperitoneal injection, for 14 days) inhibited CCN2-induced EGFR/STAT3 activation and prevented renal fibrosis in a unilateral ureteral obstruction (UUO) mouse model [1]. Additionally, OK2 administered subcutaneously at a dose of 1 mg/kg in male Sprague Dawley rats exhibited a half-life (T1/2) of 0.9 hours and a peak concentration (Cmax) of 1057.8 ng/mL [1]. Pharmacokinetic parameters for OK2 in this rat model included a T1/2 of 0.9 hours, a Cmax of 1057.8 ng/mL, and an area under the curve (AUC0-t) of 3032.0 h•ng/mL following a single subcutaneous injection [1].