AUDA is an inhibitor of sEH(IC50 values of 18 and 69 nM for the mouse and human enzymes, respectively)

sEH:18 nM (mouse), sEH:69 nM (human)

AUDA significantly inhibited PDGF-induced rat VSMC proliferation, which coincided with Pin1 suppression and heme oxygenase-1 (HO-1) upregulation.?However, exogenous 8,9-EET, 11,12-EET, and 14,15-EET treatments did not alter Pin1 or HO-1 levels and had little effect on the proliferation of rat VSMCs.?On the other hand, AUDA enhanced the PDGF-stimulated cell migration of rat VSMCs.?Furthermore, AUDA-induced activation of cyclooxygenase-2 (COX-2) and subsequent thromboxane A2 (TXA?) production were required for the enhanced migration[1].

AUDA increased the proliferation, migration, adhesion and tube formation ability of HCAECs in a dose-dependent manner.?Furthermore, in the mouse model of KD, AUDA reduced the protein expression of MMP-9, IL-1β and TNF-α, indicating that AUDA may alleviate inflammatory reactions in the coronary arteries of KD model mice[2].

Cell Line:Vascular smooth muscle cell (VSMC).Concentration:0.3, 1, 3, 10 μg/mL. Incubation Time:48 hours[1]

AUDA (i.p.; 10 mg/kg; 14 days) reduces TNF-α, MMP-9 and IL-1β expression levels.Animal Model:Male (wild-type). C57BL/6 mice (age, 4-6 weeks; weight, 18-20 g).Dosage:10 mg/kg.Administration:i.p.; 14 days[2]