CJ-42794, as a selective antagonist of EP4, less binds to EP2 and does not have binding affinity for EP1 or EP3. It displays minimal effect on numerous other receptors, channels, or enzymes. CJ-42794 delays the healing of gastric ulcers, inhibiting the upregulation of VEGF expression and angiogenesis. EP4, activated by prostaglandin E2 (PGE2), is a G-protein-coupled receptor, which plays vital roles in bone formation and resorption, cancer, and atherosclerosis via elevating the second messenger cyclic AMP (cAMP).

98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

CJ 42794

powder

DMSO : ≥ 28 mg/mL (67.66 mM)

EP2；EP4

CJ-42794 exhibited remarkable binding activity to EP4 and suppressed PGE2-triggered elevations of intracellular cAMP levels in a concentration-dependent fashion in HEK293 cells overexpressing human EP4. Moreover, CJ-42794, concentration-dependently, reversed the inhibitory effects of PGE2 on lipopolysaccharide-evoked tumor necrosis factor α production, which suggested that CJ-42794 had excellent pharmacological properties used for exploring the physiological role of EP4 .

Male Sprague-Dawley rats and C57BL/6 mice were given subcutaneously 3 and 10 mg/kg for rats, 10 mg/kg for mice once daily for 7 or 14 days. Compared to the controls, CJ-42794, in a dose-dependent manner, impaired and delayed the gastric ulcer healing in rats and mice. CJ-42794 markedly dampened the increase of VEGF expression in ulcerated mucosa of the mouse stomach and the primary gastric fibroblasts of rat.