CJ-42794

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

CJ-42794 是前列腺素 E 受体亚型 4 (EP4) 的选择性拮抗剂。它抑制 [3H]-PGE2 与人 EP4 受体的结合（平均 pKi：8.5）。

CJ-42794 is a selective antagonist of prostaglandin E receptor subtype 4 (EP4). It inhibits [3H]-PGE2 binding to the human EP4 receptor (a mean pKi: 8.5). CJ-42794 is a binding affinity that was at least 200-fold more selective for the human EP4 receptor than other human EP receptor subtypes (EP1, EP2, and EP3) (IC50 : 8.5 (pKi )).(In Vitro):EP4 in vitro: CJ-042794 competitively inhibits PGE2-evoked elevations of intracellular cAMP levels in HEK293 cells overexpressing human EP4receptor with a mean pA2 value of 8.6. CJ-042794 reverses the inhibitory effects of PGE2 on LPS-induced TNFα production in a concentration-dependent manner. (In Vivo):CJ-42794 significantly delays the ulcer healing in rats and mice and these responses were both attenuated by coadministration of CJ-42794.

CJ-042794 (CJ-042794, 0.3-5000 nM; 10 min; hEP4/HEK293 cells) inhibits the PGE2-induced elevation of cAMP in a concentration-dependent manner with a pIC50 value of 7.5.CJ-042794 (3-3000 nM; 24 h) reverses the inhibitory effects of PGE2 (10 nM) on the LPS-induced TNFα production in human whole blood (HWB) in a concentration-dependent manner with a pIC50 value of 6.4.

CJ-042794 (CJ-042794; 0.3-3 mg/kg; i.d.; once) antagonizes the HCO3 stimulatory action of AE1-329 in the duodenum.CJ-042794 (30 and 50 mg/kg; p.o.; once) does not cause any damage to the gastric mucosa of normal rats and has no gastric ulcerogenic response to cold-restraint stress.CJ-042794 (30 and 50 mg/kg; p.o.; once) does not damage the stomach and small intestine of helper arthritis rats.CJ-042794 (3-45 mg/kg; p.o.; twice daily for 14 d; Sprague-Dawley rats) promotes spontaneous healing of gastric ulcers.CJ-042794 (10 mg/kg; p.o.; daily, for 7 d) repeats administration impairs the healing of chronic gastric ulcers with a down-regulation of vascular endothelial growth factor expression in the ulcerated mucosa. Animal Model:Male Sprague-Dawley rats (200-230 g)Dosage:0.3, 1, and 3 mg/kg Administration:intradermal injection; onceResult:Attenuated the PGE2-stimulated HCO3 secretionin a dose-dependent manner and had the inhibition being 68.9% at 1 mg/kg.Animal Model:Male Sprague-Dawley rats (200-230 g)Dosage:30 and 50 mg/kg Administration:Oral administration; onceResult:Did not produce any damage in the gastrointestinal mucosa.Animal Model:Dark Agouti (DA) rats (140-160 g)Dosage:30 and 50 mg/kg Administration:Oral administration; once Result:Caused any visible damage in the gastric mucosa of normal rats.Had little injurious effect on the small intestine of arthritic rats.Animal Model:Male Sprague-Dawley rats (200-230 g)Dosage:3, 10, and 45 mg/kg Administration:Oral administration; twice daily for 14 days Result:Healed ulcers gradually within 14 days, and the ulcer score on day 17 was 1.6 mm2.Animal Model:Male Sprague-Dawley rats (200-230 g) Dosage:10 mg/kg Administration:Oral administration; daily for 7 days Result:Down-regulates the expression of VEGF and decreased the angiogenic response.

CJ-042794

Others

Other Targets

human D2 receptor| human D3 receptor| human D4 receptor

——

——

847728-01-2

413.83

C22H17ClFNO4

>98% (HPLC)

In Vitro:?DMSO : ≥ 28 mg/mL (67.66 mM)

C[C@H](NC(=O)c1cc(Cl)ccc1Oc1ccc(F)cc1)c1ccc(cc1)C(O)=O

——

(-20℃)

With Ice Pack

≥ 2 years