| CAS NO: | 847728-01-2 |
| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
| Cas No. | 847728-01-2 |
| 别名 | 4-[(1S)-1-[[5-氯-2-(4-氟苯氧基)苄基]氨基]乙基]苯甲酸,RQ-00015986 |
| 化学名 | 4-[(1S)-1-[[5-chloro-2-(4-fluorophenoxy)benzoyl]amino]ethyl]-benzoic acid |
| Canonical SMILES | FC1=CC=C(OC2=C(C(N[C@@H](C)C3=CC=C(C(O)=O)C=C3)=O)C=C(Cl)C=C2)C=C1 |
| 分子式 | C22H17ClFNO4 |
| 分子量 | 413.8 |
| 溶解度 | ≥ 11.7mg/mL in DMSO |
| 储存条件 | Store at -20℃ |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
| Shipping Condition | Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request |
| 产品描述 | Ki: 3.16 nM: antagonizes E prostanoid receptor 4 (EP4). Ki: 631 nM: antagonizes EP2. 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). In vitro: 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 [1]. In vivo: 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 [2]. References: |
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