| CAS NO: | 712313-35-4 |
| 包装 | 价格(元) |
| 1mg | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
| Cas No. | 712313-35-4 |
| 化学名 | 3-[[(3-carboxycyclohexyl)amino]carbonyl]-4-[3-[4-[4-(cyclohexyloxy)butoxy]phenyl]propoxy]-benzoic acid |
| Canonical SMILES | O=C(NC1CCCC(C(O)=O)C1)C2=CC(C(O)=O)=CC=C2OCCCC(C=C3)=CC=C3OCCCCOC4CCCCC4 |
| 分子式 | C34H45NO8 |
| 分子量 | 595.7 |
| 溶解度 | ≤5mg/ml in ethanol;20mg/ml in DMSO;20mg/ml in dimethyl formamide |
| 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 | IC50: 37.9 nM: blocks radioligand binding of leukotriene D4 (LTD4) to cysteinyl leukotriene 2 (CysLT2). IC50: 3.8 nM: antagonizes LTD4-induced intracellular calcium mobilization in a CysLT2 receptor reporter cell line. IC50: 4.4 nM: antagonizes leukotriene C4 (LTC4) -induced intracellular calcium mobilization in a CysLT2 receptor reporter cell line. HAMI3379, as a potent CysLT2 receptor antagonist, blocks radioligand binding of LTD4 to CysLT2 and CysLT1 receptor cell lines. In a CysLT2 receptor reporter cell line, HAMI3379 antagonizes LTD4- and LTC4-induced intracellular calcium mobilization. In contrast, HAMI3379 exhibits very low potency on a CysLT1 receptor reporter cell line. Additionally, HAMI3379 does not exhibit any agonistic activity on both CysLT2 and CysLT1 receptor cell lines. CysLTs LTC4 and LTD4 are potent mediators of hypersensitivity and asthma reactions. They increase the permeability of microvascular, elicit bronchoconstriction, functioning as vasoconstrictors of coronary arteries, which are transduced by CysLT1 and CysLT2. In vitro: In a murine microglial cell line (BV-2 cells), HAMI3379 effectively dampened lipopolysaccharide (LPS) -induced phagocytosis. In addition, HAMI3379 dose-dependently decreased the LPS-induced overproduction of proinflammatory cytokines which included tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 [1]. In vivo: Male Sprague–Dawley rats were injected intraperitoneally with HAMI 3379 at a dose of 0.1 mg/kg at 0, 1, 2 and 4 h. After 24 h, HAMI 3379 attenuated the acute brain injury after middle cerebral artery occlusion (MCAO). In addition, HAMI 3379 weakened the neurological deficits and decreased brain edema, infarct volume, and neuronal loss and degeneration after MACO. Moreover, HAMI 3379 blocked the release of interferon-γ, cytokines IL-1β, and TNF-α into the cerebrospinal fluid and serum after MACO [2]. References: |
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