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SC-236
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| 描述 |
SC-236 是具有口服活性的 COX-2 特异性抑制剂 (对COX-1 和COX-2 的IC50 分别为10 nM 和17.8 μM)和 PPARγ 激动剂。SC-236 可通过c-Jun 氨基端抑制激活蛋白-1 (AP-1) 活性。SC-236在小鼠模型中通过抑制ERK的磷酸化发挥抗炎作用。 |
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| 相关类别 |
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| 靶点 |
COX-2:10 nM (IC50)
COX-1:17.8 μM (IC50)
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| 体外研究 |
SC-236（15μM，30分钟）抑制非甾体抗炎药的副作用，并防止血管内皮细胞受到ALSS的炎症[1]。SC-236在HSCs中显著诱导PPARγ表达，并在荧光素酶报告子反式激活试验中作为有效的PPARγ激动剂[2]。SC-236以时间和浓度依赖的方式强烈抑制巨噬细胞活力[2]。SC-236单独或与15d-PGJ2联合，在培养的HSCs中诱导显著的促凋亡作用[2]。SC-236通过调节AP-1信号通路介导抗肿瘤作用[3]。westernblot分析[1]细胞系：vECs。浓度：15μM孵育时间：30min。结果：大鼠内皮细胞COX-2水平明显降低，IκBα水平明显升高，从而抑制ALSS诱导的NFκB活化和炎症反应。westernblot分析[2]细胞系：cos7细胞。浓度：3、10μM，孵育时间：18h（与15d-PGJ2合用）。结果：PPARγ激动剂具有浓度依赖性。 |
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| 体内研究 |
SC-236（6 mg/kg，灌胃）在CCl4处理的动物中表现出抗纤维化特性[2]。动物模型：76只成年雄性Wistar大鼠，体重200-220g（CCl4处理）[2]。剂量：6mg/kg。给药：口服，每周3次。结果：CCl4处理后大鼠肝脏COX-2蛋白表达明显增强。显著降低肝纤维化程度。显著抑制CCl4处理大鼠α-SMA的表达。 |
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| 溶解度 |
In Vitro:
DMSO : 100 mg/mL (248.89 mM; Need ultrasonic) In Vivo:
1. 请依序添加每种溶剂：?10% DMSO ?? 40% PEG300 ?? 5% Tween-80 ?? 45% saline Solubility: 2.5 mg/mL (6.22 mM); Suspended solution; Need ultrasonic 2. 请依序添加每种溶剂：?10% DMSO ?? 90% (20% SBE-β-CD in saline) Solubility: ≥ 2.5 mg/mL (6.22 mM); Clear solution 3. 请依序添加每种溶剂：?10% DMSO ?? 90% corn oil Solubility: ≥ 2.5 mg/mL (6.22 mM); Clear solution
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| 储备液 |
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| 存储 |
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| 运输 |
室温 |
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| SMILES |
O=S(C1=CC=C(N2N=C(C(F)(F)F)C=C2C3=CC=C(Cl)C=C3)C=C1)(N)=O |
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| 参考文献 |
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| 密度 | 1.5±0.1 g/cm3 |
|---|---|
| 沸点 | 543.4±60.0 °C at 760 mmHg |
| 分子式 | C16H11ClF3N3O2S |
| 分子量 | 401.791 |
| 闪点 | 282.4±32.9 °C |
| 精确质量 | 401.021271 |
| PSA | 86.36000 |
| LogP | 4.32 |
| 蒸汽压 | 0.0±1.5 mmHg at 25°C |
| 折射率 | 1.625 |
| 海关编码 | 2935009090 |
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| 中文概述 | 2935009090 其他磺（酰）胺. 增值税率:17.0% 退税率:9.0% 监管条件:无 最惠国关税:6.5% 普通关税:35.0% |
| 申报要素 | 品名, 成分含量, 用途 |
| Summary | 2935009090 other sulphonamides VAT:17.0% Tax rebate rate:9.0% Supervision conditions:none MFN tariff:6.5% General tariff:35.0% |
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Downregulation of sphingosine 1-phosphate (S1P) receptor 1 by dexamethasone inhibits S1P-induced mesangial cell migration. Biol. Chem. 396 , 803-12, (2015)
Sphingosine 1-phosphate (S1P) is generated by sphingosine kinase (SK)-1 and -2 and acts mainly as an extracellular ligand at five specific receptors, denoted S1P1-5. After activation, S1P receptors re…
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Inhibition of COX-1 attenuates the formation of thromboxane A2 and ameliorates the acute decrease in glomerular filtration rate in endotoxemic mice. Am. J. Physiol. Renal Physiol. 309 , F332-40, (2015)
Thromboxane (Tx) A2 has been suggested to be involved in the development of sepsis-induced acute kidney injury (AKI). Therefore, we investigated the impact of cyclooxygenase (COX)-1 and COX-2 activity…
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COX-2 gene dosage-dependent defects in kidney development. Am. J. Physiol. Renal Physiol. 310 , F1113-22, (2016)
Deletion of cyclooxygenase (COX)-2 causes impairment of kidney development, including hypothrophic glomeruli and cortical thinning. A critical role for COX-2 is seen 4-8 days postnatally. The present …
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HMS3262A06 |
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4-[5-(4-Chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]-benzenesulfonamide SC-58236 |
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4-[5-(4-Chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benzenesulfonamide |
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4-(5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide |
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