
TMN355
CAS No. 1186372-20-2
TMN355 ( —— )
产品货号. M22935 CAS No. 1186372-20-2
TMN355 是一种有效的亲环蛋白 A 化学抑制剂,可减少泡沫细胞形成和细胞因子分泌,用于治疗动脉粥样硬化。使用 siRNA 或化学抑制剂沉默 THP-1 细胞和人单核细胞中的亲环蛋白 A,即使在暴露于氧化 LDL 后,TMN355 也会导致脂质摄取减少 65-75%。
纯度: >98% (HPLC)






规格 | 价格/人民币 | 库存 | 数量 |
5MG | ¥1191 | 有现货 |
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10MG | ¥1847 | 有现货 |
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25MG | ¥3216 | 有现货 |
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50MG | ¥4982 | 有现货 |
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100MG | ¥7096 | 有现货 |
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500MG | ¥14418 | 有现货 |
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1G | 获取报价 | 有现货 |
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生物学信息
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产品名称TMN355
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注意事项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
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产品简述TMN355 是一种有效的亲环蛋白 A 化学抑制剂,可减少泡沫细胞形成和细胞因子分泌,用于治疗动脉粥样硬化。使用 siRNA 或化学抑制剂沉默 THP-1 细胞和人单核细胞中的亲环蛋白 A,即使在暴露于氧化 LDL 后,TMN355 也会导致脂质摄取减少 65-75%。
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产品描述TMN355 is a potent chemical inhibitor of cyclophilin A and reduces foam cell formation and cytokine secretion,and is used for atherosclerosis. Silencing cyclophilin A in THP-1 cells and human monocytes using siRNA or chemical inhibitor, TMN355 resulted in decrease in lipid uptake by 65-75% even after exposure to oxidized LDL.?The expression of scavenger receptors expressed during differentiation process, CD36 and LOX-1 were decreased (p 0.0001).?Levels of extracellular cyclophilin A and other inflammatory cytokines such as TNF-α and MCP-1also significantly reduced.?TMN 355 (0.5-10 μM;?3-9 hours) results in 75.9% reduction of cyclophilin A protein expression.?And cyclophilin A after 6 h of activation inhibited by TMN 355(1 μM).
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体外实验TMN 355 (0.5-10 μM; 3-9 hours) results in 75.9% reduction of cyclophilin A protein expression. And 1 μM TMN 355 inhibits cyclophilin A after 6 h of activation.Western Blot Analysis Cell Line:THP cell lines Concentration:0.5, 1, 2.5, 5 and 10 μM Incubation Time:3, 6 and 9 hours Result:Resulted in 75.9% reduction of cyclophilin A protein expression.
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体内实验——
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同义词——
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通路Others
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靶点Other Targets
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受体cyclophilin A
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研究领域——
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适应症——
化学信息
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CAS Number1186372-20-2
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分子量380.8
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分子式C21H14ClFN2O2
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纯度>98% (HPLC)
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溶解度DMSO:31.25 mg/mL (82.06 mM; Need ultrasonic)
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SMILESO=C(NC(NC1C2=C(C3=C1C=CC=C3)C=CC=C2)=O)C4=C(F)C=CC=C4Cl
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化学全称——
运输与储存
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储存条件(-20℃)
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运输条件With Ice Pack
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稳定性≥ 2 years
参考文献
1.Ramachandran S, et al. Cyclophilin A enhances macrophage differentiation and lipid uptake in high glucose conditions: a cellular mechanism for accelerated macro vascular disease in diabetes mellitus. Cardiovasc Diabetol. 2016 Nov 3;15(1):152.