Cytochalasin H
CAS No. 53760-19-3
Cytochalasin H ( (16-Benzyl-5,12-dihydroxy-5,7,14-trimethyl-13-methylidene-18-oxo-17-azatricyclo[9.7.0.01,15]octadeca-3,9-dien-2-yl) acetate )
产品货号. M24524 CAS No. 53760-19-3
Cytochalasin H 是肌动蛋白掺入肌丝的有效抑制剂。
纯度: >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
| 规格 | 价格/人民币 | 库存 | 数量 |
| 2MG | ¥1349 | 有现货 |
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| 5MG | ¥2261 | 有现货 |
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| 10MG | ¥3297 | 有现货 |
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| 25MG | ¥4938 | 有现货 |
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| 50MG | ¥6631 | 有现货 |
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| 100MG | ¥8577 | 有现货 |
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| 200MG | ¥11520 | 有现货 |
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| 500MG | 获取报价 | 有现货 |
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| 1G | 获取报价 | 有现货 |
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| 1 mL x 10 mM in DMSO | ¥3772 | 有现货 |
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生物学信息
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产品名称Cytochalasin H
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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Cytochalasin H 是肌动蛋白掺入肌丝的有效抑制剂。
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产品描述Cytochalasin H is a potent inhibitor of actin incorporation into filaments.
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体外实验Apoptosis AnalysisCell Line:A549 cells Concentration:0, 6.25, 12.5, 25 and 50 μM Incubation Time:48 h Result:Induced apoptosis in a dose-dependent manner in the A549 cells.Cell Cycle Analysis Cell Line:A549 cells Concentration: 0, 6.25, 12.5, 25 and 50 μM Incubation Time:48 h Result:Arrested cell cycle at the G2/M phase and sub-G1 peaks.Western Blot Analysis Cell Line:A549 cells Concentration:0, 6.25, 12.5, 25 and 50 μM Incubation Time:48 h Result:Increased the protein expression levels of Bax, P53 and cleaved caspase-3 and decreased the protein expression levels of Bcl-xL, Bcl-2 and full-length caspase-3.
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体内实验Animal Model:male Balb/cnu/nu mice with A549 xenograftDosage:2.5 mg/kg Administration:intraperitoneal injection; 3 injections/week,for 80 days Result:Attenuated tumor growth in vivo.
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同义词(16-Benzyl-5,12-dihydroxy-5,7,14-trimethyl-13-methylidene-18-oxo-17-azatricyclo[9.7.0.01,15]octadeca-3,9-dien-2-yl) acetate
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通路Others
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靶点Other Targets
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受体ET-1|MMP2
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研究领域——
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适应症——
化学信息
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CAS Number53760-19-3
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分子量493.63
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分子式C30H39NO5
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纯度>98% (HPLC)
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溶解度——
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SMILESC[C@@H]([C@@H]([C@H](Cc1ccccc1)N1)[C@@]([C@H]([C@@H]2O)/C=C/C[C@H](C)C[C@](C)(/C=C3)O)([C@@H]3OC(C)=O)C1=O)C2=C
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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.Ma Y , Xiu Z , Zhou Z , et al. Cytochalasin H Inhibits Angiogenesis via the Suppression of HIF-1α Protein Accumulation and VEGF Expression through PI3K/AKT/P70S6K and ERK1/2 Signaling Pathways in Non-Small Cell Lung Cancer Cells[J]. Journal of Cancer, 2019, 10(9).
产品手册
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