产品
编 号：F163092
分子式：C46H60N4O13S
分子量：909.05
分子式：C46H60N4O13S
分子量：909.05
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
1mg
188
In-stock
5mg
412
In-stock
10mg
616
In-stock
50mg
2112
In-stock
100mg
3360
In-stock
结构图
CAS No: 143-67-9
产品详情
生物活性：
Vinblastine sulfate is a cytotoxic alkaloid used against various cancer types. Vinblastine sulfate inhibits the formation of microtubule and suppresses nAChR with an IC50 of 8.9 μM.
体内研究：
Vinblastine is a widely used anticancer drug with undesired side effects. Its conjugation with carrier molecules could be an efficient strategy to reduce these side effects.
体外研究：
Vinblastine does not depolymerize spindle microtubules, yet it powerfully blocks mitosis (for example, IC50 0.8 nM in HeLa cells) and cells die by apoptosis. In NB4 cells, vinblastine produces alteration of p53 and DNA fragmentation. Vinblastine treatment has an antiproliferative effect via the induction of apoptosis producing Bax/Bcl-2 imbalance. Vinblastine treatment suppresses NFκB expression and depresses NFκB-DNA binding activity while maintaining JNK activation that subsequently results in apoptotic response through caspase-dependent pathway. Vinblastine is found to trigger apoptosis as evidenced by the loss of mitochondrial membrane potential, the release of both cytochrome c and apoptosis inducing factor, activation of caspase-9 and 3, and cleavage of Poly (ADP-ribose)-Polymerase.
Vinblastine sulfate is a cytotoxic alkaloid used against various cancer types. Vinblastine sulfate inhibits the formation of microtubule and suppresses nAChR with an IC50 of 8.9 μM.
体内研究：
Vinblastine is a widely used anticancer drug with undesired side effects. Its conjugation with carrier molecules could be an efficient strategy to reduce these side effects.
体外研究：
Vinblastine does not depolymerize spindle microtubules, yet it powerfully blocks mitosis (for example, IC50 0.8 nM in HeLa cells) and cells die by apoptosis. In NB4 cells, vinblastine produces alteration of p53 and DNA fragmentation. Vinblastine treatment has an antiproliferative effect via the induction of apoptosis producing Bax/Bcl-2 imbalance. Vinblastine treatment suppresses NFκB expression and depresses NFκB-DNA binding activity while maintaining JNK activation that subsequently results in apoptotic response through caspase-dependent pathway. Vinblastine is found to trigger apoptosis as evidenced by the loss of mitochondrial membrane potential, the release of both cytochrome c and apoptosis inducing factor, activation of caspase-9 and 3, and cleavage of Poly (ADP-ribose)-Polymerase.
产品资料
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