硫酸长春碱作用机制 - Medchemexpress - MCE中国

1、Product Data SheetVinblastine sulfateCat. No.: HY-13780CAS No.: 143-67-9分式: CHNOS分量: 909.05作靶点: Microtubule/Tubulin; Autophagy作通路: Cell Cycle/DNA Damage; Cytoskeleton; Autophagy储存式: 4C, protect from light* In solvent : -80C, 6 months; -20C, 1 month (protect from light)溶解性数据体外实验 DMSO : 44 mg/mL (48.4

2、0 mM)* means soluble, but saturation unknown.SolventMass1 mg 5 mg 10 mgConcentration制备储备液1 mM 1.1000 mL 5.5002 mL 11.0005 mL5 mM 0.2200 mL 1.1000 mL 2.2001 mL10 mM 0.1100 mL 0.5500 mL 1.1000 mL请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；旦配成溶液，请分装保存，避免反复冻融造成的产品失效。储备液的保存式和期限：-80C, 6 months; -20C, 1 month (protect fro

3、m light)。-80C 储存时，请在 6 个内使，-20C 储存时，请在 1 个内使。体内实验请根据您的实验动物和给药式选择适当的溶解案。以下溶解案都请先按照 In Vitro 式配制澄清的储备液，再依次添加助溶剂：为保证实验结果的可靠性，澄 的储备液可以根据储存条件，适当保存；体内实验的作液，建议您现现配，当天使； 以下溶剂前显的百分 指该溶剂在您配制终溶液中的体积占；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的式助溶1. 请依序添加每种溶剂： 10% DMSO 40% PEG300 5% Tween-80 45% salineSolubility: 2.5 mg/mL (

4、2.75 mM); Clear solution此案可获得 2.5 mg/mL (2.75 mM，饱和度未知) 的澄清溶液。以 1 mL 作液为例，取 100 L 25.0 mg/mL 的澄 DMSO 储备液加到 400 L PEG300 中，混合均匀；向上述体系中加50 L Tween-80，混合均匀；然后继续加 450 L 理盐定容 1 mL。2. 请依序添加每种溶剂： 10% DMSO 90% (20% SBE-CD in saline)Solubility: 2.5 mg/mL (2.75 mM); Clear solution此案可获得 2.5 mg/mL (2.75 mM，饱和度未

5、知) 的澄清溶液。以 1 mL 作液为例，取 100 L 25.0 mg/mL 的澄 DMSO 储备液加到 900 L 20% 的 SBE-CD 理盐溶液中，混合Page 1 of 2 www.MedChemE均匀。3. 请依序添加每种溶剂： 10% DMSO 90% corn oilSolubility: 2.5 mg/mL (2.75 mM); Clear solution此案可获得 2.5 mg/mL (2.75 mM，饱和度未知) 的澄 溶液，此案不适于实验周 期在半个以上的实验。以 1 mL 作液为例，取 100 L 25.0 mg/mL 的澄 DMSO 储备液加到 900 L 油中

6、，混合均匀。BIOLOGICAL ACTIVITY物活性 Vinblastine sulfate 值为8.9 M。种针对各种癌症类型的有细胞毒性的物碱。 长春花碱可抑制微管的形成，抑制nAChR的IC50IC & Target IC50: 8.9 M(nAChR)1体外研究 Vinblastine does not depolymerize spindle microtubules, yet it powerfully blocks mitosis (for example, IC50 0.8 nM inHeLa cells) and cells die by apoptosis2. In N

7、B4 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 NFB expression and depresses NFB-DNA binding activity while maintaining JNKactiva

8、tion that subsequently results in apoptotic response through caspase-dependent pathway3. Vinblastine isfound to trigger apoptosis as evidenced by the loss of mitochondrial membrane potential, the release of bothcytochrome c and apoptosis inducing factor, activation of caspase-9 and 3, and cleavage o

9、f Poly (ADP-ribose)-Polymerase4.体内研究 Vinblastine is a widely used anticancer drug with undesired side effects. Its conjugation with carrier molecules couldbe an efficient strategy to reduce these side effects5.户使本产品发表的科研献 Biochem Pharmacol. 2020 Mar 3:113865. Mutat Res Genet Toxicol Environ Mutagen.

10、 2016 Sep 15;808:27-37. Int J Clin Exp Pathol. 2017;10(3):3033-3042.See more customer validations on HYPERLINK www.MedChemE www.MedChemEREFERENCES1. McKay DB, et al. Nicotinic and nonnicotinic receptor-mediated actions of vinblastine. Proc Soc Exp Biol Med. 1993 Jul;203(3):372-6.2. Pandya P, et al.

11、Molecular recognition pattern of cytotoxic alkaloid vinblastine with multiple targets. J Mol Graph Model. 2014 Nov;54:1-9.3. Calvi?o E, et al. JNK and NFB dependence of apoptosis induced by vinblastine in human acute promyelocytic leukaemia cells. Cell Biochem Funct. 2015Jun;33(4):211-9.4. Selimovic

12、 D, et al. Vinblastine-induced apoptosis of melanoma cells is mediated by Ras homologous A protein (Rho A) via mitochondrial and non-mitochondrial-dependent mechanisms. Apoptosis. 2013 Aug;18(8):980-97.5. Bnczi Z, et al. Synthesis and in vitro antitumor effect of vinblastine derivative-oligoarginine conjugates. Bioconjug Chem. 2010 Nov 17;21(11):1948-55.Page 2 of 3 www.MedChemEMcePdfHeightCaution: Product has not b