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- 文献和实验
- 技术资料
- 保存条件：
见说明书
- 保质期：
＞1年
- 英文名：
Panobinostat Free Base
- 库存：
期货2-3周
- 供应商：
上海经科化学科技有限公司
- CAS号：
404950-80-7
- 规格：
5mg
供应商：上海经科化学科技有限公司
服务热线：400-0199-638
QQ:472482400(上海经科）
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本试剂(Panobinostat)
仅供科研实验使用,不得用于其他用途！
货 号：P-3703
名 称：Panobinostat
别 名：Panobinostat Free Base
C A S ：404950-80-7
分子量：349.43
分子式：C21H23N3O2
纯 度：HPLC/TLC:>99%
说 明：Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 200 mg/mL; soluble in ethanol at 5 mg/mL with warming; very poorly soluble in water; maximum solubility in plain water is estimated to be about 20-50 µM buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A.
文 献：Panobinostat inhibited histone deacetylase and induced acetylation of histone H3 and alpha-tubulin protein in human umbilical vein endothelial cells (HUVEC), which resulted in induction of G(2)-M cell cycle arrest and inhibition of HUVEC proliferation and viability. Panobinostat at noncytotoxic concentrations inhibited endothelial tube formation, Matrigel invasion, AKT activity, extracellular signal-regulated kinase 1/2 phosphorylation and chemokine receptor CXCR4 expression. It aslo reduced angiogenesis and PC-3 tumor growth in mice. Qian, D.Z., et al. "Targeting tumor angiogenesis with histone deacetylase inhibitors: the hydroxamic acid derivative LBH589." Clin. Cancer Res. 12: 634-642 (2006). After 3 days of incubation, panobinostat inhibited the proliferation of 7 of 8 tested pancreatic cell lines with a mean IC50 of 0.09 µM. Only cell line Capan-2 demonstrated an IC50 value >1 µM. Inhibition of cell growth was more marked if the incubation time was extended to 6 days. In vivo, panobinostat alone significantly decreased tumor mass and augmented the efficacy of gemcitabine. Haefner, M., et al. "Experimental treatment of pancreatic cancer with two novel histone deacetylase inhibitors." World J. Gastroenterol. 14: 3681-3692 (2008). In addition to acetylation of histone H3 and H4, panobinostat also induces acetylation of heat shock protein 90 (hsp90). Cotreatment with panobinostat and the hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG, Cat. No. A-6880) caused synergistic apoptosis of acute leukemia MV4-11 and K562 cells. This combination treatment induced apoptosis of the imatinib mesylate (IM)-refractory leukemia cells expressing Bcr-Abl with the T315I mutation. The cotreatment also brought about more apoptosis of IM-resistant primary chronic myeloid leukemia blast crisis (CML-BC) and acute myeloid leukemia (AML) cells with an activating mutation of FLT-3 than treatment with either drug alone. George, P., et al. "Combination of the histone deacetylase inhibitor LBH589 and the hsp90 inhibitor 17-AAG is highly active against human CML-BC cells and AML cells with activating mutation of FLT-3." Blood 105: 1768-1776 (2005). Treatment with LBH589 for 48 hours potently inhibited MTT uptake. IC50 values for these multiple myeloma cell lines were 5.7 nM (MM1S), 6.5 nM (MM1R), 8.1 nM (U266), 24 nM (U266LR7), and 45.5 nM (U266DOX4). Maiso, P., et al. "The histone deacetylase inhibitor LBH589 is a potent antimyeloma agent that overcomes drug resistance." Cancer Res. 66: 5781-5789 (2006). Panobinostat is well tolerated and induces clinical responses in cutaneous T-cell lymphoma (CTCL) patients. Ellis, L., et al. "Histone deacetylase inhibitor panobinostat induces clinical responses with associated alterations in gene expression profiles in cutaneous T-cell lymphoma." Clin. Cancer Res. 14: 4500-4510 (2008). QTcF prolongation was one of the dose-limiting toxicities of panobinostat but was asymptomatic and was reversed after panobinostat discontinuation. Giles, F., et al. "A phase I study of intravenous LBH589, a novel cinnamic hydroxamic acid analogue histone deacetylase inhibitor, in patients with refractory hematologic malignancies." Clin. Cancer Res. 12: 4628-4635 (2006).
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，PDX101 (Bellinostat)作为一种没有客观反应的单一疗法并不有效。在MPM动物模型中，与未治疗的小鼠相比，panobinostat治疗显著降低了肿瘤生长。迄今为止，最大的间皮瘤试验之一是VANTAGE 14。这是一项III期研究，使用的是vorinostat或安慰剂，研究对象为661名曾接受过化疗的患者。与安慰剂相比，Vorinostat并没有提高生存率，中位生存期分别为31周和27周。然而，无进展生存期得到改善，但与临床无关(来源:欧洲多学科癌症大会)。MPM细胞系,DAC诱导衰老
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Panobinostat
￥940.80
