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Buparlisib

产品编号 T1827 CAS 944396-07-0

别名: BKM120, 布帕尼西, NVP-BKM120

Buparlisib (BKM120) 是一种具有口服生物利用度的泛 I 类 PI3K 特异性口服抑制剂，对p110α/p110β/p110δ/p110γ的IC50分别为 52 nM/166 nM/116 nM/262 nM。

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Buparlisib, CAS 944396-07-0

规格	价格/CNY	货期
1 mg	￥ 233	现货
5 mg	￥ 529	现货
10 mg	￥ 788	现货
25 mg	￥ 1,190	现货
50 mg	￥ 1,730	现货
100 mg	￥ 2,570	现货
200 mg	￥ 3,820	现货
500 mg	￥ 5,730	现货
1 mL * 10 mM (in DMSO)	￥ 586	现货

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其他形式的 Buparlisib:

Buparlisib Hydrochloride
询价

选择批次

纯度: 98.4%

纯度: 98%

纯度: 96.22%

纯度: 95.32%

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生物活性

化学信息

存储 & 溶解度

参考文献

相关产品

产品描述	Buparlisib (BKM120) is an orally bioavailable specific oral inhibitor of the pan-class I PI3K (IC50s: 52/166/116/nM for p110α, p110β, and p110δ).
靶点活性	p110α:52 nM (cell free), p110γ:262 nM (cell free), p110δ:116 nM (cell free), p110β:166 nM (cell free), VPS34:2.4 μM (cell free)
体外活性	Buparlisib exhibited 50-300 nM activity for class I PI3K's, including the most common p110R mutants. Additionally, 15 exhibited lower potency against class III and class IV PI3K's, where 2, 5, >5, and >25 μM biochemical activity was observed for inhibition of VPS34, mTOR, DNAPK, and PI4K, respectively. Across all cell lines, pathway modulation and antiproliferative activity was consistent with cellular PI3K inhibition [1]. Buparlisib demonstrated anti-proliferative activity in 11 human gastric cancer cell lines by decreasing mTOR downstream signaling. But Buparlisib treatment increased p-AKT by subsequent abrogation of feedback inhibition by stabilizing insulin receptor substrate-1. In KRAS mutant gastric cancer cells, either p-ERK or p-STAT3 was also increased upon treatment of Buparlisib [2]. BKM120 induces cell growth inhibition and apoptosis in both multiple myeloma (MM) cell lines and freshly isolated primary MM cells. In addition, BKM120 shows synergistic cytotoxicity with dexamethasone in dexamethasone-sensitive MM cells. Low doses of BKM120 and dexamethasone, each of which alone has limited cytotoxicity, induce significant cell apoptosis in MM.1S and ARP-1. BKM120 exposure causes cell cycle arrest by upregulating p27 (Kip1) and downregulating cyclin D1 and induces caspase-dependent apoptosis by downregulating antiapoptotic XIAP and upregulating expression of a cytotoxic small isoform of Bim, BimS [3].
体内活性	In A2780 xenograft tumors, oral dosing of Buparlisib at 3, 10, 30, 60, and 100 mg/kg resulted in a dose-dependent modulation of pAKTSer473. Partial inhibition of pAKTser473 was observed at 3 and 10 mg/kg, and near complete inhibition was observed at doses of 30, 60, or 100 mg/kg, respectively. Inhibition of pAkt tracked well with both plasma and tumor drug exposure. pAKT modulation was also time-dependent, with >90% target modulation achieved with the 60 and 100 mg/kg dose at the 10 h time point when the plasma and tumor exposure was ca. 2 μM [1]. The treatment by Buparlisib (5 μM/kg/day) had significantly smaller tumor burdens as compared with control mice, which were measured as tumor volume and level of circulating human kappa chain. In addition, Buparlisib treatment significantly prolonged the survival of tumor-bearing mice [3].
激酶实验	Compounds to be tested were dissolved in DMSO and directly distributed into a black 384-well plate at 1.25 μL per well. To start the reaction, 25 μL of 10 nM PI3 kinase and 5 μg/mL 1-alpha-phosphatidylinositol (PI) in assay buffer (10 mM Tris pH 7.5, 5 mM MgCl2, 20 mM NaCl, 1 mM DTT and 0.05% CHAPS) were added into each well followed by 25 μL of 2 μM ATP in assay buffer. The reaction was performed until approx 50% of the ATP was depleted, and then stopped by the addition of 25 μL of KinaseGlo solution. The stopped reaction was incubated for 5 minutes and the remaining ATP was then detected via luminescence [1].
细胞实验	A2780 cells were cultured in DMEM supplemented with 10% FBS. L-glutamine, sodium pyruvate, and antibiotics. Cells were plated in the same medium at a density of 1000 cells per well, 100 ul per well into black-walled-clear-bottom plates and incubated for 3-5 hours. Test compounds supplied in DMSO (20 mM) were diluted further into DMSO (7.5 ul of 20 mM test compound in 22.5 ul DMSO. Mix well, transfer 10 ul to 20 ul DMSO, repeat until 9 concentrations have been made). The diluted test compound solution (2uL), was then added to the cell medium (500 ul) cell medium. Equal volumes of this solution (100 uL) were added to the cells in 96 well plates and incubated at 37 oC for 3 days and developed using Cell Titer Glo. Inhibition of cell proliferation was determined by luminescence read using Trilux [1].
动物实验	Six- to eight-week-old female severe combined immunodeficiency (SCID) mice were housed and monitored in the MD Anderson Cancer Center animal research facility. SCID mice were subcutaneously inoculated in the right flank with 1 million ARP-1 or MM.1S cells suspended in 50 μl phosphate-buffered saline (PBS). After palpable tumor developed (tumor diameter ≥5 mm), mice were treated with intraperitoneal injection of DMSO/PBS or BKM120 (5 μM per kg per day) for 15 days. Tumor sizes were measured every 5 days, and blood samples were collected at the same period. Tumor burdens were evaluated by measuring tumor size and detecting the circulating human kappa chain or lambda chain [3].

别名	BKM120, 布帕尼西, NVP-BKM120
分子量	410.39
分子式	C18H21F3N6O2
CAS No.	944396-07-0

存储

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

溶解度

DMSO: 76 mg/mL (185.2 mM)

H2O: Insoluble

Ethanol: 2 mg/mL

溶液配制表

可选溶剂	浓度体积质量	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.4367 mL	12.1835 mL	24.3671 mL	60.9177 mL
	5 mM	0.4873 mL	2.4367 mL	4.8734 mL	12.1835 mL
	10 mM	0.2437 mL	1.2184 mL	2.4367 mL	6.0918 mL
	20 mM	0.1218 mL	0.6092 mL	1.2184 mL	3.0459 mL
	50 mM	0.0487 mL	0.2437 mL	0.4873 mL	1.2184 mL
	100 mM	0.0244 mL	0.1218 mL	0.2437 mL	0.6092 mL

计算器

摩尔浓度计算器

稀释计算器

配液计算器

分子量计算器

质量

浓度

容积

分子量

浓度 (起始)

容积 (起始)

浓度 (终)

容积 (终)

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质量

配液浓度

参考文献

1. Burger MT, et al. Identification of NVP-BKM120 as a Potent, Selective, Orally Bioavailable Class I PI3 Kinase Inhibitor for Treating Cancer. ACS Med Chem Lett. 2011 Aug 26;2(10):774-9. 2. Park E, et al. NVP-BKM120, a novel PI3K inhibitor, shows synergism with a STAT3 inhibitor in human gastric cancer cells harboring KRAS mutations. Int J Oncol. 2012 Apr;40(4):1259-66. 3. Zheng Y, et al. Novel phosphatidylinositol 3-kinase inhibitor NVP-BKM120 induces apoptosis in myeloma cells and shows synergistic anti-myeloma activity with dexamethasone. J Mol Med (Berl). 2012 Jun;90(6):695-706. 4. Hu P, Li H, Yu X, et al. GL-V9 exerts anti-T cell malignancies effects via promoting lysosome-dependent AKT1 degradation and activating AKT1/FOXO3A/BIM axis[J]. Free Radical Biology and Medicine. 2019. 5. Wencao Zhao, Le Cao, Hanru Ying, Wenjuan Zhang, Dantong Li, Xiaolong Zhu, Wenzhi Xue, Shuang Wu, Mengye Cao, Cong Fu, Haonan Qi, Yimei Hao, Yun-Chi Tang, Jun Qin, Tao P. Zhong, Xiaoxi Lin, Luyang Yu, Xuri Li, Lin Li, Dianqing Wu & Weijun Pan . Endothelial CDS2 deficiency causes VEGFA-mediated vascular regression and tumor inhibition. Cell Research. 2019

文献引用

1. Wencao Zhao, Le Cao, Hanru Ying, Wenjuan Zhang, Dantong Li, Xiaolong Zhu, Wenzhi Xue, Shuang Wu, Mengye Cao, Cong Fu, Haonan Qi, Yimei Hao, Yun-Chi Tang, Jun Qin, Tao P. Zhong, Xiaoxi Lin, Luyang Yu, Xuri Li, Lin Li, Dianqing Wu & Weijun Pan Endothelial CDS2 deficiency causes VEGFA-mediated vascular regression and tumor inhibition. Cell Research. 2019 2. Hu P, Li H, Yu X, et al. GL-V9 exerts anti-T cell malignancies effects via promoting lysosome-dependent AKT1 degradation and activating AKT1/FOXO3A/BIM axis. Free Radical Biology and Medicine. 2019

剂量换算

对于不同动物的给药剂量换算，您也可以参考 更多...

体内实验配液计算器

请在以下方框中输入您的动物实验信息后点击计算，可以得到母液配置方法和体内配方的制备方法：比如您的给药剂量是10 mg/kg，每只动物体重20 g，给药体积100 μL，一共给药动物10 只，您使用的配方为5% DMSO+30% PEG300+5% Tween 80+60% ddH2O。那么您的工作液浓度为2 mg/mL。

母液配置方法：2 mg 药物溶于 50 μL DMSO (母液浓度为 40 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 50 μL DMSO 主液，加入 300 μL PEG300，混匀澄清，再加 50 μL Tween 80，混匀澄清，再加 600 μL ddH2O, 混匀澄清。

第一步：请输入动物实验的基本信息

剂量

mg/kg

每只动物体重

给药体积

μL

动物数量

第二步：请输入动物体内配方组成，不同的产品配方组成不同，如有配方需求，可先联系我们提供正确的体内配方。

% DMSO+

% +

% Tween 80+

% ddH₂O

%DMSO+

计算重置

计算结果如下:

工作液浓度: mg/ml;

母液配置方法: mg 药物溶于 μL DMSO (母液浓度为 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 μL DMSO 主液，加入 μL PEG300，混匀澄清，再加 μL Tween 80，混匀澄清，再加 μL ddH₂O, 混匀澄清。

备注:

要按顺序从左向右依次添加助溶剂。可配合物理方法，如涡流、超声波或热水浴使之帮助溶解。

技术支持

您可能有的问题的答案可以在抑制剂处理说明中找到，包括如何准备库存溶液，如何存储产品，以及基于细胞的分析和动物实验需要特别注意的问题。

Keywords

Buparlisib 944396-07-0 Apoptosis PI3K/Akt/mTOR signaling PI3K BKM120 Phosphoinositide 3-kinase inhibit BKM 120 Inhibitor 布帕尼西 NVP-BKM-120 BKM-120 NVP-BKM120 NVP-BKM 120 inhibitor

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Buparlisib

存储

溶解度

溶液配制表

计算器

输入分子式，点击计算，可计算出产品的分子量。

参考文献

文献引用

相关产品

相关化合物库

剂量换算

体内实验配液计算器

技术支持

Keywords