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Triciribine

产品编号 T6065 CAS 35943-35-2

别名: VD-0002, Tricyclic nucleoside, NSC 154020, 曲西立滨, API-2, TCN

Triciribine (NSC-154020) 是一种 DNA 合成抑制剂，也抑制 Akt 和 HIV-1/2，IC50分别为 130 nM 和 0.02-0.46 μM。

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Triciribine, CAS 35943-35-2

规格	价格/CNY	货期
1 mg	￥ 297	现货
2 mg	￥ 439	现货
5 mg	￥ 682	现货
10 mg	￥ 945	现货
25 mg	￥ 1,790	现货
50 mg	￥ 3,160	现货
100 mg	￥ 4,680	现货
1 mL * 10 mM (in DMSO)	￥ 756	现货

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纯度: 100%

纯度: 99.87%

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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	Triciribine (NSC-154020) is a DNA synthesis inhibitor, and it also inhibits Akt and HIV-1/2.
靶点活性	HIV-1:20 nM, Akt:130 nM
体外活性	Triciribine exhibits maximum growth inhibition around 1-10 μM and inhibits phosphorylation of Akt, as well as downstream p70S6K, to basal levels at 100 μM (IC50 = 130 nM). Triciribine shows particular promise for inhibiting growth in Nf1 and Trp53 mutant astrocytoma cells in a grade-dependent manner. The WHO II K1861-10 line is inhibited, incompletely (69% maximum inhibition), with a GI50 value of 1.7 μM for Triciribine, whereas higher-grade tumor lines (KR158, KR130, and SF295) are inhibited to a greater extent (>80% maximum inhibition) at lower GI50 values (0.4–1.1 mM). Importantly, Triciribine is much less effective at inhibiting primary astrocytes (GI5013.6 mM), suggesting that this inhibitor may show specificity for tumor cells. [1] Triciribine inihibits HIV-1with an IC50 of 20 nM. Greater than 90% inhibition is achieved at 0.1 μM and complete inhibition of syncytia formation is achieved at 5 μM. Associated cell toxicity in the same cell line for Triciribine is 46 μM, resulting in selectivity indices of 2250. Triciribine markedly inhibits HIV-1-induced p24 core antigen production, reverse transcriptase, and infectious virus production in a dose-dependent manner using HIV-1 acutedly infected CEM-SS, H9, and persistently infected H9III B and U1 cells. [2] Triciribine inhibits Akt phosphorylation at Thr308 and Ser473 and Akt activity in the human prostate cancer cell line PC-3. Triciribine sensitizes PC-3 cells to TRAIL- and anti-CD95-induced apoptosis, whereas the cells remain resistant to DNA damaging chemotherapeutics. [3] Triciribine is highly selective for Akt and does not inhibit the activation of phosphatidylinositol 3-kinase, phosphoinositide-dependent kinase-1, protein kinase C, serum and glucocorticoid-inducible kinase, protein kinase A, signal transducer and activators of transcription 3, extracellular signal-regulated kinase-1/2, or c-Jun NH2-terminal kinase. [4]
体内活性	1 mg/kg/day i.p. treated Triciribine inhibits OVCAR3, OVCAR8 and PANC1 tumor growth, which overexpressing Akt, by 90%, 88% and 80% in nude mice, respectively. However, Triciribine has little effect on the growth of OVCAR5 and COLO357 cells. [4]
激酶实验	Akt Phosphorylation Changes Assay: Cells are grown to 80%–90% confluency and stimulated for 5–10 minutes with 1–10 ng/mL of epidermal growth factor or platelet derived growth factor (PDGF)–AA with or without 10–20 mM of U0126 or LY-294002. Protein lysates (5–20 μg) are separated by 12%–15% SDS PAGE and analyzed by Western blot for Akt, phosphorylated Akt (phospho-Ser 473), MAPK, and phosphorylated MAPK (p44/42 phospho-Thr202/Tyr204) antibodies (1:1000).
细胞实验	Triciribine is evaluated for cytotoxicity by seeding CEM-SS cells at a density of 1 × 104 cells/well in growth medium, using a 96-well flat-bottom plate. Serial fivefold dilutions of Triciribine are prepared in growth medium and added to the wells as a second overlay. After a 48-hours incubation at 37 °C, the cells are pulse labeled with [3H]dThd (1 μCi per well, specific activity 20 Ci/mmol) for 6 hours and the cells are harvested to measure total DNA synthesis.(Only for Reference)

别名	VD-0002, Tricyclic nucleoside, NSC 154020, 曲西立滨, API-2, TCN
分子量	320.3
分子式	C13H16N6O4
CAS No.	35943-35-2

存储

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

溶解度

1eq. HCl: 32 mg/mL (100 mM)

DMSO: 32 mg/mL (100 mM)

溶液配制表

可选溶剂	浓度体积质量	1 mg	5 mg	10 mg	25 mg
1eq. HCl / DMSO	1 mM	3.1221 mL	15.6104 mL	31.2207 mL	78.0518 mL
	5 mM	0.6244 mL	3.1221 mL	6.2441 mL	15.6104 mL
	10 mM	0.3122 mL	1.561 mL	3.1221 mL	7.8052 mL
	20 mM	0.1561 mL	0.7805 mL	1.561 mL	3.9026 mL
	50 mM	0.0624 mL	0.3122 mL	0.6244 mL	1.561 mL
	100 mM	0.0312 mL	0.1561 mL	0.3122 mL	0.7805 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)

溶液体积

质量

配液浓度

参考文献

1. Gursel DB, et al, Nero Oncol, 2011, 13(6), 610-621. 2. Kucera LS, et al, AIDS Res Hum Retroviruses, 1993, 9(4), 307-314. 3. Dieterle A, et al, Int J Cancer , 2009, 125(4), 932-941. 4. Yang L, et al, Cancer Res, 2004, 64(13), 4394-4399.

文献引用

1. Wang G, Xu J, Ma H, et al. Phenolipid JE improves metabolic profile and inhibits gluconeogenesis via modulating AKT-mediated insulin signaling in STZ-induced diabetic mice. Pharmacological Research. 2022: 106569.

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

Triciribine 35943-35-2 Cell Cycle/Checkpoint Cytoskeletal Signaling DNA Damage/DNA Repair Microbiology/Virology PI3K/Akt/mTOR signaling Proteases/Proteasome Akt HIV Protease DNA/RNA Synthesis Inhibitor HIV VD0002 inhibit VD-0002 PKB Protein kinase B Tricyclic nucleoside NSC 154020 曲西立滨 NSC-154020 API-2 NSC154020 Human immunodeficiency virus VD 0002 API2 API 2 TCN inhibitor

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Triciribine

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