SRT 1460

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白,专注于信号通路和疾病研究领域。

SRT 1460  纯度: 98.92%

SRT 1460 是一种有效的 Sirtuin-1 (SIRT1) 激动剂,其 EC1.5 值为 2.9 μM。与对 SIRT2 和 SIRT3 (EC1.5>300 μM) 相比,SRT 1460 对 SIRT1 有很好的选择性,并且比白藜芦醇和相近 sirtuin 同系物更为有效。

SRT 1460

SRT 1460 Chemical Structure

CAS No. : 925432-73-1

规格 价格 是否有货 数量
10 mM * 1 mL in DMSO ¥1120 In-stock
5 mg ¥1000 In-stock
10 mg ¥1600 In-stock
25 mg ¥2300 In-stock
50 mg ¥3500 In-stock
100 mg ¥5300 In-stock
200 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

SRT 1460 相关产品

相关化合物库:

  • Bioactive Compound Library Plus
  • Cell Cycle/DNA Damage Compound Library
  • Epigenetics Compound Library
  • Histone Modification Research Compound Library
  • Anti-Cancer Compound Library
  • Anti-Aging Compound Library
  • Antioxidants Compound Library
  • Oxygen Sensing Compound Library
  • Glutamine Metabolism Compound Library
  • Anti-Pancreatic Cancer Compound Library

生物活性

SRT 1460, a potent Sirtuin-1 (SIRT1) activator with an EC1.5 value of 2.9 μM, shows good selectivity for activation of SIRT1 versus SIRT2 and SIRT3 (EC1.5>300 μM), and is more potent than Resveratrol and the closest sirtuin homologues[1].

IC50 & Target[1]

SIRT1

2.9 μM (EC1.5)

体外研究
(In Vitro)

SRT 1460 (2-6 μM; 72 hours) inhibits cell viability in a dose-dependent manner, with all pancreatic cancer cells being more sensitive than the control HPDE cell. The IC50s of those cells are: Patu8988t, 1.62±0.13 μM; SU86.86, 2.31±0.23 μM; Panc-1, 0.66 ±0.02 μM; HPDE, 2.39±0.29 μM[2].
SRT 1460 (5 μM; 16 hours) increases expression of the autophagy marker LC3-II[2].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay[2]

Cell Line: Patu8988t (pancreatic cancer cells), Panc-1 (pancreatic cancer cells), SU86.86 (pancreatic cancer cells), HPDE cells
Concentration: 2 μM, 4 μM, 6 μM
Incubation Time: 72 hours
Result: Inhibited cell viability in a dose-dependent manner, with all pancreatic cancer cells being more sensitive than the control HPDE cell. The IC50s of those cells were: Patu8988t, 1.62±0.13 μM; SU86.86, 2.31±0.23 μM; Panc-1, 0.66 ±0.02 μM; HPDE, 2.39±0.29 μM.

Western Blot Analysis[2]

Cell Line: Patu8988t cells
Concentration: 5 μM
Incubation Time: 16 hours
Result: SRT1460 increased expression of the autophagy marker LC3-II.

分子量

507.60

Formula

C26H29N5O4S

CAS 号

925432-73-1

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
In Vitro: 

DMSO : 10 mg/mL (19.70 mM; Need ultrasonic)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 1.9701 mL 9.8503 mL 19.7006 mL
5 mM 0.3940 mL 1.9701 mL 3.9401 mL
10 mM 0.1970 mL 0.9850 mL 1.9701 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;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效
储备液的保存方式和期限:-80°C, 6 months; -20°C, 1 month。-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方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,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议您现用现配,当天使用; 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶

  • 1.

    请依序添加每种溶剂: 10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 1.25 mg/mL (2.46 mM); Clear solution

    此方案可获得 ≥ 1.25 mg/mL (2.46 mM,饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例,取 100 μL 12.5 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中,混合均匀;向上述体系中加入50 μL Tween-80,混合均匀;然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠,完全溶解于 100 mL ddH₂O 中,得到澄清透明的生理盐水溶液

  • 2.

    请依序添加每种溶剂: 10% DMSO    90% corn oil

    Solubility: ≥ 1.25 mg/mL (2.46 mM); Clear solution

    此方案可获得 ≥ 1.25 mg/mL (2.46 mM,饱和度未知) 的澄清溶液,此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例,取 100 μL 12.5 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中,混合均匀。

*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献
  • [1]. Milne JC, et al. Small molecule activators of SIRT1 as therapeutics for the treatment of type 2 diabetes. Nature. 2007 Nov 29; 450(7170): 712–716.

    [2]. Chini CC, et al. SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway. Clin Cancer Res. 2016 May 15;22(10):2496-507.

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