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Torin 1

CAS号

1222998-36-8

分子式

C35H28F3N5O2

主要靶点

mTOR|Autophagy|PI3K|DNA-PK

仅限科研使用

Cat No : CM05234

Print datasheet

Synonyms

Autophagy|DNAPK|DNA-PK|p110γ|inhibit|Inhibitor|mTORC2|mTORC1|mTOR|Mammalian target of Rapamycin|Torin1|Torin-1|Torin 1

验证数据展示

  • CAS No.: 1222998-36-8

    Torin 1
    CAS#: 1222998-36-8

产品信息

CAS号 1222998-36-8
分子式 C35H28F3N5O2
主要靶点 mTOR|Autophagy|PI3K|DNA-PK
主要通路 PI3K/Akt/mTOR 信号通路|PI3K/Akt/mTOR 信号通路|DNA 损伤和修复|PI3K/Akt/mTOR 信号通路|自噬
分子量 607.62
纯度 99.38%， 此纯度可做参考，具体纯度与批次有关系，可咨询客服
储存条件 Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice.
别名 Autophagy|DNAPK|DNA-PK|p110γ|inhibit|Inhibitor|mTORC2|mTORC1|mTOR|Mammalian target of Rapamycin|Torin1|Torin-1|Torin 1

靶点活性

mTORC1:2 nM|mTORC2:10 nM

体内活性

方法：为检测体内抗肿瘤活性，将 Torin 1 (20 mg/kg，20% N-mentyl-2-pyrrolidone, 40% PEG400 and 40% water) 腹腔注射给携带人胶质母细胞瘤 U87MG 的 NCR nude 小鼠，每天一次，持续十天。 结果：连续给药十天导致大于 99% 的肿瘤生长抑制。停止药物治疗后，肿瘤继续生长，这表明 Torin 1 治疗主要是细胞抑制性的，并且大量肿瘤细胞在治疗过程中仍然存活。[3]

体外活性

方法：野生型 MEFs 细胞用 Torin 1 (250 nm) 处理 4 天，使用 CellTiterGlo viability assay 检测细胞增殖。 结果：250 nm Torin1 完全抑制细胞增殖。[1] 方法：人类内分泌细胞系 BON 用 Torin 1 (62.5-150 μM) 处理 3-24 h，使用 Western Blot 检测靶点蛋白表达水平。 结果：Torin1 以剂量依赖的方式增加 NT 分泌；在 Torin1 处理后 3-24 h，NT 分泌增加。Torin1 处理降低了 Akt (S473) 磷酸化，p70S6K (T389) 以及 4E-BP1 (T37/46) 的磷酸化也受到抑制。[2]

溶解度

DMSO:1 mg/mL (1.65 mM);

细胞实验

Cell viability is assessed with the CellTiter-Glo Luminescent Cell Viability Assay. On Day 0, 96-well plates are seeded with 500 cells per well and grown overnight. On Day 1, cells are treated with the appropriate compounds and subsequently analyzed on Days 3-5. For analysis, plates are incubated for 60 min at room temperature; 50 μL of CellTiter-Glo reagent is added to each well, and plates are mixed on an orbital shaker for 12 min. Luminescence is quantified on a standard plate luminometer. (Only for Reference)

参考文献

1.Thoreen CC, et al. An ATP-competitive mammalian target of rapamycin inhibitor reveals rapamycin-resistant functions of mTORCJ Biol Chem. 2009 Mar 20;284(12):8023-32.
2.Li J, et al. mTORC1 inhibition increases neurotensin secretion and gene expression through activation of the MEK/ERK/c-Jun pathway in the human endocrine cell line BON. Am J Physiol Cell Physiol. 2011 Jul;301(1):C213-26.
3.Liu Q, et al. Discovery of 1-(4-(4-propionylpiperazin-1-yl)-3-(trifluoromethyl)phenyl)-9-(quinolin-3-yl)benzo[h][1,6]naphthyridin-2(1H)-one as a highly potent, selective mammalian target of rapamycin (mTOR) inhibitor for the treatment of cancer. J Med Chem. 2010 Oct 14;53(19):7146-55.
4.Dowling RJ, et al, Science, 2010, 328(5982), 1172-1176.
5.Mitra D, Vega‐Rubin‐de‐Celis S, Royla N, et al. Abrogating GPT2 in triple negative breast cancer inhibits tumor growth and promotes autophagy[J]. International Journal of Cancer.
6.Mitra D, Vega‐Rubin‐de‐Celis S, Royla N, et al. Abrogating GPT2 in triple‐negative breast cancer inhibits tumor growth and promotes autophagy[J]. International Journal of Cancer. 2021, 148(8): 1993-2009.
7.Lu X Y, Shi X J, Hu A, et al. Feeding induces cholesterol biosynthesis via the mTORC1–USP20–HMGCR axis[J]. Nature. 2020, 588(7838): 479-484.

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