2. PI3K/Akt/mTOR Autophagy
  3. mTOR Autophagy
  4. mTORC1-IN-3

mTORC1-IN-3 是一种强效且具有选择性的 mTORC1 抑制剂，其 IC50 值为 26.38 μM。mTORC1-IN-3 可选择性地抑制 mTORC1 底物的磷酸化，而不会影响 mTORC2 底物的磷酸化。mTORC1-IN-3 能够减少细胞内脂质蓄积并诱导自噬 (autophagy)。mTORC1-IN-3 可用于癌症、免疫学、代谢性疾病和神经系统疾病的研究，如糖尿病和阿尔茨海默病。

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mTORC1-IN-3

mTORC1-IN-3 Chemical Structure

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mTORC1-IN-3 相关抗体

Top Publications Citing Use of Products

查看 mTOR 亚型特异性产品:

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mTOR mTORC1 mTORC2

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

mTORC1-IN-3 is a potent and selective mTORC1 inhibitor with an IC50 of 26.38 μM . mTORC1-IN-3 selectively inhibits the phosphorylation of mTORC1 substrates and does not without affect the phosphorylation of mTORC2 substrate. mTORC1-IN-3 can reduce cellular lipid accumulation and induce autophagy. mTORC1-IN-3 can be used for the researches of cancer, immunology, metabolic and neurological disease, such as diabetes and Alzheimer’s disease[1].

IC50 & Target[1]

mTORC1

26.38 μM (IC50)

体外研究
(In Vitro)

mTORC1-IN-3 (Compound TCG3) (10 μM, 2 h) 可选择性抑制 HepG2 细胞和小鼠原代肝细胞中 mTORC1 底物 p-p70S6K (Thr389)、p-S6 (Ser235/236) 和 p-4E-BP1 (Thr37/46) 的磷酸化，而不影响 mTORC2 底物 p-Akt(Ser473) 的磷酸化[1]。
mTORC1-IN-3 (10 μM, 24 h) 可抑制 AMPK 介导的 ULK1 (Ser757) 磷酸化，从而减少 ULK1 的激活，并在 HepG2 细胞中诱导自噬的早期阶段[1]。
mTORC1-IN-3 (10 μM, 24 h) 可减少脂肪酸诱导的 HepG2 细胞中脂滴的积累[1]。
mTORC1-IN-3 (1-30 μM, 24 h) 在 HepG2 细胞中显示出低细胞毒性[1]。
mTORC1-IN-3 (10 μM, 24 h) 可持续抑制 HEK293T、JURKAT 和 786-O 细胞中 mTORC1 底物的磷酸化[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

mTORC1-IN-3 相关抗体:

Western Blot Analysis[1]

Cell Line: HepG2 cells and mouse primary hepatocytes
Concentration: 10 μM
Incubation Time: 2 h
Result: Reduced the levels of p-p70S6K (Thr389), p-S6 (Ser235/236) and p-4E-BP1 (Thr37/46).
体内研究
(In Vivo)

mTORC1-IN-3 (Compound TCG3) (15 mg/kg，腹腔注射，胰岛素注射前 30 分钟) 可逆转 C57BL/6 小鼠中胰岛素介导的低血糖[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6 mice (male, 6-8 weeks)[1]
Dosage: 15 mg/kg
Administration: Intraperitoneally injection, 30 mins before insulin injection
Result: Reversed insulin-mediated hypoglycemiaand increased plasma glucose levels.
Inhibited insulin-induced phosphorylation of mTORC1 substrates p-S6 (Ser235/236) and p-4E-BP1 (Thr37/46) in liver.
Showed a 40% reduction in p-S6 positive area.
Showed no abnormalities or hepatocyte damage in liver.
分子量

909.84

Formula

C41H43F4N11O9
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

mTORC1-IN-3 相关分类

  • 摩尔计算器

  • 稀释计算器

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

mTORC1-IN-3mTORAutophagyMammalian target of RapamycinHepG2HypoglycemiaType 2 diabetesObesityHuntington’s DiseaseAlzheimer’sDiseaseFibrotic diseasesAutoimmune disordersCancersTuberous sclerosis (TSC)Lymphangioleiomyomatosis (LAM)Inhibitorinhibitorinhibit

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