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

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.

For research use only. We do not sell to patients.

mTORC1-IN-3

mTORC1-IN-3 Chemical Structure

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mTORC1-IN-3 Related Antibodies

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Description

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)

In Vitro

mTORC1-IN-3 (Compound TCG3) (10 μM, 2 h) selectively inhibits the phosphorylation of mTORC1 substrates p-p70S6K (Thr389), p-S6 (Ser235/236) and p-4E-BP1 (Thr37/46) in HepG2 cells and mouse primary hepatocytes, without affecting the phosphorylation of mTORC2 substrate p-Akt (Ser473)[1].
mTORC1-IN-3 (10 μM, 24 h) inhibits AMPK-mediated phosphorylation of ULK1 (Ser757) to reduce ULK1 activation and induces the early stage of autophagy in HepG2 cells[1].
mTORC1-IN-3 (10 μM, 24 h) reduces fatty acid-induced lipid droplet accumulation in HepG2 cells[1].
mTORC1-IN-3 (1-30 μM, 24 h) shows low cytotoxicity in HepG2 cells[1].
mTORC1-IN-3 (10 μM, 24 h) continuously inhibits mTORC1 substrate phosphorylation in HEK293T, JURKAT, and 786-O cells[1].

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

mTORC1-IN-3 Related Antibodies

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).
In Vivo

mTORC1-IN-3 (Compound TCG3) (15 mg/kg, i.p., 30 mins before insulin injection) reverses insulin-mediated hypoglycemia in C57BL/6 mice[1].

MedChemExpress (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.
Molecular Weight

909.84

Formula

C41H43F4N11O9
SMILES

CC1(O[C@@H]2[C@H]([C@H](O[C@@H]2O1)CN3C=C(N=N3)COCC4=C(C5=CC(C6=CN=C(N=C6)N)=CC=C5N=C4)NC7=CC=C(C(C(F)(F)F)=C7)F)OCO[C@H]8[C@H](O[C@H]9[C@@H]8OC(C)(O9)C)CN=[N+]=[N-])C
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Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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mTORC1-IN-3 Related Classifications

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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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