2. Signaling Pathways
  3. PI3K/Akt/mTOR
  4. mTOR

mTOR

Mammalian target of Rapamycin

mTOR

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mTOR (mammalian target of Rapamycin) is a protein that in humans is encoded by the mTOR gene. mTOR is a serine/threonine protein kinase that regulates cell growth, cell proliferation, cell motility, cell survival, protein synthesis, and transcription. mTOR belongs to the phosphatidylinositol 3-kinase-related kinase protein family. mTOR integrates the input from upstream pathways, including growth factors and amino acids. mTOR also senses cellular nutrient, oxygen, and energy levels. The mTOR pathway is dysregulated in human diseases, such as diabetes, obesity, depression, and certain cancers. Rapamycin inhibits mTOR by associating with its intracellular receptor FKBP12. The FKBP12-rapamycin complex binds directly to the FKBP12-Rapamycin Binding (FRB) domain of mTOR, inhibiting its activity.

mTOR Isoform Specific Products:

mTOR Isoform Comparison
Cat. No. Product Name Effect Purity Chemical Structure
  • HY-161857
    Akt/mTOR-IN-1
    		Inhibitor
    Akt/mTOR-IN-1 (Compound 8r) is an AKT/mTOR signaling pathway inhibitor exhibiting an IC50 value of 0.8 µM with anticancer activity. Akt/mTOR-IN-1 can decrease the expression of Caspase 3 and increase the expression of the autophagic protein Cyclin B1, thereby inducing cell autophagy and apoptosis. Akt/mTOR-IN-1 can be used in research related to non-small cell lung cancer (NSCLC).
    Akt/mTOR-IN-1
  • HY-161509
    PT-88
    		Inhibitor
    PT-88 is a highly selective inhibitor of mTOR (Mammalian target of rapamycin) (IC50=1.2 nM). PT-88 inhibits both mTORC1 and mTORC2 complexes, both of which are active forms of mTOR protein kinases and are closely associated with cell growth, proliferation, and survival. PT-88 can be used to study the role of mTOR in tumorigenesis and development, especially in the treatment of breast cancer.
    PT-88
  • HY-170670
    DQ661
    		Inhibitor
    DQ661 is a potent PPT1 inhibitor. DQ661 is a dimeric quinacrine autophagy inhibitor. DQ661 inhibits mTORC1 activity. DQ661 decreases the protein expression of pS6K T389, pS6 S240-244. DQ661 shows anticancer activity.
    DQ661
  • HY-P5984A
    Thioether-cyclized helix B peptide, CHBP TFA
    		Inhibitor
    Thioether-cyclized helix B peptide, CHBP (TFA) is the TFA form of Thioether-cyclized helix B peptide, CHBP (HY-P5984). Thioether-cyclized helix B peptide, CHBP (TFA) can improve metabolic stability and renoprotective effect through inducing autophagy via inhibition of mTORC1 and activation of mTORC2.
    Thioether-cyclized helix B peptide, CHBP TFA
  • HY-178192
    mTORC1-IN-3
    		Inhibitor
    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.
    mTORC1-IN-3
  • HY-172175
    HYS-072
    		Inhibitor
    HYS-072 is an orally active derivative of chrysin (HY-14589) with antitumor activity. HYS-072 induces apoptosis and autophagy by inhibiting the PI3K/AKT/mTOR signaling pathway and suppresses tumor growth in vivo in xenograft models by modulating autophagy-related pathways. HYS-072 can be used in the research of triple-negative breast cancer.
    HYS-072
  • HY-173367
    Anticancer agent 271
    		Inhibitor
    Anticancer agent 271 (compound 5C) has antiproliferative activity against lung (A549), colon (Caco-2) cancer cell lines, and human lung fibroblast (WI38) with an IC50 value of 9.18 μM on A549 cells. Anticancer agent 271 downregulates PI3K and mTOR gene expression that can be used for cancer research.
    Anticancer agent 271
  • HY-120406
    PLS-123
    		Inhibitor
    LPS-123 is a covalently irreversible BTK inhibitor with an IC50 of < 5 nM. LPS-123 simultaneously inhibits the catalytic activity of BTK at Tyr551 and its self-activation at Tyr223. LPS-123 inhibits phosphorylation of the AKT/mTOR and MAPK signaling pathways, activation of PLCγ2, ERK1/2, p38, AKT, and mTOR, and blocks the production of CCL3 and CCL4 chemokines. LPS-123 exhibits significant anti-proliferative activity against various B-cell lymphoma cell lines and effectively induces apoptosis via a caspase-dependent pathway. LPS-123 also demonstrates significant antitumor activity in the OCI-Ly7 xenograft model. LPS-123 can be used for lymphoma research.
    PLS-123
  • HY-N0112R
    Dihydromyricetin (Standard)
    		Inhibitor
    Dihydromyricetin (Standard) is the analytical standard of Dihydromyricetin. This product is intended for research and analytical applications. Dihydromyricetin is a potent inhibitor with an IC50 of 48 μM on dihydropyrimidinase. Dihydromyricetin can activate autophagy through inhibiting mTOR signaling. Dihydromyricetin suppresses the formation of mTOR complexes (mTORC1/2). Dihydromyricetin is also a potent influenza RNA-dependent RNA polymerase inhibitor with an IC50 of 22 μM.
    Dihydromyricetin (Standard)
  • HY-176435
    mTOR inhibitor-28
    		Inhibitor
    mTOR inhibitor-28 (SM-3) is a potent mTOR inhibitor. mTOR inhibitor-28 inhibits A549, H292, and H460 cells with IC50s of 72.74, 67.66, and 43.24 μM, respectively.
    mTOR inhibitor-28
  • HY-169407
    AKT-IN-24
    		Inhibitor
    KT-IN-24 (Compound M17) is a AKT allosteric inhibitor with anti-tumor activity. KT-IN-24 can target the AKT/mTOR and MEK/ERK signaling pathways and inhibit epithelial-mesenchymal transition, which has a synergistic suppressive effect on TNBC, promoting cell apoptosis while inhibiting proliferation and migration when used in combination with Trametinib (HY-10999).
    AKT-IN-24
  • HY-168893
    K882
    		Inhibitor
    K882 (Compound 4e) is a Src inhibitor, with KD of 0.315 μM. K882 induces Apoptosis. K882 inhibits XIAP and Survivin. K882 inhibits the activation of PI3K/Akt/mTOR, Jak1/Stat3, Ras/MAPK signaling pathways. K882 shows anti-tumor activity against non-small cell lung cancer.
    K882
  • HY-146200
    PI3K/mTOR Inhibitor-8
    		Inhibitor
    PI3K/mTOR Inhibitor-8 (Compound 18b) is a PI3K and mTOR dual inhibitor with IC50 values of 0.46 nM and 12 nM against PI3Kα and mTOR, respectively. PI3K/mTOR Inhibitor-8 induces HCT-116 cells apoptosis and arrests cell cycle at the G1/S phase.
    PI3K/mTOR Inhibitor-8
  • HY-159577
    Nic-15
    		Modulator
    Nic-15 (compound 4n) is an anti-constrictive agent used to antagonize the hypovascularity of pancreatic tumors. The hypovascularity allows cancer cells to adapt to the nutrient-deficient tumor microenvironment and develop drug resistance. Nic-15 can regulate the PI3K/Akt/mTOR pathway and alleviate ER stress induced by Gemcitabine (HY-17026). Nic-15 can significantly inhibit the migration and colony formation of MIA PaCa-2 and PANC-1 pancreatic cancer cells. The combination of Nic-15 and Gemcitabine can effectively solve the problem of pancreatic tumor resistance. In an in vivo xenograft model, Nic-15 can significantly enhance the efficacy of Gemcitabine.
    Nic-15
  • HY-N0486S10
    L-Leucine-18O2
    		Activator
    L-Leucine-18O2 is the 18O-labeled L-Leucine. L-Leucine is an essential branched-chain amino acid (BCAA), which activates the mTOR signaling pathway.
    L-Leucine-<sup>18</sup>O<sub>2</sub>
  • HY-151915
    ATR-IN-20
    		Inhibitor
    ATR-IN-20 is a potent ATR (ATM/ATR) inhibitor with an IC50 of 3 nM. ATR-IN-20 possess an inhibitory effect on mTOR (IC50 of 18 nM) while displaying good selectivity against PI3Kα (100 nM), ATM (100 nM), and DNA-PK (662 nM). ATR-IN-20 exhibits excellent pharmacokinetic profile (F = 30%), and has anticancer effects.
    ATR-IN-20
  • HY-178812
    PI3Kα-IN-27
    		Inhibitor
    PI3Kα-IN-27 (Compound 50b) is an orally active PI3K-α inhibitor, with an IC50 of 40 nM. PI3Kα-IN-27 effectively inhibits PAK3, p110α, phospho-mTOR and phospho-ERK1/2. PI3Kα-IN-27 induces early Apoptosis. PI3Kα-IN-27 shows anticancer activity against pancreatic cancer, lung cancer, breast cancer.
    PI3Kα-IN-27
  • HY-161856
    Antifungal agent 106
    		Inhibitor
    Antifungal agent 106 (Compound Z31) is a benzoic acid derivative and a potential fungicide against Monilinia fructicola. Antifungal agent 106 exhibits antifungal activity with an EC50 value of 11.8 mg/L. It affects hyphal growth by disrupting cell membrane integrity, leading to increased membrane permeability and release of intracellular electrolytes. Antifungal agent 106 can be used in research related to brown rot of stone fruits.
    Antifungal agent 106
  • HY-170405
    YB-3–17
    		Inhibitor
    YB-3-17 is a bifunctional molecule, that inhibits mTOR (IC50=0.22 nM) or degrades G1 to S phase transition 1 gene (GSPT1, DC50=5 nM) in a PROTAC mechanism. YB-3-17 exhibits antiproliferative activity in multi glioblastoma cell lines with IC50 of nanomolare levels. YB-3-17 exhibits antitumor efficacy in mouse models. (Pink: ligand for target protein (HY-170407); Black: linker (HY-A0102); Blue: ligand for E3 ligase Cereblon (HY-14658))
    YB-3–17
  • HY-147913
    PI3K/Akt/mTOR-IN-3
    		Inhibitor
    PI3K/Akt/mTOR-IN-3 (compound 3d) is a potent PI3K/AKT/mTOR inhibitor. PI3K/Akt/mTOR-IN-3 displays the inhibitory activity in MCF-7, HeLa and HepG2 cells, with IC50 values of 0.77, 1.23, and 4.57μM, respectively. PI3K/Akt/mTOR-IN-3 inhibits the migration of MCF-7 and HeLa cells at the concentration of 4 μM. PI3K/Akt/mTOR-IN-3 induces cell apoptosis and S phase arrest.
    PI3K/Akt/mTOR-IN-3
Cat. No. Product Name / Synonyms Application Reactivity
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Download mTOR Signaling Pathway Map.

The mammalian target of rapamycin (mTOR) signaling pathway integrates both intracellular and extracellular signals and serves as a central regulator of cell metabolism, growth, proliferation and survival[1]. mTOR is the catalytic subunit of two distinct complexes called mTORC1 and mTORC2. mTORC1 comprises DEPTOR, PRAS40, RAPTOR, mLST8, mTOR, whereas mTORC2 comprises DEPTOR, mLST8, PROTOR, RICTOR, mSIN1, mTOR[2]. Rapamycin binds to FKBP12 and inhibits mTORC1 by disrupting the interaction between mTOR and RAPTOR. mTORC1 negatively regulates autophagy through multiple inputs, including inhibitory phosphorylation of ULK1 and TFEB. mTORC1 promotes protein synthesis through activation of the translation initiation promoter S6K and through inhibition of the inhibitory mRNA cap binding 4E-BP1, and regulates glycolysis through HIF-1α. It promotes de novo lipid synthesis through the SREBP transcription factors. mTORC2 inhibits FOXO1,3 through SGK and Akt, which can lead to increased longevity. The complex also regulates actin cytoskeleton assembly through PKC and Rho kinase[3]. 

 

Growth factors: Growth factors can signal to mTORC1 through both PI3K-Akt and Ras-Raf-MEK-ERK axis. For example, ERK and RSK phosphorylate TSC2, and inhibit it.

 

Insulin Receptor: The activated insulin receptor recruits intracellular adaptor protein IRS1. Phosphorylation of these proteins on tyrosine residues by the insulin receptor initiates the recruitment and activation of PI3K. PIP3 acts as a second messenger which promotes the phosphorylation of Akt and triggers the Akt-dependent multisite phosphorylation of TSC2. TSC is a heterotrimeric complex comprised of TSC1, TSC2, and TBC1D7, and functions as a GTPase activating protein (GAP) for the small GTPase Rheb, which directly binds and activates mTORC1. mTORC2 primarily functions as an effector of insulin/PI3K signaling. 

 

Wnt: The Wnt pathway activates mTORC1. Glycogen synthase kinase 3β (GSK-3β) acts as a negative regulator of mTORC1 by phosphorylating TSC2. mTORC2 is activated by Wnt in a manner dependent on the small GTPase RAC1[4].

 

Amino acids: mTORC1 senses both lysosomal and cytosolic amino acids through distinct mechanisms. Amino acids induce the movement of mTORC1 to lysosomal membranes, where the Rag proteins reside. A complex named Ragulator, interact with the Rag GTPases, recruits them to lysosomes through a mechanism dependent on the lysosomal v-ATPase, and is essential for mTORC1 activation. In turn, lysosomal recruitment enables mTORC1 to interact with GTP-bound RHEB, the end point of growth factor. Cytosolic leucine and arginine signal to mTORC1 through a distinct pathway comprised of the GATOR1 and GATOR2 complexes.    

 

Stresses: mTORC1 responds to intracellular and environmental stresses that are incompatible with growth such as low ATP levels, hypoxia, or DNA damage. A reduction in cellular energy charge, for example during glucose deprivation, activates the stress responsive metabolic regulator AMPK, which inhibits mTORC1 both indirectly, through phosphorylation and activation of TSC2, as well as directly through the phosphorylation of RAPTOR. Sestrin1/2 are two transcriptional targets of p53 that are implicated in the DNA damage response, and they potently activate AMPK, thus mediating the p53-dependent suppression of mTOR activity upon DNA damage. During hypoxia, mitochondrial respiration is impaired, leading to low ATP levels and activation of AMPK. Hypoxia also affects mTORC1 in AMPK-independent ways by inducing the expression of REDD1, the protein products of which then suppress mTORC1 by promoting the assembly of TSC1-TSC2[2].

 

Reference:

[1]. Laplante M, et al.mTOR signaling at a glance.J Cell Sci. 2009 Oct 15;122(Pt 20):3589-94. 
[2]. Zoncu R, et al. mTOR: from growth signal integration to cancer, diabetes and ageing.Nat Rev Mol Cell Biol. 2011 Jan;12(1):21-35. 
[3]. Johnson SC, et al. mTOR is a key modulator of ageing and age-related disease.Nature. 2013 Jan 17;493(7432):338-45.
[4]. Shimobayashi M, et al. Making new contacts: the mTOR network in metabolism and signalling crosstalk.Nat Rev Mol Cell Biol. 2014 Mar;15(3):155-62.

mTOR Isoform Comparison

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