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

mTOR

Mammalian target of Rapamycin

mTOR

Related Products

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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-10219GL
    Rapamycin (GMP Like)
    		Inhibitor
    Rapamycin (Sirolimus) GMP Like is Rapamycin (HY-10219) produced by using GMP like guidelines. GMP Like small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Rapamycin is a potent and specific mTOR inhibitor.
    Rapamycin (GMP Like)
  • HY-107363
    FT-1518
    		Inhibitor 98.62%
    FT-1518 is a new generation selective, potent and oral bioavailable mTORC1 and mTORC2 inhibitor, and exhibits antitumor activity.
    FT-1518
  • HY-132902
    DEPTOR-IN-1
    		Inhibitor 99.09%
    DEPTOR-IN-1 is a novel putative DEPTOR inhibitor with a Kd value of 9.3 μM.
    DEPTOR-IN-1
  • HY-N6996R
    Methyl Eugenol (Standard)
    		Inhibitor
    Methyl Eugenol (Standard) is the analytical standard of Methyl Eugenol. This product is intended for research and analytical applications. Methyl Eugenol is a bait that has oral activity against oriental fruit fly (Hendel).Methyl Eugenol has anti-cancer and anti-inflammatory activities. Methyl Eugenol can induce Autophagy in cells. Methyl Eugenol can be used in the study of intestinal ischemia/reperfusion injury.
    Methyl Eugenol (Standard)
  • HY-124582
    NEO214
    		Activator 98.0%
    NEO214 is an autophagy inhibitor and a covalent conjugate of the PDE4 inhibitor Rolipram (HY-16900) and perillyl alcohol (HY-N7000). It has anti-cancer activity and blood-brain barrier (BBB) permeability. Over sex. NEO214 prevents autophagy-lysosome fusion, thereby blocking autophagic flux and triggering glioma cell death. The process involves mTOR activation, andTFEB(Transcription Factor EB) aggregation. NEO214 inhibitionMacroautophagy/autophagy in glioblastoma cells has the potential to overcome chemotherapy resistance in glioblastoma.
    NEO214
  • HY-143510
    RMC-4627
    		99.20%
    RMC-4627 is a selective mTORC1 inhibitor that activates 4EBP1 and inhibits tumor growth.
    RMC-4627
  • HY-15271
    WYE-687
    		Inhibitor 98.05%
    WYE-687 is an ATP-competitive mTOR inhibitor with an IC50 of 7 nM. WYE-687 concurrently inhibits activation of mTORC1 and mTORC2. WYE-687 also inhibits PI3Kα and PI3Kγ with IC50s of 81 nM and 3.11 μM, respectively.
    WYE-687
  • HY-101776A
    Desmethyl-VS-5584 hydrochloride
    		Inhibitor 98.63%
    Desmethyl-VS-5584 hydrochloride is a dimethyl analog of VS-5584, a potent and selective mTOR/< with a pyridine[2,3-d]pyrimidine structure. b>PI3KDual inhibitor.
    Desmethyl-VS-5584 hydrochloride
  • HY-124036
    DS-7423
    		Inhibitor 99.83%
    DS-7423 is a dual PI3K and mTOR inhibitor, with IC50 values of 15.6 nM, 34.9 nM for PI3Kα and mTOR, respectively. DS-7423 possesses anti-tumor activity.
    DS-7423
  • HY-N4315
    Pomiferin
    		Inhibitor 98.98%
    Pomiferin (NSC 5113) acts as an potential inhibitor of HDAC, with an IC50 of 1.05 μM, and also potently inhibits mTOR (IC50, 6.2 µM).
    Pomiferin
  • HY-N2590
    Lupenone
    		99.74%
    Lupenone is an orally active lupine-type triterpenoid that can be isolated from Musa basjoo. Lupenone Lupenone plays a role through the PI3K/Akt/mTOR and NF-κB signaling pathways. Lupenone has anti-inflammatory, antiviral, antidiabetic and anticancer activities.
    Lupenone
  • HY-N2911
    Auriculasin
    		Inhibitor 98.58%
    Auriculasin is an anticancer agent that inhibits VEGFR2, PI3K/AKT/mTOR, MAPK. Auriculasin can inhibit cell proliferation, induce cell apoptosis, and inhibit angiogenesis, and promotes mitochondrial oxidative stress and ferroptosis. Auriculasin is also active at the cannabinoid receptor CB1 with an IC50 of 8.92 μM. Auriculasin can be used in cancer research, especially related diseases such as prostate cancer and non-small cell lung cancer, as well as research on the development of anti-angiogenic drugs.
    Auriculasin
  • HY-11080A
    PKI-179 hydrochloride
    		Inhibitor 99.66%
    PKI-179 hydrochloride is a potent and orally active dual PI3K/mTOR inhibitor, with IC50s of 8 nM, 24 nM, 74 nM, 77 nM, and 0.42 nM for PI3K-α, PI3K-β, PI3K-γ, PI3K-δ and mTOR, respectively. PKI-179 hydrochloride also exhibits activity over E545K and H1047R, with IC50s of 14 nM and 11 nM, respectively. PKI-179 hydrochloride shows anti-tumor activity in vivo.
    PKI-179 hydrochloride
  • HY-114267
    Cbz-B3A
    		Inhibitor 98.63%
    Cbz-B3A is a potent and selective inhibitor of mTORC1 signaling that appear to bind to ubiquilins 1, 2, and 4, and Cbz-B3A inhibits the phosphorylation of eIF4E-binding protein 1 (4EBP1).
    Cbz-B3A
  • HY-B1787
    Sulindac sulfone
    		Inhibitor 98.10%
    Sulindac sulfone is an mTORC1 pathway inhibitor and a metabolite of Sulindac. Sulindac sulfone inhibits colon cancer cell growth and induces cell cycle arrest. Sulindac sulfone is used in cancer research.
    Sulindac sulfone
  • HY-N1163
    Tetrahydroalstonine
    		Activator 99.84%
    Tetrahydroalstonine ((-)-Tetrahydroalstonine) is an indole alkaloid and a selective α₂-adrenergic receptor antagonist. Tetrahydroalstonine exhibits certain neuroprotective effects. Tetrahydroalstonine can regulate autophagy-lysosomal function by activating the Akt/mTOR pathway, significantly reducing OGD/R-induced primary cortical neuronal injury.
    Tetrahydroalstonine
  • HY-10218R
    Everolimus (Standard)
    		Inhibitor
    Everolimus (Standard) is the analytical standard of Everolimus. This product is intended for research and analytical applications. Everolimus (RAD001) is a Rapamycin (HY-10219) derivative and a potent, selective and orally active mTOR1 inhibitor. Everolimus binds to FKBP-12 to generate an immunosuppressive complex. Everolimus inhibits tumor cells proliferation and induces cell apoptosis and autophagy. Everolimus has potent immunosuppressive and anticancer activities.
    Everolimus (Standard)
  • HY-Y0106
    2,6-Dihydroxyacetophenone
    		Inhibitor 99.56%
    2,6-Dihydroxyacetophenone, a polyphenolic derivative of Acetophenone (HY-Y0989), is an orally active mTOR inhibitor. 2,6-Dihydroxyacetophenone shows antioxidant activity. 2,6-Dihydroxyacetophenone inhibits cell growth and proliferation in CRC cells. 2,6-Dihydroxyacetophenone arrests at G0/G1 phase of cell cycle, induces apoptosis and suppresses cell migration in CRC cells. 2,6-Dihydroxyacetophenone inhibits xanthine oxidase (XOD) with an IC50 of 1.24 mM. 2,6-dihydroxyacetophenone improves uric acid metabolism in hyperuricemia mice, reduces plasma cholesterol in hypercholesterolemic rats, and inhibits lipid accumulation in HFD-induced obese mice. 2,6-Dihydroxyacetophenone can be used for the study of colorectal cancer (CRC), hyperuricemia and hypercholesterolemia.
    2,6-Dihydroxyacetophenone
  • HY-N3307
    (+)-Medioresinol
    		Agonist 98.88%
    (+)-Medioresinol is a furofuran-type lignan with antifungal and antibacterial properties. (+)-Medioresinol synergizes with antibiotics to exert antimicrobial and antibiofilm effects. (+)-Medioresinol induces intracellular ROS accumulation and mitochondrial-mediated apoptosis in Candida albicans. (+)-Medioresinol inhibits LPS (HY-D1056)-stimulated IL-12p40 production. (+)-Medioresinol is a PGC-1α activator that protects against endothelial cell pyroptosis in ischemic stroke via the PPARα-GOT1 axis. (+)-Medioresinol can be used in research on fungal and bacterial infection, inflammation, and ischemic stroke.
    (+)-Medioresinol
  • HY-171047
    Autophagy inducer 7
    		Inhibitor 99.45%
    Autophagy inducer 7 (Compound SSA) is an Autophagy and Apoptosis inducer. Autophagy inducer 7 activates autophagy by inhibiting Akt/mTOR signaling and the expression of downstream proteins. Autophagy inducer 7 suppresses DNA synthesis and causes a G0-G1 cell-cycle arrest. Autophagy inducer 7 inhibits tumor cell growth.
    Autophagy inducer 7
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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