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-Y1177
    Diphenyl disulfide
    		Inhibitor 99.96%
    Diphenyl disulfide (Phenyl disulfide) is an organic disulfide compound. Diphenyl disulfide inhibits the PI3K/AKT/mTOR pathway, and induces ferroptosis (ferroptosis), apoptosis (apoptosis) and autophagy (autophagy) in cancer cells. Diphenyl disulfide downregulates GPX4 expression, inhibits NRF2 phosphorylation, induces lipid peroxidation, promotes xCT ubiquitination, induces proteolytic cleavage of p21 Bax into p18 Bax, and suppresses cell proliferation and viability. Diphenyl disulfide can be used in research related to melanoma and breast cancer.
    Diphenyl disulfide
  • HY-10218S
    Everolimus-d4
    		Inhibitor 98.74%
    Everolimus-d4 is the deuterium labeled Everolimus. Everolimus (RAD001) is a Rapamycin 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-d<sub>4</sub>
  • HY-10681R
    Gedatolisib (Standard)
    		Inhibitor
    Gedatolisib (Standard) is the analytical standard of Gedatolisib. This product is intended for research and analytical applications. Gedatolisib (PKI-587) is a highly potent dual inhibitor of PI3Kα, PI3Kγ, and mTOR with IC50s of 0.4 nM, 5.4 nM and 1.6 nM, respectively. Gedatolisib is equally effective in both complexes of mTOR, mTORC1 and mTORC2.
    Gedatolisib (Standard)
  • 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-122665
    HTH-01-091
    		Inhibitor 99.81%
    HTH-01-091 is a potent and selective maternal embryonic leucine zipper kinase (MELK) inhibitor, with an IC50 of 10.5 nM. HTH-01-091 also inhibits PIM1/2/3, RIPK2, DYRK3, smMLCK and CLK2. HTH-01-091 can be uesd for breast cancer research.
    HTH-01-091
  • HY-13691
    MKC-1
    		Inhibitor 99.78%
    MKC-1 (Ro-31-7453) is an orally active and potent cell cycle inhibitor with broad antitumor activity. MKC-1 inhibits the Akt/mTOR pathway. MKC-1 arrests cellular mitosis and induces cell apoptosis by binding to a number of different cellular proteins including tubulin and members of the importin β family.
    MKC-1
  • HY-163199
    ASCT2-IN-2
    		Inhibitor 99.10%
    ASCT2-IN-2 (compound 25e) is an ASCT2 inhibitor with IC50 of 5.14 μM. ASCT2-IN-2 regulates amino acid metabolism as well as mTOR signaling and thereby induces cell apoptosis. ASCT2-IN-2 inhibits tumor growth.
    ASCT2-IN-2
  • HY-125927
    8-Aminoadenosine
    		Inhibitor 99.05%
    8-Aminoadenosine (8-NH2-Ado), a RNA-directed nucleoside analogue, reduces cellular ATP levels and inhibits mRNA synthesis. 8-Aminoadenosine blocks Akt/mTOR signaling and induces autophagy and apoptosis in a p53-independent manner. 8-Aminoadenosine has antitumor activity.
    8-Aminoadenosine
  • HY-175646
    AGPAT4-IN-1
    		Inhibitor 99.04%
    AGPAT4-IN-1 (Compound CL26) is a covalent AGPAT4 inhibitor with an IC50 of 795 nM. AGPAT4-IN-1 covalently binds to AGPAT4 at Cys228 and significantly inhibits acyltransferase activity, LPA-to-PA conversion and downstream mTOR/S6K pathways. AGPAT4-IN-1 sensitizes hepatocellular carcinoma (HCC) tumors to Sorafenib (HY-10201) and significantly induces apoptosis with a synergistic response. AGPAT4-IN-1 has antitumor activity and reduces tumorigenicity and stemness in HCC xenograft mouse models.
    AGPAT4-IN-1
  • HY-B0921
    Succinylsulfathiazole
    		Inhibitor 99.22%
    Succinylsulfathiazole (Succinylsulphathiazole) is a long-acting sulfonamide antibiotic with localized gut-specific antibacterial activity and is orally active. Succinylsulfathiazole inhibits bacterial folate synthesis, reduces coliform counts, suppresses intestinal bacterial growth and vitamin biosynthesis, and depletes gut folate-producing bacteria. Succinylsulfathiazole modulates hepatic mTOR signaling, diminishes cecal fermentation, decreases hepatic folate levels and total folate excretion, elevates nitrogen excretion and reduces the fermentability of certain dietary fibers. Succinylsulfathiazole induces folate deficiency and triggers biotin- and folate-related nutritional deficiency symptoms in rats and C57BL/6 mice.
    Succinylsulfathiazole
  • HY-W348485
    WRX606
    		Inhibitor
    WRX606 is an orally active nonrapalog inhibitor for mTOR complex 1 (mTORC1M). WRX606 inhibits the phosphorylation of mTORC1 substrate S6 kinase 1 (S6K1) (IC50 = 10 nM) and eukaryotic translation initiation factor 4E binding protein (p-4E-BP1) (IC50 = 0.27 μM) in MCF-7 cells. WRX606 suppresses tumor growth in mice without promotion of metastasis. WRX606 can be studied in research as an antitumor agent.
    WRX606
  • HY-118717
    mTOR inhibitor WYE-28
    		Inhibitor 99.75%
    mTOR inhibitor WYE-28 (compound 28) is a selective inhibitor of mTOR>/b< (IC50)=0.08 nM. mTOR inhibitor WYE-28 inhibits PI3Kα with an IC50 value of 6 nM. mTOR inhibitor WYE-28 shows a metabolic time (T1/2) in nude mouse microsomes of 13 min.
    mTOR inhibitor WYE-28
  • HY-134903
    (32-Carbonyl)-RMC-5552
    		Inhibitor
    (32-Carbonyl)-RMC-5552 is a potent mTOR inhibitor. (32-Carbonyl)-RMC-5552 inhibits mTORC1 and mTORC2 substrate (p-P70S6K-(T389), p-4E-BP1-(T37/36), AND p-AKT1/2/3-(S473)) phosphorylation with pIC50s of > 9, >9 and between 8 and 9, respectively (patent WO2019212990A1, example 2).
    (32-Carbonyl)-RMC-5552
  • 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 (Sirolimus; AY 22989) is a potent and specific mTOR inhibitor with an IC50 of 0.1 nM in HEK293 cells. Rapamycin binds to FKBP12 and specifically acts as an allosteric inhibitor of mTORC1. Rapamycin is an autophagy activator, an immunosuppressant.
    Rapamycin (GMP Like)
  • HY-173119
    SKLB-D18
    		Inhibitor 98.06%
    SKLB-D18 is an orally active ERK1/2/ERK5 inhibitor, with an IC50 of 38.69 nM and a Kd of 126.9 nM against human ERK1, an IC50 of 40.12 nM and a Kd of 209.8 nM against ERK2, and an IC50 of 59.72 nM and a Kd of 468.2 nM against ERK5. SKLB-D18 inhibits cancer cell proliferation, induces G0/G1 cell cycle arrest and apoptosis. SKLB-D18 reduces the levels of p-ERK5, p-RSKp90, p-c-Myc and c-Myc, and upregulates the level of p-ERK1/2, thereby inhibiting the ERK1/2/5 pathway in cells. SKLB-D18 increases LC3B-II accumulation, and decreases the levels of p62, p-mTOR and p-p70S6K. SKLB-D18 elevates the levels of ROS, lipid peroxidation and free ferrous ions, reduces the levels of NCOA4 and GPX4, and induces ferritin autophagy-dependent ferroptosis in cancer cells. SKLB-D18 exhibits antitumor activity in a triple-negative breast cancer xenograft mouse model. SKLB-D18 can be used in research related to triple-negative breast cancer.
    SKLB-D18
  • 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-109179A
    Itacnosertib hydrochloride
    		Inhibitor 99.43%
    Itacnosertib hydrochloride (TP-0184 hydrochloride) is the inhibitor for FLT3, ACVR1 (ALK2, IC50=8 nM) and JAK2 (IC50=8540 nM). Itacnosertib hydrochloride exhibits anti-leukemic activity.
    Itacnosertib hydrochloride
  • HY-N0837R
    Veratramine (Standard)
    		Inhibitor
    Veratramine (NSC17821; NSC23880) (Standard) is the analytical standard of Veratramine (HY-N0837). This product is intended for research and analytical applications. Veratramine (NSC17821; NSC23880) is an orally active inhibitor of the PI3K/Akt/mTOR signaling pathway and a SIGMAR1 modulator. Veratramine induces autophagic apoptosis of tumor cells, arrests the cell cycle at the G0/G1 phase, and inhibits epithelial-mesenchymal transition (EMT)-related proteins to reduce tumor migration. Veratramine reduces spinal cord and sciatic nerve pathological damage in a neuropathy model by inhibiting SIGMAR1 binding to NMDAR and phosphorylation of NMDAR Ser896. Veratramine has anti-tumor proliferation, apoptosis induction, anti-inflammatory and neuroprotective activities, and can be used in the study of cancers such as liver cancer and osteosarcoma, as well as diabetic peripheral neuropathy.
    Veratramine (Standard)
  • HY-N6841
    Rhodiolin
    		Inhibitor 98%
    Rhodiolin, a flavonoid, is an orally active glucose 6-phosphate isomerase (GPI) inhibitor. Rhodiolin inhibits papillary thyroid cancer (PTC) by targeting glycolysis enzyme glucose 6-phosphate isomerase GPI and suppressing PI3K/AKT/mTOR phosphorylation and induce apoptosis. Rhodiolin as a NS2B-NS3 protease inhibitor can disrupt dengue viral replication. Rhodiolin is also a potential candidate for developing anticancer strategies inhibiting CK1ε kinase. Rhodiolin can be used for the study of anti-tumor and anti-viral .
    Rhodiolin
  • HY-B1787
    Sulindac sulfone
    		Inhibitor 98.10%
    Sulindac sulfone is an orally active metabolite of Sulindac (HY-B0008). Sulindac sulfone activates PPARγ and drives transcriptional induction of SSAT by binding to the PPRE-2 element. Sulindac sulfone induces Apoptosis. Sulindac sulfone negatively regulates the function of VDAC1/2 to inhibit the mTORC1 pathway, reduces Cyclin D1 levels, and induces G1 cell cycle arrest in colon cancer cells. Sulindac sulfone exerts colon cancer preventive effects through a COX-independent mechanism. Sulindac sulfone can be used in research related to colon cancer.
    Sulindac sulfone
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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