mTOR

Mammalian target of Rapamycin

mTOR

mTOR Isoform Specific Products:

mTOR Isoform Comparison

mTOR Related Products (616)
Antibodies (14)
mTOR Signaling Pathway
mTOR Isoform Comparison

By Effects:	Inhibitors (482)

Cat. No.	Product Name	Effect	Purity	Chemical Structure

HY-N1244

Sarmentosin	Inhibitor
Sarmentosin is an activator of Nrf2. Sarmentosin inhibits mTOR signaling and induces autophagy-dependent apoptosis in human HCC cells.

HY-169960

2DII	Inhibitor	98.92%
2DII is a potent and selective mTORC2 inhibitor. 2DII selectively binds mSin1 PH domain and decreases the expression of AKT1 phosphorylation.

HY-15247R

Vistusertib (Standard)	Inhibitor
Vistusertib (Standard) is the analytical standard of Vistusertib. This product is intended for research and analytical applications. Vistusertib (AZD2014) is an ATP competitive mTOR inhibitor with an IC50 of 2.81 nM. AZD2014 inhibits both mTORC1 and mTORC2 complexes.

HY-122949

Momordicine I	Inhibitor
Momordicine I is a cucurbitane-type triterpenoids. Momordicine I suppresses glioma growth by promoting apoptosis and impairing mitochondrial oxidative phosphorylation. Momordicine I inhibits glycolysis, lipid metabolism, induces autophagy in HNC cells to suppress head and neck cancer growth. Momordicine I alleviates isoproterenol-induced cardiomyocyte hypertrophy through suppression of PLA2G6 and DGK-ζ. Momordicine I exerts its cardiovascular benefits by upregulating nitric oxide, inhibiting the activity of angiotensin-converting enzyme (ACE), activating the PI3K/Akt pathway, reducing oxidative stress and inflammation. Momordicine I inhibits AKT1, IL-6, and SRC, suggesting its potential application in type 2 diabetes.

HY-50673A

Dactolisib hydrochloride	Inhibitor	99.41%
Dactolisib (BEZ235) hydrochloride is an orally active, dual pan-class I PI3K and mTOR inhibitor for p110α/γ/δ/β and mTOR with IC₅₀ of 4 nM/5 nM/7 nM/75 nM and 20.7 nM, respectively. Dactolisib hydrochloride (BEZ235) inhibits mTORC1 and mTORC2.

HY-P11642A

Sialorphin TFA	Inhibitor
Sialorphin TFA is a neutral endopeptidase (NEP) and aminopeptidase N (APN) inhibitor that responds to androgen signals. Sialorphin TFA blocks the degradation of endogenous opioid peptides and interacts with μ-, δ-, κ-opioid receptors. Sialorphin TFA regulates the ERK/mTOR signaling pathway by inducing cell cycle arrest, enhancing ERK1/2 activity, and reducing the phosphorylation levels of mTOR, 4E-BP1, p70S6K; accordingly, Sialorphin TFA exhibits antiproliferative activity against colorectal cancer, glioma and prostate cancer cells without cytotoxicity. In addition, Sialorphin TFA also produces antinociceptive responses, regulates sexual behavior, relaxes corpus cavernosum smooth muscle, and alleviates experimental colitis. Sialorphin TFA is also a copper (II) ion-binding ligand. Sialorphin TFA has been used in mechanistic studies related to cancer, pain management and inflammatory bowel disease.

HY-123849

SN32976	Inhibitor	99.49%
SN32976 is a potent and selective class I PI3K and mTOR inhibitor with IC₅₀s of 15.1 nM, 461 nM, 110 nM, 134 nM and 194 nM for PI3Kα, PI3Kβ, PI3Kγ, PI3Kδ and mTOR, respectively. SN32976 shows high selectivity among other 442 kinases. SN32976 shows anticancer effects.

HY-109633A

PI3K/mTOR-IN-23 dihydrochloride	Inhibitor	99.70%
PI3K/mTOR-IN-23 dihydrochloride is a dual inhibitor of PI3K and mTOR with IC₅₀ values of 49 and 41 nM. PI3K/mTOR-IN-23 dihydrochloride inhibits cancer cells proliferation.

HY-N0390S7

L-Glutamine-¹⁵N₂,d₅	Inhibitor
L-Glutamine-¹⁵N₂,d₅ is the deuterium and ¹⁵N-labeled L-Glutamine (HY-N0390). L-Glutamine is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine is taken up in a Na⁺-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity.

HY-W779800

D-α-Hydroxyglutaric acid-¹³C₅ (disodium)	Inhibitor	98.87%
D-α-Hydroxyglutaric acid-¹³C₅ disodium is the ¹³C-labeled D-α-Hydroxyglutaric acid (HY-113038). D-α-Hydroxyglutaric acid ((R)-2-Hydroxyglutarate) is the principal metabolite accumulating in neurometabolic disease D-2-hydroxyglutaric aciduria. D-α-Hydroxyglutaric acid is a weak competitive antagonist of α-ketoglutarate (α-KG) and inhibits multiple α-KG-dependent dioxygenases with a K_i of 10.87 mM. D-α-Hydroxyglutaric acid increases reactive oxygen species (ROS) production. D-α-Hydroxyglutaric acid binds and inhibits ATP synthase and inhibits mTOR signaling.

HY-15271A

WYE-687 dihydrochloride	Inhibitor	≥98.0%
WYE-687 dihydrochloride is an ATP-competitive mTOR inhibitor with an IC₅₀ of 7 nM. WYE-687 dihydrochloride concurrently inhibits activation of mTORC1 and mTORC2. WYE-687 also inhibits PI3Kα and PI3Kγ with IC₅₀s of 81 nM and 3.11 μM, respectively.

HY-141805

MHY-1685	Inhibitor	99.84%
MHY-1685, a novel mammalian target of rapamycin (mTOR) inhibitor, provides opportunities to improve hCSC-based myocardial regeneration.

HY-145931

CC214-2	Inhibitor	98.41%
CC214-2 is an oral active and selective mTOR kinase inhibitor. CC214-2 targets to both of mTORC1 (pS6) and mTORC2 (pAktS473). CC214-2 induces autophagy, which is a potential target for host-directed therapy (HDT) in tuberculosis. CC214-2 exhibits synergistic bactericidal and sterilizing activity agasinst tuberculosis (TB), and shortens the treatment duration. CC214-2 also inhibits Rapamycin (HY-10219)-resistant signaling and the growth of glioblastomas in vitro and in vivo.

HY-N6651

Isocryptotanshinone	Inhibitor	≥98.0%
Isocryptotanshinone is a dual STAT3 and PTP1B (IC₅₀ = 56.1 μM) inhibitor. Isocryptotanshinone inhibits STAT3 by binding to the STAT3 SH2 domain to block phosphorylation and nuclear translocation^[1][2]. Isocryptotanshinone exerts its anti-proliferative effect via the induction of cell cycle arrest, apoptosis, and pro-death autophagy, through the regulation of STAT3, AKT/mTOR and MAPK signaling pathways. Isocryptotanshinone suppresses the xenograft gastric cancer (GC) tumor growth in BALB/c nude mice. Isocryptotanshinone can be used for cancer research, such as lung cancer, breast cancer and GC.

HY-N3628

Coronarin A	Inhibitor	≥98.0%
Coronarin A is an orally active natural compound that inhibits mTORC1 and S6K1 to increase IRS1 activity. Coronarin A shows anti-inflammatory activity and can also be used for type 2 diabetes mellitus research.

HY-109633

PI3K/mTOR-IN-23	Inhibitor	99.0%
PI3K/mTOR-IN-23 is a dual inhibitor of PI3K and mTOR with IC₅₀ values of 49 and 41 nM. PI3K/mTOR-IN-23 inhibits cancer cells proliferation.

HY-N2199

Sotetsuflavone	Inhibitor
Sotetsuflavone is a flavonoid that can be isolated from Cycas revolute. Sotetsuflavone inhibits phosphorylation of PI3K, Akt, mTOR, JNK, and p38 MAPK; modulates expression of Cyclin D1, CDK4, Bcl-2, Bax, cleaved caspases 3/9, MMP-9, TGF-β, STAT3, and β-catenin. Sotetsuflavone induces G₀/G₁ cell cycle arrest, apoptosis, autophagy, and intracellular ROS elevation, inhibits cancer cell proliferation. Sotetsuflavone inhibits tumor growth in mouse tumor xenograft models. Sotetsuflavone can be used for the research of non-small cell lung cancer and Crohn’s disease.

HY-N2423

Sinigrin hydrate	Inhibitor	99.92%
Sinigrin (Allyl-glucosinolate) hydrate is an orally active glucosinolate found in cruciferous plants. Sinigrin hydrate possesses multiple activities such as anti-cancer, antibacterial, antifungal, anti-inflammatory, antioxidant, and inhibition of fat synthesis. Sinigrin hydrate can be used in the research of tumors, inflammatory, and metabolic diseases.

HY-RS08810

MTOR Human Pre-designed siRNA Set A	Inhibitor
MTOR Human Pre-designed siRNA Set A contains three designed siRNAs for MTOR gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.

HY-N2517

Dihydroevocarpine	Inhibitor	99.62%
Dihydroevocarpine induces cytotoxicity in acute myeloid leukemia via suppressing the mTORC1/2 activity.

SLC7A5 SLC3A2 Sestrin1/2 CASTOR1 CASTOR1 GATOR2 GATOR1 FLCN-FNIP2 RagA/B RagC/D mTORC1 p14 MP1 p18 v-ATPase SLC38A9 Glucose GLUT4 DNA Damage p53 Sestrin1/2 AMPK IKKβ LKB1 RHEB FKBP12 Rapamycin mTOR mTORC1 DEPTOR RAPTOR PRAS40 mLST8 TNF Receptor TNF Growth factors GFRs: EGFRs, IGF1R, Insulin Receptor, FGFR and Met SOS SHC GRB2 IRS1 PI3K Ras Raf MEK ERK RSK TSC2 TSC1 TBC1D7 REDD1 4EBP eIF4E S6K eIF4B PDCD4 SKAR ATF4 MTHFD2 CAD HIF1α Lipin1 ULK1 UVRAG/
ATG14L TFEB ERK5 PGC1-α Autophage Proteasome
assembly SREBP Glucose
metabolism Apoptosis FOXO1,3 GRB10 S6K PTEN PDK1 Akt SGK Ion
transport Rho kinase PKC Actin/
cytoskeleton TSC2 TSC1 TBC1D7 mTOR DEPTOR RICTOR mSIN1 PROTOR mLST8 RAC1 GSK-3β Wnt mTORC2

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.

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mTOR

mTOR

mTOR Isoform Specific Products:

mTOR Isoform Specific Products:

mTOR Related Products (616)

Antibodies (14)

mTOR Signaling Pathway

mTOR Isoform Comparison

mTOR Related Products (616):