mTOR

Mammalian target of Rapamycin

mTOR

mTOR Isoform Specific Products:

mTOR Isoform Comparison

mTOR Related Products (312)
Antibodies (14)
mTOR Signaling Pathway
mTOR Isoform Comparison

By Effects:	Control (1) Inhibitors (260) Substrate (1) Antagonist (1) Activators (27) Modulators (6) p53 Inhibitor (1)

Cat. No.	Product Name	Effect	Purity	Chemical Structure

HY-N1462

Atractyloside potassium salt	Inhibitor	99.93%
Atractyloside potassium salt is a powerful and specific inhibitor of mitochondrial ADP/ATP transport. Atractyloside potassium salt inhibits chloride channels from mitochondrial membranes of rat heart. Atractyloside potassium salt activates autophagy, inhibits ANT2, mTOR and promotes the activation of p-AMPK. Atractyloside potassium salt has anti-cancer effects on non-small cell lung cancer and can inhibit liver steatosis. Atractylodesin potassium salt has nephrotoxicity.

HY-12763

GNE-317	Inhibitor	99.14%
GNE-317 is a PI3K/mTOR inhibitor, is able to cross the blood-brain barrier (BBB).

HY-10115A

PI-103 Hydrochloride	Inhibitor	98.55%
PI-103 Hydrochloride is a dual PI3K and mTOR inhibitor with IC₅₀s of 8 nM, 88 nM, 48 nM, 150 nM, 20 nM, and 83 nM for p110α, p110β, p110δ, p110γ, mTORC1, and mTORC2. PI-103 Hydrochloride also inhibits DNA-PK with an IC50 of 2 nM. PI-103 Hydrochloride induces autophagy.

HY-B0319

Tioconazole	Inhibitor	99.90%
Tioconazole (UK-20349) is a broad-spectrum antifungal imidazole derivative. Tioconazole inhibits several dermatophytes and yeasts, with MIC₅₀ values of less than 3.12 mg/L and 9 mg/L, respectively. Additionally, Tioconazole exhibits anti-parasitic activity. Tioconazole exerts anticancer activity by inhibiting the PI3K/AKT/mTOR signaling pathway and blocking autophagy. Tioconazole is applicable for research in the fields of anti-infection and anticancer therapy.

HY-100222

CZ415	Inhibitor	98.39%
CZ415 is a potent and highly selective mTOR inhibitor with a pIC₅₀ of 8.07. CZ415 inhibits mTORC1 and mTORC2 protein complex.

HY-N6996

Methyl Eugenol	Inhibitor	99.79%
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.

HY-N0107

Cyclovirobuxine D	Inhibitor	≥98.0%
Cyclovirobuxine D (CVB-D) is the main active component of the traditional Chinese medicine Buxus microphylla. Cyclovirobuxine D induces autophagy and attenuates the phosphorylation of Akt and mTOR. Cyclovirobuxine D inhibits cell proliferation of gastric cancer cells through suppression of cell cycle progression and inducement of mitochondria-mediated apoptosis. Cyclovirobuxine D is beneficial for heart failure induced by myocardial infarction.

HY-107365

PQR530	Inhibitor	99.98%
PQR530 is a potent, ATP-competitive, orally bioavailable and brain-penetrant dual pan-PI3K/mTORC1/2 inhibitor, with a subnanomolar K_d toward PI3Kα and mTOR (0.84 and 0.33 nM, respectively). Antitumor activity.

HY-N0656A

(+)-Usnic acid	Inhibitor	99.63%
(+)-Usnic acid is isolated from isolated from lichens, binds at the ATP-binding pocket of mTOR, and inhibits mTORC1/2 activity. (+)-Usnic acid inhibits the phosphorylation of mTOR downstream effectors: Akt (Ser473), 4EBP1, S6K, induces autophay, with anti-cancer and anti-inflammatory activity. (+)-Usnic acid possesses antimicrobial activity against a number of planktonic gram-positive bacteria, including Staphylococcus aureus, Enterococcus faecalis, and Enterococcus faecium.

HY-15521

ETP-46464	Inhibitor	99.55%
ETP-46464 is an effective mTOR and ATR inhibitor with IC₅₀s of 0.6 and 14 nM, respectively.

HY-156671

RMC-4998	Inhibitor
RMC-4998 is an orally active inhibitor targeting the active or GTP-bound state of the KRAS^G12C mutant. RMC-4998 can form a ternary complex with intracellular CYPA and the activated KRAS^G12C mutant, with an IC₅₀ value of 28 nM. RMC-4998 can inhibit ERK signaling in KRAS^G12C mutant cancer cells and induce apoptosis. RMC-4998 can be used for tumor research.

HY-12808

STF-118804	Inhibitor	99.72%
STF-118804 is a highly specific NAMPT inhibitor. STF-118804 activates AMPK and inhibits mTOR pathways. STF-118804 has antitumor activity against pancreatic cancer.

HY-N0486S8

L-Leucine-¹³C₆,¹⁵N	Activator	99.90%
L-Leucine-¹³C₆,¹⁵N is the ¹³C- and ¹⁵N-labeled L-Leucine. L-Leucine is an essential branched-chain amino acid (BCAA), which activates the mTOR signaling pathway[1].

HY-14581

Palomid 529	Inhibitor	99.37%
Palomid 529 is a potent inhibitor of mTORC1 and mTORC2 complexes.

HY-16962A

CC-115 hydrochloride	Inhibitor	98.03%
CC-115 hydrochloride is a potent and dual DNA-PK and mTOR kinase inhibitor with IC₅₀s of 13 nM and 21 nM, respectively. CC-115 blocks both mTORC1 and mTORC2 signaling.

HY-15272

WAY-600	Inhibitor	99.75%
WAY-600 is a potent, ATP-competitive, and selective mTOR inhibitor with an IC₅₀ of 9 nM for recombinant mTOR enzyme. WAY-600 blocks mTOR complex 1/2 (mTORC1/2) assemble and activation.

HY-W016412

Coenzyme Q0	Inhibitor	99.88%
Coenzyme Q0 (CoQ0) is a potent, oral active ubiquinone compound can be derived from Antrodia cinnamomea. Coenzyme Q0 induces apoptosis and autophagy, suppresses of HER-2/AKT/mTOR signaling to potentiate the apoptosis and autophagy mechanisms. Coenzyme Q0 regulates NFκB/AP-1 activation and enhances Nrf2 stabilization in attenuation of inflammation and redox imbalance. Coenzyme Q0 has anti-angiogenic activity through downregulation of MMP-9/NF-κB and upregulation of HO-1 signaling.

HY-100026

PQR620	Inhibitor	98.01%
PQR620 is an orally bioavailable and selective brain penetrant inhibitor of mTORC1/2.

HY-15248

GDC-0349	Inhibitor	98.02%
GDC-0349 is a potent and selective ATP-competitive mTOR inhibitor with a K_i of 3.8 nM. GDC-0349 inhibits of both mTORC1 and mTORC2 complexes.

HY-10219R

Rapamycin (Standard)	Inhibitor
Rapamycin (Standard) is the analytical standard of Rapamycin. This product is intended for research and analytical applications. 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.

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 (312)

Antibodies (14)

mTOR Signaling Pathway

mTOR Isoform Comparison

mTOR Related Products (312):