mTOR

Mammalian target of Rapamycin

mTOR

mTOR Isoform Specific Products:

mTOR Isoform Comparison

mTOR Related Products (437)
Antibodies (14)
mTOR Signaling Pathway
mTOR Isoform Comparison

By Effects:	Control (1) Inhibitors (350) Substrate (1) Agonists (9) Degrader (1) Antagonist (1) Activators (41) Modulators (6) p53 Inhibitor (1)

Cat. No.	Product Name	Effect	Purity	Chemical Structure

HY-N2217R

Rotundic acid (Standard)	Inhibitor
Rotundic acid (Standard) is the analytical standard of Rotundic acid. This product is intended for research and analytical applications. Rotundic acid, a triterpenoid obtained from Ilex rotunda Thunb., induces DNA damage and cell apoptosis in hepatocellular carcinoma through AKT/mTOR and MAPK Pathways. Rotundic acid possesses anti-inflammatory and cardio-protective abilities.

HY-N10754

Aschantin	Inhibitor
Aschantin, a bisepoxylignan, can be isolated from Magnolia biondii. Aschantin has antiplasmodial, Ca²⁺-antagonistic, platelet activating factor-antagonistic, and chemopreventive activities. Aschantin is a mTOR kinase inhibitor. Aschantin is also an inhibitor of Cytochrome P450 and UGT enzyme.

HY-155376

mTOR inhibitor-14	Inhibitor
mTOR inhibitor-14 (compound 14c) is a potent mTOR inhibitor. mTOR inhibitor-14 also shows minimal CYP2C8 inhibition. mTOR inhibitor-14 can inhibit tumor growth.

HY-17654

BIEGi-1	Inhibitor
BIEGi-1 is an EGFR inhibitor. BIEGi-1 effectively disrupts the EGFR-Rheb interaction in cells. BIEGi-1 robustly inhibits EGFR kinase activity (reduces p-Y1068-EGFR) as well as mTORC1 activation (reduces p-T389-S6K1) in EGFR-mutant cells. BIEGi-1 shows strong antiproliferative effects on EGFR-mutant PC9 and HCC827 cells with IC₅₀ values of 17 nM and 20 nM, respectively. BIEGi-1 can be used for the study of cancers harboring EGFR mutations, such as non-small cell lung cancer (NSCLC).

HY-173141

mTOR inhibitor-26	Inhibitor
mTOR inhibitor-26 (Compound HPT-11) is an inhibitor of mTOR with an IC₅₀ of 0.7 nM. It effectively inhibits the proliferation of AML cell lines Molm-13 and MV-4-11. mTOR inhibitor-26 exhibits antitumor activity and favorable metabolic stability, making it a promising candidate for cancer research.

HY-13610

N1,N11-Diethylnorspermine	Inhibitor
N1,N11-Diethylnorspermine is a synthetic analog of the naturally occurring polyamine spermine, can induce polyamine depletion and inhibit tumor cell growth. N1,N11-Diethylnorspermine activates polyamine catabolism and downregulates mTOR protein. N1,N11-Diethylnorspermine induces the release of cytochrome c from mitochondria, resulting in activation of caspase 3. N1,N11-Diethylnorspermine tetrahydrochloride kills glioblastoma multiforme (GBM) through induction of SSAT (spermidine/spermine N1-acetyltransferase) coupled with H₂O₂ production.

HY-137315S

TML-6-d₃
TML-6-d₃ is the deuterium labeled TML-6. TML-6, an orally active curcumin derivative, inhibits the synthesis of the β-amyloid precursor protein and β-amyloid (Aβ). TML-6 can upregulate Apo E, suppress NF-κB and mTOR, and increase the activity of the anti-

HY-B0168BS

Levomilnacipran-d₅ hydrochloride	Activator
Levomilnacipran-d5 ((1S,2R)-Milnacipran-d5) hydrochloride is deuterium labeled Levomilnacipran hydrochloride (HY-B0168B). Levomilnacipran ((1S,2R)-Milnacipran) hydrochloride is the enantiomer of Milnacipran (HY-B0168) and a strong substrate of P-gp that can cross the blood-brain barrier. Levomilnacipran hydrochloride is a serotonin and norepinephrine reuptake inhibitor, with IC₅₀ values of 10.5 nM and 19.0 nM, and K_i values of 92.2 nM and 1.2 nM for human norepinephrine transporter (NET) and serotonin transporter (SERT), respectively. Levomilnacipran hydrochloride has antidepressant and anxiolytic activities. Levomilnacipran hydrochloride can be used for the research of depression.

HY-15269

PP30	Inhibitor
PP30, a TORKinib, is a potent, selective, and ATP-competitive inhibitor of mTOR with an IC₅₀ of 80 nM.

HY-147966

HDAC-IN-43	Inhibitor
HDAC-IN-43 is a potent HDAC 1/3/6 inhibitor with IC₅₀ values of 82, 45, and 24 nM, respectively. HDAC-IN-43 is a weak PI3K/mTOR inhibitors with IC₅₀ values of 3.6 and 3.7 μM, respectively. HDAC-IN-43 shows broad anti-proliferative activity .

HY-163511

PI3K/Akt/mTOR-IN-4	Inhibitor
PI3K/Akt/mTOR-IN-4 (compound 4r) is a potent PI3K/Akt/mTOR and tubulin polymerization inhibitor. PI3K/Akt/mTOR-IN-4 induce apoptosis and cell cycle arrest at G2/M phase. PI3K/Akt/mTOR-IN-4 decreases the expression of p-PI3K, p-Akt, and p-mTOR, β-tubulin.

HY-N0404R

Sinigrin (Standard)	Inhibitor
Sinigrin (Standard) (Allyl-glucosinolate (Standard)) is the analytical standard of Sinigrin (HY-N0404). This product is intended for research and analytical applications. Sinigrin (Allyl-glucosinolate) is an orally active glucosinolate found in cruciferous plants. Sinigrin possesses multiple activities such as anti-cancer, antibacterial, antifungal, anti-inflammatory, antioxidant, and inhibition of fat synthesis. Sinigrin can be used in the research of tumors, inflammatory, and metabolic diseases.

HY-152238

PI3K/mTOR Inhibitor-12	Inhibitor
PI3K/mTOR Inhibitor-12 is a potent, orally active and selective PI3K/mTOR inhibitor with IC₅₀ values of 0.06 nM and 3.12 nM for PI3Kα and mTOR, respectively. PI3K/mTOR Inhibitor-12 has antitumor activity. PI3K/mTOR Inhibitor-12 has lower liver toxicity.

HY-150061

NVP-BBD130	Inhibitor
NVP-BBD130 is a potent, stable, ATP-competitive and orally active dual PI3K and mTOR inhibitor. NVP-BBD130 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

HY-172259

Toyaburgine	Inhibitor
Toyaburgine is a unique isoquinoline compound that exhibits anti-tumor activity. It packs a punch by disrupting the PI3K/AKT/mTOR signaling pathway, causing significant morphological changes and cell death in MIA PaCa-2 cells. On top of that, it puts the brakes on cell migration and colony formation. This compound is showing a lot of promise in the realm of pancreatic cancer research.

HY-W339757

Dioctanoylphosphatidic acid sodium
Dioctanoylphosphatidic acid sodium functions as a modulator of phagocyte respiratory burst, acts as a precursor to diacylglycerol and lysophosphatidic acid, and influences the phosphorylation of the mammalian target of rapamycin (mTOR) while enhancing the viability of gallbladder carcinoma cells treated with histone deacetylase inhibitors (HDACIs); it is derived from glycerophospholipid through the action of phospholipase D.

HY-N0047R

Polyphyllin I (Standard)	Inhibitor
Polyphyllin I (Standard) is the analytical standard of Polyphyllin I. This product is intended for research and analytical applications. Polyphyllin I is a bioactive constituent extracted from Paris polyphylla, has strong anti-tumor activity. Polyphyllin I is an activator of the JNK signaling pathway and is an inhibitor of PDK1/Akt/mTOR signaling. Polyphyllin I induces autophagy, G2/M phase arrest and apoptosis.

HY-15268

PP487	Inhibitor
PP487 is a dual inhibitor of tyrosine kinase/PI(3)Ks with IC₅₀ values of 0.017 μM, 0.072 μM, 0.004 μM, 0.01 μM, 0.55 μM, 0.22 μM, and < 0.01 μM against DNA-PK, mTOR, Hck, Src, EGFR, EphB4, and PDGFR, respectively. PP487 can be used for cancer research.

HY-N0735R

Phellodendrine chloride (Standard)	Agonist
Phellodendrine chloride (Standard) is the analytical standard of Phellodendrine chloride (HY-N0735). Phellodendrine chloride is an orally active plant alkaloid. Phellodendrine chloride inhibits the proliferation of KRAS-mutated pancreatic cancer cells by suppressing macropinocytosis and glutamine metabolism, inducing ROS accumulation and mitochondrial apoptosis. Phellodendrine chloride promotes autophagy by activating the AMPK/mTOR pathway, alleviating intestinal damage in ulcerative colitis. Phellodendrine chloride can alleviate gouty arthritis by inhibiting the IL-6/STAT3 signaling pathway. Phellodendrine chloride suppresses allergic reactions by altering the conformation of MRGPRB3/MRGPRX2 protein, thereby inhibiting the activation of PKC and subsequent downstream MAPK and NF-κB signaling. Phellodendrine chloride inhibits the AKT/NF-κB pathway and down-regulates the expression of COX-2, thereby protecting zebrafish embryos from oxidative stress. Phellodendrine chloride has an anti-major depressive disorder (MDD) effect by down-regulating CHRM1, HTR1A, and the PI3K/Akt signaling pathway.

HY-RS08812

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

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 (437)

Antibodies (14)

mTOR Signaling Pathway

mTOR Isoform Comparison

mTOR Related Products (437):