mTOR

Mammalian target of Rapamycin

mTOR

mTOR Isoform Specific Products:

mTOR Isoform Comparison

mTOR Related Products (613)
Antibodies (14)
mTOR Signaling Pathway
mTOR Isoform Comparison

By Effects:	Inhibitors (479)

Cat. No.	Product Name	Effect	Purity	Chemical Structure

HY-N9942

Physalin A	Inhibitor	99.63%
Physalin A is a biologically active withanolide. Physalin A shows anti-inflammatory, antifibrotic and ameliorative effects on autophagy in models of disc degeneration. Physalin A has antitumor activity and can induce apoptosis, ROS production and G2/M phase cell cycle arrest. Besides. Physalin A can significantly increase the activity of quinone reductase and increase the expression of detoxifying enzymesc.

HY-10219S1

Rapamycin-¹³C,d₃	Inhibitor
Rapamycin-¹³C,d₃ (Sirolimus-¹³C,d₃) is the ¹³C and deuterium labeled Rapamycin (HY-10219). Rapamycin 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.

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.

HY-137315

TML-6	Inhibitor	98.34%
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-oxidative Nrf2 gene. TML-6 has the potential for Alzheimer’s disease (AD) research.

HY-172423

Darlifarnib	Inhibitor
Darlifarnib (KO-2806) is an orally active farnesyl transferase inhibitor. Darlifarnib inhibits the mTORC1 signaling pathway, thereby enhancing the anti-angiogenic properties of tyrosine kinase inhibitors. When used in combination with anti-VEGFR tyrosine kinase inhibitors, Darlifarnib promotes renal cell carcinoma tumor regression and inhibits tumor neovascularization. Darlifarnib sensitizes renal cell carcinoma tumors that progress after anti-VEGFR TKI treatment.

HY-147284

PI3K-IN-37	Inhibitor	99.0%
PI3K-IN-37 (Example 84.1) is a PI3K α/β/δ inhibitor with IC₅₀s of 6, 8, 4 nM, respectively. PI3K-IN-37 can also inhibit mTOR (IC₅₀=4 nM).

HY-10620

PI3K-IN-22	Inhibitor	99.50%
PI3K-IN-22 is a PI3Kα/mTOR dual kinase inhibitor. PI3K-IN-22 has IC₅₀s of 0.9, 0.6 nM for PI3Kα and mTOR, respectively. PI3K-IN-22 can be used for the research of cancer.

HY-N11709

Theasaponin E1	Inhibitor	99.0%
Theasaponin E1 is an orally effective tea saponin. Theasaponin E1 inhibits the proliferation of cancer cells by activating apoptosis. Theasaponin E1 inhibits angiogenesis in ovarian cancer cells and HUVECs by reducing the expression of VEGF. Theasaponin E1 upregulates the phosphorylation level of ATM protein and the expression level of PTEN protein in cancer cells, decreases the phosphorylation levels of Akt, mTOR, p70S6K and 4E-BP1 proteins, downregulates the expression of HIF-1α and NF-κB, and reduces the protein expression of Notch ligands Dll4 and Jagged1. Theasaponin E1 exerts neuroprotective effects by inhibiting the activity of acetylcholinesterase, activating α-secretase and neprilysin, reducing the concentration of Aβ, and inhibiting the activities of β-secretase and γ-secretase. Theasaponin E1 exhibits toxic effects on cancer cells and quinone reductase-inducing activity, and inhibits tumor growth in vivo. Theasaponin E1 induces ferroptosis in Pomacea canaliculata by synergistically disrupting cholesterol homeostasis and sphingolipid metabolism. Theasaponin E1 possesses anti-biofilm activity against Candida albicans. Theasaponin E1 can be used in the research of ovarian cancer, obesity, Alzheimer's disease and fungal infections.

HY-110109

ETP-45658	Inhibitor	98.97%
ETP-45658 is a potent PI3K inhibitor, with IC₅₀s of 22.0 nM, 39.8 nM, 129.0 nM and 717.3 nM for PI3Kα, PI3Kδ, PI3Kβ and PI3Kγ, respectively. ETP-45658 also can inhibit DNA-PK (IC₅₀=70.6 nM) and mTOR (IC₅₀=152.0 nM). ETP-45658 can be used for the research of cancer.

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.

HY-174066

SI-W052	Inhibitor	98.0%
SI-W052 is an orally active, brain-penetrant and selective small-molecule inhibitor targeting mTOR and TEX264. SI-W052 activates autophagy by inhibiting mTOR phosphorylation and enhances TEX264 expression to promote ER turnover, suppressing LPS-induced release of inflammatory factors (TNF-α, IL-6). SI-W052 is promising for research of Alzheimer’s disease (AD)-associated neuroinflammation.

HY-176761

NSC647889	Inhibitor	99.28%
NSC647889 is an apoptosis and autophagy inducer. NSC647889 induces apoptosis, inhibits mTOR pathway and abrogates DNA synthesis. NSC647889 triggers LC3-positive vesicle formation, modulates AKT and 4EBP1 phosphorylation and shows heightened caspase-3 activation in multicellular spheroids. NSC647889 can be used for the research of solid cancer tumour, head-neck carcinoma, and colorectal cancer.

HY-153120A

PI3K/mTOR Inhibitor-13 sodium	Inhibitor	98.11%
PI3K/mTOR Inhibitor-13 sodium is an orally active dual inhibitor of phosphoinositol 3-kinase (PI3K) and mTOR kinase. PI3K/mTOR Inhibitor-13 sodium has potential applications in sexual diseases, solid tumor and idiopathic pulmonary fibrosis (IPF).

HY-15269

PP30	Inhibitor
PP30 is a potent, selective, ATP-competitive mTOR inhibitor with an IC₅₀ of 80 nM. PP30 blocks insulin-stimulated phosphorylation of Akt at residues S473 and T308, preventing the full activation of Akt. PP30 is applicable for cancer research.

HY-156671A

RMC-4998 formic	Inhibitor	99.02%
RMC-4998 formic is an orally active inhibitor targeting the active or GTP-bound state of the KRAS^G12C mutant. RMC-4998 formic can form a ternary complex with intracellular CYPA and the activated KRAS^G12C mutant, with an IC₅₀ value of 28 nM. RMC-4998 formic can inhibit ERK signaling in KRAS^G12C mutant cancer cells and induce apoptosis. RMC-4998 formic can be used for non-small cell lung cancer (NSCLC) research.

HY-155066

FD274	Inhibitor	99.45%
FD274 is a highly potent PI3K/mTOR dual inhibitor with IC₅₀s of 0.65 nM, 1.57 nM, 0.65 nM, 0.42 nM, and 2.03 nM against PI3Kα/β/γ/δ and mTOR, respectively. FD274 exhibits significant anti-proliferation of AML cell lines (HL-60 and MOLM-16). FD274 arrests HL-60 cell cycle at G1 phase and increases apoptosis. FD274 demonstrates dose-dependent inhibition of tumor growth in the HL-60 xenograft model. FD274 has the potential for acute myeloid leukemia research.

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).

HY-N12124

Monascuspiloin	Inhibitor
Monascuspiloin (Monascinol) exhibits anti-androgenic activity with an IC₅₀ of 7 μM. Monascuspiloin inhibits viability of PC-3 and LNCaP with IC₅₀ of 45 and 47 μM. Monascuspiloin induces apoptosis in LNCaP through inhibition of Akt/mTOR signaling pathway, induces autophagy through activation AMPK signaling pathway and arrest cell cycle at G2/M phase in PC-3. Monascuspiloin exhibits antitumor efficacy in mice.

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.

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 (613)

Antibodies (14)

mTOR Signaling Pathway

mTOR Isoform Comparison

mTOR Related Products (613):