1. PI3K/Akt/mTOR MAPK/ERK Pathway Cell Cycle/DNA Damage
  2. mTOR Ribosomal S6 Kinase (RSK) Akt DNA-PK
  3. eALM1137

eALM1137 is a mTOR inhibitor with an IC50 of 4.8 nM. eALM1137 mediates dual inhibition of the mTORC1 and mTORC2 signaling pathways, and inhibits DNA-PK (IC50=77 nM). eALM1137 exhibits antiproliferative and cytostatic activities, and induces G1 cell cycle arrest. eALM1137 is applicable to the research of glioblastoma multiforme.

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eALM1137

eALM1137 Chemical Structure

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Description

eALM1137 is a mTOR inhibitor with an IC50 of 4.8 nM. eALM1137 mediates dual inhibition of the mTORC1 and mTORC2 signaling pathways, and inhibits DNA-PK (IC50=77 nM). eALM1137 exhibits antiproliferative and cytostatic activities, and induces G1 cell cycle arrest. eALM1137 is applicable to the research of glioblastoma multiforme[1].

IC50 & Target

mTORC1

 

mTORC2

 

In Vitro

eALM1137 (0.1-1000 nM; 5 days) potently inhibits U87-MG glioblastoma cell proliferation with an EC50 of 5.1 nM after 5 days of treatment[1].
eALM1137 (0.1-1000 nM; 5 days) potently inhibits T98G glioblastoma cell proliferation with an EC50 of 11 nM after 5 days of treatment[1].
eALM1137 (3 nM, 10 nM, 30 nM, 100 nM, 300 nM) dose-dependently inhibits mTORC1 and mTORC2 signaling in U87-MG and T98G glioblastoma cells, with marked reduction of phosphorylated S6 and Akt at concentrations ≥30 nM[1].
eALM1137 (10-8-10-5 M; 3 days) potently inhibits NPE glioblastoma stem cell proliferation with an EC50 of 85 nM after 3 days of treatment, exerting cytostatic rather than cytotoxic effects[1].
eALM1137 (300 nM; 24 h) inhibits mTORC1 and mTORC2 signaling in NPE glioblastoma stem cells after 24 h of treatment at 300 nM, while inducing compensatory activation of the RAF-MEK-ERK pathway[1].
eALM1137 (0.03 μM, 0.1 μM, 0.3 μM, 1 μM, 3 μM, 10 μM; 3 days) induces dose-dependent G1-phase cell cycle arrest in E21 patient-derived glioblastoma stem cells after 3 days of treatment[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay[1]

Cell Line: U87-MG glioblastoma multiforme cells
Concentration: 0.1-1000 nM
Incubation Time: 5 days
Result: Suppressed U87-MG cell proliferation with an EC50 of 5.1 nM.
Showed stronger potency than reference compound sapanisertib (EC50=7.5 nM).

Cell Cycle Analysis[1]

Cell Line: E21 patient-derived mesenchymal glioblastoma stem cells expressing FUCCI cell cycle reporter
Concentration: 0.03 μM, 0.1 μM, 0.3 μM, 1 μM, 3 μM, 10 μM
Incubation Time: 3 days
Result: Induced a strong G1-phase cell cycle arrest in a dose-dependent manner.
Caused significant increases in the percentage of G1-phase cells relative to DMSO control at all tested concentrations.
Molecular Weight

450.49

Formula

C22H26N8O3

SMILES

O=C(N1CCC(CN2N=C(C3=CC=C(OC(N)=N4)C4=C3)C5=C(N)N=CN=C52)CC1)OC(C)C

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation
References
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    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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eALM1137
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HY-183250
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