APS-2-79 hydrochloride

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APS-2-79 hydrochloride is a KSR-dependent MEK antagonist. APS-2-79 inhibits ATP^biotin binding to KSR2 within the KSR2-MEK1 complexe with an IC₅₀ of 120 nM. APS-2-79 makes the stabilization of the KSR inactive state antagonizes oncogenic Ras-MAPK signaling.

For research use only. We do not sell to patients.

APS-2-79 hydrochloride Chemical Structure

CAS No. : 2002381-31-7

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Other In-stock Forms of APS-2-79 hydrochloride:

APS-2-79

Other Forms of APS-2-79 hydrochloride:

APS-2-79 In-stock

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MEK1 MEK2 MEK5 MEK

Biological Activity
Protocol
Purity & Documentation
References
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Description

IC₅₀ & Target^[1]

KSR2

120 nM (IC₅₀)

MEK1

In Vitro

APS-2-79 (5 μM) suppresses KSR-stimulated MEK and ERK phosphorylation in 293H cells^[1].
APS-2-79 (1 μM) enhances the efficacy of the clinical MEK inhibitor trametinib within cancer cell lines containing K-Ras mutations^[1]

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

Molecular Weight

423.89

Formula

C₂₃H₂₂ClN₃O₃

CAS No.

2002381-31-7

SMILES

CC1=CC(OC2=CC=CC=C2)=CC=C1NC3=C4C=C(OC)C(OC)=CC4=NC=N3.Cl

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

Handling Instructions (2659 KB)

References

[1]. Dhawan NS, et al. Small molecule stabilization of the KSR inactive state antagonizes oncogenic Ras signalling. Nature. 2016 Sep 1;537(7618):112-116. [Content Brief]

Cell Assay
^[1]

Cell viability assays are performed in 96 well plates. Optimal cell densities for 96 well plate assays are determined to obtain linear growth over the time course of assays. A549, HCT-116, A375, SK-MEL-239, COLO-205, LOVO, SK-MEL-2, CALU-6, MEWO, SW620 and SW1417 cells are plated at 500 cells per well and treated with inhibitors (e.g., APS-2-79; 100-3,000 nM) for 72hrs before measuring viability. H2087 and HEPG2 cells are plated at 2000 cells per well, and treated with inhibitors (e.g., APS-2-79; 100-3,000 nM) for 72hrs. Cell viability is measured using Resazurin, and the percent cell viability is determined by normalizing inhibitor-treated samples to DMSO controls^[1].

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

References

[1]. Dhawan NS, et al. Small molecule stabilization of the KSR inactive state antagonizes oncogenic Ras signalling. Nature. 2016 Sep 1;537(7618):112-116. [Content Brief]