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In Vitro：
APS-2-79 inhibits BRAF and CRAF phosphorylation of MEK in a KSR-dependent manner. APS-2-79 does not affect BRAF(V600E)-induced MAPK activation in cells. APS-2-79 impedes KSR-stimulated MAPK signalling within cells through wild-type and MEK equally. APS-2-79 synergizes with trametinib specifically in Ras-mutant cells compared to the HER-family and SRC-family inhibitors lapatinib and sarcatinib. APS-2-79 increases the potency of several MEK inhibitors specifically within Ras-mutant cell lines by antagonizing release of negative feedback signalling, demonstrating the potential of targeting KSR to improve the efficacy of current MAPK inhibitors. The IC50 value of APS-2-79 against ATPbiotin probe-labelling of KSR2 is 120 nM[1].

Fields：
APS-2-79 is a novel modulator of KSR-dependent MAPK signalling,KSR2,IC50=120 nM

Specificity：
Target: ERK. Fields: APS-2-79 is a novel modulator of KSR-dependent MAPK signalling,KSR2,IC50=120 nM

Source：
Rabbit

Dilution：
WB 1:500-2000

Concentration：
>98%

Storage Stability：
2 years -20°C Powder, 2 weeks4°C in DMSO,6 months-80°C in DMSO

Other Name：
APS 2 79,APS279,APS-279

MolecularWeight(Da)：
387.16

References：
[1]. Dhawan NS, et al. Small molecule stabilization of the KSR inactive state antagonizes oncogenic Ras signalling. Nature. 2016 Aug 24;537(7618):112-116.

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