Catalog No. size PriceQuantity
M6512-2 2mg solid $81
M6512-10 10mg solid $316



Product Information:

APS-2-79 is a KSR-dependent MAPK modulator. APS-2-79 modulates KSR-dependent MAPK signalling by antagonizing RAF heterodimerization as well as the conformational changes required for phosphorylation and activation of KSR-bound MEK (mitogen-activated protein kinase kinase). APS-2-79 increased 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. Co-targeting of enzymatic and scaffolding activities within Ras-MAPK signalling complexes is a therapeutic strategy for overcoming Ras-driven cancers.


Chemical Formula: C23H21N3O3


Exact Mass: 387.1583


Molecular Weight: 387.439


Elemental Analysis: C, 71.30; H, 5.46; N, 10.85; O, 12.39





APS 2-79



APS 279



Chemical Name: 



InChi Key:



InChi Code: 



Smiles Code:




Technical Data:


Appearance: Solid powder

Purity: >98% (or refer to the Certificate of Analysis)

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.

Storage Condition: Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).

Solubility: Soluble in DMSO

Shelf Life: >2 years if stored properly

Drug Formulation: This drug may be formulated in DMSO

Stock Solution Storage: 0 - 4 C for short term (days to weeks), or -20 C for long term (months).

HS Tariff Code: 2934.99.9001


In Vitro:

APS-2-79 (1 μM) shifts the cell viability dose response to Trametinib in Ras-mutant cell lines HCT-116 and A549, but not BRAF mutant cell lines SK-MEL-239 and A375. Although the cellular effects of APS-2-79 alone are modest, combination analysis over full concentration matrices reveal that kinase suppressor of Ras (KSR)-inactive state (KSRi) synergizes with Trametinib, and other MEK inhibitors, specifically in KRAS mutant cell lines. APS-3-77, and additional control compounds, do not demonstrate Ras-mutant-specific synergy, supporting the hypothesis that the enhanced activity of Trametinib when combined with APS-2-79 depends on co-modulation of KSR.





  1. KSR Mutations Guide Development of RAS Pathway Antagonists. Cancer Discov. 2016 Oct;6(10):1079. PubMed PMID: 27591198.


  1. Dhawan NS, Scopton AP, Dar AC. Small molecule stabilization of the KSR inactive state antagonizes oncogenic Ras signalling. Nature. 2016 Aug 24;537(7618):112-116. doi: 10.1038/nature19327. [Epub ahead of print] PubMed PMID: 27556948.


Products are for research use only. Not for human use.

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