ras/erk activation

XRP44X (XRP 44X) is a potent inhibitor of Ras-Net (Elk-3) pathway.

UC-857993, a selective SOS1-Ras inhibitor (Kd=14.7 μM, His6-SOS1cat), effectively suppresses catalytic activity. In addition to inhibiting ERK and Ras activation, it also hampers the growth of mouse embryonic fibroblasts (MEFs).

Pseudoginsenoside Rh2 has cytotoxicity, it induces mitochondrial apoptosis in A549 cells and is responsible for excessive activation of the Ras Raf ERK p53 pathway. (20Z) -Pseudoginsenoside Rh2 and (20E)-Pseudoginsenoside Rh2 have antioxidative activity.

POP-3MB (compound 1b) acts as an inhibitor of ICMT, displaying an IC50 value of 2.5 μM. This compound not only alters the subcellular localization of K-Ras but also impedes Ras activation and inhibits Erk phosphorylation [1].

Son of sevenless homolog 1 (Sos1) is a guanine nucleotide exchange factor (GEF) that directs the exchange of Ras-GDP to Ras-GTP by binding to SH3 domains of the growth factor receptor-bound protein 2 (Grb2), leading to the activation of ERK. Ras inhibitory peptide is a synthetic peptide that contains the sequence PVPPR, which corresponds to a region within human Sos1 that interacts with an SH3 domain of Grb2. It specifically blocks the interaction of the GEF with Grb2, preventing an interaction that is essential for Ras activation by receptor tyrosine kinases, including epidermal growth factor receptor.

Pimasertib HCl is an orally bioavailable small-molecule inhibitor of MEK1 and MEK2 (MEK1/2) with potential antineoplastic activity. Pimasertib selectively binds to and inhibits the activity of MEK1/2, preventing the activation of MEK1/2-dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK1/2 (MAP2K1/K2) are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.