ERKs (Extracellular-signal-regulated kinases) are widely expressed protein kinase intracellular signalling molecules that are involved in functions including the regulation of meiosis, mitosis, and postmitotic functions in differentiated cells. Many different stimuli, including growth factors, cytokines, virus infection, ligands for heterotrimeric G protein-coupled receptors, transforming agents, and carcinogens, activate the ERK pathway. In the MAPK/ERK pathway, Ras activates c-Raf, followed by mitogen-activated protein kinase kinase (abbreviated as MKK, MEK, or MAP2K) and then MAPK1/2 (below). Ras is typically activated by growth hormones through receptor tyrosine kinases and GRB2/SOS, but may also receive other signals. ERKs are known to activate many transcription factors, such as ELK1, and some downstream protein kinases. Disruption of the ERK pathway is common in cancers, especially Ras, c-Raf and receptors such as HER2.
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KO-947 is a potent and selective inhibitor of ERK1/2 kinase in biochemical, cellular and in vivo antitumor activity assays; blocks ERK signaling and proliferation of tumor cells exhibiting dysregulation of MAPK pathway signaling, including mutations in BRAF, NRAS or KRAS, at low nanomolar concentrations.
A potent, highly selective ERK5 inhibitor with IC50 of 8 nM; shows little affinity for BRD4 (Kd=3.6 uM); clearly inhibits the EGF-stimulated, phosphorylated form of ERK5 in HeLa cells.
LY-3214996 is a novel potent, selective, orally active ERK1/2 inhibitor with IC50 of 5 nM for both enzymes in biochemical assays; potently inhibits cellular phospho-RSK1 in BRAF and RAS mutant cancer cell lines; demonstrates inhibition of cell proliferation, general sensitivitity against tumor cells with MAPK pathway alterations including BRAF, NRAS or KRAS mutation; significantly inhibits tumor growth in vivo and is well tolerated in BRAF or NRAS mutant melanoma, BRAF or KRAS mutant colorectal, lung and pancreatic cancer xenografts or PDX models.
CC-90003 (CC90003) is a potent and selective, covalent ERK1/2 inhibitor with IC50 of 10-20 nM, demonstrates excellent selectivity in a 258-kinase biochemical assay panel; potently inhibits 27 growth of KRAS mutant cell lines with GI50 of <1 uM, also is active against 28 of 37 (76%) KRAS-mutant cancer cell lines, shows cytotoxic effects in KRAS mutant PDAC, lung cancer and CRC cell lines, does not significantly inhibit proliferation of normal lung fibroblasts or bronchial epithelial cells; decreases colony formation ex-vivo and inhibits tumor growth in vivo of KRAS mutant PDX models, induces full regression and prevents regrowth of KRAS mutant Lung PDX model when combined with Docetaxel.
AZD0364 (AZD-0364) is a potent, selective, orally active ERK1/2 inhibitor for treatment of NSCLC.
Tauroursodeoxycholic acid (TUDCA) is a neuroprotective bile conjugate; inhibits nuclear factor-kappa B (NF-κB) activation in glial cells; shows anti-inflammatory effect by inducing TGF-β pathway; inhibits TNFα-induced lipolysis.
DEL-22379 is a small molecule inhibitor of ERK dimerization with IC50 of 0.5 uM, without affecting ERK phosphorylation; prevents tumorigenesis by RAS-ERK pathway oncogenes.
FR 180204 is a potent, selective, ATP-competitive ERK inhibitor with Ki of 0.31 and 0.14 uM for ERK1 and ERK2, respectively; inhibits TGFβ-induced luciferase-expression in mink lung epithelial Mv1Lu cells, decreases plasma anti-CII antibody levels and attenuates delayed-type hypersensitivity in CII-immunized DBA/1 mice, also inhibits in vitro CII-induced proliferation of lymph node cells prepared from CII-immunized mice; enhances apoptotic and anti-proliferative effects of Akt inhibitor API-1 in human DLD-1 and LoVo colorectal cancer cells.
VX-11e is apotent, selective, and orally bioavailable inhibitor of ERK2 with Ki of <2 nM; shows >200-fold selectivity over GSK3, Aurora A, CDK2, FLT3, etc; significantly inhibits CKAP2 overexpression-induced cell proliferation, migration and invasion in SiHa cells.
SCH772984 is a novel potent and selective inhibitor of ERK1/ERK2 with IC50 of 4 nM/1 nM, respectively; is highly selective, with only seven kinases of 300 showing >50% inhibition at 1 uM; prevents MEK-mediated ERK phosphorylation, reduces pCRAF S289/S296/S301 phosphorylation; has nanomolar cellular potency in tumor cells with mutations in BRAF, NRAS, or KRAS and induces tumor regressions in xenograft models.
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