erk 1

ERK1/2 inhibitor 1 is a potent, orally bioavailable compound that exhibits 60% inhibition at 1 nM and has an IC50 of 3.0 nM against ERK1 and ERK2, respectively.

ERK1/2 inhibitor 12 (compound 76.3) is an ERK1/2 inhibitor that suppresses ERK-mediated phosphorylation of caspase-9 and p90Rsk-1 kinases. It exhibits anticancer properties and is applicable in cancer research.

ERK1/2 Inhibitor 3, a potent inhibitor of ERK1/2, plays a crucial role in the signal transduction pathway by targeting the Mitogen-activated protein kinase (MAPK) family, specifically the extracellular signal-regulated kinase (ERK). Given its significant impact, this compound holds promise for research or prevention efforts related to cancer, inflammation, or other proliferative diseases[1].

ERK1/2 Inhibitor 9 (Probe 1), a covalent antagonist of ERK1/2, exhibits sub-micromolar efficacy in cellular assays (A375 GI50=0.47 μM) and facilitates the reduction of phospho-ERK1/2 levels. When conjugated with trans-cyclo-octene (TCO) and Tz-Thalidomide (tetrazine-tagged Thalidomide), it forms the corresponding ERK-CLIPTAC, promoting targeted ERK1/2 degradation [1].

ERK1/2 inhibitor 13 (Compound 21y) is an orally bioavailable ERK inhibitor that targets ERK1 and ERK2, with IC50 values of 91.71 nM and 97.87 nM, respectively. It effectively suppresses the proliferation of cancer cell lines MCF-7, 4T1, MDA-MB-468, and HCC1970 with IC50 values of 0.67 μM, 2.76 μM, 2.15 μM, and 1.68 μM, respectively. Additionally, it inhibits cancer cell migration, induces apoptosis and autophagy in MCF-7 cells, and demonstrates anti-tumor and anti-metastatic effects in a 4T1 xenograft mouse model.

ERK1/2 inhibitor 10 (Compound 36c) is a potent inhibitor of ERK1 and ERK2, with IC50 values of 0.11 nM and 0.08 nM, respectively. It effectively hinders the phosphorylation of downstream substrates p90RSK and c-Myc. Additionally, ERK1/2 inhibitor 10 induces apoptosis and incomplete autophagy-related cell death. This compound demonstrates significant antitumor efficacy in models of triple-negative breast cancer and colorectal cancer harboring BRAF and RAS mutations.

ERK1/2 inhibitor 7 is a potent inhibitor of ERK, with an IC50 of 0.94 nM for ERK2.

ERK1/2 inhibitor 8 is a potent ERK inhibitor, targeting ERK2 with an IC50 of 0.48 nM.

ERK1/2 inhibitor 6 is a potent inhibitor of ERK1/2, showing potential for studying or preventing cancer, inflammation, and other proliferative diseases.

ERK1/2 inhibitor 5 is a potent inhibitor of ERK1/2, with potential applications in investigating or preventing cancer, inflammation, and other proliferative diseases.

p44/42 MAPK (Erk1/2) (137F5) Rabbit mAb #4695R is a useful organic compound for research related to life sciences and the catalog number is T64587.

Phospho-p44/42 MAPK (Erk1/2) (Thr202/Tyr204) (20G11) Rabbit mAb #4376R is a useful organic compound for research related to life sciences and the catalog number is T64608.

SCH772984 is an ERK inhibitor that inhibits ERK1 and ERK2 (IC50=4/1 nM) and is highly selective and ATP-competitive. SCH772984 exhibits antitumor activity against BRAF or RAS mutant cells.

MK-8353 (SCH900353) is a potent, selective, and orally available inhibitor of ERK1/2 with IC50 values of 23.0 nM and 8.8 nM, respectively.

AY 77 (Unk-Cha-Chg-NH2) is a potent and selective PAR2 agonist. AY 77 showed selectivity for Ca2+ and ERK1/2 signaling (ec50 value of Ca2+ release was 40 nM and ec50 value of ERK1/2 phosphorylation was 2 μM). AY 77 can promote migration of human breast cancer cells in vitro.

Notoginsenoside R1 (Sanchinoside R1) has been shown to exhibit antioxidant, antiapoptotic, anti-inflammatory, and immune-stimulatory properties.

Selumetinib (AZD6244) is a MEK1/2 inhibitor that inhibits MEK1 (IC50=14 nM) with potent selectivity and is non-ATP-competitive. Selumetinib has antitumor activity and is used for the treatment of neurofibromatosis type 1 (NF1).

Rineterkib (ERK-IN-1) is an inhibitor of RAF and ERK1/2 activating mutations in the MAPK pathway.

CC-90003 is a selective inhibitor of ERK 1/2. It has antitumor activity.

DMU-212 is a methylated derivative of resveratrol with antimitotic, anti-proliferative, antioxidant, and apoptosis-promoting activities. It induces mitotic arrest, apoptosis, and activation of ERK1/2 protein and has oral activity[1][2]. DMU-212 (0.3125-40 μM) inhibits the growth of human melanoma cells (A375, MeWo, Bro, M5)[1]. At concentrations of 30-50 μM over 24 hours, it upregulates cell cycle inhibitors, induces apoptosis, and activates ERK in A375 cells[1]. DMU-212 also induces G2/M arrest and apoptosis in cancer cells[1]. In a xenograft model of human ovarian cancer with six-week-old SCID female mice (20-24 g), DMU-212 (50 mg/kg, administered orally three times a week for 14 days) inhibits tumor growth[2]. [1]. Vasilis Pericles Androutsopoulos, et al. Activation of ERK1/2 is required for the antimitotic activity of the resveratrol analogue 3,4,5,4'-tetramethoxystilbene (DMU-212) in human melanoma cells. Exp Dermatol. 2015 Aug;24(8):632-4. [2]. Hanna Piotrowska, et al. DMU-212 inhibits tumor growth in xenograft model of human ovarian cancer. Biomed Pharmacother. 2014 May;68(4):397-400.

Temuterkib (LY3214996) is a potent and selective, orally available inhibitor of the extracellular signal-regulated kinase (ERK) 1 and 2, with potential antineoplastic activity.

Pluripotin (SC1) (SC1), which keep embryonic stem cell (ESC) self-renewal, is a dual inhibitor of extracellular signal-regulated kinase 1 (ERK1, MAPK3) and RasGAP.

mSIRK (G-Protein βγ Binding Peptide) is a cell-permeable activator of ERK 1/2 with an EC50 of 2.5-5 μM. It disrupts the interaction between the α and βγ subunits, facilitating α subunit dissociation without inducing nucleotide exchange [1].

ERK1/2 inhibitor 2 (ASTX029) is a selective and orally bioavailable extracellular signal-regulated kinases 1 and 2 (ERK 1/2) inhibitor, with potential antineoplastic activity.