erk-1/2 inhibitor 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 11 (compound L6) is a dual inhibitor of ERK1/2 that promotes the accumulation of DSBs and the degradation of ERK1/2 expression. This compound decreases BCL-2 levels and induces DNA damage by inhibiting PARP and ERK1/2. Additionally, ERK1/2 inhibitor 11 activates caspase 3 to induce apoptosis.

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.

Yoda 1 is an agonist of the Piezo1 channel that agonizes human- and mouse-derived Piezo1 (EC50=17.1/26.6 μM). Yoda 1 is also an inhibitor of glycine transporter protein 2 (GlyT2).

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

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

ERK-IN-2, an ERK2 inhibitor, exhibits an IC50 value of 1.8 nM. At doses greater than 10 μM, it may induce off-target toxicity and/or activity [1].

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

SOS1-IN-17 (Compound 8d) is an orally active inhibitor targeting the SOS1-KRASG12C interaction, with an IC50 of 5.1 nM. It suppresses ERK phosphorylation in DLD-1 cells with an IC50 of 18 nM and demonstrates antiproliferative activity in KRASG12C-mutant Mia-Paca-2 cells, with an IC50 of 0.11 μM. In mouse models, SOS1-IN-17 shows antitumor efficacy against pancreatic cancer.

Rineterkib hydrochloride (compound B) is an orally active RAF and ERK1/2 inhibitor used in treating proliferative diseases characterized by activating mutations in the MAPK pathway, particularly KRAS-mutant NSCLC, BRAF-mutant NSCLC, KRAS-mutant pancreatic cancer, KRAS-mutant colorectal cancer (CRC), and KRAS-mutant ovarian cancer[1].

Jaceosidin has anti-oxidative activity. Jaceosidin has anti-inflammatory activity, also a microglial inhibitor with anti-neuroinflammation activity. aceosidin has anticancer activity, modulates the ERK/ATM/Chk1/2 pathway, leading to inactivation of the Cd

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

Verrucarin A (Muconomycin A) is a Type D macrocyclic mycotoxin. Verrucarin A (VA), derived from the pathogen fungus Myrothecium verrucaria, is a protein synthesis inhibitor that inhibits the growth of leukemia cell lines and activates caspases, apoptosis, and inflammatory signaling in macrophages. It effectively increases the phosphorylation of p38 MAPK and diminishes the phosphorylation of ERK/Akt. Additionally, Verrucarin A causes cell cycle deregulation through the induction of p21 and p53 [1] [2].

CAFESTOL is a ERK inhibitor for AP-1-targeted activity against PGE2 production and the mRNA expression of cyclooxygenase (COX)-2 in LPS-activated RAW264.7 cells. Cafestol has strong inhibitory activity on PGE2 production by suppressing the NF-kB activation pathway.

KRAS inhibitor-12 (compound 6-1) is a potent inhibitor of KRAS G12C (IC50: 0.537 μM), exhibiting p-ERK inhibition in MIA PaCA-2 and A549 cells with IC50 values of 1.3 and 3.7 μM, respectively. KRAS inhibitor-12 has potential for study in pancreatic, colorectal, and lung cancers.

Calpain-2-IN-1 (Formula 1A) is a selective calpain-2 inhibitor with Ki values of 181 nM for calpain-1 and 7.8 nM for calpain-2, applicable for neurodegenerative diseases and other synaptic dysfunction disorders.

Multi-kinase-IN-2 is an orally active inhibitor of angiokinases. multi-kinase-IN-2 significantly inhibits the activity of angiokinases such as VEGFR-1/2/3, PDGFRα/β, FGFR-1, LYN and c-KIT kinases. -IN-2 significantly attenuates phosphorylation of AKT and ERK proteins, induces apoptosis and has anticancer effects.

Butein is a cAMP-specific PDE inhibitor, protein tyrosine kinase inhibitor, and SIRT1 activator. It sensitizes HeLa cells to Cisplatin by targeting FoxO3a via the AKT and ERK/p38 MAPK pathways.

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].

Paluratide (LUNA18) is a reversible cyclic peptide KRAS inhibitor with the advantages of oral availability and cell permeability for the treatment of kras-mutant cancers, which inhibits cancer cell proliferation by phosphorylating ERK and AKT, and also inhibits the interaction of RAS with guanine nucleotide exchange factors (GEFs).

Laxiflorin B, a novel selective inhibitor of ERK 1/2 derived from herbal sources, exhibits antitumor activity [1].