erk1/2 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.

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 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.

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).

1. 2,5-Dihydroxyacetophenone (Quinacetophenone) possess anti-anxiety, and neuroprotective qualities. 2. 2,5-Dihydroxyacetophenone (Quinacetophenone) reatment can induce a sustained activation of JNK, ERK1/2, and p38 MAPKs, it also can potentiate the pro-apoptotic and anti-proliferative effects of bortezomib in U266 cells. 3. 2,5-Dihydroxyacetophenone (Quinacetophenone) has anti-inflammatory activity in activated macrophages, raising the possibility that this compound has a therapeutic potential for inflammatory conditions. 4. 2,5-Dihydroxyacetophenone (Quinacetophenone) is an uncompetitive inhibitor of murine tyrosinase (K(I) 0.28mm), it strongly inhibits both melanogenesis and cellular tyrosinase activity in vitro in 3-isobutyl-1-methylxanthin-stimulated B16 mouse melanoma cells or in vivo in zebrafish and mouse models.

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

Fasudil (HA-1077) is a potent inhibitor of ROCK1, PKA, PKC, and MLCK.

FLT3/VEGFR2-IN-1 (Compound 26) is a potent inhibitor of FLT3, VEGFR2, and HDAC, exhibiting IC50 values of 14.5 nM, 3.9 nM, and 30.8 nM against FLT3, VEGFR2, and HDAC1, respectively. It effectively inhibits the phosphorylation of STAT3 and ERK1/2, as well as the proliferation of leukemia cells. FLT3/VEGFR2-IN-1 demonstrates antitumor activity and is applicable in research on acute myeloid leukemia.

BRAFV600E/JNK-IN-1 (Compound 14c) is an inhibitor of JNK1, JNK2, JNK3, and BRAFV600E, with IC50 values of 0.51 μM, 0.53 μM, 1.02 μM, and 0.009 μM, respectively. It also inhibits the phosphorylation of MEK1/2 and ERK1/2. Additionally, BRAFV600E/JNK-IN-1 suppresses tumor cell proliferation, NO release, and PGE2 production, exhibiting both antitumor and anti-inflammatory activities.

Cantharidic acid is a selective inhibitor of protein phosphatase 2 (PP2A) and protein phosphatase 1 (PP1). It impedes cell viability by upregulating the ERK1/2, p38, and JNK1/2 pathways, causes cell cycle arrest at the sub-G1 phase, and induces apoptosis in NPC-39 and HONE-1 cells.

APS03118 is an orally effective, potent, and highly selective RET inhibitor. It broadly inhibits RET fusions and various mutations (including G810, V804, L730, and Y806 variants), with IC50 values generally below 1 nM (0.0952 nM for the wild type; mutation IC50s range from 0.00438 to 5.72 nM), demonstrating significant inhibitory activity against RETG810 mutations. APS03118 effectively suppresses the entire RET signaling pathway, including RET, Shc, and ERK1/2, and shows more than 20-fold selectivity over most off-target kinases, excluding FLT3 and YES. In vivo, APS03118 induces complete tumor regression in KIF5B-RET and CCDC6-RET V804M PDX mouse models and significantly extends survival in intracranial CCDC6-RET metastatic mouse models. This compound is applicable for research on RET-driven cancers resistant to selective RET inhibitors (SRI).

EGFR-IN-113 (compound II-1) is an EGFR kinase inhibitor with an IC50 of 14.79 μM. It induces apoptosis and inhibits cell proliferation by downregulating the Akt and Erk1/2 signaling pathways. EGFR-IN-113 is applicable in research on EGFR-driven cancers, such as lung cancer, pancreatic cancer, and breast cancer.

SCH772984 HCl is a selective inhibitor of ERK1/2 that displays behaviors of both type I and type II kinase inhibitors, with IC50s of 4 and 1 nM, respectively. SCH772984 HCl has nanomolar cellular potency in tumor cells with mutations in BRAF, NRAS, or KRA

PHPS1 is an inhibitor of Shp2. PHPS1 efficiently inhibits activation of Erk1/2 by the leukemia-associated Shp2 mutant, Shp2-E76K, and blocks the anchorage-independent growth of a variety of human tumor cell lines.

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].

RWJ-56110 dihydrochloride is a potent, selective, peptide-mimetic inhibitor of PAR-1 activation and internalization (binding IC50=0.44 μM), showing no effect on PAR-2, PAR-3, or PAR-4. It inhibits the aggregation of human platelets induced by SFLLRN-NH2 (IC50=0.16 μM) and thrombin (IC50=0.34 μM), with high selectivity relative to U46619. RWJ-56110 dihydrochloride also blocks angiogenesis and the formation of new vessels in vivo, and induces cell apoptosis[1][2].