erk in 3

ERK-IN-3 (ASN007 free base) is a potent and orally active inhibitor of ERK. It inhibits ERK1/2 with low single-digit nM IC50 values. It can be used for the research of cancers driven by RAS mutations.

ERK-IN-3 benzenesulfonate is a potent and orally active inhibitor of ERK . ERK-IN-3 benzenesulfonate inhibits ERK1/2 with low single-digit nM IC 50 values. ERK-IN-3 benzenesulfonate can be used for the research of cancers driven by 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].

PI3K/AKT/ERK/CREB activator 1 is an orally active agent that stimulates the PI3K/AKT/ERK/CREB signaling pathway. It supports neuronal survival and function, enhances neuron proliferation, and revives the activity of damaged neurons, while also aiding in synapse formation. By reducing pro-inflammatory cytokine levels, it alleviates neuroinflammation and preserves synaptic ultrastructure, thereby restoring spatial memory in Alzheimer's disease models. PI3K/AKT/ERK/CREB activator 1 serves as a valuable tool for Alzheimer's disease research.

ERK5-IN-3 is a selective and potent inhibitor of ERK5 (extracellular signal-associated kinase 5) (IC50: 6 nM). ERK5-IN-3 exhibits anti-proliferative effects on Hela cells (IC50: 31 nM).

PERK-IN-3 is a potent inhibitor of PERK (IC50 of 7.4 nM).

EF24 (3,5-Bis[(2-fluorophenyl)Methylene]-4-piperidinone) treatment increases the levels of activated caspase 3 and 9, and decreases the phosphorylated forms of MEK1 and ERK. EF24 shows potent anti-tumor activity in oral squamous cell carcinoma (OSCC) via deactivation of the MAPK/ERK signaling pathway.

Eicosapentaenoic Acid is an ω-3 fatty acid and an inhibitor of fatty acid synthase (FASN). Eicosapentaenoic Acid promotes DNA demethylation in the reexpression of the tumor suppressor gene CCAAT/ enhancer-binding protein δ (C/EBPδ). Eicosapentaenoic Acid activates the RAS/ERK/C/EBPβ pathway in U937 leukemia cells through demethylation of the CpG island of H-RAS intron 1. Eicosapentaenoic Acid promotes the relaxation of vascular smooth muscle cells and vasodilation.

3-Methoxytyramine (3-O-methyl Dopamine) is a cellular metabolite of dopamine (3-hydroxytyramine), a neuromodulator that induces behavioral effects, induces significant ERK and CREB phosphorylation, and is capable of inducing a complex set of aberrant involuntary movements in acutely depleted dopamine-containing mice.

MAPK-IN-3 (Compound 4a) is an antiproliferative agent demonstrating significant inhibitory effects on KYSE 30, HCT 116, and HGC 27 cell lines, with IC50 values of 0.57 μM, 3.27 μM, and 2.28 μM, respectively. This compound arrests the cell cycle via a p53-dependent mechanism and induces apoptosis through a p53-independent pathway. It reduces the expression of cell cycle-related proteins, such as Cyclin D1 and Cyclin B1, while increasing pro-apoptotic proteins like cleaved PARP, cleaved caspase-7, and cleaved caspase-9. MAPK-IN-3 also decreases anti-apoptotic proteins such as Bcl-2, elevates ROS levels in KYSE 30 cells, and enhances the expression of ROS-related MAPK pathway members, including p-ERK, p-p38, and p-JNK.

7,4'-Dimethoxy-3-hydroxyflavone is an orally active PAR4 antagonist. This compound inhibits PAR4-mediated human platelet aggregation with an IC50 of 1.4 μM. It disrupts PAR4-mediated aggregation and related signaling pathways, including NF-κB, Ca2+/protein kinase C (PKC), Akt, ERK, and p38. In a streptozotocin (STZ)-induced diabetic mouse model, 7,4'-Dimethoxy-3-hydroxyflavone inhibits vascular PAR4 expression, improves endothelial dysfunction, and reduces oxidative stress. Additionally, it prevents thrombosis in mice without affecting bleeding time.

PT-262 is a potent Rho-associated protein kinase (ROCK) inhibitor with an IC50 value of approximately 5 μM, and it induces mitochondrial membrane potential loss, enhances caspase-3 activation, and promotes apoptosis, while concurrently inhibiting ERK and CDC2 phosphorylation through a p53-independent signaling pathway, disrupting cytoskeletal organization and cell migration, and collectively exerting broad anticancer activity that makes PT-262 a valuable tool for mechanistic cancer biology and signal transduction research.

Darinaparsin is a dimethylated arsenic linked to glutathione. It is cytotoxic to DU145, LNCaP, and PC3 prostate cancer cells (IC50s = 5-10 µM) and patient-derived primary prostate cancer cells (IC50s = 2.5-20 µM), as well as Jurkat T cell lymphoma and L540 Hodgkin lymphoma cells (IC50s = 2.7 and 1.3 µM, respectively). [1][2] It decreases the tumor-initiating subpopulation in DU145 and PC3 cells and halts the cell cycle in the G2/M phase. Darinaparsin decreases transcription of Gli-2, a transcription factor that mediates Sonic hedgehog signaling, when used at a concentration of 1.5 but not 3 µM. It decreases SHP1 phosphatase activity and increases ERK phosphorylation. [2] Darinaparsin reduces tumor growth in DU145 and PC3 prostate cancer mouse xenograft models when administered at a dose of 100 mg/kg every other day.[1]

(E)-SIS3 (SIS3) is a Smad3 inhibitor (IC50=3 μM) and is selective. (E)-SIS3 inhibits the differentiation of fibroblasts into myofibroblasts via TGF-β1.

HNMPA-(AM)3 inhibits activation of ERK phosphorylation and stimulation of ecdysteroid production by prothyrotropin (PTTH). Furthermore, HNMPA-(AM)3 had inhibitory effects on ecdysteroid production (IC50=14.2 μM) and insulin receptor activity (IC50=14.2 μM and 200 μM, in mosquitoes and mammals, respectively).

Resolvin D5 is an oxidised lipid mediator derived from docosahexaenoic acid (DHA) with anti-inflammatory properties. It inhibits the production of interleukin-6 (IL-6) and chemokine CCL5 in LPS-stimulated THP-1 cells via the ERK-NF-κB signalling pathway.

1. β,β-Dimethylacrylshikonin (Dimethylacrylshikonin) is a promising agent for developing an improved strategy for radiotherapy against tumors. (a) Injection of Dimethylacrylshikonin combined with IR treatment significantly suppressed tumor growth of the HCT-116 xenograft. (b) Dimethylacrylshikonin significantly suppressed the growth of H(22) transplantable hepatoma, and induced the activation of caspase-3 . (c) Dimethylacrylshikonin inhibited growth of gastric cancer SGC-791 cells by inducing ERK signaling pathway. 2. Dimethylacrylshikonin inhibits the proliferation of MCF-7 cells in vitro by inducing apoptosis through the downregulation of Bcl-2, upregulation of Bax and partial inactivation of the NF-κB pathway.

1. Prunetin (Prunusetin) significantly reduces serum levels of inflammatory cytokines and mortality in mice challenged with lipopolysaccharide. 2. Prunetin mediates anti-obesity/adipogenesis effects by suppressing obesity-related transcription through a feedback mechanism that regulates the expression of adiponectin, adipoR1, adipoR2, and AMPK. 3. Prunetin and biochanin A are potent reducers of NF-κB and ERK activation, zonula occludens 1 tyrosine phosphorylation, and metalloproteinase-mediated shedding activity, which may account for the barrier-improving ability of these isoflavones. 4. Prunetin significantly suppresses ATP-induced mucin secretion from cultured RTSE cells; Prunetin inhibits the production of MUC5AC mucin protein induced by EGF or PMA from NCI-H292 cells; Prunetin also inhibits the expression of MUC5AC mucin gene induced by EGF or PMA from NCI-H292 cells.

1. Oleandrin (Folinerin), the principal cardiac glycoside component of PBI-524, can quantitatively account for regulation of BDNF at both the protein and transcriptional levels. 2. Oleandrin are known to inhibit the Na, K-ATPase pump, resulting in a consequent increase in calcium influx in heart muscle. 3. Oleandrin has stronger anti-proliferative activity in undifferentiated CaCO-2 cells (IC50, 8.25 nM) , causes an autophagic cell death and altered ERK phosphorylation in undifferentiated.

KRAS inhibitor-15 (compound 3-19) is a potent inhibitor of KRAS G12C with an IC50 of 0.954 μM. It exhibits p-ERK inhibition in MIA PaCA-2 and A549 cells with IC50s of 2.03 μM and >33.3 μM, respectively. KRAS inhibitor-15 has potential for study in pancreatic, colorectal, and lung cancers.

KRAS inhibitor-16 (compound 3-11) is a potent inhibitor of KRAS G12C (IC50: 0.457 μM) and exhibits p-ERK inhibition in MIA PaCA-2 and A549 cells with IC50s of 3.06 and 11.1 μM, respectively. KRAS inhibitor-16 has potential for study in pancreatic, colorectal, and lung cancers.

KRAS inhibitor-18 (compound 3-10) is a potent inhibitor of KRAS G12C (IC50: 4.74 μM) and exhibited p-ERK inhibition in MIA PaCA-2 and A549 cells with IC50s of 66.4 μM and 11.1 μM, respectively. KRAS inhibitor-18 has potential for pancreatic, colorectal, and lung cancer studies.

KRAS inhibitor-17 (compound 3-9) is a potent inhibitor of KRAS G12C with an IC50 of 3.37 μM. It exhibits p-ERK inhibition with an IC50 of 9.25 μM in MIA PaCA-2 cells and greater than 33.3 μM in A549 cells. KRAS inhibitor-17 has potential applications in the study of pancreatic, colorectal, and lung cancers.

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.