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.

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.

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.

(E)-SIS3 (SIS3), a selective Smad3 inhibitor, can attenuate TGF-β1-dependent Smad3 phosphorylation and DNA binding. It has no effect on p38 MAPK, Smad2, ERK or PI3K signaling. It also inhibits TGF-β1-induced myofibroblast differentiation of dermal fibroblasts and inhibits TGF-β2-induced endothelial cell differentiation in iPSCs.

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.

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.

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]

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).

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.

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.

1. Farrerol has antioxidative activity.2. Farrerol modulates TAP and BNBD5 gene expression in mammary gland, enhances bMEC defense against S. aureus infection and could be useful in protection against bovine mastitis. 3. Farrerol inactivates KEAP-1 or act

1. Mulberroside has nephroprotective, hypoglycemic, and antidiabetic effects. 2. Mulberroside A is a glycosylated stilbene of oxyresveratrol; thus, the deglycosylation of Mulberroside A resulted in enhanced inhibition of melanogenesis. 3. Mulberroside A has anti-inflammatory antiapoptotic effects. by decreasing the expressions of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 and inhibiting the activation of NALP3, caspase-1, and nuclear factor-κB and the phosphorylation of extracellular signal-regulated protein kinases, the c-Jun N-terminal kinase, and p38.

1. Nardosinone has inhibitory effect on Ang II-induced hypertrophy in H9c2 cells, might be mediated by targeting PI3K Akt and MEK ERK signaling pathways. 2. Nardosinone could protect against the neuronal injury exposed to OGD, which may be relevant to the

Theobromine-d6 is intended for use as an internal standard for the quantification of theobromine by GC- or LC-MS. Theobromine is a methylxanthine alkaloid and derivative of caffeine that has been found in cocoa beans and has diverse biological activities. It is an adenosine A1 receptor antagonist. Theobromine increases AMPK phosphorylation and inhibits adipocyte differentiation, ERK and JNK phosphorylation, and IL-6 and TNF-α production in 3T3-L1 preadipocytes cultured in differentiation medium. It inhibits decreases in renal cortex SIRT1 activity and increases in NADPH oxidase-dependent reactive oxygen species (ROS) production, as well as reduces kidney hypertrophy and albuminuria in a spontaneously hypertensive rat model of streptozotocin-induced diabetes when administered at a dose of 5 mg kg per day.3 Theobromine is toxic to dogs with an LD50 value of 250 to 500 mg kg.

Eicosapentaenoic Acid (EPA) sodium, an orally active omega-3 long-chain polyunsaturated fatty acid (ω-3 LC-PUFA), demonstrates a unique ability to demethylate DNA, thereby facilitating the re-expression of the tumor suppressor gene CCAAT enhancer-binding protein δ (C EBPδ). This compound also activates the RAS ERK C EBPβ pathway by demethylating H-Ras intron 1 CpG island in U937 leukemia cells and promotes the relaxation of vascular smooth muscle cells, leading to vasodilation.

CYP1B1-IN-3 is a potent, selective inhibitor of CYP1B1, exhibiting IC50 values of 6.6 nM for CYP1B1, 347.3 nM for CYP1A1, and >10000 nM for CYP1A2. It also impedes cell migration and invasion, and inhibits the P-gp, AKT ERK, FAK SRC, and EMT pathways [1].

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].

PLM-101 is an anticancer compound orally active against acute myeloid leukemia by targeting FLT3 and RET. It impedes RET function, promoting autophagic breakdown of FLT3, and suppresses the PI3K and Ras ERK pathways, contributing to its anti-leukemic effects. The compound's antitumor efficacy is demonstrated in both a mouse MV4-11 flank xenograft model (doses of 3 and 10 mg kg; po) and an allogeneic xenograft mouse model (dose of 40 mg kg; po) [1].