About 23 results found for searched term "ERK-IN-4" (0.126 seconds)
| Cat.No. | Name | Target |
|---|---|---|
| M49693 | ERK-IN-4 | ERK |
| ERK-IN-4 is an ERK inhibitor binds preferentially to ERK2 with a Kd of 5 μM. | ||
| M49702 | ERK1/2 inhibitor 4 | ERK |
| ERK1/2 inhibitor 5 is a potent inhibitor of ERK1/2. | ||
| M49709 | ERK5-IN-4 | ERK |
| ERK5-IN-4 is a potent and selective inhibitor of extracellular signal-related kinase 5 (ERK5). | ||
| M56015 | PERK-IN-4 | PERK |
| PERK-IN-4 is a potent and selective PERK (protein kinase R (PKR)-like endoplasmic reticulum kinase) inhibitor with an IC 50 of 0.3 nM. | ||
| M2734 | GSK2606414 | PERK |
| GSK2606414 is an orally available, potent, and selective PERK inhibitor with IC50 of 0.4 nM, displaying at least 100-fold selectivity over the other EIF2AKs assayed. | ||
| M3642 | FR 180204 | ERK |
| FR 180204 is an ATP-competitive, selective ERK inhibitor with Ki of 0.31 μM and 0.14 μM for ERK1 And ERK2, respectively. | ||
| M4819 | XMD17-109 | ERK |
| ERK5-IN-1 | ||
| XMD17-109 (ERK5-IN-1) is a novel, specific inhibitor of ERK-5 with an EC50 value of 4.2 μM in HEK293 cells. | ||
| M6160 | Bohemine | CDK |
| Bohemine is A selective CDK inhibitor with IC50 of 4.6 μM, 83 μM and 2.7 μM against Cdk2/ Cyclin E, Cdk2/ Cyclin A and Cdk9/cyclin T1, respectively. Bohemine also inhibited ERK2, IC50 was 52 μM, and inhibited CDK1, CDK4 and CDK6. Bohemine is also a purine analogue and has a wide range of anticancer activities. | ||
| M7792 | EF-24 | ERK |
| EF24 | ||
| EF-24 is an NF-kB inhibitor with great anti-tumor efficacy and oral bioavailability via deactivation of the MAPK/ERK signaling pathway in oral squamous cell carcinoma (OSCC). EF24 is active against melanoma and breast cancer cell lines with GI50 values of 0.7 μM and 0.8 μM, respectively. | ||
| M19411 | Cafestol | ERK |
| 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 activatio䲧瓰Ỵ瓱��㧀 | ||
| M20614 | NSC-87877 disodium salt | Phosphatase |
| NSC-87877 disodium is a cell-permeable inhibitor of both SHP-1 and SHP-2 with IC50 values of 355 and 318 nM respectively. NSC-87877 disodium salt also inhibits EGF-induced Erk1/2 activation in HEK293 cells and significantly reduces MDA-MB-468 cell viability/proliferation. | ||
| M28985 | AMG PERK 44 | PERK |
| AMG PERK 44 is an orally active and highly selective PERK inhibitor with an IC50 of 6 nM. AMG PERK 44 has 1000-fold and 160-fold selectivity over GCN2 (IC50=7300 nM) and B-Raf (IC50 >1000 nM), respectively. AMG PERK 44 induces autophagy. | ||
| M29047 | YF-452 | VEGFR/PDGFR |
| YF-452 is a potent inhibitor of vascular endothelial growth factor receptor 2 (VEGFR2). YF-452 remarkably inhibits the migration, invasion and tube-like structure formation of human umbilical vein endothelial cells (HUVECs) with little toxicity. YF-452 inhibits VEGF-induced phosphorylation of VEGFR2 kinase and the downstream protein kinases including extracellular signal regulated kinase (ERK), focal adhesion kinase (FAK) and Src. YF-452 is a potential antiangiogenic agent candidate for cancer research. | ||
| M29655 | EtDO-P4 | Others |
| EtDO-P4 is a nanomolar inhibitor of glycosphingolipid (GSL) synthesis. EtDO-P4 suppresses activation of the EGFR-induced ERK pathway and various receptor tyrosine kinases (RTKs). EtDO-P4 can be used for various types of cancer, including Burkitt’s lymphoma. | ||
| M30835 | Lipoxin A4 | IL Receptor/Related |
| LXA4 | ||
| Lipoxin A4 (LXA4), an endogenous lipoxygenase-derived eicosanoid mediator, has potent dual pro-resolving and anti-inflammatory properties. Lipoxin A4 inhibits proliferation and inflammatory cytokine/chemokine production of human epidermal keratinocytes (NHEKs) associated with the ERK1/2 and NF-kB pathways. Lipoxin A4 inhibits serum amyloid A (SAA)-mediated IL-8 release with an IC50 value of 25.74 nM. | ||
| M42116 | ERK-IN-7 | ERK |
| ERK-IN-7, an analogue of SHR2415, is a potent ERK inhibitor with IC50 of 5 nM and 7 nM against ERK1 and ERK2, respectively. | ||
| M45398 | MSU-42011 | RAR/RXR |
| MSU-42011 is an orally active retinoid X receptor-like (RXR) agonist that potently inhibits the expression of iNOS as well as p-ERK protein levels. In addition, MSU-42011 has immunomodulatory and antitumor activities for cancer research. | ||
| M49692 | ERK1/2 inhibitor 7 | ERK |
| ERK1/2 inhibitor 7 is a potent ERK inhibitor with an IC50 of 0.94 nM for ERK2. | ||
| M49696 | ADTL-EI1712 | ERK |
| ADTL-EI1712 is a potent, orally active, and selective dual-target inhibitor of ERK1 and ERK5, inhibition rates of ERK1/5 at 1 μM are 93.54% and 89.35%, respectively. | ||
| M49705 | ERK1/2 inhibitor 8 | ERK |
| ERK1/2 inhibitor 8 is a potent ERK inhibitor with an IC50 of 0.48 nM for ERK2. | ||
| M49707 | ERK2-IN-3 | ERK |
| ERK2-IN-3 is a inhibitor of ERK2, and inhibits Erk2WT and Erk2DS1 activation loop phosphorylation, with IC50 of 5 μM and 42 nM, respectively. | ||
| M54671 | BTX-6654 | PROTAC |
| BTX-6654 is a targeted and specific cerebellar-based bifunctional SOS1 PROTAC degrader.BTX-6654 reduces the downstream signaling markers pERK and pS6 and displays antiproliferative activity in a wide range of KRAS-mutant cells. In two KRAS G12C xenograft models, BTX-6654 degraded SOS1 in a dose-dependent manner correlating with tumor growth inhibition, additionally exhibiting synergy with KRAS and MEK inhibitors. | ||
| M54609 | Capmatinib dihydrochloride hydrate | c-Met |
| INC280 dihydrochloride hydrate; INCB-28060 dihydrochloride hydrate | ||
| Capmatinib dihydrochloride hydrate is a potent, orally active, selective, ATP-competitive c-Met kinase inhibitor (IC50=0.13 nM) that inhibits the phosphorylation of c-MET, as well as downstream effector proteins of the c-MET pathway, such as ERK1/2, AKT, FAK, In addition, Capmatinib dihydrochloride hydrate effectively inhibited the proliferation and migration of c-Met-dependent tumor cells, induced apoptosis, and demonstrated antitumor activity in a mouse model of tumor. Capmatinib dihydrochloride hydrate is mainly metabolized by CYP3A4 and aldehyde oxidase. | ||
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