MEK-IN-4 is a MEK inhibitor that can be used to study inflammatory diseases and cancer.

MEK/PI3K-IN-2 (compound 6s), a potent inhibitor of both MEK and PI3K, demonstrates IC50 values of 352 nM (MEK1), 107 nM (PI3Kα), and 137 nM (PI3Kδ). This compound effectively reduces pAKT and pERK1/2 levels, exhibiting anti-proliferative activity against various tumor cell lines [1].

MEK inhibitor is a potent MEK inhibitor with antitumor potency.

MEK-IN-6 (Example 69), a potent MEK inhibitor, effectively inhibits ERK1/2 (Thr202/Tyr204) phosphorylation in A375 cells, with an IC50 of 2 nM, making it valuable for cancer research [1].

MEK-IN-6 hydrate (compound 69), a MEK inhibitor, exhibits an IC50 value of 2 nM in A375 cells [1].

MEK-IN-1 is a MEK inhibitor.

MEK4 inhibitor-1 is a newly developed compound specifically designed to inhibit the activity of MEK4, a key enzyme involved in pancreatic adenocarcinoma, with an IC 50 value of 61 nM.

MEK-IN-5, a potent MEK inhibitor and nitric oxide (NO) donor, effectively decreases pMEK and pERK levels in a dose-dependent and time-dependent fashion. Additionally, it induces apoptosis in MDA-MB-231 cells.

MEK/PI3K-IN-1 (compound 6r) is a potent inhibitor targeting both MEK and PI3K, exhibiting IC50 values of 124 nM for MEK1, 130 nM for PI3Kα, and 236 nM for PI3Kδ. It effectively reduces levels of pAKT and pERK1/2, demonstrating anti-proliferative effects on various tumor cell lines [1].

Myristoyl-MEK1 Derived Peptide Inhibitor 1, the myristoylated variant of MEK1 Derived Peptide Inhibitor 1, effectively inhibits ERK activation, demonstrating an inhibitory concentration (IC50) of 10 μM [1].

Antiproliferative Against-3 (comp 33) demonstrates significant activity against Hela (IC 50 = 0.21 µM), A549 (IC 50 = 0.39 µM), and MCF-7 (IC 50 = 0.33 µM) cell lines. Additionally, it induces apoptosis in a dose-dependent manner by arresting A549 cells in the G1 phase.

PROTAC MEK1 Degrader-1, a targeted protein degradation agent, combines a MEK1 inhibitor with a von Hippel-Lindau ligand to effectively inhibit ERK1/2 phosphorylation. With a pIC50 value of 7.0, it exhibits antiproliferative activity against A375 cells [1].

MEK4 Inhibitor-2, a novel MEK4 inhibitor, demonstrates efficacy against pancreatic adenocarcinoma, exhibiting an IC50 value of 83 nM.

MEK1 Derived Peptide Inhibitor 1, a peptide inhibitor, prevents the in vitro activation of ERK2 by MEK1, exhibiting an inhibitory concentration (IC 50) of 30 μM. It is utilized in the study of cell-permeable [1].

STE-MEK1(13), a cell-permeable ERK1/2 inhibitor with IC50 values ranging from 13 to 30 μM, impedes the phosphorylation of ERK1/2, as demonstrated in studies [1] [2].

MEK1/2-IN-2 is a potent, ATP-competitive MEK1/2 inhibitor that exhibits equal inhibitory effects on wild-type MEK1/2 and a group of MEK1/2 mutant cells.

GDC-0623 (RG 7421) is a potent and ATP-uncompetitive MEK1 inhibitor with Ki of 0.13 nM. Phase 1.

Bermekimab (MABp1) is a humanized monoclonal antibody against interleukin-1α (IL-1α).Bermekimab has potential anti-inflammatory activity to prevent skin inflammation.

Bimekizumab (Anti-Human IL17A/IL-17F Recombinant Antibody), a humanized monoclonal antibody, selectively neutralizes IL-17A and IL-17F, both of which promote osteogenic differentiation in human periosteum-derived cells (hPDC). Consequently, Bimekizumab inhibits inflammation-driven osteogenic differentiation [1].

Refametinib R enantiomer (RDEA119 R enantiomer) is an MEK inhibitor with an EC50 of 2.0-15 nM.Refametinib (R enantiomer) has anticancer activity and can be used in cancer research.

PAF (C16) is a potent MAPK and MEK/ERK activator that induces increased vascular permeability. PAF (C16) (PAF (C16)) is a platelet-activating factor, a phospholipid-derived mediator and a ligand for PAF G protein-coupled receptor (PAFR). PAF (C16) has shown anti-apoptotic and anti-inflammatory activity in vitro, inhibiting Caspase-dependent apoptosis by interacting with its receptor (PAF-R) to perform cell signaling.

iMDK quarterhydrate is a potent PI3K inhibitor that inhibits the growth factor MDK (also known as midkine or MK). iMDK quarterhydrate synergistically inhibits non-small cell lung cancer (NSCLC) with MEK inhibitors without harming normal cells and mice.

PD 198306 is a selective inhibitor of MAPK/ERK-kinase (MEK) with antihyperalgesic effects. PD 198306 reduces the Streptozocin-induced increase in the level of active ERK1.

Refametinib (RDEA119) (RDEA119, Bay 86-9766) is an effective, ATP non-competitive and specific inhibitor of MEK1/2 (IC50: 19/47 nM).

Lidocaine hydrochloride (Lignocaine hydrochloride) is a local anesthetic and cardiac depressant used as an antiarrhythmic agent. Its actions are more intense and its effects more prolonged than those of PROCAINE but its duration of action is shorter than that of BUPIVACAINE or PRILOCAINE.

U0126, an effective and selective non-competitive inhibitor of MAP kinase, inhibits MEK-1 and MEK-2 with IC50 values of 0.07 and 0.06 μM respectively. U0126 inhibits autophagy and mitophagy.

U0126-EtOH (U0126 Ethanol) is a non-ATP competitive specific inhibitor of MEK1/2 (IC50: 0.07/0.06 μM).

Trametinib (GSK1120212) is a MEK inhibitor that inhibits MEK1 and MEK2 (IC50=0.7/0.9 nM) with ATP non-competitive and oral activity. Trametinib activates autophagy and induces apoptosis.

Mirdametinib (PD325901) is an MEK inhibitor (IC50=0.33 nM) with selective, non-ATP-competitive, and oral activity. Mirdametinib exhibits antitumor activity by inhibiting p-ERK1/2 expression and inducing apoptosis.

PD98059 is an MEK inhibitor that inhibits MEK1 and MEK2 (IC50=2/50 μM) and is non-ATP-competitive. PD98059 is also antagonistic as a ligand for AHR. PD98059 inhibits autophagy.

Cobimetinib (GDC-0973) is a selective inhibitor of mitogen-activated protein kinase kinase (MEK) (IC50: 0.9 nM). Cobimetinib specifically binds to and inhibits the catalytic activity of MEK1, resulting in inhibition of extracellular signal-related kinase 2 (ERK2) phosphorylation and activation and decreased tumor cell proliferation.

Selumetinib (AZD6244) (AZD6244) is an effective, specific inhibitor of MEK1 and ERK1/2 phosphorylation (IC50: 14/10 nM).

AZD8330 (ARRY-704) is a novel, selective, non-ATP competitive MEK 1/2 inhibitor with IC50 of 7 nM. Phase 1.

Vem-L-Cy5 (compound 3), a Vemurafenib-based BRAF inhibitor conjugated with the near-infrared (NIR) fluorophore cyanine-5 (Cy5), selectively targets the BRAF V600E mutation and inhibits MEK phosphorylation. This compound demonstrates cell permeability and has been shown to inhibit the growth of various cancer cell types [1].

MS934, a novel VHL-recruiting MEK 1/2 degrader, exhibits potent anti-proliferative effects on HT-29 cell growth, achieving a GI50 of 0.023 μM. It holds potential for researching various human cancers including melanoma, non-small cell lung cancer (NSCLC), colorectal cancer, primary brain tumors, and hepatocellular carcinoma [1].

Cobimetinib R-enantiomer is the less active R-enantiomer of Cobimetinib which is a selective MEK inhibitor.

Potent, selective and competitive corticotropin-releasing factor CRF2 receptor antagonist (Kd values are 1.4 and 153.6 nM for binding to mouse CRF2β and rat CRF1 receptors respectively). Inhibits sauvagine-stimulated cAMP accumulation in HEK-mCRF2β cells

Tpl2 kinase inhibitor is an inhibitor of tumor progression locus 2 (Tpl2; IC50= 0.05 μM).1It is selective for Tpl2 over MEK, p38 MAPK, Src, MK2, and PKC (IC50s = >40, 180, >400, 110, and >400 μM, respectively). Tpl2 kinase inhibitor inhibits LPS-induced TNF-α production in isolated human monocytes and whole blood (IC50s = 0.7 and 8.5 μM, respectively). It enhances differentiation induced by calcitriol in HL-60 and U937 leukemia cells when used at a concentration of 5 μM.2Tpl2 kinase inhibitor (5 μM) inhibits the proliferation of KG-1a leukemia cells.3 1.Garvin, L.K., Green, N., Hu, Y., et al.Inhibition of Tpl2 kinase and TNF-α production with 1,7-naphthyridine-3-carbonitriles: Synthesis and structure-activity relationshipsBioor. Med. Chem. Lett.15(23)5288-5292(2005) 2.Wang, X., and Studzinski, G.P.Expression of MAP3 kinase COT1 is up-regulated by 1,25-dihydroxyvitamin D3 in parallel with activated c-jun during differentiation of human myeloid leukemia cellsJ. Steroid. Biochem. Mol. Biol.121(1-2)395-398(2010) 3.Wang, X., Gocek, E., Novik, V., et al.Inhibition of Cot1/Tlp2 oncogene in AML cells reduces ERK5 activation and up-regulates p27Kip1 concomitant with enhancement of differentiation and cell cycle arrest induced by silibinin and 1,25-dihydroxyvitamin D3Cell Cycle9(22)4542-4551(2010)

NSC 80538 is an inhibitor of MEK Kinase PB1 Domains in multiplex HTS assays.

Lidocaine Hydrochloride hydrate is an amide local anesthetic, has anti-inflammatory property.

Inactive analog of U0126(MEK-1/2 inhibitor), used as a negative control

EBI-1051 is a highly potent and orally efficacious inhibitor of MEK (IC50: 3.9 nM).

G-38963 is a potent and highly specific MEK inhibitor (MEKi).

GSK1790627, the N-deacetylated metabolite of Trametinib, represents an orally active MEK inhibitor that promotes autophagy and triggers apoptosis [1].

G-573 is an allosteric inhibitor of MEK that is both potent and selective. The IC(50) value for pERK inhibition in HCT116 tumours by G-573 was estimated to be 0.406  µM. The IC(50) values for tumour growth inhibition in HCT116 and H2122 were estimated to be 3.43 and 2.56 µM, respectively. ED(50) estimates in HCT116 and H2122 mouse xenograft models were estimated to be ~4.6 and 1.9 mg/kg/day, respectively.

G-479 is an potent MEK inhibitor. Structurally, G-479 is an analogue of GDC-0623 (or so-call Me-Too drug). G-479 with polarity distributed throughout the molecule was shown improved bioactivity over GDC-0623 in many aspects.

Balamapimod is a reversible inhibitor of Ras/Raf/MEK. It also has a potential anti-tumor activity.

The Survival of Motor Neurons (SMN) protein participates in RNA splicing. Decreases in SMN, typically a consequence of defects in the smn1 gene, result in the death of motor neurons and lead to the neurodegenerative disease, spinal muscular atrophy (SMA). Cuspin-1 is a small molecule upregulator of SMN that has been shown in vitro to increase levels of SMN in SMA patient fibroblasts by 50% at 18 μM. Its mechanism of action is thought to involve increased phosphorylation of ERK to initiate Ras-Raf-MEK signaling, which results in an increased rate of SMN translation.

BAY-846 is an allosteric MEK inhibitor with long half-lives, high bioavailabilities, low brain penetration potential and high efficacy in a K-Ras-mutated A549 xenograft model.

ST-168 is a potent inhibitor of PI3K and MEK. ST-168 displays improved PI3K and MEK1 isoform inhibition. ST-168 demonstrated a 2.8-, 2.7-, 23-, and 2.5-fold improved inhibition toward the PI3Kα, PI3Kβ, PI3Kδ, and PI3Kγ isoforms and a 2.2-fold improvement