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Results for "

MEK-IN-1

" in MedChemExpress (MCE) Product Catalog:

31

Inhibitors & Agonists

1

Fluorescent Dye

1

Biochemical Assay Reagents

2

Natural
Products

2

Isotope-Labeled Compounds

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-145702
    MAP855

    		MEK ERK Cancer
    MAP855 is a highly potent, selective, ATP-competitive and orally active MEK1/2 kinase inhibitor (MEK1 ERK2 cascade IC50=3 nM, pERK EC50=5 nM). MAP855 shows equipotent inhibition of wild-type and mutant MEK1/2 [1].
    MAP855
  • HY-12058
    AZD8330
    5+ Cited Publications

    ARRY-424704; ARRY-704

    		 MEK Cancer
    AZD8330 (ARRY-424704) is a potent, uncompetitive MEK1/MEK2 inhibitor, with an IC50 of 7 nM.
    AZD8330
  • HY-15202
    Binimetinib
    30+ Cited Publications

    MEK162; ARRY-162; ARRY-438162

    		 MEK Autophagy Cancer
    Binimetinib (MEK162) is an oral and selective MEK1/2 inhibitor. Binimetinib (MEK162) inhibits MEK with an IC50 of 12 nM.
    Binimetinib
  • HY-12042
    Pimasertib
    5+ Cited Publications

    AS703026; MSC1936369B

    		 MEK Cancer
    Pimasertib (AS703026) is a highly selective, ATP non-competitive allosteric orally available MEK1/2 inhibitor [1] .
    Pimasertib
  • HY-14719
    RO4987655
    5 Publications Verification

    CH4987655

    		 MEK Cancer
    RO4987655 is an orally active and highly selective MEK inhibitor with an IC50 of 5.2 nM for inhibition of MEK1/MEK2.
    RO4987655
  • HY-U00312
    MEK-IN-1

    		MEK Cancer
    MEK-IN-1 is a MEK inhibitor extracted from patent WO2008076415A1.
    MEK-IN-1
  • HY-145701
    MEK1/2-IN-2

    		MEK Cancer
    MEK1/2-IN-2 is a potent ATP-competitive MEK1/2 inhibitor and shows equipotent inhibition of WT MEK1/2 and a panel of MEK1/2 mutant cell lines [1].
    MEK1/2-IN-2
  • HY-12447
    SMK-17

    		MEK Apoptosis Cancer
    SMK-17 is a selective, non-ATP-competitive MEK1/MEK2 inhibitor with IC50s of 62 nM and 56 nM, respectively. SMK-17 binds to the allosteric pocket of MEK1/2. SMK-17 induces apoptosis in tumor cell lines harboring β-catenin mutations [1].
    SMK-17
  • HY-12042A
    Pimasertib hydrochloride

    AS703026 hydrochloride; MSC1936369B hydrochloride

    		 MEK Cancer
    Pimasertib hydrochloride is a highly selective, ATP non-competitive allosteric orally available MEK1/2 inhibitor [1] .
    Pimasertib hydrochloride
  • HY-13303
    RO 4927350

    		MEK Cancer
    RO 4927350 is a potent and selective non-ATP-competitive MEK1/2 inhibitor. RO 4927350 exhibits significant antitumor efficacy in a broad spectrum of tumor models [1].
    RO 4927350
  • HY-126048
    JTP-70902

    		MEK Cancer
    JTP-70902, a p15 INK4b-inductive compound, is a MEK1/2 inhibitor. JTP-70902 exhibits potent antitumor effect [1].
    JTP-70902
  • HY-50706
    Selumetinib
    Maximum Cited Publications
    65 Publications Verification

    AZD6244; ARRY-142886

    		 MEK Apoptosis Cancer
    Selumetinib (AZD6244) is selective, non-ATP-competitive oral MEK1/2 inhibitor, with an IC50 of 14 nM for MEK1. Selumetinib (AZD6244) inhibits ERK1/2 phosphorylation.
    Selumetinib
  • HY-14691
    Refametinib
    10+ Cited Publications

    BAY 869766; RDEA119

    		 MEK Cancer
    Refametinib (BAY 869766; RDEA119) is an orally available, potent, non-ATP-competitive, selective, allosteric MEK1/MEK2 inhibitor with IC50s of 19 nM and 47 nM, respectively.
    Refametinib
  • HY-15202R
    Binimetinib (Standard)

    		MEK Autophagy Cancer
    Binimetinib (Standard) is the analytical standard of Binimetinib. This product is intended for research and analytical applications. Binimetinib (MEK162) is an oral and selective MEK1/2 inhibitor. Binimetinib (MEK162) inhibits MEK with an IC50 of 12 nM.
    Binimetinib (Standard)
  • HY-15202S3
    Binimetinib-d4

    MEK162-d4; ARRY-162-d4; ARRY-438162-d4

    		 Isotope-Labeled Compounds Autophagy MEK Cancer
    Binimetinib-d4 (MEK162-d4) is deuterium labeled Binimetinib. Binimetinib (MEK162) is an oral and selective MEK1/2 inhibitor. Binimetinib (MEK162) inhibits MEK with an IC50 of 12 nM.
    Binimetinib-d4
  • HY-15202S1
    Binimetinib-d3

    MEK162-d3; ARRY-162-d3; ARRY-438162-d3

    		 Isotope-Labeled Compounds MEK Autophagy Cancer
    Binimetinib-d3 (MEK162-d3) is deuterium labeled Binimetinib. Binimetinib (MEK162) is an oral and selective MEK1/2 inhibitor. Binimetinib (MEK162) inhibits MEK with an IC50 of 12 nM [1].
    Binimetinib-d3
  • HY-10254G
    Mirdametinib

    PD0325901; PD325901

    		 MEK Cancer
    Mirdametinib (PD0325901) (GMP) is Mirdametinib (HY-10254) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Mirdametinib is an orally active, selective and non-ATP-competitive MEK inhibitor .
    Mirdametinib
  • HY-18086
    TCS PIM-1 1
    4 Publications Verification

    SC 204330

    		 Pim Cancer
    TCS PIM-1 1 (SC 204330) is a potent, selective and ATP-competitive Pim-1 kianse inhibitor with an IC50 of 50 nM, displays good selectivity over Pim-2 and MEK1/MEK2 (IC50s >20000 nM) [1].
    TCS PIM-1 1
  • HY-12062
    PD318088
    1 Publications Verification

    		 MEK Cancer
    PD318088 is a potent, allosteric and non-ATP competitive MEK1/2 inhibitor, an analog of PD184352 (HY-50295). PD318088 binds simultaneously with ATP in a region of the MEK1 active site that is adjacent to the ATP-binding site. PD318088 can be used for cancer research [1].
    PD318088
  • HY-113592
    ERK-IN-4

    		ERK Cancer
    ERK-IN-4 is an ERK inhibitor binds preferentially to ERK2 with a Kd of 5 μM. ERK-IN-4 specificity inhibits ERK Rsk-1 and Elk-1 phosphorylation. ERK-IN-4 has little effect on ERK protein phosphorylation by its upstream activator MEK1/2 [1].
    ERK-IN-4
  • HY-131295
    PD0325901-O-C2-dioxolane
    2 Publications Verification

    		 MEK Ligands for Target Protein for PROTAC Cancer
    PD0325901-O-C2-dioxolane has main portion of MEK inhibitor PD0325901. PD0325901-O-C2-dioxolane and a ligand of VHL or CRBN E3 ligase can be used in the synthesis of MEK1/2 degrader [1].
    PD0325901-O-C2-dioxolane
  • HY-130642
    (S,R,S)-AHPC-Me-C10-Br

    		E3 Ligase Ligand-Linker Conjugates Cancer
    (S,R,S)-AHPC-Me-C10-Br is a synthesized E3 ligase ligand-linker conjugate. (S,R,S)-AHPC-Me-C10-Br incorporates a VHL E3 ligase linker and MS432 based on the MEK1/2 inhibitor PD0325901 [1].
    (S,R,S)-AHPC-Me-C10-Br
  • HY-B0023
    Azelnidipine
    2 Publications Verification

    CS 905

    		 Calcium Channel MEK Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    Azelnidipine (CS 905) is a dihydropyridine calcium channel blocker that is effective orally. Azelnidipine inhibits the intracellular calcium ion flow and lower blood pressure by selectively blocking L-type calcium channel on the membrane of vascular smooth muscle. Azelnidipine inhibits esophageal squamous cell carcinoma proliferation by targeting MEK1/2. Azelnidipine also has anti-inflammatory, antioxidant and neuroprotective effects [1] .
    Azelnidipine
  • HY-13425
    Deguelin
    5+ Cited Publications

    (-)-DeguelIN; (-)-cis-DeguelIN

    		 Akt Autophagy Apoptosis Cancer
    Deguelin, a naturally occurring rotenoid, acts as a chemopreventive agent by blocking multiple pathways like PI3K-Akt, IKK-NF-κB, and MAPK-mTOR-survivin-mediated apoptosis. Deguelin binding to Hsp90 leads to a decreased expression of numerous oncogenic proteins, including MEK1/2, Akt, HIF1α, COX-2, and NF-κB.
    Deguelin
  • HY-120485
    Raxofelast

    IRFI-016

    		 p38 MAPK ERK PKC Cardiovascular Disease
    Raxofelast (IRFI-016) is an antioxidant agent in various models of ischemia-reperfusion injury. Raxofelast has antiproliferative activity in H2O2-stimulated rat aortic smooth muscle cells. Raxofelast attenuates the activation of mitogen-activating protein kinase (MAPK), ERK kinase 1, 2 (MEK1,2) and protein kinase C (PKC) without affecting Ras expression [1].
    Raxofelast
  • HY-107417
    Hypothemycin

    		VEGFR MEK FLT3 PDGFR ERK Cancer
    Hypothemycin, a fungal polyketide, is a multikinase inhibitor with Kis of 10/70 nM, 17/38 nM, 90 nM, 900 nM/1.5 μM, and 8.4/2.4 μM for VEGFR2/VEGFR1, MEK1/MEK2, FLT-3, PDGFRβ/PDGFRα, and ERK1/ERK2, respectively [1] .
    Hypothemycin
  • HY-10338A
    Foretinib phosphate

    		c-Met/HGFR VEGFR Cancer
    Foretinib phosphate is an orally bioavailable small molecule with potential anti-tumor activity. Foretinib phosphate can selectively inhibit hepatocyte growth factor (HGF) receptor c-MET and vascular endothelial growth factor receptor 2 (VEGFR2), thereby potentially inhibiting tumor angiogenesis, tumor cell proliferation and metastasis. Foretinib phosphate shows different anti-cancer activity from cabozantinib in lung cancer cells and has stronger inhibitory effects on targets such as MEK1/2, FER and AURKB [1].
    Foretinib phosphate
  • HY-15196
    TAK-285
    2 Publications Verification

    		 EGFR Cancer
    TAK-285 is a potent, selective, ATP-competitive and orally active HER2 and EGFR(HER1) inhibitor with IC50 of 17 nM and 23 nM, respectively. TAK-285 is >10-fold selectivity for HER1/2 than HER4, and less potent to MEK1/5, c-Met, Aurora B, Lck, CSK etc. TAK-285 has effective antitumor activity [1]. TAK-285 can cross the blood-brain barrier (BBB) .
    TAK-285
  • HY-173153
    BRAFV600E/JNK-IN-1

    		JNK PERK MEK NO Synthase Inflammation/Immunology Cancer
    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. BRAFV600E/JNK-IN-1 can inhibit the phosphorylation of MEK1/2 and ERK1/2. In addition, BRAFV600E/JNK-IN-1 can inhibit tumor cell proliferation, NO release and PGE2 production, and has anti-tumor and anti-inflammatory activities [1].
    BRAFV600E/JNK-IN-1
  • HY-132844
    Tunlametinib

    HL-085

    		 MEK Cancer
    Tunlametinib is a highly selective, orally active MEK1/2 inhibitor (IC50=1.9 nM, MEK1). Tunlametinib blocks the RAS-RAF-MEK-ERK signaling pathway, arrests tumor cell cycle and promotes apoptosis. Tunlametinib potently inhibits the proliferation of RAS/RAF mutant cancer cells (such as BRAF V600E, KRAS G12C mutant cells). Tunlametinib shows synergistic anti-tumor effects with BRAF/KRAS G12C/SHP2 inhibitors, Docetaxel (HY-B0011). Tunlametinib can be used to study targeted therapy for RAS/RAF mutation-driven malignancies (such as melanoma, colorectal cancer, and non-small cell lung cancer) [1] .
    Tunlametinib
  • HY-147245
    Basroparib

    STP1002

    		 PARP Cancer
    Basroparib (STP1002) is a selective, orally active inhibitor of tankyrase (TNKS1/TNKS2) with IC50 of 29.94 nM and 3.68 nM for TNKS1 and TNKS2, respectively. Basroparib has an IC50 of >10 μM for PARP1. Basroparib binds to TNKS, stabilizes AXIN1/2 proteins, blocks Wnt/β-catenin signaling pathway, inhibits tumor cell proliferation and induces apoptosis, while reducing cancer stem cell properties. Basroparib can be used in colorectal cancer (CRC) studies with KRAS mutations (such as G12V/G12D) to overcome acquired resistance to MEK inhibitors. STP1002 has synergistic antitumor activity with MEK inhibitors .
    Basroparib