MEK

シグナル伝達経路

研究分野

阻害剤の選択性比較

カタログ番号	製品カタログ	溶解度(25°C)
カタログ番号	製品カタログ	水	DMSO	アルコール
S1008	Selumetinib (AZD6244)	<1 mg/mL	91 mg/mL	<1 mg/mL
S1036	Mirdametinib (PD0325901)	<1 mg/mL	96 mg/mL	40 mg/mL
S2673	Trametinib (GSK1120212)	<1 mg/mL	22 mg/mL	'<1 mg/mL
S1102	U0126-EtOH	<1 mg/mL	85 mg/mL	'<1 mg/mL
S1020	PD184352 (CI-1040)	<1 mg/mL	96 mg/mL	14 mg/mL
S4484	Trametinib DMSO solvate	<1 mg/mL	50 mg/mL	''<1 mg/mL
S1177	PD98059	<1 mg/mL	14 mg/mL	<1 mg/mL
S1531	BIX 02189	<1 mg/mL	60 mg/mL	80 mg/mL
S1475	Pimasertib (AS-703026)	<1 mg/mL	86 mg/mL	<1 mg/mL
S1392	Pelitinib (EKB-569)	<1 mg/mL	13 mg/mL	<1 mg/mL
S1530	BIX 02188	<1 mg/mL	43 mg/mL	3 mg/mL
S2617	TAK-733	<1 mg/mL	101 mg/mL	<1 mg/mL
S2134	AZD8330	<1 mg/mL	92 mg/mL	92 mg/mL
S7007	Binimetinib (MEK162)	<1 mg/mL	88 mg/mL	<1 mg/mL
S1568	PD318088	<1 mg/mL	112 mg/mL	14 mg/mL
S2310	Honokiol (NSC 293100)	<1 mg/mL	53 mg/mL	''''<1 mg/mL
S1066	SL-327	<1 mg/mL	67 mg/mL	7 mg/mL
S1089	Refametinib (RDEA119)	<1 mg/mL	100 mg/mL	100 mg/mL
S2326	Myricetin	<1 mg/mL	63 mg/mL	9 mg/mL
S7843	BI-847325	<1 mg/mL	19 mg/mL	1 mg/mL
S8041	Cobimetinib (GDC-0973)	<1 mg/mL	100 mg/mL	47 mg/mL
S7170	RO5126766 (CH5126766)	<1 mg/mL	94 mg/mL	'<1 mg/mL
S7553	GDC-0623	<1 mg/mL	91 mg/mL	5 mg/mL
S8355	APS-2-79 HCl	<1 mg/mL	97 mg/mL	32 mg/mL

亜型選択性的な製品

MEK製品

All (24) MEK阻害剤(23) MEK拮抗剤(1)

製品コード	製品説明	文献中Selleckの製品使用例	お客様のフィードバック
S1008	Selumetinib (AZD6244) Selumetinib (AZD6244, ARRY-142886) is a potent, highly selective MEK inhibitor with IC50 of 14 nM for MEK1 and Kd value of 530 nM for MEK2. It also inhibits ERK1/2 phosphorylation with IC50 of 10 nM, no inhibition to p38α, MKK6, EGFR, ErbB2, ERK2, B-Raf, etc. Selumetinib suppresses cell proliferation, migration and trigger apoptosis. Phase 3.	Nat Cell Biol, 2021, 23(4):377-390 J Extracell Vesicles, 2021, 10(8):e12091 Cancer Res, 2021, canres.1895.2020	Stimulation response of p37d-expressing cells. (c) Western blot of 5 min serum stimulated HEK-293 cells stably expressing p37d, p110d or control, with the presence of inhibitors as indicated at the top.
S1036	Mirdametinib (PD0325901) Mirdametinib (PD0325901) is a selective and non ATP-competitive MEK inhibitor with IC50 of 0.33 nM in cell-free assays, roughly 500-fold more potent than CI-1040 on phosphorylation of ERK1 and ERK2. Phase 2.	Nature, 2021, 10.1038/s41586-020-03085-8 Cell, 2021, 184(11):2843-2859.e20 Immunity, 2021, S1074-7613(21)00403-9	Phosphorylation of PPARg in epididymal white adipose tissue in ob/ob mice after treatment with MEK inhibitors. Gene expression in ob/ob epididymal white adipose tissue after treatment with vehicle or either of two MEK inhibitors, PD0325901 or GSK1120212 (n = 7, 7 and 8, respectively). Areas under the curve and gene expression were analysed by analysis of variance.
S2673	Trametinib (GSK1120212) Trametinib (GSK1120212, JTP-74057, Mekinist) is a highly specific and potent MEK1/2 inhibitor with IC50 of 0.92 nM/1.8 nM in cell-free assays, no inhibition of the kinase activities of c-Raf, B-Raf, ERK1/2. Trametinib activates autophagy and induces apoptosis.	Nature, 2021, 10.1038/s41586-021-03916-2 Nat Biotechnol, 2021, 10.1038/s41587-021-00837-3 Cancer Cell, 2021, S1535-6108(21)00383-4	ERK phosphorylates FBW7 at T205. PANC-1 cells were pretreated with the proteasome inhibitor MG132 and trametinib, as indicated, overnight before harvest. Endogenous FBW7 phosphorylation status was examined by immunoblot analysis after immunoprecipitates (IP).
S1102	U0126-EtOH U0126-EtOH is a highly selective inhibitor of MEK1/2 with IC50 of 0.07 μM/0.06 μM in cell-free assays, 100-fold higher affinity for ΔN3-S218E/S222D MEK than PD98059. U0126 inhibits autophagy and mitophagy with antiviral activity.	J Am Chem Soc, 2021, 10.1021/jacs.1c05386 Sci Adv, 2021, 7(36):eabi9787 Theranostics, 2021, 11(3):996-1015	Cells were stimulated with TPA (10 nM) for 15 min in the presence of the indicated concentrations of U0126. Samples were collected and analyzed by Western blot to detect phosphorylated p42/p44 MAPK.
S1020	PD184352 (CI-1040) PD184352 (CI-1040) is an ATP non-competitive MEK1/2 inhibitor with IC50 of 17 nM in cell-based assays, 100-fold more selective for MEK1/2 than MEK5. PD184352 (CI-1040) selectively induces apoptosis. Phase 2.	Cell Syst, 2021, S2405-4712(21)00111-3 Elife, 2021, 10e66596 JCI Insight, 2021, 149137	Melanoma cell viability and in vivo growth by cyclindependent kinase 2/4 inhibition. Western blot analysis for c-Jun, phosphorylated-ERK1/2 (Thr202/Tyr204) (p-ERK1/2), and total ERK1/2 protein levels was done for human melanoma cell lines treated with the BRAFV600E inhibitor GDC-0879 (1 μM), or MEK inhibitors CI-1040 (1 μM), U0126 (1 μM), and PD98059 (10 μM) for 18 hours.
S4484^新	Trametinib DMSO solvate Trametinib (GSK1120212, JTP-74057, Mekinist) DMSO solvate is a highly specific and potent MEK1/2 inhibitor with IC50 of 0.92 nM/1.8 nM in cell-free assay. Trametinib activates autophagy and induces apoptosis.
S1177	PD98059 PD98059 is a non-ATP competitive MEK inhibitor with IC50 of 2 μM in a cell-free assay, specifically inhibits MEK-1-mediated activation of MAPK; does not directly inhibit ERK1 or ERK2. PD98059 is a ligand for the aryl hydrocarbon receptor (AHR) and functions as an AHR antagonist.	Immunity, 2021, S1074-7613(20)30538-0 Mol Cell, 2021, S1097-2765(21)00269-0 Cell Rep, 2021, 35(13):109331	Activation of a TLR2eERK1/2 pathway in MDDC. (C) MDDC were either untreated or treated with C. pneumoniae alone or in the presence of the ERK1/2 inhibitor PD98059 for 48 h. IL-12p70 and IL-10 release in culture media was assessed by ELISA. (D) MDDC were treated as in panel C for 48 h and then cocultured with purified allogeneic CD3t T cells. On day 12, supernatants were collected, and secreted cytokines were measured by ELISA.
S1531	BIX 02189 BIX02189 is a selective inhibitor of MEK5 with IC50 of 1.5 nM, also inhibits ERK5 catalytic activity with IC50 of 59 nM in cell-free assays, and does not inhibit closely related kinases MEK1, MEK2, ERK2, and JNK2.	Cell Stem Cell, 2021, 28(2):257-272.e11 Cancers (Basel), 2021, 13(6)1205 Sci Rep, 2021, 11(1):17764	Expression of iNOS, Fra-1, Fra-2, JunB, JunD, and FosB in PMN. (A) PMN were treated with or without SB203580 (40 μM), BIX02189 (30 μM), or SP600125 (40 μM) for 1 h before addition of NDMA (0.74 μg/μl). The cytoplasmic and nuclear fractions obtained from the cells were used to detect iNOS, Fra-1, Fra-2, JunB, JunD, and FosB protein levels by Western blot. The results shown are representative of five independent experiments.
S1475	Pimasertib (AS-703026) Pimasertib (AS-703026, MSC1936369B, SAR 245509) is a highly selective, potent, ATP non-competitive allosteric inhibitor of MEK1/2 with IC50 of 5 nM-2 μM in MM cell lines. Phase 2.	Sci Rep, 2021, 11(1):9161 STAR Protoc, 2021, 2(1):100300 Cancer Cell, 2020, 37(6):834-849.e13	Western blot analysis showing HSP27 up-regulation on treatment of MKN-45 cells with the 2 indicated MEK1/2 kinase inhibitors (AS703026: 0.5 uM; PD98059: 10 uM) for the indicated time. Inset: effectiveness of the inhibitors in reducing Erk1/2 phosphorylation.
S1392	Pelitinib (EKB-569) Pelitinib (EKB-569) is a potent irreversible EGFR inhibitor with IC50 of 38.5 nM. Pelitinib (EKB-569) also slightly inhibits Src, MEK/ERK and ErbB2 with IC50s of 282 nM, 800 nM and 1255 nM, respectively. Phase2.	Mol Cancer Ther, 2020, 5;molcanther.1131.2019 Nat Cell Biol, 2019, 21(6):778-790 Korean J Parasitol, 2017, 55(5):491-503	HBMEC were preincubated with the indicated concentrations of either ErB1/2/4 inhibitor (Pelitinib; EKB-569), and cells were then infected for 4 h with the unencapsulated strain, MC58 siaD. The numbers of adherent (black bars) and invasive (gray bars) bacteria were determined in a gentamicin protection assay. The graphs show the percentages of adhesion and invasion of inhibitor-treated cells, relative to control cells (means 盨D of three independent experiments performed in duplicate). *, P < 0.05.
S1530	BIX 02188 BIX02188 is a selective inhibitor of MEK5 with IC50 of 4.3 nM, also inhibits ERK5 catalytic activity with IC50 of 810 nM, and does not inhibit closely related kinases MEK1, MEK2, ERK2, and JNK2.	Cell Stem Cell, 2021, 28(2):257-272.e11 Nat Immunol, 2018, 19(3):233-245 J Leukoc Biol, 2016, 99(1):143-52	Retrograde NGF increased BDNF expression in sensory neurons, which was mediated by the MEK/ERK pathway. In two-compartmented DRG-nerve culture, NGF (50 ng/mL) was added to the chamber containing the sensory axonal terminals. The expression of BDNF was examined in the DRG neuronal soma located in another chamber. After 12 h of NGF treatment, the level of BDNF was increased in the sensory neuronal cell bodies by 3 fold (compare B to A) when compared to control (E). The role of the MEK/ERK pathway in retrograde NGF-triggered BDNF up-regulation was determined by pre-treatment of the ganglia with inhibitors U0126 (C), PD98059 (D) or BIX02188 (E). All inhibitors signiﬁcantly reduced NGF-evoked BDNF up-regulation in the ganglia when compared to vehicle treatment (F). Results were from 4 independent experiments for each treatment. Bar=80 μm. *, p＜0.05 vs all groups.
S2617	TAK-733 TAK-733 is a potent and selective MEK allosteric site inhibitor for MEK1 with IC50 of 3.2 nM, inactive to Abl1, AKT3, c-RAF, CamK1, CDK2, c-Met, etc. Phase 1.	Curr Protoc, 2021, 1(6):e180 Nature, 2019, 569(7757):509-513 Mol Cancer, 2019,	Effect of MEK inhibitor TAK-733 in A549 cells. A549 cells were incubated with increasing concentrations of TAK-733 for 2 h. The cell lysates were harvested and phosphorylation of indicated proteins was determined by Western blotting.
S2134	AZD8330 AZD8330 (ARRY704) is a novel, selective, non-ATP competitive MEK 1/2 inhibitor with IC50 of 7 nM. Phase 1.	Curr Protoc, 2021, 1(6):e180 Int J Clin Oncol, 2020, 19 Nature, 2019, 569(7757):509-513	iKras p53L/+ cells were treated with AZD8330 (50 nM), BKM120 (150 nM), or Rapamycin (20 nM) for 18 hr. As control, cells were cultured in the presence or absence of doxycycline for 24 hr, and cell lysates were blotted for phospho-Akt, phospho-Erk, phospho-S6, and Myc.
S7007	Binimetinib (MEK162) Binimetinib (MEK162, ARRY-162, ARRY-438162) is a potent inhibitor of MEK1/2 with IC50 of 12 nM in a cell-free assay. Binimetinib induces G1 cell cycle arrest and apoptosis in human NSCLC cell lines and induces autophagy. Phase 3.	Nat Commun, 2021, 12(1):3707 Neuro Oncol, 2021, 23(5):770-782 Cell Death Dis, 2021, 12(1):85	Whole-cell lysates from NRAS- or BRAF-mutant melanoma cells treated with encorafenib or/and binimetinib or DMSO as a control for 24 hours were subjected to Western blot analysis to detect pERK, ERK, andb-actin. The experiment shown is a representative of three independent experiments.
S1568	PD318088 PD318088 is a non-ATP competitive allosteric MEK1/2 inhibitor, binds simultaneously with ATP in a region of the MEK1 active site that is adjacent to the ATP-binding site.	Curr Protoc, 2021, 1(6):e180 Nature, 2019, 569(7757):509-513 Nat Commun, 2019, 10(1):2197	After starved in serum-free medium for 24h, T47D cells incubated with the indicated concentrations of PD318088 for 3h,followed by 20-minute stimolation of 100ng/ml EGF.
S2310	Honokiol (NSC 293100) Honokiol (NSC 293100) is the active principle of magnolia extract that inhibits Akt-phosphorylation and promotes ERK1/2 phosphorylation. Honokiol causes G0/G1 phase arrest, induces apoptosis, and autophagy via the ROS/ERK1/2 signaling pathway. Honokiol inhibits hepatitis C virus (HCV) infection. Phase 3.	Cell Death Dis, 2021, 12(9):847 Front Cell Dev Biol, 2021, 9:619475 Am J Cancer Res, 2021, 11(6):3039-3054	(B) Cleaved PARP, Bax and Bcl2 protein expression was evaluated by immunoblotting of KRAS mutant cells lysates after 48 h of honokiol (10, 20, 40, and 60 μM) treatment. ∗∗P < 0.01 and ∗∗∗P < 0.001 for comparison between control group and honokiol-treated group.
S1066	SL-327 SL327 is a selective inhibitor for MEK1/2 with IC50 of 0.18 μM/ 0.22 μM, no activity towards Erk1, MKK3, MKK4, c-JUN, PKC, PKA, or CamKII;capable of transport through the blood-brain barrier.	Nat Commun, 2020, 25;11(1):1556 Neuroscience, 2020, 430:1-11 Nat Commun, 2019, 10(1):2016
S1089	Refametinib (RDEA119) Refametinib (RDEA119, Bay 86-9766) is a potent, ATP non-competitive and highly selective inhibitor of MEK1 and MEK2 with IC50 of 19 nM and 47 nM, respectively.	Genome Med, 2021, 13(1):116 Int J Mol Sci, 2021, 22(13)6727 J Transl Med, 2021, 19(1):184	RDEA119 (1 µM) or JTP-74057 (0.1 µM) abolished the effects of G1 on DAPK1 and NR2B phosphorylation.
S2326	Myricetin Myricetin, a natural flavonoid with antioxidant and anti tumor properties, is a novel inhibitor of MEK1 activity and transformation of JB6 P+ mouse epidermal cells. It also inhibits PI3Kγ with Kd of 0.17 μM.	Molecules, 2021, 26(5)1210 Front Med (Lausanne), 2020, 7:71 Int J Mol Sci, 2020, 21(14):5025
S7843	BI-847325 BI-847325 is an orally bioavailable, and selective dual MEK/Aurora kinase inhibitor with IC50 of 3 nM, 25 nM, 15 nM, 25 nM, and 4 nM for Xenopus laevis Aurora B, human Aurora A and Aurora C, as well as human MEK1 and MEK2, respectively. Phase 1.	Sci Rep, 2021, 11(1):9161 Curr Protoc, 2021, 1(6):e180 Nature, 2019, 569(7757):509-513
S8041	Cobimetinib (GDC-0973) Cobimetinib (GDC-0973, RG7420) is a potent and highly selective MEK1 inhibitor with IC50 of 4.2 nM, showing more than 100-fold selectively for MEK1 over MEK2 and showed no significant inhibition when tested against a panel of more than 100 of serine-threonine and tyrosine kinases. Cobimetinib induces apoptosis. Phase 3.	Clin Cancer Res, 2021, 10.1158/1078-0432.CCR-21-2660 EMBO Mol Med, 2021, e13466 Cell Rep, 2021, 35(8):109157	Three types of selective inhibitors of MAPK signaling produce expected differential kinase inhibition and activation responses in HCT116 colorectal cancer cells. HCT116 cells were treated with 250 nM of GDC-0973, GDC-0623, SCH772984 or DMSO for 1, 4, or 24 h. In the washout samples, cells were drug treated for 24 h, then changed into fresh media and harvested after 0.5 or 2 h. Lysates were used for Western blots of total and phosphorylated MEK, ERK, and RSK; blotting for COX IV was used as the loading control.
S7170	RO5126766 (CH5126766) RO5126766 (CH5126766, VS 6766, CKI-27, R-7304, RG-7304) is a dual RAF/MEK inhibitor with IC50 of 8.2 nM,19 nM, 56 nM, and 160 nM for BRAF V600E, BRAF, CRAF, and MEK1, respectively. Phase 1.	Cancer Sci, 2021, 112(10):4026-4036 Nature, 2020, 588(7838):509-514 Mol Cell, 2020, 80(1):164-174.e4
S7553	GDC-0623 GDC-0623 (G-868) is a potent and ATP-uncompetitive MEK1 inhibitor with K_i of 0.13 nM. Phase 1.	Curr Protoc, 2021, 1(6):e180 Nature, 2019, 569(7757):509-513 Cell Rep, 2019, 29(3):573-588	Three types of selective inhibitors of MAPK signaling produce expected differential kinase inhibition and activation responses in HCT116 colorectal cancer cells. HCT116 cells were treated with 250nM of GDC-0973, GDC-0623, SCH772984 or DMSO for 1, 4, or 24 hours. In the washout samples, cells were drug treated for 24 hours, then changed into fresh media and harvested after 0.5 or 2 hours. Lysates were used for western blots of total and phosphorylated MEK, ERK and RSK; blotting for COX IV was used as the loading control.
S8355	APS-2-79 HCl APS-2-79 is a MAPK antagonist that modulating KSR-dependent MAPK signalling by antagonizing RAF heterodimerization as well as the conformational changes required for phosphorylation and activation of KSR-bound MEK.	Sci Adv, 2019, 5(11):eaax4249 Exp Ther Med, 2018, 15(6):5269-5274	Detection of the effects of letrozole and the MAPK pathway on the proliferation of GC-1 spg cells by BrdU. MAPK, mitogen-activated protein kinase; spg, spermatogonia; BrdU, bromodeoxyuridine

製品コード	製品説明	文献中Selleckの製品使用例	お客様のフィードバック
S1008	Selumetinib (AZD6244) Selumetinib (AZD6244, ARRY-142886) is a potent, highly selective MEK inhibitor with IC50 of 14 nM for MEK1 and Kd value of 530 nM for MEK2. It also inhibits ERK1/2 phosphorylation with IC50 of 10 nM, no inhibition to p38α, MKK6, EGFR, ErbB2, ERK2, B-Raf, etc. Selumetinib suppresses cell proliferation, migration and trigger apoptosis. Phase 3.	Nat Cell Biol, 2021, 23(4):377-390 J Extracell Vesicles, 2021, 10(8):e12091 Cancer Res, 2021, canres.1895.2020	Stimulation response of p37d-expressing cells. (c) Western blot of 5 min serum stimulated HEK-293 cells stably expressing p37d, p110d or control, with the presence of inhibitors as indicated at the top.
S1036	Mirdametinib (PD0325901) Mirdametinib (PD0325901) is a selective and non ATP-competitive MEK inhibitor with IC50 of 0.33 nM in cell-free assays, roughly 500-fold more potent than CI-1040 on phosphorylation of ERK1 and ERK2. Phase 2.	Nature, 2021, 10.1038/s41586-020-03085-8 Cell, 2021, 184(11):2843-2859.e20 Immunity, 2021, S1074-7613(21)00403-9	Phosphorylation of PPARg in epididymal white adipose tissue in ob/ob mice after treatment with MEK inhibitors. Gene expression in ob/ob epididymal white adipose tissue after treatment with vehicle or either of two MEK inhibitors, PD0325901 or GSK1120212 (n = 7, 7 and 8, respectively). Areas under the curve and gene expression were analysed by analysis of variance.
S2673	Trametinib (GSK1120212) Trametinib (GSK1120212, JTP-74057, Mekinist) is a highly specific and potent MEK1/2 inhibitor with IC50 of 0.92 nM/1.8 nM in cell-free assays, no inhibition of the kinase activities of c-Raf, B-Raf, ERK1/2. Trametinib activates autophagy and induces apoptosis.	Nature, 2021, 10.1038/s41586-021-03916-2 Nat Biotechnol, 2021, 10.1038/s41587-021-00837-3 Cancer Cell, 2021, S1535-6108(21)00383-4	ERK phosphorylates FBW7 at T205. PANC-1 cells were pretreated with the proteasome inhibitor MG132 and trametinib, as indicated, overnight before harvest. Endogenous FBW7 phosphorylation status was examined by immunoblot analysis after immunoprecipitates (IP).
S1102	U0126-EtOH U0126-EtOH is a highly selective inhibitor of MEK1/2 with IC50 of 0.07 μM/0.06 μM in cell-free assays, 100-fold higher affinity for ΔN3-S218E/S222D MEK than PD98059. U0126 inhibits autophagy and mitophagy with antiviral activity.	J Am Chem Soc, 2021, 10.1021/jacs.1c05386 Sci Adv, 2021, 7(36):eabi9787 Theranostics, 2021, 11(3):996-1015	Cells were stimulated with TPA (10 nM) for 15 min in the presence of the indicated concentrations of U0126. Samples were collected and analyzed by Western blot to detect phosphorylated p42/p44 MAPK.
S1020	PD184352 (CI-1040) PD184352 (CI-1040) is an ATP non-competitive MEK1/2 inhibitor with IC50 of 17 nM in cell-based assays, 100-fold more selective for MEK1/2 than MEK5. PD184352 (CI-1040) selectively induces apoptosis. Phase 2.	Cell Syst, 2021, S2405-4712(21)00111-3 Elife, 2021, 10e66596 JCI Insight, 2021, 149137	Melanoma cell viability and in vivo growth by cyclindependent kinase 2/4 inhibition. Western blot analysis for c-Jun, phosphorylated-ERK1/2 (Thr202/Tyr204) (p-ERK1/2), and total ERK1/2 protein levels was done for human melanoma cell lines treated with the BRAFV600E inhibitor GDC-0879 (1 μM), or MEK inhibitors CI-1040 (1 μM), U0126 (1 μM), and PD98059 (10 μM) for 18 hours.
S4484^新	Trametinib DMSO solvate Trametinib (GSK1120212, JTP-74057, Mekinist) DMSO solvate is a highly specific and potent MEK1/2 inhibitor with IC50 of 0.92 nM/1.8 nM in cell-free assay. Trametinib activates autophagy and induces apoptosis.
S1177	PD98059 PD98059 is a non-ATP competitive MEK inhibitor with IC50 of 2 μM in a cell-free assay, specifically inhibits MEK-1-mediated activation of MAPK; does not directly inhibit ERK1 or ERK2. PD98059 is a ligand for the aryl hydrocarbon receptor (AHR) and functions as an AHR antagonist.	Immunity, 2021, S1074-7613(20)30538-0 Mol Cell, 2021, S1097-2765(21)00269-0 Cell Rep, 2021, 35(13):109331	Activation of a TLR2eERK1/2 pathway in MDDC. (C) MDDC were either untreated or treated with C. pneumoniae alone or in the presence of the ERK1/2 inhibitor PD98059 for 48 h. IL-12p70 and IL-10 release in culture media was assessed by ELISA. (D) MDDC were treated as in panel C for 48 h and then cocultured with purified allogeneic CD3t T cells. On day 12, supernatants were collected, and secreted cytokines were measured by ELISA.
S1531	BIX 02189 BIX02189 is a selective inhibitor of MEK5 with IC50 of 1.5 nM, also inhibits ERK5 catalytic activity with IC50 of 59 nM in cell-free assays, and does not inhibit closely related kinases MEK1, MEK2, ERK2, and JNK2.	Cell Stem Cell, 2021, 28(2):257-272.e11 Cancers (Basel), 2021, 13(6)1205 Sci Rep, 2021, 11(1):17764	Expression of iNOS, Fra-1, Fra-2, JunB, JunD, and FosB in PMN. (A) PMN were treated with or without SB203580 (40 μM), BIX02189 (30 μM), or SP600125 (40 μM) for 1 h before addition of NDMA (0.74 μg/μl). The cytoplasmic and nuclear fractions obtained from the cells were used to detect iNOS, Fra-1, Fra-2, JunB, JunD, and FosB protein levels by Western blot. The results shown are representative of five independent experiments.
S1475	Pimasertib (AS-703026) Pimasertib (AS-703026, MSC1936369B, SAR 245509) is a highly selective, potent, ATP non-competitive allosteric inhibitor of MEK1/2 with IC50 of 5 nM-2 μM in MM cell lines. Phase 2.	Sci Rep, 2021, 11(1):9161 STAR Protoc, 2021, 2(1):100300 Cancer Cell, 2020, 37(6):834-849.e13	Western blot analysis showing HSP27 up-regulation on treatment of MKN-45 cells with the 2 indicated MEK1/2 kinase inhibitors (AS703026: 0.5 uM; PD98059: 10 uM) for the indicated time. Inset: effectiveness of the inhibitors in reducing Erk1/2 phosphorylation.
S1392	Pelitinib (EKB-569) Pelitinib (EKB-569) is a potent irreversible EGFR inhibitor with IC50 of 38.5 nM. Pelitinib (EKB-569) also slightly inhibits Src, MEK/ERK and ErbB2 with IC50s of 282 nM, 800 nM and 1255 nM, respectively. Phase2.	Mol Cancer Ther, 2020, 5;molcanther.1131.2019 Nat Cell Biol, 2019, 21(6):778-790 Korean J Parasitol, 2017, 55(5):491-503	HBMEC were preincubated with the indicated concentrations of either ErB1/2/4 inhibitor (Pelitinib; EKB-569), and cells were then infected for 4 h with the unencapsulated strain, MC58 siaD. The numbers of adherent (black bars) and invasive (gray bars) bacteria were determined in a gentamicin protection assay. The graphs show the percentages of adhesion and invasion of inhibitor-treated cells, relative to control cells (means 盨D of three independent experiments performed in duplicate). *, P < 0.05.
S1530	BIX 02188 BIX02188 is a selective inhibitor of MEK5 with IC50 of 4.3 nM, also inhibits ERK5 catalytic activity with IC50 of 810 nM, and does not inhibit closely related kinases MEK1, MEK2, ERK2, and JNK2.	Cell Stem Cell, 2021, 28(2):257-272.e11 Nat Immunol, 2018, 19(3):233-245 J Leukoc Biol, 2016, 99(1):143-52	Retrograde NGF increased BDNF expression in sensory neurons, which was mediated by the MEK/ERK pathway. In two-compartmented DRG-nerve culture, NGF (50 ng/mL) was added to the chamber containing the sensory axonal terminals. The expression of BDNF was examined in the DRG neuronal soma located in another chamber. After 12 h of NGF treatment, the level of BDNF was increased in the sensory neuronal cell bodies by 3 fold (compare B to A) when compared to control (E). The role of the MEK/ERK pathway in retrograde NGF-triggered BDNF up-regulation was determined by pre-treatment of the ganglia with inhibitors U0126 (C), PD98059 (D) or BIX02188 (E). All inhibitors signiﬁcantly reduced NGF-evoked BDNF up-regulation in the ganglia when compared to vehicle treatment (F). Results were from 4 independent experiments for each treatment. Bar=80 μm. *, p＜0.05 vs all groups.
S2617	TAK-733 TAK-733 is a potent and selective MEK allosteric site inhibitor for MEK1 with IC50 of 3.2 nM, inactive to Abl1, AKT3, c-RAF, CamK1, CDK2, c-Met, etc. Phase 1.	Curr Protoc, 2021, 1(6):e180 Nature, 2019, 569(7757):509-513 Mol Cancer, 2019,	Effect of MEK inhibitor TAK-733 in A549 cells. A549 cells were incubated with increasing concentrations of TAK-733 for 2 h. The cell lysates were harvested and phosphorylation of indicated proteins was determined by Western blotting.
S2134	AZD8330 AZD8330 (ARRY704) is a novel, selective, non-ATP competitive MEK 1/2 inhibitor with IC50 of 7 nM. Phase 1.	Curr Protoc, 2021, 1(6):e180 Int J Clin Oncol, 2020, 19 Nature, 2019, 569(7757):509-513	iKras p53L/+ cells were treated with AZD8330 (50 nM), BKM120 (150 nM), or Rapamycin (20 nM) for 18 hr. As control, cells were cultured in the presence or absence of doxycycline for 24 hr, and cell lysates were blotted for phospho-Akt, phospho-Erk, phospho-S6, and Myc.
S7007	Binimetinib (MEK162) Binimetinib (MEK162, ARRY-162, ARRY-438162) is a potent inhibitor of MEK1/2 with IC50 of 12 nM in a cell-free assay. Binimetinib induces G1 cell cycle arrest and apoptosis in human NSCLC cell lines and induces autophagy. Phase 3.	Nat Commun, 2021, 12(1):3707 Neuro Oncol, 2021, 23(5):770-782 Cell Death Dis, 2021, 12(1):85	Whole-cell lysates from NRAS- or BRAF-mutant melanoma cells treated with encorafenib or/and binimetinib or DMSO as a control for 24 hours were subjected to Western blot analysis to detect pERK, ERK, andb-actin. The experiment shown is a representative of three independent experiments.
S1568	PD318088 PD318088 is a non-ATP competitive allosteric MEK1/2 inhibitor, binds simultaneously with ATP in a region of the MEK1 active site that is adjacent to the ATP-binding site.	Curr Protoc, 2021, 1(6):e180 Nature, 2019, 569(7757):509-513 Nat Commun, 2019, 10(1):2197	After starved in serum-free medium for 24h, T47D cells incubated with the indicated concentrations of PD318088 for 3h,followed by 20-minute stimolation of 100ng/ml EGF.
S2310	Honokiol (NSC 293100) Honokiol (NSC 293100) is the active principle of magnolia extract that inhibits Akt-phosphorylation and promotes ERK1/2 phosphorylation. Honokiol causes G0/G1 phase arrest, induces apoptosis, and autophagy via the ROS/ERK1/2 signaling pathway. Honokiol inhibits hepatitis C virus (HCV) infection. Phase 3.	Cell Death Dis, 2021, 12(9):847 Front Cell Dev Biol, 2021, 9:619475 Am J Cancer Res, 2021, 11(6):3039-3054	(B) Cleaved PARP, Bax and Bcl2 protein expression was evaluated by immunoblotting of KRAS mutant cells lysates after 48 h of honokiol (10, 20, 40, and 60 μM) treatment. ∗∗P < 0.01 and ∗∗∗P < 0.001 for comparison between control group and honokiol-treated group.
S1066	SL-327 SL327 is a selective inhibitor for MEK1/2 with IC50 of 0.18 μM/ 0.22 μM, no activity towards Erk1, MKK3, MKK4, c-JUN, PKC, PKA, or CamKII;capable of transport through the blood-brain barrier.	Nat Commun, 2020, 25;11(1):1556 Neuroscience, 2020, 430:1-11 Nat Commun, 2019, 10(1):2016
S1089	Refametinib (RDEA119) Refametinib (RDEA119, Bay 86-9766) is a potent, ATP non-competitive and highly selective inhibitor of MEK1 and MEK2 with IC50 of 19 nM and 47 nM, respectively.	Genome Med, 2021, 13(1):116 Int J Mol Sci, 2021, 22(13)6727 J Transl Med, 2021, 19(1):184	RDEA119 (1 µM) or JTP-74057 (0.1 µM) abolished the effects of G1 on DAPK1 and NR2B phosphorylation.
S2326	Myricetin Myricetin, a natural flavonoid with antioxidant and anti tumor properties, is a novel inhibitor of MEK1 activity and transformation of JB6 P+ mouse epidermal cells. It also inhibits PI3Kγ with Kd of 0.17 μM.	Molecules, 2021, 26(5)1210 Front Med (Lausanne), 2020, 7:71 Int J Mol Sci, 2020, 21(14):5025
S7843	BI-847325 BI-847325 is an orally bioavailable, and selective dual MEK/Aurora kinase inhibitor with IC50 of 3 nM, 25 nM, 15 nM, 25 nM, and 4 nM for Xenopus laevis Aurora B, human Aurora A and Aurora C, as well as human MEK1 and MEK2, respectively. Phase 1.	Sci Rep, 2021, 11(1):9161 Curr Protoc, 2021, 1(6):e180 Nature, 2019, 569(7757):509-513
S8041	Cobimetinib (GDC-0973) Cobimetinib (GDC-0973, RG7420) is a potent and highly selective MEK1 inhibitor with IC50 of 4.2 nM, showing more than 100-fold selectively for MEK1 over MEK2 and showed no significant inhibition when tested against a panel of more than 100 of serine-threonine and tyrosine kinases. Cobimetinib induces apoptosis. Phase 3.	Clin Cancer Res, 2021, 10.1158/1078-0432.CCR-21-2660 EMBO Mol Med, 2021, e13466 Cell Rep, 2021, 35(8):109157	Three types of selective inhibitors of MAPK signaling produce expected differential kinase inhibition and activation responses in HCT116 colorectal cancer cells. HCT116 cells were treated with 250 nM of GDC-0973, GDC-0623, SCH772984 or DMSO for 1, 4, or 24 h. In the washout samples, cells were drug treated for 24 h, then changed into fresh media and harvested after 0.5 or 2 h. Lysates were used for Western blots of total and phosphorylated MEK, ERK, and RSK; blotting for COX IV was used as the loading control.
S7170	RO5126766 (CH5126766) RO5126766 (CH5126766, VS 6766, CKI-27, R-7304, RG-7304) is a dual RAF/MEK inhibitor with IC50 of 8.2 nM,19 nM, 56 nM, and 160 nM for BRAF V600E, BRAF, CRAF, and MEK1, respectively. Phase 1.	Cancer Sci, 2021, 112(10):4026-4036 Nature, 2020, 588(7838):509-514 Mol Cell, 2020, 80(1):164-174.e4
S7553	GDC-0623 GDC-0623 (G-868) is a potent and ATP-uncompetitive MEK1 inhibitor with K_i of 0.13 nM. Phase 1.	Curr Protoc, 2021, 1(6):e180 Nature, 2019, 569(7757):509-513 Cell Rep, 2019, 29(3):573-588	Three types of selective inhibitors of MAPK signaling produce expected differential kinase inhibition and activation responses in HCT116 colorectal cancer cells. HCT116 cells were treated with 250nM of GDC-0973, GDC-0623, SCH772984 or DMSO for 1, 4, or 24 hours. In the washout samples, cells were drug treated for 24 hours, then changed into fresh media and harvested after 0.5 or 2 hours. Lysates were used for western blots of total and phosphorylated MEK, ERK and RSK; blotting for COX IV was used as the loading control.

製品コード	製品説明	文献中Selleckの製品使用例	お客様のフィードバック
S8355	APS-2-79 HCl APS-2-79 is a MAPK antagonist that modulating KSR-dependent MAPK signalling by antagonizing RAF heterodimerization as well as the conformational changes required for phosphorylation and activation of KSR-bound MEK.	Sci Adv, 2019, 5(11):eaax4249 Exp Ther Med, 2018, 15(6):5269-5274	Detection of the effects of letrozole and the MAPK pathway on the proliferation of GC-1 spg cells by BrdU. MAPK, mitogen-activated protein kinase; spg, spermatogonia; BrdU, bromodeoxyuridine

製品コード

製品説明

文献中Selleckの製品使用例

お客様のフィードバック

S8355

APS-2-79 HCl

APS-2-79 is a MAPK antagonist that modulating KSR-dependent MAPK signalling by antagonizing RAF heterodimerization as well as the conformational changes required for phosphorylation and activation of KSR-bound MEK.

Sci Adv, 2019, 5(11):eaax4249

Exp Ther Med, 2018, 15(6):5269-5274

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MEK

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