MEK

シグナル伝達経路

研究分野

阻害剤の選択性比較
溶解度

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	PD0325901	<1 mg/mL	96 mg/mL	40 mg/mL
S1020	PD184352 (CI-1040)	<1 mg/mL	96 mg/mL	14 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
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, ARRY-162, ARRY-438162)	<1 mg/mL	88 mg/mL	<1 mg/mL
S1568	PD318088	<1 mg/mL	112 mg/mL	14 mg/mL
S2310	Honokiol	<1 mg/mL	53 mg/mL	<1 mg/mL
S1089	Refametinib (RDEA119, Bay 86-9766)	<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, RG7420)	<1 mg/mL	100 mg/mL	47 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 (18) MEK阻害剤(17) 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) 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. Phase 3.	Nature, 2012, 487(7408):505-9 Nature, 2016, 10.1038/nature19347 Nature, 2010, 468(7326):968-72	Left: BRAFV600E A375 cells expressing pLKO or shMED12 vectors were cultured in the absence or presence of 2.5 μM PLX4032 or 0.5 μM AZD6244. The cells were fixed, stained, and photographed after 10 (untreated) or 28 days (treated). Right: A375 cells expressing pLKO or shMED12 vectors were grown in the absence or presence of 1 μM PLX4032 or 0.5 μM AZD6244 for 6 hr.
S1036	PD0325901 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, 2015, 10.1038/nature14413 Nature, 2015, 517(7534):391-5 Nature, 2016, 539(7629):452-455	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.
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. Phase 2.	Science, 2011, 331(6019):912-6 Nat Genet, 2011, 44(2):133-9 Cancer Discov, 2013, 3(9):1058-71	The inhibitor PD173074 (A) or PD184352 (B) was administered to one uterine horn of Hand2d/d mice on day 3 of pregnancy (n = 5). The other horn served as vehicle-treated control. Uterine horns were collected on the morning of day 4, and sections were subjected to IHC to detect p-FRS2, p-ERK1/2, and Ki-67. (C) IHC of pERa and Muc-1 in uterine sections of Hand2d/d mice treated with PD173074 or PD184352.
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.	Nature, 2016, 10.1038/nature19347 Hepatology, 2013, 59(4):1262-72 Nat Commun, 2015, 10.1038/ncomms9390	a-c, Inhibitors of BRAFV600E (PLX4032) and MEK1/2 (PD98059 or AZD6244) increase PGC1α and ID2 expression (a, b) and repress integrin expression and signalling (b, c). Cells were treated with indicated concentration of inhibitors for 6 h (a, b) or 24 h (c). d, e, PLX4032 increases the interaction between ID2 and TCF4 (d) and decreases the occupancy of TCF4 at the promoters of integrin genes (e). f–g, PGC1α and ID2 are partially required for PLX4032-mediated inhibition of invasion and metastasis. For in vitro assays (f), A375 cells were incubated with 1 μM PLX4032 for 10 h. Images represent one picture captured per membrane with the scale bar representing 200 μm. Values in a, b, e and f represent mean±s.d. of independent biological triplicates; P<0.05 and *P<0.01 by Student's t-test in a, b, e, f.
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.	J Neurochem, 2014, 129(6):980-7 Neurobiol Aging, 2014, 35(3):669-79 Biochim Biophys Acta, 2014, 1843(5):945-54
S1475	Pimasertib (AS-703026) Pimasertib (AS-703026) 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.	Blood, 2016, 127(9):1138-50 Nat Commun, 2015, 6:6683 Mol Psychiatry, 2019, 10.1038/s41380-018-0325-9	Western blot of brains of mice (WT mice received p.o. administration of 1, 2, or 5 mg/kg pimasertib. Data are means±SD; n54; p<0.05, p<0.01, p<0.001, **p<0.0001.
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.	Mol Cancer, 2014, 13:40 Cardiovasc Res, 2015, 105(1):86-95 Cardiovasc Res, 2015, 105(1):86-95	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.	Nat Commun, 2016, 7:13701 Mol Cancer Ther, 2014, 13(2):353-63 Int J Clin Exp Pathol, 2013, 6(10):2082-91	(c) Fold induction of apoptotic cells after 3-day compound or vehicle (DMSO) treatment, as measured by annexin V positivity. Error bars indicate s.d.'s (n=4). P<0.01, *P<0.001, two-way ANOVA with Holm Sidak multiple comparisons correction.
S2134	AZD8330 AZD8330 is a novel, selective, non-ATP competitive MEK 1/2 inhibitor with IC50 of 7 nM. Phase 1.	Cell, 2012, 32(34):4034-42 Nature, 2014, 514(7524):628-32 Genes Cancer, 2015, 6(11-12):503-12	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, ARRY-162, ARRY-438162) Binimetinib (MEK162, ARRY-162, ARRY-438162) is a potent inhibitor of MEK1/2 with IC50 of 12 nM in a cell-free assay. Phase 3.	Nature, 2017, 550(7674):133-136 Clin Cancer Res, 2017, 23(20):6203-6214 Eur J Cancer, 2018, 89:90-101	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, and b-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.		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 Honokiol is the active principle of magnolia extract that inhibits Akt-phosphorylation and promotes ERK1/2 phosphorylation. Phase 3.	SENSOR ACTUAT B-CHEM, 2012, Jin Akagi Front Pharmacol, 2017, 10.3389/fphar.2017.00199 Mol Med Rep, 2018, 17(1):1683-1689	(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.
S1089	Refametinib (RDEA119, Bay 86-9766) 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.	EBioMedicine, 2017, 15:90-99 J Neurosci, 2012, 32(14):4887-900 Am J Cancer Res, 2016, 6(10):2235-2251	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.
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.
S8041	Cobimetinib (GDC-0973, RG7420) 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. Phase 3.	Nature, 2019, 567(7749):521-524 Cancer Discov, 2015, 10.1158/2159-8290.CD-15-0913 Cancer Discov, 2016, 6(2):154-65	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.
S7553	GDC-0623 GDC-0623 is a potent and ATP-uncompetitive MEK1 inhibitor with K_i of 0.13 nM. Phase 1.	Mol Cell Proteomics, 2017, 16(2):265-277	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.	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) 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. Phase 3.	Nature, 2012, 487(7408):505-9 Nature, 2016, 10.1038/nature19347 Nature, 2010, 468(7326):968-72	Left: BRAFV600E A375 cells expressing pLKO or shMED12 vectors were cultured in the absence or presence of 2.5 μM PLX4032 or 0.5 μM AZD6244. The cells were fixed, stained, and photographed after 10 (untreated) or 28 days (treated). Right: A375 cells expressing pLKO or shMED12 vectors were grown in the absence or presence of 1 μM PLX4032 or 0.5 μM AZD6244 for 6 hr.
S1036	PD0325901 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, 2015, 10.1038/nature14413 Nature, 2015, 517(7534):391-5 Nature, 2016, 539(7629):452-455	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.
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. Phase 2.	Science, 2011, 331(6019):912-6 Nat Genet, 2011, 44(2):133-9 Cancer Discov, 2013, 3(9):1058-71	The inhibitor PD173074 (A) or PD184352 (B) was administered to one uterine horn of Hand2d/d mice on day 3 of pregnancy (n = 5). The other horn served as vehicle-treated control. Uterine horns were collected on the morning of day 4, and sections were subjected to IHC to detect p-FRS2, p-ERK1/2, and Ki-67. (C) IHC of pERa and Muc-1 in uterine sections of Hand2d/d mice treated with PD173074 or PD184352.
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.	Nature, 2016, 10.1038/nature19347 Hepatology, 2013, 59(4):1262-72 Nat Commun, 2015, 10.1038/ncomms9390	a-c, Inhibitors of BRAFV600E (PLX4032) and MEK1/2 (PD98059 or AZD6244) increase PGC1α and ID2 expression (a, b) and repress integrin expression and signalling (b, c). Cells were treated with indicated concentration of inhibitors for 6 h (a, b) or 24 h (c). d, e, PLX4032 increases the interaction between ID2 and TCF4 (d) and decreases the occupancy of TCF4 at the promoters of integrin genes (e). f–g, PGC1α and ID2 are partially required for PLX4032-mediated inhibition of invasion and metastasis. For in vitro assays (f), A375 cells were incubated with 1 μM PLX4032 for 10 h. Images represent one picture captured per membrane with the scale bar representing 200 μm. Values in a, b, e and f represent mean±s.d. of independent biological triplicates; P<0.05 and *P<0.01 by Student's t-test in a, b, e, f.
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.	J Neurochem, 2014, 129(6):980-7 Neurobiol Aging, 2014, 35(3):669-79 Biochim Biophys Acta, 2014, 1843(5):945-54
S1475	Pimasertib (AS-703026) Pimasertib (AS-703026) 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.	Blood, 2016, 127(9):1138-50 Nat Commun, 2015, 6:6683 Mol Psychiatry, 2019, 10.1038/s41380-018-0325-9	Western blot of brains of mice (WT mice received p.o. administration of 1, 2, or 5 mg/kg pimasertib. Data are means±SD; n54; p<0.05, p<0.01, p<0.001, **p<0.0001.
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.	Mol Cancer, 2014, 13:40 Cardiovasc Res, 2015, 105(1):86-95 Cardiovasc Res, 2015, 105(1):86-95	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.	Nat Commun, 2016, 7:13701 Mol Cancer Ther, 2014, 13(2):353-63 Int J Clin Exp Pathol, 2013, 6(10):2082-91	(c) Fold induction of apoptotic cells after 3-day compound or vehicle (DMSO) treatment, as measured by annexin V positivity. Error bars indicate s.d.'s (n=4). P<0.01, *P<0.001, two-way ANOVA with Holm Sidak multiple comparisons correction.
S2134	AZD8330 AZD8330 is a novel, selective, non-ATP competitive MEK 1/2 inhibitor with IC50 of 7 nM. Phase 1.	Cell, 2012, 32(34):4034-42 Nature, 2014, 514(7524):628-32 Genes Cancer, 2015, 6(11-12):503-12	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, ARRY-162, ARRY-438162) Binimetinib (MEK162, ARRY-162, ARRY-438162) is a potent inhibitor of MEK1/2 with IC50 of 12 nM in a cell-free assay. Phase 3.	Nature, 2017, 550(7674):133-136 Clin Cancer Res, 2017, 23(20):6203-6214 Eur J Cancer, 2018, 89:90-101	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, and b-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.		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 Honokiol is the active principle of magnolia extract that inhibits Akt-phosphorylation and promotes ERK1/2 phosphorylation. Phase 3.	SENSOR ACTUAT B-CHEM, 2012, Jin Akagi Front Pharmacol, 2017, 10.3389/fphar.2017.00199 Mol Med Rep, 2018, 17(1):1683-1689	(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.
S1089	Refametinib (RDEA119, Bay 86-9766) 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.	EBioMedicine, 2017, 15:90-99 J Neurosci, 2012, 32(14):4887-900 Am J Cancer Res, 2016, 6(10):2235-2251	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.
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.
S8041	Cobimetinib (GDC-0973, RG7420) 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. Phase 3.	Nature, 2019, 567(7749):521-524 Cancer Discov, 2015, 10.1158/2159-8290.CD-15-0913 Cancer Discov, 2016, 6(2):154-65	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.
S7553	GDC-0623 GDC-0623 is a potent and ATP-uncompetitive MEK1 inhibitor with K_i of 0.13 nM. Phase 1.	Mol Cell Proteomics, 2017, 16(2):265-277	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.	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.

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

研究分野別

製品類型

MEK

シグナル伝達経路

研究分野

亜型選択性的な製品

MEK製品