MEK

信号経路図

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
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
S8355	APS-2-79 HCl	<1 mg/mL	97 mg/mL	32 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
S1066	SL-327	<1 mg/mL	67 mg/mL	7 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

亜型選択性的な製品

MEK阻害剤(20)
MEK拮抗剤(1)
新MEK製品

製品コード	製品説明	文献中の使用例	お客様のフィードバック
S1008	Selumetinib (AZD6244) Selumetinib (AZD6244)は一種の有効で、高度選択性的なMEK1阻害剤で、無細胞試験でIC50値が14 nMですが、ERK1/2リン酸化も抑制する時のIC50値が10 nMになって、p38α、MKK6、EGFR、ErbB2、ERK2とB-Raf等を抑制する作用がありません。臨床3期。	Nature, 2012, 487(7408):505-9 Nature, 2010, 468(7326):968-72 Nature, 2016, 10.1038/nature19347	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は一種の選択性的で、非ATP競争性的なMEK阻害剤で、無細胞試験でIC50値が0.33 nMですが、ERK1とERK2のリン酸化を抑制する作用はCI-1040より500倍左右が高くなります。臨床2期。	Nature, 2015, 10.1038/nature14413 Nature, 2015, 517(7534):391-5 Cell, 2015, 160(1-2):161-76	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)は一種の高度特異性的で、有効なMEK1/2阻害剤で、無細胞試験でIC50値が0.92 nM/1.8 nMですが、c-Raf、B-RafとERK1/2を抑制する活性がありません。	Nature, 2014, 510(7504):283-7 Nature, 2015, 517(7534):391-5 Nature, 2014, 508(7494):118-22	SMYD3 knockout augments the effects of the MEK1/2 inhibitor Trametinib (GSK1120212) in vivo. Representative serial HE staining and IHC for pERK1/2, a marker of Ras activity, and MUC5, a marker of PanIN lesions. All scale bars, 50 um.
S1102	U0126-EtOH U0126-EtOHは一種の高度選択性的なMEK1/2阻害剤で、無細胞試験でIC50値が0.07 μM/0.06 μMですが、ΔN3-S218E/S222D MEKに作用する亲和力はPD098059に作用する親和力より100倍が高くなります。	Cell, 2013, 153(4):840-54 Nat Genet, 2011, 44(2):133-9 J Natl Cancer Inst, 2012, 104(21):1673-9	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.
S1020	PD184352 (CI-1040) PD184352 (CI-1040)は一種のATP非競争性的なMEK1/2阻害剤で、細胞試験でIC50値が17nMですが、MEK1/2に作用する選択性はMEK5に作用する選択性より100倍が高くなります。臨床2期。	Science, 2011, 331(6019):912-6 Nat Genet, 2011, 44(2):133-9 Cancer Cell, 2016, 10.1016/j.ccell.2016.01.006	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は一種の非ATP競争性的なMEK阻害剤で、無細胞試験でIC50値が2μMですが、MEK-1が媒介したMAPKの活性を特異性的に抑制して、ERK1或いはERK2を直接に抑制しません。	Nature, 2016, 10.1038/nature19347 J Natl Cancer Inst, 2012, 104(21):1673-9 Hepatology, 2013, 59(4):1262-72	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は一種の選択性的なMEK5阻害剤で、無細胞試験でIC50値が1.5 nMですが、ERK5触媒活性も抑制して、このIC50値が59 nMになりますが、密接関連のキナーゼMEK1、MEK2、ERK2とJNK2を抑制しません。	Neurobiol Aging, 2014, 35(3):669-79 Am J Pathol, 2013, 183(6):1758-68 J Biol Chem, 2014, 289(9):6311-22
S1475	Pimasertib (AS-703026) Pimasertib (AS-703026)は一種の高度選択性的で、有効で、ATP非競争性的なMEK1/2構造変容阻害剤で、MM細胞の中にIC50値が5 nM-2μMです。臨床2期。	Nat Commun, 2015, 6:6683 FASEB J, 2014, 10.1096/fj.13-247924 Oncotarget, 2016, 7(4):4265-78	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.
S1530	BIX 02188 BIX02188は一種の選択性的なMEK5阻害剤で、IC50値が4.3 nMですが、ERK5触媒活性も抑制して、このIC50値が810 nMになって、密接関連のキナーゼMEK1、MEK2、ERK2とJNK2を抑制しません。	Cardiovasc Res, 2015, 105(1):86-95 Cardiovasc Res, 2015, 105(1):86-95 Exp Neurol, 2012, 238(2):209-17	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は一種の有効で、選択性的なMEK構造変容阻害剤で、MEK1に作用するIC50値が3.2 nMですが、Abl1、AKT3、c-RAF、CamK1、CDK2とc-Met等の活性を抑制します。臨床1期。	Nat Commun, 2016, 7:13701 Oncotarget, 2014, 5(20):9609-18 Mol Cancer Ther, 2014, 13(2):353-63	(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は一種の新たで、選択性的で、非ATP競争性的なMEK 1/2阻害剤で、IC50値が7 nMです。臨床1期。	Cell, 2012, 32(34):4034-42 Oncotarget, 2016, 7(13):16273-81	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)は一種の有効なMEK1/2阻害剤で、無細胞試験でIC50値が12nMです。臨床3期。	Stem Cells, 2015, 10.1002/stem.1990 Mol Oncol, 2014, 8(3):544-54 Tumour Biol, 2015, 10.1007/s13277-015-3244-2	Cells seeded in 96-well plates (2,000-3,000 cells per well) were cultured in triplicate with or without graded concentrations of MEK1/2 plus/minus 100 μg/mL cetuximab, which were not renewed during the entire period of cell exposure. For each pair of columns, the height of the left columns represents the sum of the toxic effect of each agent and, therefore, the expected toxicity if their effects were additive when used in combination. The total height of the right columns represents the observed toxicity when the agents were used in combination. The difference between the heights of the paired columns reflects the magnitude of antagonism or synergism on cell toxicity between MEK1/2 inhibitors and cetuximab in NRAS^+/+ (left panels) and NRAS^Q61K/+ (right panels) cells. Results are shown as mean (columns) ± SD (error bars) from at least three experiments in which triplicate wells were analyzed.
S1568	PD318088 PD318088は一種の非ATP競争性的で、MEK1/2構造変容阻害剤ですが、同時に、ATP結合サイトと近隣のMEK1活性サイト地域にATPと結合します。		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は木蘭の有効な成分ですが、Aktリン酸化を抑制し、ERK1/2リン酸化を促進します。臨床3期。	Sensor actuat B-chem, 2012, Jin Akagi Front Pharmacol, 2017, 10.3389/fphar.2017.00199	(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は一種の選択性的なMEK1/2阻害剤で、IC50値が0.18μM/0.22μMですが、Erk1、MKK3、MKK4、c-JUN、PKC、PKA及びCamKIIを抑制する活性がなくて、血脳障壁（barrier）を透すことができます。
S1089	Refametinib (RDEA119, Bay 86-9766) Refametinib (RDEA119, Bay 86-9766)は一種の有効で、ATP非競争性的で、高度選択性的なMEK1とMEK2阻害剤で、このIC50値が19 nMと47 nMです。	J Neurosci, 2012, 32(14):4887-900 Am J Cancer Res, 2016, 6(10):2235-2251 Sci Rep, 2016, 6:35444	RDEA119 (1 µM) or JTP-74057 (0.1 µM) abolished the effects of G1 on DAPK1 and NR2B phosphorylation.
S2326	Myricetin Myricetin is a naturally occurring flavonol, a flavonoid found in many grapes, berries, fruits, vegetables, herbs, as well as other plants.
S7843	BI-847325 BI-847325は一種の経口生物利用可能で、選択性的な二重MEK/オーロラキナーゼ阻害剤です。BI-847325はアフリカツメガエル（Xenopus laevis）オーロラB、人間オーロラAとオーロラC、及び人間MEK1とMEK2に作用する時のIC50値が3 nM、25 nM、15 nM、25 nMと4 nMそれぞれに分かれます。臨床1期。
S8041	Cobimetinib (GDC-0973, RG7420) Cobimetinib (GDC-0973, RG7420)は一種の有効で、高度選択性的なMEK1阻害剤で、IC50値が4.2 nMです。臨床3期。	Cancer Discov, 2015, 10.1158/2159-8290.CD-15-0913 Mol Cell Proteomics, 2017, 16(2):265-277 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は1種の有効的で、 ATP非競争性のMEK1阻害剤で、 Ki値は0.13 nMです。臨床1期。
S8355^新	APS-2-79 HCl APS-2-79は一種のMAPK拮抗剤ですが、拮抗RAFのヘテロ二量体化（heterodimerization）及びKSRが結合したMEKのリン酸化と活性化に対するニーズによるコンフォメーション変化（conformational change）を通じて、 KSRが依頼するMAPK信号経路を調節します。

製品コード	製品説明	文献中の使用例	お客様のフィードバック
S1008	Selumetinib (AZD6244) Selumetinib (AZD6244)は一種の有効で、高度選択性的なMEK1阻害剤で、無細胞試験でIC50値が14 nMですが、ERK1/2リン酸化も抑制する時のIC50値が10 nMになって、p38α、MKK6、EGFR、ErbB2、ERK2とB-Raf等を抑制する作用がありません。臨床3期。	Nature, 2012, 487(7408):505-9 Nature, 2010, 468(7326):968-72 Nature, 2016, 10.1038/nature19347	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は一種の選択性的で、非ATP競争性的なMEK阻害剤で、無細胞試験でIC50値が0.33 nMですが、ERK1とERK2のリン酸化を抑制する作用はCI-1040より500倍左右が高くなります。臨床2期。	Nature, 2015, 10.1038/nature14413 Nature, 2015, 517(7534):391-5 Cell, 2015, 160(1-2):161-76	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)は一種の高度特異性的で、有効なMEK1/2阻害剤で、無細胞試験でIC50値が0.92 nM/1.8 nMですが、c-Raf、B-RafとERK1/2を抑制する活性がありません。	Nature, 2014, 510(7504):283-7 Nature, 2015, 517(7534):391-5 Nature, 2014, 508(7494):118-22	SMYD3 knockout augments the effects of the MEK1/2 inhibitor Trametinib (GSK1120212) in vivo. Representative serial HE staining and IHC for pERK1/2, a marker of Ras activity, and MUC5, a marker of PanIN lesions. All scale bars, 50 um.
S1102	U0126-EtOH U0126-EtOHは一種の高度選択性的なMEK1/2阻害剤で、無細胞試験でIC50値が0.07 μM/0.06 μMですが、ΔN3-S218E/S222D MEKに作用する亲和力はPD098059に作用する親和力より100倍が高くなります。	Cell, 2013, 153(4):840-54 Nat Genet, 2011, 44(2):133-9 J Natl Cancer Inst, 2012, 104(21):1673-9	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.
S1020	PD184352 (CI-1040) PD184352 (CI-1040)は一種のATP非競争性的なMEK1/2阻害剤で、細胞試験でIC50値が17nMですが、MEK1/2に作用する選択性はMEK5に作用する選択性より100倍が高くなります。臨床2期。	Science, 2011, 331(6019):912-6 Nat Genet, 2011, 44(2):133-9 Cancer Cell, 2016, 10.1016/j.ccell.2016.01.006	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は一種の非ATP競争性的なMEK阻害剤で、無細胞試験でIC50値が2μMですが、MEK-1が媒介したMAPKの活性を特異性的に抑制して、ERK1或いはERK2を直接に抑制しません。	Nature, 2016, 10.1038/nature19347 J Natl Cancer Inst, 2012, 104(21):1673-9 Hepatology, 2013, 59(4):1262-72	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は一種の選択性的なMEK5阻害剤で、無細胞試験でIC50値が1.5 nMですが、ERK5触媒活性も抑制して、このIC50値が59 nMになりますが、密接関連のキナーゼMEK1、MEK2、ERK2とJNK2を抑制しません。	Neurobiol Aging, 2014, 35(3):669-79 Am J Pathol, 2013, 183(6):1758-68 J Biol Chem, 2014, 289(9):6311-22
S1475	Pimasertib (AS-703026) Pimasertib (AS-703026)は一種の高度選択性的で、有効で、ATP非競争性的なMEK1/2構造変容阻害剤で、MM細胞の中にIC50値が5 nM-2μMです。臨床2期。	Nat Commun, 2015, 6:6683 FASEB J, 2014, 10.1096/fj.13-247924 Oncotarget, 2016, 7(4):4265-78	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.
S1530	BIX 02188 BIX02188は一種の選択性的なMEK5阻害剤で、IC50値が4.3 nMですが、ERK5触媒活性も抑制して、このIC50値が810 nMになって、密接関連のキナーゼMEK1、MEK2、ERK2とJNK2を抑制しません。	Cardiovasc Res, 2015, 105(1):86-95 Cardiovasc Res, 2015, 105(1):86-95 Exp Neurol, 2012, 238(2):209-17	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は一種の有効で、選択性的なMEK構造変容阻害剤で、MEK1に作用するIC50値が3.2 nMですが、Abl1、AKT3、c-RAF、CamK1、CDK2とc-Met等の活性を抑制します。臨床1期。	Nat Commun, 2016, 7:13701 Oncotarget, 2014, 5(20):9609-18 Mol Cancer Ther, 2014, 13(2):353-63	(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は一種の新たで、選択性的で、非ATP競争性的なMEK 1/2阻害剤で、IC50値が7 nMです。臨床1期。	Cell, 2012, 32(34):4034-42 Oncotarget, 2016, 7(13):16273-81	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)は一種の有効なMEK1/2阻害剤で、無細胞試験でIC50値が12nMです。臨床3期。	Stem Cells, 2015, 10.1002/stem.1990 Mol Oncol, 2014, 8(3):544-54 Tumour Biol, 2015, 10.1007/s13277-015-3244-2	Cells seeded in 96-well plates (2,000-3,000 cells per well) were cultured in triplicate with or without graded concentrations of MEK1/2 plus/minus 100 μg/mL cetuximab, which were not renewed during the entire period of cell exposure. For each pair of columns, the height of the left columns represents the sum of the toxic effect of each agent and, therefore, the expected toxicity if their effects were additive when used in combination. The total height of the right columns represents the observed toxicity when the agents were used in combination. The difference between the heights of the paired columns reflects the magnitude of antagonism or synergism on cell toxicity between MEK1/2 inhibitors and cetuximab in NRAS^+/+ (left panels) and NRAS^Q61K/+ (right panels) cells. Results are shown as mean (columns) ± SD (error bars) from at least three experiments in which triplicate wells were analyzed.
S1568	PD318088 PD318088は一種の非ATP競争性的で、MEK1/2構造変容阻害剤ですが、同時に、ATP結合サイトと近隣のMEK1活性サイト地域にATPと結合します。		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は木蘭の有効な成分ですが、Aktリン酸化を抑制し、ERK1/2リン酸化を促進します。臨床3期。	Sensor actuat B-chem, 2012, Jin Akagi Front Pharmacol, 2017, 10.3389/fphar.2017.00199	(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は一種の選択性的なMEK1/2阻害剤で、IC50値が0.18μM/0.22μMですが、Erk1、MKK3、MKK4、c-JUN、PKC、PKA及びCamKIIを抑制する活性がなくて、血脳障壁（barrier）を透すことができます。
S1089	Refametinib (RDEA119, Bay 86-9766) Refametinib (RDEA119, Bay 86-9766)は一種の有効で、ATP非競争性的で、高度選択性的なMEK1とMEK2阻害剤で、このIC50値が19 nMと47 nMです。	J Neurosci, 2012, 32(14):4887-900 Am J Cancer Res, 2016, 6(10):2235-2251 Sci Rep, 2016, 6:35444	RDEA119 (1 µM) or JTP-74057 (0.1 µM) abolished the effects of G1 on DAPK1 and NR2B phosphorylation.
S2326	Myricetin Myricetin is a naturally occurring flavonol, a flavonoid found in many grapes, berries, fruits, vegetables, herbs, as well as other plants.
S7843	BI-847325 BI-847325は一種の経口生物利用可能で、選択性的な二重MEK/オーロラキナーゼ阻害剤です。BI-847325はアフリカツメガエル（Xenopus laevis）オーロラB、人間オーロラAとオーロラC、及び人間MEK1とMEK2に作用する時のIC50値が3 nM、25 nM、15 nM、25 nMと4 nMそれぞれに分かれます。臨床1期。
S8041	Cobimetinib (GDC-0973, RG7420) Cobimetinib (GDC-0973, RG7420)は一種の有効で、高度選択性的なMEK1阻害剤で、IC50値が4.2 nMです。臨床3期。	Cancer Discov, 2015, 10.1158/2159-8290.CD-15-0913 Mol Cell Proteomics, 2017, 16(2):265-277 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は1種の有効的で、 ATP非競争性のMEK1阻害剤で、 Ki値は0.13 nMです。臨床1期。

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S8355^新	APS-2-79 HCl APS-2-79は一種のMAPK拮抗剤ですが、拮抗RAFのヘテロ二量体化（heterodimerization）及びKSRが結合したMEKのリン酸化と活性化に対するニーズによるコンフォメーション変化（conformational change）を通じて、 KSRが依頼するMAPK信号経路を調節します。

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S8355^新

APS-2-79 HCl

APS-2-79は一種のMAPK拮抗剤ですが、拮抗RAFのヘテロ二量体化（heterodimerization）及びKSRが結合したMEKのリン酸化と活性化に対するニーズによるコンフォメーション変化（conformational change）を通じて、 KSRが依頼するMAPK信号経路を調節します。

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MEK

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亜型選択性的な製品