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) | ||
|---|---|---|---|---|
| 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
| 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. |
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 |
PD0325901PD0325901 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. |
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. |
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. |
|
| S1177 |
PD98059PD98059 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. |
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 02189BIX02189 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. |
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) 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. |
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 02188BIX02188 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. |
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-733TAK-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. |
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 |
AZD8330AZD8330 is a novel, selective, non-ATP competitive MEK 1/2 inhibitor with IC50 of 7 nM. Phase 1. |
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. |
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 |
PD318088PD318088 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 |
HonokiolHonokiol is the active principle of magnolia extract that inhibits Akt-phosphorylation and promotes ERK1/2 phosphorylation. Phase 3. |
(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. |
RDEA119 (1 µM) or JTP-74057 (0.1 µM) abolished the effects of G1 on DAPK1 and NR2B phosphorylation.
|
|
| S2326 |
MyricetinMyricetin, 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-847325BI-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. |
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-0623GDC-0623 is a potent and ATP-uncompetitive MEK1 inhibitor with Ki of 0.13 nM. Phase 1. |
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 HClAPS-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. |
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. |
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 |
PD0325901PD0325901 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. |
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. |
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. |
|
| S1177 |
PD98059PD98059 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. |
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 02189BIX02189 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. |
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) 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. |
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 02188BIX02188 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. |
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-733TAK-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. |
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 |
AZD8330AZD8330 is a novel, selective, non-ATP competitive MEK 1/2 inhibitor with IC50 of 7 nM. Phase 1. |
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. |
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 |
PD318088PD318088 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 |
HonokiolHonokiol is the active principle of magnolia extract that inhibits Akt-phosphorylation and promotes ERK1/2 phosphorylation. Phase 3. |
(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. |
RDEA119 (1 µM) or JTP-74057 (0.1 µM) abolished the effects of G1 on DAPK1 and NR2B phosphorylation.
|
|
| S2326 |
MyricetinMyricetin, 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-847325BI-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. |
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-0623GDC-0623 is a potent and ATP-uncompetitive MEK1 inhibitor with Ki of 0.13 nM. Phase 1. |
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 HClAPS-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. |
2019, 5(11):eaax4249 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
|
