c-Met

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
S1068	Crizotinib (PF-02341066)	<1 mg/mL	9 mg/mL	<1 mg/mL
S1119	Cabozantinib (XL184, BMS-907351)	<1 mg/mL	100 mg/mL	<1 mg/mL
S1111	Foretinib (GSK1363089)	<1 mg/mL	100 mg/mL	<1 mg/mL
S1070	PHA-665752	<1 mg/mL	128 mg/mL	<1 mg/mL
S1080	SU11274	<1 mg/mL	92 mg/mL	2 mg/mL
S7564	SAR125844	˂1 mg/mL	11 mg/mL	˂1 mg/mL
S9308	Pulsatilla saponin D	-1 mg/mL	100 mg/mL	-1 mg/mL
S1112	SGX-523	<1 mg/mL	3 mg/mL	<1 mg/mL
S1561	BMS-777607	<1 mg/mL	47 mg/mL	<1 mg/mL
S2753	Tivantinib (ARQ 197)	<1 mg/mL	73 mg/mL	<1 mg/mL
S1114	JNJ-38877605	<1 mg/mL	37 mg/mL	<1 mg/mL
S1094	PF-04217903	<1 mg/mL	5 mg/mL	<1 mg/mL
S1361	MGCD-265 analog	<1 mg/mL	104 mg/mL	<1 mg/mL
S2788	Capmatinib (INCB28060)	<1 mg/mL	2 mg/mL	<1 mg/mL
S1124	BMS-754807	<1 mg/mL	92 mg/mL	92 mg/mL
S2201	BMS-794833	<1 mg/mL	94 mg/mL	<1 mg/mL
S1316	AMG-208	<1 mg/mL	0.25 mg/mL	<1 mg/mL
S2774	MK-2461	<1 mg/mL	99 mg/mL	<1 mg/mL
S2859	Golvatinib (E7050)	<1 mg/mL	20 mg/mL	<1 mg/mL
S2747	AMG-458	<1 mg/mL	21 mg/mL	<1 mg/mL
S2761	NVP-BVU972	<1 mg/mL	68 mg/mL	68 mg/mL
S8167	AMG 337	<1 mg/mL	95 mg/mL	95 mg/mL
S7014	Merestinib (LY2801653)	<1 mg/mL	100 mg/mL	100 mg/mL
S8404	S49076	<1 mg/mL	87 mg/mL	<1 mg/mL
S3759	Norcantharidin	-1 mg/mL	33 mg/mL	-1 mg/mL
S7669	NPS-1034	<1 mg/mL	100 mg/mL	4 mg/mL
S7674	HMPL-504(AZD6094, Volitinib)	<1 mg/mL	16 mg/mL	<1 mg/mL

c-Met製品

All (27) c-Met阻害剤(27) 新c-Met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
S1068	Crizotinib (PF-02341066) Crizotinib (PF-02341066) is a potent inhibitor of c-Met and ALK with IC50 of 11 nM and 24 nM in cell-based assays, respectively.	Nature, 2016, 534(7609):647-51 Nature, 2012, 487(7408):505-9 Nat Med, 2011, 17(9):1116-20	(c) Western blot analyses of p-Akt (Ser473) and p-S6RP (Ser235 and Ser236) in two RCT-E565 transplanted tumors treated with vehicle or PF02341066. Samples were isolated 4 h after the last dose from mice treated with PF02341066 for 3 d. (d) Responses of RCT-E565 transplanted tumors in athymic mice to PF02341066 or vehicle. Data are means ±s.e.m. (each group, n = 6). P < 0.005, *P < 0.001 (Student^,s t test).
S1119	Cabozantinib (XL184, BMS-907351) Cabozantinib (XL184, BMS-907351) is a potent VEGFR2 inhibitor with IC50 of 0.035 nM and also inhibits c-Met, Ret, Kit, Flt-1/3/4, Tie2, and AXL with IC50 of 1.3 nM, 4 nM, 4.6 nM, 12 nM/11.3 nM/6 nM, 14.3 nM and 7 nM in cell-free assays, respectively.	Nature, 2017, 543(7647):728-732 Cancer Discov, 2018, 8(7):836-849 Cancer Discov, 2014, 4(7):816-27	Level of phospho-proteins in RTK and PI3K/Akt/mTOR pathways in treated tumors, detected with western blot. (c) Phospho-Erk and phospho-S6 intensity in MDSCs when co-transfected with ERK2 and p70S6K, detected with western blot.
S1111	Foretinib (GSK1363089) Foretinib (GSK1363089) is an ATP-competitive inhibitor of HGFR and VEGFR, mostly for Met and KDR with IC50 of 0.4 nM and 0.9 nM in cell-free assays. Less potent against Ron, Flt-1/3/4, Kit, PDGFRα/β and Tie-2, and little activity to FGFR1 and EGFR. Phase 2.	Nat Genet, 2012, 44(8):852-60 Clin Cancer Res, 2018, 24(10):2357-2369 Clin Cancer Res, 2015, 21(10):2379-87	D. Effects of erlotinib and inhibitors of PI3K, MEK, MET or IGF-1R on phosphorylation of AKT and ERK in ER3 cells.
S1070	PHA-665752 PHA-665752 is a potent, selective and ATP-competitive c-Met inhibitor with IC50 of 9 nM in cell-free assays, >50-fold selectivity for c-Met than RTKs or STKs.	Nat Genet, 2012, 44(8):852-60 Cancer Discov, 2013, 3(12):1404-15 Cell Res, 2015, 10.1038/cr.2015.16	A, representative Western blot analyses of samples obtained from NSCLC cells exposed to 1 umol/L erlotinib or PHA-665,752 for 6 hours. Levels of total and phosphorylated forms of EGFR, MET, and HER3. B, representative Western blot analyses of samples obtained as described in A showing the levels of EGFR downstream signaling mediators. Protein samples obtained from untreated and treated cells were separated by SDS-PAGE and immunoblotted with each antibody. Tubulin served to ensure equal loading.
S1080	SU11274 SU11274 is a selective Met inhibitor with IC50 of 10 nM in cell-free assays, no effects on PGDFRβ, EGFR or Tie2.	Nat Med, 2012, 18(7):1118-22 Clin Cancer Res, 2014, 20(22):5796-807 Clin Cancer Res, 2013, 19(16):4371-82	Inhibition of c-MET sensitizes PTEN deficient tumor cells to EGFR TKI-induced apoptosis. PTEN deficient TGFα-EGFR^WT;InkΔ2/3-/-;PTEN^lox GBM tumor cells were treated with gefitinib (10 uM) and/or the c-MET kinase inhibitor SU11274 (10 uM). Immunoblot analysis of total cell lysates from TGFα-EGFR^WT;InkΔ2/3-/-;PTEN^lox GBM tumor cells treated with the indicated inhibitors using c-MET and c-MET phosphotyrosine 1234,1235 antibodies. Anti β-tubulin probing is used as an internal loading control.
S7564^新	SAR125844
S9308^新	Pulsatilla saponin D Pulsatilla saponin D, isolated from the root of Pulsatilla koreana, targets c-Met and exerts antiangiogenic and antitumor activities.
S1112	SGX-523 SGX-523 is a selective Met inhibitor with IC50 of 4 nM, no activity to BRAFV599E, c-Raf, Abl and p38α. Phase 1.	Am J Respir Crit Care Med, 2016, 10.1164/rccm.201509-1878OC J Hepatol, 2014, 60(1):143-51 Nat Commun, 2016, 7:10690
S1561	BMS-777607 BMS-777607 is a Met-related inhibitor for c-Met, Axl, Ron and Tyro3 with IC50 of 3.9 nM, 1.1 nM, 1.8 nM and 4.3 nM in cell-free assays, 40-fold more selective for Met-related targets versus Lck, VEGFR-2, and TrkA/B, and more than 500-fold greater selectivity versus all other receptor and non receptor kinases. Phase 1/2.	J Clin Invest, 2014, 124(11):4737-52 Cancer Res, 2018, 10.1158/0008-5472.CAN-18-1106 J Pathol, 2015, 237(1):14-24	IHC for phospho-Neu Y1248 in tumors, 1 hour after lapatinib treatment (day 1, d1), and day 7 (d7), 1 hour after final treatment with BMS-777607. Representative images are shown.
S2753	Tivantinib (ARQ 197) Tivantinib (ARQ 197) is the first non-ATP-competitive c-Met inhibitor with K_i of 0.355 μM in a cell-free assay, little activity to Ron, and no inhibition to EGFR, InsR, PDGFRα or FGFR1/4. Phase 3.	Clin Cancer Res, 2017, pii: clincanres.3118.2016 J Exp Clin Cancer Res, 2015, 34:118 Cell Signal, 2013, 25(12):2652-60	Effect of tivantinib on the mitotic index was compared with the antimitotic drugs paclitaxel and vinblastine after overnight treatment of the HLE cell line with two different concentrations of each drug
S1114	JNJ-38877605 JNJ-38877605 is an ATP-competitive inhibitor of c-Met with IC50 of 4 nM, 600-fold selective for c-Met than 200 other tyrosine and serine-threonine kinases. Phase 1.	Nature, 2015, 10.1038/nature14407 Gut, 2014, 10.1136/gutjnl-2013-305257 Clin Cancer Res, 2017, 10.1158/1078-0432.CCR-16-3118	Inducers of EMT. (A) Expression of Hgf, Egf, and Tgfb1 genes in RETAAD tumors analyzed by qRT-PCR. Hgf and Tgfb1 are preferentially expressed in PMN-MDSC, while Egf is preferentially expressed in tumor cells. Data are from four individual experiments using sorted fractions of PMNMDSC and melanoma cells. Bars represent mean 6 SD. (B) NBT-II cells (100 cells per well) were plated for 4 d to allow for colony growth and were pretreated for 24 h with inhibitors before the addition of PMN-MDSC. After co-culture with PMN-MDSCs in the presence of inhibitors, cells were fixed and stained with anti-rat desmoplakin. Green, Desmoplakin; red, H2b (nuclear stain). PD153035-EGFR inhibitor, JNJ38877605-c-met (HGFR) inhibitor, and SB525334-TGF-bR1 inhibitor. Images are representative of three independent experiments.
S1094	PF-04217903 PF-04217903 is a selective ATP-competitive c-Met inhibitor with IC50 of 4.8 nM in A549 cell line, susceptible to oncogenic mutations (no activity to Y1230C mutant). Phase 1.	J Clin Invest, 2016, 126(6):2181-90 Clin Cancer Res, 2014, 20(17):4559-73 Clin Cancer Res, 2015, 21(1):166-74	(A) p-MET, p-eIF4E, and p-ERK1/2 levels in S462 cells 24 hours after treatment with 1 μM PF04217903 and 750 nM PD901. (B) Change in cell number after treatment with 1 μM PF04217903 (PF903) and/or 750 nM PD901. Graph represents the average log2 of fold change in cell number 72 hours after treatment relative to time 0 (mean ± SD, n = 3).
S1361	MGCD-265 analog MGCD-265 is a potent, multi-target and ATP-competitive inhibitor of c-Met and VEGFR1/2/3 with IC50 of 1 nM, 3 nM/3 nM/4 nM, respectively; also inhibits Ron and Tie2. Phase 1/2.	Cancer Lett, 2013, 340(1):43-50 Int J Clin Exp Pathol, 2013, 6(10):2082-91 Mol Cancer Ther, 2018, 17(7):1526-1539	c-MET/RON inhibitors restore sensitivity to lapatinib in SK-BR-3-LR cells. The concentration used was 0.1 uM for crizotinib, MGCD-265, XL880, sunitinib, dasatinib, TAE-684, and RON inhibitor I. Columns, means; bars, SEMs (n = 3). The phosphorylation of HER2, AKT and ERK1/2 was determined by Western blotting.
S2788	Capmatinib (INCB28060) Capmatinib (INCB28060) is a novel, ATP-competitive inhibitor of c-MET with IC50 of 0.13 nM in a cell-free assay, inactive against RONβ, as well as EGFR and HER-3. Phase 1.	Clin Cancer Res, 2017, 23(21):6661-6672 Dev Cell, 2014, 29(4):421-36 Mol Cancer Ther, 2018, 17(4):751-762	Western blots of MET and Akt for parental, crizotinib-resistant, or capmatinib-resistant cells treated for 4 hours with a range of doses of capmatinib, crizotinib, or glesatinib (G-I).
S1124	BMS-754807 BMS-754807 is a potent and reversible inhibitor of IGF-1R/InsR with IC50 of 1.8 nM/1.7 nM in cell-free assays, less potent to Met, Aurora A/B, TrkA/B and Ron, and shows little activity to Flt3, Lck, MK2, PKA, PKC etc. Phase 2.	Clin Cancer Res, 2013, 19(11):2984-94 Cancer Res, 2014, 74(20):5866-77 Mol Cell Biol, 2015, 35(7):1182-96
S2201	BMS-794833 BMS-794833 is a potent ATP competitive inhibitor of Met/VEGFR2 with IC50 of 1.7 nM/15 nM, also inhibits Ron, Axl and Flt3 with IC50 of <3 nM; a prodrug of BMS-817378. Phase 1.
S1316	AMG-208 AMG 208 is a highly selective c-Met inhibitor with IC50 of 9 nM. Phase 1.
S2774	MK-2461 MK-2461 is a potent, multi-targeted inhibitor for c-Met(WT/mutants) with IC50 of 0.4-2.5 nM, less potent to Ron, Flt1; 8- to 30-fold greater selectivity of c-Met targets versus FGFR1, FGFR2, FGFR3, PDGFRβ, KDR, Flt3, Flt4, TrkA, and TrkB. Phase 1/2. .	Mol Cell Biochem, 2018, 449(1-2):1-8	Both V-H cells and V-J cells are treated with MK-2461, XL-184 or ABT-869, respectively. (i-k) Western blot analysis of sFlt-1 expression after incubation with three VEGF-A receptor inhibitors or in the control.
S2859	Golvatinib (E7050) Golvatinib (E7050) is a dual c-Met and VEGFR-2 inhibitor with IC50 of 14 nM and 16 nM, does not inhibit bFGF-stimulated HUVEC growth (up to 1000 nM). Phase 1/2.	Cancer Sci, 2017, 108(7):1378-1385 Mol Cancer Ther, 2017, 16(3):506-515 Cancer Med, 2017, 6(12):2972-2983	PC-9/LMC-GR cells (2 × 105 cells/well) were incubated in 6-well plates with various concentrations of gefitinib with or without crizotinib (1 μmol/L) or golvatinib (1 μmol/L) for 1 hour. Cell lysate were obtained and subjected to immunoblotting with antibodies toward the indicated molecules.
S2747	AMG-458 AMG 458 is a potent c-Met inhibitor with K_i of 1.2 nM, ~350-fold selectivity for c-Met than VEGFR2 in cells.
S2761	NVP-BVU972 NVP-BVU972 is a selective and potent Met inhibitor with IC50 of 14 nM.
S8167	AMG 337 AMG 337 is an oral, small molecule, ATP-competitive, highly selective inhibitor of the MET receptor.
S7014	Merestinib (LY2801653) LY2801653 is a type-II ATP competitive, slow-off inhibitor of MET tyrosine kinase with a dissociation constant (Ki) of 2 nM, a pharmacodynamic residence time (Koff) of 0.00132 min(-1) and t1/2 of 525 min.	PLoS One, 2018, 13(4):e0194730
S8404	S49076 S49076 is a novel, potent inhibitor of MET, AXL/MER, and FGFR1/2/3 with IC50 values below 20 nmol/L.
S3759	Norcantharidin Norcantharidin is a synthetic anticancer compound which is a dual inhibitor for c-Met and EGFR in human colon cancers.
S7669	NPS-1034 NPS-1034 is a dual Met/Axl inhibitor with IC50 of 48 nM and 10.3 nM, respectively.
S7674	HMPL-504(AZD6094, Volitinib) Savolitinib (volitinib, AZD6094, HMPL-504) is a novel, potent, and selective MET inhibitor currently in clinical development in various indications, including PRCC. The IC50 values of this compound for c-Met and p-Met are 5 nM and 3 nM, respectively. It shows exquisite selectivity for c-Met over 274 kinase.

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
S1068	Crizotinib (PF-02341066) Crizotinib (PF-02341066) is a potent inhibitor of c-Met and ALK with IC50 of 11 nM and 24 nM in cell-based assays, respectively.	Nature, 2016, 534(7609):647-51 Nature, 2012, 487(7408):505-9 Nat Med, 2011, 17(9):1116-20	(c) Western blot analyses of p-Akt (Ser473) and p-S6RP (Ser235 and Ser236) in two RCT-E565 transplanted tumors treated with vehicle or PF02341066. Samples were isolated 4 h after the last dose from mice treated with PF02341066 for 3 d. (d) Responses of RCT-E565 transplanted tumors in athymic mice to PF02341066 or vehicle. Data are means ±s.e.m. (each group, n = 6). P < 0.005, *P < 0.001 (Student^,s t test).
S1119	Cabozantinib (XL184, BMS-907351) Cabozantinib (XL184, BMS-907351) is a potent VEGFR2 inhibitor with IC50 of 0.035 nM and also inhibits c-Met, Ret, Kit, Flt-1/3/4, Tie2, and AXL with IC50 of 1.3 nM, 4 nM, 4.6 nM, 12 nM/11.3 nM/6 nM, 14.3 nM and 7 nM in cell-free assays, respectively.	Nature, 2017, 543(7647):728-732 Cancer Discov, 2018, 8(7):836-849 Cancer Discov, 2014, 4(7):816-27	Level of phospho-proteins in RTK and PI3K/Akt/mTOR pathways in treated tumors, detected with western blot. (c) Phospho-Erk and phospho-S6 intensity in MDSCs when co-transfected with ERK2 and p70S6K, detected with western blot.
S1111	Foretinib (GSK1363089) Foretinib (GSK1363089) is an ATP-competitive inhibitor of HGFR and VEGFR, mostly for Met and KDR with IC50 of 0.4 nM and 0.9 nM in cell-free assays. Less potent against Ron, Flt-1/3/4, Kit, PDGFRα/β and Tie-2, and little activity to FGFR1 and EGFR. Phase 2.	Nat Genet, 2012, 44(8):852-60 Clin Cancer Res, 2018, 24(10):2357-2369 Clin Cancer Res, 2015, 21(10):2379-87	D. Effects of erlotinib and inhibitors of PI3K, MEK, MET or IGF-1R on phosphorylation of AKT and ERK in ER3 cells.
S1070	PHA-665752 PHA-665752 is a potent, selective and ATP-competitive c-Met inhibitor with IC50 of 9 nM in cell-free assays, >50-fold selectivity for c-Met than RTKs or STKs.	Nat Genet, 2012, 44(8):852-60 Cancer Discov, 2013, 3(12):1404-15 Cell Res, 2015, 10.1038/cr.2015.16	A, representative Western blot analyses of samples obtained from NSCLC cells exposed to 1 umol/L erlotinib or PHA-665,752 for 6 hours. Levels of total and phosphorylated forms of EGFR, MET, and HER3. B, representative Western blot analyses of samples obtained as described in A showing the levels of EGFR downstream signaling mediators. Protein samples obtained from untreated and treated cells were separated by SDS-PAGE and immunoblotted with each antibody. Tubulin served to ensure equal loading.
S1080	SU11274 SU11274 is a selective Met inhibitor with IC50 of 10 nM in cell-free assays, no effects on PGDFRβ, EGFR or Tie2.	Nat Med, 2012, 18(7):1118-22 Clin Cancer Res, 2014, 20(22):5796-807 Clin Cancer Res, 2013, 19(16):4371-82	Inhibition of c-MET sensitizes PTEN deficient tumor cells to EGFR TKI-induced apoptosis. PTEN deficient TGFα-EGFR^WT;InkΔ2/3-/-;PTEN^lox GBM tumor cells were treated with gefitinib (10 uM) and/or the c-MET kinase inhibitor SU11274 (10 uM). Immunoblot analysis of total cell lysates from TGFα-EGFR^WT;InkΔ2/3-/-;PTEN^lox GBM tumor cells treated with the indicated inhibitors using c-MET and c-MET phosphotyrosine 1234,1235 antibodies. Anti β-tubulin probing is used as an internal loading control.
S7564^新	SAR125844
S9308^新	Pulsatilla saponin D Pulsatilla saponin D, isolated from the root of Pulsatilla koreana, targets c-Met and exerts antiangiogenic and antitumor activities.
S1112	SGX-523 SGX-523 is a selective Met inhibitor with IC50 of 4 nM, no activity to BRAFV599E, c-Raf, Abl and p38α. Phase 1.	Am J Respir Crit Care Med, 2016, 10.1164/rccm.201509-1878OC J Hepatol, 2014, 60(1):143-51 Nat Commun, 2016, 7:10690
S1561	BMS-777607 BMS-777607 is a Met-related inhibitor for c-Met, Axl, Ron and Tyro3 with IC50 of 3.9 nM, 1.1 nM, 1.8 nM and 4.3 nM in cell-free assays, 40-fold more selective for Met-related targets versus Lck, VEGFR-2, and TrkA/B, and more than 500-fold greater selectivity versus all other receptor and non receptor kinases. Phase 1/2.	J Clin Invest, 2014, 124(11):4737-52 Cancer Res, 2018, 10.1158/0008-5472.CAN-18-1106 J Pathol, 2015, 237(1):14-24	IHC for phospho-Neu Y1248 in tumors, 1 hour after lapatinib treatment (day 1, d1), and day 7 (d7), 1 hour after final treatment with BMS-777607. Representative images are shown.
S2753	Tivantinib (ARQ 197) Tivantinib (ARQ 197) is the first non-ATP-competitive c-Met inhibitor with K_i of 0.355 μM in a cell-free assay, little activity to Ron, and no inhibition to EGFR, InsR, PDGFRα or FGFR1/4. Phase 3.	Clin Cancer Res, 2017, pii: clincanres.3118.2016 J Exp Clin Cancer Res, 2015, 34:118 Cell Signal, 2013, 25(12):2652-60	Effect of tivantinib on the mitotic index was compared with the antimitotic drugs paclitaxel and vinblastine after overnight treatment of the HLE cell line with two different concentrations of each drug
S1114	JNJ-38877605 JNJ-38877605 is an ATP-competitive inhibitor of c-Met with IC50 of 4 nM, 600-fold selective for c-Met than 200 other tyrosine and serine-threonine kinases. Phase 1.	Nature, 2015, 10.1038/nature14407 Gut, 2014, 10.1136/gutjnl-2013-305257 Clin Cancer Res, 2017, 10.1158/1078-0432.CCR-16-3118	Inducers of EMT. (A) Expression of Hgf, Egf, and Tgfb1 genes in RETAAD tumors analyzed by qRT-PCR. Hgf and Tgfb1 are preferentially expressed in PMN-MDSC, while Egf is preferentially expressed in tumor cells. Data are from four individual experiments using sorted fractions of PMNMDSC and melanoma cells. Bars represent mean 6 SD. (B) NBT-II cells (100 cells per well) were plated for 4 d to allow for colony growth and were pretreated for 24 h with inhibitors before the addition of PMN-MDSC. After co-culture with PMN-MDSCs in the presence of inhibitors, cells were fixed and stained with anti-rat desmoplakin. Green, Desmoplakin; red, H2b (nuclear stain). PD153035-EGFR inhibitor, JNJ38877605-c-met (HGFR) inhibitor, and SB525334-TGF-bR1 inhibitor. Images are representative of three independent experiments.
S1094	PF-04217903 PF-04217903 is a selective ATP-competitive c-Met inhibitor with IC50 of 4.8 nM in A549 cell line, susceptible to oncogenic mutations (no activity to Y1230C mutant). Phase 1.	J Clin Invest, 2016, 126(6):2181-90 Clin Cancer Res, 2014, 20(17):4559-73 Clin Cancer Res, 2015, 21(1):166-74	(A) p-MET, p-eIF4E, and p-ERK1/2 levels in S462 cells 24 hours after treatment with 1 μM PF04217903 and 750 nM PD901. (B) Change in cell number after treatment with 1 μM PF04217903 (PF903) and/or 750 nM PD901. Graph represents the average log2 of fold change in cell number 72 hours after treatment relative to time 0 (mean ± SD, n = 3).
S1361	MGCD-265 analog MGCD-265 is a potent, multi-target and ATP-competitive inhibitor of c-Met and VEGFR1/2/3 with IC50 of 1 nM, 3 nM/3 nM/4 nM, respectively; also inhibits Ron and Tie2. Phase 1/2.	Cancer Lett, 2013, 340(1):43-50 Int J Clin Exp Pathol, 2013, 6(10):2082-91 Mol Cancer Ther, 2018, 17(7):1526-1539	c-MET/RON inhibitors restore sensitivity to lapatinib in SK-BR-3-LR cells. The concentration used was 0.1 uM for crizotinib, MGCD-265, XL880, sunitinib, dasatinib, TAE-684, and RON inhibitor I. Columns, means; bars, SEMs (n = 3). The phosphorylation of HER2, AKT and ERK1/2 was determined by Western blotting.
S2788	Capmatinib (INCB28060) Capmatinib (INCB28060) is a novel, ATP-competitive inhibitor of c-MET with IC50 of 0.13 nM in a cell-free assay, inactive against RONβ, as well as EGFR and HER-3. Phase 1.	Clin Cancer Res, 2017, 23(21):6661-6672 Dev Cell, 2014, 29(4):421-36 Mol Cancer Ther, 2018, 17(4):751-762	Western blots of MET and Akt for parental, crizotinib-resistant, or capmatinib-resistant cells treated for 4 hours with a range of doses of capmatinib, crizotinib, or glesatinib (G-I).
S1124	BMS-754807 BMS-754807 is a potent and reversible inhibitor of IGF-1R/InsR with IC50 of 1.8 nM/1.7 nM in cell-free assays, less potent to Met, Aurora A/B, TrkA/B and Ron, and shows little activity to Flt3, Lck, MK2, PKA, PKC etc. Phase 2.	Clin Cancer Res, 2013, 19(11):2984-94 Cancer Res, 2014, 74(20):5866-77 Mol Cell Biol, 2015, 35(7):1182-96
S2201	BMS-794833 BMS-794833 is a potent ATP competitive inhibitor of Met/VEGFR2 with IC50 of 1.7 nM/15 nM, also inhibits Ron, Axl and Flt3 with IC50 of <3 nM; a prodrug of BMS-817378. Phase 1.
S1316	AMG-208 AMG 208 is a highly selective c-Met inhibitor with IC50 of 9 nM. Phase 1.
S2774	MK-2461 MK-2461 is a potent, multi-targeted inhibitor for c-Met(WT/mutants) with IC50 of 0.4-2.5 nM, less potent to Ron, Flt1; 8- to 30-fold greater selectivity of c-Met targets versus FGFR1, FGFR2, FGFR3, PDGFRβ, KDR, Flt3, Flt4, TrkA, and TrkB. Phase 1/2. .	Mol Cell Biochem, 2018, 449(1-2):1-8	Both V-H cells and V-J cells are treated with MK-2461, XL-184 or ABT-869, respectively. (i-k) Western blot analysis of sFlt-1 expression after incubation with three VEGF-A receptor inhibitors or in the control.
S2859	Golvatinib (E7050) Golvatinib (E7050) is a dual c-Met and VEGFR-2 inhibitor with IC50 of 14 nM and 16 nM, does not inhibit bFGF-stimulated HUVEC growth (up to 1000 nM). Phase 1/2.	Cancer Sci, 2017, 108(7):1378-1385 Mol Cancer Ther, 2017, 16(3):506-515 Cancer Med, 2017, 6(12):2972-2983	PC-9/LMC-GR cells (2 × 105 cells/well) were incubated in 6-well plates with various concentrations of gefitinib with or without crizotinib (1 μmol/L) or golvatinib (1 μmol/L) for 1 hour. Cell lysate were obtained and subjected to immunoblotting with antibodies toward the indicated molecules.
S2747	AMG-458 AMG 458 is a potent c-Met inhibitor with K_i of 1.2 nM, ~350-fold selectivity for c-Met than VEGFR2 in cells.
S2761	NVP-BVU972 NVP-BVU972 is a selective and potent Met inhibitor with IC50 of 14 nM.
S8167	AMG 337 AMG 337 is an oral, small molecule, ATP-competitive, highly selective inhibitor of the MET receptor.
S7014	Merestinib (LY2801653) LY2801653 is a type-II ATP competitive, slow-off inhibitor of MET tyrosine kinase with a dissociation constant (Ki) of 2 nM, a pharmacodynamic residence time (Koff) of 0.00132 min(-1) and t1/2 of 525 min.	PLoS One, 2018, 13(4):e0194730
S8404	S49076 S49076 is a novel, potent inhibitor of MET, AXL/MER, and FGFR1/2/3 with IC50 values below 20 nmol/L.
S3759	Norcantharidin Norcantharidin is a synthetic anticancer compound which is a dual inhibitor for c-Met and EGFR in human colon cancers.
S7669	NPS-1034 NPS-1034 is a dual Met/Axl inhibitor with IC50 of 48 nM and 10.3 nM, respectively.
S7674	HMPL-504(AZD6094, Volitinib) Savolitinib (volitinib, AZD6094, HMPL-504) is a novel, potent, and selective MET inhibitor currently in clinical development in various indications, including PRCC. The IC50 values of this compound for c-Met and p-Met are 5 nM and 3 nM, respectively. It shows exquisite selectivity for c-Met over 274 kinase.

研究分野別

製品類型

c-Met

シグナル伝達経路

研究分野

c-Met製品