c-Met

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
S1068	Crizotinib (PF-02341066)	<1 mg/mL	9 mg/mL	'<1 mg/mL
S1119	Cabozantinib (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
S9620	TPX-0022	<1 mg/mL	<1 mg/mL	'''5 mg/mL
S5190	Crizotinib hydrochloride	97 mg/mL	97 mg/mL	''97 mg/mL
S0361	AMG-1	<1 mg/mL	100 mg/mL	60 mg/mL
S6899	Licochalcone 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
S1244	Amuvatinib (MP-470)	<1 mg/mL	32 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
S4001	Cabozantinib malate (XL184)	<1 mg/mL	100 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
S7067	Tepotinib (EMD 1214063)	<1 mg/mL	5 mg/mL	''<1 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
S0540	BAY-474	<1 mg/mL	58 mg/mL	4 mg/mL
S8570	RXDX-106 (CEP-40783)	<1 mg/mL	10 mg/mL	'2 mg/mL
S8854	JNJ-38877618(OMO-1)	<1 mg/mL	10 mg/mL	'2 mg/mL
S8404	S49076	<1 mg/mL	87 mg/mL	'<1 mg/mL
S9308	Pulsatilla saponin D	-1 mg/mL	100 mg/mL	-1 mg/mL
S6870	Ningetinib	<1 mg/mL	20 mg/mL	'<1 mg/mL
S6762	Bozitinib (PLB-1001)	<1 mg/mL	85 mg/mL	'2.5 mg/mL
S9662	UNC2025	<1 mg/mL	100 mg/mL	''60 mg/mL
S7564	SAR125844	˂1 mg/mL	11 mg/mL	'˂1 mg/mL
S3759	Norcantharidin	-1 mg/mL	33 mg/mL	-1 mg/mL
S6412	Altiratinib	<1 mg/mL	100 mg/mL	'<1 mg/mL
S7669	NPS-1034	<1 mg/mL	100 mg/mL	'4 mg/mL
S8676	Glumetinib (SCC244)	<1 mg/mL	11 mg/mL	'<1 mg/mL
S7674	Savolitinib (AZD6094)	<1 mg/mL	16 mg/mL	''<1 mg/mL
S5115	Sodium L-ascorbyl-2-phosphate	64 mg/mL	<1 mg/mL	'-1 mg/mL

c-Met製品

All (43) c-Met阻害剤(42)

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. It is also a potent ROS1 inhibitor with Ki value less than 0.025 nM. Crizotinib induces autophagy through inhibition of the STAT3 pathway in multiple lung cancer cell lines.	Cell, 2021, 184(10):2649-2664.e18 Nat Commun, 2021, 12(1):5006 Cancer Lett, 2021, 522:119-128	(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 (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. Cabozantinib induces PUMA-dependent apoptosis in colon cancer cells via AKT/GSK-3β/NF-κB signaling pathway.	Clin Cancer Res, 2021, 27(9):2533-2548 Cancers (Basel), 2021, 13(3)E372 Cancers (Basel), 2021, 13(14)3635	Effects of AXL inhibitors on induction of pAKT and rescue of pERK following AXL overexpression. R428, 500 nmol/L; XL184, 3 umol/L; XL880, 100 nmol/L; in the presence or absence of 2 umol/L PLX4720. shAXL is a positive control.
S1111	Foretinib (GSK1363089) Foretinib (GSK1363089, EXEL-2880, XL-880, GSK089) is an ATP-competitive inhibitor of HGFR and VEGFR, mostly for Met (c-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 (c-Kit), PDGFRα/β and Tie-2, and little activity to FGFR1 and EGFR. Phase 2.	Cancers (Basel), 2021, 13(3)E372 Mol Carcinog, 2021, 60(7):481-496 Hum Cell, 2021, 10.1007/s13577-021-00579-z	c-MET/RON inhibitors restore sensitivity to lapatinib in SK-BR-3-LR cells. Cell growth was determined using the sulforhodamine B assay. The concentration used was 0.1 uM for crizotinib, MGCD-265, XL880, sunitinib, dasatinib, and TAE-684I. The phosphorylation of HER2, AKT and ERK1/2 was determined by Western blotting.
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.	Cancers (Basel), 2021, 13(16)4133 Oncogenesis, 2021, 10(3):25 Sci Rep, 2021, 11(1):5468	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 (PKI-SU11274) is a selective Met (c-Met) inhibitor with IC50 of 10 nM in cell-free assays, no effects on PGDFRβ, EGFR or Tie2. SU11274 induces autophagy, apoptosis and cell cycle arrest.	Cell Chem Biol, 2021, S2451-9456(21)00303-2 J Orthop Translat, 2021, 27:9-16 J Biol Chem, 2020, 23 pii: jbc	Effect of crizotinib, tivantinib, and SU11274 on levels of c-MET phosphorylation and downstream signaling pathway in SW1736 and TL3 thyroid cancer cells. Cells were prestarved in culture medium containing 0.5% FBS (24 hour) ?either crizotinib or tivantinib (0.1, 1.0, and 10 umol/L) or SU11274 (10 umol/L), and stimulated with 20 ng/mL recombinant human HGF for 10 minutes before lysates were made for Western blotting. A series of c-MET downstream signaling pathway proteins and phosphor proteins were detected using Western blotting. β-Actin was used as a loading balance control.
S9620^新	TPX-0022 TPX-0022 (CSF1R-IN-2) is a potent inhibitor of MET/CSF1R/SRC with enzymatic kinase inhibition IC50s of 0.14 nM, 0.71 nM and 0.12 nM, respectively. TPX-0022 modulates the tumor immune microenvironment in preclinical models.
S5190^新	Crizotinib hydrochloride Crizotinib (PF-02341066) hydrochloride (Xalkori) inhibits tyrosine phosphorylation of c-Met and nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK) with IC50 of of 11 nM and 24 nM in cell-based assays, respectively. Crizotinib hydrochloride is also a potent ROS1 inhibitor with Ki less than 0.025 nM. Crizotinib induces autophagy through inhibition of the STAT3 pathway in multiple lung cancer cell lines.	Nat Commun, 2021, 12(1):5006 Cancer Lett, 2021, 522:119-128 Mol Cancer Ther, 2021, molcanther.0965.2020
S0361^新	AMG-1 AMG-1 (c-Met/RON Dual Kinase Inhibitor, RON-IN-1) is a potent inhibitor of human c-Met and RON with IC50 of 4 nM and 9 nM, respectively.
S6899^新	Licochalcone D Licochalcone D (Lico D, LCD, LD), a flavonoid isolated from a Chinese medicinal plant Glycyrrhiza inflata, has antioxidant, anti-inflammatory and anti-cancer properties. Licochalcone D inhibit phosphorylation of NF-κB p65 in LPS signaling pathway. Licochalcone D inhibits JAK2, EGFR and MET activities and induces ROS-dependent apoptosis. Licochalcone D also induces caspases activation and poly (ADP-ribose) polymerase (PARP) cleavage.
S1112	SGX-523 SGX-523 is a selective Met (c-Met) inhibitor with IC50 of 4 nM, no activity to BRAFV599E, c-Raf, Abl and p38α. Phase 1.	J Pathol, 2020, 250(2):205-216 Acta Pharmacol Sin, 2020, 10.1038/s41401-019-0336-3 Neurooncol Adv, 2020, 2(1):vdaa067	Association of c-Met phosphorylation and s-Met generation in EBC-1 xenograft tumor. Mice were treated with SGX523 at 10 mg/kg, 3 mg/kg, 0.1 mg/kg, at 0 h and 8 h point, respectively. Plasma and tumor lysates were collected using the method described in "Materials and methods"section at 24 h time point. The bar and line in the figure represents the average phosphorylation rate of c-Met and s-Met in subgroups, respectively. Each subgroup consists of four mice with tumor volume around 600 mm³.
S1561	BMS-777607 BMS-777607 (BMS 817378) 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.	Oncogene, 2021, 10.1038/s41388-021-01869-4 J Cell Mol Med, 2021, 10.1111/jcmm.16261 Cell Metab, 2020, 4;31(2):406-421 e7	Numbers of clonogenic cells from L3.6pl cells and CSCs^＋24/44/ESAin duplicate were counted. Clonogenic growth from the cell control was set as 100%.
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. Tivantinib (ARQ 197) induces a G2/M arrest and apoptosis. Phase 3.	Eur J Pharmacol, 2021, 906:174214 Hum Cell, 2021, 10.1007/s13577-021-00579-z Oncotarget, 2021, 12(7):674-685	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.	Oncogenesis, 2021, 10(3):25 Acta Biochim Biophys Sin (Shanghai), 2021, gmab026 Angiogenesis, 2021, 10.1007/s10456-021-09771-z	(B) RPE50 cells were untreated (-), treated with 50 nM of HGF or EGF or 50 ng/ml HB-EGF coupled with DMSO or various inhibitors as indicated for 0.5 h.
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.	Cell Chem Biol, 2019, 10.1016/j.chembiol.2019.06.003 Neoplasia, 2019, 22(1):1-9 Sci Rep, 2019, 9(1):606	Clonogenicity of LXFA 526L and LXFA 1647L with titration of the MET inhibitor PF-04217903 and combination of PF-04217903 at 0.1 uM with 0.66 uM cetuximab.
S1244	Amuvatinib (MP-470) Amuvatinib (MP-470, HPK 56) is a potent and multi-targeted inhibitor of c-Kit, PDGFRα and Flt3 with IC50 of 10 nM, 40 nM and 81 nM, respectively. Amuvatinib suppresses c-MET and c-RET. Amuvatinib is also active as a DNA repair protein Rad51 inhibitor with antineoplastic activity. Phase 2.	Hum Cell, 2021, 10.1007/s13577-021-00579-z Hum Cell, 2020, 10.1007/s13577-020-00420-z PLoS Genet, 2016, 12(9):e1006279	Inactivation of AXL by MP470 reverses epithelial to mesenchymal transition. Immunoblot analyses of lysates from TGFβ/TNFα- treated MCF10A cells treated with varying amounts of MP470 for 72 hours.
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.	Elife, 2019, 8e47460 Protein Cell, 2019, 10(3):161-177 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, INC280, NVP-INC280) 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. Capmatinib (INCB28060) inhibits Wnt/β-catenin and EMT signaling pathways and induces apoptosis in diffuse gastric cancer positive for c-MET amplification. Phase 1.	Cancer Lett, 2021, 519:328-342 Cancer Lett, 2021, 512:51-59 Cancers (Basel), 2021, 13(3)E372	(a) MET inhibition by INCB28060 prevents HGF-induced MET phosphorylation in MDA-MB231 and HCC-1954 cells. After one hour preincubation with INC2B8060, BC cells were stimulated with HGF for one hour. Phosphorylation of MET and total MET were determined by western blot and quantified by densitometric analysis. Results are expressed as percentage of unstimulated and untreated cells (negative control).
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 (c-Met), Aurora A/B, TrkA/B and Ron, and shows little activity to Flt3, Lck, MK2, PKA, PKC etc. Phase 2.	Front Oncol, 2021, 11:650052 Life Sci, 2021, 267:118977 Sci China Life Sci, 2021, 10.1007/s11427-020-1836-7
S2201	BMS-794833 BMS-794833 is a potent ATP competitive inhibitor of Met (c-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 dual c-Met and RON inhibitor with IC50 of 9 nM for c-Met.
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 Carcinog, 2021, 60(7):481-496 G3 (Bethesda), 2021, 11(10)jkab265 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.
S4001	Cabozantinib malate (XL184) Cabozantinib malate (XL184) is the malate of Cabozantinib, a potent VEGFR2 inhibitor with IC50 of 0.035 nM and also inhibits c-Met, Ret (c-Ret), Kit (c-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. Cabozantinib malate (XL184) induces apoptosis.	Clin Cancer Res, 2021, 27(9):2533-2548 Cancers (Basel), 2021, 13(14)3635 J Clin Endocrinol Metab, 2021, dgab020	Effects of AXL inhibitors on induction of pAKT and rescue of pERK following AXL overexpression. R428, 500 nmol/L; XL184, 3 umol/L; XL880, 100 nmol/L; in the presence or absence of 2 umol/L PLX4720. shAXL is a positive 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, 2020, 111(10):3813-3823 Nephron, 2020, 1-12 Cell, 2019, 178(6):1478-1492	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 (c-Met) inhibitor with IC50 of 14 nM.	PLoS Biol, 2021, 19(5):e3001263
S7067	Tepotinib (EMD 1214063) Tepotinib (EMD 1214063, MSC2156119) is a potent and selective c-Met inhibitor with IC50 of 4 nM, >200-fold selective for c-Met than IRAK4, TrkA, Axl, IRAK1, and Mer. Tepotinib (EMD 1214063) induces autophagy. Phase 1.	Transl Lung Cancer Res, 2020, 9(5):1810-1821 Int J Mol Sci, 2020, 21(21)E7905 CU Digital Repository, 2020, N/A	Ectopic expression of a RNAi-resistant SMARCE1 cDNA resensitizes SMARCE1-knockdown cells to MET inhibition in MET-amplified NSCLC cells. The above-described cells were grown in the absence or presence of 300 nM Crizotinib, 150 nM EMD1214063, or 150 nM PHA665752. Cells were then fixed, stained and photographed after 12 days (untreated) or 28 days (treated).
S8167	AMG 337 AMG 337 is an oral, small molecule, ATP-competitive, highly selective inhibitor of the Met (c-Met) receptor with an IC50 of 1 nM.	Cancer Cell, 2019, 36(1):35-50
S7014	Merestinib (LY2801653) Merestinib (LY2801653) is a type-II ATP competitive, slow-off inhibitor of Met (c-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. Merestinib (LY2801653) also inhibits MST1R, AXL, ROS1, MKNK1/2, FLT3, MERTK, DDR1 and DDR2 with IC50 of 11 nM, 2 nM, 23 nM, 7 nM, 7 nM, 10 nM, 0.1 nM and 7 nM, respectively.	J Clin Invest, 2021, 131(11)146987 Front Oncol, 2020, 12;10:700 Cancer Commun (Lond), 2020, 11
S0540	BAY-474 BAY-474 is an inhibitor of tyrosine-protein kinase c-Met and can act as an epigenetics probe.
S8570	RXDX-106 (CEP-40783) RXDX-106 (CEP-40783) is an orally-available, potent and selective TAM(TYRO3, AXL, MER)/Met (c-Met) inhibitor displaying low nanomolar biochemical activity and slow (T1/2 >120 min) inhibitor off-rate in peptide phosphorylation assays and in vitro kinase binding assays, respectively.	Clin Cancer Res, 2021, 27(9):2533-2548 J Clin Invest, 2018, 128(11):5034-5055
S8854	JNJ-38877618(OMO-1) JNJ-38877618 (OMO-1) is a potent, highly selective, orally bioavailable Met (c-Met) kinase inhibitor with binding affinity (Kd) of 1.4 nM and enzyme inhibitory activity against wt and M1268T mutant Met (c-Met) (2 and 3 nM IC50).
S8404	S49076 S49076 is a novel, potent inhibitor of Met (c-Met), AXL/MER, and FGFR1/2/3 with IC50 values below 20 nmol/L.	Mol Brain, 2020, 4;13(1):66
S9308	Pulsatilla saponin D Pulsatilla saponin D (SB365), isolated from the root of Pulsatilla koreana, targets c-Met and exerts antiangiogenic and antitumor activities.
S6870	Ningetinib Ningetinib (CT-053, DE-120, CT053PTSA) is a potent, orally bioavailable inhibitor of tyrosine kinase with IC50 of 6.7 nM, 1.9 nM and <1.0 nM for c-Met, VEGFR2 and Axl, respectively. Ningetinib exhibits antitumor activity.
S6762	Bozitinib (PLB-1001) Bozitinib (PLB-1001, CBT-101, APL-101, CBI-3103) is a highly selective ATP-competitive c-Met inhibitor with blood-brain barrier permeability. Bozitinib (PLB-1001) selectively inhibits MET-altered tumor cells in preclinical models.
S9662	UNC2025 UNC2025 is a potent and orally active dual inhibitor of FLT3 and MER with IC50 of 0.35 nM and 0.46 nM, respectively. UNC2025 also inhibits AXL, TRKA, TRKC, QIK, TYRO3, SLK, NuaK1, Kit (c-Kit) and Met (c-Met) with IC50 of 1.65 nM, 1.67 nM, 4.38 nM, 5.75 nM, 5.83 nM, 6.14 nM, 7.97 nM, 8.18 nM and 364 nM, respectively.	Front Immunol, 2020, 11:564133 Cell Signal, 2014, 26(1):149-61
S7564	SAR125844 SAR125844 is a potent intravenously active and highly selective Met (c-Met) kinase inhibitor, displaying nanomolar activity against the wild-type kinase (IC50 value of 4.2 nmol/L) and H1094Y, Y1235D, M1250T, L1195V, and D1228H kinase domain mutants (IC50 values of 0.22, 1.7, 6.5, 65, and 81 nmol/L, respectively).
S3759	Norcantharidin Norcantharidin (Endothall anhydride) is a synthetic anticancer compound which is a dual inhibitor for c-Met and EGFR in human colon cancers.
S6412	Altiratinib Altiratinib (DCC-2701) is a potent single-digit nanomolar inhibitor of TRK, Met (c-Met), TIE2, and VEGFR2 kinases with IC50 vaules of 0.9 nM, 4.6 nM, and 0.8 nM for TRKA, B, and C, respectively. It inhibits Met (c-Met) and Met (c-Met) mutant with IC50 values in the range of 0.3-6 nM.
S7669	NPS-1034 NPS-1034 is a dual Met (c-Met)/Axl inhibitor with IC50 of 48 nM and 10.3 nM, respectively.	J Med Chem, 2021, 64(6):3165-3184
S8676	Glumetinib (SCC244) Glumetinib (SCC244) is a potent and highly selective c-Met inhibitor with an IC50 of 0.42 ± 0.02 nmol/L. Glumetinib has greater than 2,400-fold selectivity for c-Met over those 312 kinases evaluated, including the c-Met family member RON and highly homologous kinases Axl, Mer, and TyrO3.
S7674	Savolitinib (AZD6094) 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.	Phytomedicine, 2021, 80:153355 J Exp Clin Cancer Res, 2021, 40(1):69 Nature, 2020, 580(7801):136-141
S5115	Sodium L-ascorbyl-2-phosphate Sodium L-ascorbyl-2-phosphate (Sodium ascorbyl monophosphate, Sodium ascorbyl phosphate, SAP) is specifically produced for use as a stabilized source of vitamin C in cosmetic products. It is used in skin care recipes for UV protection, collagen production, as an antioxidant and for its skin lightening and brightening effects.	Stem Cell Res Ther, 2021, 12(1):48

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. It is also a potent ROS1 inhibitor with Ki value less than 0.025 nM. Crizotinib induces autophagy through inhibition of the STAT3 pathway in multiple lung cancer cell lines.	Cell, 2021, 184(10):2649-2664.e18 Nat Commun, 2021, 12(1):5006 Cancer Lett, 2021, 522:119-128	(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 (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. Cabozantinib induces PUMA-dependent apoptosis in colon cancer cells via AKT/GSK-3β/NF-κB signaling pathway.	Clin Cancer Res, 2021, 27(9):2533-2548 Cancers (Basel), 2021, 13(3)E372 Cancers (Basel), 2021, 13(14)3635	Effects of AXL inhibitors on induction of pAKT and rescue of pERK following AXL overexpression. R428, 500 nmol/L; XL184, 3 umol/L; XL880, 100 nmol/L; in the presence or absence of 2 umol/L PLX4720. shAXL is a positive control.
S1111	Foretinib (GSK1363089) Foretinib (GSK1363089, EXEL-2880, XL-880, GSK089) is an ATP-competitive inhibitor of HGFR and VEGFR, mostly for Met (c-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 (c-Kit), PDGFRα/β and Tie-2, and little activity to FGFR1 and EGFR. Phase 2.	Cancers (Basel), 2021, 13(3)E372 Mol Carcinog, 2021, 60(7):481-496 Hum Cell, 2021, 10.1007/s13577-021-00579-z	c-MET/RON inhibitors restore sensitivity to lapatinib in SK-BR-3-LR cells. Cell growth was determined using the sulforhodamine B assay. The concentration used was 0.1 uM for crizotinib, MGCD-265, XL880, sunitinib, dasatinib, and TAE-684I. The phosphorylation of HER2, AKT and ERK1/2 was determined by Western blotting.
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.	Cancers (Basel), 2021, 13(16)4133 Oncogenesis, 2021, 10(3):25 Sci Rep, 2021, 11(1):5468	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 (PKI-SU11274) is a selective Met (c-Met) inhibitor with IC50 of 10 nM in cell-free assays, no effects on PGDFRβ, EGFR or Tie2. SU11274 induces autophagy, apoptosis and cell cycle arrest.	Cell Chem Biol, 2021, S2451-9456(21)00303-2 J Orthop Translat, 2021, 27:9-16 J Biol Chem, 2020, 23 pii: jbc	Effect of crizotinib, tivantinib, and SU11274 on levels of c-MET phosphorylation and downstream signaling pathway in SW1736 and TL3 thyroid cancer cells. Cells were prestarved in culture medium containing 0.5% FBS (24 hour) ?either crizotinib or tivantinib (0.1, 1.0, and 10 umol/L) or SU11274 (10 umol/L), and stimulated with 20 ng/mL recombinant human HGF for 10 minutes before lysates were made for Western blotting. A series of c-MET downstream signaling pathway proteins and phosphor proteins were detected using Western blotting. β-Actin was used as a loading balance control.
S9620^新	TPX-0022 TPX-0022 (CSF1R-IN-2) is a potent inhibitor of MET/CSF1R/SRC with enzymatic kinase inhibition IC50s of 0.14 nM, 0.71 nM and 0.12 nM, respectively. TPX-0022 modulates the tumor immune microenvironment in preclinical models.
S5190^新	Crizotinib hydrochloride Crizotinib (PF-02341066) hydrochloride (Xalkori) inhibits tyrosine phosphorylation of c-Met and nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK) with IC50 of of 11 nM and 24 nM in cell-based assays, respectively. Crizotinib hydrochloride is also a potent ROS1 inhibitor with Ki less than 0.025 nM. Crizotinib induces autophagy through inhibition of the STAT3 pathway in multiple lung cancer cell lines.	Nat Commun, 2021, 12(1):5006 Cancer Lett, 2021, 522:119-128 Mol Cancer Ther, 2021, molcanther.0965.2020
S0361^新	AMG-1 AMG-1 (c-Met/RON Dual Kinase Inhibitor, RON-IN-1) is a potent inhibitor of human c-Met and RON with IC50 of 4 nM and 9 nM, respectively.
S6899^新	Licochalcone D Licochalcone D (Lico D, LCD, LD), a flavonoid isolated from a Chinese medicinal plant Glycyrrhiza inflata, has antioxidant, anti-inflammatory and anti-cancer properties. Licochalcone D inhibit phosphorylation of NF-κB p65 in LPS signaling pathway. Licochalcone D inhibits JAK2, EGFR and MET activities and induces ROS-dependent apoptosis. Licochalcone D also induces caspases activation and poly (ADP-ribose) polymerase (PARP) cleavage.
S1112	SGX-523 SGX-523 is a selective Met (c-Met) inhibitor with IC50 of 4 nM, no activity to BRAFV599E, c-Raf, Abl and p38α. Phase 1.	J Pathol, 2020, 250(2):205-216 Acta Pharmacol Sin, 2020, 10.1038/s41401-019-0336-3 Neurooncol Adv, 2020, 2(1):vdaa067	Association of c-Met phosphorylation and s-Met generation in EBC-1 xenograft tumor. Mice were treated with SGX523 at 10 mg/kg, 3 mg/kg, 0.1 mg/kg, at 0 h and 8 h point, respectively. Plasma and tumor lysates were collected using the method described in "Materials and methods"section at 24 h time point. The bar and line in the figure represents the average phosphorylation rate of c-Met and s-Met in subgroups, respectively. Each subgroup consists of four mice with tumor volume around 600 mm³.
S1561	BMS-777607 BMS-777607 (BMS 817378) 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.	Oncogene, 2021, 10.1038/s41388-021-01869-4 J Cell Mol Med, 2021, 10.1111/jcmm.16261 Cell Metab, 2020, 4;31(2):406-421 e7	Numbers of clonogenic cells from L3.6pl cells and CSCs^＋24/44/ESAin duplicate were counted. Clonogenic growth from the cell control was set as 100%.
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. Tivantinib (ARQ 197) induces a G2/M arrest and apoptosis. Phase 3.	Eur J Pharmacol, 2021, 906:174214 Hum Cell, 2021, 10.1007/s13577-021-00579-z Oncotarget, 2021, 12(7):674-685	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.	Oncogenesis, 2021, 10(3):25 Acta Biochim Biophys Sin (Shanghai), 2021, gmab026 Angiogenesis, 2021, 10.1007/s10456-021-09771-z	(B) RPE50 cells were untreated (-), treated with 50 nM of HGF or EGF or 50 ng/ml HB-EGF coupled with DMSO or various inhibitors as indicated for 0.5 h.
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.	Cell Chem Biol, 2019, 10.1016/j.chembiol.2019.06.003 Neoplasia, 2019, 22(1):1-9 Sci Rep, 2019, 9(1):606	Clonogenicity of LXFA 526L and LXFA 1647L with titration of the MET inhibitor PF-04217903 and combination of PF-04217903 at 0.1 uM with 0.66 uM cetuximab.
S1244	Amuvatinib (MP-470) Amuvatinib (MP-470, HPK 56) is a potent and multi-targeted inhibitor of c-Kit, PDGFRα and Flt3 with IC50 of 10 nM, 40 nM and 81 nM, respectively. Amuvatinib suppresses c-MET and c-RET. Amuvatinib is also active as a DNA repair protein Rad51 inhibitor with antineoplastic activity. Phase 2.	Hum Cell, 2021, 10.1007/s13577-021-00579-z Hum Cell, 2020, 10.1007/s13577-020-00420-z PLoS Genet, 2016, 12(9):e1006279	Inactivation of AXL by MP470 reverses epithelial to mesenchymal transition. Immunoblot analyses of lysates from TGFβ/TNFα- treated MCF10A cells treated with varying amounts of MP470 for 72 hours.
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.	Elife, 2019, 8e47460 Protein Cell, 2019, 10(3):161-177 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, INC280, NVP-INC280) 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. Capmatinib (INCB28060) inhibits Wnt/β-catenin and EMT signaling pathways and induces apoptosis in diffuse gastric cancer positive for c-MET amplification. Phase 1.	Cancer Lett, 2021, 519:328-342 Cancer Lett, 2021, 512:51-59 Cancers (Basel), 2021, 13(3)E372	(a) MET inhibition by INCB28060 prevents HGF-induced MET phosphorylation in MDA-MB231 and HCC-1954 cells. After one hour preincubation with INC2B8060, BC cells were stimulated with HGF for one hour. Phosphorylation of MET and total MET were determined by western blot and quantified by densitometric analysis. Results are expressed as percentage of unstimulated and untreated cells (negative control).
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 (c-Met), Aurora A/B, TrkA/B and Ron, and shows little activity to Flt3, Lck, MK2, PKA, PKC etc. Phase 2.	Front Oncol, 2021, 11:650052 Life Sci, 2021, 267:118977 Sci China Life Sci, 2021, 10.1007/s11427-020-1836-7
S2201	BMS-794833 BMS-794833 is a potent ATP competitive inhibitor of Met (c-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 dual c-Met and RON inhibitor with IC50 of 9 nM for c-Met.
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 Carcinog, 2021, 60(7):481-496 G3 (Bethesda), 2021, 11(10)jkab265 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.
S4001	Cabozantinib malate (XL184) Cabozantinib malate (XL184) is the malate of Cabozantinib, a potent VEGFR2 inhibitor with IC50 of 0.035 nM and also inhibits c-Met, Ret (c-Ret), Kit (c-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. Cabozantinib malate (XL184) induces apoptosis.	Clin Cancer Res, 2021, 27(9):2533-2548 Cancers (Basel), 2021, 13(14)3635 J Clin Endocrinol Metab, 2021, dgab020	Effects of AXL inhibitors on induction of pAKT and rescue of pERK following AXL overexpression. R428, 500 nmol/L; XL184, 3 umol/L; XL880, 100 nmol/L; in the presence or absence of 2 umol/L PLX4720. shAXL is a positive 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, 2020, 111(10):3813-3823 Nephron, 2020, 1-12 Cell, 2019, 178(6):1478-1492	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 (c-Met) inhibitor with IC50 of 14 nM.	PLoS Biol, 2021, 19(5):e3001263
S7067	Tepotinib (EMD 1214063) Tepotinib (EMD 1214063, MSC2156119) is a potent and selective c-Met inhibitor with IC50 of 4 nM, >200-fold selective for c-Met than IRAK4, TrkA, Axl, IRAK1, and Mer. Tepotinib (EMD 1214063) induces autophagy. Phase 1.	Transl Lung Cancer Res, 2020, 9(5):1810-1821 Int J Mol Sci, 2020, 21(21)E7905 CU Digital Repository, 2020, N/A	Ectopic expression of a RNAi-resistant SMARCE1 cDNA resensitizes SMARCE1-knockdown cells to MET inhibition in MET-amplified NSCLC cells. The above-described cells were grown in the absence or presence of 300 nM Crizotinib, 150 nM EMD1214063, or 150 nM PHA665752. Cells were then fixed, stained and photographed after 12 days (untreated) or 28 days (treated).
S8167	AMG 337 AMG 337 is an oral, small molecule, ATP-competitive, highly selective inhibitor of the Met (c-Met) receptor with an IC50 of 1 nM.	Cancer Cell, 2019, 36(1):35-50
S7014	Merestinib (LY2801653) Merestinib (LY2801653) is a type-II ATP competitive, slow-off inhibitor of Met (c-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. Merestinib (LY2801653) also inhibits MST1R, AXL, ROS1, MKNK1/2, FLT3, MERTK, DDR1 and DDR2 with IC50 of 11 nM, 2 nM, 23 nM, 7 nM, 7 nM, 10 nM, 0.1 nM and 7 nM, respectively.	J Clin Invest, 2021, 131(11)146987 Front Oncol, 2020, 12;10:700 Cancer Commun (Lond), 2020, 11
S0540	BAY-474 BAY-474 is an inhibitor of tyrosine-protein kinase c-Met and can act as an epigenetics probe.
S8570	RXDX-106 (CEP-40783) RXDX-106 (CEP-40783) is an orally-available, potent and selective TAM(TYRO3, AXL, MER)/Met (c-Met) inhibitor displaying low nanomolar biochemical activity and slow (T1/2 >120 min) inhibitor off-rate in peptide phosphorylation assays and in vitro kinase binding assays, respectively.	Clin Cancer Res, 2021, 27(9):2533-2548 J Clin Invest, 2018, 128(11):5034-5055
S8854	JNJ-38877618(OMO-1) JNJ-38877618 (OMO-1) is a potent, highly selective, orally bioavailable Met (c-Met) kinase inhibitor with binding affinity (Kd) of 1.4 nM and enzyme inhibitory activity against wt and M1268T mutant Met (c-Met) (2 and 3 nM IC50).
S8404	S49076 S49076 is a novel, potent inhibitor of Met (c-Met), AXL/MER, and FGFR1/2/3 with IC50 values below 20 nmol/L.	Mol Brain, 2020, 4;13(1):66
S9308	Pulsatilla saponin D Pulsatilla saponin D (SB365), isolated from the root of Pulsatilla koreana, targets c-Met and exerts antiangiogenic and antitumor activities.
S6870	Ningetinib Ningetinib (CT-053, DE-120, CT053PTSA) is a potent, orally bioavailable inhibitor of tyrosine kinase with IC50 of 6.7 nM, 1.9 nM and <1.0 nM for c-Met, VEGFR2 and Axl, respectively. Ningetinib exhibits antitumor activity.
S6762	Bozitinib (PLB-1001) Bozitinib (PLB-1001, CBT-101, APL-101, CBI-3103) is a highly selective ATP-competitive c-Met inhibitor with blood-brain barrier permeability. Bozitinib (PLB-1001) selectively inhibits MET-altered tumor cells in preclinical models.
S9662	UNC2025 UNC2025 is a potent and orally active dual inhibitor of FLT3 and MER with IC50 of 0.35 nM and 0.46 nM, respectively. UNC2025 also inhibits AXL, TRKA, TRKC, QIK, TYRO3, SLK, NuaK1, Kit (c-Kit) and Met (c-Met) with IC50 of 1.65 nM, 1.67 nM, 4.38 nM, 5.75 nM, 5.83 nM, 6.14 nM, 7.97 nM, 8.18 nM and 364 nM, respectively.	Front Immunol, 2020, 11:564133 Cell Signal, 2014, 26(1):149-61
S7564	SAR125844 SAR125844 is a potent intravenously active and highly selective Met (c-Met) kinase inhibitor, displaying nanomolar activity against the wild-type kinase (IC50 value of 4.2 nmol/L) and H1094Y, Y1235D, M1250T, L1195V, and D1228H kinase domain mutants (IC50 values of 0.22, 1.7, 6.5, 65, and 81 nmol/L, respectively).
S3759	Norcantharidin Norcantharidin (Endothall anhydride) is a synthetic anticancer compound which is a dual inhibitor for c-Met and EGFR in human colon cancers.
S6412	Altiratinib Altiratinib (DCC-2701) is a potent single-digit nanomolar inhibitor of TRK, Met (c-Met), TIE2, and VEGFR2 kinases with IC50 vaules of 0.9 nM, 4.6 nM, and 0.8 nM for TRKA, B, and C, respectively. It inhibits Met (c-Met) and Met (c-Met) mutant with IC50 values in the range of 0.3-6 nM.
S7669	NPS-1034 NPS-1034 is a dual Met (c-Met)/Axl inhibitor with IC50 of 48 nM and 10.3 nM, respectively.	J Med Chem, 2021, 64(6):3165-3184
S8676	Glumetinib (SCC244) Glumetinib (SCC244) is a potent and highly selective c-Met inhibitor with an IC50 of 0.42 ± 0.02 nmol/L. Glumetinib has greater than 2,400-fold selectivity for c-Met over those 312 kinases evaluated, including the c-Met family member RON and highly homologous kinases Axl, Mer, and TyrO3.
S7674	Savolitinib (AZD6094) 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.	Phytomedicine, 2021, 80:153355 J Exp Clin Cancer Res, 2021, 40(1):69 Nature, 2020, 580(7801):136-141

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S5115	Sodium L-ascorbyl-2-phosphate Sodium L-ascorbyl-2-phosphate (Sodium ascorbyl monophosphate, Sodium ascorbyl phosphate, SAP) is specifically produced for use as a stabilized source of vitamin C in cosmetic products. It is used in skin care recipes for UV protection, collagen production, as an antioxidant and for its skin lightening and brightening effects.	Stem Cell Res Ther, 2021, 12(1):48

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S5115

Sodium L-ascorbyl-2-phosphate

Sodium L-ascorbyl-2-phosphate (Sodium ascorbyl monophosphate, Sodium ascorbyl phosphate, SAP) is specifically produced for use as a stabilized source of vitamin C in cosmetic products. It is used in skin care recipes for UV protection, collagen production, as an antioxidant and for its skin lightening and brightening effects.

Stem Cell Res Ther, 2021, 12(1):48

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c-Met

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c-Met製品