c-Met is a receptor for HGF (Hepatocyte growth factor) which is essential during many biological processes. The HGF / MET pathway is an excellent target for anti-cancer therapies. Activation of MET results in the recruitment of scaffolding proteins like Gab1 and Grb2, leading to the recruitment of SH2-domain containing signal transducers that in turn activate a number of pathways, like MAPK or PI3K. Branching morphogenesis, the most complex biological response induced by Met requires all signaling pathways and targets including MAPK, Gab1, Grb2, PI3K, Shp2, SH2 (Src-homology-2), Sos (son-of-sevenless), and PLC (phospholipase C).
c-Met inhibitors
| Cat.No. | Product Name | Information | Product Use Citations | Product Validations |
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| S7067 | Tepotinib | Tepotinib 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. This compound induces autophagy. Phase 1. |
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| E4606 | Dihexa | Dihexa (PNB-0408), an oligopeptide drug, is an orally active and blood-brain barrier-permeable analogue of angiotensin IV. It binds to hepatocyte growth factor (HGF) with high affinity and potentiates its activity at its receptor, c-Met. This compound can also be used as a therapeutic potential in the treatment of Alzheimer’s disease. | ||
| 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. This compound 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. |
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| S1119 | Cabozantinib (XL184) | A potent VEGFR2 inhibitor with IC50 of 0.035 nM, Cabozantinib (XL184) 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. It induces PUMA-dependent apoptosis in colon cancer cells via AKT/GSK-3β/NF-κB signalling pathway. |
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| S1068 | PF-02341066 (Crizotinib) | Crizotinib 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. |
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| 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. |
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| 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. |
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| S1111 | Foretinib | Foretinib 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. |
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| S2788 | Capmatinib (INC280) | Capmatinib 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 signalling pathways and induces apoptosis in diffuse gastric cancer positive for c-MET amplification. Phase 1. |
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| 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. This compound induces autophagy, apoptosis and cell cycle arrest. |
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