The MET receptor, also known as hepatocyte growth factor receptor (HGFR), is a proto-oncogenic receptor tyrosine kinase. The endogenous ligand for MET is hepatocyte growth factor/scatter factor (HGF), a disulfide-linked heterodimeric molecule.
Inhibitors |
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Cat No | Product Name / Activity |
4368 | Crizotinib |
Potent c-MET/ALK inhibitor | |
6056 | GSK 1363089 |
Potent inhibitor of MET, VEGFR2, Ron and AXL | |
1683 | K 252a |
Receptor tyrosine kinase inhibitor, inhibits MET | |
5369 | Norleual |
Highly potent HGF/c-MET inhibitor; also AT4 antagonist | |
4239 | PF 04217903 mesylate |
Highly selective MET inhibitor | |
2693 | PHA 665752 |
Potent and selective MET inhibitor | |
5356 | SGX 523 |
Selective and potent c-MET kinase inhibitor | |
4101 | SU 11274 |
Selective inhibitor of MET kinase activity | |
3037 | SU 5416 |
MET inhibitor. Also inhibits KIT, RET, VEGFR and FLT3 | |
5422 | XL 184 |
Potent c-MET inhibitor; also inhibits other RTKs |
The MET receptor, also known as hepatocyte growth factor receptor (HGFR), is a proto-oncogenic receptor tyrosine kinase. The endogenous ligand for the MET receptor is hepatocyte growth factor/scatter factor (HGF), a disulfide-linked heterodimeric molecule produced predominantly by mesenchymal cells.
In the adult, MET receptor expression is limited to stem and progenitor cells and is necessary for wound healing and hepatocyte regeneration. In the embryo, MET receptors are expressed on cells of epithelial origin. They are essential for invasive growth and mediate epithelial-mesenchymal transition (EMT).
Aberrant activation of the HGF/MET pathway leads to a variety of cancers. MET receptor mutations are associated with poor prognosis as they can trigger tumor growth, angiogenesis and metastasis.
Tocris offers the following scientific literature for MET Receptors to showcase our products. We invite you to request* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.