Abl Kinase
The Abl family of non-receptor tyrosine kinases includes c-Abl (Abelson tyrosine kinase) and Arg (Abl2) subtypes. c-Abl is localized at many subcellular sites including the nucleus, cytoplasm, mitochondria and endoplasmic reticulum, where it interacts with several proteins.
Abl Kinase Inhibitors |
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|---|---|
| Cat. No. | 产品名称/活性 |
| 4274 | AP 24534 |
| Potent multi-kinase and pan-Bcr-Abl inhibitor | |
| 4361 | Bosutinib |
| Dual Src-Abl inhibitor; antiproliferative | |
| 6793 | Dasatinib |
| Highly potent pan-Src/Bcr-Abl inhibitor | |
| 4908 | GNF 5 |
| Selective allosteric inhibitor of Bcr-Abl; analog of GNF 2 (Cat. No. 4399) | |
| 5607 | GNF 7 |
| Potent Abl Kinase inhibitor; also inhibits Ras signaling; GCK and Ack1 | |
| 5906 | Imatinib mesylate |
| Potent and selective v-Abl tyrosine kinase inhibitor; also inhibits PDGFR and c-kit | |
| 3063 | 1-Naphthyl PP1 |
| Inhibitor of c-Abl, v-Src and c-Fyn | |
| 4730 | PPY A |
| Potent inhibitor of Abl T315l mutant and wild-type Abl kinases | |
Degraders |
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| Cat. No. | 产品名称/活性 |
| 7265 | GMB 475 |
| BCR-ABL1 kinase Degrader; inhibits proliferation of CML cells | |
The Abl family of non-receptor tyrosine kinases includes c-Abl (Abelson tyrosine kinase) and Arg (Abl2) subtypes. c-Abl is localized at several subcellular sites including the nucleus, cytoplasm, mitochondria and endoplasmic reticulum, where it interacts with a large variety of cellular proteins including signaling adaptors, kinases, phosphatases, cell cycle regulators, transcription factors and cytoskeletal proteins.
Due to its diverse range of targets, c-Abl has been implicated in many cellular processes including regulation of cell growth and survival, oxidative stress and DNA-damage responses, and actin dynamics and cell migration. The Abl family have significant structural homology to the Src tyrosine kinase family, but have a unique long carboxy-terminal extension that contains protein-protein interaction sites and acts as the binding site for targets such as ATM, p53 and pRb. c-Abl is medically important as there is a causal link between the Abl-Bcr fusion protein (caused by a t(9,22) translocation) and development of chronic myeloid leukemia.