ALK, a member of the insulin receptor superfamily and a receptor tyrosine kinase, is primarily expressed in the brain and is thought to play a role in cognition and neuronal development. Adenosine triphosphate (ATP) and a gamma-phosphate group are transferred via ALK to a tyrosine residue on a substrate protein. As a result, it causes the tyrosine residues in its substrate proteins to phosphorylate. Different enzymes (kinases and phosphatases) catalyze the important protein reactions of phosphorylation and dephosphorylation, which are essential to many cellular processes.
ALK gene activation results from fusion with other oncogenes (NPM, EML4, TIM, etc.) or gene amplification, mutation, or protein overexpression and contributes to the development of several human cancers, including anaplastic large cell lymphoma, lung cancer, inflammatory myofibroblastic tumors, and neuroblastoma. ALK is a transmembrane tyrosine kinase receptor that dimerizes and then autophosphorylates the intracellular kinase domain in response to ligand binding to its extracellular domain. Specific inhibitors, like Crizotinib, Ceritinib, Alectinib, etc., have shown to be highly effective in treating ALK-positive non-small cell lung cancer in particular when it becomes activated in cancer.
| Structure | Cat No. | Product Name | CAS No. | Product Description |
|---|---|---|---|---|
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V69266 | TL13-22 | 2229036-65-9 | TL13-22, a negative control (NC) of TL13-12, is a potent ALK inhibitor (antagonist) with IC50 of 0.54 nM. |
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V18838 | X-376 | 1365267-27-1 | X-376 (an analog ofEnsartinib or X-396) is a novel, potent and highly selectiveALK inhibitor with IC50of 0.61 nM and the potential to be used for treating non-small cell lung cancer. |
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