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 |
|---|---|---|---|---|
|
V69256 | Alectinib-d8 (CH5424802-d8; RO5424802-d8; AF802-d8) | 1256585-15-5 | Alectinib-d8 is the deuterated form of Alectinib. |
|
V69260 | ALK-IN-12 | 1197958-53-4 | ALK-IN-12 is a potent and orally bioactive ALK inhibitor (antagonist) with IC50 of 0.18 nM. |
|
V69264 | ALK-IN-13 | 1197953-88-0 | ALK-IN-13 is an ALK inhibitor from patent US20130225528A1, example 19. |
|
V69265 | ALK-IN-21 | 2901889-01-6 | ALK-IN-21 (Compound B10) is a potent ALK inhibitor (antagonist) with IC50s of 4.59 nM, 2.07 nM and 5.95 nM for ALKWT, ALKL1196M and ALKG1202R respectively. |
|
V69247 | ALK-IN-27 | 2739866-40-9 | ALK-IN-27 (compound 1) is a potent ALK inhibitor. |
|
V87981 | ALK-IN-27 TFA | ALK-IN-27 TFA is the TFA salt form of ALK-IN-27. | |
|
V69257 | ALK-IN-5 | 2351929-66-1 | ALK-IN-5 is a selective, brain barrier-permeable/penetrable (ALK) kinase inhibitor (antagonist) with IC50 of 2.9 nM. |
|
V69258 | ALK-IN-9 | 2359662-39-6 | ALK-IN-9 (compound 40) is a potent ALK inhibitor. |
|
V69262 | ALK/EGFR-IN-2 | 2730432-75-2 | ALK/EGFR-IN-2 is a potent dual (bifunctional) inhibitor of ALK and EGFR. |
|
V69259 | ALK/EGFR-IN-3 | 2730432-72-9 | ALK/EGFR-IN-3 is a dual (bifunctional) inhibitor of ALK and EGFR. |
|
V85845 | ALK/ROS1-IN-3 | ||
|
V85477 | ALK/ROS1-IN-4 | 2649878-59-9 | |
|
V85468 | ALK/ROS1-IN-4 hydrate | ||
|
V69268 | ALK2-IN-5 | 2414149-20-3 | ALK2-IN-5 is a pyrazolopyrimidine compound and an ALK2 inhibitor. |
|
V87984 | ALK5-IN-79 | 2725056-38-0 | ALK5-IN-79 (compound 57) is an ALK inhibitor with anticancer activity by blocking the TGF-β1/SMAD signaling pathway. |
|
V86154 | CEP-28122 mesylate hydrochloride | 1354545-57-5 | |
|
V69255 | CJ-2360 | 2226742-61-4 | CJ-2360 is a potent oral ALK inhibitor (antagonist) with IC50s of 2.2, 4.0, 8.8, 6.3 and 8.9 nM against wild-type ALK and F1197M, G1269A, L1196M and S1206Y ALK mutants, respectively. |
|
V69269 | Con B-1 | 2415537-51-6 | ConB-1 is a selective ALK inhibitor (antagonist) with low toxicity to normal cells. |
|
V69252 | CPD-1224 | 2891620-68-9 | CPD-1224 is an orally bioavailable ALK inhibitor and an ALK inhibitor analogue coupled to cereblon ligand. |
|
V69253 | Envonalkib | 1621519-26-3 | This product is discontinued due to commercial reason. Envonalkib is a potent and orally bioactive ALK inhibitor (antagonist) with IC50s of 1.96 nM, 35.1 nM and 61.3 nM against WT and mutant L1196M and G1269S-ALK, respectively. |
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