ALK
Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase (RTK) that was first identified in anaplastic large cell lymphoma (ALCL) as part of the fusion protein NPM-ALK. ALK has been implicated in the pathogenesis of many types of cancer.
ALK Inhibitors |
|
|---|---|
| Cat. No. | Product Name / Activity |
| 5310 | ASP 3026 |
| Potent anaplastic lymphoma kinase (ALK) inhibitor; also potent ACK inhibitor | |
| 6905 | Ceritinib |
| Highly potent ALK inhibitor; also potently inhibits IR, IGF1R, STK22D and FLT3 | |
| 4368 | Crizotinib |
| Potent c-MET/ALK inhibitor | |
| 5111 | GSK 1838705 |
| Potent ALK inhibitor; also IR and IGF1R inhibitor | |
| 5098 | KRCA 0008 |
| Potent Ack1 and ALK dual inhibitor; orally bioavailable | |
| 1614 | SB 431542 |
| Potent, selective inhibitor of TGF-βRI, ALK4 and ALK7 | |
| 3263 | SB 505124 |
| Selective inhibitor of TGF-βRI, ALK4 and ALK7 | |
Degraders |
|
| Cat. No. | Product Name / Activity |
| 6745 | TL 13-112 |
| Selective ALK Degrader | |
| 6744 | TL 13-12 |
| Selective ALK Degrader | |
Controls |
|
| Cat. No. | Product Name / Activity |
| 6746 | TL 13-110 |
| Negative control for TL 13-112 (Cat. No. 6745) | |
| 6747 | TL 13-22 |
| Negative control for TL 13-12 (Cat. No. 6744) | |
Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase (RTK) that was first identified in anaplastic large cell lymphoma (ALCL) as part of the fusion protein NPM-ALK. ALK is highly expressed throughout the central and peripheral nervous system during development, with levels decreasing following gestation. Low levels of ALK protein are however, expressed in the adult CNS, whilst ALK transcripts have also been identified in the periphery.
The physiological role of ALK has yet to be determined, although due to its expression profile it has been postulated to be involved in neuronal differentiation. ALK has two putative endogenous ligands, midkine (MK) and leiotrophin (PTN), which have both been implicated in neurite growth and have similar expression profiles to ALK. Ligand binding to ALK initiates homodimerization and autophosphorylation of the three tyrosine residues within the kinase domain, which results in tyrosine kinase activation. Downstream effectors of ALK tyrosine kinase activity have been shown to include the Ras-ERK, PI 3-K-Akt, JAK-STAT and NF-κB signaling pathways. In the absence of ligand binding ALK is inactive, with its expression promoting apoptosis. Conversely, when ALK is activated through either ligand binding or as part of an ALK fusion protein, apoptosis is decreased.
The expression of many ALK fusion oncogenes have been implicated in the pathogenesis of many types of cancer. Examples include NPM-ALK, EML4-ALK and CLTLC-ALK which have been described in ALCL, non-small cell lung cancer (NSCLC) and diffuse large B cell lymphoma (DLBCL) respectively. ALK fusion proteins consist of a C-terminus composed of the intracellular tyrosine kinase domain of ALK and an N-terminus derived from the partner protein. The partner protein has been shown to induce constitutive kinase activation by mediating ALK dimerization. ALK is also involved in oncogenesis through overexpression and gain-of-function mutations. ALK is overexpressed in NSCLC, melanoma and certain types of breast cancer, amongst others, whilst point mutations in the ALK kinase domain have been implicated in neuroblastoma development.
External sources of pharmacological information for ALK :
Literature for ALK
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