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BIOMARKER:

ALK F1174V

i
Other names: NBLST3, CD246, Anaplastic Lymphoma Kinase, Anaplastic Lymphoma Kinase (Ki-1), CD246 Antigen, Mutant Anaplastic Lymphoma Kinase, ALK, ALK Receptor Tyrosine Kinase, Anaplastic Lymphoma Receptor Tyrosine Kinase, ALK Tyrosine Kinase Receptor
Entrez ID:
10ms
A computational examination of the therapeutic advantages of fourth-generation ALK inhibitors TPX-0131 and repotrectinib over third-generation lorlatinib for NSCLC with ALK F1174C/L/V mutations. (PubMed, Front Mol Biosci)
This comparative study of the potential binding effects of fourth-generation inhibitors TPX-0131 and repotrectinib and third-generation inhibitor LOR for ALK F1174C/L/V mutations revealed the atomistic insights of the binding mechanism. These computational findings enable us to carry out further research for the clinical implementation of fourth-generation ALK inhibitors on ALK-positive NSCLC.
Journal
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ALK (Anaplastic lymphoma kinase)
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ALK positive • ALK rearrangement • ALK mutation • ALK F1174C • ALK F1174V
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Lorbrena (lorlatinib) • Augtyro (repotrectinib) • TPX-0131
over4years
Drug resistance mechanisms in Japanese ALK positive NSCLC and the clinical responses based on the resistant mechanisms. (PubMed, Cancer Sci)
After alectinib failure, G1202R and I1171N mutations were detected in 7 of 15 specimens. G1202R, F1174V and G1202R, and P-gp overexpression were observed in 3 of 7 samples after ceritinib treatment. L1196M + G1202R, a compound mutation, was detected in 1 specimen after lorlatinib treatment...In conclusion, resistance to ALK-TKIs based on secondary mutation in this study was similar to that in previous reports, except for crizotinib resistance. The appropriate treatment matching resistance mechanisms contributes to the efficacy of multiple ALK-TKI treatment strategies.
Clinical • Journal
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ALK (Anaplastic lymphoma kinase)
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ALK G1202R • ALK C1156Y • ALK G1269A • ALK I1171N • ALK I1171T • ALK F1174V • ALK L1196M
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Xalkori (crizotinib) • Alecensa (alectinib) • Lorbrena (lorlatinib) • Zykadia (ceritinib)