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Crizotinib acts as ABL1 inhibitor combining ATP-binding with allosteric inhibition and is active against native BCR-ABL1 and its resistance and compound mutants BCR-ABL1(T315I) and BCR-ABL1(T315I-E255K)
Resistance remains the major clinical challenge for the therapy of Philadelphia chromosome–positive (Ph+) leukemia. With the exception of ponatinib, all approved tyrosine kinase inhibitors (TKIs) are unable to inhibit the common “gatekeeper” mutation T315I. Here we investigated the therapeutic poten...
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| Publicat a: | Ann Hematol |
|---|---|
| Autors principals: | , , , , , , , , , , , , |
| Format: | Artigo |
| Idioma: | Inglês |
| Publicat: |
Springer Berlin Heidelberg
2021
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| Matèries: | |
| Accés en línia: | https://ncbi.nlm.nih.gov/pmc/articles/PMC8285356/ https://ncbi.nlm.nih.gov/pubmed/34110462 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1007/s00277-020-04357-z |
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