Nilotinib: A second-generation tyrosine kinase inhibitor for chronic myeloid leukemia
Leukemia Research, ISSN: 0145-2126, Vol: 34, Issue: 2, Page: 129-134
2010
- 56Citations
- 65Captures
- 6Mentions
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations56
- Citation Indexes56
- 56
- CrossRef31
- Captures65
- Readers65
- 65
- Mentions6
- References5
- Wikipedia5
- Blog Mentions1
- Blog1
Review Description
Imatinib mesylate is currently the standard of care for chronic myeloid leukemia (CML) patients in early chronic phase. However, the emergence of resistance and intolerance has dampened the enthusiasm for this drug. To overcome this phenomenon, different strategies have been developed, including novel targeted agents. Nilotinib, formerly known as AMN107, is a second-generation tyrosine kinase inhibitor 30-fold more potent than imatinib, with high affinity and selectivity on BCR/ABL, and also active against a wide range of mutant clones, except T315I mutation. Phase II trials of nilotinib showed high activity in imatinib-resistant or intolerant CML patients, whereas front-line treatment of the disease in chronic phase demonstrated rapid and stable cytogenetic responses and increasing molecular responses. We here review the development of nilotinib and the efficacy data in phase II and front-line trials. The aim of this review is to evaluate the pharmacology, pharmacokinetic and pharmacodynamic properties of the drug and the recent results of clinical trials performed in patients with CML and Ph+ acute lymphoblastic leukemia (ALL).
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0145212609004408; http://dx.doi.org/10.1016/j.leukres.2009.08.031; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=74849116614&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/19783301; https://linkinghub.elsevier.com/retrieve/pii/S0145212609004408; https://dx.doi.org/10.1016/j.leukres.2009.08.031
Elsevier BV
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