Nilotinib

Tyrosine kinase inhibitors

MECHANISM OF ACTION

Cellular TKI that targets BCR-ABL kinase. Hepatic metabolism

MECHANISM OF KIDNEY INJURY

Water/electrolyte disturbances

CLINICAL KIDNEY SYNDROME

Hypertension, Cardiac arrhythmia

CARDIOVASCULAR ADVERSE EFFECTS

Prolongation of the QT interval, myocardial ischemia -- https://doi.org/10.1182/blood.V110.11.735.735 and PMID: 26837842

LYTE ABNORMALITIES

Hyperkalemia, Hypocalcemia, Hypokalemia

RISK FACTORS

MITIGATION STRATEGIES

Unclear if it truly causes kidney injury, likely less so than other TKI/VEGF

SUGGESTIONS

Check urine analysis for cyrstals, WBC, RBC, etc, Confirm electrolyte derangement and address as needed.

NOTES/COMMENTS

98%

PHARMACOKINETICS

Molecular Weight

529.5245 g/mol

Volume of Distribution

579 L

Plasma Protein Binding

Metabolism

Hepatic; oxidation and hydroxylation, via CYP3A4 to inactive metabolites

Bioavailability

50%; increased to 82% when administered 30 minutes after a high-fat meal

Half-life elimination

17 hours

Time to peak

3 hours

Excretion

Feces (93%; 69% as parent drug)

Dialyzable?

REF:

PMID: 34976304
https://www.lumc.nl/sub/4010/att/1683422/1896506

PATHOLOGY SLIDES:

ENTRY UPDATES:

Raad Chowdhury

MN/USA

Sep 25, 2022

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