Population pharmacokinetics of cabazitaxel in patients with advanced solid tumors
Cancer Chemotherapy and Pharmacology, ISSN: 0344-5704, Vol: 71, Issue: 3, Page: 681-692
2013
- 39Citations
- 41Captures
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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.
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Metrics Details
- Citations39
- Citation Indexes39
- 39
- CrossRef24
- Captures41
- Readers41
- 41
Article Description
Purpose: To develop a population pharmacokinetic (PK) model for cabazitaxel in patients with advanced solid tumors and examine the influence of demographic and baseline parameters. Methods: One hundred and seventy patients who received cabazitaxel (10-30 mg/m, 1-h IV infusion) every 7 or 21 days in five Phase I-III studies were analyzed by non-linear mixed-effect modeling (NONMEM VI). Model evaluation comprised non-parametric bootstrap and visual predictive checks. Results: Cabazitaxel PK was best described by a linear three-compartment model with: first-order elimination; interindividual variability on clearance (CL), central volume of distribution (V1), and all intercompartmental rate constants except K21; interoccasion variability in CL and V1; proportional residual error of 27.8 %. Cabazitaxel CL was related to body surface area (BSA) and tumor type (breast cancer; finding confounded by study). Typical CL for a non-breast cancer patient with a BSA of 1.84 m was 48.5 L/h, with V1 26.0 L, steady-state volume of distribution 4,870 L and alpha, beta, and gamma half-lives of 4.4 min, 1.6, and 95 h, respectively. Sex, height, weight, age, Caucasian race, renal/hepatic function, and cytochrome P450 inducer use did not significantly further explain the PK of cabazitaxel. Bootstrap and posterior predictive checks confirmed the adequacy of the model. Conclusions: Cabazitaxel PK appears unaffected by most baseline patient factors, and the influence of BSA on CL is addressed in practice by BSA-dependent doses. This analysis suggests consistent cabazitaxel PK and exposure across most solid tumor types, although the potential influence of breast cancer on CL requires further confirmation. © 2013 The Author(s).
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84875863196&origin=inward; http://dx.doi.org/10.1007/s00280-012-2058-9; http://www.ncbi.nlm.nih.gov/pubmed/23299792; http://link.springer.com/10.1007/s00280-012-2058-9; https://dx.doi.org/10.1007/s00280-012-2058-9; https://link.springer.com/article/10.1007/s00280-012-2058-9
Springer Nature
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