Matthijs M. Tibben

The Netherlands Cancer Institute

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Jos H. Beijnen

The Netherlands Cancer Institute

Hilde Rosing

The Netherlands Cancer Institute

Jan H.M. Schellens

The Netherlands Cancer Institute

Alwin D. R. Huitema

Princess Máxima Center

Alfred H. Schinkel

The Netherlands Cancer Institute

L. van Andel

The Netherlands Cancer Institute

Maria C. Lebre

The Netherlands Cancer Institute

A. Gebretensae

The Netherlands Cancer Institute

Sjoerd Rodenhuis

The Netherlands Cancer Institute

Nancy H.C. Loos

The Netherlands Cancer Institute

Cooperative Institutions

The Netherlands Cancer Institute

108

Oncode Institute

Slotervaartziekenhuis

Utrecht University

University Medical Center Utrecht

PharmaMar (Spain)

Dutch Cancer Society

Erasmus MC

Academic Medical Center

Amsterdam University Medical Centers

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Inductively coupled plasma mass spectrometric analysis of the total amount of platinum in DNA extracts from peripheral blood mononuclear cells and tissue from patients treated with cisplatin

Analytical and Bioanalytical Chemistry (2008)

E. E. M. Brouwers Matthijs M. Tibben Dick Pluim Hilde Rosing Henk Boot

10.1007/s00216-008-2034-8

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Citations (48)

Simultaneous quantification of abemaciclib and its active metabolites in human and mouse plasma by UHPLC–MS/MS

Journal of Pharmaceutical and Biomedical Analysis (2021)

Alejandra Martínez-Chávez Matthijs M. Tibben Karen A.M. de Jong Hilde Rosing Alfred H. Schinkel

Abemaciclib is the third cyclin-dependent kinase 4 and 6 inhibitor approved for the treatment of advanced or metastatic breast cancer. In humans, abemaciclib is extensively metabolized by CYP3A4 with the formation of three active metabolites: N-desethylabemaciclib (M2), hydroxyabemaciclib (M20) and hydroxy-N-desethylabemaciclib (M18). These metabolites showed similar potency compared to the parent drug and were significantly abundant in plasma circulation. Thus, M2, M20, and M18 may contribute to the clinical activity of abemaciclib. For this reason, an UHPLC–MS/MS method for the simultaneous quantification of abemaciclib and its active metabolites in human and mouse plasma was developed and validated to support further clinical or preclinical investigations on this drug. Samples were processed by protein precipitation with acetonitrile, followed by supernatant dilution and filtration. Chromatographic separation was performed on a Kinetex C18 column (150 × 2.1 mm ID, 2.6 μm) using gradient elution with 10 mM ammonium bicarbonate in water (eluent A) and in methanol-water (9:1, v/v, eluent B). This method was selective, linear, accurate and precise within the range of 1−600 ng/mL for abemaciclib, 0.5−300 ng/mL for M2 and M20, and 0.2−120 ng/mL for M18. Furthermore, stability of the analytes in human and mouse plasma samples in several conditions was demonstrated. Finally, this assay was successfully used in a preclinical pharmacokinetic study, where abemaciclib and its active metabolites were identified and quantified. Inter-species differences between human and mouse samples were encountered, especially in the formation of M20, where isomers of this compound were detected in mouse plasma, but not in human plasma. This was confirmed by high resolution-mass spectrometry (HR-MS) measurements.

Protein precipitation

Active metabolite

10.1016/j.jpba.2021.114225

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Citations (19)

Sensitive gas chromatographic determination of the cyclophosphamide metabolite 2-dechloroethylcyclophosphamide in human plasma

Journal of Chromatography B Biomedical Sciences and Applications (2001)

Alwin D. R. Huitema Cindy Reinders Matthijs M. Tibben Sjoerd Rodenhuis Jos H. Beijnen

Bioanalysis

Solid phase extraction

Sample Preparation

10.1016/s0378-4347(01)00178-5

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Citations (10)

Mechanism of the Pharmacokinetic Interaction between Methotrexate and Benzimidazoles

Cancer Research (2004)

Pauline Breedveld Noam Zelcer Dick Pluim Özgür Sönmezer Matthijs M. Tibben

The antifolate drug methotrexate (MTX) is transported by breast cancer resistance protein (BCRP; ABCG2) and multidrug resistance-associated protein1-4 (MRP1-4; ABCC1-4). In cancer patients, coadministration of benzimidazoles and MTX can result in profound MTX-induced toxicity coinciding with an increase in the serum concentrations of MTX and its main metabolite 7-hydroxymethotrexate. We hypothesized that benzimidazoles interfere with the clearance of MTX and/or 7-hydroxymethotrexate by inhibition of the ATP-binding cassette drug transporters BCRP and/or MRP2, two transporters known to transport MTX and located in apical membranes of epithelia involved in drug disposition. First, we investigated the mechanism of interaction between benzimidazoles (pantoprazole and omeprazole) and MTX in vitro in membrane vesicles from Sf9 cells infected with a baculovirus containing human BCRP or human MRP2 cDNA. In Sf9-BCRP vesicles, pantoprazole and omeprazole inhibited MTX transport (IC50 13 microm and 36 microm, respectively). In Sf9-MRP2 vesicles, pantoprazole did not inhibit MTX transport and at high concentrations (1 mm), it even stimulated MTX transport 1.6-fold. Secondly, we studied the transport of pantoprazole in MDCKII monolayers transfected with mouse Bcrp1 or human MRP2. Pantoprazole was actively transported by Bcrp1 but not by MRP2. Finally, the mechanism of the interaction was studied in vivo using Bcrp1-/- mice and wild-type mice. Both in wild-type mice pretreated with pantoprazole to inhibit Bcrp1 and in Bcrp1-/- mice that lack Bcrp1, the clearance of i.v. MTX was decreased significantly 1.8- to 1.9-fold compared with the clearance of i.v. MTX in wild-type mice. The conclusion is as follows: benzimidazoles differentially affect transport of MTX mediated by BCRP and MRP2. Competition for BCRP may explain the clinical interaction between MTX and benzimidazoles.

Abcg2

Pantoprazole

ABCC1

Antifolate

Fexofenadine

10.1158/0008-5472.can-03-4062

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Citations (230)

A mechanism-based pharmacokinetic model for the cytochrome P450 drug-drug interaction between cyclophosphamide and thioTEPA and the autoinduction of cyclophosphamide.

Journal of Pharmacokinetics and Pharmacodynamics (2001)

Alwin D. R. Huitema Ron A. A. Mathôt Matthijs M. Tibben Sjoerd Rodenhuis Jos H. Beijnen

ThioTEPA

Active metabolite

Carboplatin

10.1023/a:1011543508731

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Citations (46)

Development and validation of a liquid chromatography-tandem mass spectrometry assay for the quantification of lurbinectedin in human plasma and urine

Journal of Pharmaceutical and Biomedical Analysis (2018)

L. van Andel Hilde Rosing Rubin Lubomirov Pablo Avilés Salvador Fudio

10.1016/j.jpba.2018.05.053

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Citations (4)

Validation of a Therapeutic Drug Monitoring Strategy for Thiotepa in a High-Dose Chemotherapy Regimen

Therapeutic Drug Monitoring (2001)

Alwin D. R. Huitema Ron A. A. Mathôt Matthijs M. Tibben Sjoerd Rodenhuis Jos H. Beijnen

Thiotepa is an alkylating agent widely used in high-dose chemotherapy. The pharmacokinetics of thiotepa and its main metabolite tepa show a wide interpatient variability, which may be responsible for the interpatient variability in toxicity. The aim of this study was to develop and validate a pharmacokinetically guided dosing strategy with the sum of the thiotepa and tepa area under the concentration-time curve (AUC) as the target parameter. A total of 46 patients received 77 courses of chemotherapy with thiotepa (80–120 mg/m 2 per day) divided into two daily 30-minute infusions in combination with cyclophosphamide and carboplatin. Patients received up to three courses of chemotherapy. The interpatient, course-to-course, day-to-day, and residual variability in the pharmacokinetics of thiotepa and tepa were estimated with a population analysis with the software program NONMEM. The planned strategy consisted of the collection of blood samples on day 1 and either day 3 or day 4 of each 4-day course. The thiotepa dose was planned to be adjusted on day 3 of each course and before the start of a new course on the basis of Bayesian predictions of the pharmacokinetics with data of day 1 and/or the possible previous course. The prediction procedure was validated by dividing the dataset into an index and validation set. The Bayesian predictions of the validation set were compared with true AUC values generated with individual fits of each course. The performance of the complete strategy was tested with a simulation procedure in 1,000 patients. Interpatient variability and course-to-course variability were in the same order (±20%); day-to-day variability was less (±15%). The sampling strategy resulted in predictions of the AUC without bias with acceptable precision (±20%). The simulation showed that variability in exposure was effectively decreased by the dosing strategy. This strategy resulted in a reduction in the variability of the exposure to thiotepa and tepa and can be implemented in a clinical study.

ThioTEPA

Carboplatin

Regimen

Therapeutic Drug Monitoring

NONMEM

10.1097/00007691-200112000-00010

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Citations (11)

Validated method for the determination of the novel organo-ruthenium anticancer drug NAMI-A in human biological fluids by Zeeman atomic absorption spectrometry

Fresenius Journal of Analytical Chemistry (2001)

Mirjam Crul H.J.G.D. van den Bongard Matthijs M. Tibben Olaf van Tellingen Gianni Sava

Matrix (chemical analysis)

Sample Preparation

10.1007/s002160000662

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Citations (19)

Overestimation of the effect of (fos)aprepitant on intravenous dexamethasone pharmacokinetics requires adaptation of the guidelines for children with chemotherapy-induced nausea and vomiting

Supportive Care in Cancer (2022)

A. Laura Nijstad Evelien de Vos‐Kerkhof Catherine F. Enters-Weijnen Marianne D. van de Wetering Wim J. E. Tissing

Chemotherapy-induced nausea and vomiting (CINV) are common side effects in pediatric oncology treatment. Besides 5-HT3-antagonists, both dexamethasone and aprepitant are cornerstone drugs in controlling these side effects. Based on results of adult studies, the dexamethasone dose is reduced by 50% when combined with aprepitant, because of a drug-drug interaction, even though data on the interaction in children is lacking. The current study was developed to investigate the effect of aprepitant on dexamethasone clearance (CL) in children, in order to assess if dexamethasone dose reduction for concomitant use of aprepitant is appropriate in the current antiemetic regimen.In total, 65 children (0.6-17.9 years), receiving intravenous or oral antiemetic therapy (dexamethasone ± aprepitant) as standard of care, were included. 305 dexamethasone plasma concentrations were determined using LC-MS/MS. An integrated dexamethasone and aprepitant pharmacokinetic model was developed using non-linear mixed effects modelling in order to investigate the effect of aprepitant administration on dexamethasone CL.In this population, dexamethasone CL in patients with concomitant administration of aprepitant was reduced by approximately 30% of the uninhibited CL (23.3 L/h (95% confidence interval 20.4-26.0)). This result is not consistent with the results of adult studies (50% reduction). This difference was not age dependent, but might be related to the route of administration of dexamethasone. Future studies are needed to assess the difference in oral/intravenous dexamethasone.When dexamethasone is given intravenously as a component of triple therapy to prevent CINV in children, we advise to reduce the dexamethasone dose by 30% instead of 50%.

Aprepitant

Concomitant

10.1007/s00520-022-07423-6

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Citations (5)

Phase I and pharmacological trial of lapatinib in combination with gemcitabine in patients with advanced breast cancer

Investigational New Drugs (2015)

Ruud van der Noll Willem M. Smit A.N.M. Wymenga David S. Boss Mayer B. Grob

Summary Background Lapatinib has proven efficacy as monotherapy and in combination with capecitabine in patients with metastatic breast cancer (MBC) overexpressing HER2 and/or EGFR. Gemcitabine also has anti-tumor activity in MBC and a favourable toxicity profile. In this phase I study lapatinib and gemcitabine were combined. Methods Female patients with advanced BC were given lapatinib once daily (QD) in 28-day cycles with gemcitabine administered on day 1, 8 and 15. Physical examinations, vital signs and blood sampling for hematology, clinical chemistry and pharmacokinetics (PK) and radiological assessments of disease were performed at regular intervals. Results In total, 33 patients were included. Six dose-limiting toxicities were observed, mostly grade 3 increases in liver function tests. Most common toxicities were fatigue (73 %), nausea (70 %), diarrhea (58 %), increases in ALAT and ASAT (55 and 52 %, respectively) and rash (46 %). The maximum tolerated dose was lapatinib 1250 mg QD with gemcitabine 1000 mg/m 2 . Lapatinib and gemcitabine PK did not appear to be influenced by each other. Anti-tumor activity was observed with one patient (4 %) showing complete response and six (23 %) partial response. Conclusion Despite a slightly increased toxicity profile compared to their respective monotherapies, lapatinib and gemcitabine can be safely combined while showing signs of anti-tumor activity.

Lapatinib

10.1007/s10637-015-0281-z

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Citations (12)