Literature DB >> 28497258

Clinical Pharmacokinetics and Mass Balance of Veliparib in Combination with Temozolomide in Subjects with Nonhematologic Malignancies.

Silpa Nuthalapati1, Wijith Munasinghe2, Vincent Giranda3, Hao Xiong4.   

Abstract

BACKGROUND AND OBJECTIVES: Veliparib is an orally active potent poly(ADP-ribose) polymerase (PARP) inhibitor currently in phase III clinical trials in solid tumors. This phase I study evaluated the pharmacokinetics and mass balance of veliparib administered alone and in combination with temozolomide, and assessed any potential pharmacokinetic drug-drug interaction between veliparib and temozolomide.
METHODS: This was an open-label, dose-escalation study of veliparib in combination with temozolomide in 42 subjects with nonhematologic malignancies. Veliparib was administered orally at doses ranging from 10 to 80 mg twice daily on days 1-7, and temozolomide was administered orally at 150-200 mg/m2 once daily on days 1-5 of each 28-day cycle. The pharmacokinetics of veliparib, its M8 metabolite, and temozolomide, as well as urinary excretion of unchanged veliparib and its M8 metabolite, were determined.
RESULTS: Mean veliparib maximum observed plasma concentration (C max) and area under the plasma concentration-time curve for the first 6 h postdose (AUC6) values increased dose proportionally in the veliparib 10-80 mg twice-daily dose range. The urinary recovery of veliparib dose as the unchanged parent compound alone and together with the M8 metabolite was 73 ± 18 and 90 ± 22%, respectively, over a 12-h dosing interval on day 6 of Cycle 1. Veliparib and temozolomide pharmacokinetic exposures were not affected when administered together.
CONCLUSIONS: Veliparib is a Biopharmaceutical Classification System (BCS) Class 1 compound, with no less than 90% of the dose absorbed and an oral bioavailability of at least 73%. Veliparib is primarily eliminated by renal excretion. Veliparib exhibited linear pharmacokinetics in the 10-80 mg twice-daily dose range. No pharmacokinetic interaction was observed when veliparib and temozolomide were administered together. CLINICAL TRIAL REGISTRATION NUMBER: NCT00526617.

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Year:  2018        PMID: 28497258     DOI: 10.1007/s40262-017-0547-z

Source DB:  PubMed          Journal:  Clin Pharmacokinet        ISSN: 0312-5963            Impact factor:   6.447


  21 in total

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Authors:  S Piantadosi; J D Fisher; S Grossman
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3.  Some practical improvements in the continual reassessment method for phase I studies.

Authors:  S N Goodman; M L Zahurak; S Piantadosi
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4.  Poly(ADP-ribose) polymerase-2 (PARP-2) is required for efficient base excision DNA repair in association with PARP-1 and XRCC1.

Authors:  Valérie Schreiber; Jean-Christophe Amé; Pascal Dollé; Inès Schultz; Bruno Rinaldi; Valérie Fraulob; Josiane Ménissier-de Murcia; Gilbert de Murcia
Journal:  J Biol Chem       Date:  2002-04-10       Impact factor: 5.157

5.  ABT-888, an orally active poly(ADP-ribose) polymerase inhibitor that potentiates DNA-damaging agents in preclinical tumor models.

Authors:  Cherrie K Donawho; Yan Luo; Yanping Luo; Thomas D Penning; Joy L Bauch; Jennifer J Bouska; Velitchka D Bontcheva-Diaz; Bryan F Cox; Theodore L DeWeese; Larry E Dillehay; Debra C Ferguson; Nayereh S Ghoreishi-Haack; David R Grimm; Ran Guan; Edward K Han; Rhonda R Holley-Shanks; Boris Hristov; Kenneth B Idler; Ken Jarvis; Eric F Johnson; Lawrence R Kleinberg; Vered Klinghofer; Loren M Lasko; Xuesong Liu; Kennan C Marsh; Thomas P McGonigal; Jonathan A Meulbroek; Amanda M Olson; Joann P Palma; Luis E Rodriguez; Yan Shi; Jason A Stavropoulos; Alan C Tsurutani; Gui-Dong Zhu; Saul H Rosenberg; Vincent L Giranda; David J Frost
Journal:  Clin Cancer Res       Date:  2007-05-01       Impact factor: 12.531

6.  Liquid chromatography-mass spectrometric assay for the quantitation in human plasma of ABT-888, an orally available, small molecule inhibitor of poly(ADP-ribose) polymerase.

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7.  Mechanistic Dissection of PARP1 Trapping and the Impact on In Vivo Tolerability and Efficacy of PARP Inhibitors.

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Review 8.  The effects of deregulated DNA damage signalling on cancer chemotherapy response and resistance.

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9.  A phase 1 study evaluating the pharmacokinetics and preliminary efficacy of veliparib (ABT-888) in combination with carboplatin/paclitaxel in Japanese subjects with non-small cell lung cancer (NSCLC).

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Journal:  Cancer Chemother Pharmacol       Date:  2015-10-03       Impact factor: 3.333

10.  Trapping of PARP1 and PARP2 by Clinical PARP Inhibitors.

Authors:  Junko Murai; Shar-yin N Huang; Benu Brata Das; Amelie Renaud; Yiping Zhang; James H Doroshow; Jiuping Ji; Shunichi Takeda; Yves Pommier
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Review 1.  PARP Inhibitors in the Treatment of Triple-Negative Breast Cancer.

Authors:  Jill J J Geenen; Sabine C Linn; Jos H Beijnen; Jan H M Schellens
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Journal:  Cancer Chemother Pharmacol       Date:  2018-11-20       Impact factor: 3.333

Review 3.  PARP Inhibition in Cancer: An Update on Clinical Development.

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4.  A Population Pharmacokinetic Meta-Analysis of Veliparib, a PARP Inhibitor, Across Phase 1/2/3 Trials in Cancer Patients.

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