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Yuichi Sugiyama

The University of Tokyo

5 papers in the library · 524 citations · publishing 2010-2020

Papers

Identification of the Rate-Determining Process in the Hepatic Clearance of Atorvastatin in a Clinical Cassette Microdosing Study

Clinical Pharmacology & Therapeutics August 10, 2011 Kazuya Maeda, Yasumasa Ikeda, Tomoe Fujita et al. 207 citations

Atorvastatin, a cholesterol-lowering drug, is cleared from the body by being taken up into the liver via organic anion transporting polypeptides (OATPs) and then broken down by the enzyme CYP3A4. A clinical study using a microdose cocktail given to eight healthy volunteers showed that blocking OATPs with rifampicin increased atorvastatin's exposure 12-fold, while blocking CYP3A4 with itraconazole had no effect. This demonstrates that hepatic uptake via OATPs, not metabolism by CYP3A4, is the dominant process for eliminating atorvastatin at a subtherapeutic dose.

Microdosing Clinical Study: Pharmacokinetic, Pharmacogenomic (SLCO2B1), and Interaction (Grapefruit Juice) Profiles of Celiprolol Following the Oral Microdose and Therapeutic Dose

The Journal of Clinical Pharmacology May 19, 2011 Ichiro Ieiri, Yohei Doi, Kazuya Maeda et al. 106 citations

In 30 healthy volunteers matched for SLCO2B1 genotype, the effect of a genetic variant on the body's exposure to celiprolol depended on the dose. At a therapeutic dose (100 mg), people with two copies of the *3 variant had a lower average area under the concentration-time curve (AUC) of 775 ng·h/mL compared with 1097 ng·h/mL for those with one copy (*1/*3) and 1547 ng·h/mL for those with none (*1/*1). At a microdose (97.5 µg), these genotype differences disappeared. Dose-normalized AUC was much lower at the microdose, suggesting saturation of an efflux transporter at the therapeutic dose explains why the genetic effect only appears at that higher dose.

Phase 0/microdosing approaches: time for mainstream application in drug development?

Nature Reviews Drug Discovery September 8, 2020 Tal Burt, Graeme Young, Wooin Lee et al. 101 citations

Phase 0 approaches, including microdosing, are early-stage clinical trials that test very low, subtherapeutic doses of new drugs in humans to gather safety and pharmacological data before larger studies. Traditionally used to assess pharmacokinetics, these methods now also help understand a drug's mechanism of action and pharmacodynamics. Phase 0 trials can improve the selection of drug candidates for further development, making the process safer, cheaper, quicker, and more informed. While challenges like extrapolating results to therapeutic doses and managing development timelines remain, the authors suggest that phase 0 approaches should be considered for most drug development scenarios.

Impact of microdosing clinical study — Why necessary and how useful?

Advanced Drug Delivery Reviews October 14, 2010 Yuichi Sugiyama, Shinji Yamashita 60 citations

Microdose clinical studies, which administer less than 100 μg of a test compound, allow selection of drug candidates with favorable pharmacokinetic profiles in humans while minimizing risk of harmful events. However, the low dose may produce different pharmacokinetic profiles than at therapeutic doses, and no efficacy or safety information is obtained from such studies. Combining microdose study data with physiologically based pharmacokinetic (PBPK) model analysis of in vitro metabolism, transport, and binding enables accurate prediction of therapeutic-dose pharmacokinetics. Positron emission tomography molecular imaging can further provide efficacy and safety information. Coordinating these methodologies is expected to innovate drug discovery and development.

Nonlinear Pharmacokinetics of Oral Quinidine and Verapamil in Healthy Subjects: A Clinical Microdosing Study

Clinical Pharmacology & Therapeutics June 29, 2011 Kazuya Maeda, Junichi Takano, Yasumasa Ikeda et al. 50 citations

Microdosing studies help identify early pharmacokinetic properties of drugs in humans, but nonlinearity between microdose and therapeutic dose due to saturation of metabolic enzymes and transporters is a concern. In healthy subjects, verapamil and quinidine, substrates of MDR1 and CYP3A4, showed dose-dependent pharmacokinetics. Dose-normalized AUC values increased 2.6-fold for quinidine and 2.3-fold for verapamil at therapeutic doses compared to microdoses, suggesting saturation of MDR1 and/or CYP3A4 in the small intestine causes nonlinearity.