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347 results on '"Jeong, Seung-Hyun"'

57. A population pharmacokinetic model for individualized regimens of finasteride according to CYP3A5genotype and liver function

Author

Jang, Ji-Hun, Jeong, Seung-Hyun, and Lee, Yong-Bok

Abstract

Purpose: Finasteride, a 5α-reductase inhibitor, is used in clinical practice to treat benign prostatic hyperplasia and androgenetic alopecia. However, scientific and quantitative dosage regimen studies for finasteride are lacking. This study explored effective finasteride covariates related to inter-individual pharmacokinetic (PK) variability through population PK modeling and their quantitative correlations. Methods: We used bioequivalence PK results from healthy Korean males for modeling. We considered the physiological and biochemical parameters obtained from each individual and CYP3A5genotyping information in the covariate search process. We investigated the genetic polymorphisms of CYP3A5and alanine transaminase (ALT) as effective covariates for clearance (CL/F) in inter-individual finasteride PK variability. Results: The homozygous (*3/*3) CYP3A5*3allele had approximately 34% lower CL/F than the *1allele carriers (*1/*1and *1/*3), and the CL/F decreased as ALT increased. The established model explained the data sets of multiple-dose groups and subjects derived from external sources. The model simulation revealed that the mean finasteride plasma or serum concentration at steady state was significantly increased by approximately 1.59–1.83 fold with the *3/*3genotype of CYP3A5, and the ALT level was higher than 40 IU/L. Conclusion: This suggests that the CYP3A5genotype is *3allele homozygous or that, with increased hepatic impairment, continued exposure to high doses of finasteride can lead to adverse side effects. It was quantitatively confirmed that the dosage might have to be adjusted, considering the CYP3A5and ALT genotypes. Thus, this study will aid in the clinical application of finasteride.

Published
2023
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61. Language Bindings for Spatio-Temporal Database Programming in Tripod

Author

Griffiths, Tony, Paton, Norman W., Fernandes, Alvaro A. A., Jeong, Seung-Hyun, Djafri, Nassima, Kanade, Takeo, editor, Kittler, Josef, editor, Kleinberg, Jon M., editor, Mattern, Friedemann, editor, Mitchell, John C., editor, Naor, Moni, editor, Nierstrasz, Oscar, editor, Pandu Rangan, C., editor, Steffen, Bernhard, editor, Sudan, Madhu, editor, Terzopoulos, Demetri, editor, Tygar, Dough, editor, Vardi, Moshe Y., editor, Weikum, Gerhard, editor, Williams, Howard, editor, and MacKinnon, Lachlan, editor

Published
2004
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67. Dosage exploration of meloxicam according to CYP2C9 genetic polymorphisms based on a population pharmacokinetic‐pharmacodynamic model.

Author

Jang, Ji‐Hun, Jeong, Seung‐Hyun, and Lee, Yong‐Bok

Subjects
*GENETIC polymorphisms, *INHIBITION (Chemistry), *INDIVIDUALIZED medicine, *PHARMACOKINETICS
Abstract

Background: Meloxicam, used for treating inflammatory diseases, shows large differences in metabolism according to CYP2C9 genetic polymorphisms; however, there are few studies on dose regimen setting based on quantitative predictions. Objective: The aim of this study was to determine the appropriate meloxicam dose regimen for each genotype through population pharmacokinetic‐pharmacodynamic modeling of meloxicam by considering CYP2C9 genetic polymorphisms. Methods: For modeling, previously reported pharmacokinetic (plasma concentration)‐pharmacodynamic (inhibition of thromboxane B2 generation) data of meloxicam were collected for CYP2C9 genetic polymorphisms (n = 43). And these data were mainly used in the modeling process. Through simulations of the established models, steady‐state pharmacokinetic‐pharmacodynamic profiles were obtained according to meloxicam multiple exposures for each CYP2C9 genotype, and predictions were made based on dose regimen changes. Results: Genetic polymorphisms of CYP2C9 were identified as key covariates that significantly affected pharmacokinetic variability of meloxicam between individuals. The developed meloxicam population pharmacokinetic‐pharmacodynamic model predicted pharmacokinetic results of the 7.5 mg meloxicam administration groups (n = 26) for CYP2C9*1/*1 and *1/*3 as an external validation. The results of model simulation revealed that the differences were 2.39–5.42 times for steady‐state mean plasma concentrations and 1.21–1.71 times for the degree of inhibition of thromboxane B2 generation following multiple exposures for CYP2C9*1/*1 versus *1/*13, *1/*3, and *3/*3. This suggested that thromboxane B2 inhibition following increased plasma exposure to meloxicam differed significantly according to CYP2C9 genetic polymorphisms. The dose of meloxicam in CYP2C9*1/*13, *1/*3, and *3/*3 was randomly adjusted to 1.6–15 mg to approximate the mean thromboxane B2 inhibition for CYP2C9*1/*1 at steady state, the dose intervals varied from 24 h to 48 h. Conclusions: The results suggested that clinical dose adjustment of meloxicam would be necessary to account for CYP2C9 genetic polymorphisms and reduce side effects. This study suggests a clearer direction for setting up clinical therapy based on personalized medicine and quantitative predictions for meloxicam. [ABSTRACT FROM AUTHOR]

Published
2023
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