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  1. Article: Physiologically based pharmacokinetic modeling of candesartan related to CYP2C9 genetic polymorphism in adult and pediatric patients

    Jung, Eui Hyun / Cho, Chang-Keun / Kang, Pureum / Park, Hye-Jung / Lee, Yun Jeong / Bae, Jung‑Woo / Choi, Chang-Ik / Jang, Choon-Gon / Lee, Seok-Yong

    Archives of pharmacal research. 2021 Dec., v. 44, no. 12

    2021  

    Abstract: Candesartan cilexetil is an angiotensin II receptor blocker and it is widely used to treat hypertension and heart failure. This drug is a prodrug that rapidly converts to candesartan after oral administration. Candesartan is metabolized by cytochrome ... ...

    Abstract Candesartan cilexetil is an angiotensin II receptor blocker and it is widely used to treat hypertension and heart failure. This drug is a prodrug that rapidly converts to candesartan after oral administration. Candesartan is metabolized by cytochrome P450 2C9 (CYP2C9) enzyme or uridine diphosphate glucurinosyltransferase 1A3, or excreted in an unchanged form through urine, biliary tract and feces. We investigated the effect of genetic polymorphism of CYP2C9 enzyme on drug pharmacokinetics using physiologically based pharmacokinetic (PBPK) modeling. In addition, by introducing the age and ethnicity into the model, we developed a model that can propose an appropriate dosage regimen taking into account the individual characteristics of each patient. To evaluate the suitability of the model, the results of a clinical trial on twenty-two healthy Korean subjects and their CYP2C9 genetic polymorphism data was applied. In this study, PK-Sim® was used to develop the PBPK model of candesartan.
    Keywords adults ; biliary tract ; clinical trials ; cytochrome P-450 ; drugs ; feces ; genetic polymorphism ; heart failure ; hypertension ; models ; nationalities and ethnic groups ; oral administration ; patients ; pharmacokinetics ; research ; uridine diphosphate ; urine
    Language English
    Dates of publication 2021-12
    Size p. 1109-1119.
    Publishing place Pharmaceutical Society of Korea
    Document type Article
    ZDB-ID 447623-2
    ISSN 1976-3786 ; 0253-6269
    ISSN (online) 1976-3786
    ISSN 0253-6269
    DOI 10.1007/s12272-021-01363-1
    Database NAL-Catalogue (AGRICOLA)

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  2. Article: Physiologically based pharmacokinetic (PBPK) modeling for prediction of celecoxib pharmacokinetics according to CYP2C9 genetic polymorphism

    Kim, Young-Hoon / Kang, Pureum / Cho, Chang‑Keun / Jung, Eui Hyun / Park, Hye-Jeong / Lee, Yun Jeong / Bae, Jung‑Woo / Jang, Choon-Gon / Lee, Seok-Yong

    Archives of pharmacal research. 2021 July, v. 44, no. 7

    2021  

    Abstract: Celecoxib is a non-steroidal anti-inflammatory drug (NSAID) and a representative selective cyclooxygenase (COX)-2 inhibitor, which is commonly prescribed for osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, acute pain, and primary ... ...

    Abstract Celecoxib is a non-steroidal anti-inflammatory drug (NSAID) and a representative selective cyclooxygenase (COX)-2 inhibitor, which is commonly prescribed for osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, acute pain, and primary dysmenorrhea. It is mainly metabolized by CYP2C9 and partly by CYP3A4 after oral administration. Many studies reported that CYP2C9 genetic polymorphism has significant effects on the pharmacokinetics of celecoxib and the occurrence of adverse drug reactions. The aim of this study was to develop a physiologically based pharmacokinetic (PBPK) model of celecoxib according to CYP2C9 genetic polymorphism for personalized pharmacotherapy. Initially, a clinical pharmacokinetic study was conducted where a single dose (200 mg) of celecoxib was administered to 39 healthy Korean subjects with CYP2C9*1/*1 or CYP2C9*1/*3 genotypes to obtain data for PBPK development. Based on the conducted pharmacokinetic study and a previous pharmacokinetic study involving subjects with CYP2C9*1/*13 and CYP2C9*3/*3 genotype, PBPK model for celecoxib was developed. A PBPK model for CYP2C9*1/*1 genotype group was developed and then scaled to other genotype groups (CYP2C9*1/*3, CYP2C9*1/*13 and CYP2C9*3/*3). After model development, model validation was performed with comparison of five pharmacokinetic studies. As a result, the developed PBPK model of celecoxib successfully described the pharmacokinetics of each CYP2C9 genotype group and its predicted values were within the acceptance criterion. Additionally, all the predicted values were within two-fold error range in comparison to the previous pharmacokinetic studies. This study demonstrates the possibility of determining the appropriate dosage of celecoxib for each individual through the PBPK modeling with CYP2C9 genomic information. This approach could contribute to the reduction of adverse drug reactions of celecoxib and enable precision medicine.
    Keywords genetic polymorphism ; genomics ; genotype ; model validation ; models ; nonsteroidal anti-inflammatory agents ; oral administration ; osteoarthritis ; pain ; pharmacokinetics ; precision medicine ; prediction ; prostaglandin synthase ; research ; rheumatoid arthritis
    Language English
    Dates of publication 2021-07
    Size p. 713-724.
    Publishing place Pharmaceutical Society of Korea
    Document type Article
    ZDB-ID 447623-2
    ISSN 1976-3786 ; 0253-6269
    ISSN (online) 1976-3786
    ISSN 0253-6269
    DOI 10.1007/s12272-021-01346-2
    Database NAL-Catalogue (AGRICOLA)

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  3. Article ; Online: Physiologically based pharmacokinetic (PBPK) modeling of flurbiprofen in different CYP2C9 genotypes

    Whang, Sang-Sup / Cho, Chang‑Keun / Jung, Eui Hyun / Kang, Pureum / Park, Hye Jung / Lee, Yun Jeong / Choi, Chang-Ik / Bae, Jung‑Woo / Kim, Hyung Sik / Jang, Choon-Gon / Lee, Seok-Yong

    Arch. Pharm. Res.. 2022 Aug., v. 45, no. 8 p.584-595

    2022  

    Abstract: The aim of this study was to establish the physiologically based pharmacokinetic (PBPK) model of flurbiprofen related to CYP2C9 genetic polymorphism and describe the pharmacokinetics of flurbiprofen in different CYP2C9 genotypes. PK-Sim® software was ... ...

    Abstract The aim of this study was to establish the physiologically based pharmacokinetic (PBPK) model of flurbiprofen related to CYP2C9 genetic polymorphism and describe the pharmacokinetics of flurbiprofen in different CYP2C9 genotypes. PK-Sim® software was used for the model development and validation. A total of 16 clinical pharmacokinetic data for flurbiprofen in different CYP2C9 genotypes, dose regimens, and age groups were used for the PBPK modeling. Turnover number (kcₐₜ) of CYP2C9 values were optimized to capture the observed profiles in different CYP2C9 genotypes. In the simulation, predicted fraction metabolized by CYP2C9, fraction excreted to urine, bioavailability, and volume of distribution were similar to previously reported values. Predicted plasma concentration-time profiles in different CYP2C9 genotypes were visually similar to the observed profiles. Predicted AUCᵢₙf in CYP2C9*1/*2, CYP2C9*1/*3, and CYP2C9*3/*3 genotypes were 1.44-, 2.05-, and 3.67-fold higher than the CYP2C9*1/*1 genotype. The ranges of fold errors for AUCᵢₙf, Cₘₐₓ, and t₁/₂ were 0.84–1.00, 0.61–1.22, and 0.74–0.94 in development and 0.59–0.98, 0.52–0.97, and 0.61–1.52 in validation, respectively, which were within the acceptance criterion. Thus, the PBPK model was successfully established and described the pharmacokinetics of flurbiprofen in different CYP2C9 genotypes, dose regimens, and age groups. The present model could guide the decision-making of tailored drug administration strategy by predicting the pharmacokinetics of flurbiprofen in various clinical scenarios.
    Keywords bioavailability ; computer software ; decision making ; drugs ; genetic polymorphism ; genotype ; models ; pharmacokinetics ; urine
    Language English
    Dates of publication 2022-08
    Size p. 584-595.
    Publishing place Pharmaceutical Society of Korea
    Document type Article ; Online
    ZDB-ID 447623-2
    ISSN 1976-3786 ; 0253-6269
    ISSN (online) 1976-3786
    ISSN 0253-6269
    DOI 10.1007/s12272-022-01403-4
    Database NAL-Catalogue (AGRICOLA)

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  4. Article: Targeted Inhibition of O-Linked β-N-Acetylglucosamine Transferase as a Promising Therapeutic Strategy to Restore Chemosensitivity and Attenuate Aggressive Tumor Traits in Chemoresistant Urothelial Carcinoma of the Bladder.

    Lee, Hye Won / Kang, Mi Ju / Kwon, Young-Ju / Abdi Nansa, Sama / Jung, Eui Hyun / Kim, Sung Han / Lee, Sang-Jin / Jeong, Kyung-Chae / Kim, Youngwook / Cheong, Heesun / Seo, Ho Kyung

    Biomedicines

    2022  Volume 10, Issue 5

    Abstract: Acquisition of acquired chemoresistance during treatment cycles in urothelial carcinoma of the bladder (UCB) is the major cause of death through enhancing the risk of cancer progression and metastasis. Elevated glucose flux through the abnormal ... ...

    Abstract Acquisition of acquired chemoresistance during treatment cycles in urothelial carcinoma of the bladder (UCB) is the major cause of death through enhancing the risk of cancer progression and metastasis. Elevated glucose flux through the abnormal upregulation of O-linked β-N-acetylglucosamine (O-GlcNAc) transferase (OGT) controls key signaling and metabolic pathways regulating diverse cancer cell phenotypes. This study showed that OGT expression levels in two human UCB cell models with acquired resistance to gemcitabine and paclitaxel were significantly upregulated compared with those in parental cells. Reducing hyper-O-GlcNAcylation by OGT knockdown (KD) markedly facilitated chemosensitivity to the corresponding chemotherapeutics in both cells, and combination treatment with OGT-KD showed more severe growth defects in chemoresistant sublines. We subsequently verified the suppressive effects of OGT-KD monotherapy on cell migration/invasion in vitro and xenograft tumor growth in vivo in chemoresistant UCB cells. Transcriptome analysis of these cells revealed 97 upregulated genes, which were enriched in multiple oncogenic pathways. Our final choice of suspected OGT glycosylation substrate was VCAN, S1PR3, PDGFRB, and PRKCG, the knockdown of which induced cell growth defects. These findings demonstrate the vital role of dysregulated OGT activity and hyper-O-GlcNAcylation in modulating treatment failure and tumor aggression in chemoresistant UCB.
    Language English
    Publishing date 2022-05-18
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines10051162
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Physiologically based pharmacokinetic (PBPK) modeling of flurbiprofen in different CYP2C9 genotypes.

    Whang, Sang-Sup / Cho, Chang-Keun / Jung, Eui Hyun / Kang, Pureum / Park, Hye-Jung / Lee, Yun Jeong / Choi, Chang-Ik / Bae, Jung-Woo / Kim, Hyung Sik / Jang, Choon-Gon / Lee, Seok-Yong

    Archives of pharmacal research

    2022  Volume 45, Issue 8, Page(s) 584–595

    Abstract: The aim of this study was to establish the physiologically based pharmacokinetic (PBPK) model of flurbiprofen related to CYP2C9 genetic polymorphism and describe the pharmacokinetics of flurbiprofen in different CYP2C9 genotypes. PK-Sim® software was ... ...

    Abstract The aim of this study was to establish the physiologically based pharmacokinetic (PBPK) model of flurbiprofen related to CYP2C9 genetic polymorphism and describe the pharmacokinetics of flurbiprofen in different CYP2C9 genotypes. PK-Sim® software was used for the model development and validation. A total of 16 clinical pharmacokinetic data for flurbiprofen in different CYP2C9 genotypes, dose regimens, and age groups were used for the PBPK modeling. Turnover number (k
    MeSH term(s) Computer Simulation ; Cytochrome P-450 CYP2C9/genetics ; Cytochrome P-450 CYP2C9/metabolism ; Flurbiprofen/pharmacokinetics ; Genotype ; Models, Biological
    Chemical Substances Flurbiprofen (5GRO578KLP) ; Cytochrome P-450 CYP2C9 (EC 1.14.13.-)
    Language English
    Publishing date 2022-08-26
    Publishing country Korea (South)
    Document type Journal Article
    ZDB-ID 447623-2
    ISSN 1976-3786 ; 0253-6269
    ISSN (online) 1976-3786
    ISSN 0253-6269
    DOI 10.1007/s12272-022-01403-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Effects of paroxetine on the pharmacokinetics of atomoxetine and its metabolites in different CYP2D6 genotypes

    Jung, Eui Hyun / Lee, Yun Jeong / Kim, Dong-Hyun / Kang, Pureum / Lim, Chang Woo / Cho, Chang-Keun / Jang, Choon-Gon / Lee, Seok-Yong / Bae, Jung-Woo

    Archives of pharmacal research. 2020 Dec., v. 43, no. 12

    2020  

    Abstract: The aim of this study was to investigate the effects of paroxetine, a potent inhibitor of CYP2D6, on the pharmacokinetics of atomoxetine and its two metabolites, 4-hydroxyatomoxetine and N-desmethylatomoxetine, in different CYP2D6 genotypes. Twenty-six ... ...

    Abstract The aim of this study was to investigate the effects of paroxetine, a potent inhibitor of CYP2D6, on the pharmacokinetics of atomoxetine and its two metabolites, 4-hydroxyatomoxetine and N-desmethylatomoxetine, in different CYP2D6 genotypes. Twenty-six healthy subjects were recruited and divided into CYP2D6*wt/*wt (*wt=*1 or *2, n = 10), CYP2D6*wt/*10 (n = 9), and CYP2D6*10/*10 groups (n = 7). In atomoxetine phase, all subjects received a single oral dose of atomoxetine (20 mg). In paroxetine phase, after administration of a single oral dose of paroxetine (20 mg) for six consecutive days, all subjects received a single oral dose of atomoxetine with paroxetine. Plasma concentrations of atomoxetine and its metabolites were determined up to 24 h after dosing. During atomoxetine phase, there were significant differences in Cₘₐₓ and AUC₀₋₂₄ of atomoxetine and N-desmethylatomoxetine among three genotype groups, whereas significant differences were not found in relation to CYP2D6*10 allele after administration of paroxetine. AUC ratios of 4-hydroxyatomoxetine and N-desmethylatomoxetine to atomoxetine were significantly different among three genotype groups during atomoxetine phase (all, P < 0.001), but after paroxetine treatment significant differences were not found. After paroxetine treatment, AUC₀₋₂₄ of atomoxetine was increased by 2.3-, 1.7-, and 1.3-fold, in CYP2D6*wt/*wt, CYP2D6*wt/*10, and CYP2D6*10/*10 groups in comparison to atomoxetine phase, respectively. AUC ratio of 4-hydroxyatomoxetine to atomoxetine in each group was significantly decreased, whereas AUC ratio of N-desmethylatomoxetine to atomoxetine significantly increased after administration of paroxetine. In conclusion, paroxetine coadministration significantly affected pharmacokinetic parameters of atomoxetine and its two metabolites, 4-hydroxyatomoxetine and N-desmethylatomoxetine. When atomoxetine was administered alone, Cₘₐₓ, AUC₀₋₂₄ and CL/F of atomoxetine were significantly different among the three CYP2D6 genotype groups. However, after paroxetine coadministration, no significant differences in these pharmacokinetic parameters were observed among the CYP2D6 genotype groups.
    Keywords alleles ; genotype ; metabolites ; oral administration ; pharmacokinetics ; research
    Language English
    Dates of publication 2020-12
    Size p. 1356-1363.
    Publishing place Pharmaceutical Society of Korea
    Document type Article
    Note NAL-AP-2-clean
    ZDB-ID 447623-2
    ISSN 1976-3786 ; 0253-6269
    ISSN (online) 1976-3786
    ISSN 0253-6269
    DOI 10.1007/s12272-020-01300-8
    Database NAL-Catalogue (AGRICOLA)

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  7. Article: Physiologically based pharmacokinetic modeling of candesartan related to CYP2C9 genetic polymorphism in adult and pediatric patients.

    Jung, Eui Hyun / Cho, Chang-Keun / Kang, Pureum / Park, Hye-Jung / Lee, Yun Jeong / Bae, Jung-Woo / Choi, Chang-Ik / Jang, Choon-Gon / Lee, Seok-Yong

    Archives of pharmacal research

    2021  Volume 44, Issue 12, Page(s) 1109–1119

    Abstract: Candesartan cilexetil is an angiotensin II receptor blocker and it is widely used to treat hypertension and heart failure. This drug is a prodrug that rapidly converts to candesartan after oral administration. Candesartan is metabolized by cytochrome ... ...

    Abstract Candesartan cilexetil is an angiotensin II receptor blocker and it is widely used to treat hypertension and heart failure. This drug is a prodrug that rapidly converts to candesartan after oral administration. Candesartan is metabolized by cytochrome P450 2C9 (CYP2C9) enzyme or uridine diphosphate glucurinosyltransferase 1A3, or excreted in an unchanged form through urine, biliary tract and feces. We investigated the effect of genetic polymorphism of CYP2C9 enzyme on drug pharmacokinetics using physiologically based pharmacokinetic (PBPK) modeling. In addition, by introducing the age and ethnicity into the model, we developed a model that can propose an appropriate dosage regimen taking into account the individual characteristics of each patient. To evaluate the suitability of the model, the results of a clinical trial on twenty-two healthy Korean subjects and their CYP2C9 genetic polymorphism data was applied. In this study, PK-Sim® was used to develop the PBPK model of candesartan.
    MeSH term(s) Adult ; Age Factors ; Angiotensin II Type 1 Receptor Blockers/pharmacokinetics ; Asians/genetics ; Benzimidazoles/pharmacokinetics ; Biphenyl Compounds/pharmacokinetics ; Child ; Child, Preschool ; Cytochrome P-450 CYP2C9/genetics ; Female ; Humans ; Infant ; Male ; Models, Biological ; Polymorphism, Genetic ; Tetrazoles/pharmacokinetics ; Young Adult
    Chemical Substances Angiotensin II Type 1 Receptor Blockers ; Benzimidazoles ; Biphenyl Compounds ; Tetrazoles ; CYP2C9 protein, human (EC 1.14.13.-) ; Cytochrome P-450 CYP2C9 (EC 1.14.13.-) ; candesartan cilexetil (R85M2X0D68)
    Language English
    Publishing date 2021-11-24
    Publishing country Korea (South)
    Document type Journal Article
    ZDB-ID 447623-2
    ISSN 1976-3786 ; 0253-6269
    ISSN (online) 1976-3786
    ISSN 0253-6269
    DOI 10.1007/s12272-021-01363-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Effects of steady-state clarithromycin on the pharmacokinetics of zolpidem in healthy subjects.

    Lee, Choong-Min / Jung, Eui Hyun / Byeon, Ji-Yeong / Kim, Se-Hyung / Jang, Choon-Gon / Lee, Yun Jeong / Lee, Seok-Yong

    Archives of pharmacal research

    2019  Volume 42, Issue 12, Page(s) 1101–1106

    Abstract: Zolpidem is extensively metabolized by CYP3A4, CYP2C9 and CYP1A2. Previous studies demonstrated that pharmacokinetics of zolpidem was affected by CYP inhibitors, but not by short-term treatment of clarithromycin. The objective of this study was to ... ...

    Abstract Zolpidem is extensively metabolized by CYP3A4, CYP2C9 and CYP1A2. Previous studies demonstrated that pharmacokinetics of zolpidem was affected by CYP inhibitors, but not by short-term treatment of clarithromycin. The objective of this study was to investigate the effects of steady-state clarithromycin on the pharmacokinetics of zolpidem in healthy subjects. In the control phase, 33 subjects received a single dose of zolpidem (5 mg). One week later, in the clarithromycin phase, the subjects received clarithromycin (500 mg) twice daily for 5 days to reach steady state concentrations, followed by zolpidem (5 mg) and clarithromycin (500 mg). In each phase, plasma concentrations of zolpidem were evaluated up to 12 h after drug administration by using liquid chromatography-tandem mass spectrometry method. In the clarithromycin phase, mean total area under the curve of zolpidem (AUC
    MeSH term(s) Administration, Oral ; Adult ; Clarithromycin/administration & dosage ; Clarithromycin/blood ; Clarithromycin/pharmacokinetics ; Drug Combinations ; Healthy Volunteers ; Humans ; Male ; Republic of Korea ; Young Adult ; Zolpidem/administration & dosage ; Zolpidem/blood ; Zolpidem/pharmacokinetics
    Chemical Substances Drug Combinations ; Zolpidem (7K383OQI23) ; Clarithromycin (H1250JIK0A)
    Language English
    Publishing date 2019-12-09
    Publishing country Korea (South)
    Document type Journal Article
    ZDB-ID 447623-2
    ISSN 1976-3786 ; 0253-6269
    ISSN (online) 1976-3786
    ISSN 0253-6269
    DOI 10.1007/s12272-019-01201-5
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  9. Article: Physiologically based pharmacokinetic (PBPK) modeling for prediction of celecoxib pharmacokinetics according to CYP2C9 genetic polymorphism.

    Kim, Young-Hoon / Kang, Pureum / Cho, Chang-Keun / Jung, Eui Hyun / Park, Hye-Jeong / Lee, Yun Jeong / Bae, Jung-Woo / Jang, Choon-Gon / Lee, Seok-Yong

    Archives of pharmacal research

    2021  Volume 44, Issue 7, Page(s) 713–724

    Abstract: Celecoxib is a non-steroidal anti-inflammatory drug (NSAID) and a representative selective cyclooxygenase (COX)-2 inhibitor, which is commonly prescribed for osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, acute pain, and primary ... ...

    Abstract Celecoxib is a non-steroidal anti-inflammatory drug (NSAID) and a representative selective cyclooxygenase (COX)-2 inhibitor, which is commonly prescribed for osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, acute pain, and primary dysmenorrhea. It is mainly metabolized by CYP2C9 and partly by CYP3A4 after oral administration. Many studies reported that CYP2C9 genetic polymorphism has significant effects on the pharmacokinetics of celecoxib and the occurrence of adverse drug reactions. The aim of this study was to develop a physiologically based pharmacokinetic (PBPK) model of celecoxib according to CYP2C9 genetic polymorphism for personalized pharmacotherapy. Initially, a clinical pharmacokinetic study was conducted where a single dose (200 mg) of celecoxib was administered to 39 healthy Korean subjects with CYP2C9*1/*1 or CYP2C9*1/*3 genotypes to obtain data for PBPK development. Based on the conducted pharmacokinetic study and a previous pharmacokinetic study involving subjects with CYP2C9*1/*13 and CYP2C9*3/*3 genotype, PBPK model for celecoxib was developed. A PBPK model for CYP2C9*1/*1 genotype group was developed and then scaled to other genotype groups (CYP2C9*1/*3, CYP2C9*1/*13 and CYP2C9*3/*3). After model development, model validation was performed with comparison of five pharmacokinetic studies. As a result, the developed PBPK model of celecoxib successfully described the pharmacokinetics of each CYP2C9 genotype group and its predicted values were within the acceptance criterion. Additionally, all the predicted values were within two-fold error range in comparison to the previous pharmacokinetic studies. This study demonstrates the possibility of determining the appropriate dosage of celecoxib for each individual through the PBPK modeling with CYP2C9 genomic information. This approach could contribute to the reduction of adverse drug reactions of celecoxib and enable precision medicine.
    MeSH term(s) Administration, Oral ; Celecoxib/administration & dosage ; Celecoxib/adverse effects ; Celecoxib/pharmacokinetics ; Cyclooxygenase 2 Inhibitors/administration & dosage ; Cyclooxygenase 2 Inhibitors/adverse effects ; Cyclooxygenase 2 Inhibitors/pharmacokinetics ; Cytochrome P-450 CYP2C9/genetics ; Cytochrome P-450 CYP2C9/metabolism ; Drug-Related Side Effects and Adverse Reactions/genetics ; Drug-Related Side Effects and Adverse Reactions/prevention & control ; Healthy Volunteers ; Humans ; Models, Biological ; Pharmacogenomic Variants ; Precision Medicine/methods
    Chemical Substances Cyclooxygenase 2 Inhibitors ; CYP2C9 protein, human (EC 1.14.13.-) ; Cytochrome P-450 CYP2C9 (EC 1.14.13.-) ; Celecoxib (JCX84Q7J1L)
    Language English
    Publishing date 2021-07-25
    Publishing country Korea (South)
    Document type Clinical Trial ; Journal Article
    ZDB-ID 447623-2
    ISSN 1976-3786 ; 0253-6269
    ISSN (online) 1976-3786
    ISSN 0253-6269
    DOI 10.1007/s12272-021-01346-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Correction to: Relationship between plasma exposure of zolpidem and CYP2D6 genotype in healthy Korean subjects.

    Jung, Eui Hyun / Lee, Choong-Min / Byeon, Ji-Yeong / Shin, Hyo-Bin / Oh, Kyung-Yul / Cho, Chang-Keun / Lim, Chang Woo / Jang, Choon-Gon / Lee, Seok-Yong / Lee, Yun Jeong

    Archives of pharmacal research

    2021  Volume 44, Issue 3, Page(s) 323

    Language English
    Publishing date 2021-01-30
    Publishing country Korea (South)
    Document type Published Erratum
    ZDB-ID 447623-2
    ISSN 1976-3786 ; 0253-6269
    ISSN (online) 1976-3786
    ISSN 0253-6269
    DOI 10.1007/s12272-020-01302-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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