Drug Metabolism and Personalized Therapy

Official journal of the European Society of Pharmacogenomics and Personalised Therapy

ISSN: 2363-8915

First published: December 1, 1980

Editor-in-chief: Adrián Llerena

About this journal

Objective
Drug Metabolism and Personalized Therapy (DMPT) is a peer-reviewed journal, and is abstracted/indexed in relevant major Abstracting Services. It provides up-to-date research articles, reviews and opinion papers in the wide field of drug metabolism research, covering established, new and potential drugs, environmentally toxic chemicals, the mechanisms by which drugs may interact with each other and with biological systems, and the pharmacological and toxicological consequences of these interactions and drug metabolism and excretion.

Topics

drug metabolizing enzymes
pharmacogenetics and pharmacogenomics
biochemical pharmacology
molecular pathology
clinical pharmacology
pharmacokinetics and drug-drug interactions
immunopharmacology
neuropsychopharmacology

Article formats
Research Articles, Reviews and Mini Reviews, Opinion Papers, Short Communications, letters to the Editor, Case Reports, Editorials

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Your benefits:

Comprehensive approach to drug metabolism research
State-of-the-art research results
Renowned editorial board
High quality peer-review

Drug Metabolism and Personalized Therapy is the official journal of the European Society of Pharmacogenomics and Personalised Therapy (ESPT).

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Founded in 1981 until 2014: Drug Metabolism and Drug Interactions

From 2015 onwards: Drug Metabolism and Personalized Therapy

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Volume 35 Issue 4

December 2020

Related expression of TRKA and P75 receptors and the changing copy number of MYC-oncogenes determine the sensitivity of brain tumor cells to the treatment of the nerve growth factor in combination with cisplatin and temozolomide

Alexandr N. Chernov, Diana A. Alaverdian, Oleg S. Glotov, Michael V. Talabaev, Stanislav P. Urazov, Sergei G. Shcherbak, Alessandra Renieri, Elisa Frullanti, Olga Shamova September 4, 2020

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Abstract

Objectives Oncological diseases are an urgent medical and social problem. The chemotherapy induces not only the death of the tumor cells but also contributes to the development of their multidrug resistance and death of the healthy cells and tissues. In this regard, the search for the new pharmacological substances with anticancer activity against drug-resistant tumors is of utmost importance. In the present study we primarily investigated the correlation between the expression of TrkA and p75 receptors with the nerve growth factor (NGF) and cisplatin or temozolomide sensitivity of anaplastic astrocytoma (AA), glioblastoma (GB) and medulloblastoma (MB) cell cultures. We then evaluated the changing of copy numbers of MYCC and MYCN and its correlation with cytotoxicity index (CI) in MB cells under NGF exposition. Methods The primary cell cultures were obtained from the tumor biopsy samples of the patients with AA (n=5), GB (n=7) or MB (n=25) prior to radiotherapy and chemotherapy. The cytotoxicity effect of NGF and its combinations with cisplatin or temozolomide, the relative expression of TrkA and p75 receptors, its correlations with CI in AA, GB and MB primary cell cultures were studied by trypan blue cytotoxicity assay and immunofluorescence staining respectively. The effect of NGF on MYCC and MYCN copy numbers in MB cell cultures was studied by fluorescence in situ hybridization. Results We found that the expression of TrkA and p75 receptors (p=0.03) and its ratio (p=0.0004) depends on the sensitivity of AA and GB cells to treatment with NGF and its combinations with cisplatin or temozolomide. NGF reduces (p<0.05) the quantity of MB cells with six or eight copies of MYCN and three or eight copies of MYCC . Besides, NGF increases (p<0.05) the quantity of MB cells containing two copies of both oncogenes. The negative correlation (r=−0.65, p<0.0001) is established between MYCC average copy numbers and CI of NGF in MB cells. Conclusions The relative expression of NGF receptors (TrkA/p75) and its correlation with CI of NGF and its combinations in AA and GB cells point to the mechanism involving a cell death signaling pathway. NGF downregulates (p<0.05) some increased copy numbers of MYCC and MYCN in the human MB cell cultures, and upregulates normal two copies of both oncogenes (p<0.05).

Understanding COVID-19 in the light of epidemic disease described in Unani medicine

Md Anzar Alam, Mohd Aleemuddin Quamri, Ghulamuddin Sofi, Umme Ayman, Shabnam Ansari, Mariyam Ahad September 24, 2020

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Abstract

Unani system of medicine is based on the humoral theory postulated by Hippocrates, according to him the state of body health and disease are regulated by qualitative and quantitative equilibrium of four humours. Amraz-e-Waba is an umbrella term which is used in Unani medicine for all types of epidemics (smallpox, measles, plague, Hameer Saifi , influenza, Nipaha, Ebola, Zika, and 2019 novel coronavirus, etc.) mostly fatal in nature. The coronavirus disease 2019 (COVID-19) is a severe acute respiratory infection, and the pathogenesis and clinical features resemble with those of Nazla-e-Wabaiya (influenza) and Zatul Riya (pneumonia) which were well described many years ago in Unani text such as high-grade fever, headache, nausea and vomiting, running nose, dry cough, respiratory distress, alternate and small pulse, asthenia, foul smell from breath, insomnia, frothy stool, syncope, coldness in both upper and lower extremities, etc. The World Health Organization declared COVID-19 as a global emergency pandemic. Unani scholars like Hippocrates (370–460 BC), Galen (130–200 AD), Rhazes (865–925 AD), and Avicenna (980–1037 AD) had described four etiological factors for Amraz-e-Waba viz., change in quality of air, water, Earth, and celestial bodies, accordingly mentioned various preventive measures to be adopted during epidemics such as restriction of movement, isolation or “ quarantena ”, and fumigation with loban ( Styrax benzoin W. G. Craib ex Hartwich.), sandalwood ( Santalum album L.), Zafran ( Crocus sativus L.), myrtle ( Myrtus communis L.), and roses ( Rosa damascena Mill.) and use of vinegar ( sirka ) and antidotes ( Tiryaq ) as prophylaxis, and avoiding consumption of milk, oil, sweet, meat, and alcohol. This review focuses and elaborates on the concept, prevention, and probable management of COVID-19 in the light of Amraz-e-Waba . Highlights – Coronavirus disease 2019 (COVID-19) has been declared a global emergency by the World Health Organization. – According to Unani literature, COVID-19 is a type of Amraz-e-Waba or Nazla-e-Wabaiya. – Amraz-e-Waba are contagious, and some of them spreads rapidly, and are fatal also. – People with malign humours and diminished immunity are more susceptible to Amraz-e-Waba. During Amraz-e-Waba , social distancing, restriction of movement, use of disinfectants, and fumigation and use of vinegar, and anti-dotes as prophylaxis.

NUDT15 polymorphism explains serious toxicity to azathioprine in Indian patients with chronic immune thrombocytopenia and autoimmune hemolytic anemia: a case series

Anup J. Devasia, Raveen Stephen Stallon Illangeswaran, Infencia Xavier Raj, Biju George, Poonkuzhali Balasubramanian August 24, 2020

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Abstract

Objectives Azathioprine (AZA) is a commonly used immunosuppressant in patients with autoimmune diseases. The toxic side effect to AZA (myelosuppression, hair loss, and oral ulcers) are highly unpredictable which can be life threatening if not identified earlier and dose adjustments made or the drug is withdrawn. Case presentation Here we report a case series of five patients with severe toxicity while on treatment with AZA for autoimmune hemolytic anemia (n=1) and Immune thrombocytopenia (n=4). The common thiopurine methyltransferase (TPMT) variants (TPMT*2, *3A, *3B) were not present in these patients. However, all these patients had the NUDT15 415C>T variant that has been reported to explain serious toxicity to thioguanine in Asian patients. Conclusions Our report suggests pre-emptive genotype-based dosing of AZA could reduce adverse toxicity and hence better outcome.

Methyl jasmonate delays the latency to anoxic convulsions by normalizing the brain levels of oxidative stress biomarkers and serum corticosterone contents in mice with repeated anoxic stress

Abayomi Ololade Adelaja, Oluwafemi Gabriel Oluwole, Oritoke Modupe. Aluko, Solomon Umukoro September 4, 2020

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Abstract

Objectives Repeated exposure to anoxic stress damages the brain through cortisol-mediated increases in oxidative stress and cellular-antioxidants depletion. Thus, compounds with antioxidant property might confer protection against anoxic stress-induced brain injuries. In this study, we further examined the protective effect of methyl jasmonate (MJ), a potent anti-stress agent against anoxic stress-induced convulsions in mice. Methods Thirty-six male Swiss mice randomized into six groups (n=6) were given MJ (25, 50 and 100 mg/kg, i.p.) or vehicle (10 mL/kg, i.p.) 30 min before 15 min daily exposure to anoxic stress for 7 days. The latency(s) to anoxic convulsion was recorded on day 7. The blood glucose and serum corticosterone levels were measured afterwards. The brains were also processed for the determination of malondialdehyde, nitrite, and glutathione levels. Results Methyl jasmonate (MJ) delayed the latency to anoxic convulsion and reduced the blood glucose and serum corticosterone levels. The increased malondialdehyde and nitrite contents accompanied by decreased glutathione concentrations in mice with anoxic stress were significantly attenuated by MJ. Conclusions These findings further showed that MJ possesses anti-stress property via mechanisms relating to the reduction of serum contents of corticosterone and normalization of brain biomarker levels of oxidative stress in mice with anoxic stress.

Diosmin attenuates schizophrenia-like behavior, oxidative stress, and acetylcholinesterase activity in mice

Aya-Ebi Okubo Eneni, Benneth Ben-Azu, Abayomi Mayowa Ajayi, Adegbuyi Oladele Aderibigbe October 15, 2020

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Abstract

Objectives Diosmin (DSM), commonly isolated from various plants, is a citrus nutrient that has been shown to increase intracellular antioxidant capacity and assuage symptoms associated with neurological disorders. Deficiency in the antioxidant system has been implicated in the pathogenesis of schizophrenia. The use of antioxidants as neuroprotectants to suppress schizophrenia pathology is increasingly being sought. Hence, this study investigated the effects of DSM on schizophrenia-like behavior and the underlying changes in biomarkers of oxidative stress and acetylcholinesterase (AChE) activity in mice. Methods The acute antipsychotic effect of DSM (25, 50, and 100 mg/kg, intraperitoneally [i.p.]), haloperidol (1 mg/kg, i.p.), and risperidone (RIS) (0.5 mg/kg, i.p.) was investigated on stereotyped behaviors induced by apomorphine (2 mg/kg, i.p.) and ketamine (10 mg/kg, i.p.). The effect of DSM on ketamine-induced hyperlocomotion, immobility enhancement, and its woodblock cataleptogenic potential was evaluated. Also, the subacute antipsychotic potential of DSM was assessed following intraperitoneal injection of DSM (25–100 mg/kg, i.p.) alone and in combination with ketamine (20 mg/kg, i.p.) for 10 days. The behaviors of the animals were assessed in the open-field, Y-maze, and forced swim tests. Brains of the animals were afterward processed for spectrophotometric assay of oxidative stress and AChE contents. Results DSM (25, 50, and 100 mg/kg) attenuated apormorphine-induced stereotypy and devoid of cataleptogenic effect. DSM and RIS reversed acute and subacute ketamine-induced schizophrenia-like behaviors. Disomin alone increased cognitive function and reduced despair-like phenotype. Furthermore, DSM increased superoxide dismutase and glutathione and decreased malondialdehyde and AChE levels in naïve and ketamine schizophrenic mice. Conclusions DSM prevents schizophrenia-like behavior, attenuates oxidative stress, and AChE activity in naïve and ketamine schizophrenic mice.

Pharmacogenetics of antipsychotics in adolescents with acute psychotic episode during first 14 days after admission: effectiveness and safety evaluation

Dmitriy V. Ivashchenko, Sofi Z. Khoang, Bakhu V. Makhmudova, Nina I. Buromskaya, Pavel V. Shimanov, Roman V. Deitch, Kristina A. Akmalova, Grigoriy N. Shuev, Irina V. Dorina, Marina I. Nastovich, Eugenia N. Shagovenko, Elena A. Grishina, Lyudmila M. Savchenko, Yuriy S. Shevchenko, Dmitriy A. Sychev August 24, 2020

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Abstract

Objectives Prediction of the antipsychotic’s effectiveness is a relevant topic in the field of personalized medicine. Methods The research design of this study is a prospective observation with posthoc analysis of associations of genetic polymorphisms with safety parameters and effectiveness of antipsychotic therapy. We observed 53 adolescents with an acute psychotic episode which were prescribed antipsychotics for 14 days. We evaluated the effectiveness of antipsychotics with the Positive and Negative Symptoms Scale and the safety with the UKU Side Effects Rating Scale, Simpson-Angus Scale, and Barnes Akathisia rating scale. We genotyped CYP3A4*22 (rs2740574), CYP3A5*3 (6986A>G, rs7767746), CYP2D6*4, *9, *10 (rs3892097, rs1065852), ABCB1 1236C>T (rs1128503), 2677G>T/A (rs2032582), 3435C>T (rs1045642), DRD2 (rs1800497), DRD4 (rs1800955), HTR2A (rs6313) by the real-time polymerase chain reaction method. Results We found significantly more frequent “increased dream activity” between CYP2D6 intermediate metabolizers and normal metabolizers (54 vs. 22%; p=0.043). The «increased duration of sleep» was more often observed in homozygotes TT of ABCB1 2677G>T/A (50 vs. 15.8%, p=0.006) and TT of 3435C>T (41.7 vs. 8.2%, p=0.007). Conclusions We found that CYP2D6 and ABCB1 polymorphisms were associated with the safety of antipsychotics in adolescents with an acute psychotic episode.

Using a pharmacogenetic clinical decision support system to improve psychopharmacotherapy dosing in patients with affective disorders

Michael Zastrozhin, Valentin Skryabin, Alexander Sorokin, Oleg Buzik, Inessa Bedina, Elena Grishina, Kristina Ryzhikova, Valery Shipitsyn, Evgeny Bryun, Dmitry Sychev September 1, 2020

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Abstract

Objectives Although pharmacogenetic tests provide the information on a genotype and the predicted phenotype, these tests do not themselves provide the interpretation of data for a physician. Currently, there are approximately two dozen pharmacogenomic clinical decision support systems (CDSSs) used in psychiatry. Implementation of the CDSSs forming the recommendations on drug and dose selection according to the results of pharmacogenetic testing is an urgent task. Fulfillment of this task will allow increasing the efficacy of therapy and decreasing the risk of undesirable side effects. Methods The study included 118 male patients (48 in the main group and 70 in the control group) with affective disorders and comorbid alcohol use disorder. To evaluate the efficacy and safety of therapy, several international psychometric scales and rating scales to measure side effects were used. Genotyping was performed using the real-time polymerase chain reaction with allele-specific hybridization. Pharmacogenetic testing results were interpreted using free software PGX2 (LLE Medicine, Russian Federation, Biomedical Cluster of Skolkovo, Moscow Innovative Cluster; www.pgx2.com). Results The statistically significant differences across the scores on psychometric scales were revealed. For instance, the total score on the Hamilton Rating Scale for Depression by day 9 was 9.0 [8.0; 10.0] for the main group and 11.0 [10.0; 12.0] (p<0.001) for the control group and by day 16 it was 4.0 [2.0; 6.0] for the main group and 14.0 [13.0; 14.0] (p<0.001) for the control group. The UKU Side-Effect Rating Scale (UKU) also revealed a statistically significant difference. The total score on the UKU scale by day 9 was 4.0 [4.0; 5.0] for the main group and 5.0 [5.0; 6.0] (p<0.001) for the control group and by day 16 this difference grew significantly: 3.0 [0.0; 4.2] for the main group and 9.0 [7.0; 11.0] (p<0.001) for the control group. Conclusions Pharmacogenetic-guided personalization of the drug dose in patients with affective disorders and comorbid alcohol use disorder can reduce the risk of undesirable side effects and pharmacoresistance. It allows recommending the use of pharmacogenetic CDSSs for optimizing drug dosage.

Genotype-driven pharmacokinetic simulations of warfarin levels in Puerto Ricans

Stephanie Reyes-González, Camila de las Barreras, Gledys Reynaldo, Leyanis Rodríguez-Vera, Cornelis Vlaar, Vilmali Lopez Mejias, Jean-Christophe M. Monbaliu, Torsten Stelzer, Victor Mangas, Jorge Duconge August 18, 2020

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Abstract

Objectives The inter-individual variability of warfarin dosing has been linked to genetic polymorphisms. This study was aimed at performing genotype-driven pharmacokinetic (PK) simulations to predict warfarin levels in Puerto Ricans. Methods Analysis of each individual dataset was performed by one-compartmental modeling using WinNonlin®v6.4. The k e of warfarin given a cytochrome P450 2C9 ( CYP2C9 ) genotype ranged from 0.0189 to 0.0075 h −1 . K a and V d parameters were taken from literature. Data from 128 subjects were divided into two groups (i.e., wild-types and carriers) and statistical analyses of PK parameters were performed by unpaired t-tests. Results In the carrier group (n=64), 53 subjects were single-carriers and 11 double-carriers (i.e., *2/*2, *2/*3, *2/*5, *3/*5, and *3/*8). The mean peak concentration (Cmax) was higher for wild-type (0.36±0.12 vs. 0.32±0.14 mg/L). Likewise, the average clearance (CL) parameter was faster among non-carriers (0.22±0.03 vs. 0.17±0.05 L/h; p=0.0001), with also lower area under the curve (AUC) when compared to carriers (20.43±6.97 vs. 24.78±11.26 h mg/L; p=0.025). Statistical analysis revealed a significant difference between groups with regard to AUC and CL, but not for Cmax. This can be explained by the variation of k e across different genotypes. Conclusions The results provided useful information for warfarin dosing predictions that take into consideration important individual PK and genotyping data.

A study of the pharmacokinetics of moxifloxacin by the dynamics of its distribution in the blood plasma and saliva of healthy volunteers: a comparative analysis and possible extrapolation methods

Svetlana N. Kondratenko, Irina V. Zolkina, Eugenia V. Shikh September 2, 2020

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Abstract

Objectives The pharmacokinetics of moxifloxacin in plasma and saliva was investigated in this study. Methods The pharmacokinetics of two specialty drugs of moxifloxacin – reference (Ref) and test (Test) preparation – was studied in 18 healthy volunteers after a single oral dose of 400 mg. Results It was found that the concentration of moxifloxacin in saliva 3–24 h after taking the drugs was statistically significantly higher than that in plasma. A high correlation was observed between the concentration of moxifloxacin in plasma and saliva of volunteers after taking of Ref and Test. Some pharmacokinetic parameters, calculated by the concentration of moxifloxacin in saliva and plasma, are statistically different. A technique is proposed for extrapolating the concentration of moxifloxacin in plasma according to its concentration in saliva using the established linear relationship between the moxifloxacin in plasma and saliva of volunteers in time interval of 3–24 h after taking Ref. Based on the obtained extrapolated concentration of moxifloxacin, the pharmacokinetic parameters were calculated for two studied drugs and did not statistically differ from the parameters calculated according to the data in plasma. Conclusions The developed method of concentration extrapolation allows the use of saliva for pharmacokinetic studies of the tablet preparations of moxifloxacin.

Prognostic indicators in critically ill poisoned patients: development of a risk-prediction nomogram

Alireza Amirabadizadeh, Samaneh Nakhaee, Firoozeh Jahani, Sima Soorgi, Christopher O. Hoyte, Omid Mehrpour September 29, 2020

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Abstract

Objectives The prognosis of acutely poisoned patients is a significant concern for clinical toxicologists. In this study, we sought to determine the clinical and laboratory findings that can contribute to predicting the medical outcomes of poisoned patients admitted to intensive care units (ICUs). Methods This retrospective study was performed from January 2009 to January 2016 in the ICU of Vali-e-Asr Hospital in Birjand, Iran. We included all patients with the diagnosis of acute poisoning admitted to the ICU. Demographic data, laboratory results, the Sequential Organ Failure Assessment (SOFA), and acute physiology score + age points + chronic health points (APACHE) II, and the Simplified Acute Physiology Score (SAPS) II, and outcome were collected. Univariate analysis (Mann–Whitney or t-test), multiple logistic regression, receiver operating characteristics (ROC) curve analysis, and Pearson’s correlation test were performed using SPSS, STATA/SE 13.0, and Nomolog software programs. Results The multiple logistic regression analysis revealed that five factors were significant for predicting mortality including age (OR 95% CI: 1.1[1.05–1.12], p<0.001), Glasgow Coma Score (GCS) (OR 95% CI: 0.71[0.6–0.84], p<0.001), white blood cell (WBC) count (OR 95% CI: 1.1[1.01–1.12], p=0.04), serum sodium (Na) (OR 95% CI: 1.08[1.01–1.15], p=0.02), and creatinine levels (Cr) (OR 95% CI: 1.86 [1.23–2.81], p=0.003). We generated a five-variable risk-prediction nomogram which could both predict mortality risk and identify high-risk patients. Conclusions Age, GCS, WBC, serum creatinine, and sodium levels are the best prognostic factors for mortality in poisoned patients admitted to the ICU. The APACHE II score can discriminate between non-survivors and survivors. The nomogram developed in the current study can provide a more precise, quick, and simple analysis of risks, thereby enabling the users to predict mortality and identify high-risk patients.

The need of the clinical implementation of pharmacogenetics in European health services for routine drug prescription. What’s next? An urgent clinical unmet need for patients

Miquel Taron, Adrián Llerena, Vangelis G. Manolopoulos, Cristina Rodriguez-Antona, Sanja Stankovic, Ron H.N. van Schaik November 13, 2020

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Genetic influence of DPYD*9A polymorphism on plasma levels of 5-fluorouracil and subsequent toxicity after oral administration of capecitabine in colorectal cancer patients of South Indian origin

Ashok Varma, Mathaiyan Jayanthi, Biswajit Dubashi, Deepak Gopal Shewade, Rajan Sundaram September 23, 2020

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Abstract

Objectives High interindividual variability was reported with capecitabine toxicities among colorectal cancer (CRC) patients. DPYD*9A polymorphism was reported responsible for grade 3 or 4 toxicities. Finding the phenotypic association between DPYD*9A polymorphism and 5-fluorouracil (5-FU) plasma levels will give a better prediction for toxicity susceptibility. Methods A total of 145 CRC patients were included in the final analysis. Each patient received capecitabine of 1,000 mg/m 2 twice daily for the first 14 days of a 21 day cycle. 5-FU levels were measured at two-time points 2 and 3 h post capecitabine administration across the 1st and 4th cycles of chemotherapy. 5-FU levels were measured using liquid chromatography and tandem mass spectrometry (LC-MS/MS). Genotyping analysis was done by real-time PCR (RT-PCR). Results The mean 5-FU drug levels measured during the 1st cycle at time points 2 and 3 h were found to be 267 ng/mL ± (29) and 124 ng/mL ± (22) respectively. Whereas, the observed 5-FU levels in the 4th cycle were 275 ng/mL ± (28) and 130 ng/mL ± (26) respectively. Patients with 5-FU levels in the range of 281–320 and 141–160 ng/mL at 2 and 3 h respectively showed a higher risk for the hand-foot syndrome (HFS) and thrombocytopenia. No association was found between DPYD*9A polymorphism and 5-FU drug levels measured at time point 2 h across both the cycles. However, the drug levels measured at 3 h were found to be significantly different across the DPYD*9A genotypes. Individuals with GG genotype showed significantly higher 5-FU levels when compared to AA genotype. Conclusions DPYD*9A polymorphism had a significant influence on the plasma levels of 5-FU after capecitabine administration. The 5-FU levels measured at 3 h corresponding to elimination t 1/2 was significantly higher in patients with GG genotype compared AA genotype.

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Volume 35 (2020)

Volume 34 (2019)

Volume 33 (2018)

Volume 32 (2017)

Volume 31 (2016)

Volume 30 (2015)

Volume 29 (2014)

Volume 28 (2013)

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Volume 26 (2011)

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Volume 10 (1992)

Volume 9 (1991)

Volume 8 (1990)

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Volume 7 (1989)

Volume 6 (1988)

Volume 5 (1987)

Volume 4 (1982)

Volume 3 (1981)

Cite Score	2.4
SCImago Journal Rank	0.282
Source Normalized Impact per Paper	0.476

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Editorial

Editor-in-Chief
Adrián LLerena
CICAB Clinical Research Center, Extremadura University Hospital, Badajoz, Spain
allerena@unex.es

Associate Editor
Vangelis G. Manolopoulos, Dept. of Pharmacology, Democritus University of Thrace Medical School, Alexandroupolis, Greece

Editorial Board
Mongi Benjeddou, Dept. of Biotechnology, University of the Western Cape, Cape Town, South Africa
Bing Chen, Shanghai, Dept. of Laboratory Medicine, Jiaotong University, Shanghai, P.R. China
Jaroslav Hubacek, Centre for Experimental Medicine, Institute for Clinical and Experimental Medicine
Magnus Ingelman-Sundberg, Dept. of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
Giorgio D. Kotzalidis, Dept. of Neurosciences, Mental Health, and Sensory Organs, Sapienza University, Rome, Italy
Janja Marc, Faculty of Pharmacy, University of Ljubljana, Ljubljana, Slovenia
Urs A. Meyer, Dept. of Pharmacology, Biocenter of the University of Basel, Basel, Switzerland
Sujit Nair, Pharmaceutical Sciences, University of Mumbai, Mumbai, India
Charity Nofziger, Insitute of Pharmacology and Toxicology, Paracelsus Medical University, Salzburg, Austria
Ana Peiró, University General Hospital of Alicante, Alicante, Spain
Georgia Ragia, Laboratory of Pharmacology, Democritus University of Thrace, Alexandroupolis, Greece
Jae-Gook Shin, Pharmacogenomics Research Center, Inje University College of Medicine, Busan, South Korea
Maurizio Simmaco, Dept. of Neurosciences, Faculty of Medicine & Psychology, Sapienza University of Rome, Rome, Italy
Sanja Stankovic, Faculty of Biology, University of Belgrade, Belgrade, Serbia
Enrique Terán, School of Medicine, Universidad San Francisco de Quito, Quito, Ecuador
Ron H.N. van Schaik, Dept. of Clinical Chemistry, Erasmus Medical Center, Rotterdam, The Netherlands
Sophie Visvikis-Siest, INSERM U525, University of Lorraine, Nancy, France

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