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1. Associations between (pharmaco-)genetic markers and postoperative pain after inguinal hernia repair – a prospective study protocol

Author: Wiss, Florine M., Dietz, Ulrich, Thalheimer, Andreas, Lamm, Sebastian, Rosenberg, Robert, Allemann, Samuel S., zu Schwabedissen, Henriette E. Meyer, Bollinger, Anna, and Lampert, Markus L.
Published: 2024
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2. Pharmacogenotyping disproves genetic cause of drug-related problems in family history: a case report

Author: Bollinger, Anna, Hersberger, Kurt E., Meyer zu Schwabedissen, Henriette E., Allemann, Samuel S., and Stäuble, Céline K.
Published: 2024
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3. Increased coproporphyrin serum levels in healthy volunteers treated with the cholesterol uptake inhibitor ezetimibe

Author: Jonny Kinzi, Markus Grube, Isabell Seibert, Werner Siegmund, and Henriette E. Meyer zu Schwabedissen
Subjects: Therapeutics. Pharmacology, RM1-950, Public aspects of medicine, RA1-1270
Abstract: Abstract Ezetimibe undergoes glucuronidation that results in the active metabolite ezetimibe phenoxy‐glucuronide (ezetimibe‐glucuronide). This phase‐II metabolite was shown to interact with the clinically relevant hepatic transporter organic anion transporting polypeptide (OATP) 1B1. In recent years, coproporphyrin I (CPI) was established as a Tier 1 biomarker for OATP1B‐mediated interactions among other endogenous substrates like CPIII. To evaluate whether levels of the biomarker are affected by ezetimibe treatment, we assessed the impact of ezetimibe and ezetimibe‐glucuronide on OATP1B1‐mediated transport of CPs in vitro. Then, we quantified CP levels in serum samples of healthy volunteers treated with a single oral dose of ezetimibe (20 mg) alone or in combination with rifampin (600 mg). Results from our in vitro experiments showed a significant reduction in cellular CPI accumulation in the presence of ezetimibe‐glucuronide with an IC50 of 1.97 μM [95% CI: 1.04 to 3.96], while CPIII accumulation was impacted by 10 μM and above. In the in vivo study, we observed peak CP concentrations 1.33 h after dosing, which is closest to the tmax of the ezetimibe metabolite. Co‐administration of ezetimibe with rifampin resulted in even higher serum CP levels. The AUC0–24h of CPI and CPIII increased two‐ and threefold, respectively, after concomitant dosing compared to ezetimibe alone. Moreover, we quantified CP levels in cumulative urine from both study phases where the renally excreted amount (Ae) of CPI and CPIII increased after ezetimibe and rifampin co‐administration compared to ezetimibe alone. In conclusion, our findings indicate that rifampin co‐administration results in additional inhibition of OATP1B1 in vivo.
Published: 2024
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4. Pharmacogenetic testing and counselling in the community pharmacy: mixed-methods study of a new pharmacist-led service

Author: Jeiziner, Chiara, Meyer zu Schwabedissen, Henriette E., Hersberger, Kurt E., and Allemann, Samuel S.
Published: 2023
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5. Q.ANTUM NEO with LECO Exceeding 25.5 % cell Efficiency

Author: Mette, Ansgar, Hörnlein, Stefan, Stenzel, Florian, Hönig, René, Höger, Ingmar, Schaper, Martin, Petter, Kai, Junghänel, Matthias, Klenke, Christian, Weihrauch, Anika, Ploigt, Hans-Christoph, Kwon, Ohjin, Schönmann, Antje, Tobail, Osama, Kim, Kyunghun, Schwabedissen, Axel, Kauert, Maximilian, Duncker, Klaus, Faulwetter-Quandt, Björn, Scharf, Jessica, Cieslak, Janko, Kersten, Friederike, Lee, Benjamin, Kristensen, Sissel Tind, Schnelting, Olaf, Baer, Carsten, Queck, Martina, Zimmermann, Gregor, Burtone, Lorenzo, Niebergall, Larissa, Schütze, Matthias, Schulz, Susanne, Fischer, Markus, Peters, Stefan, Fertig, Fabian, and Müller, Jörg W.
Published: 2024
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6. The effect of itraconazole, a strong CYP3A4 inhibitor, on the pharmacokinetics of the first‐in‐class ACKR3/CXCR7 antagonist, ACT‐1004‐1239

Author: Christine Huynh, Jasper Dingemanse, Henriette E. Meyer zu Schwabedissen, Marlene Fonseca, and Patricia N. Sidharta
Subjects: Therapeutics. Pharmacology, RM1-950, Public aspects of medicine, RA1-1270
Abstract: Abstract Cytochrome P450 (CYP) 3A4 is an enzyme involved in the metabolism of many drugs that are currently on the market and is therefore a key player in drug–drug interactions (DDIs). ACT‐1004‐1239 is a potent and selective, first‐in‐class ACKR3/CXRC7 antagonist being developed as a treatment for demyelinating diseases including multiple sclerosis. Based on the human absorption, distribution, metabolism, and excretion (ADME) study results, ACT‐1004‐1239 is predominantly metabolized by CYP3A4. This study investigated the effect of the strong CYP3A4 inhibitor, itraconazole, on the pharmacokinetics of single‐dose ACT‐1004‐1239 in healthy male subjects. In the open‐label, fixed‐sequence DDI study, a total of 16 subjects were treated. Each subject received a single dose of 10 mg ACT‐1004‐1239 (Treatment A) in the first period followed by concomitant administration of multiple doses of 200 mg itraconazole and a single dose of 10 mg ACT‐1004‐1239 in the second period. We report a median of difference in tmax (90% confidence interval, CI) of 0.5 h (0.0, 1.0) comparing both treatments. The geometric mean ratio (GMR) (90% CI) of Cmax and AUC0−∞ was 2.16 (1.89, 2.47) and 2.77 (2.55, 3.00), respectively. The GMR (90% CI) of t1/2 was 1.46 (1.26, 1.70). Both treatments were well‐tolerated with an identical incidence in subjects reporting treatment‐emergent adverse events (TEAE). The most frequently reported TEAEs were headache and nausea. In conclusion, ACT‐1004‐1239 is classified as a moderately sensitive CYP3A4 substrate (i.e., increase of AUC ≥2‐ to
Published: 2024
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7. The influence of OATP2B1 and atorvastatin on coproporphyrin isomers in rats

Author: Jonny Kinzi, Markus Grube, Janine Hussner, Isabell Seibert, Matthias Hamburger, and Henriette E. Meyer zu Schwabedissen
Subjects: OATP2B1, Coproporphyrin, Atorvastatin, Therapeutics. Pharmacology, RM1-950
Abstract: Coproporphyrin I (CPI) and III (CPIII) are discussed as biomarkers for organic anion transporting polypeptides (OATPs). We report on CPI and CPIII levels in wildtype, rSlco2b1-knockout, and SLCO2B1-humanized rats at baseline and after administration of atorvastatin, an inhibitor of the CPIII-specific rOATP2B1/hOATP2B1 and the CPI/CPIII-transporting rOATP1B2. OATP-inhibition by atorvastatin leads to significantly increased CPI and CPIII serum levels. However, basal CP serum levels in rSlco2b1-knockout animals were significantly lower (CPI), or unaffected (CPIII). In the presence of atorvastatin, this genotype effect was abolished. In conclusion, our results indicate an unexpected impact of OATP2B1 on CP serum levels in rats.
Published: 2023
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8. Various effects of repeated rifampin dosing on coproporphyrin levels in humans

Author: Jonny Kinzi, Markus Grube, Karin Brecht, Isabell Seibert, Werner Siegmund, and Henriette E. Meyer zu Schwabedissen
Subjects: Therapeutics. Pharmacology, RM1-950, Public aspects of medicine, RA1-1270
Abstract: Abstract In recent years, the identification of endogenous substrates as biomarkers became an uprising topic. Particularly coproporphyrins (CPs), byproducts of heme biosynthesis, are intensely investigated as biomarkers for predicting interactions with the organic anion transporting polypeptide (OATP) 1B transporters. In the context of drug–drug interactions, several preclinical and clinical studies assessed the effect of the OATP1B‐index inhibitor rifampin on CPI levels. However, rifampin is not only a “perpetrator” drug of transporters but is also known for its interaction with the nuclear receptor pregnane X receptor (PXR) leading to the efficient induction of PXR‐target genes. These include hemoproteins like cytochrome P450 enzymes but also the δ‐aminolevulinate synthase 1, which is the rate‐limiting enzyme in heme biosynthesis. In this study, we showed that quantification of CPs in clinical serum samples was possible after long‐term storage at −20°C. We quantified CPI, CPIII, and heme levels in clinical serum samples (at selected timepoints) that originated from a trial investigating the interaction potential of repeated rifampin administration in 12 healthy participants. In samples collected at the assumed time to maximum concentration of rifampin, higher CP levels were observed compared to baseline. Increased levels persisted even 14 h after discontinuation of rifampin. No impact on heme serum levels was observed. We found a correlation between CP isomers at baseline and at 14 h after rifampin intake. In summary, we show that multiple doses of rifampin affect CP levels. However, besides inhibition of hepatic OATP function there is evidence for an interaction with CP levels beyond the transporter level.
Published: 2023
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9. Recurrent high creatine kinase levels under clozapine treatment - a case report assessing a suspected adverse drug reaction

Author: Florine M. Wiss, Samuel S. Allemann, Henriette E. Meyer zu Schwabedissen, Céline K. Stäuble, Thorsten Mikoteit, and Markus L. Lampert
Subjects: therapeutic drug monitoring, pharmacogenetic, adverse drug reaction, adherence, clozapine, CYP2D6, Psychiatry, RC435-571
Abstract: Suspected adverse drug reactions (ADRs) during treatment with clozapine often prompt therapeutic drug monitoring (TDM) in clinical practice. Currently, there is no official recommendation for pharmacogenetic (PGx) testing in the context of clozapine therapy. In this case report, we demonstrate and discuss the challenges of interpreting PGx and TDM results highlighting the possibilities and limitations of both analytical methods. A 36-year-old male patient with catatonic schizophrenia was treated with clozapine. He experienced multiple hospitalizations due to elevated creatine kinase (CK) levels (up to 9000 U/L, reference range: 30-200 U/L). With no other medical explanation found, physicians suspected clozapine-induced ADRs. However, plasma levels of clozapine were consistently low or subtherapeutic upon admission, prompting us to conduct a PGx analysis and retrospectively review the patient’s TDM data, progress notes, and discharge reports. We investigated two possible hypotheses to explain the symptoms despite low clozapine plasma levels: Hypothesis i. suggested the formation and accumulation of a reactive intermediate metabolite due to increased activity in cytochrome P450 3A5 and reduced activity in glutathione S-transferases 1, leading to myotoxicity. Hypothesis ii. proposed under-treatment with clozapine, resulting in ineffective clozapine levels, leading to a rebound effect with increased catatonic symptoms and CK levels. After considering both data sources (PGx and TDM), hypothesis ii. appeared more plausible. By comprehensively assessing all available TDM measurements and examining them in temporal correlation with the drug dose and clinical symptoms, we observed that CK levels normalized when clozapine plasma levels were raised to the therapeutic range. This was achieved through hospitalization and closely monitored clozapine intake. Therefore, we concluded that the symptoms were not an ADR due to altered clozapine metabolism but rather the result of under-treatment. Interpreting TDM and PGx results requires caution. Relying solely on isolated PGx or single TDM values can result in misinterpretation of drug reactions. We recommend considering the comprehensive patient history, including treatment, dosages, laboratory values, clinic visits, and medication adherence.
Published: 2024
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10. Towards >25% Efficiency of Passivating-Contact Solar Cells in Mass Production

Author: Benjamin Lee, Florian Stenzel, Ralf Albrecht, Carsten Baer, Tabitha Ballmann, Janko Cieslak, Klaus Duncker, Björn Faulwetter-Quandt, Fabian Fertig, Markus Fischer, Ingmar Höger, Rene Hönig, Stefan Hörnlein, Kati Hübener, Enrico Jarzembowski, Matthias Junghänel, Michael Kaiser, Maximilian Kauert, Cangming Ke, Friederike Kersten, Kyunghun Kim, Christian Klenke, Matthias Köhler, Sissel Kristensen, Ohjin Kwon, Ronny Lantzsch, Ansgar Mette, Yvonne Neumann, Larissa Niebergall, Stefan Peters, Kai Petter, Hans-Christoph Ploigt, Britta Pohl-Hampel, Martina Queck, Tomasz Rudolph, Martin Schaper, Jessica Scharf, Michael Schley, Antje Schönmann, Susanne Schulz, Matthias Schütze, Axel Schwabedissen, Anika Weihrauch, Tino Wieczorek, and Jörg Müller
Subjects: Silicon Solar Cells, Passivating Contacts, Mass Production, Renewable energy sources, TJ807-830
Abstract: We report efficiencies of >24% being consistently achieved in mass-production of passivating-contact solar cells. Furthermore, the certified efficiency of cells from our pilot line has reached 25.3% with 730 mV open-circuit voltage. An analysis of the cell performance, including simulations, shows that the cells’ rear-side is nearly ideal, while there remains potential for further optimization of the front emitter and passivation.
Published: 2024
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11. Genotyping of Patients with Adverse Drug Reaction or Therapy Failure: Database Analysis of a Pharmacogenetics Case Series Study

Author: Bollinger A, Stäuble CK, Jeiziner C, Wiss FM, Hersberger KE, Lampert ML, Meyer zu Schwabedissen HE, and Allemann SS
Subjects: pharmacogenomics, pgx, personalized medicine, clinical pharmacy, clinical practice, medication review, Therapeutics. Pharmacology, RM1-950
Abstract: Anna Bollinger,1 Céline K Stäuble,1,2 Chiara Jeiziner,1 Florine M Wiss,1,2 Kurt E Hersberger,1 Markus L Lampert,1,2 Henriette E Meyer zu Schwabedissen,1 Samuel S Allemann1 1Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland; 2Institute of Hospital Pharmacy, Solothurner Spitäler AG, Olten, SwitzerlandCorrespondence: Anna Bollinger, Department of Pharmaceutical Sciences, University of Basel, Klingelbergstrasse 50, Basel, 4056, Switzerland, Tel +41 61 207 66 31, Email a.bollinger@unibas.chPurpose: Pharmacogenetics (PGx) is an emerging aspect of personalized medicine with the potential to increase efficacy and safety of pharmacotherapy. However, PGx testing is still not routinely integrated into clinical practice. We conducted an observational case series study where PGx information from a commercially available panel test covering 30 genes was integrated into medication reviews. The aim of the study was to identify the drugs that are most frequently object of drug-gene-interactions (DGI) in the study population.Patients and Methods: In out-patient and in-patient settings, we recruited 142 patients experiencing adverse drug reaction (ADR) and/or therapy failure (TF). Collected anonymized data from the individual patient was harmonized and transferred to a structured database.Results: The majority of the patients had a main diagnosis of a mental or behavioral disorder (ICD-10: F, 61%), of musculoskeletal system and connective tissue diseases (ICD-10: M, 21%), and of the circulatory system (ICD-10: I, 11%). The number of prescribed medicines reached a median of 7 per person, resulting in a majority of patients with polypharmacy (≥ 5 prescribed medicines, 65%). In total, 559 suspected DGI were identified in 142 patients. After genetic testing, an association with at least one genetic variation was confirmed for 324 suspected DGI (58%) caused by 64 different drugs and 21 different genes in 141 patients. After 6 months, PGx-based medication adjustments were recorded for 62% of the study population, whereby differences were identified in subgroups.Conclusion: The data analysis from this study provides valuable insights for the main focus of further research in the context of PGx. The results indicate that most of the selected patients in our sample represent suitable target groups for PGx panel testing in clinical practice, notably those taking drugs for mental or behavioral disorder, circulatory diseases, immunological diseases, pain-related diseases, and patients experiencing polypharmacy.Keywords: pharmacogenomics, PGx, personalized medicine, clinical pharmacy, clinical practice, medication review
Published: 2023

12. Protease-activated receptor 2 deficient mice develop less angiotensin II induced left ventricular hypertrophy but more cardiac fibrosis.

Author: Albrecht Meyer Zu Schwabedissen, Silvia Vergarajauregui, Marko Bertog, Kerstin Amann, Felix B Engel, and Christoph Daniel
Subjects: Medicine, Science
Abstract: AimsActivation of Protease Activated Receptor 2 (PAR2) has been shown to be involved in regulation of injury-related processes including inflammation, fibrosis and hypertrophy. In this study we will investigate the role of PAR2 in cardiac injury in a mouse model of hypertension using continuous infusion with angiotensin II.MethodsHypertension was induced in 12 weeks old wildtype (wt, n = 8) and PAR2 deficient mice (n = 9) by continuous infusion with angiotensin II for 4 weeks using osmotic minipumps. At the end, hearts were collected for analysis of left ventricular hypertrophy (LVH), myocardial capillary supply, fibrosis and localization of PAR2 expression using histological, immunohistological and mRNA expression analysis techniques. In addition, rat cardiac fibroblasts were treated with angiotensin II and PAR2 was inhibited by a blocking antibody and the PAR2 inhibitor AZ3451.ResultsCardiac PAR2 mRNA expression was downregulated by 40±20% in wt mice treated with AngII compared to untreated controls. Four weeks after AngII treatment, LVH was significantly increased in AngII-treated wt mice compared to similarly treated PAR2-deficient animals as determined by relative heart weight, left ventricular cross-sectional area, and analysis of ventricular lumen area determined on sections. Treatment of wt mice resulted in an approximately 3-fold increase in cardiac expression of FGF23, which was 50% lower in PAR2-deficient animals compared to wt animals and therefore no longer significantly different from expression levels in untreated control mice. In contrast, cardiac interstitial fibrosis was significantly higher in PAR2-deficient mice compared to similar treated wt controls, as assessed by Sirius Red staining (>3-fold) and collagen IV staining (>2-fold). Additional experiments with isolated cardiac fibroblasts showed induction of pro-fibrotic genes when treated with PAR2 inhibitors.ConclusionIn angiotensin II-induced cardiac injury, PAR2 deficiency has an ambivalent effect, enhancing fibrosis on the one hand, but reducing LVH on the other.
Published: 2024
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13. Utilization of Drugs with Pharmacogenetic Dosing Recommendations in Switzerland: A Descriptive Study Using the Helsana Database

Author: Wittwer NL, Meier CR, Huber CA, Meyer zu Schwabedissen HE, Allemann S, and Schneider C
Subjects: pgx, drug use, claims data, pharmacoepidemiology, Therapeutics. Pharmacology, RM1-950
Abstract: Nina L Wittwer,1,2 Christoph R Meier,1– 3 Carola A Huber,4 Henriette E Meyer zu Schwabedissen,1 Samuel Allemann,1,&ast; Cornelia Schneider1,2,&ast; 1Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland; 2Hospital Pharmacy, University Hospital Basel, Basel, Switzerland; 3Boston Collaborative Drug Surveillance Program, Lexington, MA, USA; 4Department of Health Sciences, Helsana Insurance Group, Zürich, Switzerland&ast;These authors contributed equally to this workCorrespondence: Samuel Allemann, Pharmaceutical Care Research Group University of Basel, Department of Pharmaceutical Sciences, Klingelbergstrasse 50, Basel, 4056, Switzerland, Tel +41 61 207 61 76, Email s.allemann@unibas.chPurpose: In Switzerland 167 drugs on the market contain information about pharmacogenetics in their drug label (PGx drug). Preemptive pharmacogenetic testing is reimbursed by health care insurance for only seven drugs (abacavir, carbamazepine, 6-mercaptopurine, azathioprine, 5-fluorouracil, capecitabine, and irinotecan) although, it is proposed to be a cost-effective approach to personalized medicine. The aim of this study was to describe the use of PGx drugs and their corresponding genes in Switzerland.Methods: We identified 90 drugs with dosing recommendations from the Pharmacogenetic Knowledgebase involving 24 genes. We assessed the utilization of those drugs between 2016 and 2020, using claims data from a large Swiss insurance company (Helsana).Results: Of 841 491 persons with drug claims during the whole study period, 78.7% were exposed to PGx drugs. Ibuprofen, pantoprazole, and tramadol had the highest number of users. Seven genes (CYP2C19, CYP2C9, CYP2D6, SLCO1B1, HLA-B, MT-RNR1, and VKORC1) were responsible for over 95% of all potential drug-gene interactions.Conclusion: The prevalence of PGx drug prescriptions is high in the Swiss population. Therefore, intensified preemptive testing may be a useful option as a substantial amount of the Swiss population might benefit.Keywords: PGx, drug use, claims data, pharmacoepidemiology
Published: 2022

14. Management of biliary obstruction in patients with newly diagnosed alveolar echinococcosis: a Swiss retrospective cohort study

Author: Sandra Müller, Soleen Ghafoor, Cordula Meyer zu Schwabedissen, Felix Grimm, Fritz Ruprecht Murray, Lars Husmann, Nadine Stanek, Peter Deplazes, Christoph Schlag, Andreas E. Kremer, Christoph Gubler, Cäcilia S. Reiner, David Semela, Beat Müllhaupt, and Ansgar Deibel
Subjects: Medicine
Abstract: BACKGROUND AND STUDY AIMS: Alveolar echinococcosis, an orphan zoonosis affecting the liver, is of increasing concern worldwide. Most symptomatic cases present at an advanced and inoperable stage, sometimes with biliary obstruction prompting biliary tract interventions. These are, however, associated with a high risk of infectious complications. The aim of this retrospective study was to compare the effectiveness and safety of conservative and interventional treatment approaches in patients with newly diagnosed alveolar echinococcosis and biliary obstruction. PATIENTS AND METHODS: Alveolar echinococcosis patients treated at two referral centres in Switzerland, presenting with hyperbilirubinaemia (total bilirubin >1.5 Upper Limit of Normal) at diagnosis were included, unless another underlying aetiology, i.e. common bile duct stones or decompensated cirrhosis, was identified. Patients were divided into two groups, according to whether they initially received a biliary tract intervention. The primary endpoint was normalisation of bilirubin levels within a 6-month period. Secondary endpoints included, among others, the occurrence of early and late biliary complications, the need for biliary tract interventions during follow-up and overall duration of hospital stays for treatment initiation and for biliary complications. RESULTS: 28 patients were included in this study, of whom 17 received benzimidazole therapy alone and 11 additionally received a biliary tract intervention. Baseline characteristics did not differ between groups. All but one patient in each group achieved the primary endpoint (p=0.747). Biliary tract intervention was associated with faster laboratory improvement (t1/2 1.3 vs 3.0 weeks), but also with more frequent early biliary complications (7/11 vs 1/17, p=0.002) and longer initial hospital stay (18 days vs 7 days, p=0.007). CONCLUSION: Biliary obstruction in patients with newly diagnosed alveolar echinococcosis can be treated effectively with benzimidazole therapy alone. Biliary tract intervention, on the other hand, is associated with a high complication rate and should probably be reserved for patients with insufficient response to benzimidazole therapy.
Published: 2023
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15. Is Pharmacogenetic Panel Testing Applicable to Low-Dose Methotrexate in Rheumatoid Arthritis? – A Case Report

Author: Jeiziner C, Allemann SS, Hersberger KE, and Meyer zu Schwabedissen HE
Subjects: pharmacogenetics (pgx), abcb1, slc19a1, mthfr, rheumatoid arthritis, methotrexate (mtx), Therapeutics. Pharmacology, RM1-950
Abstract: Chiara Jeiziner,1 Samuel S Allemann,1 Kurt E Hersberger,1 Henriette E Meyer zu Schwabedissen2 1Pharmaceutical Care Research Group, Department Pharmaceutical Sciences, University of Basel, Basel, Switzerland; 2Biopharmacy, Department Pharmaceutical Sciences, University of Basel, Basel, SwitzerlandCorrespondence: Chiara Jeiziner, Pharmaceutical Care Research Group, Department Pharmaceutical Sciences, University of Basel, Klingelbergstrasse 50, Basel, 4056, Switzerland, Tel +41 61 207 61 80, Email chiara.jeiziner@unibas.chPurpose: Pharmacogenetic (PGx) panel testing could help to determine the heritable component of a rheumatoid arthritis (RA) patient’s susceptibility for therapy failure and/or adverse drug reactions (ADRs) from methotrexate (MTX). Considering the literature mentioning the potential applicability of PGx panel testing within MTX regimens, we discuss the case of a patient who was treated with MTX, suffered from ADRs, and obtained a reactive PGx panel testing.Genotyping: We used a commercial PGx panel test involving the ABC-transporters P-glycoprotein (P-gp; gene: ABCB1), and breast cancer resistance protein (BCRP; gene: ABCG2), the solute carriers reduced folate carrier 1 (RFC1; gene: SLC19A1), and organic anion transporting polypeptide 1B1 (OATP1B1; gene: SLCO1B1), and the enzymes inosine triphosphatase (ITPA), and glutathione transferase P1 (GSTP1). In addition, we genotyped the patient for the enzymes 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase (AICAR)/inosine monophosphate (IMP) cyclohydrolase (gene name: ATIC), gamma-glutamyl hydrolase (gene name: GGH) and methylenetetrahydrofolate reductase (gene name: MTHFR).Results: The PGx profile of the patient revealed genetic variants in SLC19A1, ABCB1, and MTHFR, which may explain the ADRs experienced during the treatment with MTX and a potentially lower efficacy of MTX. Based on our interpretation of the PGx profile, we recommended the patient to avoid MTX in the future.Conclusion: The MTX pathway is complex, which makes the interpretation of genetic variants affecting metabolism challenging. A reactive PGx panel test was applicable to explain ADRs experienced during MTX treatment for a patient with RA. However, the clinical utility of PGx-guided MTX treatment in a primary care setting is still limited. In order to base a recommendation for MTX on PGx data, we need genome-wide association studies, large prospective multicenter studies and PGx studies, which analyze different multi-gene haplotypes and gene-drug-drug interactions for MTX.Keywords: pharmacogenetics, PGx, ABCB1, SLC19A1, MTHFR, rheumatoid arthritis, methotrexate, MTX
Published: 2022

16. Zahlungsdienste und E-Geld-Geschäft

Author: Meyer zu Schwabedissen, Gustav, primary, Dörner, Barbara, additional, and Schenkel, Bénédict, additional
Published: 2022
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17. Protease-activated receptor 2 deficient mice develop less angiotensin II induced left ventricular hypertrophy but more cardiac fibrosis.

Author: Meyer zu Schwabedissen, Albrecht, Vergarajauregui, Silvia, Bertog, Marko, Amann, Kerstin, Engel, Felix B., and Daniel, Christoph
Subjects: LEFT ventricular hypertrophy, PROTEASE-activated receptors, GENE expression, HEART fibrosis, CARDIAC hypertrophy
Abstract: Aims: Activation of Protease Activated Receptor 2 (PAR2) has been shown to be involved in regulation of injury-related processes including inflammation, fibrosis and hypertrophy. In this study we will investigate the role of PAR2 in cardiac injury in a mouse model of hypertension using continuous infusion with angiotensin II. Methods: Hypertension was induced in 12 weeks old wildtype (wt, n = 8) and PAR2 deficient mice (n = 9) by continuous infusion with angiotensin II for 4 weeks using osmotic minipumps. At the end, hearts were collected for analysis of left ventricular hypertrophy (LVH), myocardial capillary supply, fibrosis and localization of PAR2 expression using histological, immunohistological and mRNA expression analysis techniques. In addition, rat cardiac fibroblasts were treated with angiotensin II and PAR2 was inhibited by a blocking antibody and the PAR2 inhibitor AZ3451. Results: Cardiac PAR2 mRNA expression was downregulated by 40±20% in wt mice treated with AngII compared to untreated controls. Four weeks after AngII treatment, LVH was significantly increased in AngII-treated wt mice compared to similarly treated PAR2-deficient animals as determined by relative heart weight, left ventricular cross-sectional area, and analysis of ventricular lumen area determined on sections. Treatment of wt mice resulted in an approximately 3-fold increase in cardiac expression of FGF23, which was 50% lower in PAR2-deficient animals compared to wt animals and therefore no longer significantly different from expression levels in untreated control mice. In contrast, cardiac interstitial fibrosis was significantly higher in PAR2-deficient mice compared to similar treated wt controls, as assessed by Sirius Red staining (>3-fold) and collagen IV staining (>2-fold). Additional experiments with isolated cardiac fibroblasts showed induction of pro-fibrotic genes when treated with PAR2 inhibitors. Conclusion: In angiotensin II-induced cardiac injury, PAR2 deficiency has an ambivalent effect, enhancing fibrosis on the one hand, but reducing LVH on the other. [ABSTRACT FROM AUTHOR]
Published: 2024
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18. Impact of the clinically approved Petasites hybridus extract Ze 339 on intestinal mechanisms involved in the handling of histamine

Author: Mettler, Lina G., Brecht, Karin, Butterweck, Veronika, and Meyer zu Schwabedissen, Henriette E.
Published: 2022
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19. Development of the Swiss Database for dosing medicinal products in pediatrics

Author: Tilen, Romy, Panis, Dalibor, Aeschbacher, Samuel, Sabine, Thomas, Meyer zu Schwabedissen, Henriette E., and Berger, Christoph
Published: 2022
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20. TOP-140 Evolution of clinical presentation, treatment and prognosis of patients with alveolar echinococcosis treated at the university hospital Zurich: a 50-year experience

Author: Deibel, Ansgar, primary, Kindler, Yannick, additional, Mita, Rubens, additional, Ghafoor, Soleen, additional, Schwabedissen, Cordula Meyer zu, additional, Schweiger, Alexander, additional, Grimm, Felix, additional, Reinehr, Michael, additional, Weber, Achim, additional, Reiner, Cäcilia, additional, Kremer, Andreas E., additional, Petrowsky, Henrik, additional, Clavien, Pierre-Alain, additional, Deplazes, Peter, additional, von Felten, Stefanie, additional, and Mullhaupt, Beat, additional
Published: 2024
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21. A face‐to‐face comparison of the BBB cell models hCMEC/D3 and hBMEC for their applicability to adenoviral expression of transporters

Author: Taggi, Valerio, primary, Schäfer, Anima M., additional, Dolce, Asaél, additional, and Meyer zu Schwabedissen, Henriette E., additional
Published: 2024
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22. Pharmacist-guided pre-emptive pharmacogenetic testing in antidepressant therapy (PrePGx): study protocol for an open-label, randomized controlled trial

Author: Céline K. Stäuble, Markus L. Lampert, Samuel Allemann, Martin Hatzinger, Kurt E. Hersberger, Henriette E. Meyer zu Schwabedissen, Christian Imboden, and Thorsten Mikoteit
Subjects: Pharmacogenomics, Depression, Antidepressant, Pharmaceutical care, Psychiatry, Medicine (General), R5-920
Abstract: Abstract Background It is known that only 50% of patients diagnosed with major depressive disorders (MDD) respond to the first-line antidepressant treatment. Accordingly, there is a need to improve response rates to reduce healthcare costs and patient suffering. One approach to increase rates of treatment response might be the integration of pharmacogenetic (PGx) testing to stratify antidepressant drug selection. The goal of PGx assessments is to identify patients who have an increased risk to experience adverse drug reactions or non-response to specific drugs. Especially for antidepressants, there is compiling evidence on PGx influencing drug exposure as well as response. Methods This study is an open-label, randomized controlled trial conducted in two study centers in Switzerland: (1) the Psychiatric Clinic of Solothurn and (2) the Private Clinic Wyss in Münchenbuchsee. Adult inpatients diagnosed with a unipolar moderate or severe depressive episode are recruited at clinic admission and are included in the study. If the adjustment to a new antidepressant pharmacotherapy is necessary, the participants are randomized to either Arm A (intervention group) or Arm B (control group). If no new antidepressant pharmacotherapy is introduced the participants will be followed up in an observational arm. The intervention is the service of pharmacist-guided pre-emptive PGx testing to support clinical decision making on antidepressant selection and dosing. As a comparison, in the control group, the antidepressant pharmacotherapy is selected by the treating physician according to current treatment guidelines (standard of care) without the knowledge of PGx test results and support of clinical pharmacists. The primary outcome of this study compares the response rates under antidepressant treatment after 4 weeks between intervention and control arm. Discussion The findings from this clinical trial are expected to have a direct impact on inter-professional collaborations for the handling and use of PGx data in psychiatric practice. Trial registration ClinicalTrials.gov NCT04507555 . Registered on August 11, 2020. Swiss National Clinical Trials Portal SNCTP000004015 . Registered August 18, 2020.
Published: 2021
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23. SwissPKcdw – A clinical data warehouse for the optimization of pediatric dosing regimens

Author: Roland Goers, Diana Coman Schmid, Vera F. Jäggi, Paolo Paioni, Michal J. Okoniewski, Althea Parker, Beat Bangerter, Sofia Georgakopoulou, Thierry Sengstag, Julia Bielicki, Romy Tilen, Swen Vermeul, Stefanie D. Krämer, Christoph Berger, Bernd Rinn, and Henriette E. Meyer zu Schwabedissen
Subjects: Therapeutics. Pharmacology, RM1-950
Abstract: Abstract Clinical trials have been performed mainly in adults and accordingly the necessary information is lacking for pediatric patients, especially regarding dosage recommendation for approved drugs. This gap in information could be filled with results from pharmacokinetic (PK) modeling, based on data collected in daily clinical routine. In order to make this data accessible and usable for research, the Swiss Pharmacokinetics Clinical Data Warehouse (SwissPKcdw) project has been set up, including a clinical data warehouse (CDW) and the regulatory framework for data transfer and use within. Embedded into the secure BioMedIT network, the CDW can connect to various data providers and researchers in order to collaborate on the data securely. Due to its modularity, partially containerized deployment and open‐source software, each of the components can be extended, modified, and re‐used for similar projects that require integrated data management, data analysis, and web tools in a secure scientific data and information technology (IT) environment. Here, we describe a collaborative and interprofessional effort to implement the aforementioned infrastructure between several partners from medical health care and academia. Furthermore, we describe a real‐world use case where blood samples from pediatric patients were analyzed for the presence of genetic polymorphisms and the results were aggregated and further analyzed together with the health‐related patient data in the SwissPKcdw.
Published: 2021
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24. Differences in transport function of the human and rat orthologue of the Organic Anion Transporting Polypeptide 2B1 (OATP2B1)

Author: Hussner, Janine, Foletti, Annalise, Seibert, Isabell, Fuchs, Anja, Schuler, Eveline, Malagnino, Vanessa, Grube, Markus, and Meyer zu Schwabedissen, Henriette E.
Published: 2021
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25. Target engagement of the first-in-class CXCR7 antagonist ACT-1004-1239 following multiple-dose administration in mice and humans

Author: Huynh, Christine, Brussee, Janneke M., Pouzol, Laetitia, Fonseca, Marlene, Meyer zu Schwabedissen, Henriette E., Dingemanse, Jasper, and Sidharta, Patricia N.
Published: 2021
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26. HLA‐associated adverse drug reactions ‐ scoping review

Author: Chiara Jeiziner, Ursina Wernli, Katja Suter, Kurt E. Hersberger, and Henriette E. Meyer zu Schwabedissen
Subjects: Therapeutics. Pharmacology, RM1-950, Public aspects of medicine, RA1-1270
Abstract: Abstract Alleles of the human leukocyte antigen (HLA) system have been associated with the occurrence of idiosyncratic adverse drug reactions (ADRs). Accordingly, it is assumed that pre‐emptive testing for the presence of certain HLA alleles (HLA‐typing) could prevent these ADRs in carriers. In order to perceive the current evidence for HLA‐associated ADRs, we conducted a scoping review according to the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA). The literature search on PubMed and on Embase was carried out on the July 8 and 9, 2020, respectively. To be included in the scoping review, the studies had to investigate an association of any HLA‐associated ADR with any small molecule approved and available on the Swiss market. We considered English and German primary literature published since 2002. A total of 149 studies were included, whereof most were retrospective, whereas one was a prospective randomized controlled trial. The majority of the studies (n = 33) described the association of HLA‐B*15:02 with carbamazepine. It was not possible to directly compare the studies, as they were too heterogeneous in terms of the ADR definition, the HLA alleles, the number of participants, and the study types. Therefore, we summarized the results in a descriptive manner. Even if an interpretation of the outcomes remains open, the descriptive overview revealed the prevailing complexity and uncertainty in the field. For the future, consistent definitions on the different phenotypes need to be established and applied and the reporting of association studies should follow a harmonized structure.
Published: 2021
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27. OATP2B1 – The underrated member of the organic anion transporting polypeptide family of drug transporters?

Author: Kinzi, Jonny, Grube, Markus, and Meyer zu Schwabedissen, Henriette E.
Published: 2021
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28. Erratum: Genetic loci associated with heart rate variability and their effects on cardiac disease risk.

Author: Nolte, Ilja, Munoz, M, Tragante, Vinicius, Amare, Azmeraw, Jansen, Rick, Vaez, Ahmad, von der Heyde, Benedikt, Avery, Christy, Bis, Joshua, Dierckx, Bram, van Dongen, Jenny, Gogarten, Stephanie, Goyette, Philippe, Hernesniemi, Jussi, Huikari, Ville, Hwang, Shih-Jen, Jaju, Deepali, Kerr, Kathleen, Kluttig, Alexander, Krijthe, Bouwe, Kumar, Jitender, van der Laan, Sander, Lyytikäinen, Leo-Pekka, Maihofer, Adam, Minassian, Arpi, van der Most, Peter, Müller-Nurasyid, Martina, Nivard, Michel, Salvi, Erika, Stewart, James, Thayer, Julian, Verweij, Niek, Wong, Andrew, Zabaneh, Delilah, Zafarmand, Mohammad, Abdellaoui, Abdel, Albarwani, Sulayma, Albert, Christine, Alonso, Alvaro, Ashar, Foram, Auvinen, Juha, Axelsson, Tomas, Baker, Dewleen, de Bakker, Paul, Barcella, Matteo, Bayoumi, Riad, Bieringa, Rob, Boomsma, Dorret, Boucher, Gabrielle, Britton, Annie, Christophersen, Ingrid, Dietrich, Andrea, Ehret, George, Ellinor, Patrick, Eskola, Markku, Felix, Janine, Floras, John, Franco, Oscar, Friberg, Peter, Gademan, Maaike, Geyer, Mark, Giedraitis, Vilmantas, Hartman, Catharina, Hemerich, Daiane, Hofman, Albert, Hottenga, Jouke-Jan, Huikuri, Heikki, Hutri-Kähönen, Nina, Jouven, Xavier, Junttila, Juhani, Juonala, Markus, Kiviniemi, Antti, Kors, Jan, Kumari, Meena, Kuznetsova, Tatiana, Laurie, Cathy, Lefrandt, Joop, Li, Yong, Li, Yun, Liao, Duanping, Limacher, Marian, Lin, Henry, Lindgren, Cecilia, Lubitz, Steven, Mahajan, Anubha, McKnight, Barbara, Zu Schwabedissen, Henriette, Milaneschi, Yuri, Mononen, Nina, Morris, Andrew, Nalls, Mike, Navis, Gerjan, Neijts, Melanie, Nikus, Kjell, North, Kari, OConnor, Daniel, Ormel, Johan, Perz, Siegfried, Peters, Annette, and Psaty, Bruce
Abstract: This corrects the article DOI: 10.1038/ncomms15805.
Published: 2017

29. Genetic loci associated with heart rate variability and their effects on cardiac disease risk.

Author: Nolte, Ilja M, Munoz, M Loretto, Tragante, Vinicius, Amare, Azmeraw T, Jansen, Rick, Vaez, Ahmad, von der Heyde, Benedikt, Avery, Christy L, Bis, Joshua C, Dierckx, Bram, van Dongen, Jenny, Gogarten, Stephanie M, Goyette, Philippe, Hernesniemi, Jussi, Huikari, Ville, Hwang, Shih-Jen, Jaju, Deepali, Kerr, Kathleen F, Kluttig, Alexander, Krijthe, Bouwe P, Kumar, Jitender, van der Laan, Sander W, Lyytikäinen, Leo-Pekka, Maihofer, Adam X, Minassian, Arpi, van der Most, Peter J, Müller-Nurasyid, Martina, Nivard, Michel, Salvi, Erika, Stewart, James D, Thayer, Julian F, Verweij, Niek, Wong, Andrew, Zabaneh, Delilah, Zafarmand, Mohammad H, Abdellaoui, Abdel, Albarwani, Sulayma, Albert, Christine, Alonso, Alvaro, Ashar, Foram, Auvinen, Juha, Axelsson, Tomas, Baker, Dewleen G, de Bakker, Paul IW, Barcella, Matteo, Bayoumi, Riad, Bieringa, Rob J, Boomsma, Dorret, Boucher, Gabrielle, Britton, Annie R, Christophersen, Ingrid, Dietrich, Andrea, Ehret, George B, Ellinor, Patrick T, Eskola, Markku, Felix, Janine F, Floras, John S, Franco, Oscar H, Friberg, Peter, Gademan, Maaike GJ, Geyer, Mark A, Giedraitis, Vilmantas, Hartman, Catharina A, Hemerich, Daiane, Hofman, Albert, Hottenga, Jouke-Jan, Huikuri, Heikki, Hutri-Kähönen, Nina, Jouven, Xavier, Junttila, Juhani, Juonala, Markus, Kiviniemi, Antti M, Kors, Jan A, Kumari, Meena, Kuznetsova, Tatiana, Laurie, Cathy C, Lefrandt, Joop D, Li, Yong, Li, Yun, Liao, Duanping, Limacher, Marian C, Lin, Henry J, Lindgren, Cecilia M, Lubitz, Steven A, Mahajan, Anubha, McKnight, Barbara, Zu Schwabedissen, Henriette Meyer, Milaneschi, Yuri, Mononen, Nina, Morris, Andrew P, Nalls, Mike A, Navis, Gerjan, Neijts, Melanie, Nikus, Kjell, North, Kari E, O'Connor, Daniel T, Ormel, Johan, Perz, Siegfried, Peters, Annette, and Psaty, Bruce M
Subjects: Humans, Heart Diseases, Genetic Predisposition to Disease, RGS Proteins, Potassium Channels, Muscle Proteins, Risk Factors, Cohort Studies, Blood Pressure, Heart Rate, Polymorphism, Single Nucleotide, Quantitative Trait Loci, European Continental Ancestry Group, Genome-Wide Association Study, Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels, Cardiovascular, Genetics, Heart Disease
Abstract: Reduced cardiac vagal control reflected in low heart rate variability (HRV) is associated with greater risks for cardiac morbidity and mortality. In two-stage meta-analyses of genome-wide association studies for three HRV traits in up to 53,174 individuals of European ancestry, we detect 17 genome-wide significant SNPs in eight loci. HRV SNPs tag non-synonymous SNPs (in NDUFA11 and KIAA1755), expression quantitative trait loci (eQTLs) (influencing GNG11, RGS6 and NEO1), or are located in genes preferentially expressed in the sinoatrial node (GNG11, RGS6 and HCN4). Genetic risk scores account for 0.9 to 2.6% of the HRV variance. Significant genetic correlation is found for HRV with heart rate (-0.74g
Published: 2017

30. Pharmacogenetic information in Swiss drug labels – a systematic analysis

Author: Jeiziner, C., Suter, K., Wernli, U., Barbarino, J. M., Gong, L., Whirl-Carrillo, M., Klein, T. E., Szucs, T. D., Hersberger, K. E., and Meyer zu Schwabedissen, H. E.
Published: 2021
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31. Endogenous Coproporphyrin I and III are Altered in Multidrug Resistance-Associated Protein 2-Deficient (TR−) Rats

Author: Bezençon, Jacqueline, Saran, Chitra, Hussner, Janine, Beaudoin, James J., Zhang, Yueping, Shen, Hong, Fallon, John K., Smith, Philip C., Meyer zu Schwabedissen, Henriette E., and Brouwer, Kim L.R.
Published: 2021
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32. Increased coproporphyrin serum levels in healthy volunteers treated with the cholesterol uptake inhibitor ezetimibe.

Author: Kinzi, Jonny, Grube, Markus, Seibert, Isabell, Siegmund, Werner, and Meyer zu Schwabedissen, Henriette E.
Subjects: ORGANIC anion transporters, ANTICHOLESTEREMIC agents, EZETIMIBE, GLUCURONIDATION, RIFAMPIN
Abstract: Ezetimibe undergoes glucuronidation that results in the active metabolite ezetimibe phenoxy‐glucuronide (ezetimibe‐glucuronide). This phase‐II metabolite was shown to interact with the clinically relevant hepatic transporter organic anion transporting polypeptide (OATP) 1B1. In recent years, coproporphyrin I (CPI) was established as a Tier 1 biomarker for OATP1B‐mediated interactions among other endogenous substrates like CPIII. To evaluate whether levels of the biomarker are affected by ezetimibe treatment, we assessed the impact of ezetimibe and ezetimibe‐glucuronide on OATP1B1‐mediated transport of CPs in vitro. Then, we quantified CP levels in serum samples of healthy volunteers treated with a single oral dose of ezetimibe (20 mg) alone or in combination with rifampin (600 mg). Results from our in vitro experiments showed a significant reduction in cellular CPI accumulation in the presence of ezetimibe‐glucuronide with an IC50 of 1.97 μM [95% CI: 1.04 to 3.96], while CPIII accumulation was impacted by 10 μM and above. In the in vivo study, we observed peak CP concentrations 1.33 h after dosing, which is closest to the tmax of the ezetimibe metabolite. Co‐administration of ezetimibe with rifampin resulted in even higher serum CP levels. The AUC0–24h of CPI and CPIII increased two‐ and threefold, respectively, after concomitant dosing compared to ezetimibe alone. Moreover, we quantified CP levels in cumulative urine from both study phases where the renally excreted amount (Ae) of CPI and CPIII increased after ezetimibe and rifampin co‐administration compared to ezetimibe alone. In conclusion, our findings indicate that rifampin co‐administration results in additional inhibition of OATP1B1 in vivo. [ABSTRACT FROM AUTHOR]
Published: 2024
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33. Enriching Medication Review with a Pharmacogenetic Profile – A Case of Tamoxifen Adverse Drug Reactions

Author: Jeiziner C, Stäuble CK, Lampert ML, Hersberger KE, and Meyer zu Schwabedissen HE
Subjects: pharmacogenetics (pgx), cyp2d6, cyp2c9, cyp2c19, medication review, tamoxifen, Therapeutics. Pharmacology, RM1-950
Abstract: Chiara Jeiziner,1 Céline K Stäuble,1,2 Markus L Lampert,1 Kurt E Hersberger,1 Henriette E Meyer zu Schwabedissen2 1Pharmaceutical Care Research Group, Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland; 2Biopharmacy, Department of Pharmaceutical Sciences, University of Basel, Basel, SwitzerlandCorrespondence: Chiara JeizinerPharmaceutical Care Research Group; University of Basel, Petersplatz 14, Postfach 2148, Basel, 4001, SwitzerlandTel +41 61 207 61 80Email chiara.jeiziner@unibas.chAbstract: Pharmacogenotyping is applied to determine the hereditable component of a patient’s susceptibility to experience therapy failure and/or adverse drug reactions (ADRs). We present the case of a female patient diagnosed with breast cancer and treated with tamoxifen as recurrence therapy who experienced various ADRs. Pharmacogenotyping revealed variants in the cytochrome P450 (CYP) enzymes CYP2D6, CYP2C9, and CYP2C19. The observed genotype was associated with a risk for lower tamoxifen efficacy. Aside from the tamoxifen therapy, the comedication was reviewed for the influence of the patient’s pharmacogenetic profile. As a result of this pharmacist-led medication review with pharmacogenetic analyses, concrete genotype-driven recommendations for the treating gynecologist were compiled. This case revealed the added value of a large pharmacogenetic panel and the complexity of integrating a pharmacogenetic profile into a recommendation.Keywords: pharmacogenetics, PGx, CYP2D6, CYP2C9, CYP2C19, medication review, tamoxifen
Published: 2021

34. Case report: Non-response to fluoxetine in a homozygous 5-HTTLPR S-allele carrier of the serotonin transporter gene

Author: Céline K. Stäuble, Rebecca Meier, Markus L. Lampert, Thorsten Mikoteit, Martin Hatzinger, Samuel S. Allemann, Kurt E. Hersberger, and Henriette E. Meyer zu Schwabedissen
Subjects: pharmacogenetics, depression, pharmaceutical care, SLC6A4, 5-HTT, ABCB1, Psychiatry, RC435-571
Abstract: We report the case of a 50-year-old male with major depressive disorder (MDD) to illustrate the challenge of finding effective antidepressant pharmacotherapy and the role that the patient’s genetic makeup may play. Recent treatment attempts before clinic admission included venlafaxine and fluoxetine. Venlafaxine was discontinued due to lack of response, and subsequently switched to fluoxetine based on pharmacogenotyping of the P-glycoprotein transporter (P-gp, encoded by ABCB1) by the outpatient psychiatrist. Despite steady state serum levels within the therapeutic range, the patient did not benefit from fluoxetine either, necessitating admission to our clinic. Here a clinical pharmacist-led medication review including additional pharmacogenetic (PGx) analysis resulted in the change of the antidepressant therapy to bupropion. Under the new regimen, established in the in-patient-setting, the patient remitted. However, based on the assessed pharmacokinetics-related gene variants, including CYPs and ABCB1, non-response to fluoxetine could not be conclusively explained. Therefore, we retrospectively selected the serotonin transporter (SERT1, encoded by SLC6A4) for further genetic analysis of pharmacodynamic variability. The patient presented to be a homozygous carrier of the short allele variant in the 5-HTTLPR (S/S) located within the SLC6A4 promoter region, which has been associated with a reduced expression of the SERT1. This case points out the potential relevance of panel PGx testing considering polymorphisms in genes of pharmacokinetic as well as pharmacodynamic relevance.
Published: 2022
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35. Genetic variants of SLCO1B7 are of relevance for the transport function of OATP1B3-1B7

Author: Meyer zu Schwabedissen, Henriette E., Seibert, Isabell, Grube, Markus, Alter, Claudio L., Siegmund, Werner, and Hussner, Janine
Published: 2020
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36. Relevance of the CXCR4/CXCR7-CXCL12 axis and its effect in pathophysiological conditions

Author: Huynh, Christine, Dingemanse, Jasper, Meyer zu Schwabedissen, Henriette E., and Sidharta, Patricia N.
Published: 2020
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37. The surgical safety checklist and patient outcomes after surgery: a prospective observational cohort study, systematic review and meta-analysis

Author: Pearse, Rupert M., Beattie, Scott, Clavien, Pierre-Alain, Demartines, Nicolas, Fleisher, Lee A., Grocott, Mike, Haddow, James, Hoeft, Andreas, Holt, Peter, Moreno, Rui, Pritchard, Naomi, Rhodes, Andrew, Wijeysundera, Duminda, Wilson, Matt, Ahmed, Tahania, Everingham, Kirsty, Hewson, Russell, Januszewska, Marta, Phull, Mandeep-Kaur, Halliwell, Richard, Shulman, Mark, Myles, Paul, Schmid, Werner, Hiesmayr, Michael, Wouters, Patrick, de Hert, Stefan, Lobo, Suzana, Fang, Xiangming, Rasmussen, Lars, Futier, Emmanuel, Biais, Matthieu, Venara, Aurélien, Slim, Karem, Sander, Michael, Koulenti, Despoina, Arvaniti, Kostoula, Chan, Mathew, Kulkarni, Atul, Chandra, Susilo, Tantri, Aida, Geddoa, Emad, Abbas, Muntadhar, Della Rocca, Giorgio, Sivasakthi, Datin, Mansor, Marzida, Luna, Pastor, Bouwman, Arthur, Buhre, Wolfgang, Beavis, Vanessa, Campbell, Douglas, Short, Tim, Osinaike, Tunde, Matos, Ricardo, Grigoras, Ioana, Kirov, Mikhail, Protsenko, Denis, Biccard, Bruce, Aldecoa, Cesar, Chew, Michelle, Hofer, Christoph, Hubner, Martin, Ditai, James, Szakmany, Tamas, Fleisher, Lee, Ferguson, Marissa, MacMahon, Michael, Cherian, Ritchie, Currow, Helen, Kanathiban, Kathirgamanathan, Gillespie, David, Pathmanathan, Edward, Phillips, Katherine, Reynolds, Jenifer, Rowley, Joanne, Douglas, Jeanene, Kerridge, Ross, Garg, Sameer, Bennett, Michael, Jain, Megha, Alcock, David, Terblanche, Nico, Cotter, Rochelle, Leslie, Kate, Stewart, Marcelle, Zingerle, Nicolette, Clyde, Antony, Hambidge, Oliver, Rehak, Adam, Cotterell, Sharon, Huynh, Wilson Binh Quan, McCulloch, Timothy, Ben-Menachem, Erez, Egan, Thomas, Cope, Jennifer, Fellinger, Paul, Haisjackl, Markus, Haselberger, Simone, Holaubek, Caroline, Lichtenegger, Paul, Scherz, Florian, Hoffer, Franz, Cakova, Veronika, Eichwalder, Andreas, Fischbach, Norbert, Klug, Reinhold, Schneider, Elisabeth, Vesely, Martin, Wickenhauser, Reinhart, Grubmueller, Karl Gernot, Leitgeb, Marion, Lang, Friedrich, Toro, Nancy, Bauer, Marlene, Laengle, Friedrich, Haberl, Claudia, Mayrhofer, Thomas, Trybus, Christoph, Buerkle, Christian, Forstner, Karin, Germann, Reinhard, Rinoesl, Harald, Schindler, Elke, Trampitsch, Ernst, Bogner, Gerhard, Dankl, Daniel, Duenser, Martin, Fritsch, Gerhard, Gradwohl-Matis, Ilse, Hartmann, Andreas, Hoelzenbein, Thomas, Jaeger, Tarkan, Landauer, Franz, Lindl, Gregor, Lux, Michael, Steindl, Johannes, Stundner, Ottokar, Szabo, Christian, Bidgoli, Jawad, Verdoodt, Hans, Forget, Patrice, Kahn, David, Lois, Fernande, Momeni, Mona, Prégardien, Caroline, Pospiech, Audrey, Steyaert, Arnaud, Veevaete, Laurent, De Kegel, Dirk, De Jongh, Karen, Foubert, Luc, Smitz, Carine, Vercauteren, Marcel, Poelaert, Jan, Van Mossevelde, Veerle, Abeloos, Jacques, Bouchez, Stefaan, Coppens, Marc, De Baerdemaeker, Luc, Deblaere, Isabel, De Bruyne, Ann, Fonck, Kristine, Heyse, Bjorn, Jacobs, Tom, Lapage, Koen, Moerman, Anneliese, Neckebroek, Martine, Parashchanka, Aliaksandra, Roels, Nathalie, Van Den Eynde, Nancy, Vandenheuvel, Michael, Limmen, JurgenVan, Vanluchene, Ann, Vanpeteghem, Caroline, Wyffels, Piet, Huygens, Christel, Vandenbempt, Punitha, Van de Velde, Marc, Dylst, Dimitri, Janssen, Bruno, Schreurs, Evelien, Aleixo, Fábia Berganton, Candido, Keulle, Batista, Hugo Dias, Guimarães, Mario, Guizeline, Jaqueline, Hoffmann, João, Lobo, Francisco Ricardo Marques, Nascimento, Vinícius, Nishiyama, Katia, Pazetto, Lucas, Souza, Daniela, Rodrigues, Rodrigo Souza, Vilela dos Santos, Ana Maria, Jardim, Jaquelline, Sá Malbouisson, Luiz Marcelo, Silva, Joao, Nascimento Junior, Paulo do, Baio, Thalissa Hermínia, Pereira de Castro, Gabriel Isaac, Watanabe Oliveira, Henri Roger, Amendola, Cristina Prata, Cardoso, Gutemberg, Ortega, Daniela, Brotto, Ana Flavia, De Oliveira, Mirella Cristine, Réa-Neto, Álvaro, Dias, Fernando, Travi, Maria Eduarda, Zerman, Luiza, Azambuja, Pedro, Knibel, Marcos Freitas, Martins, Antonio, Almeida, William, Neto, Calim Neder, Tardelli, Maria Angela, Caser, Eliana, Machado, Marcio, Aguzzoli, Crisitiano, Baldisserotto, Sérgio, Tabajara, Fernanda Beck, Bettega, Fernanda, Rodrigues Júnior, La Hore Correa, de Gasperi, Julia, Faina, Lais, Nolasco, Marcos Farias, Ferreira da Costa Fischer, Bruna, Fosch de Campos Ferreira, Mariana, Hartmann, Cristina, Kliemann, Marta, Hubert Ribeiro, Gustavo Luis, Fraga, Julia Merladete, Netto, Thiago Motta, Pozza, Laura Valduga, Wendling, Paulo Rafael, Azevedo, Caroline, Garcia, Juliana, Lopes, Marcel, Maia, Bernardo, Maselli, Paula, Melo, Ralph, Mendes, Weslley, Neves, Matheus, Ney, Jacqueline, Piras, Claudio, Applewhaite, Christopher, Carr, Adrienne, Chow, Lorraine, Duttchen, Kaylene, Foglia, Julena, Greene, Michael, Hinther, Ashley, Houston, Kendra, McCormick, Thomas Jared, Mikhayel, Jennifer, Montasser, Sam, Ragan, Alex, Suen, Andrew, Woolsey, Adrianna, Yu, Hai Chuan, Funk, Duane, Kowalski, Stephen, Legaspi, Regina, McDonald, Heather, Siddiqui, Faisal, Pridham, Jeremy, Rowe, Bernadette, Sampson, Sonia, Thiessen, Barton, Zbitnew, Geoff, Bernard, Andre, George, Ronald, Jones, Philip, Moor, Rita, Siddiqui, Naveed, Wolfer, Alexandra, Tran, Diem, Winch, Denyse, Dobson, Gary, McCormick, Thomas, Montasser, Osama, Hall, Richard, Baghirzada, Leyla, Curley, Gerard, Dai, Si Yuan, Hare, Gregory, Lee, Esther, Shastri, Uma, Tsui, Albert, Yagnik, Anmol, Alvares, Danielle, Choi, Stephen, Dwyer, Heather, Flores, Kathrina, McCartney, Colin, Somascanthan, Priya, Carroll, Jo, Pazmino-Canizares, Janneth, Ami, Noam, Chan, Vincent, Perlas, Anahi, Argue, Ruth, Huang, Yang, Lavis, Katie, Mayson, Kelly, Cao, Ying, Gao, Hong, Hu, Tingju, Lv, Jie, Yang, Jian, Yang, Yang, Zhong, Yi, Zhou, Jing, Zou, Xiaohua, He, Miao, Li, Xiaoying, Luo, Dihuan, Wang, Haiying, Yu, Tian, Chen, Liyong, Wang, Lijun, Cai, Yunfei, Cao, Zhongming, Li, Yanling, Lian, Jiaxin, Sun, Haiyun, Wang, Sheng, Wang, Zhipeng, Wang, Kenru, Zhu, Yi, Du, Xindan, Fan, Hao, Fu, Yunbin, Huang, Lixia, Huang, Yanming, Hwan, Haifang, Luo, Hong, Qu, Pi-Sheng, Tao, Fan, Wang, Zhen, Wang, Guoxiang, Wang, Shun, Zhang, Yan, Zhang, Xiaolin, Chen, Chao, Wang, Weixing, Liu, Zhengyuan, Fan, Lihua, Tang, Jing, Chen, Yijun, Chen, Yongjie, Han, Yangyang, Huang, Changshun, Liang, Guojin, Shen, Jing, Wang, Jun, Yang, Qiuhong, Zhen, Jungang, Zhou, Haidong, Chen, Junping, Chen, Zhang, Li, Xiaoyu, Meng, Bo, Ye, Haiwang, Zhang, Xiaoyan, Bi, Yanbing, Cao, Jianqiao, Guo, Fengying, Lin, Hong, Liu, Yang, Lv, Meng, Shi, Pengcai, Song, Xiumei, Sun, Chuanyu, Sun, Yongtao, Wang, Yuelan, Wang, Shenhui, Zhang, Min, Chen, Rong, Hou, Jiabao, Leng, Yan, Meng, Qing-tao, Qian, Li, Shen, Zi-ying, Xia, Zhong-yuan, Xue, Rui, Zhang, Yuan, Zhao, Bo, Zhou, Xian-jin, Chen, Qiang, Guo, Huinan, Guo, Yongqing, Qi, Yuehong, Wang, Zhi, Wei, Jianfeng, Zhang, Weiwei, Zheng, Lina, Bao, Qi, Chen, Yaqiu, Chen, Yijiao, Fei, Yue, Hu, Nianqiang, Hu, Xuming, Lei, Min, Li, Xiaoqin, Lv, Xiaocui, Miao, Fangfang, Ouyang, Lingling, Qian, Lu, Shen, Conyu, Sun, Yu, Wang, Yuting, Wang, Dong, Wu, Chao, Xu, Liyuan, Yuan, 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Cristina, Tosa, Flaviu, Tranca, Sebastian, Copotoiu, Sanda Maria, Ungureanu, Liviu Lucian, Harsan, Cristian Remus, Papurica, Marius, Cernea, Daniela Denisa, Dragoescu, Nicoleta Alice, CarmenVaida, Laura Aflori, Ciobotaru, Oana Roxana, Aignatoaie, Mariana, Carp, Cristina Paula, Cobzaru, Isabelle, Mardare, Oana, Purcarin, Bianca, Tutunaru, Valentin, Ionita, Victor, Arustei, Mirela, Codita, Anisoara, Busuioc, Mihai, Chilinciuc, Ion, Ciobanu, Cristina, Belciu, Ioana, Tincu, Eugen, Blaj, Mihaela, Grosu, Ramona - Mihaela, Sandu, Gigel, Bruma, Dana, Corneci, Dan, Dutu, Madalina, Krepil, Adriana, Copaciu, Elena, Dumitrascu, Clementina Oana, Jemna, Ramona, Mihaescu, Florentina, Petre, Raluca, Tudor, Cristina, Ursache, Elena, Kulikov, Alexander, Lubnin, Andrey, Grigoryev, Evgeny, Pugachev, Stanislav, Tolmasov, Alexander, Hussain, Ayyaz, Ilyina, Yana, Roshchina, Anna, Iurin, Aleksandr, Chazova, Elena, Dunay, Artem, Karelov, Alexey, Khvedelidze, Irina, Voldaeva, Olga, Belskiy, Vladislav, Dzhamullaev, Parvin, Grishkowez, Elena, Kretov, Vladimir, Levin, Valeriy, Molkov, Aleksandr, Puzanov, Sergey, Samoilenko, Aleksandr, Tchekulaev, Aleksandr, Tulupova, Valentina, Utkin, Ivan, Allorto, Nikki Leigh, Bishop, David Gray, Builu, Pierre Monji, Cairns, Carel, Dasrath, Ashish, de Wet, Jacques, Hoedt, Marielle den, Grey, Ben, Hayes, Morgan Philip, Küsel, Belinda Senta, Shangase, Nomcebo, Wise, Robert, Cacala, Sharon, Farina, Zane, Govindasamy, Vishendran, Kruse, Carl-Heinz, Lee, Carolyn, Marais, Leonard, Naidoo, Thinagrin Dhasarthun, Rajah, Chantal, Rodseth, Reitze Nils, Ryan, Lisa, von Rhaden, Richard, Adam, Suwayba, Alphonsus, Christella, Ameer, Yusuf, Anderson, Frank, Basanth, Sujith, Bechan, Sudha, Bhula, Chettan, Biccard, Bruce M., Biyase, Thuli, Buccimazza, Ines, Cardosa, Jorge, Chen, James, Daya, Bhavika, Drummond, Leanne, Elabib, Ali, Abdel Goad, Ehab Helmy, Goga, Ismail E., Goga, Riaz, Harrichandparsad, R., Hodgson, Richard E., Jordaan, J., Kalafatis, Nicky, Kampik, Christian, Landers, A.T., Loots, Emil, Madansein, Rajhmum, Madaree, Anil, Madiba, Thandinkosi E., Manzini, Vukani T., Mbuyisa, Mbali, Moodley, Rajan, Msomi, Mduduzi, Mukama, Innocent, Naidoo, Desigan, Naidoo, Rubeshan, Naidu, Tesuven K., Ntloko, Sindiswa, Padayachee, Eneshia, Padayachee, Lucelle, Phaff, Martijn, Pillay, Bala, Pillay, Desigan, Pillay, Lutchmee, Ramnarain, Anupa, Ramphal, Suren R., Ryan, Paul, Saloojee, Ahmed, Sebitloane, Motshedisi, Sigcu, Noluyolo, Taylor, Jenna L., Torborg, Alexandra, Visser, Linda, Anderson, Philip, Conradie, Alae, de Swardt, Mathew, de Villiers, Martin, Eikman, Johan, Liebenberg, Riaan, Mouton, Johan, Paton, Abbey, van der Merwe, Louwrence, Wilscott-Davids, Candice, Barrett, Wendy Joan, Bester, Marlet, de Beer, Johan, Geldenhuys, Jacques, Gouws, Hanni, Potgieter, Jan-Hendrik, Strydom, Magdel, WilberforceTurton, Edwin, Chetty, Rubendraj R., Chirkut, Subash, Cronje, Larissa, de Vasconcellos, Kim, Dube, Nokukhanya Z., Gama, N. Sibusiso, Green, Garyth M., Green-Thompson, Randolph, Kinoo, Suman Mewa, Kistnasami, Prenolin, Maharaj, Kapil, Moodley, Manogaran S., Mothae, Sibongile J., Naidoo, Ruvashni, Aslam F Noorbhai, M., Rughubar, Vivesh, Reddy, Jenendhiran, Singh, Avesh, Skinner, David L., Smith, Murray J., Singh, Bhagwan, Misra, Ravi, Naidoo, Maheshwar, Ramdharee, Pireshin, Selibea, Yvonne, Sewpersad, Selina, Sham, Shailendra, Wessels, Joseph D., Africander, Cucu, Bejia, Tarek, Blakemore, Stephen P., Botes, Marisa, Bunwarie, Bimalshakth, Hernandez, Carlos B., Jeeraz, Mohammud A., Legutko, Dagmara A., Lopez, Acela G., De Meyer, Jenine N., Muzenda, Tanaka, Naidoo, Noel, Patel, Maryam, Pentela, Rao, Junge, Marina, Mansoor, Naj, Rademan, Lana, Scislowski, Pawel, Seedat, Ismail, van den Berg, Bianca, van der Merwe, Doreen, van Wyk, Steyn, Govender, Komalan, Naicker, Darshan, Ramjee, Rajesh, Saley, Mueen, Kuhn, Warren Paul, Matos-Puig, Roel, Alberto Lisi, Zaheer Moolla, Perez, Gisela, Beltran, Anna Valle, Lozano, Angels, Navarro, Carlos Delgado, Duca, Alejandro, Ernesto, Ernesto Pastor Martinez, Ferrando, Carlos, Fuentes, Isabel, García-Pérez, Maria Luisa, Gracia, Estefania, Palomares, Ana Izquierdo, Katime, Antonio, Miñana, Amanda, Incertis, Raul Raul, Romero, Esther, Romero Garcia, Carolina Soledad, Rubio, Concepcion, Artiles, Tania Socorro, Soro, Marina, Valls, Paola, Laguarda, Gisela Alaman, Benavent, Pau, Cuenca, Vicente Chisbert, Cueva, Andreu, Lafuente, Matilde, Parra, Asuncion Marques, Rodrigo, Alejandra Romero, Sanchez-Morcillo, Silvia, Tormo, Sergi, Redondo, Francisco Javier, De Andrés Ibanez, José Antonio, Diago, Lorena Gómez, José Hernández Cádiz, Maria, Manuel, Granell Gil, Peris, Raquel, Saiz, Cristina, Vivo, Jose Tatay, Soto, Maria Teresa Tebar, Brunete, Tamara, Cancho, David, Delgado García, David R., Zamudio, Diana, Del Valle, Santiago Garcia, Serrano, M. Luz, Alonso, Eduardo, Anillo, Victor, Maseda, Emilio, Salgado, Patricia, Suarez, Luis, Suarez-de-la-Rica, Alejandro, Villagrán, María José, Alonso, José Ignacio, Cabezuelo, Estefania, Garcia-Saiz, Irene, Lopez del Moral, Olga, Martín, Silvia, Gonzalez, Alba Perez, Doncel, Ma Sherezade Tovar, Vera, Martin Agüero, José Ávila Sánchez, Francisco, Castaño, Beatriz, Moreira, Beatriz Castaño, Risco, Sahely Flores, Martín, Daniel Paz, Martín, Fernando Pérez, Poza, Paloma, Ruiz, Adela, Serna Martínez, Wilson Fabio, Vicente, Bárbara Vázquez, Dominguez, Saul Velaz, Fernández, Salvador, Munoz-López, Alfonso, Bernat, Maria Jose, Mas, Arantxa, Planas, Kenneth, Jawad, Monir, Saeed, Yousif, Hedin, Annika, Levander, Helena, Holmström, Sandra, Lönn, David, Zoerner, Frank, Åkring, Irene, Widmark, Carl, Zettergren, Jan, Liljequist, Victor Aspelund, Nystrom, Lena, Odeberg-Wernerman, Suzanne, Oldner, Anders, Fagerlund, Malin Jonsson, Reje, Patrik, Lyckner, Sara, Sperber, Jesper, Adolfsson, Anne, Klarin, Bengt, Ögren, Katrin, Barras, Jean-Pierre, Bührer, Thomas, Despotidis, Vasileios, Helmy, Naeder, Holliger, Stephan, Raptis, Dimitri Aristotle, Schmid, Roger, Meyer, Antoine, Jaquet, Yves, Kessler, Ulf, Muradbegovic, Mirza, Nahum, Solange R., Rotunno, Teresa, Schiltz, Boris, Voruz, François, Worreth, Marc, Christoforidis, Dimitri, Popeskou, Sotirios Georgios, Furrer, Markus, Prevost, Gian Andrea, Stocker, Andrea, Lang, Klaus, Breitenstein, Stefan, Ganter, Michael T., Geisen, Martin, Soll, Christopher, Korkmaz, Michelle, Lubach, Iris, Schmitz, Michael, Meyer zu Schwabedissen, Moritz, Moritz, Meyer zu Schwabedissen, Zingg, Urs, Hillermann, Thomas, Wildi, Stefan, Pinto, Bernardo Bollen, Walder, Bernhard, Mariotti, Giustina, Slankamenac, Ksenija, Namuyuga, Mirioce, Kyomugisha, Edward, Kituuka, Olivia, Shikanda, Anne Wesonga, Kakembo, Nasser, Tom, Charles Otim, Antonina, Webombesa, Bua, Emmanuel, Ssettabi, Eden Michael, Epodoi, Joseph, Kabagenyi, Fiona, Kirya, Fred, Dempsey, Ged, Seasman, Colette, Nawaz Khan, Raja Basit, Kurasz, Claire, Macgregor, Mark, Shawki, Burhan, Francis, Daren, Hariharan, Vimal, Chau, Simon, Ellis, Kate, Butt, Georgina, Chicken, Dennis-Wayne, Christmas, Natasha, Allen, Samantha, Daniel, Gayatri Daniel, Dempster, Angie, Kemp, Juliette, Matthews, Lewis, Mcglone, Philip, Tambellini, Joanne, Trodd, Dawn, Freitas, Katie, Garg, Atul, Gupta, Janesh Kumar, Karpate, Shilpaja, Kulkarni, Aditi, O'Hara, Chloe, Troko, Jtroko, Angus, Kirsty, Bradley, Jacqueline, Brennan, Emma, Brooks, Carolyn, Brown, Janette, Brown, Gemma, Finch, Amanda, Gratrix, Karen, Hesketh, Sue, Hill, Gillian, Jeffs, Carol, Morgan, Maureen, Pemberton, Chris, Slawson, Nicola, Spickett, Helen, Swarbrick, Gemma, Thomas, Megan, Van Duyvenvoorde, Greta, Brennan, Andrew, Briscoe, Richard, Cooper, Sarah, Lawton, Tom, Northey, Martin, Senaratne, Rashmi, Stanworth, Helen, Burrows, Lorna, Cain, Helen, Craven, Rachael, Davies, Keith, Jonas, Attila, Pachucki, Marcin, Walkden, Graham, Davies, Helen, Gudaca, Mariethel, Hobrok, Maria, Arawwawala, Dilshan, Fergey, Lauren, Gardiner, Matthew, Gunn, Jacqueline, Johnson, Lyndsay, Lofting, Amanda, Lyle, Amanda, Neela, Fiona Mc, Smolen, Susan, Topliffe, Joanne, Williams, Sarah, Bland, Martin, Balaji, Packianathaswamy, Kaura, Vikas, Lanka, Prasad, Smith, Neil, Ahmed, Ahmed, Myatt, John, Shenoy, Ravikiran, Soon, Wai Cheong, Tan, Jessica, Karadia, Sunny, Self, James, Durant, Emma, Tripathi, Shiva, Bullock, Clare, Campbell, Debbie, Ghosh, Alison, Hughes, Thomas, Zsisku, Lajos, Bengeri, Sheshagiri, Cowton, Amanda, Khalid, Mohammed Shazad, Limb, James, McAdam, Colin, Porritt, Mandy, Rafi, M. Amir, Shekar, Priya, Adams, David, Harden, Catherine, Hollands, Heidi, King, Angela, March, Linda, Minto, Gary, Patrick, Abigail, Squire, Rosalyn, Waugh, Darren, Kumara, Paramesh, Simeson, Karen, Yarwood, Jamie, Browning, Julie, Hatton, Jonathan, Julian, Howes, Mitra, Atideb, Newton, Maria, Pernu, Pawan Kootelu, Wilson, Alison, Commey, Thelma, Foot, Helen, Glover, Lyn, Gupta, Ajay, Lancaster, Nicola, Levin, Jill, Mackenzie, Felicity, Mestanza, Claire, Nofal, Emma, Pout, Lauren, Varden, Rosanna, Wild, Jonathan, Jones, Stephanie, Moreton, Sarah, Pulletz, Mark, Davies, Charlotte, Martin, Matthew, Thomas, Sian, Burns, Karen, McArthur, Carol, Patel, Panna, Lau, Gary, Rich, Natalie, Davis, Fiona, Lyons, Rachel, Port, Beth, Prout, Rachel, Smith, Christopher, Adelaja, Yemi, Bennett, Victoria, Bidd, Heena, Dumitrescu, Alexandra, Murphy, Jacqui Fox, Keen, Abigail, Mguni, Nhlanhla, Ong, Cheng, Adams, George, Boshier, Piers, Brown, Richard, Butryn, Izabella, Chatterjee, Jayanta, Freethy, Alexander, Lockwood, Geoffrey, Tsakok, Maria, Tsiligiannis, Sophia, Peat, William, Stephenson, Lorraine, Bradburn, Mike, Pick, Sara, Cunha, Pedro, Olagbaiye, Olufemi, Tayeh, Salim, Packianathaswamy, Balaji, Abernethy, Caroline, Balasubramaniam, Madhu, Bennett, Rachael, Bolton, David, Martinson, Victoria, Naylor, Charde, Bell, Stephanie, Heather, Blaylock, Kushakovsky, Vlad, Alcock, Liam, Alexander, Hazel, Anderson, Colette, Baker, Paul, Brookes, Morag, Cawthorn, Louise, Cirstea, Emanuel, Clarkson, Rachel, Colling, Kerry, Coulter, Ian, Das, Suparna, Haigh, Kathryn, Hamdan, Alhafidz, Hugill, Keith, Kottam, Lucksy, Lisseter, Emily, Mawdsley, Matthew, McGivern, Julie, Padala, Krishnaveni, Phelps, Victoria, Ramesh kumar, Vineshykaa, Stewart, Kirsten, Towse, Kayley, Tregonning, Julie, Vahedi, Ali, Walker, Alycon, Baines, Duncan, Bilolikar, Anjali, Chande, Shiv, Copley, Edward, Dunk, Nigel, Kulkarni, Raghavendra, Kumar, Pawan, Metodiev, Yavor, Ncomanzi, Dumisani, Raithatha, Bhavesh, Raymode, Parizade, Szafranski, Jan, Twohey, Linda, Watt, Philip, Weatherall, Lucie, Weatherill, J., Whitman, Zoe, Wighton, Elinor, Abayasinghe, Chamika, Chan, Alexander, Darwish, Sharif, Gill, James, Glasgow, Emma, Hadfield, Daniel, Harris, Clair, Hopkins, Phil, Kochhar, Arun, Kunst, Gudrun, Mellis, Clare, Pool, Andrew, Riozzi, Paul, Selman, Andrew, Smith, Emma-Jane, Vele, Liana, Gercek, Yuksel, Guy, Kramer, Holden, Douglas, Watson, Nicholas, Whysall, Karen, Andreou, Prematie, Hales, Dawn, Thompson, Jonathan, Bowrey, Sarah, McDonald, Shara, Gilmore, Jemma, Hills, Vicky, Kelly, Chan, Kelly, Sinead, Lloyd, Geraint, Abbott, Tom, Gall, Lewis, Torrance, Hew, Vivian, Mark, Berntsen, Emer, Nolan, Tracey, Turner, Angus, Vohra, Akbar, Brown, Andrew, Clark, Richard, Coughlan, Elaine, Daniel, Conway, Patvardhan, Chinmay, Pearson, Rachel, Predeep, Sheba, Saad, Hesham, Shanmugam, Mohanakrishnan, Varley, Simon, Wylie, Katharine, Cooper, Lucy, Makowski, Arystarch, Misztal, Beata, Moldovan, Eliza, Pegg, Claire, Donovan, Andrew, Foot, Jayne, Large, Simon, Claxton, Andrew, Netke, Bhagyashree, Armstrong, Richard, Calderwood, Claire, Kwok, Andy, Mohr, Otto, Oyeniyi, Peter, Patnaik, Lisa, Post, Benjamin, Ali, Sarah, Arshad, Homa, Baker, Gerard, Brenner, Laura, Brincat, Maximilian, Brunswicker, Annemarie, Cox, Hannah, Cozar, Octavian Ionut, Cheong, Edward, Durst, Alexander, Fengas, Lior, Flatt, Jim, Glister, Georgina, Narwani, Vishal, Photi, Evangelos, Rankin, Adeline, Rosbergen, Melissa, Tan, Mark, Beaton, Ceri, Horn, Rachel, Hunt, Jane, Rousseau, Guy, Stancombe, Lucia, Absar, Mohammed, Allsop, Joanne, Drinkwater, Zoe, Hodgkiss, Tracey, Smith, Kirsty, Brown, Jamie, Alexander-Sefre, Farhad, Campey, Lorraine, Dudgeon, Lucy, Hall, Kathryn, Hitchcock, Rachael, James, Lynne, Smith, Kate, Winstone, Ulrika, Ahmad, Norfaizan, Bauchmuller, Kris, Harrison, Jonathan, Jeffery, Holly, Miller, Duncan, Pinder, Angela, Pothuneedi, Sailaja, Rosser, Jonathan, Sanghera, Sumayer, Swift, Diane, Walker, Rachel, Bester, Delia, Cavanagh, Sarah, Cripps, Heather, Daniel, Harvey, Lynch, Julie, Paton, Alison, Pyke, Shirley, Scholefield, John, Whitworth, Helen, Bottrill, Fiona, Ramalingam, Ganesh, Webb, Stephen, Akerman, Nik, Antill, Philip, Bourner, Lynsey, Buckley, Sarah, Castle, Gail, Charles, Rob, Eggleston, Christopher, Foster, Rebecca, Gill, Satwant, Lindley, Kate, Lklouk, Mohamed, Lowery, Tracey, Martin, Oliver, Milne, David, O'Connor, Patrick, Ratcliffe, Andrew, Rose, Alastair, Smith, Annie, Varma, Sandeep, Ward, Jackie, Barcraft-Barnes, Helena, Camsooksai, Julie, Colvin, Carolyn, Reschreiter, Henrik, Tbaily, Lee, Venner, Nicola, Hamilton, Caroline, Kelly, Lewis, Toth-Tarsoly, Piroska, Dodsworth, Kerry, Foord, Denise, Gordon, Paul, Hawes, Elizabeth, Lamb, Nikki, Mouland, Johanna, Nightingale, Jeremy, Rose, Steve, Schrieber, Joe, Al'Amri, Khalid, Aladin, Hafiz, Arshad, Mohammed Asif, Barraclough, James, Bentley, Conor, Bergin, Colin, Carrera, Ronald, Clarkson, Aisling, Collins, Michelle, Cooper, Lauren, Denham, Samuel, Griffiths, Ewen, Ip, Peter, Jeyanthan, Somasundaram, Joory, Kavita, Kaur, Satwant, Marriott, Paul, Mitchell, Natalie, Nagaiah, Sukumar, Nilsson, Annette, Parekh, Nilesh, Pope, Martin, Seager, Joseph, Serag, Hosam, Tameem, Alifia, Thomas, Anna, Thunder, Joanne, Torrance, Andrew, Vohra, Ravinder, Arlo whitehouse, Wong, Tony, Blunt, Mark, Wong, Kate, Giles, Julian, Reed, Isabelle, Weller, Debbie, Bell, Gillian, Birch, Julie, Damant, Rose, Maiden, Jane, Mewies, Clare, Prince, Claire, Radford, Jane, Reynolds, Tim, Balain, Birender, Banerjee, Robin, Barnett, Andrew, Burston, Ben, Davies, Kirsty, Edwards, Jayne, Evans, Chris, Ford, David, Gallacher, Pete, Hill, Simon, Jaffray, David, Karlakki, Sudheer, Kelly, Cormac, Kennedy, Julia, Kiely, Nigel, Lewthwaite, Simon, Marquis, Chris, Ockendon, Matthew, Phillips, Stephen, Pickard, Simon, Richardson, James, Roach, Richard, Smith, Tony, Spencer-Jones, Richard, Steele, Niall, Steen, Julie, Van Liefland, Marck, White, Steve, Faulds, Matthew, Harris, Meredyth, Kelly, Carrie, Nicol, Scott, Pearson, Sally Anne, Chukkambotla, Srikanth, Andrew, Alyson, Attrill, Elizabeth, Campbell, Graham, Datson, Amanda, Fouracres, Anna, Graterol, Juan, Graves, Lynne, Hong, Bosun, Ishimaru, Alexander, Karthikeyan, Arvind, King, Helen, Lawson, Tom, Lee, Gregory, Lyons, Saoirse, Hall, Andrew Macalister, Mathoulin, Sophie, Mcintyre, Eilidh, Mclaughlin, Danny, Mulcahy, Kathleen, Paddle, Jonathan, Ratcliffe, Anna, Robbins, James, Sung, Weilin, Tayo, Adeoluwa, Trembath, Lisa, Venugopal, Suneetha, Walker, Robert, Wigmore, Geoffrey, Boereboom, Catherine, Downes, Charlotte, Humphries, Ryan, Melbourne, Susan, Smith, Coral, Tou, Samson, Ullah, Shafa, Batchelor, Nick, Boxall, Leigh, Broomby, Rupert, Deen, Tariq, Hellewell, Alistair, Helliwell, Laurence, Hutchings, Melanie, Hutchins, David, Keenan, Samantha, Mackie, Donna, Potter, Alison, Smith, Frances, Stone, Lucy, Thorpe, Kevin, Wassall, Richard, Woodgate, Andrew, Baillie, Shelley, Campbell, Tara, James, Sarah, King, Chris, Marques de Araujo, Daniela, Martin, Daniel, Morkane, Clare, Neely, Julia, Rajendram, Rajkumar, Burton, Megan, James, Kathryn, Keevil, Edward, Minik, Orsolya, Morgan, Jenna, Musgrave, Anna, Rajanna, Harish, Roberts, Tracey, Adamson, Michael, Jumbe, Sandra, Kendall, Jennie, Muthuswamy, Mohan Babu, Anderson, Charlotte, Cruikshanks, Andrew, Wrench, Ian, Zeidan, Lisa, Ardern, Diane, Harris, Benjamin, Hellstrom, Johanna, Martin, Jane, Thomas, Richard, Varsani, Nimu, Brown, Caroline Wrey, Docherty, Philip, Gillies, Michael, McGregor, Euan, Usher, Helen, Craig, Jayne, Smith, Andrew, Ahmad, Tahania, Bodger, Phoebe, Creary, Thais, Fowler, Alexander, Hewson, Russ, Ijuo, Eke, Jones, Timothy, Kantsedikas, Ilya, Lahiri, Sumitra, McLean, Aaron Lawson, Niebrzegowska, Edyta, Phull, Mandeep, Wang, Difei, Wickboldt, Nadine, Baldwin, Jacqueline, Doyle, Donna, Mcmullan, Sean, Oladapo, Michelle, Owen, Thomas, Williams, Alexandra, Daniel, Hull, Gregory, Peter, Husain, Tauqeer, Kirk-Bayley, Justin, Mathers, Edward, Montague, Laura, Harper, Mark, White, Stuart, Jack, James, Ridley, Carrie, Avis, Joanne, Cook, Tim, Dali-Kemmery, Lola, Kerslake, Ian, Lambourne, Victoria, Pearson, Annabel, Boyd, Christine, Callaghan, Mark, Lawson, Cathy, McCrossan, Roopa, Nesbitt, Vanessa, O'connor, Laura, Scott, Julia, Sinclair, Rhona, Farid, Nahla, Morgese, Ciro, Bhatia, Kailash, Karmarkar, Swati, Ahmed, Jamil, Branagan, Graham, Hutton, Monica, Swain, Andrew, Brookes, Jamie, Cornell, Jonathan, Dolan, Rachael, Hulme, Jonathan, Jansen van Vuuren, Amanda, Jowitt, Tom, Kalashetty, Gunasheela, Lloyd, Fran, Patel, Kiran, Sherwood, Nicholas, Brown, Lynne, Chandler, Ben, Deighton, Kerry, Emma, Temlett, Haunch, Kirsty, Cheeseman, Michelle, Dent, Kathy, Garg, Sanjeev, Gray, Carol, Hood, Marion, Jones, Dawn, Juj, Joanne, Rao, Roshan, Walker, Tara, Al Anizi, Mashel, Cheah, Clarissa, Cheing, Yushio, Coutinho, Francisco, Gondo, Prisca, Hadebe, Bernard, Hove, Mazvangu Onie, Ahamed khader, Krishnachetty, Bobby, Rhodes, Karen, Sokhi, Jagdish, Baker, Katie-Anne, Bertram, Wendy, Looseley, Alex, Mouton, Ronelle, Hanna, George, Arnold, Glenn, Arya, Shobhit, Balfoussia, Danai, Baxter, Linden, Harris, James, Jones, Craig, Knaggs, Alison, Markar, Sheraz, Perera, Anisha, Scott, Alasdair, Shida, Asako, Sirha, Ravneet, Wright, Sally, Frost, Victoria, Gray, Catherine, Andrews, Emma, Arrandale, Lindsay, Barrett, Stephen, Cifra, Elna, Cooper, Mariese, Dragnea, Dragos, Elna, Cifra, Maclean, Jennifer, Meier, Sonja, Milliken, Donald, Munns, Christopher, Ratanshi, Nadir, Ramessur, Suneil, Salvana, Abegail, Watson, Anthony, Ali, Hani, Campbell, Gill, Critchley, Rebecca, Endersby, Simon, Hicks, Catherine, Liddle, Alison, Pass, Marc, Ritchie, Charlotte, Thomas, Charlotte, Too, Lingxi, Welsh, Sarah, Gill, Talvinder, Johnson, Joanne, Reed, Joanne, Davis, Edward, Papadopoullos, Sam, Attwood, Clare, Biffen, Andrew, Boulton, Kerenza, Gray, Sophie, Hay, David, Mills, Sarah, Montgomery, Jane, Riddell, Rory, Simpson, James, Bhardwaj, Neeraj, Paul, Elaine, Uwubamwen, Nosakhare, Alexander, Maini, Arrich, James, Arumugam, Swarna, Blackwood, Douglas, Boggiano, Victoria, Brown, Robyn, Chan, Yik Lam, Chatterjee, Devnandan, Chhabra, Ashok, Christian, Rachel, Costelloe, Hannah, Matthewman, Madeline Coxwell, Dalton, Emma, Darko, Julia, Davari, Maria, Dave, Tejal, Deacon, Matthew, Deepak, Shantal, Edmond, Holly, Ellis, Jessica, El-Sayed, Ahmed, Eneje, Philip, English, Rose, Ewe, Renee, Foers, William, Franklin, John, Gallego, Laura, Garrett, Emily, Goldberg, Olivia, Goss, Harry, Greaves, Rosanna, Harris, Rudy, Hennings, Charles, Jones, Eleanor, Kamali, Nelson, Kokkinos, Naomi, Lewis, Carys, Lignos, Leda, Malgapo, Evaleen Victoria, Malik, Rizwana, Milne, Andrew, Mulligan, John-Patrick, Nicklin, Philippa, Palipane, Natasha, Parsons, Thomas, Piper, Rebecca, Prakash, Rohan, Ramesh, Byron, Rasip, Sarah, Reading, Jacob, Rela, Mariam, Reyes, Anna, Stephens, Robert, Rooms, Martin, Shah, Karishma, Simons, Henry, Solanki, Shalil, Spowart, Emma, Stevens, Amy, Thomas, Christopher, Waggett, Helena, Yassaee, Arrash, Kennedy, Anthony, Scott, Sara, Somanath, Sameer, Berg, Andrew, Hernandez, Miguel, Nanda, Rajesh, Tank, Ghanshyambhai, Wilson, Natalie, Wilson, Debbie, Al-Soudaine, Yassr, Baldwin, Matthew, Cornish, Julie, Davies, Zoe, Davies, Leigh, Edwards, Marc, Frewer, Natasha, Gallard, Sian, Glasbey, James, Harries, Rhiannon, Hopkins, Luke, Kim, Taeyang, Koompirochana, Vilavan, Lawson, Simon, Lewis, Megan, Makzal, Zaid, Scourfield, Sarah, Ahmad, Yousra, Bates, Sarah, Blackwell, Clare, Bryant, Helen, Collins, Hannah, Coulter, Suzanne, Cruickshank, Ross, Daniel, Sonya, Daubeny, Thomas, Edwards, Mark, Golder, Kim, Hawkins, Lesley, Helen, Bryant, Hinxman, Honor, Levett, Denny, Salmon, Karen, Seaward, Leanne, Skinner, Ben, Tyrell, Bryony, Wadams, Beverley, Walsgrove, Joseph, Dickson, Jane, Constantin, Kathryn, Karen, Markwell, O'Brien, Peter, O'Donohoe, Lynn, Payne, Hannah, Sundayi, Saul, Walker, Elaine, Brooke, Jenny, Cardy, Jon, Humphreys, Sally, Kessack, Laura, Kubitzek, Christiane, Kumar, Suhas, Cotterill, Donna, Hodzovic, Emil, Hosdurga, Gurunath, Miles, Edward, Saunders, Glenn, Campbell, Marta, Chan, Peter, Jemmett, Kim, Raj, Ashok, Naik, Aditi, Oshowo, Ayo, Ramamoorthy, Rajarajan, Shah, Nimesh, Sylvan, Axel, Blyth, Katharine, Burtenshaw, Andrew, Freeman, David, Johnson, Emily, Lo, Philip, Martin, Terry, Plunkett, Emma, Wollaston, Julie, Allison, Joanna, Carroll, Christine, Craw, Nicholas, Craw, Sarah, Pitt-Kerby, Tressy, Rowland-Axe, Rebecca, Spurdle, Katie, McDonald, Andrew, Simon, Davies, Sinha, Vivek, Smith, Thomas, Banner-Goodspeed, Valerie, Boone, Myles, Campbell, Kathleen, Lu, Fengxin, Scannell, Joseph, Sobol, Julia, Balajonda, Naraida, Clemmons, Karen, Conde, Carlos, Elgasim, Magdi, Funk, Bonita, Hall, Roger, Hopkins, Thomas, Olaleye, Omowunmi, Omer, Omer, Pender, Michelle, Porto, Angelo, Stevens, Alice, Waweru, Peter, Yeh, Erlinda, Bodansky, Daniella, Evans, Adam, Kleopoulos, Steven, Maril, Robert, Mathney, Edward, Sanchez, Angela, Tinuoye, Elizabeth, Bateman, Brian, Eng, Kristen, Jiang, Ning, Ladha, Karim, Needleman, Joseph, Chen, Lee-lynn, Lane, Rondall, Robinowitz, David, Ghushe, Neil, Irshad, Mariam, O'Connor, John, Patel, Samir, Takemoto, Steven, Wallace, Art, Mazzeffi, Michael, Rock, Peter, Wallace, Karin, Zhu, Xiaomao, Chua, Pandora, Mattera, Matthew, Sharar, Rebecca, Thilen, Stephan, Treggiari, Miriam, Morgan, Angela, Sofjan, Iwan, Subramaniam, Kathirvel, Avidan, Michael, Maybrier, Hannah, Muench, Maxwell, Wildes, Troy, Abbott, T.E.F., Ahmad, T., Phull, M.K., Fowler, A.J., Hewson, R., Biccard, B.M., Chew, M.S., Gillies, M., and Pearse, R.M.
Published: 2018
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38. Recurrent high creatine kinase levels under clozapine treatment - a case report assessing a suspected adverse drug reaction

Author: Wiss, Florine M., primary, Allemann, Samuel S., additional, Meyer zu Schwabedissen, Henriette E., additional, Stäuble, Céline K., additional, Mikoteit, Thorsten, additional, and Lampert, Markus L., additional
Published: 2024
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39. A Clinical Practice Perspective on the Evaluation of OATP1B1‐associated Drug Interactions

Author: Stäuble, Céline K., primary, Lampert, Markus L., additional, Allemann, Samuel S., additional, and Meyer zu Schwabedissen, Henriette E., additional
Published: 2024
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40. Information in summaries of product characteristics about use in children is limited and needs standardisation: a systematic analysis in Switzerland

Author: Tilen, Romy, primary, Berger, Christoph, additional, Allemann, Samuel, additional, and Meyer zu Schwabedissen, Henriette, additional
Published: 2024
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41. Humanization ofSLCO2B1in Rats Increases rCYP3A1 Protein Expression but Not the Metabolism of Erlotinib to OSI-420

Author: Rysz, Marta, primary, Schäfer, Anima M., additional, Paloumpis, Nikolaos, additional, Kinzi, Jonny, additional, Brecht, Karin, additional, Seibert, Isabell, additional, Schmidlin, Seraina, additional, In-Albon, Katja, additional, Ricklin, Daniel, additional, and Meyer zu Schwabedissen, Henriette E., additional
Published: 2024
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42. Vitamin D moderates the interaction between 5-HTTLPR and childhood abuse in depressive disorders

Author: Sarah Bonk, Johannes Hertel, Helena U. Zacharias, Jan Terock, Deborah Janowitz, Georg Homuth, Matthias Nauck, Henry Völzke, Henriette Meyer zu Schwabedissen, Sandra Van der Auwera, and Hans Jörgen Grabe
Subjects: Medicine, Science
Abstract: Abstract A complex interplay between genetic and environmental factors determines the individual risk of depressive disorders. Vitamin D has been shown to stimulate the expression of the tryptophan hydroxylase 2 (TPH2) gene, which is the rate-limiting enzyme for serotonin production in the brain. Therefore, we investigate the hypothesis that serum vitamin D levels moderate the interaction between the serotonin transporter promotor gene polymorphism (5-HTTLPR) and childhood abuse in depressive disorders. Two independent samples from the Study of Health in Pomerania (SHIP-LEGEND: n = 1 997; SHIP-TREND-0: n = 2 939) were used. Depressive disorders were assessed using questionnaires (BDI-II, PHQ-9) and interview procedures (DSM-IV). Besides serum vitamin D levels (25(OH)D), a functional polymorphism (rs4588) of the vitamin D-binding protein is used as a proxy for 25(OH)D. S-allele carriers with childhood abuse and low 25(OH)D levels have a higher mean BDI-II score (13.25) than those with a higher 25(OH)D level (9.56), which was not observed in abused LL-carriers. This significant three-way interaction was replicated in individuals with lifetime major depressive disorders when using the rs4588 instead of 25(OH)D (p = 0.0076 in the combined sample). We conclude that vitamin D relevantly moderates the interaction between childhood abuse and the serotonergic system, thereby impacting vulnerability to depressive disorders.
Published: 2020
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43. Spectroscopic Properties, Conformation and Structure of Difluorothiophosphoryl Isocyanate in the Gaseous and Solid Phase

Author: Dr. Jan Schwabedissen, Pia C. Trapp, Dr. Hans‐Georg Stammler, Prof. Dr. Norbert W. Mitzel, Zhuang Wu, Xianxu Chu, and Prof. Dr. Xiaoqing Zeng
Subjects: difluorothiophosphoryl isocyanate, gas electron diffraction, X-ray diffraction, vibrational spectroscopy, photodecomposition, Chemistry, QD1-999
Abstract: Abstract Difluorothiophosphoryl isocyanate, F2P(S)NCO was characterized with UV/vis, NMR, IR (gas and Ar‐matrix), and Raman (liquid) spectroscopy. Its molecular structure was also established by means of gas electron diffraction (GED) and single crystal X‐ray diffraction (XRD) in the gas phase and solid state, respectively. The analysis of the spectroscopic data and molecular structures is complemented by extensive quantum‐chemical calculations. Theoretically, the Cs symmetric syn‐conformer is predicted to be the most stable conformation. Rotation about the P−N bond requires about 9 kJ mol−1 and the predicted existence of an anti‐conformer is dependent on the quantum‐chemical method used. This syn‐orientation of the isocyanate group is the only one found in the gas phase and contained likewise in the crystal. The overall molecular structure is very similar in gas and solid, despite in the solid state the molecules arrange through intramolecular O⋅⋅⋅F contacts into layers, which are further interconnected by S⋅⋅⋅N, S⋅⋅⋅C and C⋅⋅⋅F contacts. Additionally, the photodecomposition of F2P(S)NCO to form CO, F2P(S)N, and F2PNCO is observed in the solid Ar‐matrix.
Published: 2020
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44. Structures and Properties of trans‐1,3,3,3‐Tetrafluoro‐ propene (HFO‐1234ze) and 2,3,3,3‐Tetrafluoropropene (HFO‐1234yf) Refrigerants

Author: Dr. Jan Schwabedissen, Timo Glodde, Dr. Yury V. Vishnevskiy, Dr. Hans‐Georg Stammler, Lukas Flierl, Prof. Dr. Andreas J. Kornath, and Prof. Dr. Norbert W. Mitzel
Subjects: refrigerants, high-angle X-ray diffraction, vibrational spectra, matrix isolation, combustion analysis, Chemistry, QD1-999
Abstract: Abstract The refrigerant trans‐1,3,3,3‐tetrafluoropropene (HFO‐1234ze) is used as a replacement for former cooling agents that have been phased‐out due to their global warming potential or ozone depleting potential. Although it is used on a large scale, only a few vibrational data and no structural data of HFO‐1234ze are known. We report structure determinations based on low‐temperature single‐crystal X‐ray diffraction data as well as gas‐phase diffraction data of HFO‐1234ze and HFO‐1234yf (2,3,3,3‐tetrafluoropropene). Furthermore, vibrational spectra of HFO‐1234ze in all phases are described. The results are discussed together with quantum‐chemical calculations on the PBE0/cc‐pVTZ level of theory. Combustion experiments of HFO‐1234ze show carbonyl difluoride, carbon dioxide and hydrogen fluoride to be the main combustion products.
Published: 2020
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45. Absorption, Metabolism, and Excretion of ACT-1004-1239, a First-In-Class CXCR7 Antagonist: In Vitro, Preclinical, and Clinical Data

Author: Christine Huynh, Swen Seeland, Jerome Segrestaa, Carmela Gnerre, Jens Hogeback, Henriette E. Meyer zu Schwabedissen, Jasper Dingemanse, and Patricia N. Sidharta
Subjects: CXCR7, ADME, accelerator mass spectrometry, microtracer, CYP3A4, 14C-ACT-1004-1239, Therapeutics. Pharmacology, RM1-950
Abstract: ACT-1004-1239 is a potent, selective, first-in-class CXCR7 antagonist, which shows a favorable preclinical and clinical profile. Here we report the metabolites and the metabolic pathways of ACT-1004-1239 identified using results from in vitro and in vivo studies. Two complementary in vitro studies (incubation with human liver microsomes in the absence/presence of cytochrome P450- [CYP] specific chemical inhibitors and incubation with recombinant CYPs) were conducted to identify CYPs involved in ACT-1004-1239 metabolism. For the in vivo investigations, a microtracer approach was integrated in the first-in-human study to assess mass balance and absorption, distribution, metabolism, and excretion (ADME) characteristics of ACT-1004-1239. Six healthy male subjects received orally 100 mg non-radioactive ACT-1004-1239 together with 1 μCi 14C-ACT-1004-1239. Plasma, urine, and feces samples were collected up to 240 h post-dose and 14C-drug-related material was measured with accelerator mass spectrometry. This technique was also used to construct radiochromatograms of pooled human samples. Metabolite structure elucidation of human-relevant metabolites was performed using high performance liquid chromatography coupled with high resolution mass spectrometry and facilitated by the use of rat samples. CYP3A4 was identified as the major CYP catalyzing the formation of M1 in vitro. In humans, the cumulative recovery from urine and feces was 84.1% of the dose with the majority being eliminated via the feces (69.6%) and the rest via the urine (14.5%). In human plasma, two major circulating metabolites were identified, i.e., M1 and M23. Elimination via M1 was the only elimination pathway that contributed to ≥25% of ACT-1004-1239 elimination. M1 was identified as a secondary amine metabolite following oxidative N-dealkylation of the parent. M23 was identified as a difluorophenyl isoxazole carboxylic acid metabolite following central amide bond hydrolysis of the parent. Other metabolites observed in humans were A1, A2, and A3. Metabolite A1 was identified as an analog of M1 after oxidative defluorination, whereas both, A2 and A3, were identified as a reduced analog of M1 and parent, respectively, after addition of two hydrogen atoms at the isoxazole ring. In conclusion, CYP3A4 contributes to a relevant extent to ACT-1004-1239 disposition and two major circulating metabolites were observed in humans.Clinical Trial Registration: (https://clinicaltrials.gov/ct2/show/NCT03869320) ClinicalTrials.gov Identifier NCT03869320.
Published: 2022
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46. Evaluation of a structured treatment discontinuation in patients with inoperable alveolar echinococcosis on long-term benzimidazole therapy: A retrospective cohort study.

Author: Ansgar Deibel, Daniel Stocker, Cordula Meyer Zu Schwabedissen, Lars Husmann, Philipp Andreas Kronenberg, Felix Grimm, Peter Deplazes, Cäcilia S Reiner, and Beat Müllhaupt
Subjects: Arctic medicine. Tropical medicine, RC955-962, Public aspects of medicine, RA1-1270
Abstract: ObjectivesAlveolar echinococcosis (AE) is an orphan zoonosis of increasing concern in endemic areas, including Europe. It frequently presents in an advanced, inoperable stage, that requires life-long parasitostatic benzimidazole therapy. In some patients, long-term therapy leads to negative anti-Em18 antibody ELISA and PET. It is disputed, whether these patients are truly cured and treatment can be safely discontinued. Our aim was to retrospectively assess long-term outcome of 34 patients with inoperable AE who participated in a previous study to determine feasibility of benzimidazole treatment cessation.MethodsRetrospective analysis of medical charts was undertaken in all 34 AE patients who participated in our previous study. Of particular interest were AE recurrence or other reasons for re-treatment in patients who stopped benzimidazole therapy and whether baseline clinical and laboratory parameters help identify of patients that might qualifiy for treatment cessation. Additionally, volumetric measurement of AE lesions on contrast-enhanced cross-sectional imaging was performed at baseline and last follow-up in order to quantify treatment response.Results12 of 34 patients stopped benzimidazole therapy for a median of 131 months. 11 of these patients showed stable or regressive AE lesions as determined by volumetric measurement. One patient developed progressive lesions with persistently negative anti-Em18 antibody ELISA but slight FDG-uptake in repeated PET imaging. At baseline, patients who met criteria for treatment cessation demonstrated higher lymphocyte count and lower total IgE.ConclusionTreatment cessation is feasible in inoperable AE patients, who demonstrate negative anti-Em18 antibody ELISA and PET on follow-up. Close monitoring including sectional imaging is strongly advised.
Published: 2022
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47. The nuclear receptors PXR and LXR are regulators of the scaffold protein PDZK1

Author: Ferreira, Celio, Meyer, Ramona, and Meyer zu Schwabedissen, Henriette E.
Published: 2019
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48. Impact of OATP2B1 on Pharmacokinetics of Atorvastatin Investigated in rSlco2b1-Knockout and SLCO2B1-Knockin Rats▪

Author: Kinzi, Jonny, Hussner, Janine, Seibert, Isabell, Vythilingam, Mirubagini, Vonwyl, Celina, Gherardi, Clarisse, Detampel, Pascal, Schwardt, Oliver, Ricklin, Daniel, and Meyer zu Schwabedissen, Henriette E.
Abstract: The organic anion transporting polypeptide (OATP) 2B1 is considered an emerging drug transporter that is found expressed in pharmacokinetically relevant organs such as the liver, small intestine, and kidney. Despite its interaction with various substrate drugs, the understanding of its in vivo relevance is still limited. In this study, we first validated the interaction of atorvastatin with rat OATP2B1 using transiently transfected HeLa cells. Moreover, we characterized our rSlco2b1-knockout and SLCO2B1-knockin rats for mRNA, protein expression, and localization of OATP2B1 in the liver, small intestine, and kidney. The transporter showed the highest expression in the liver followed by the small intestine. In humanized rats, human OATP2B1 is localized on the sinusoidal membrane of hepatocytes. In enterocytes of wild-type and humanized rats, the transporter was detected in the luminal membrane with the vast majority being localized subapical. Subsequently, we assessed atorvastatin pharmacokinetics in male wild-type, rSlco2b1-knockout, and SLCO2B1-knockin rats after a single-dose administration (orally and intravenously). Investigating the contribution of rat OATP2B1 or human OATP2B1 to oral atorvastatin pharmacokinetics revealed no differences in concentration-time profiles or pharmacokinetic parameters. However, when comparing the pharmacokinetics of atorvastatin after intravenous administration in SLCO2B1-humanized rats and knockout animals, notable differences were observed. In particular, the systemic exposure (area under the curve) decreased by approximately 40% in humanized animals, whereas the clearance was 57% higher in animals expressing human OATP2B1. These findings indicate that human OATP2B1 influences pharmacokinetics of atorvastatin after intravenous administration, most likely by contributing to the hepatic uptake.
Published: 2024
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49. Structure and photochemistry of di-tert-butyldiphosphatetrahedrane

Author: Hierlmeier, Gabriele, primary, Kutta, Roger Jan, additional, Coburger, Peter, additional, Stammler, Hans-Georg, additional, Schwabedissen, Jan, additional, Mitzel, Norbert W., additional, Dimitrova, Maria, additional, Berger, Raphael J. F., additional, Nuernberger, Patrick, additional, and Wolf, Robert, additional
Published: 2024
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50. The effect of itraconazole, a strong CYP3A4 inhibitor, on the pharmacokinetics of the first‐in‐class ACKR3/CXCR7 antagonist, ACT‐1004‐1239.

Author: Huynh, Christine, Dingemanse, Jasper, Meyer zu Schwabedissen, Henriette E., Fonseca, Marlene, and Sidharta, Patricia N.
Subjects: CYTOCHROME P-450 CYP3A, PHARMACOKINETICS, CYTOCHROME P-450, DRUG metabolism, ENZYME metabolism, ITRACONAZOLE, NATALIZUMAB
Abstract: Cytochrome P450 (CYP) 3A4 is an enzyme involved in the metabolism of many drugs that are currently on the market and is therefore a key player in drug–drug interactions (DDIs). ACT‐1004‐1239 is a potent and selective, first‐in‐class ACKR3/CXRC7 antagonist being developed as a treatment for demyelinating diseases including multiple sclerosis. Based on the human absorption, distribution, metabolism, and excretion (ADME) study results, ACT‐1004‐1239 is predominantly metabolized by CYP3A4. This study investigated the effect of the strong CYP3A4 inhibitor, itraconazole, on the pharmacokinetics of single‐dose ACT‐1004‐1239 in healthy male subjects. In the open‐label, fixed‐sequence DDI study, a total of 16 subjects were treated. Each subject received a single dose of 10 mg ACT‐1004‐1239 (Treatment A) in the first period followed by concomitant administration of multiple doses of 200 mg itraconazole and a single dose of 10 mg ACT‐1004‐1239 in the second period. We report a median of difference in tmax (90% confidence interval, CI) of 0.5 h (0.0, 1.0) comparing both treatments. The geometric mean ratio (GMR) (90% CI) of Cmax and AUC0−∞ was 2.16 (1.89, 2.47) and 2.77 (2.55, 3.00), respectively. The GMR (90% CI) of t1/2 was 1.46 (1.26, 1.70). Both treatments were well‐tolerated with an identical incidence in subjects reporting treatment‐emergent adverse events (TEAE). The most frequently reported TEAEs were headache and nausea. In conclusion, ACT‐1004‐1239 is classified as a moderately sensitive CYP3A4 substrate (i.e., increase of AUC ≥2‐ to <5‐fold), and this should be considered in further clinical studies if CYP3A4 inhibitors are concomitantly administered. [ABSTRACT FROM AUTHOR]
Published: 2024
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