Journal articles: 'Pharmacokinetic interactions'

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Taylor, David. "Pharmacokinetic interactions involving clozapine." British Journal of Psychiatry 171, no. 2 (August 1997): 109–12. http://dx.doi.org/10.1192/bjp.171.2.109.

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BackgroundMetabolism of clozapine is complex and not fully understood. Pharmacokinetic interactions with other drugs have been described but, in some cases, their mechanism is unknown.MethodPublished trials and case reports relevant to the human metabolism of clozapine and to suspected pharmacokinetic interactions were reviewed.ResultsMetabolism of clozapine appears to be largely controlled by the function of the hepatic cytochrome p4501A2 (CYPIA2). Compounds which induce CYPIA2 activity (carbamazepine, tobacco smoke) may reduce plasma clozapine levels. Inhibitors of CYPIA2 (caffeine, erythromycin) have the opposite effect. Drugs which inhibit the hepatic cytochrome p4502D6 (CYP2D6) have also been reported to elevate plasma clozapine levels. The mechanism of this interaction is unclear.ConclusionsThe co-administration of clozapine and compounds reported to alter its metabolism should be avoided where possible. A host of other interactions can be predicted and so caution should be exercised when co-administering drugs which affect the function of CYPIA2 and CYP2D6. The pharmacokinetics of clozapine require further investigation so that its safe use can be assured.

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Keirns, J., T. Sawamoto, M. Holum, D. Buell, W. Wisemandle, and A. Alak. "Steady-State Pharmacokinetics of Micafungin and Voriconazole after Separate and Concomitant Dosing in Healthy Adults." Antimicrobial Agents and Chemotherapy 51, no. 2 (November 20, 2006): 787–90. http://dx.doi.org/10.1128/aac.00673-06.

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ABSTRACT We assessed the pharmacokinetics and interactions of steady-state micafungin (Mycamine) or placebo with steady-state voriconazole in 35 volunteers. The 90% confidence intervals around the least-squares mean ratios for micafungin pharmacokinetic parameters and placebo-corrected voriconazole pharmacokinetic parameters were within the 80%-to-125% limits, indicating an absence of drug interaction.

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Soyata, Amelia, Aliya Nur Hasanah, and Taofik Rusdiana. "Interaction of Warfarin with Herbs Based on Pharmacokinetic and Pharmacodynamic Parameters." Indonesian Journal of Pharmaceutics 2, no. 2 (June 5, 2020): 69. http://dx.doi.org/10.24198/idjp.v2i2.27289.

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Warfarin is an oral anticoagulant that has been widely used and has strong efficacy, but the use of warfarin is still a concern because of its narrow therapeutic index which cause interactions when co-administration with drugs, herbs or food. This interaction can affect the pharmacokinetics and pharmacodynamics of warfarin and the most fatal effect from warfarin interactions is bleeding. In this review article data on warfarin-herbs interactions were collected based on pharmacokinetic parameters (AUC0-∞, Cmax, T1/2, Cl/F, and V/F), while pharmacodynamic parameters (International normalized ratio (INR), platelet aggregation, AUC INR and Protombine Time). As a result some herbs had significant interactions with warfarin. Herbs that affect warfarin pharmacokinetic were Danshen gegen, echinacea, St. John's wort and caffeine and herbs that affect pharmacodynamic were policosanol, Ginkgo biloba, cranberry, St. John's wort, ginseng, pomegranate, Psidium guajava and curcumin, so co-administration warfarin with herbs need to be considered.Keywords: Warfarin, Interactions, Herbs, Pharmacokinetics, Pharmacodynamics

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Costache, Irina-Iuliana, Anca Miron, Monica Hăncianu, Viviana Aursulesei, Alexandru Dan Costache, and Ana Clara Aprotosoaie. "Pharmacokinetic Interactions between Cardiovascular Medicines and Plant Products." Cardiovascular Therapeutics 2019 (September 2, 2019): 1–19. http://dx.doi.org/10.1155/2019/9402781.

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The growing use of plant products among patients with cardiovascular pharmacotherapy raises the concerns about their potential interactions with conventional cardiovascular medicines. Plant products can influence pharmacokinetics or/and pharmacological activity of coadministered drugs and some of these interactions may lead to unexpected clinical outcomes. Numerous studies and case reports showed various pharmacokinetic interactions that are characterized by a high degree of unpredictability. This review highlights the pharmacokinetic clinically relevant interactions between major conventional cardiovascular medicines and plant products with an emphasis on their putative mechanisms, drawbacks of herbal products use, and the perspectives for further well-designed studies.

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ERESHEFSKY, LARRY, STEPHEN R. SAKLAD, MARK D. WATANABE, CHESTER M. DAVIS, and MICHAEL W. JANN. "Thiothixene Pharmacokinetic Interactions." Journal of Clinical Psychopharmacology 11, no. 5 (October 1991): 296???301. http://dx.doi.org/10.1097/00004714-199110000-00004.

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Hartshorn, Edward A. "Pharmacokinetic Drug Interactions." Journal of Pharmacy Technology 1, no. 5 (September 1985): 193–99. http://dx.doi.org/10.1177/875512258500100505.

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Eichelbaum, Michel. "Pharmacokinetic Drug Interactions." Journal of Clinical Pharmacology 26, no. 6 (July 8, 1986): 469–73. http://dx.doi.org/10.1002/j.1552-4604.1986.tb03560.x.

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Pukrittayakamee, Sasithon, Joel Tarning, Podjanee Jittamala, Prakaykaew Charunwatthana, Saranath Lawpoolsri, Sue J. Lee, Warunee Hanpithakpong, et al. "Pharmacokinetic Interactions between Primaquine and Chloroquine." Antimicrobial Agents and Chemotherapy 58, no. 6 (March 31, 2014): 3354–59. http://dx.doi.org/10.1128/aac.02794-13.

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ABSTRACTChloroquine combined with primaquine has been the standard radical curative regimen forPlasmodium vivaxandPlasmodium ovalemalaria for over half a century. In an open-label crossover pharmacokinetic study, 16 healthy volunteers (4 males and 12 females) aged 20 to 47 years were randomized into two groups of three sequential hospital admissions to receive a single oral dose of 30 mg (base) primaquine, 600 mg (base) chloroquine, and the two drugs together. The coadministration of the two drugs did not affect chloroquine or desethylchloroquine pharmacokinetics but increased plasma primaquine concentrations significantly (P≤ 0.005); the geometric mean (90% confidence interval [CI]) increases were 63% (47 to 81%) in maximum concentration and 24% (13 to 35%) in total exposure. There were also corresponding increases in plasma carboxyprimaquine concentrations (P≤ 0.020). There were no significant electrocardiographic changes following primaquine administration, but there was slight corrected QT (QTc) (Fridericia) interval lengthening following chloroquine administration (median [range] = 6.32 [−1.45 to 12.3] ms;P< 0.001), which was not affected by the addition of primaquine (5.58 [1.74 to 11.4] ms;P= 0.642). This pharmacokinetic interaction may explain previous observations of synergy in preventingP. vivaxrelapse. This trial was registered at ClinicalTrials.gov under reference number NCT01218932.

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Cohen, Lawrence J., and C. Lindsay DeVane. "Clinical Implications of Antidepressant Pharmacokinetics and Pharmacogenetics." Annals of Pharmacotherapy 30, no. 12 (December 1996): 1471–80. http://dx.doi.org/10.1177/106002809603001216.

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OBJECTIVE: To review available data on pharmacokinetic and pharmacogenetic influences on the response to antidepressant therapy, analyze the mechanisms for and clinical significance of pharmacokinetic and pharmacogenetic differences, and explain the implications of pharmacokinetics and pharmacogenetics for patient care. DATA SOURCES: A MEDLINE search of English-language clinical studies, abstracts, and review articles on antidepressant pharmacokinetics, pharmacogenetics, and drug interactions was used to identify pertinent literature. DATA SYNTHESIS: The pharmacokinetic profiles of selected antidepressants are reviewed and the impact of hepatic microsomal enzymes on antidepressant metabolism is considered. How phenotypic differences influence the metabolism of antidepressant drug therapy is addressed. To evaluate the clinical implications of these pharmacokinetic and pharmacogenetic considerations, the findings of studies designed to elucidate drug interactions involving antidepressant agents are discussed. CONCLUSIONS: Differences in antidepressant plasma concentrations, and possibly safety, are caused by polymorphism in the genes that encode some of the cytochrome P450 isoenzymes that metabolize antidepressants. The isoenzymes 1A2, 2C9/19, 2D6, and 3A4 are the major enzymes that catalyze antidepressant metabolic reactions. Antidepressants can be either substrates or inhibitors of these enzymes, which also metabolize many other pharmacologic agents. Although the cytochrome enzymes that metabolize antidepressants have not been fully characterized, interaction profiles of the newer antidepressants are becoming more clearly defined. Determining patient phenotypes is not practical in the clinical setting, but an awareness of the possibility of genetic polymorphism in antidepressant metabolism may help explain therapeutic failure or toxicity, help predict the likelihood of drug interactions, and help clinicians better manage antidepressant drug therapy.

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Marvanova, Marketa. "Pharmacokinetic characteristics of antiepileptic drugs (AEDs)." Mental Health Clinician 6, no. 1 (January 1, 2016): 8–20. http://dx.doi.org/10.9740/mhc.2015.01.008.

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Abstract Antiepileptic drugs (AEDs) are routinely prescribed for the management of a variety of neurologic and psychiatric conditions, including epilepsy and epilepsy syndromes. Physiologic changes due to aging, pregnancy, nutritional status, drug interactions, and diseases (ie, those involving liver and kidney function) can affect pharmacokinetics of AEDs. This review discusses foundational pharmacokinetic characteristics of AEDs currently available in the United States, including clobazam but excluding the other benzodiazepines. Commonalities of pharmacokinetic properties of AEDs are discussed in detail. Important differences among AEDs and clinically relevant pharmacokinetic interactions in absorption, distribution, metabolism, and/or elimination associated with AEDs are highlighted. In general, newer AEDs have more predictable kinetics and lower risks for drug interactions. This is because many are minimally or not bound to serum proteins, are primarily renally cleared or metabolized by non–cytochrome P450 isoenzymes, and/or have lower potential to induce/inhibit various hepatic enzyme systems. A clear understanding of the pharmacokinetic properties of individual AEDs is essential in creating a safe and effective treatment plan for a patient.

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Rodin, Steven M., and Brian F. Johnson. "Pharmacokinetic Interactions with Digoxin." Clinical Pharmacokinetics 15, no. 4 (October 1988): 227–44. http://dx.doi.org/10.2165/00003088-198815040-00003.

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Glue, Paul, Christopher R. Banfield, James L. Perhach, Gary G. Mather, Jagdish K. Racha, and Rene H. Levy. "Pharmacokinetic Interactions with Felbamate." Clinical Pharmacokinetics 33, no. 3 (September 1997): 214–24. http://dx.doi.org/10.2165/00003088-199733030-00004.

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Niemi, Mikko, Janne T. Backman, Martin F. Fromm, Pertti J. Neuvonen, and Kari T. Kivist?? "Pharmacokinetic Interactions with Rifampicin." Clinical Pharmacokinetics 42, no. 9 (2003): 819–50. http://dx.doi.org/10.2165/00003088-200342090-00003.

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Bialer, Meir, Dennis R. Doose, Bindu Murthy, Christopher Curtin, Shean-Sheng Wang, Roy E. Twyman, and Stefan Schwabe. "Pharmacokinetic Interactions of Topiramate." Clinical Pharmacokinetics 43, no. 12 (2004): 763–80. http://dx.doi.org/10.2165/00003088-200443120-00001.

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Scheen, Andr?? J. "Pharmacokinetic Interactions with Thiazolidinediones." Clinical Pharmacokinetics 46, no. 1 (2007): 1–12. http://dx.doi.org/10.2165/00003088-200746010-00001.

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&NA;. "Olanzapine + fluvoxamine: pharmacokinetic interactions." Inpharma Weekly &NA;, no. 1362 (November 2002): 20. http://dx.doi.org/10.2165/00128413-200213620-00050.

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Reinoso, R. F., A. Sánchez Navarro, M. J. García, and J. R. Prous. "Pharmacokinetic interactions of statins." Methods and Findings in Experimental and Clinical Pharmacology 23, no. 10 (2001): 541. http://dx.doi.org/10.1358/mf.2001.23.10.677120.

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Baciewicz, Anne M., and Frank A. Baciewicz. "Cyclosporine pharmacokinetic drug interactions." American Journal of Surgery 157, no. 2 (February 1989): 264–71. http://dx.doi.org/10.1016/0002-9610(89)90541-2.

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Kalam, Muhammad Nasir, Muhammad Fawad Rasool, Asim Ur Rehman, and Naveed Ahmed. "Clinical Pharmacokinetics of Propranolol Hydrochloride: A Review." Current Drug Metabolism 21, no. 2 (June 11, 2020): 89–105. http://dx.doi.org/10.2174/1389200221666200414094644.

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Background: Nobel laureate Sir James Black’s molecule, propranolol, still has broad potential in cardiovascular diseases, infantile haemangiomas and anxiety. A comprehensive and systematic review of the literature for the summarization of pharmacokinetic parameters would be effective to explore the new safe uses of propranolol in different scenarios, without exposing humans and using virtual-human modeling approaches. Objective: This review encompasses physicochemical properties, pharmacokinetics and drug-drug interaction data of propranolol collected from various studies. Methods: Clinical pharmacokinetic studies on propranolol were screened using Medline and Google Scholar databases. Eighty-three clinical trials, in which pharmacokinetic profiles and plasma time concentration were available after oral or IV administration, were included in the review. Results: The study depicts that propranolol is well absorbed after oral administration. It has dose-dependent bioavailability, and a 2-fold increase in dose results in a 2.5-fold increase in the area under the curve, a 1.3-fold increase in the time to reach maximum plasma concentration and finally, 2.2 and 1.8-fold increase in maximum plasma concentration in both immediate and long-acting formulations, respectively. Propranolol is a substrate of CYP2D6, CYP1A2 and CYP2C19, retaining potential pharmacokinetic interactions with co-administered drugs. Age, gender, race and ethnicity do not alter its pharmacokinetics. However, in renal and hepatic impairment, it needs a dose adjustment. Conclusion: Physiochemical and pooled pharmacokinetic parameters of propranolol are beneficial to establish physiologically based pharmacokinetic modeling among the diseased population.

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Ahmane, Amel, Hocine Gacem, Karim Boulesbiaat, and Meriem Boullelli. "Pharmacokinetic interactions: from mechanisms to clinical relevance." Batna Journal of Medical Sciences (BJMS) 1, no. 2 (December 31, 2014): 85–95. http://dx.doi.org/10.48087/bjmstf.2014.1209.

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Among the various types of known drug interactions, those involving pharmacokinetic processes are more complex and dangerous. From digestive pH changes to plasma protein binding and induction or inhibition phenomena; current data used to define, with precision, the sites of interaction. The enzymes involved in metabolism, the transporters involved in tissue distribution and excretion of drugs, and nuclear receptors that regulate the expression of these enzymes and transporters are keys determinants that should be defined for each drug. The clinical relevance of a pharmacokinetic interaction is related to the magnitude of changes in drug concentrations and pharmacological properties of these. Good knowledge of the pharmacokinetic properties of drugs and the mechanisms involved in the genesis of these interactions is, then, needed to prevent and avoid theme.

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Goswami, Suchandra, Shivangi Saxena, Shalini Yadav, Diptendu Goswami, Koushik Brahmachari, Sruti Karmakar, Biswajit Pramanik, and Sunil Brahmachari. "Review of Curcumin and Its Different Formulations: Pharmacokinetics, Pharmacodynamics and Pharmacokinetic-Pharmacodynamic Interactions." OBM Integrative and Complementary Medicine 07, no. 04 (December 27, 2022): 1–35. http://dx.doi.org/10.21926/obm.icm.2204057.

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Curcumin, the yellow principle of the Indian Turmeric, ‘Haldi’ has recently attracted renewed interest in the field of experimental medicine with pleiotropic activity. This review has emphasized three pharmaceutical studies of interest: the pharmacokinetics, pharmacology, and pharmacodynamics of curcumin. In this review, we attempted to review the general pharmacokinetics profile, pharmacokinetic interactions, and pharmacokinetic-pharmacodynamic interactions of curcumin and its formulations. Different species of turmeric in India, as well as their cultivars, different forms of curcumin, and harvesting methods have also been discussed. Furthermore, pharmacokinetic studies of the interaction of curcumin and its different formulations with efflux transporters such as P-glycoprotein, ABC-transporter protein, multidrug-resistant protein, and cytochrome p450 metabolism enzymes have been broadly explained following data from preclinical and clinical trials reported in the literature. A few interesting chemical interactions between curcumin and its metabolites with the receptor have also been described. The pharmacological activities of curcumin and its related formulations and products have been reviewed in a few targeted disease pathologies of national concern, such as cancer, gastroduodenal disorder, immunodeficiency, liver disease, ophthalmology, diabetes and osteoarthritis among other metabolic diseases, and microbial and viral infections. The pharmacodynamics of curcumin, especially regarding the potassium/calcium ion channel pathway, apoptosis, calcium signaling pathway, endoplasmic reticulum stress, and other intracellular signaling pathways, have been documented. Lastly, the use of curcumin as a cosmetic and the value chain analysis of turmeric products, as well as curcumin, have also been placed appropriately. A total of 174 publications were reviewed and, overall, this review tried to cover various important therapeutic aspects of curcumin, which can generate new research interest in general.

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Liang, Liuyi, Xin Jin, Jinjing Li, Rong Li, Xinyi Jiao, Yuanyuan Ma, Rui Liu, and Zheng Li. "A Comprehensive Review of Pharmacokinetics and Pharmacodynamics in Animals: Exploration of Interaction with Antibiotics of Shuang-Huang- Lian Preparations." Current Topics in Medicinal Chemistry 22, no. 2 (February 2022): 83–94. http://dx.doi.org/10.2174/1568026621666211012111442.

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: As a traditional Chinese medicine (TCM), Shuang-Huang-Lian (SHL) has been widely used for treating infectious diseases of the respiratory tract such as encephalitis, pneumonia, and asthma. During the past few decades, considerable research has focused on pharmacological action, pharmacokinetic interaction with antibiotics, and clinical applications of SHL. A huge and more recent body of pharmacokinetic studies support the combination of SHL and antibiotics have different effects such as antagonism and synergism. SHL has been one of the best-selling TCM products. However, there is no systematic review of SHL preparations, ranging from protection against respiratory tract infections to interaction with antibiotics. Since their important significance in clinical therapy, the pharmacodynamics, pharmacokinetics, and interactions with antibiotics of SHL were reviewed and discussed. In addition, this review attempts to explore the possible potential mechanism of SHL preparations in the prevention and treatment of COVID-19. We are concerned about the effects of SHL against viruses and bacteria, as well as its interactions with antibiotics in an attempt to provide a new strategy for expanding the clinical research and medication of SHL preparations.

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Czyrski, Andrzej, Matylda Resztak, Paweł Świderski, Jan Brylak, and Franciszek K. Główka. "The Overview on the Pharmacokinetic and Pharmacodynamic Interactions of Triazoles." Pharmaceutics 13, no. 11 (November 19, 2021): 1961. http://dx.doi.org/10.3390/pharmaceutics13111961.

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Second generation triazoles are widely used as first-line drugs for the treatment of invasive fungal infections, including aspergillosis and candidiasis. This class, along with itraconazole, voriconazole, posaconazole, and isavuconazole, is characterized by a broad range of activity, however, individual drugs vary considerably in safety, tolerability, pharmacokinetics profiles, and interactions with concomitant medications. The interaction may be encountered on the absorption, distribution, metabolism, and elimination (ADME) step. All triazoles as inhibitors or substrates of CYP isoenzymes can often interact with many drugs, which may result in the change of the activity of the drug and cause serious side effects. Drugs of this class should be used with caution with other agents, and an understanding of their pharmacokinetic profile, safety, and drug-drug interaction profiles is important to provide effective antifungal therapy. The manuscript reviews significant drug interactions of azoles with other medications, as well as with food. The PubMed and Google Scholar bases were searched to collect the literature data. The interactions with anticonvulsants, antibiotics, statins, kinase inhibitors, proton pump inhibitors, non-nucleoside reverse transcriptase inhibitors, opioid analgesics, benzodiazepines, cardiac glycosides, nonsteroidal anti-inflammatory drugs, immunosuppressants, antipsychotics, corticosteroids, biguanides, and anticoagulants are presented. We also paid attention to possible interactions with drugs during experimental therapies for the treatment of COVID-19.

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Botts, Sheila R., and Cara Alfaro. "Antidepressant Drug Interactions." Journal of Pharmacy Practice 14, no. 6 (December 2001): 467–77. http://dx.doi.org/10.1177/089719001129040964.

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Second-generation antidepressants are more selective in their pharmacological mechanisms and offer fewer side effects and a safer toxicological profile than cyclic antidepressants and monoamine oxidase inhibitors. While the risk for pharmacodynamic interactions is more limited than with older agents with broader receptor effects, the risks for pharmacokinetic interactions is greater. The capacity of selective serotonin reuptake inhibitors to inhibit the metabolic activity of cytochrome P450 isozyme system has spurred over a decade of intense psychopharmacological and pharmacogenetics research to better the understanding of the significance of these interactions. Clinicians have had to increase their knowledge and understanding of drug interaction potential to better manage patients receiving these newer antidepressants. The following is a review of both pharmacodynamic and pharmacokinetic drug-drug interactions with antidepressants.

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Lesko, L. J. "Pharmacokinetic Drug Interactions with Amiodarone." Clinical Pharmacokinetics 17, no. 2 (August 1989): 130–40. http://dx.doi.org/10.2165/00003088-198917020-00005.

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Venkatesan, K. "Pharmacokinetic Drug Interactions with Rifampicin." Clinical Pharmacokinetics 22, no. 1 (January 1992): 47–65. http://dx.doi.org/10.2165/00003088-199222010-00005.

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Periti, Piero, Teresita Mazzei, Enrico Mini, and Andrea Novelli. "Pharmacokinetic Drug Interactions of Macrolides." Clinical Pharmacokinetics 23, no. 2 (August 1992): 106–31. http://dx.doi.org/10.2165/00003088-199223020-00004.

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Riva, Roberto, Fiorenzo Albani, Manuela Contin, and Agostino Baruzzi. "Pharmacokinetic Interactions Between Antiepileptic Drugs." Clinical Pharmacokinetics 31, no. 6 (December 1996): 470–93. http://dx.doi.org/10.2165/00003088-199631060-00005.

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Giao, Phantrong, and Peter J. de Vries. "Pharmacokinetic Interactions of Antimalarial Agents." Clinical Pharmacokinetics 40, no. 5 (2001): 343–73. http://dx.doi.org/10.2165/00003088-200140050-00003.

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Unger, Matthias. "Pharmacokinetic drug interactions involvingGinkgo biloba." Drug Metabolism Reviews 45, no. 3 (July 19, 2013): 353–85. http://dx.doi.org/10.3109/03602532.2013.815200.

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Somogyi, Andrew, and Murray Muirhead. "Pharmacokinetic Interactions of Cimetidine 1987." Clinical Pharmacokinetics 12, no. 5 (May 1987): 321–66. http://dx.doi.org/10.2165/00003088-198712050-00002.

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Oesterheld, Jessica R., Scott C. Armstrong, and Kelly L. Cozza. "Ecstasy: Pharmacodynamic and Pharmacokinetic Interactions." Psychosomatics 45, no. 1 (March 2004): 84–87. http://dx.doi.org/10.1176/appi.psy.45.1.84.

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Pleuvry, Barbara J. "Pharmacodynamic and pharmacokinetic drug interactions." Anaesthesia & Intensive Care Medicine 6, no. 4 (April 2005): 129–33. http://dx.doi.org/10.1383/anes.6.4.129.63634.

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Blei, Andres. "Pharmacokinetic-Hemodynamic Interactions in Cirrhosis." Seminars in Liver Disease 6, no. 04 (November 1986): 299–308. http://dx.doi.org/10.1055/s-2008-1040612.

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Back, David, Sara Gibbons, and Saye Khoo. "Pharmacokinetic Drug Interactions with Nevirapine." JAIDS Journal of Acquired Immune Deficiency Syndromes 34 (September 2003): S8—S14. http://dx.doi.org/10.1097/00126334-200309011-00003.

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Tarirai, Clemence, Alvaro M. Viljoen, and Josias H. Hamman. "Herb–drug pharmacokinetic interactions reviewed." Expert Opinion on Drug Metabolism & Toxicology 6, no. 12 (November 11, 2010): 1515–38. http://dx.doi.org/10.1517/17425255.2010.529129.

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Brüggemann, Roger J. M., Jan-Willem C. Alffenaar, Nicole M. A. Blijlevens, Eliane M. Billaud, Jos G. W. Kosterink, Paul E. Verweij, and David M. Burger. "Pharmacokinetic drug interactions of azoles." Current Fungal Infection Reports 2, no. 1 (March 2008): 20–27. http://dx.doi.org/10.1007/s12281-008-0004-4.

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Zerjav, Sylvia, Gordon Tse, and Michael J. W. Scott. "Review of Duloxetine and Venlafaxine in Depression." Canadian Pharmacists Journal / Revue des Pharmaciens du Canada 142, no. 3 (May 2009): 144–52. http://dx.doi.org/10.3821/1913-701x-142.3.144.

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Objectives: To compare the efficacy and pharmacologic, pharmacokinetic, drug interaction and adverse effect profiles of duloxetine and venlafaxine. Methods: A systematic review of the literature pertaining to duloxetine and venlafaxine was conducted using a computer-aided search of MEDLINE and EMBASE for the period January 1988 to May 2008 with the following search terms: venlafaxine and duloxetine and depression, clinical studies, pharmacology, drug interactions, pharmacokinetics, adverse effects, safety, case reports and review articles. Results: Duloxetine and venlafaxine have comparable efficacy and share similar pharmacologic profiles but differ somewhat in their pharmacokinetic profiles, drug interactions and adverse effects. Both agents block the reuptake of serotonin and norepinephrine and both are substrates for the cytochrome P450 2D6 isoenzyme; however, duloxetine inhibits these enzymes to a moderate extent, whereas venlafaxine is only a weak inhibitor. Furthermore, duloxetine is more extensively bound to protein than venlafaxine. Venlafaxine is more likely to elevate blood pressure in a dose-related manner. Both duloxetine and venlafaxine have the potential to cause hepatic injury. Conclusions: Although venlafaxine and duloxetine have similar efficacy in the treatment of depression, differences in their adverse effects and pharmacokinetic profiles suggest that one agent may be preferred over the other in certain patient groups.

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Choi, Min-Koo, and Im-Sook Song. "Pharmacokinetic Drug–Drug Interactions and Herb–Drug Interactions." Pharmaceutics 13, no. 5 (April 23, 2021): 610. http://dx.doi.org/10.3390/pharmaceutics13050610.

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Rapp, Robert P. "Pharmacokinetics and Pharmacodynamics of Intravenous and Oral Azithromycin: Enhanced Tissue Activity and Minimal Drug Interactions." Annals of Pharmacotherapy 32, no. 7-8 (July 1998): 785–93. http://dx.doi.org/10.1345/aph.17299.

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OBJECTIVE: To review the pharmacokinetics and pharmacodynamics of oral and intravenous azithromycin compared with other macrolide antibiotics, and to evaluate these differences and their relation to clinical effectiveness. DATA SOURCE: A MEDLINE search (1966–May 1998) was performed to identify applicable English-language clinical, animal, and microbiologic studies pertaining to pharmacokinetic and pharmacodynamic parameters. STUDY SELECTION: Relevant studies concerning microbiology, pharmacokinetics, tissue concentrations, pharmacodynamics, and the clinical effects of these parameters were selected. DATA SYNTHESIS: The structural modification that distinguishes the azalide antibiotics from the macrolide antibiotics is responsible for the pharmacokinetic and pharmacodynamic behavior of azithromycin, resulting in the high and sustained tissue and intracellular concentrations seen with this agent. Drug delivery to the site of infection by phagocytes and fibroblasts is the hallmark of azithromycin's tissue-directed pharmacodynamics, allowing for convenient once-daily, 5-day regimens for most infections that respond to oral therapy and 7–10 days for more serious infections requiring initial intravenous therapy. Metabolism is via hepatic pathways other than cytochrome P450, thus minimizing the risk of drug interactions. CONCLUSIONS: Compared with other macrolide antibiotics, the unique pharmacokinetic and pharmacodynamic features of azithromycin offer the potential for improved efficacy and safety from drug interactions. These attributes, combined with its once-daily dosing schedule, make azithromycin suitable for the treatment of many types of bacterial infection.

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Hofmeister, Craig C., Xiaoxia Yang, Flavia Pichiorri, Ping Chen, Darlene M. Rozewski, Amy J. Johnson, Seungsoo Lee, et al. "Phase I Trial of Lenalidomide and CCI-779 in Patients With Relapsed Multiple Myeloma: Evidence for Lenalidomide–CCI-779 Interaction via P-Glycoprotein." Journal of Clinical Oncology 29, no. 25 (September 1, 2011): 3427–34. http://dx.doi.org/10.1200/jco.2010.32.4962.

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Purpose Multiple myeloma (MM) is an incurable plasma-cell neoplasm for which most treatments involve a therapeutic agent combined with dexamethasone. The preclinical combination of lenalidomide with the mTOR inhibitor CCI-779 has displayed synergy in vitro and represents a novel combination in MM. Patients and Methods A phase I clinical trial was initiated for patients with relapsed myeloma with administration of oral lenalidomide on days 1 to 21 and CCI-779 intravenously once per week during a 28-day cycle. Pharmacokinetic data for both agents were obtained, and in vitro transport and uptake studies were conducted to evaluate potential drug-drug interactions. Results Twenty-one patients were treated with 15 to 25 mg lenalidomide and 15 to 20 mg CCI-779. The maximum-tolerated dose (MTD) was determined to be 25 mg lenalidomide with 15 mg CCI-779. Pharmacokinetic analysis indicated increased doses of CCI-779 resulted in statistically significant changes in clearance, maximum concentrations, and areas under the concentration-time curves, with constant doses of lenalidomide. Similar and significant changes for CCI-779 pharmacokinetics were also observed with increased lenalidomide doses. Detailed mechanistic interrogation of this pharmacokinetic interaction demonstrated that lenalidomide was an ABCB1 (P-glycoprotein [P-gp]) substrate. Conclusion The MTD of this combination regimen was 25 mg lenalidomide with 15 mg CCI-779, with toxicities of fatigue, neutropenia, and electrolyte wasting. Pharmacokinetic and clinical interactions between lenalidomide and CCI-779 seemed to occur, with in vitro data indicating lenalidomide was an ABCB1 (P-gp) substrate. To our knowledge, this is the first report of a clinically significant P-gp–based drug-drug interaction with lenalidomide.

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Albitar, Orwa, Sabariah Noor Harun, Hadzliana Zainal, Baharudin Ibrahim, and Siti Maisharah Sheikh Ghadzi. "Population Pharmacokinetics of Clozapine: A Systematic Review." BioMed Research International 2020 (January 8, 2020): 1–10. http://dx.doi.org/10.1155/2020/9872936.

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Background and Objective. Clozapine is a second-generation antipsychotic drug that is considered the most effective treatment for refractory schizophrenia. Several clozapine population pharmacokinetic models have been introduced in the last decades. Thus, a systematic review was performed (i) to compare published pharmacokinetics models and (ii) to summarize and explore identified covariates influencing the clozapine pharmacokinetics models. Methods. A search of publications for population pharmacokinetic analyses of clozapine either in healthy volunteers or patients from inception to April 2019 was conducted in PubMed and SCOPUS databases. Reviews, methodology articles, in vitro and animal studies, and noncompartmental analysis were excluded. Results. Twelve studies were included in this review. Clozapine pharmacokinetics was described as one-compartment with first-order absorption and elimination in most of the studies. Significant interindividual variations of clozapine pharmacokinetic parameters were found in most of the included studies. Age, sex, smoking status, and cytochrome P450 1A2 were found to be the most common identified covariates affecting these parameters. External validation was only performed in one study to determine the predictive performance of the models. Conclusions. Large pharmacokinetic variability remains despite the inclusion of several covariates. This can be improved by including other potential factors such as genetic polymorphisms, metabolic factors, and significant drug-drug interactions in a well-designed population pharmacokinetic model in the future, taking into account the incorporation of larger sample size and more stringent sampling strategy. External validation should also be performed to the previously published models to compare their predictive performances.

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Karlina, M. V., V. M. Kosman, V. G. Makarov, M. N. Makarova, S. V. Morozov, E. E. Gushchina, and N. V. Zhuravskaya. "Pharmacokinetic Interactions of Phenosanic Acid with Valproic Acid and Carbamazepine in Dogs." Safety and Risk of Pharmacotherapy 10, no. 4 (December 29, 2022): 420–33. http://dx.doi.org/10.30895/2312-7821-2022-10-4-420-433.

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Phenosanic acid prevents convulsions, reduces the frequency of epileptic seizures, and improves cognitive, intellectual and mnestic functions in patients with epilepsy. Therefore, phenosanic acid-based medicinal products are promising candidates for inclusion in combination antiepileptic therapy. In order to combine medicinal products rationally and ensure that the therapy is safe, it is useful to study the pharmacokinetic interaction of medicinal products planned for clinical co-administration.The aim of the study was to examine single-dose pharmacokinetic interactions between Dibufelon® 200 mg capsules (PIQ-PHARMA LLC, Russia) and two medicinal products planned for clinical co-application with it, namely, valproic acid and carbamazepine, in sexually mature dogs.Materials and methods: the study included medicinal products of phenosanic acid (Dibufelon® 200 mg capsules by PIQ-PHARMA LLC, Russia), valproic acid (300 mg prolonged-release film-coated tablets), and carbamazepine (200 mg tablets). The medicinal products were administered to beagle dogs (2 groups of 9 males each) as a single oral dose separately and in the following combinations: phenosanic acid with valproic acid and phenosanic acid with carbamazepine. Dose selection involved adjusting maximum human therapeutic doses using interspecies conversion factors. Phenosanic acid was administered at a dose of 24 mg/kg; valproic acid and carbamazepine were administered at a dose of 60 mg/kg. Blood sampling took place at baseline and in 0.5, 0.75, 1, 2, 4, 6, 8, 10, and 24 h after dosing. Plasma concentrations of active substances were determined by HPLC-UV. Pharmacokinetic interactions were evaluated by changes in the main pharmacokinetic parameters (Сmax, Тmax, AUC0-24, MRT, Т1/2).Results: the study demonstrated rapid gastrointestinal absorption and prolonged systemic circulation of phenosanic acid administered separately (Tmax 2–4 h, T1/2 13–28 h) and combined with valproic acid (Tmax 2 h, T1/2 22 h). When administered with carbamazepine, phenosanic acid was eliminated from the systemic blood flow faster (T1/2 7.4 h).Conclusions: co-administration of phenosanic acid and valproic acid medicinal products had no significant effect on their respective pharmacokinetics. Whereas, the combination of phenosanic acid and carbamazepine demonstrated a significant decrease in the Tmax values of phenosanic acid and the MRT values of carbamazepine. The pharmacokinetic changes suggestive of a possible interaction between phenosanic acid and carbamazepine need further clinical investigation.

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Cattaneo, Dario, Cristina Gervasoni, and Alberto Corona. "The Issue of Pharmacokinetic-Driven Drug-Drug Interactions of Antibiotics: A Narrative Review." Antibiotics 11, no. 10 (October 13, 2022): 1410. http://dx.doi.org/10.3390/antibiotics11101410.

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Patients in intensive care units (ICU) are at high risk to experience potential drug-drug interactions (pDDIs) because of the complexity of their drug regimens. Such pDDIs may be driven by pharmacokinetic or pharmacodynamic mechanisms with clinically relevant consequences in terms of treatment failure or development of drug-related adverse events. The aim of this paper is to review the pharmacokinetic-driven pDDIs involving antibiotics in ICU adult patients. A MEDLINE Pubmed search for articles published from January 2000 to June 2022 was completed matching the terms “drug-drug interactions” with “pharmacokinetics”, “antibiotics”, and “ICU” or “critically-ill patients”. Moreover, additional studies were identified from the reference list of retrieved articles. Some important pharmacokinetic pDDIs involving antibiotics as victims or perpetrators have been identified, although not specifically in the ICU settings. Remarkably, most of them relate to the older antibiotics whereas novel molecules seem to be associated with a low potential for pDDIs with the exceptions of oritavancin as potential perpetrator, and eravacicline that may be a victim of strong CYP3A inducers. Personalized therapeutic drug regimens by means of available web-based pDDI checkers, eventually combined with therapeutic drug monitoring, when available, have the potential to improve the response of ICU patients to antibiotic therapies.

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Fuhr, Uwe, Chih-hsuan Hsin, Xia Li, Wafaâ Jabrane, and Fritz Sörgel. "Assessment of Pharmacokinetic Drug–Drug Interactions in Humans: In Vivo Probe Substrates for Drug Metabolism and Drug Transport Revisited." Annual Review of Pharmacology and Toxicology 59, no. 1 (January 6, 2019): 507–36. http://dx.doi.org/10.1146/annurev-pharmtox-010818-021909.

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Pharmacokinetic parameters of selective probe substrates are used to quantify the activity of an individual pharmacokinetic process (PKP) and the effect of perpetrator drugs thereon in clinical drug–drug interaction (DDI) studies. For instance, oral caffeine is used to quantify hepatic CYP1A2 activity, and oral dagibatran etexilate for intestinal P-glycoprotein (P-gp) activity. However, no probe substrate depends exclusively on the PKP it is meant to quantify. Lack of selectivity for a given enzyme/transporter and expression of the respective enzyme/transporter at several sites in the human body are the main challenges. Thus, a detailed understanding of the role of individual PKPs for the pharmacokinetics of any probe substrate is essential to allocate the effect of a perpetrator drug to a specific PKP; this is a prerequisite for reliably informed pharmacokinetic models that will allow for the quantitative prediction of perpetrator effects on therapeutic drugs, also in respective patient populations not included in DDI studies.

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Li, Ying, Yin Wu, Ya-Jing Li, Lu Meng, Cong-Yang Ding, and Zhan-Jun Dong. "Effects of Silymarin on the In Vivo Pharmacokinetics of Simvastatin and Its Active Metabolite in Rats." Molecules 24, no. 9 (April 28, 2019): 1666. http://dx.doi.org/10.3390/molecules24091666.

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Herein, the effect of silymarin pretreatment on the pharmacokinetics of simvastatin in rats was evaluated. To ensure the accuracy of the results, a rapid and sensitive UPLC–MS/MS method was established for simultaneous quantification of simvastatin (SV) and its active metabolite simvastatin acid (SVA). This method was applied for studying the pharmacokinetic interactions in rats after oral co-administration of silymarin (45 mg/kg) and different concentrations of SV. The major pharmacokinetic parameters, including Cmax, tmax, t1/2, mean residence time (MRT), elimination rate constant (λz) and area under the concentration-time curve (AUC0–12h), were calculated using the non-compartmental model. The results showed that the co-administration of silymarin and SV significantly increased the Cmax and AUC0–12h of SVA compared with SV alone, while there was no significant difference with regards to Tmax and t1/2. However, SV pharmacokinetic parameters were not significantly affected by silymarin pretreatment. Therefore, these changes indicated that drug-drug interactions may occur after co-administration of silymarin and SV.

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Hoetdmans, Richard MW. "Pharmacology of Antiretroviral Drugs." Antiviral Therapy 4, no. 3_suppl (April 1, 1998): 29–41. http://dx.doi.org/10.1177/135965359900403s01.

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In this paper, an overview of the pharmacokinetics of currently available antiretroviral drugs is provided. Included in this article are the agents zidovudine, stavudine, zalcitabine, lamivudine, didanosine, abacavir, nevirapine, delavirdine, efavirenz, saquinavir, indinavir, ritonavir and nelfinavir. Key pharmacokinetic parameters, drug penetration in body compartments and drug interactions are discussed for each agent.

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Petrykiv, S., L. De Jonge, and M. Arts. "Interactions between SSRI's and statins: Clinical relevance versus statistical significance." European Psychiatry 41, S1 (April 2017): S757—S758. http://dx.doi.org/10.1016/j.eurpsy.2017.01.1418.

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IntroductionDepression and hypercholesterolemia are two of the most commonly treated conditions in the developed countries, while the lipid–lowering agents and antidepressants are among the most widely prescribed drugs in the world. There is a common concern that selective serotonin reuptake inhibitors (SSRIs) can trigger statin adverse effects, especially myopathy. However, the supporting evidence originates from studies in-vitro and big epidemiological studies. Recent pharmacokinetic insights indicate that the magnitude of pharmacokinetic interaction between SSRIs and statins is likely to be below the threshold for clinical significance.Objectives and aimsExplorative study on pharmacokinetic effects of SSRIs on statin drugs.MethodsWe performed a detailed literature review through PubMed, EMBASE and Cochran's Library to assess the clinical relevance of combined SSRIs and statin use. To address pharmacokinetic interactions between two drug groups, we focused on:– cytochrome P450 enzyme metabolism of statins;– CYP enzyme inhibition by SSRIs;– SSRIs–statin drug interactions;– non-CYP pharmacokinetic pathways.ResultsWith regard to pharmacokinetic drug interactions and the risk of statin related myopathy, escitalopram, citalopram, and paroxetine are to be safe in co-therapy with all statins. Rosuvastatin and pravastatin are almost certain to be safe in co-therapy with all SSRIs. Fluoxetine and sertraline are also likely to be safe, even when combined with atorvastatin, simvastatin, and lovastatin.ConclusionThough the absolute risk of concomitant use of SSRIs with statins seems to be negligible, even this risk can be minimized by using lower statin doses and monitoring the patient.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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Coelho, Maria Miguel, Carla Fernandes, Fernando Remião, and Maria Elizabeth Tiritan. "Enantioselectivity in Drug Pharmacokinetics and Toxicity: Pharmacological Relevance and Analytical Methods." Molecules 26, no. 11 (May 23, 2021): 3113. http://dx.doi.org/10.3390/molecules26113113.

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Enzymes, receptors, and other binding molecules in biological processes can recognize enantiomers as different molecular entities, due to their different dissociation constants, leading to diverse responses in biological processes. Enantioselectivity can be observed in drugs pharmacodynamics and in pharmacokinetic (absorption, distribution, metabolism, and excretion), especially in metabolic profile and in toxicity mechanisms. The stereoisomers of a drug can undergo to different metabolic pathways due to different enzyme systems, resulting in different types and/or number of metabolites. The configuration of enantiomers can cause unexpected effects, related to changes as unidirectional or bidirectional inversion that can occur during pharmacokinetic processes. The choice of models for pharmacokinetic studies as well as the subsequent data interpretation must also be aware of genetic factors (such as polymorphic metabolic enzymes), sex, patient age, hepatic diseases, and drug interactions. Therefore, the pharmacokinetics and toxicity of a racemate or an enantiomerically pure drug are not equal and need to be studied. Enantioselective analytical methods are crucial to monitor pharmacokinetic events and for acquisition of accurate data to better understand the role of the stereochemistry in pharmacokinetics and toxicity. The complexity of merging the best enantioseparation conditions with the selected sample matrix and the intended goal of the analysis is a challenge task. The data gathered in this review intend to reinforce the importance of the enantioselectivity in pharmacokinetic processes and reunite innovative enantioselective analytical methods applied in pharmacokinetic studies. An assorted variety of methods are herein briefly discussed.

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Liu, Mou-Ze, Yue-Li Zhang, Mei-Zi Zeng, Fa-Zhong He, Zhi-Ying Luo, Jian-Quan Luo, Jia-Gen Wen, Xiao-Ping Chen, Hong-Hao Zhou, and Wei Zhang. "Pharmacogenomics and Herb-Drug Interactions: Merge of Future and Tradition." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/321091.

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The worldwide using of herb products and the increasing potential herb-drug interaction issue has raised enthusiasm on discovering the underlying mechanisms. Previous review indicated that the interactions may be mediated by metabolism enzymes and transporters in pharmacokinetic pathways. On the other hand, an increasing number of studies found that genetic variations showed some influence on herb-drug interaction effects whereas these genetic factors did not draw much attention in history. We highlight that pharmacogenomics may involve the pharmacokinetic or pharmacodynamic pathways to affect herb-drug interaction. We are here to make an updated review focused on some common herb-drug interactions in association with genetic variations, with the aim to help safe use of herbal medicines in different individuals in the clinic.

Journal articles on the topic 'Pharmacokinetic interactions'

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