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Amorphous solid dispersion (ASD) is a powerful formulation technology to improve oral absorption of poorly soluble drugs. Despite their being in existence for more than half a century, controlling ASD performance is still regarded as difficult because of ASD’s natural non-equilibrium. However, recent significant advances in ASD knowledge and technology may enable a much broader use of ASD technology. This Special Issue, which includes 3 reviews and 6 original articles, focuses on recent progresses in ASD technology in hopes of helping to accelerate developmental studies in the pharmaceutical industry. In striving for a deep understanding of ASD non-equilibrium behavior, the Special issue also delves into and makes progress in the theory of soft-matter dynamics.
thermodynamic modeling --- molecular dynamics simulation --- poorly soluble drugs --- amorphous solid dispersions --- dissolution enhancement --- crystallization tendency --- continuous processing --- stability --- milling --- granulation --- thermal analysis --- amorphous --- ball milling --- pharmaceutical glass --- dissolution --- rebamipide --- poloxamer --- classification --- polyelectrolytes --- amorphisation --- self-assembly --- dissolution rate --- miscibility --- bioavailability --- solubility --- evaporation --- mesoporous --- polyelectrolyte excipient matrix --- polymer --- bicaludamide --- phase diagram --- Weibull dissolution model --- spectroscopic techniques --- anticancer drugs --- manufacturing methods --- nucleation --- molecular complex --- nanoaggregates --- enrofloxacin --- accelerated stability test --- solubility enhancement --- amorphous solid dispersion --- tadalafil --- process development --- amorphous polymeric salt --- Wood’s apparatus --- hot melt extrusion --- solid dispersions --- intrinsic dissolution rate --- solid dispersion --- interaction --- crystallization --- spray drying --- characterization --- ciprofloxacin
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Drug–drug interactions (DDIs) cause a drug to affect other drugs, leading to reduced drug efficacy or increased toxicity of the affected drug. Some well-known interactions are known to be the cause of adverse drug reactions (ADRs) that are life threatening to the patient. Traditionally, DDI have been evaluated around the selective action of drugs on specific CYP enzymes. The interaction of drugs with CYP remains very important in drug interactions but, recently, other important mechanisms have also been studied as contributing to drug interaction including transport- or UDP-glucuronyltransferase as a Phase II reaction-mediated DDI. In addition, novel mechanisms of regulating DDIs can also be suggested. In the case of the substance targeted for interaction, not only the DDIs but also the herb–drug or food–drug interactions have been reported to be clinically relevant in terms of adverse side effects. Reporting examples of drug interactions on a marketed drug or studies on new mechanisms will be very helpful for preventing the side effects of the patient taking these drugs. This Special Issue aims to highlight current progress in understanding both the clinical and nonclinical interactions of commercial drugs and the elucidation of the mechanisms of drug interactions.
tadalafil --- ticagrelor --- drug-drug interaction --- pharmacokinetics --- plasma concentration --- CYP3A4 --- Loxoprofen --- CYP3A --- Dexamethasone --- Ketoconazole --- CYP2D6 --- O-desmethyltramadol --- physiologically-based pharmacokinetics --- tramadol --- (‒)-sophoranone --- CYP2C9 --- potent inhibition --- in vitro --- in vivo --- drug interaction --- low permeability --- high plasma protein binding --- biflavonoid --- cytochrome P450 --- drug interactions --- selamariscina A --- uridine 5′-diphosphoglucuronosyl transferase --- tissue-specific --- systemic exposure --- P-glycoprotein (P-gp) --- organic anion transporting polypeptide 1A2 (OATP1A2) --- Rumex acetosa --- fexofenadine --- chronic kidney disease --- drug–drug interactions --- polypharmacy --- adverse drug reactions --- Lexicomp --- subset analysis --- signal detection algorithms --- spontaneous reporting systems --- mechanism-based inhibition --- competitive inhibition --- non-competitive inhibition --- substrate --- inhibitor --- cytochromes P450 --- OATP1B1 --- OATP1B3 --- tyrosine kinase inhibitors --- drug-drug interactions --- migraine --- lasmiditan --- gepants --- monoclonal antibodies --- CYP1A1 --- CYP1A2 --- drug–drug interaction --- expression --- metabolism --- regulation --- drug transporter --- ubiquitination --- ixazomib --- DDI --- computational prediction --- in silico --- QSAR --- drug metabolism --- ADME --- CYP --- metabolic DDI --- P450 --- 1A2 --- 2B6 --- 2C19 --- 2C8 --- 2C9 --- 2D6 --- 3A4
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Drug–drug interactions (DDIs) cause a drug to affect other drugs, leading to reduced drug efficacy or increased toxicity of the affected drug. Some well-known interactions are known to be the cause of adverse drug reactions (ADRs) that are life threatening to the patient. Traditionally, DDI have been evaluated around the selective action of drugs on specific CYP enzymes. The interaction of drugs with CYP remains very important in drug interactions but, recently, other important mechanisms have also been studied as contributing to drug interaction including transport- or UDP-glucuronyltransferase as a Phase II reaction-mediated DDI. In addition, novel mechanisms of regulating DDIs can also be suggested. In the case of the substance targeted for interaction, not only the DDIs but also the herb–drug or food–drug interactions have been reported to be clinically relevant in terms of adverse side effects. Reporting examples of drug interactions on a marketed drug or studies on new mechanisms will be very helpful for preventing the side effects of the patient taking these drugs. This Special Issue aims to highlight current progress in understanding both the clinical and nonclinical interactions of commercial drugs and the elucidation of the mechanisms of drug interactions.
Research & information: general --- Biology, life sciences --- tadalafil --- ticagrelor --- drug-drug interaction --- pharmacokinetics --- plasma concentration --- CYP3A4 --- Loxoprofen --- CYP3A --- Dexamethasone --- Ketoconazole --- CYP2D6 --- O-desmethyltramadol --- physiologically-based pharmacokinetics --- tramadol --- (‒)-sophoranone --- CYP2C9 --- potent inhibition --- in vitro --- in vivo --- drug interaction --- low permeability --- high plasma protein binding --- biflavonoid --- cytochrome P450 --- drug interactions --- selamariscina A --- uridine 5′-diphosphoglucuronosyl transferase --- tissue-specific --- systemic exposure --- P-glycoprotein (P-gp) --- organic anion transporting polypeptide 1A2 (OATP1A2) --- Rumex acetosa --- fexofenadine --- chronic kidney disease --- drug–drug interactions --- polypharmacy --- adverse drug reactions --- Lexicomp --- subset analysis --- signal detection algorithms --- spontaneous reporting systems --- mechanism-based inhibition --- competitive inhibition --- non-competitive inhibition --- substrate --- inhibitor --- cytochromes P450 --- OATP1B1 --- OATP1B3 --- tyrosine kinase inhibitors --- drug-drug interactions --- migraine --- lasmiditan --- gepants --- monoclonal antibodies --- CYP1A1 --- CYP1A2 --- drug–drug interaction --- expression --- metabolism --- regulation --- drug transporter --- ubiquitination --- ixazomib --- DDI --- computational prediction --- in silico --- QSAR --- drug metabolism --- ADME --- CYP --- metabolic DDI --- P450 --- 1A2 --- 2B6 --- 2C19 --- 2C8 --- 2C9 --- 2D6 --- 3A4
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