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000075925 0247_ $$2doi$$a10.3389/fphys.2018.00678
000075925 0248_ $$2sideral$$a106846
000075925 037__ $$aART-2018-106846
000075925 041__ $$aeng
000075925 100__ $$aGrandi, E.
000075925 245__ $$aEditorial: Safety Pharmacology - Risk Assessment QT Interval Prolongation and Beyond
000075925 260__ $$c2018
000075925 5060_ $$aAccess copy available to the general public$$fUnrestricted
000075925 5203_ $$aThe scope of safety pharmacology is to predict whether a drug is likely to cause potentially lethal adverse effects if administered to humans. While safety pharmacology has broadened its interests in recent years to the whole cardiovascular, respiratory, and central nervous systems (and is now extending to other body functions), a major focus since its inception has been assessing drug-induced prolongation in the QT interval—a surrogate biomarker for torsades de pointes (TdP) liability. Because the vast majority of drugs that can cause QT prolongation inhibit hERG channels, current regulatory guidelines concerning cardiac safety recommend that all compounds are evaluated in vitro for their hERG inhibitory potency (Redfern et al., 2003) and in vivo for their ability to cause QT/QTc interval prolongation (Food and Drug Administration, 2005) in an appropriate animal model and in humans. However, it has now become apparent that QT/QTc prolongation and hERG block are an insufficient proxy for TdP risk. While the current approach based on these markers has been successful in terms of preventing TdP risk, this regulatory paradigm might lead to withdrawal from the drug development pipeline and clinical use of potentially safe drugs. There is therefore a crucial need to develop a more accurate assessment of proarrhythmic potential of drugs...
000075925 536__ $$9info:eu-repo/grantAgreement/ES/MINECO/DPI2016-75458-R$$9This project has received funding from the European Union’s Horizon 2020 research and innovation program under grant agreement No H2020 638284-MODELAGE$$9info:eu-repo/grantAgreement/EC/H2020/638284/EU/Is your heart aging well? A systems biology approach to characterize cardiac aging from the cell to the body surface/MODELAGE$$9info:eu-repo/grantAgreement/ES/DGA-FEDER/T39-17R-BSICoS
000075925 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000075925 590__ $$a3.201$$b2018
000075925 591__ $$aPHYSIOLOGY$$b25 / 81 = 0.309$$c2018$$dQ2$$eT1
000075925 592__ $$a1.153$$b2018
000075925 593__ $$aPhysiology (medical)$$c2018$$dQ2
000075925 593__ $$aPhysiology$$c2018$$dQ2
000075925 655_4 $$ainfo:eu-repo/semantics/other$$vinfo:eu-repo/semantics/publishedVersion
000075925 700__ $$aMorotti, S.
000075925 700__ $$0(orcid)0000-0002-1960-407X$$aPueyo, E.$$uUniversidad de Zaragoza
000075925 700__ $$aRodriguez, B.
000075925 7102_ $$15008$$2800$$aUniversidad de Zaragoza$$bDpto. Ingeniería Electrón.Com.$$cÁrea Teoría Señal y Comunicac.
000075925 773__ $$g9 (2018), 678 [5 pp]$$pFront. physiol.$$tFRONTIERS IN PHYSIOLOGY$$x1664-042X
000075925 8564_ $$s186103$$uhttps://zaguan.unizar.es/record/75925/files/texto_completo.pdf$$yVersión publicada
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000075925 951__ $$a2021-08-20-08:36:33
000075925 980__ $$aARTICLE