Flecainide: A new antiarrhythmic drug

Mueller, Romano; Baur, H

doi:10.1002/clc.4960090102

Cited by 10 publications

(2 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Flecainide is a well‐characterized sodium channel–blocking agent18–20 commonly used to treat cardiac arrhythmias 21. We propose that the partial blockade of Na + currents by flecainide averts a deleterious axoplasmic accumulation of Na + at sites of inflammation, which, in turn, prevents a damaging increase in intraaxonal calcium.…”

Section: Discussionmentioning

confidence: 99%

Atypical squamous cells of undetermined significance on cervical smears

Cheung

Szeto

et al. 2004

Cancer

View full text Add to dashboard Cite

Axonal degeneration is a major cause of permanent neurological deficit in multiple sclerosis (MS), but no current therapies for the disease are known to be effective at axonal protection. Here, we examine the ability of a sodium channel–blocking agent, flecainide, to reduce axonal degeneration in an experimental model of MS, chronic relapsing experimental autoimmune encephalomyelitis (CR‐EAE). Rats with CR‐EAE were treated with flecainide or vehicle from either 3 days before or 7 days after inoculation (dpi) until termination of the experiment at 28 to 30 dpi. Morphometric examination of neurofilament‐labeled axons in the spinal cord of CR‐EAE animals showed that both flecainide treatment regimens resulted in significantly higher numbers of axons surviving the disease (83 and 98% of normal) compared with controls (62% of normal). These findings indicate that flecainide and similar agents may provide a novel therapy aimed at axonal protection in MS and other neuroinflammatory disorders.

show abstract

Section: Discussionmentioning

confidence: 99%

Atypical squamous cells of undetermined significance on cervical smears

Cheung

Szeto

et al. 2004

Cancer

View full text Add to dashboard Cite

show abstract

“…Flecainide is an antiarrhythmic drug known to cause taste dysfunction. Flecainide, a widely used antiarrhythmic drug, prevents supraventricular and ventricular arrhythmias, paroxysmal atrial fibrillation and flutter (Mueller & Baur, 1986). The main antiarrhythmic action of this drug is thought to be due to the inhibition of voltage-gated sodium channels (SCN5A), which slows the conduction of electrical impulses within the heart and prolongs the refractory period of ventricular and atrial myocytes (Liu et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

The Antiarrhythmic Drug Flecainide Enhances Aversion to HCl in Mice

Kawabata,

Takai,

Sanematsu

et al. 2023

eNeuro

View full text Add to dashboard Cite

Drug-induced taste disorders reduce quality of life, but little is known about the molecular mechanisms by which drugs induce taste disturbances. In this study, we investigated the short-term and long-term effects of the antiarrhythmic drug flecainide, which is known to cause taste dysfunction. Analyses of behavioral responses (licking tests) revealed that mice given a single intraperitoneal injection of flecainide exhibited a significant reduction in preference for a sour tastant (HCl) but not for other taste solutions (NaCl, quinine, sucrose, KCl and monopotassium glutamate) when compared with controls. Mice administered a single dose of flecainide also had significantly higher taste nerve responses to HCl but not to other taste solutions. Compared with controls, mice administered flecainide once-daily for 30 d showed a reduced preference for HCl without any changes in the behavioral responses to other taste solutions. The electrophysiological experiments using HEK293T cells transiently expressing otopetrin-1 (Otop1; the mouse sour taste receptor) showed that flecainide did not alter the responses to HCl. Taken together, our results suggest that flecainide specifically enhances the response to HCl in mice during short-term and long-term administration. Although further studies will be needed to elucidate the molecular mechanisms, these findings provide new insights into the pathophysiology of drug-induced taste disorders.

show abstract

Axonal protection using flecainide in experimental autoimmune encephalomyelitis

Bechtold

Kapoor

Smith

2004

Annals of Neurology

181

View full text Add to dashboard Cite

Axonal degeneration is a major cause of permanent neurological deficit in multiple sclerosis (MS), but no current therapies for the disease are known to be effective at axonal protection. Here, we examine the ability of a sodium channel-blocking agent, flecainide, to reduce axonal degeneration in an experimental model of MS, chronic relapsing experimental autoimmune encephalomyelitis (CR-EAE). Rats with CR-EAE were treated with flecainide or vehicle from either 3 days before or 7 days after inoculation (dpi) until termination of the experiment at 28 to 30 dpi. Morphometric examination of neurofilament-labeled axons in the spinal cord of CR-EAE animals showed that both flecainide treatment regimens resulted in significantly higher numbers of axons surviving the disease (83 and 98% of normal) compared with controls (62% of normal). These findings indicate that flecainide and similar agents may provide a novel therapy aimed at axonal protection in MS and other neuroinflammatory disorders.

show abstract

Flecainide: A new antiarrhythmic drug

Cited by 10 publications

References 25 publications

Atypical squamous cells of undetermined significance on cervical smears

Atypical squamous cells of undetermined significance on cervical smears

The Antiarrhythmic Drug Flecainide Enhances Aversion to HCl in Mice

Axonal protection using flecainide in experimental autoimmune encephalomyelitis

Contact Info

Product

Resources

About