Page last updated: 2024-11-06

ibutilide

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Description

Ibutilide is a class III antiarrhythmic drug used to treat atrial fibrillation and atrial flutter. It is a potent blocker of the rapid delayed rectifier potassium current (IKr) and has a lesser effect on the sodium current. Ibutilide is administered intravenously and has a rapid onset of action. It is effective in converting atrial fibrillation to sinus rhythm and in maintaining sinus rhythm. Ibutilide is studied because it is a highly effective and rapid-acting antiarrhythmic agent. It is also being investigated for its potential use in other cardiac arrhythmias, such as ventricular tachycardia.'

ibutilide: RN & structure in first source; RN refers to the fumarate salt [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID60753
CHEMBL ID533
CHEBI ID5856
SCHEMBL ID3719856
MeSH IDM0184268

Synonyms (46)

Synonym
ibutilide [inn:ban]
ibutilidum [inn-latin]
ibutilida [inn-spanish]
122647-31-8
ibutilide
C07753
n-(4-{4-[ethyl(heptyl)amino]-1-hydroxybutyl}phenyl)methanesulfonamide
DB00308
n-(4-(4-(ethylheptylamino)-1-hydroxybutyl)phenyl)methanesulfonamide
130350-52-6
bdbm50131432
n-{4-[4-(ethyl-heptyl-amino)-1-hydroxy-butyl]-phenyl}-methanesulfonamide
n-(4-(4-(ethyl(heptyl)amino)-1-hydroxybutyl)phenyl)methanesulfonamide
n-[4-[4-[ethyl(heptyl)amino]-1-hydroxybutyl]phenyl]methanesulfonamide
CHEMBL533 ,
chebi:5856 ,
ibutilide (inn)
D08060
2436vx1u9b ,
ibutilidum
ibutilida
unii-2436vx1u9b
FT-0631106
gtpl7200
ibutilide [inn]
ibutilide [who-dd]
ibutilide [vandf]
ibutilide [mi]
methanesulfonamide, n-(4-(4-(ethylheptylamino)-1-hydroxybutyl)phenyl)-
SCHEMBL3719856
n-[4-[4-(ethylheptylamino)-1-hydroxybutyl]phenyl]methanesulfonamide
[2-(3-methyl-pyrazol-1-yl)-ethylsulfanyl]-aceticacid
methanesulfonamide, n-[4-[4-(ethylheptylamino)-1-hydroxybutyl]phenyl]-
AB01568246_01
DTXSID20861271
Q3791612
100632-81-3
HMS3741K11
NCGC00181771-02
HY-B0387A
CS-0103328
EN300-708804
ibutilid
ibutilida (inn-spanish)
ibutilidum (inn-latin)
c01bd05

Research Excerpts

Overview

Ibutilide is a rapid-acting antiarrhythmic drug with worldwide use for conversion of recent-onset atrial fibrillation. It appears to be an effective and well tolerated drug in octogenarian patients.

ExcerptReferenceRelevance
"Ibutilide is a class III antiarrhythmic indicated for pharmacological cardioversion of recent-onset AF/AFL."( Efficacy and safety of ibutilide for chemical cardioversion of atrial fibrillation and atrial flutter in cancer patients.
Agarwal, R; Bickford, CL; Durand, JB; Lenihan, DJ; Urbauer, DL, 2014
)
1.43
"Ibutilide is a rapid-acting antiarrhythmic drug with worldwide use for conversion of recent-onset atrial fibrillation. "( Vernakalant is superior to ibutilide for achieving sinus rhythm in patients with recent-onset atrial fibrillation: a randomized controlled trial at the emergency department.
Domanovits, H; Herkner, H; Laggner, AN; Niederdoeckl, J; Schuetz, N; Simon, A; Skyllouriotis, E; Spiel, AO; Weiser, C, 2017
)
2.19
"Ibutilide is a class III antiarrhythmic drug, frequently used for conversion of atrial fibrillation and flutter. "( Pre-injection of magnesium sulfate enhances the efficacy of ibutilide for the conversion of typical but not of atypical persistent atrial flutter.
Hofmann, R; Hönig, S; Kammler, J; Kypta, A; Leisch, F; Schmitt, B; Steinwender, C, 2010
)
2.05
"Ibutilide is a class III antiarrhythmic agent indicated for cardioversion of atrial fibrillation and atrial flutter to sinus rhythm (SR). "( Effect of high doses of magnesium on converting ibutilide to a safe and more effective agent.
Antonatos, D; Babalis, D; Christou, A; Kafkas, N; Katsanos, S; Nikolaou, N; Patsilinakos, S; Spanodimos, S, 2010
)
2.06
"Ibutilide is a newer class-III antiarrhythmic agent approved for clinical use. "( Effects of ibutilide on inhibiting heart rate and rapidly terminating atrial flutter in canine.
Guo, J; Li, X; Liu, P; Sun, J; Zhang, P, 2011
)
2.2
"Ibutilide is a novel class III antiarrhythmic agent used for the rapid cardioversion of atrial fibrillation or atrial flutter."( Ibutilide in rapid conversion of atrial flutter in octogenarians.
Antonicelli, R; Recanatini, A; Testarmata, P, 2002
)
2.48
"Ibutilide appears to be an effective and well tolerated drug for rapid conversion of recent-onset atrial flutter in octogenarian patients, and may represent a valid approach in the acute management of atrial flutter in this particular set of patients."( Ibutilide in rapid conversion of atrial flutter in octogenarians.
Antonicelli, R; Recanatini, A; Testarmata, P, 2002
)
3.2
"Ibutilide is a class III antiarrhythmic agent used for the termination of atrial fibrillation and atrial flutter. "( Ibutilide-induced long QT syndrome and torsade de pointes.
Cosme-Thormann, BF; Gowda, RM; Khan, IA; Patlola, RR; Punukollu, G; Sacchi, TJ; Tejani, FH; Vasavada, BC,
)
3.02
"Ibutilide is a class III antiarrhythmic drug used for pharmacological cardioversion of recent-onset atrial fibrillation and flutter. "( Use of ibutilide for cardioversion of recent-onset atrial fibrillation and flutter in elderly.
Gowda, RM; Khan, IA; Mendoza, C; Punukollu, G; Sacchi, TJ; Vasavada, BC; Wilbur, SL,
)
2.03
"Ibutilide is an intravenous class III antiarrhythmic agent that has been shown to be effective in converting acute onset atrial fibrillation/flutter in stable medical and cardio-surgical patients. "( Ibutilide for rapid conversion of atrial fibrillation or flutter in a mixed critically ill patient population.
Delle Karth, G; Geppert, A; Gwechenberger, M; Haumer, M; Heinz, G; Meyer, B; Schillinger, M; Siostrzonek, P, 2005
)
3.21
"Ibutilide is an effective treatment for conversion of acute tachycardic atrial fibrillation/flutter in critically ill patients. "( Ibutilide for rapid conversion of atrial fibrillation or flutter in a mixed critically ill patient population.
Delle Karth, G; Geppert, A; Gwechenberger, M; Haumer, M; Heinz, G; Meyer, B; Schillinger, M; Siostrzonek, P, 2005
)
3.21
"Ibutilide is a 'pure' class III antiarrhythmic drug, used intravenously against atrial flutter and fibrillation. "( Ibutilide--recent molecular insights and accumulating evidence for use in atrial flutter and fibrillation.
Doggrell, SA; Hancox, JC, 2005
)
3.21
"Ibutilide is an anti arrhythmic indicated for the cardioversion of atrial fibrillation and flutter where the onset is less than 48 hours."( Rapid cardioversion of new onset atrial fibrillation with ibutilide in the emergency department.
Cummins, FH; Fahy, GJ; Ryan, DT, 2005
)
1.29
"Ibutilide is a class III antiarrhythmic drug, frequently used for conversion of atrial fibrillation and flutter. "( Efficacy and safety of ibutilide for the conversion of monomorphic atrial tachycardia.
Eidher, U; Freihoff, F; Kaltenbrunner, W; Steinbach, K, 2006
)
2.09
"Ibutilide is a type III antiarrhythmic agent approved for the pharmacologic conversion of atrial fibrillation (AF) and atrial flutter (AFl). "( Ibutilide to expedite ED therapy for recent-onset atrial fibrillation flutter.
McPherson, CA; Mountantonakis, SE; Moutzouris, DA; Papaioannou, GN; Tiu, RV, 2006
)
3.22
"Ibutilide is a selective class III antiarrhythmic agent which when administered intravenously can terminate AF and Af."( Conversion efficacy of intravenous ibutilide compared with intravenous amiodarone in patients with recent-onset atrial fibrillation and atrial flutter.
Chaveles, JI; Dagadaki, OK; Kafkas, NV; Kelesidis, KM; Mertzanos, GA; Papageorgiou, KI; Patsilinakos, SP, 2007
)
1.34
"Ibutilide is a class III antiarrhythmic drug that is used for the cardioversion of atrial arrhythmias, but it can cause torsades de pointes. "( The role of amiodarone in recent-onset atrial fibrillation after ibutilide has failed to restore sinus rhythm.
Bonios, M; Exarchos, P; Kogias, J; Melexopoulou, C; Sideris, S; Tsatiris, K, 2007
)
2.02
"Ibutilide is a class III antiarrhythmic agent used for the cardioversion of atrial flutter or atrial fibrillation."( Pharmacokinetic and pharmacodynamic properties of a single intravenous dose of ibutilide fumarate: a phase I, randomized, open-label, increasing-dose study in healthy Chinese men.
Hua, L; Huang, Y; Li, Y; Tian, L, 2007
)
1.29
"Ibutilide is an action potential-prolonging antiarrhythmic currently in clinical trials. "( Ibutilide, a methanesulfonanilide antiarrhythmic, is a potent blocker of the rapidly activating delayed rectifier K+ current (IKr) in AT-1 cells. Concentration-, time-, voltage-, and use-dependent effects.
Roden, DM; Snyders, DJ; Yang, T, 1995
)
3.18
"Ibutilide fumarate is an investigational class III antiarrhythmic agent that prolongs repolarization by increasing the slow inward sodium current and by blocking the delayed rectifier current. "( Efficacy of intravenous ibutilide for rapid termination of atrial fibrillation and atrial flutter: a dose-response study.
Ellenbogen, KA; Meissner, MC; Perry, KT; Sager, PT; Stambler, BS; Vanderlugt, JT; Wakefield, LK; Wesley, RC; Wood, MA; Zoble, RG, 1996
)
2.04
"Ibutilide fumarate is a new class III intravenous antiarrhythmic agent indicated for the acute termination of atrial fibrillation and flutter. "( Electrophysiology and pharmacology of ibutilide.
Gibson, JK; Lee, KS; Naccarelli, GV; VanderLugt, J, 1996
)
2.01
"Ibutilide is a new intravenous agent that safely and rapidly converts atrial fibrillation and atrial flutter to sinus rhythm."( Efficacy of ibutilide for termination of atrial fibrillation and flutter.
Clemo, HF; Ellenbogen, KA; Stambler, BS; VanderLugt, JT; Wood, MA, 1996
)
1.39
"Ibutilide fumarate is a new antiarrhythmic agent recently approved for the conversion of atrial flutter (AFl) and atrial fibrillation (AF) to normal sinus rhythm. "( Ibutilide: a new class III antiarrhythmic agent.
Antal, EG; Cropp, JS; Talbert, RL,
)
3.02
"Ibutilide is an intravenous, selective class III antiarrhythmic agent that is effective for conversion of atrial fibrillation or flutter."( Acute hemodynamic effects of intravenous ibutilide in patients with or without reduced left ventricular function.
Beckman, KJ; Camm, JA; Ellenbogen, KA; Kadish, AH; Perry, KT; Stambler, BS; VanderLugt, JT, 1997
)
1.28
"Ibutilide appears to be an effective alternative to other antiarrhythmic agents for rapid conversion of arrhythmias to normal sinus rhythm in hemodynamically stable patients."( Ibutilide: a new class III antiarrhythmic agent.
Granberry, MC, 1998
)
2.46
"Ibutilide fumarate is an intravenous (IV) class III antiarrhythmic agent that has been shown to be significantly more effective than placebo in the pharmacologic conversion of atrial flutter and fibrillation to sinus rhythm. "( Conversion efficacy and safety of intravenous ibutilide compared with intravenous procainamide in patients with atrial flutter or fibrillation.
Carberry, PA; Dunn, GH; Kowey, PR; Lewis, WR; Perry, KT; Stambler, B; Vanderlugt, JT; Volgman, AS, 1998
)
2
"Ibutilide is a Vaughan-Williams class III antiarrhythmic agent approved for intravenous use for the rapid termination of recent-onset AF or AFl. "( Ibutilide: an antiarrhythmic agent for the treatment of atrial fibrillation or flutter.
Howard, PA, 1999
)
3.19
"Ibutilide appears to be an effective alternative method for rapid conversion of recent-onset AF or AFl. "( Ibutilide: an antiarrhythmic agent for the treatment of atrial fibrillation or flutter.
Howard, PA, 1999
)
3.19
"Ibutilide is a useful and safe treatment alternative for the atrial arrhythmias that occur after cardiac surgery."( Efficacy and safety of ibutilide fumarate for the conversion of atrial arrhythmias after cardiac surgery.
Ahern, T; Denker, S; Kowey, PR; Mattioni, T; Perry, KT; Torchiana, D; VanderLugt, JT; Wakefield, LK, 1999
)
2.06
"Ibutilide is a compound with Class III effects marketed for rapid conversion of atrial fibrillation and atrial flutter. "( The effect of ibutilide on retrograde accessory pathway conduction.
Cohen, M; Sorbera, C, 2000
)
2.11
"Ibutilide is an effective and well tolerated drug for the rapid termination of Afb or Afl of recent onset associated with symptomatic and/or hemodynamically unstable disorders, and it is most efficacious (> or = 90%) when the atrial arrhythmia is < or = 1 week in duration. "( Acute management of atrial fibrillation and atrial flutter in the critical care unit: should it be ibutilide?
Sedighi, A; Varriale, P, 2000
)
1.97
"Ibutilide is a Vaughan-Williams class III antiarrhythmic agent approved for chemical cardioversion of acute onset atrial fibrillation/flutter. "( Termination of acute wide QRS complex atrial fibrillation with ibutilide.
Dhruva, NN; Sobel, RM, 2000
)
1.99
"Ibutilide is a potent blocker of the rapid delayed rectifier K(+) current, I(Kr)."( Electrophysiological effects of ibutilide on the delayed rectifier K(+) current in rabbit sinoatrial and atrioventricular node cells.
Giles, WR; Habuchi, Y; Sato, N; Tanaka, H, 2000
)
1.31
"Ibutilide is an intravenous Class III antidysrhythmic approved for the treatment of recent onset atrial fibrillation or atrial flutter. "( Ibutilide: a class III rapidly acting antidysrhythmic for atrial fibrillation or atrial flutter.
Rogers, KC; Wolfe, DA, 2001
)
3.2
"Ibutilide is a class III drug that is used for the cardioversion of atrial arrhythmias, but it can cause torsade de pointes. "( Chemical cardioversion of atrial fibrillation or flutter with ibutilide in patients receiving amiodarone therapy.
Chatterjee, K; Cheng, J; Glatter, K; Kayser, S; Modin, G; Scheinman, MM; Yang, Y, 2001
)
1.99
"Ibutilide is a novel class III antiarrhythmic agent used for the termination of atrial flutter and atrial fibrillation. "( [Severe ibutilide-induced arrhythmia in patients with heart failure].
Amlie, JP; Harg, P; Madsen, S, 2001
)
2.19

Effects

Ibutilide has been shown to prolong repolarization times and increase the risk of ventricular tachyarrhythmias. It has a conversion rate of up to 75% to 80% in recent-onset atrial fibrillation and flutter. I butilide (I) has been reported to block I(k) and to delay inactivation of the slow Na(+) current (S-Na)

ExcerptReferenceRelevance
"Ibutilide has a conversion rate of up to 75% to 80% in recent-onset atrial fibrillation and flutter; the conversion rate is higher for atrial flutter than for atrial fibrillation."( Safety and efficacy of ibutilide in cardioversion of atrial flutter and fibrillation.
George, LK; Koshy, SK; Nair, M,
)
1.16
"Ibutilide has been shown to reduce left atrial surface area exhibiting CFAE."( The modified stepwise ablation guided by low-dose ibutilide in chronic atrial fibrillation trial (The MAGIC-AF Study).
Aryana, A; Barrett, CD; d'Avila, A; Dukkipati, SR; Heist, EK; Kim, YH; Mangrum, JM; Michaud, GF; Parides, MK; Reddy, VY; Singh, SM; Thorpe, KE, 2016
)
1.41
"Ibutilide has been shown to prolong repolarization times and increase the risk of ventricular tachyarrhythmias particularly in patients with structural heart disease. "( Ibutilide-induced changes in the temporal lability of ventricular repolarization in patients with and without structural heart disease.
Angkeow, P; Berger, RD; Calkins, H; Cheng, A; Dalal, D; Fetics, BJ; Spragg, DD; Tomaselli, GF, 2009
)
3.24
"Ibutilide has a conversion rate of up to 75% to 80% in recent-onset atrial fibrillation and flutter; the conversion rate is higher for atrial flutter than for atrial fibrillation."( Safety and efficacy of ibutilide in cardioversion of atrial flutter and fibrillation.
George, LK; Koshy, SK; Nair, M,
)
1.16
"Ibutilide has been commonly used for pharmacologic cardioversion of atrial fibrillation and flutter in clinical settings. "( Ibutilide decreases defibrillation threshold by the reduction of activation pattern complexity during ventricular fibrillation in canine hearts.
Gu, G; Jin, Q; Lin, CJ; Pang, Y; Shen, WF; Wu, LQ; Zhang, N; Zhou, J, 2012
)
3.26
"Ibutilide has no significant advantage over amiodarone for the conversion of atrial fibrillation to sinus rhythm in either time to conversion or conversion overall, but severe hypotension was not seen with ibutilide."( Ibutilide versus amiodarone in atrial fibrillation: a double-blinded, randomized study.
Bernard, EO; Candinas, R; Germann, R; Scharf, C; Schmid, ER; Schmidlin, D, 2003
)
3.2
"Ibutilide has been shown to terminate atrial flutter and fibrillation in animal studies, with some risk of ventricular pro-arrhythmia."( Ibutilide--recent molecular insights and accumulating evidence for use in atrial flutter and fibrillation.
Doggrell, SA; Hancox, JC, 2005
)
2.49
"Ibutilide (I) has been reported to block I(k) and to delay inactivation of the slow Na(+) current (S-Na). "( The actions of ibutilide and class Ic drugs on the slow sodium channel: new insights regarding individual pharmacologic effects elucidated through combination therapies.
Blitzer, M; Reiffel, JA, 2000
)
2.1

Actions

Ibutilide could suppress sinus atrial node and the atrioventricular node function. Can cause torsades de pointes in rabbit model of proarrhythmia dependent on formation of early afterdepolarizations.

ExcerptReferenceRelevance
"Ibutilide could suppress sinus atrial node and the atrioventricular node function. "( [The study of inhibiting heart rate and rapidly terminating atrial flutter of ibutilide on canine].
Guo, JH; Li, XY; Liu, P; Sun, JL; Yi, Z; Zhang, P, 2009
)
2.02
"Ibutilide can cause torsades de pointes in a rabbit model of proarrhythmia dependent on the formation of early afterdepolarizations."( Electrophysiology and pharmacology of ibutilide.
Gibson, JK; Lee, KS; Naccarelli, GV; VanderLugt, J, 1996
)
1.29

Treatment

Ibutilide pretreatment facilitates transthoracic defibrillation and decreases the energy requirement of electrical cardioversion by both monophasic and biphasic shocks. Pretreatment with ibutilide resulted in significantly higher conversion rates than placebo.

ExcerptReferenceRelevance
"Ibutilide treatment was successful in all patients, with the arrhythmia recurring early in 1 patient."( Safety and efficacy of ibutilide in heart transplant recipients.
Benza, RL; Bourge, RC; Franco, V; Kirklin, JK; McGiffin, DC; Pamboukian, SV; Rayburn, BK; Smallfield, M; Tallaj, JA, 2009
)
1.38
"Ibutilide pretreatment facilitates transthoracic defibrillation and decreases the energy requirement of electrical cardioversion by both monophasic and biphasic shocks."( Safety and efficacy of ibutilide in cardioversion of atrial flutter and fibrillation.
George, LK; Koshy, SK; Nair, M,
)
1.16
"ibutilide treatment, up to 2 mg, and Group 2-ATP, with "burst" and "ramp" pacing protocols."( Efficacy and safety of ibutilide vs. transoesophageal atrial pacing for the termination of type I atrial flutter.
Bettiol, F; Bisceglia, I; Fera, MS; Gaudio, C; Giovannini, E; Mazza, A; Pulignano, G; Tanzi, P, 2004
)
1.36
"Pretreatment with ibutilide before electrical defibrillation has a conversion rate of 100% compared with 72% with no pretreatment."( Safety and efficacy of ibutilide in cardioversion of atrial flutter and fibrillation.
George, LK; Koshy, SK; Nair, M,
)
0.77
"Pretreatment with ibutilide was associated with a reduction in the mean energy required for defibrillation (166+/-80 J, as compared with 228+/-93 J without pretreatment; P<0.001)."( Facilitating transthoracic cardioversion of atrial fibrillation with ibutilide pretreatment.
Goyal, R; Knight, BP; Michaud, GF; Morady, F; Oral, H; Souza, JJ; Strickberger, SA, 1999
)
0.86
"Treatment with ibutilide resulted in significantly higher conversion rates than placebo, and efficacy was dose related (placebo 15%; ibutilide 0.25 mg 40%, 0.5 mg 47%, and 1.0 mg 57%)."( Efficacy and safety of ibutilide fumarate for the conversion of atrial arrhythmias after cardiac surgery.
Ahern, T; Denker, S; Kowey, PR; Mattioni, T; Perry, KT; Torchiana, D; VanderLugt, JT; Wakefield, LK, 1999
)
0.95

Toxicity

Ibutilide is effective and safe for acute termination of atrial fibrillation or atrial flutte. The most serious adverse effect of ibutilide was non-sustained monomorphic ventricular tachycardia.

ExcerptReferenceRelevance
" Noncardiovascular adverse effects of ibutilide were similar in frequency to those with placebo."( Safety and risk/benefit analysis of ibutilide for acute conversion of atrial fibrillation/flutter.
Kowey, PR; Luderer, JR; VanderLugt, JT, 1996
)
0.84
" Since a no observed adverse effect level (NOAEL) was not found, a second teratology study was performed."( Developmental toxicity of ibutilide fumarate in rats after oral administration.
Marks, TA; Terry, RD, 1996
)
0.59
" Hypotension was the major adverse effect seen with procainamide."( Conversion efficacy and safety of intravenous ibutilide compared with intravenous procainamide in patients with atrial flutter or fibrillation.
Carberry, PA; Dunn, GH; Kowey, PR; Lewis, WR; Perry, KT; Stambler, B; Vanderlugt, JT; Volgman, AS, 1998
)
0.56
"Ibutilide is effective and safe for acute termination of atrial fibrillation or atrial flutter."( Conversion efficacy and safety of repeated doses of ibutilide in patients with atrial flutter and atrial fibrillation. Study Investigators.
Abi-Mansour, P; Carberry, PA; Dunn, GH; Henthorn, RW; McCowan, RJ; Perry, KT, 1998
)
1.99
"Ibutilide is a useful and safe treatment alternative for the atrial arrhythmias that occur after cardiac surgery."( Efficacy and safety of ibutilide fumarate for the conversion of atrial arrhythmias after cardiac surgery.
Ahern, T; Denker, S; Kowey, PR; Mattioni, T; Perry, KT; Torchiana, D; VanderLugt, JT; Wakefield, LK, 1999
)
2.06
" Serious cardiovascular adverse events were documented in six patients; of those patients, five had baseline QTc intervals above 440 msec, two experienced ventricular fibrillation, and four experienced symptomatic bradycardia (range 49-60 beats/minute) requiring medical intervention."( Safety and effectiveness of ibutilide in a community hospital.
Donaldson, AR; Taylor, CT, 2001
)
0.6
" Duration of arrhythmia, left atrial (LA) size, ejection fraction (EF), time to conversion, QTc interval, and adverse drug events were determined."( Ibutilide: efficacy and safety in atrial fibrillation and atrial flutter in a general cardiology practice.
Conti, CR; Eversole, A; Hancock, W; Johns, T; Lopez, LM, 2001
)
1.75
" Complications are rare and without long-term adverse effects."( Ibutilide: efficacy and safety in atrial fibrillation and atrial flutter in a general cardiology practice.
Conti, CR; Eversole, A; Hancock, W; Johns, T; Lopez, LM, 2001
)
1.75
"To test whether the use of ibutilide as a first-choice drug and of amiodarone as a second-line treatment provides a rapid, effective, and safe algorithm for conversion of recent-onset AF or AFl to sinus rhythm (SR), 85 consecutively recruited patients (59 women; mean age 69."( Conversion of recent-onset atrial fibrillation or flutter with amiodarone after ibutilide has failed: a rapid, efficient, and safe algorithm.
Dilaveris, P; Gialafos, E; Giannopoulos, G; Stefanadis, C; Synetos, A, 2005
)
0.85
"The combination of ibutilide as a first-choice drug and of amiodarone infusion in the case of ibutilide failure provides an effective, rapid, and safe algorithm for restoration of SR in patients with AF or AFl of recent onset."( Conversion of recent-onset atrial fibrillation or flutter with amiodarone after ibutilide has failed: a rapid, efficient, and safe algorithm.
Dilaveris, P; Gialafos, E; Giannopoulos, G; Stefanadis, C; Synetos, A, 2005
)
0.88
"The use of IB in patients receiving amiodarone or propafenone for AFL or AF is equally effective and safe as the use of IB alone."( Efficacy and safety of ibutilide for cardioversion of atrial flutter and fibrillation in patients receiving amiodarone or propafenone.
Fragakis, N; Katsaris, G; Kozirakis, M; Maligkos, G; Papadopoulos, N; Papanastasiou, S; Tsaritsaniotis, E, 2005
)
0.64
"5 million adverse drug reaction (ADR) reports for 8620 drugs/biologics that are listed for 1191 Coding Symbols for Thesaurus of Adverse Reaction (COSTAR) terms of adverse effects."( Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
Benz, RD; Contrera, JF; Kruhlak, NL; Matthews, EJ; Weaver, JL, 2004
)
0.32
" It is also safe in the conversion of chronic atrial fibrillation/flutter among patients receiving oral amiodarone therapy."( Safety and efficacy of ibutilide in cardioversion of atrial flutter and fibrillation.
George, LK; Koshy, SK; Nair, M,
)
0.44
" The most serious adverse effect of ibutilide was non-sustained monomorphic ventricular tachycardia (3/49,6."( [Efficacy and safety of ibutilide for conversion of atrial fibrillation/flutter].
Ma, C; Xiang, M; Yang, Y; Yu, Z; Zhang, S, 2013
)
0.97
"Intravenous ibutilide is a safe and effective agent for cardioversion of recent-onset AF/AFL."( [Efficacy and safety of ibutilide for conversion of atrial fibrillation/flutter].
Ma, C; Xiang, M; Yang, Y; Yu, Z; Zhang, S, 2013
)
1.08
"Overall, ibutilide is safe and effective in cancer patients when used for acute cardioversion of AF/AFL."( Efficacy and safety of ibutilide for chemical cardioversion of atrial fibrillation and atrial flutter in cancer patients.
Agarwal, R; Bickford, CL; Durand, JB; Lenihan, DJ; Urbauer, DL, 2014
)
1.13
" We seek to describe patient characteristics, ibutilide administration patterns, cardioversion rates, and adverse outcomes in the community emergency department (ED) setting."( Ibutilide Effectiveness and Safety in the Cardioversion of Atrial Fibrillation and Flutter in the Community Emergency Department.
Ballard, DW; Lugovskaya, N; Nagam, MR; Reed, ME; Rome, AM; Stevenson, MD; Vinson, DR; Warton, EM, 2018
)
2.18
" TdP is a potentially serious adverse event that requires careful monitoring."( Safety and Efficacy of Ibutilide for Acute Pharmacological Cardioversion of Rheumatic Atrial Fibrillation.
Banavalikar, B; Deshpande, S; Nireshwalia, A; Padmanabhan, D; Reddy, SS; Shenthar, J; Valappil, SP,
)
0.44

Pharmacokinetics

ExcerptReferenceRelevance
" As the dose increased, pharmacokinetic differences between the enantiomers were observed."( Pharmacokinetics of ibutilide and its enantiomers in dogs.
Hsu, CY; Walters, RR, 1996
)
0.62
"This study assessed the pharmacokinetic (PK) and pharmacodynamic properties and tolerability of a single intravenous dose of ibutilide fumarate in healthy Chinese men."( Pharmacokinetic and pharmacodynamic properties of a single intravenous dose of ibutilide fumarate: a phase I, randomized, open-label, increasing-dose study in healthy Chinese men.
Hua, L; Huang, Y; Li, Y; Tian, L, 2007
)
0.77
" pharmacokinetic data on 670 drugs representing, to our knowledge, the largest publicly available set of human clinical pharmacokinetic data."( Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
Lombardo, F; Obach, RS; Waters, NJ, 2008
)
0.35
"Multicenter, prospective pharmacokinetic study."( Pharmacokinetics of ibutilide in patients with heart failure due to left ventricular systolic dysfunction.
Amankwa, K; Borzak, S; Coram, R; Flockhart, DA; Kingery, JR; Kovacs, RJ; Overholser, BR; Sowinski, KM; Tisdale, JE; Wroblewski, HA; Zipes, DP, 2008
)
0.67
"92), or half-life (12."( Pharmacokinetics of ibutilide in patients with heart failure due to left ventricular systolic dysfunction.
Amankwa, K; Borzak, S; Coram, R; Flockhart, DA; Kingery, JR; Kovacs, RJ; Overholser, BR; Sowinski, KM; Tisdale, JE; Wroblewski, HA; Zipes, DP, 2008
)
0.67

Compound-Compound Interactions

ExcerptReferenceRelevance
" Class III antiarrhythmic drugs may interact with other drugs by two major processes: pharmacodynamic and pharmacokinetic interactions."( Potentially significant drug interactions of class III antiarrhythmic drugs.
DeBisschop, M; Lower, DL; Martin, LG; Yamreudeewong, W, 2003
)
0.32

Bioavailability

ExcerptReferenceRelevance
"6% oral bioavailability in the rat at a dose of 10 mg/kg, as determined in separate studies."( Developmental toxicity of ibutilide fumarate in rats after oral administration.
Marks, TA; Terry, RD, 1996
)
0.59

Dosage Studied

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of ibutilide are reviewed. Magnesium dosing intensity appeared to be an important determinant of ib utilide efficacy. The 4 grams dose associated with a threefold increase in the odds of successful chemical conversion (AOR; 2.5%)

ExcerptRelevanceReference
" Agents were compared over dosage ranges that produced maximal increases in QTc interval and monophasic action potential duration (MAPD)."( Comparative assessment of ibutilide, D-sotalol, clofilium, E-4031, and UK-68,798 in a rabbit model of proarrhythmia.
Brunden, MN; Buchanan, LV; Gibson, JK; Kabell, G, 1993
)
0.59
" The two ibutilide dosing regimens did not differ in conversion efficacy (44% versus 49%)."( Efficacy and safety of repeated intravenous doses of ibutilide for rapid conversion of atrial flutter or fibrillation. Ibutilide Repeat Dose Study Investigators.
Ellenbogen, KA; Perry, KT; Stambler, BS; VanderLugt, JT; Wakefield, LK; Wood, MA, 1996
)
0.96
" Although statistically significant differences were not detected, scoliosis was also found in the 10 mg/kg/day group (3 fetuses in 2 litters), along with a significant dose-response trend for this malformation."( Developmental toxicity of ibutilide fumarate in rats after oral administration.
Marks, TA; Terry, RD, 1996
)
0.59
"The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of ibutilide are reviewed."( Ibutilide: a new class III antiarrhythmic agent.
Granberry, MC, 1998
)
1.96
" These observations suggest that additional studies are warranted to determine if ibutilide dosing regiments can be optimized."( Atrial electrophysiological effects of ibutilide infusion in humans.
Langberg, JJ; Schwartz, RA, 2000
)
0.8
" There appeared to be a dose-response relationship between Ic dose and its effects on QTc prolongation."( The actions of ibutilide and class Ic drugs on the slow sodium channel: new insights regarding individual pharmacologic effects elucidated through combination therapies.
Blitzer, M; Reiffel, JA, 2000
)
0.66
" Two different propafenone dosage regimens were used according to the duration of the presenting arrhythmia: patients with paroxysmal arrhythmia (n = 48) received 600 mg loading dose, and patients with chronic arrhythmia (n = 56) were receiving 150 mg three times a day as stable-dose pre-treatment."( Ibutilide added to propafenone for the conversion of atrial fibrillation and atrial flutter.
Chiladakis, JA; Kalogeropoulos, A; Manolis, AS; Patsouras, N, 2004
)
1.77
" Multivariate logistic regression analysis was used to determine the impact of magnesium on ibutilide efficacy as well as the impact of magnesium dosing intensity on ibutilide efficacy."( Intravenous magnesium sulfate enhances the ability of intravenous ibutilide to successfully convert atrial fibrillation or flutter.
Coleman, CI; Kluger, J; Tercius, AJ; White, CM, 2007
)
0.8
" Continuous electrocardiographic monitoring was performed, and 12-lead electrocardiograms were recorded before dosing and at defined times from the start of infusion until 24 hours after dosing."( Pharmacokinetic and pharmacodynamic properties of a single intravenous dose of ibutilide fumarate: a phase I, randomized, open-label, increasing-dose study in healthy Chinese men.
Hua, L; Huang, Y; Li, Y; Tian, L, 2007
)
0.57
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Drug Classes (2)

ClassDescription
organic amino compoundA compound formally derived from ammonia by replacing one, two or three hydrogen atoms by organyl groups.
benzenesAny benzenoid aromatic compound consisting of the benzene skeleton and its substituted derivatives.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Pathways (1)

PathwayProteinsCompounds
Ibutilide Action Pathway478

Protein Targets (5)

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Voltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)IC50 (µMol)62.50000.00032.63119.0000AID1207745
Voltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)IC50 (µMol)62.50000.00032.59559.0000AID1207745
Potassium voltage-gated channel subfamily H member 2Homo sapiens (human)IC50 (µMol)0.01300.00091.901410.0000AID161281; AID240820; AID243151; AID408340; AID576612
Voltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)IC50 (µMol)62.50000.00032.63119.0000AID1207745
Voltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)IC50 (µMol)62.50000.00032.25459.6000AID1207745
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (62)

Processvia Protein(s)Taxonomy
visual perceptionVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
detection of light stimulus involved in visual perceptionVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
calcium ion import across plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
calcium ion transportVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
adenylate cyclase-modulating G protein-coupled receptor signaling pathwayVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
sensory perception of soundVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
positive regulation of adenylate cyclase activityVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
positive regulation of calcium ion transportVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
regulation of atrial cardiac muscle cell membrane repolarizationVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
calcium ion importVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
calcium ion transmembrane transportVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
cardiac muscle cell action potential involved in contractionVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
membrane depolarization during cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
membrane depolarization during SA node cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
regulation of heart rate by cardiac conductionVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
regulation of potassium ion transmembrane transporter activityVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
regulation of potassium ion transmembrane transportVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
calcium ion import across plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
regulation of heart rate by cardiac conductionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of heart rate by hormonePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of membrane potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
positive regulation of DNA-templated transcriptionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion homeostasisPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
cardiac muscle contractionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of membrane repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of ventricular cardiac muscle cell membrane repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
cellular response to xenobiotic stimulusPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
ventricular cardiac muscle cell action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane depolarization during action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarization during action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarization during cardiac muscle cell action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of heart rate by cardiac conductionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion export across plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarization during ventricular cardiac muscle cell action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
negative regulation of potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
positive regulation of potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
negative regulation of potassium ion export across plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion import across plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
skeletal system developmentVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
extraocular skeletal muscle developmentVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
calcium ion transportVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
muscle contractionVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
striated muscle contractionVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
endoplasmic reticulum organizationVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
myoblast fusionVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
neuromuscular junction developmentVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
skeletal muscle adaptationVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
positive regulation of muscle contractionVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
skeletal muscle fiber developmentVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
release of sequestered calcium ion into cytosolVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
calcium ion transmembrane transportVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
cellular response to caffeineVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
calcium ion import across plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
immune system developmentVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
positive regulation of cytosolic calcium ion concentrationVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
heart developmentVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
regulation of cardiac muscle contraction by regulation of the release of sequestered calcium ionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
embryonic forelimb morphogenesisVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
camera-type eye developmentVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
positive regulation of adenylate cyclase activityVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
positive regulation of muscle contractionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
calcium ion transport into cytosolVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
cardiac conductionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
calcium ion transmembrane transport via high voltage-gated calcium channelVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
calcium ion transmembrane transportVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
cardiac muscle cell action potential involved in contractionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
membrane depolarization during cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
membrane depolarization during AV node cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
cell communication by electrical coupling involved in cardiac conductionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
regulation of heart rate by cardiac conductionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
regulation of ventricular cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
membrane depolarization during atrial cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
calcium ion import across plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (24)

Processvia Protein(s)Taxonomy
voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
metal ion bindingVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
high voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
high voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
protein bindingVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
ankyrin bindingVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
metal ion bindingVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
alpha-actinin bindingVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
voltage-gated calcium channel activity involved in cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
voltage-gated calcium channel activity involved SA node cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
transcription cis-regulatory region bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
inward rectifier potassium channel activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
delayed rectifier potassium channel activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
protein bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
ubiquitin protein ligase bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
identical protein bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
protein homodimerization activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
C3HC4-type RING finger domain bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel activity involved in cardiac muscle cell action potential repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
scaffold protein bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
protein bindingVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
calmodulin bindingVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
high voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
small molecule bindingVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
metal ion bindingVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
molecular function activator activityVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
high voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated calcium channel activity involved in cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
protein bindingVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
calmodulin bindingVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
high voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
metal ion bindingVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
alpha-actinin bindingVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated calcium channel activity involved in cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated calcium channel activity involved in AV node cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (18)

Processvia Protein(s)Taxonomy
photoreceptor outer segmentVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
membraneVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
perikaryonVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1FHomo sapiens (human)
plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
Z discVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
L-type voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1D Homo sapiens (human)
plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
cell surfacePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
perinuclear region of cytoplasmPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel complexPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
inward rectifier potassium channel complexPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
cytoplasmVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
sarcoplasmic reticulumVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
T-tubuleVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
I bandVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
L-type voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1SHomo sapiens (human)
cytoplasmVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
postsynaptic densityVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
membraneVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
Z discVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
dendriteVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
perikaryonVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
postsynaptic density membraneVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
L-type voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (87)

Assay IDTitleYearJournalArticle
AID62777Conduction time from Q wave to T wave of lead II electrocardiogram corrected for heart rate was tested in dogs at a dose of 0.3 mg/kg through intravenous administration. (baseline value- 352+/-7)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID62668Conduction time for ventricular refractory period of the second premature stimulus was tested in dogs at a dose of 1.0 mg/kg through intravenous administration. (baseline value- 123+/-4)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID101861Metabolic stability in relative to 31E observed on incubation with human liver microsomes; not evaluated2001Journal of medicinal chemistry, Mar-29, Volume: 44, Issue:7
Progress toward the development of a safe and effective agent for treating reentrant cardiac arrhythmias: synthesis and evaluation of ibutilide analogues with enhanced metabolic stability and diminished proarrhythmic potential.
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID425652Total body clearance in human2009Journal of medicinal chemistry, Aug-13, Volume: 52, Issue:15
Physicochemical determinants of human renal clearance.
AID1220558Fraction unbound in Beagle dog brain homogenates at 1 uM after 6 hrs by equilibrium dialysis method2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Species independence in brain tissue binding using brain homogenates.
AID62395Compound was tested in vivo in dogs at a dose of 0.1 mg/kg through intravenous route and time at which nonsustained ventricular arrhythmias were induced was recorded.(Base line value-1)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID167090Mean dose at which EADs (early after depolarizations) began to develop in rabbits2001Journal of medicinal chemistry, Mar-29, Volume: 44, Issue:7
Progress toward the development of a safe and effective agent for treating reentrant cardiac arrhythmias: synthesis and evaluation of ibutilide analogues with enhanced metabolic stability and diminished proarrhythmic potential.
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID62513Compound was tested in vivo in dogs at a dose of 0.3 mg/kg through intravenous route and time at which nonsustained ventricular arrhythmias were induced was recorded.(Base line value-1)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID1220560Fraction unbound in human occipital cortex at 1 uM after 6 hrs by equilibrium dialysis method2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Species independence in brain tissue binding using brain homogenates.
AID167091Mean dose at which PVTs (Polymorphic ventricular tachyarrhythmias) were observed in rabbits2001Journal of medicinal chemistry, Mar-29, Volume: 44, Issue:7
Progress toward the development of a safe and effective agent for treating reentrant cardiac arrhythmias: synthesis and evaluation of ibutilide analogues with enhanced metabolic stability and diminished proarrhythmic potential.
AID1220556Fraction unbound in CD-1 mouse brain homogenates at 1 uM after 6 hrs by equilibrium dialysis method2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Species independence in brain tissue binding using brain homogenates.
AID588216FDA HLAED, serum glutamic oxaloacetic transaminase (SGOT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID62510Compound was tested in vivo in dogs at a dose of 0.1 mg/kg through intravenous route and time at which ventricular fibrillation was induced was recorded.(Base line value-6)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID167477Tested for effective refractory period measured at a pacing rate of 1 Hz in vitro with rabbit heart tissue preparations.1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID166938Mean dose of test compound at which a statistically significant increase was first observed and the dose for the maximum increase in MAPD90 in rabbits (0.5-1.0)2001Journal of medicinal chemistry, Mar-29, Volume: 44, Issue:7
Progress toward the development of a safe and effective agent for treating reentrant cardiac arrhythmias: synthesis and evaluation of ibutilide analogues with enhanced metabolic stability and diminished proarrhythmic potential.
AID540213Half life in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID588217FDA HLAED, serum glutamic pyruvic transaminase (SGPT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID540211Fraction unbound in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID62666Conduction time for ventricular refractory period of the second premature stimulus was tested in dogs at a dose of 0.3 mg/kg through intravenous administration. (baseline value- 123+/-4)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID588215FDA HLAED, alkaline phosphatase increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID167478Tested for effective refractory period measured at a pacing rate of 3 Hz in vitro with rabbit heart tissue preparations.1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID588218FDA HLAED, lactate dehydrogenase (LDH) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID588214FDA HLAED, liver enzyme composite activity2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID62661Conduction time for ventricular refractory period of the first premature stimulus was tested in dogs at a dose of 1.0 mg/kg through intravenous administration. (baseline value- 137+/-4)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID62532Compound was tested in vivo in dogs at a dose of 1.0 mg/kg through intravenous route and time at which ventricular arrhythmias were not indicible was recorded.(Base line value-1)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID167695In vivo evaluation of potential efficacy observed as the maximum increase in QTc interval from the methoxamine infusion baseline in rabbits2001Journal of medicinal chemistry, Mar-29, Volume: 44, Issue:7
Progress toward the development of a safe and effective agent for treating reentrant cardiac arrhythmias: synthesis and evaluation of ibutilide analogues with enhanced metabolic stability and diminished proarrhythmic potential.
AID540212Mean residence time in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1220555Fraction unbound in Sprague-Dawley rat brain homogenates at 1 uM after 6 hrs by equilibrium dialysis method2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Species independence in brain tissue binding using brain homogenates.
AID240820Inhibitory concentration against IKr potassium channel2004Bioorganic & medicinal chemistry letters, Sep-20, Volume: 14, Issue:18
The pharmacophore hypotheses of I(Kr) potassium channel blockers: novel class III antiarrhythmic agents.
AID62785Conduction time from the His bundle to the onset of ventricular depolarizations was tested in dogs at a dose of 0.1 mg/kg through intravenous administration. (baseline value- 17+/-1 )1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID62792Conduction time from the atrium to His bundle was tested in dogs at a dose of 0.1 mg/kg through intravenous administration. (baseline value- 73+/-3 )1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID62796Conduction time from the atrium to His bundle was tested in dogs at a dose of 1.0 mg/kg through intravenous administration. (baseline value- 73+/-3 )1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID62787Conduction time from the His bundle to the onset of ventricular depolarizations was tested in dogs at a dose of 0.3 mg/kg through intravenous administration. (baseline value- 17+/-1 )1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID62659Conduction time for ventricular refractory period of the first premature stimulus was tested in dogs at a dose of 0.3 mg/kg through intravenous administration. (baseline value- 137+/-4)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID165521Tested for conduction time measured at a pacing rate of 1 Hz in vitro with rabbit heart tissue preparations.1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID62789Conduction time from the His bundle to the onset of ventricular depolarizations was tested in dogs at a dose of 1.0 mg/kg through intravenous administration. (baseline value- 17+/-1 )1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID588219FDA HLAED, gamma-glutamyl transferase (GGT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID1220559Fraction unbound in cynomolgus monkey brain homogenates at 1 uM after 6 hrs by equilibrium dialysis method2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Species independence in brain tissue binding using brain homogenates.
AID425653Renal clearance in human2009Journal of medicinal chemistry, Aug-13, Volume: 52, Issue:15
Physicochemical determinants of human renal clearance.
AID540210Clearance in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID540209Volume of distribution at steady state in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID62794Conduction time from the atrium to His bundle was tested in dogs at a dose of 0.3 mg/kg through intravenous administration. (baseline value- 73+/-3 )1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID1207745Inhibition of Cav1.2 current measured using QPatch automatic path clamp system in CHO cells expressing Cav1.2, beta-2 and alpha-2/delta-1 subunits2013Scientific reports, , Volume: 3MICE models: superior to the HERG model in predicting Torsade de Pointes.
AID167844Ratio of the number of rabbits that developed early after depolarization to the total number of rabbits evaluated.(4/4)2001Journal of medicinal chemistry, Mar-29, Volume: 44, Issue:7
Progress toward the development of a safe and effective agent for treating reentrant cardiac arrhythmias: synthesis and evaluation of ibutilide analogues with enhanced metabolic stability and diminished proarrhythmic potential.
AID167699Tested for rate automaticity measured in beats per minute from unpaced right atria of rabbit heart.1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID62523Compound was tested in vivo in dogs at a dose of 0.3 mg/kg through intravenous route and time at which ventricular fibrillation was induced was recorded.(Base line value-6)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID62527Compound was tested in vivo in dogs at a dose of 1.0 mg/kg through intravenous route and time at which nonsustained ventricular arrhythmias were induced was recorded.(Base line value-1)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID62671Conduction time from Q wave to T wave of lead II electrocardiogram corrected for heart rate was tested in dogs at a dose of 0.1 mg/kg through intravenous administration. (baseline value- 352+/-7)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID161281Inhibition of human Potassium channel HERG expressed in mammalian cells2003Bioorganic & medicinal chemistry letters, Aug-18, Volume: 13, Issue:16
Prediction of hERG potassium channel affinity by traditional and hologram qSAR methods.
AID62642Compound was tested in vivo in dogs at a dose of 1.0 mg/kg through intravenous route and time at which ventricular fibrillation was induced was recorded.(Base line value-6)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID167855Ratio of the number of rabbits that developed polymorphic ventricular tachycardia to the total number of rabbits evaluated. (2/16)2001Journal of medicinal chemistry, Mar-29, Volume: 44, Issue:7
Progress toward the development of a safe and effective agent for treating reentrant cardiac arrhythmias: synthesis and evaluation of ibutilide analogues with enhanced metabolic stability and diminished proarrhythmic potential.
AID62517Compound was tested in vivo in dogs at a dose of 0.3 mg/kg through intravenous route and time at which sustained ventricular arrhythmias were induced was recorded.(Base line value-3)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1220554Fraction unbound in Wistar Han rat brain homogenates at 1 uM after 6 hrs by equilibrium dialysis method2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Species independence in brain tissue binding using brain homogenates.
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID576612Inhibition of human ERG2011European journal of medicinal chemistry, Feb, Volume: 46, Issue:2
Predicting hERG activities of compounds from their 3D structures: development and evaluation of a global descriptors based QSAR model.
AID62504Compound was tested in vivo in dogs at a dose of 0.1 mg/kg through intravenous route and time at which sustained ventricular arrhythmias were induced was recorded.(Base line value-3)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID1220557Fraction unbound in Hartley guinea pig brain homogenates at 1 uM after 6 hrs by equilibrium dialysis method2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Species independence in brain tissue binding using brain homogenates.
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID62778Conduction time from Q wave to T wave of lead II electrocardiogram corrected for heart rate was tested in dogs at a dose of 1.0 mg/kg through intravenous administration. (baseline value- 352+/-7)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID62664Conduction time for ventricular refractory period of the second premature stimulus was tested in dogs at a dose of 0.1 mg/kg through intravenous administration. (baseline value- 123+/-4)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID62506Compound was tested in vivo in dogs at a dose of 0.1 mg/kg through intravenous route and time at which ventricular arrhythmias were not indicible was recorded.(Base line value-1)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID166983Maximum increase in the ventricular monophasic action potential duration at 90% repolarization from the methoxamine infusion baseline in rabbits2001Journal of medicinal chemistry, Mar-29, Volume: 44, Issue:7
Progress toward the development of a safe and effective agent for treating reentrant cardiac arrhythmias: synthesis and evaluation of ibutilide analogues with enhanced metabolic stability and diminished proarrhythmic potential.
AID167087Mean dose of test compound at which a statistically significant increase was first observed and the dose for the maximum increase in QTc interval in rabbits (0.25-5.0)2001Journal of medicinal chemistry, Mar-29, Volume: 44, Issue:7
Progress toward the development of a safe and effective agent for treating reentrant cardiac arrhythmias: synthesis and evaluation of ibutilide analogues with enhanced metabolic stability and diminished proarrhythmic potential.
AID62657Conduction time for ventricular refractory period of the first premature stimulus was tested in dogs at a dose of 0.1 mg/kg through intravenous administration. (baseline value- 137+/-4)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID165640Tested for conduction time measured at a pacing rate of 3 Hz in vitro with rabbit heart tissue preparations.1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID167622Tested for force of contraction measured in mg at a pacing rate of 2 Hz in vitro with rabbit heart tissue preparations.1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID62519Compound was tested in vivo in dogs at a dose of 0.3 mg/kg through intravenous route and time at which ventricular arrhythmias were not indicible was recorded.(Base line value-1)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID408340Inhibition of human ERG expressed in CHO cells by whole cell patch clamp technique2008Bioorganic & medicinal chemistry, Jun-01, Volume: 16, Issue:11
Support vector machines classification of hERG liabilities based on atom types.
AID62531Compound was tested in vivo in dogs at a dose of 1.0 mg/kg through intravenous route and time at which sustained ventricular arrhythmias were induced was recorded.(Base line value-3)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity.
AID243151Inhibitory concentration against potassium channel HERG2005Bioorganic & medicinal chemistry letters, Jun-02, Volume: 15, Issue:11
A discriminant model constructed by the support vector machine method for HERG potassium channel inhibitors.
AID1347411qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1346751Human Kv11.1 (Voltage-gated potassium channels)2003Bioorganic & medicinal chemistry letters, Aug-18, Volume: 13, Issue:16
Prediction of hERG potassium channel affinity by traditional and hologram qSAR methods.
AID1346751Human Kv11.1 (Voltage-gated potassium channels)2004Molecular pharmacology, Aug, Volume: 66, Issue:2
Structural determinants of HERG channel block by clofilium and ibutilide.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (260)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's70 (26.92)18.2507
2000's140 (53.85)29.6817
2010's43 (16.54)24.3611
2020's7 (2.69)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 57.55

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index57.55 (24.57)
Research Supply Index5.83 (2.92)
Research Growth Index4.43 (4.65)
Search Engine Demand Index94.99 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (57.55)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials58 (20.71%)5.53%
Reviews50 (17.86%)6.00%
Case Studies23 (8.21%)4.05%
Observational1 (0.36%)0.25%
Other148 (52.86%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (8)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Panoramic ECGi to Guide Ablation of Non-Paroxysmal AF: Effect of Ibutilide on AF Source Location and Organization [NCT03370536]1 participants (Actual)Interventional2017-11-01Terminated(stopped due to 1 patient enrolled (consented) but screen failed. Study stopped as unable to enroll.)
Novel Approaches for Minimizing Drug-Induced QT Interval Lengthening [NCT04675788]Phase 483 participants (Anticipated)Interventional2021-09-02Recruiting
Atrial Fibrillation Mechanism Analysis Through Ibutilide Administration During Pulmonary Vein Ablation. [NCT00589992]50 participants (Anticipated)Interventional2007-10-31Recruiting
Modified Stepwise Ablation Guided by Low Dose Ibutilide in Chronic Atrial Fibrillation [NCT01014741]200 participants (Actual)Interventional2009-10-31Completed
Influence of Testosterone Administration on Drug-Induced QT Interval Prolongation and Torsades de Pointes [NCT02513940]Phase 414 participants (Actual)Interventional2016-05-31Completed
Vernakalant Versus Ibutilide In Recent-Onset Atrial Fibrillation [NCT01447862]Phase 4101 participants (Actual)Interventional2011-10-31Completed
Novel Approaches for Minimizing Drug-Induced QT Interval Lengthening: Reducing the Risk of Drug-Induced QT Interval Lengthening in Women [NCT03834883]Phase 440 participants (Anticipated)Interventional2019-03-26Recruiting
Influence of Progesterone Administration on Drug-Induced QT Interval Prolongation and Torsades de Pointes [NCT01929083]Phase 219 participants (Actual)Interventional2013-04-30Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT01014741 (4) [back to overview]Procedure Time
NCT01014741 (4) [back to overview]Radiofrequency Ablation Time
NCT01014741 (4) [back to overview]AF Termination
NCT01014741 (4) [back to overview]Number of Participants With 1 Year Freedom From AF / AT
NCT01929083 (10) [back to overview]Area Under the QTcI - Time Curve (AUEC)
NCT01929083 (10) [back to overview]Baseline (Pre-Ibutilide) QTcI Intervals
NCT01929083 (10) [back to overview]Maximum (Peak) Serum Ibutilide Concentrations During Progesterone and Placebo Phases
NCT01929083 (10) [back to overview]Maximum % Change From Baseline in QTcI Intervals Following Ibutilide Administration
NCT01929083 (10) [back to overview]Maximum Individual-corrected QT Interval (QTcI)
NCT01929083 (10) [back to overview]Ratio of Serum Progesterone:Estradiol Concentrations During the Progesterone and Placebo Phases
NCT01929083 (10) [back to overview]Serum Estradiol Concentrations During the Progesterone and Placebo Phases
NCT01929083 (10) [back to overview]Serum Progesterone Concentrations During Progesterone and Placebo Phases
NCT01929083 (10) [back to overview]Adverse Effects Associated With Ibutilide in the Progesterone and Placebo Phases
NCT01929083 (10) [back to overview]Incidence of Progesterone-associated Adverse Effects Compared to Placebo
NCT02513940 (5) [back to overview]Area Under the QTF Versus Time Curve for 0-1 Hour Following Ibutilide 0.003 mg/kg
NCT02513940 (5) [back to overview]Baseline (Pre-ibutilide) Individualized Rate-corrected QT Interval (QTF)
NCT02513940 (5) [back to overview]Maximum Percent Change From Pretreatment Value in QTF Following Ibutilide 0.003 mg/kg
NCT02513940 (5) [back to overview]Maximum QTF Following Ibutilide 0.003 mg/kg
NCT02513940 (5) [back to overview]Number of Participants With Adverse Effects Associated With Testosterone, Progesterone and Placebo

Procedure Time

Overall procedure duration (NCT01014741)
Timeframe: at time of the procedure

Interventionminutes (Mean)
Ibutilide Arm316
Placebo Arm321

[back to top]

Radiofrequency Ablation Time

(NCT01014741)
Timeframe: at time of the procedure

Interventionminutes (Mean)
Ibutilide Arm99
Placebo Arm104

[back to top]

AF Termination

AF termination with complex fractionated atrial electrograms (CFAE) ablation (NCT01014741)
Timeframe: at time of the procedure

,
Interventionparticipants (Number)
yesno
Ibutilide Arm6639
Placebo Arm5243

[back to top]

Number of Participants With 1 Year Freedom From AF / AT

Freedom from atrial arrhythmia after repeat procedures with or without drugs (NCT01014741)
Timeframe: one year

,
Interventionparticipants (Number)
yesno
Ibutilide Arm6527
Placebo Arm6231

[back to top]

Area Under the QTcI - Time Curve (AUEC)

(NCT01929083)
Timeframe: From beginning of 10-minute ibutilide infusion to 1 hour following ibutilide infusion

Interventionms*hr (Mean)
Progesterone497
Placebo510

[back to top]

Baseline (Pre-Ibutilide) QTcI Intervals

(NCT01929083)
Timeframe: After 7 days of progesterone or placebo, prior to receiving IV ibutilide

Interventionms (Mean)
Progesterone412
Placebo419

[back to top]

Maximum (Peak) Serum Ibutilide Concentrations During Progesterone and Placebo Phases

(NCT01929083)
Timeframe: Within 1 hour following ibutilide administration (0, 15 & 30 minutes and 1 hours.)

Interventionpg/mL (Mean)
Progesterone1247
Placebo1172

[back to top]

Maximum % Change From Baseline in QTcI Intervals Following Ibutilide Administration

(NCT01929083)
Timeframe: After 7 days of progesterone or placebo

Interventionpercentage change from baseline value (Mean)
Progesterone7.5
Placebo9.3

[back to top]

Maximum Individual-corrected QT Interval (QTcI)

QT intervals will be corrected as follows: Prior to randomization, subjects will come to the Indiana Clinical Research Center for a 12-hour stay, during which three ECGs, one minute apart, will be obtained at the following times: 0, 15 & 30 minutes, and 1, 2, 4, 6, 8, and 12 hours. Subjects will be discharged, and then return then next morning for the 24 hour ECG. QT and RR intervals will be used to determine each subject's individual rate-corrected QT interval (QTcI) using the parabolic model QT = β•RRα, where RR is the interval between adjacent QRS complexes, and α and β are subject-specific correction factors. (NCT01929083)
Timeframe: 0, 15 & 30 minutes, and 1, 2, 4, 6, 8, and 12 hours post-ibutilide administration

Interventionms (Mean)
Progesterone443
Placebo458

[back to top]

Ratio of Serum Progesterone:Estradiol Concentrations During the Progesterone and Placebo Phases

(NCT01929083)
Timeframe: After 7 days of progesterone or placebo

InterventionRatio (Mean)
Progesterone205
Placebo18

[back to top]

Serum Estradiol Concentrations During the Progesterone and Placebo Phases

(NCT01929083)
Timeframe: Following 7 days of progesterone or placebo

Interventionpg/mL (Mean)
Progesterone89.3
Placebo71.8

[back to top]

Serum Progesterone Concentrations During Progesterone and Placebo Phases

(NCT01929083)
Timeframe: After 7 days of progesterone or placebo

Interventionng/mL (Mean)
Progesterone16.2
Placebo1.2

[back to top]

Adverse Effects Associated With Ibutilide in the Progesterone and Placebo Phases

(NCT01929083)
Timeframe: Within 8 hours following ibutilide administration

,
Interventionpercentage of participants (Number)
Bradycardia (HR < 60 bpm)Burning at infusion siteTransient QTc interval > 500 ms
Placebo1266
Progesterone2070

[back to top]

Incidence of Progesterone-associated Adverse Effects Compared to Placebo

(NCT01929083)
Timeframe: During 7 days of treatment with oral progesterone or placebo

,
Interventionpercentage of participants (Number)
Fatigue/general malaiseHeadacheMood changesBreast tendernessHypotensionVertigo requiring discontinuation
Placebo660000
Progesterone3813131366

[back to top]

Area Under the QTF Versus Time Curve for 0-1 Hour Following Ibutilide 0.003 mg/kg

"Prolonged QT interval is a marker of increased risk of the ventricular arrhythmia known as torsades de pointes, which can cause sudden cardiac death. Three 12-lead ECGs were obtained ~ 1 minute apart immediately at the end of the ibutilide infusion and at 5, 10, 15, 20, 30, and 45 minutes and 1, 2, 4, 6, and 8 hours post-infusion. QT intervals were measured from ECG lead II by one investigator (E.T.M.) who was blinded to the subjects' assigned treatment phases. QT intervals were measured using computerized high-resolution electronic calipers. QT and RR intervals at each time point were averaged over 3 consecutive complexes. The end of the T-wave was determined via the tangent method. Area under the QTF curve was calculated using the trapezoidal rule and reflects overall QTF interval exposure over time." (NCT02513940)
Timeframe: 1 hour following ibutilide administration

Interventionms·hr (Mean)
Testosterone471
Progesterone480
Placebo483

[back to top]

Baseline (Pre-ibutilide) Individualized Rate-corrected QT Interval (QTF)

QT interval is an electrocardiogram (ECG) measure of ventricular repolarization. Prolonged QT interval is a marker of increased risk of the ventricular arrhythmia known as torsades de pointes, which can cause sudden cardiac death. QT intervals were measured from ECG lead II by one investigator (E.T.M.) who was blinded to the subjects' assigned treatment phases. QT intervals were measured using computerized high-resolution electronic calipers (EP Calipers 1.6). QT and RR intervals at each time point were averaged over 3 consecutive complexes. The end of the T-wave was determined via the tangent method. Only clearly discernable QT intervals were measured. QT intervals vary with heart rate, and therefore must be corrected for heart rate. QT intervals were corrected using the Fridericia (QTF) method. The baseline QTF assesses the influence of testosterone and progesterone on naturally-occurring (before ibutilide administration) QTF (NCT02513940)
Timeframe: Following 7 days of testosterone, progesterone or placebo

Interventionms (Mean)
Testosterone393
Progesterone399
Placebo399

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Maximum Percent Change From Pretreatment Value in QTF Following Ibutilide 0.003 mg/kg

QT interval is an ECG measure of ventricular repolarization. Prolonged QT interval is a marker of increased risk of the ventricular arrhythmia known as torsades de pointes, which can cause sudden cardiac death. Three 12-lead ECGs were obtained ~ 1 minute apart immediately at the end of the ibutilide infusion and at 5, 10, 15, 20, 30, and 45 minutes and 1, 2, 4, 6, and 8 hours post-infusion. QT intervals were measured from ECG lead II by one investigator (E.T.M.) who was blinded to the subjects' assigned treatment phases. QT intervals were measured using computerized high-resolution electronic calipers. QT and RR intervals at each time point were averaged over 3 consecutive complexes. The end of the T-wave was determined via the tangent method. QT intervals were corrected using the Fridericia (QTF) method. (NCT02513940)
Timeframe: Within 8 hours of ibutilide administration

InterventionPercent change (Mean)
Testosterone5.6
Progesterone5.9
Placebo6.1

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Maximum QTF Following Ibutilide 0.003 mg/kg

QT interval is an ECG measure of ventricular repolarization. Prolonged QT interval is a marker of increased risk of the ventricular arrhythmia known as torsades de pointes, which can cause sudden cardiac death. Three 12-lead ECGs were obtained ~ 1 minute apart immediately at the end of the ibutilide infusion and at 5, 10, 15, 20, 30, and 45 minutes and 1, 2, 4, 6, and 8 hours post-infusion. QT intervals were measured from ECG lead II by one investigator (E.T.M.) who was blinded to the subjects' assigned treatment phases. QT intervals were measured using computerized high-resolution electronic calipers. QT and RR intervals at each time point were averaged over 3 consecutive complexes. The end of the T-wave was determined via the tangent method. QT intervals vary with heart rate, and therefore must be corrected for heart rate. QT intervals were corrected using the Fridericia (QTF) method. Maximum QTF is the longest QTF measured following ibutilide at any time point. (NCT02513940)
Timeframe: Within 8 hours following ibutilide administration

Interventionms (Mean)
Testosterone416
Progesterone425
Placebo426

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Number of Participants With Adverse Effects Associated With Testosterone, Progesterone and Placebo

Adverse effects were assessed by study investigators using telephone calls during the 7-day treatment period in each phase, as well as by asking participants about adverse effects on ibutilide administration days (NCT02513940)
Timeframe: During 7 day administration periods

,,
InterventionParticipants (Count of Participants)
FatigueRash on gel application site
Placebo01
Progesterone10
Testosterone00

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