Page last updated: 2024-11-04

zonisamide

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Description

Zonisamide: A benzisoxazole and sulfonamide derivative that acts as a CALCIUM CHANNEL blocker. It is used primarily as an adjunctive antiepileptic agent for the treatment of PARTIAL SEIZURES, with or without secondary generalization. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

zonisamide : A 1,2-benzoxazole compound having a sulfamoylmethyl substituent at the 3-position. [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]

Cross-References

ID SourceID
PubMed CID5734
CHEMBL ID750
CHEBI ID10127
SCHEMBL ID35458
MeSH IDM0077929

Synonyms (126)

Synonym
BIDD:GT0708
AC-1413
BIDD:PXR0183
HMS3269F21
AB00876297-10
BRD-K48300629-001-03-8
tremode
e-2090 ,
excegran
ad-810n
trerief
ad-810
pd 110843
1,2-benzisoxazole-3-methanesulfonamide
hsdb 7293
zonegran
zonisamida [spanish]
3-(sulfamoylmethyl)-1,2-benzisoxazole
zonisamidum [latin]
brn 1077076
excegram
ci-912
ci 912
ad 810
c8h8n2o3s
exceglan
C07504
68291-97-4
zonisamide
DB00909
spr_2
benzo[d]isoxazol-3-yl-methanesulfonamide
bdbm10888
zonisamide, 1
zonisamide (zns)
NCGC00159319-02
zonisamide, zns
1,2-benzoxazol-3-ylmethanesulfonamide
chembl750 ,
excegran (tn)
zonisamide (jp17/usp/inn)
D00538
MLS001306491
NCGC00159319-03
smr000596519
MLS001195632
HMS2089O07
zonisade
n03ax15
pd-110843
1-(1,2-benzisoxazol-3-yl)methanesulfonamide
CHEBI:10127 ,
zonisamida
zonisamidum
1-(1,2-benzoxazol-3-yl)methanesulfonamide
AKOS001312269
A836085
HMS3259N09
STK711131
(1,2-benzoxazol-3-yl)methanesulfonamide
EN300-50288
459384h98v ,
unii-459384h98v
zonisamide [usan:usp:inn:ban:jan]
cas-68291-97-4
tox21_111569
dtxcid7026023
dtxsid9046023 ,
BBL010040
HMS2235L13
FT-0675931
FT-0601524
benzo[d]isoxazol-3-ylmethanesulfonamide
S1445
gtpl7047
zonisamide [jan]
zonisamide [hsdb]
zonisamide [orange book]
zonisamide [usp-rs]
zonisamide [ema epar]
zonisamide [vandf]
zonisamide [usp monograph]
zonisamide [who-dd]
zonisamide [usan]
zonisamide [mi]
zonisamide [mart.]
zonisamide [inn]
CCG-220669
CS-1888
HY-B0124
NC00637
SCHEMBL35458
NCGC00159319-04
tox21_111569_1
KS-1142
AB00876297-09
1,2-benzisoxazol-3-ylmethanesulfonamide
Q-201948
HB0675
Z0026
AB00876297_11
zonisamide pound>>ci-912 pound>>pd 110843
SR-01000837537-3
SR-01000837537-2
SR-01000837537-8
sr-01000837537
HMS3657E03
C76163
zonisamide 1.0 mg/ml in methanol
HMS3714E19
Z223042524
SW199135-2
HMS3677L09
mfcd00865316
Q219957
BCP28480
HMS3413L09
HMS3884I17
HMS3742M15
BZ164593
zonisamide (mart.)
zonisamidum (latin)
zonisamide (usp-rs)
benzo(d)isoxazol-3-yl-methanesulfonamide
zonisamide (usan:usp:inn:ban:jan)
zonisamide (usp monograph)

Research Excerpts

Overview

Zonisamide (ZNS) is an anticonvulsant which is used to treat the symptoms of epilepsy. Zonisamide is a new anti-epileptic drug whose mechanism of action is associated with neurotransmission systems also involved in the pathogenesis of addiction.

ExcerptReferenceRelevance
"Zonisamide (ZNS) is a new generation antiepileptic drug (AED) used in refractory epilepsy. "( Effectiveness of zonisamide in childhood refractory epilepsy.
Aslan, M; Gungor, S, 2022
)
2.5
"Zonisamide appears to be a new treatment option for patients with PD and DLB."( Zonisamide's Efficacy and Safety on Parkinson's Disease and Dementia with Lewy Bodies: A Meta-Analysis and Systematic Review.
Jiang, Z; Kong, L; Liu, H; Wang, Z; Xi, J; Yu, X, 2022
)
2.89
"Zonisamide (ZNS) is an anticonvulsant which is used to treat the symptoms of epilepsy. "( Reproductive toxic effects and possible mechanisms of zonisamide in male rats.
Atli-Eklioglu, O; Aydogan-Kılıc, G; Baysal, M; Ilgin, S; Karaduman, AB; Kilic, V; Ucarcan, S, 2019
)
2.21
"Zonisamide is an antiepileptic drug developed in Japan, where its therapeutic effects on PD were also discovered and developed."( [Parkinson's Disease: amantadine, zonisamide, dabrafenib].
Okamoto, T, 2019
)
1.51
"Zonisamide is an antiepileptic drug with a perspective of a broader use. "( The effect of zonisamide on memory processes - A preclinical study.
Krupa-Burtnik, A; Pietrzak, B; Zwierzyńska, E, 2020
)
2.36
"Zonisamide is a nondopaminergic antiparkinsonian drug that can improve "wearing-off" although response to the treatment varies between individuals."( Genome-wide association study identifies zonisamide responsive gene in Parkinson's disease patients.
Ando-Kanagawa, Y; Cha, PC; Murata, M; Satake, W; Toda, T; Yamamoto, K, 2020
)
1.55
"Zonisamide is an anti-epileptic medication with multiple mechanisms of action and a favorable safety profile. "( The Application of Zonisamide to Patients Suffering from Dementia with Lewy Bodies: Emerging Clinical Data.
Leverenz, JB; Tousi, B, 2021
)
2.39
"Zonisamide is a new anti-epileptic drug whose mechanism of action is associated with neurotransmission systems also involved in the pathogenesis of addiction. "( The Impact of Zonisamide on the Development and Course of Alcohol Dependence in Rabbits. A pharmaco-EEG study.
Kordala, A; Krupa-Burtnik, A; Pietrzak, B; Zwierzynska, E, 2017
)
2.26
"Zonisamide (ZNS) is an effective drug for not only motor symptoms but also non-motor symptoms in Parkinson's disease. "( Zonisamide inhibits monoamine oxidase and enhances motor performance and social activity.
Asano, T; Hikawa, R; Takahashi, R; Uemura, MT; Yamakado, H, 2017
)
3.34
"Zonisamide is a new-generation anticonvulsant antiepileptic drug metabolized primarily in the liver, with subsequent elimination via the renal route."( Pharmacometabolomics applied to zonisamide pharmacokinetic parameter prediction.
Borobia, AM; Carcás Sansuan, AJ; Dapía, I; Díaz, L; Frías, J; García Bartolomé, A; García, I; Guerra, P; Martínez-Ávila, JC; Tong, HY, 2018
)
2.21
"Zonisamide is an established antiepileptic with a multifactorial mechanism of action which has shown to be useful in other headache disorders such as migraine."( Zonisamide for Cluster Headache Prophylaxis: A Case Series.
Holland, LC; Limmer, AL; Loftus, BD, 2019
)
2.68
"Zonisamide appears to be an effective prophylactic treatment for patients with chronic and episodic cluster headache disorders. "( Zonisamide for Cluster Headache Prophylaxis: A Case Series.
Holland, LC; Limmer, AL; Loftus, BD, 2019
)
3.4
"Zonisamide is an antiepileptic drug firstly approved in Europe as add-on therapy in adult patients with partial seizures and recently as monotherapy."( [Zonisamide in the epilepsy treatment: a literature review from add-on therapy to monotherapy].
Serrano-Castro, PJ; Villanueva, V, 2013
)
2.74
"Oral zonisamide (Zonegran(®)) is a benzisoxazole derivative chemically unrelated to other antiepileptic agents. "( Zonisamide: a review of its use in the management of adults with partial seizures.
Hoy, SM, 2013
)
2.35
"Zonisamide is an antiepileptic drug mainly used in patients with refractory epilepsy. "( [Bilateral urolithiasis with zonisamide developed for a short period of time in a 10-year-old girl with intractable epilepsy].
Hirobe, M; Nishinaka, K; Sato, S; Takahashi, S; Tsukamoto, T, 2013
)
2.12
"Oral zonisamide (Zonegran®) is a benzisoxazole derivative chemically unrelated to other antiepileptic drugs (AEDs). "( Zonisamide: a review of its use as adjunctive therapy in the management of partial seizures in pediatric patients aged ≥6 years.
Hoy, SM, 2014
)
2.36
"Zonisamide (ZNM) is an antiepileptic drug that is used as an adjunctive therapy in the treatment of adults with partial seizures. "( A simple and accurate liquid chromatography-tandem mass spectrometry method for quantification of zonisamide in plasma and its application to a pharmacokinetic study.
Matar, KM, 2014
)
2.06
"Zonisamide is a new antiepileptic drug used in childhood intractable seizures."( Zonisamide attenuates hyperoxia-induced apoptosis in the developing rat brain.
Bayram, E; Karaoğlu, P; Kumral, A; Kurul, SH; Ozbal, S; Topçu, Y; Tuğyan, K; Yılmaz, O; Yiş, U, 2014
)
2.57
"Zonisamide is a new generation antiepileptic drug (AED) widely used in children with refractory epilepsy, although until recently, it was used to a large extent as off-label or unlicensed medication due to the lack of evidence-based studies. "( Zonisamide: pharmacokinetics, efficacy, and adverse events in children with epilepsy.
Dahlin, M; Ohman, I; Wallander, KM, 2014
)
3.29
"Zonisamide (ZNS) is an antiepileptic drug with a broad spectrum of action mechanisms. "( Long-term retention rate of zonisamide in patients with epilepsy: an observational study.
Choi, K; Kim, DW; Moon, HS; Oh, J,
)
1.87
"Zonisamide is an option for the treatment of intractable seizures with favorable seizure control in children and adolescents."( Efficacy and safety of zonisamide in Thai children and adolescents with intractable seizures.
Khongkhatithum, C; Thampratankul, L; Visudtibhan, A, 2015
)
1.45
"Zonisamide is a structurally related anticonvulsant that is a promising agent for the treatment of AD and may have greater tolerability than topiramate."( Zonisamide, topiramate, and levetiracetam: efficacy and neuropsychological effects in alcohol use disorders.
Ciraulo, DA; Colaneri, L; Devine, E; Knapp, CM; Oscar-Berman, M; Putnam, M; Richambault, C; Richardson, MA; Sarid-Segal, O; Streeter, CC; Surprise, C; Waters, M, 2015
)
2.58
"Zonisamide is a relatively new sulfonamide derivative indicated for epilepsy and used off-label for migraines."( Zonisamide-induced angle closure and myopic shift.
Weiler, DL, 2015
)
2.58
"Zonisamide (ZNS) is a second-generation antiepileptic drug with a unique structure and multiple mechanisms of action."( The safety and long-term efficacy of zonisamide as adjunctive therapy for focal epilepsy.
Schulze-Bonhage, A, 2015
)
1.41
"Zonisamide is an orally administered antiepileptic drug that was first approved for clinical use in Japan in 1989. "( Zonisamide: Review of Recent Clinical Evidence for Treatment of Epilepsy.
Chen, TC; Chuang, YC; Dash, A; Huang, CW; Jou, SB; Kwan, SY, 2015
)
3.3
"Zonisamide is a sulfonamide drug used primarily for the treatment of partial seizures in adults. "( Complete Recovery After Acute Zonisamide Overdose in an Adolescent Female.
McStay, C; Pierce, R; Riley, C, 2018
)
2.21
"Zonisamide (ZNS) is an anticonvulsant (AC) that contains a sulpha moiety potentially triggering hypersensitivity syndrome reactions (HSR). "( Predicting possible zonisamide hypersensitivity syndrome.
Cohen, L; Kessas, M; Lee, AW; Malkiewicz, IM; Neuman, MG; Shear, NH, 2008
)
2.11
"Zonisamide (ZNS) is a multi-target antiepileptic drug reported to be efficient in the treatment of both partial and generalized seizures, with T-type Ca(2+) channel blockade being one of its proposed mechanisms of action. "( Zonisamide block of cloned human T-type voltage-gated calcium channels.
Hescheler, J; Jin, W; Matar, N; Schneider, T; Weiergräber, M; Wrubel, H, 2009
)
3.24
"Zonisamide (ZNS) is an antiepileptic drug (AED) with broad spectrum action that demonstrated a good efficacy in controlling seizures as add-on in adult and pediatric epilepsy. "( Efficacy and tolerability of zonisamide as add-on in brain tumor-related epilepsy: preliminary report.
Carapella, CM; Dinapoli, L; Jandolo, B; Maschio, M; Pompili, A; Saveriano, F; Vidiri, A, 2009
)
2.09
"Zonisamide appeared to be a reasonably effective and generally well-tolerated antiepileptic drug in a heterogeneous group of 57 children with poorly controlled epilepsy and provides another treatment option for children with refractory seizures."( Effectiveness and tolerability of zonisamide in children with epilepsy: a retrospective review.
Appleton, RE; Kneen, R; Martland, TR; Tan, HJ, 2010
)
2.08
"Zonisamide is an FDA-approved antiepileptic drug that blocks voltage-dependent Na(+) channels and T-type Ca(2+) channels and improves clinical outcome in Parkinson's disease (PD) patients when used as an adjunct to other PD therapies. "( The antiepileptic drug zonisamide inhibits MAO-B and attenuates MPTP toxicity in mice: clinical relevance.
Buckley, B; Sonsalla, PK; Winnik, B; Wong, LY, 2010
)
2.11
"Zonisamide is an antiepileptic drug with multiple mechanisms of action, corresponding to efficacy in diverse epilepsy syndromes."( Zonisamide in the treatment of epilepsy.
Schulze-Bonhage, A, 2010
)
2.52
"Zonisamide is a second generation antiepileptic drug available in France since 2005. "( [Therapeutic drug monitoring of zonisamide].
Bentué-Ferrer, D; Tribut, O; Verdier, MC,
)
1.86
"Zonisamide is an anticonvulsant medication with GABAergic, glutamatergic, and monoaminergic effects. "( Placebo-controlled trial of zonisamide for the treatment of alcohol dependence.
Arias, AJ; Covault, J; Feinn, R; Kranzler, HR; Oncken, C, 2010
)
2.1
"Zonisamide (ZNS) is an antiepileptic drug (AED) that has been associated with psychiatric adverse events (PAE) and cognitive adverse events (CAE); controlled studies evaluating these adverse events are limited. "( Zonisamide discontinuation due to psychiatric and cognitive adverse events: a case-control study.
Beniak, TE; Birnbaum, AK; Leppik, IE; Marino, SE; Walczak, TS; White, JR, 2010
)
3.25
"Zonisamide is an antiepileptic drug that also improves the cardinal symptoms of Parkinson's disease. "( Zonisamide-induced long-lasting recovery of dopaminergic neurons from MPTP-toxicity.
Choudhury, ME; Kubo, M; Kyaw, WT; Matsuda, S; Moritoyo, T; Nagai, M; Nishikawa, N; Nomoto, M; Yabe, H, 2011
)
3.25
"Zonisamide is an antiepileptic drug that acts on voltage-sensitive sodium and calcium channels, with a modulatory effect on GABA-mediated neuronal inhibition and an inhibitory effect on carbonic anhydrase. "( Moderate toxic effects following acute zonisamide overdose.
Ceschi, A; Hofer, KE; Kullak-Ublick, GA; Kupferschmidt, H; Rauber-Lüthy, C; Trachsel, C, 2011
)
2.08
"Zonisamide (ZNS) is an antiepileptic drug (AED) with multiple putative mechanisms of action. "( The long-term retention of zonisamide in a large cohort of people with epilepsy at a tertiary referral centre.
Bartolini, E; Bell, GS; Catarino, CB; Duncan, JS; Sander, JW; Yuen, AW, 2011
)
2.11
"Zonisamide is a broad spectrum antiepileptic drug with multiple mechanisms of action which has been recently approved in the US and Europe as an adjunctive therapy for refractory partial seizures in adults."( Drug safety evaluation of zonisamide for the treatment of epilepsy.
Cincotta, M; Tramacere, L; Zaccara, G, 2011
)
2.11
"Zonisamide is a second-generation antiepileptic drug (AED) that has broad-spectrum efficacy, a favorable side-effect profile and simpler dosing than earlier drugs."( Zonisamide in the treatment of epilepsy.
Holder, JL; Wilfong, AA, 2011
)
2.53
"Zonisamide is an anti-seizure medication that is indicated for adjunctive therapy in the treatment of partial seizures. "( Psychosis induced by zonisamide: a case report and review of the literature.
Abdoh, M; Melgar, TA; Mersfelder, TL,
)
1.89
"Zonisamide is an antiepileptic drug associated with weight loss."( A randomized, placebo-controlled study of zonisamide to prevent olanzapine-associated weight gain.
Guerdjikova, AI; Keck, PE; Martens, B; McCoy, J; McElroy, SL; Moeller, D; Mori, N; Winstanley, E, 2012
)
1.36
"Zonisamide is an anticonvulsant used as an adjunctive treatment for partial seizures. "( Zonisamide-induced psychosis in a patient with bipolar disorder and narcolepsy.
Opler, LA; Platt, EM; Platt, JE,
)
3.02
"Zonisamide is a benzisoxazole derivative, chemically unrelated to other antiepileptic drugs, that appears to have multiple mechanisms of action, including inhibition of Na(+) channels and reduction of T-type Ca(2+) currents. "( Zonisamide: its pharmacology, efficacy and safety in clinical trials.
Ben-Menachem, E; Brodie, MJ; Chouette, I; Giorgi, L, 2012
)
3.26
"Zonisamide is a marketed antiepileptic drug that has serotonergic and dopaminergic activity in addition to blockade of sodium and calcium channels. "( Zonisamide for weight loss in obese adults: a randomized controlled trial.
Franciscy, DM; Gadde, KM; Krishnan, KR; Wagner, HR, 2003
)
3.2
"Zonisamide is an antiepileptic drug developed and first marketed in Japan in 1989. "( Oligohydrosis and fever in pediatric patients treated with zonisamide.
Kapcala, LP; Knudsen, JF; Racoosin, JA; Thambi, LR, 2003
)
2
"Zonisamide (ZNS) is a new antiepileptic drug (AED) efficient in treating refractory epilepsy."( Zonisamide: a new antiepileptic drug.
Borowicz, KK; Czuczwar, SJ; Kimber-Trojnar, Z; Małek, R; Piskorska, B; Sobieszek, G,
)
2.3
"Zonisamide is a novel antiepileptic drug associated with weight loss."( Zonisamide in the treatment of binge-eating disorder: an open-label, prospective trial.
Hudson, JI; Keck, PE; Kotwal, R; McElroy, SL; Nelson, EB, 2004
)
2.49
"Zonisamide is a new type of benzisoxazole derivative, first marketed in Japan in 1989. "( Overview of Japanese experience-controlled and uncontrolled trials.
Yagi, K, 2004
)
1.77
"Zonisamide is a benzisoxazole-based compound first synthesized in the early 1970s by the research laboratories of Dainippon Pharmaceutical Company in Osaka, Japan. "( Review of zonisamide development in Japan.
Seino, M, 2004
)
2.17
"Zonisamide is a synthetic 1,2-benzisoxazole-3-methanesulfonamide with anticonvulsant properties. "( Zonisamide: chemistry, mechanism of action, and pharmacokinetics.
Leppik, IE, 2004
)
3.21
"Zonisamide is an antiepilepsy drug (AED) with both sodium and calcium channel-blocking properties. "( Review of United States and European clinical trials of zonisamide in the treatment of refractory partial-onset seizures.
Faught, E, 2004
)
2.01
"Zonisamide is an antiepileptic agent that is indicated as adjunctive therapy for the treatment of partial seizures in adults. "( Zonisamide and associated oligohidrosis and hyperthermia.
James, S; Leong, R; Low, PA; Peschel, T; Rothstein, A, 2004
)
3.21
"Zonisamide is a novel anticonvulsant drug with multiple mechanisms of action, many of which may confer efficacy in the treatment of migraine headaches. "( Open-label zonisamide for refractory migraine.
Armentbright, AD; Drake, ME; Greathouse, NI; Renner, JB,
)
1.96
"Zonisamide is a broad-spectrum antiepilepsy drug indicated for the adjunctive treatment of partial seizures in adults."( Zonisamide monotherapy for epilepsy in children and young adults.
Wilfong, AA, 2005
)
2.49
"Zonisamide is a broad-spectrum antiepilepsy drug approved in the United States for the adjunctive treatment of partial seizures in adults with epilepsy. "( Use of zonisamide in pediatric patients.
Brotherton, T; Santos, CC, 2005
)
2.23
"Zonisamide is an antiepileptic drug used as adjunctive therapy for refractory partial seizures in adults. "( Zonisamide: review of its use in epilepsy therapy.
Zareba, G, 2005
)
3.21
"Zonisamide is an antiepileptic drug with preliminary studies suggesting some efficacy in the adult headache population."( Zonisamide prophylaxis in refractory pediatric headache.
Kring, D; Pakalnis, A, 2006
)
2.5
"Zonisamide (ZNS) is a new AED effective in the treatment of refractory epilepsy and since it is only prescribed in polytherapy regimens, its interactions with other AEDs is of particular importance."( Interactions between zonisamide and conventional antiepileptic drugs in the mouse maximal electroshock test model.
Borowicz, KK; Czuczwar, SJ; Luszczki, JJ; Patsalos, PN; Ratnaraj, N; Sobieszek, G, 2007
)
1.38
"Zonisamide is a new antiepileptic drug with multiple mechanisms of action and a favourable pharmacokinetic profile. "( Zonisamide for migraine prophylaxis in refractory patients.
Ashkenazi, A; Benlifer, A; Korenblit, J; Silberstein, SD, 2006
)
3.22
"Zonisamide is an adjuvant for the treatment of patients with partial epilepsy, with or without secondary generalisation. "( [New medications; zonisamide].
Cohen, AF; van Bronswijk, H, 2006
)
2.11
"Zonisamide is a novel antiepileptic drug associated with weight loss."( Zonisamide in the treatment of binge eating disorder with obesity: a randomized controlled trial.
D'Alessio, DA; Guerdjikova, AI; Hudson, JI; Keck, PE; Kotwal, R; Lake, KA; McElroy, SL; Nelson, EB; Welge, JA, 2006
)
2.5
"Zonisamide is a novel AED that has a broad combination of complementary mechanisms of action, which may offer a clinical advantage over other antiepileptic agents."( Clinical pharmacology and mechanism of action of zonisamide.
Biton, V,
)
1.11
"Zonisamide is an antiepileptic drug widely used to treat seizures worldwide. "( Zonisamide for the treatment of Parkinson's disease.
Miwa, H, 2007
)
3.23
"Zonisamide is an antiepileptic with several potential mechanisms of action."( Zonisamide for essential tremor.
Ondo, WG,
)
2.3
"Zonisamide (ZNS) is an anticonvulsant drug known to affect various neuronal channels and transmitter systems. "( Antiepileptic activity of zonisamide on hippocampal CA3 neurons does not depend on carbonic anhydrase inhibition.
Leniger, T; Splettstösser, F; Thöne, J; Wiemann, M, 2008
)
2.09
"Zonisamide is a 1,2 benzisoxazole derivative and the first agent of this chemical class to be developed as an antiepileptic drug. "( Zonisamide. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in epilepsy.
Peters, DH; Sorkin, EM, 1993
)
3.17
"Zonisamide is an effective antiepileptic drug for add-on treatment of refractory partial epilepsy."( Zonisamide for add-on treatment of refractory partial epilepsy: a European double-blind trial.
Bauer, G; Blankenhorn, V; Deisenhammer, E; Despland, A; Egli, M; Jacob, R; Klinger, D; Loiseau, P; Schmidt, D; Stenzel, E, 1993
)
2.45
"Zonisamide is a new drug with broad-spectrum antiepileptic activity against partial as well as generalized seizures. "( Long-term effects of zonisamide in the treatment of epilepsy in children with intellectual disability.
Cho, K; Iinuma, K; Kajii, N; Minami, T; Tachi, N, 1998
)
2.06
"Zonisamide (ZNS) is a relatively new antiepileptic medication currently available in Japan. "( Zonisamide: a new antiepileptic drug.
Mathews, S; Oommen, KJ,
)
3.02
"Zonisamide (ZNS) is a broad-spectrum antiepileptic drug in both animal models of epilepsy and patients with epilepsy. "( Zonisamide.
Leppik, IE, 1999
)
3.19
"Zonisamide is a sulfonamide antiepilepsy drug with sodium and calcium channel-blocking actions. "( Randomized controlled trial of zonisamide for the treatment of refractory partial-onset seizures.
Ayala, R; Faught, E; Leppik, IE; Montouris, GG, 2001
)
2.04
"Zonisamide (ZNS) is a generally well tolerated anticonvulsant that has beneficial effects on Parkinson's disease (PD). "( Zonisamide has beneficial effects on Parkinson's disease patients.
Horiuchi, E; Kanazawa, I; Murata, M, 2001
)
3.2
"Zonisamide (ZNS) is an antiepileptic drug developed in Japan. "( Regional accumulation of 14C-zonisamide in rat brain during kainic acid-induced limbic seizures.
Akaike, K; Fukumoto, S; Imamura, S; Takigawa, M; Tanaka, S; Tojo, H, 2001
)
2.04
"Zonisamide is a novel anticonvulsant that is structurally and mechanistically unique, compared with other antiepilepsy drugs. "( Zonisamide in pediatric epilepsy: review of the Japanese experience.
Glauser, TA; Pellock, JM, 2002
)
3.2
"Zonisamide is a new antiepileptic drug which has a wide range of antiepileptic efficacy. "( [Zonisamide induced tremor--report of two cases].
Taira, T, 1992
)
2.64
"Zonisamide is a novel anticonvulsant that prevents seizures in laboratory animals and in man. "( Blockade of sustained repetitive action potentials in cultured spinal cord neurons by zonisamide (AD 810, CI 912), a novel anticonvulsant.
Macdonald, RL; Rock, DM; Taylor, CP,
)
1.8
"Zonisamide (CI-912) is an experimental antiepileptic drug. "( Comparative pharmacokinetics of zonisamide (CI-912) in epileptic patients on carbamazepine or phenytoin monotherapy.
Buchanan, RA; Friel, PN; Levy, RH; McLean, JR; Ojemann, LM; Shastri, RA; Wilensky, AJ, 1986
)
2

Effects

Zonisamide (Zonegran) has a similar pharmacologic profile to topiramate, which has been shown to reduce smoking, but is better tolerated. Zonisamide has a long T1/2 enabling once-daily dosing and linear pharmacokinetics. Plasma levels of commonly administered AEDs and oral contraceptives are unaffected by concomitant zonisamide.

Zonisamide has shown efficacy as adjunct therapy for the management of motor symptoms in patients with Parkinson's disease (PD) Zonisamide was found to improve the symptoms of PD in a patient who had both epilepsy and PD. It has been reported to have protective effects on epilepsy and Parkinson’s disease.

ExcerptReferenceRelevance
"Zonisamide (Zonegran) has a similar pharmacologic profile to topiramate, which has been shown to reduce smoking, but is better tolerated."( Zonisamide Reduces Withdrawal Symptoms But Does Not Enhance Varenicline-Induced Smoking Cessation.
Dunn, KE; Kim, C; Marcus, TF; Schroeder, JR; Umbricht, A; Vandrey, R, 2016
)
2.6
"Zonisamide has a pharmacokinetic profile favorable for clinical use."( Zonisamide: chemistry, mechanism of action, and pharmacokinetics.
Leppik, IE, 2004
)
2.49
"Zonisamide has a long T1/2 enabling once-daily dosing, linear pharmacokinetics and minimal interaction with other drugs; plasma levels of commonly administered AEDs and oral contraceptives are unaffected by concomitant zonisamide."( Introduction to zonisamide.
Baulac, M, 2006
)
1.4
"Zonisamide has a broader therapeutic range than other antiepileptic drugs."( Neuropharmacology of zonisamide, a new antiepileptic drug.
Hammond, EJ; McLean, JR; Perchalski, RJ; Wilder, BJ, 1987
)
1.31
"Zonisamide has exhibited neuroprotective activities toward adult rat DRG neurons in vitro and therefore, we aimed to assess its potential efficacy against OHP-induced neurotoxicity."( Pretreatment with Zonisamide Mitigates Oxaliplatin-Induced Toxicity in Rat DRG Neurons and DRG Neuron-Schwann Cell Co-Cultures.
Sango, K; Takaku, S, 2022
)
1.78
"Zonisamide (ZNS) has shown anti-apoptosis effects in recent studies."( Neuroprotective effects of zonisamide on cerebral ischemia injury via inhibition of neuronal apoptosis.
Chen, R; Chen, Y; He, J; He, W; Xie, Y; Yang, Y; Zhang, X, 2021
)
1.64
"Zonisamide has shown efficacy as adjunct therapy for the management of motor symptoms in patients with Parkinson's disease (PD)."( The Application of Zonisamide to Patients Suffering from Dementia with Lewy Bodies: Emerging Clinical Data.
Leverenz, JB; Tousi, B, 2021
)
1.67
"Zonisamide has been suggested as a potentially useful agent for the treatment of ET but there is uncertainty about its efficacy and safety."( Zonisamide for essential tremor.
Bruno, E; Colosimo, C; Filippini, G; Nicoletti, A; Quattrocchi, G; Zappia, M, 2017
)
2.62
"Zonisamide has been in use for epilepsy and it was serendipitously found to improve the symptoms of PD in a patient who had both epilepsy and PD."( Zonisamide: a review of the clinical and experimental evidence for its use in Parkinson's disease.
Gokhale, DV; Grover, ND; Limaye, RP; Patil, TR,
)
2.3
"Zonisamide has efficacy as an add-on treatment in people with drug-resistant partial epilepsy. "( Zonisamide add-on for drug-resistant partial epilepsy.
Carmichael, K; Lakhan, SE; Marson, AG; Parikh, P; Pulman, J, 2013
)
3.28
"Zonisamide has recently been approved in Europe for the adjunctive treatment of partial seizures (with or without secondary generalisation) in adolescents and children aged ≥6 years."( Safety and tolerability of zonisamide in paediatric patients with epilepsy.
Auvin, S; Cross, JH; Giorgi, L; Patten, A, 2014
)
2.14
"Zonisamide has been reported to have protective effects on epilepsy and Parkinson׳s disease and to work via various mechanisms of action, such as inhibition of monoamine oxidase-B and enhancement of tyrosine hydroxylase. "( Zonisamide suppresses endoplasmic reticulum stress-induced neuronal cell damage in vitro and in vivo.
Hara, H; Hashizume, T; Ishisaka, M; Shimazawa, M; Tsujii, S, 2015
)
3.3
"Zonisamide has been associated with weight loss in children and adults."( Effects of adjunctive zonisamide treatment on weight and body mass index in children with partial epilepsy.
Giorgi, L; Lagae, L; Meshram, C; Patten, A, 2015
)
2.17
"Zonisamide (Zonegran) has a similar pharmacologic profile to topiramate, which has been shown to reduce smoking, but is better tolerated."( Zonisamide Reduces Withdrawal Symptoms But Does Not Enhance Varenicline-Induced Smoking Cessation.
Dunn, KE; Kim, C; Marcus, TF; Schroeder, JR; Umbricht, A; Vandrey, R, 2016
)
2.6
"Zonisamide has neuroprotective effects though inhibition of quinoprotein and increasing the levels of GSH and Mn SOD."( [Therapy of Parkinson's disease--up to date].
Murata, M, 2008
)
1.07
"Zonisamide has demonstrated good efficacy and tolerability in patients refractory to topiramate and shows a prolonged half life, which improves compliance."( [The role of the neuromodulators in the preventive treatment of migraine].
Pascual-Gómez, J,
)
0.85
"Zonisamide has also been shown to reduce alcohol intake in rodents and in risky drinkers in the context of a laboratory study."( Placebo-controlled trial of zonisamide for the treatment of alcohol dependence.
Arias, AJ; Covault, J; Feinn, R; Kranzler, HR; Oncken, C, 2010
)
1.38
"Zonisamide has multiple modes of action, and its effects on Parkinson's disease include activation of dopamine synthesis, inhibition of monoamine oxidase, inhibition of T-type calcium channels and inhibition of an indirect pathway in the basal ganglia through the δ opioid receptor."( Zonisamide: a new drug for Parkinson's disease.
Murata, M, 2010
)
2.52
"Zonisamide (ZNS) has proved effective for motor symptoms in PD and it may be also useful in the field of ICDs."( Zonisamide in managing impulse control disorders in Parkinson's disease.
Anciones, B; Bermejo, PE; Ruiz-Huete, C, 2010
)
2.52
"Zonisamide, which has several putative pharmacologic mechanisms of action, is a member of the carbonic anhydrase inhibitor drug group."( Zonisamide ameliorates symptoms of secondary paroxysmal dystonia.
Borenstein, MJ; Egel, RT; Hoganson, GE; Katerji, MA, 2010
)
2.52
"Zonisamide has several CNS dose-dependent, metabolic and idiosyncratic adverse effects. "( Drug safety evaluation of zonisamide for the treatment of epilepsy.
Cincotta, M; Tramacere, L; Zaccara, G, 2011
)
2.11
"Zonisamide has been proven as an effective drug for the recovery of degenerating dopaminergic neurons in the animal models of Parkinson's disease. "( Zonisamide up-regulated the mRNAs encoding astrocytic anti-oxidative and neurotrophic factors.
Choudhury, ME; Iwaki, H; Kubo, M; Kyaw, WT; Nagai, M; Nishikawa, N; Nomoto, M; Sugimoto, K; Tanaka, J; Tsujii, T, 2012
)
3.26
"Zonisamide has also been shown to have favourable long-term retention rates, an important indication of its overall effectiveness."( Zonisamide: its pharmacology, efficacy and safety in clinical trials.
Ben-Menachem, E; Brodie, MJ; Chouette, I; Giorgi, L, 2012
)
2.54
"Zonisamide has a pharmacokinetic profile favorable for clinical use."( Zonisamide: chemistry, mechanism of action, and pharmacokinetics.
Leppik, IE, 2004
)
2.49
"Zonisamide has been commercially available in Japan since 1989, and became available in the United States for treatment of adults over the age of 12 with partial-onset seizures in March 2000."( Review of United States and European clinical trials of zonisamide in the treatment of refractory partial-onset seizures.
Faught, E, 2004
)
1.29
"Zonisamide has multiple mechanisms of action, which may explain widespread reports of its utility in focal epilepsy and generalized epilepsy, and for nonseizure disorders such as headache and neuropathic pain."( Zonisamide: newer antiepileptic agent with multiple mechanisms of action.
Biton, V, 2004
)
2.49
"Zonisamide has efficacy as an add-on treatment in people with drug-resistant partial epilepsy. "( Zonisamide add-on for drug-resistant partial epilepsy.
Chadwick, DW; Marson, AG, 2005
)
3.21
"Zonisamide (Zonegran) has been used extensively worldwide (>2 million patient-years experience) for the effective treatment of a broad range of epilepsy indications. "( Zonisamide as adjunctive therapy for refractory partial seizures.
Brodie, MJ, 2006
)
3.22
"Zonisamide has a long T1/2 enabling once-daily dosing, linear pharmacokinetics and minimal interaction with other drugs; plasma levels of commonly administered AEDs and oral contraceptives are unaffected by concomitant zonisamide."( Introduction to zonisamide.
Baulac, M, 2006
)
1.4
"Zonisamide has no clinically relevant effects on the pharmacokinetics of other commonly used AEDs, however, co-administration with cytochrome P450 3A4 (CYP3A4) inducers or inhibitors may change zonisamide's pharmacokinetic profile."( Efficacy and safety of adjunctive zonisamide therapy for refractory partial seizures.
Baulac, M; Leppik, IE, 2007
)
1.34
"Zonisamide and bupropion have been investigated for weight reduction in obese adults. "( Combination therapy of zonisamide and bupropion for weight reduction in obese women: a preliminary, randomized, open-label study.
Foust, MS; Gadde, KM; Wagner, HR; Yonish, GM, 2007
)
2.09
"Zonisamide has demonstrated efficacy equivalent to that of carbamazepine in patients with (mainly) partial seizures, and to that of valproic acid in a small study of children (n = 32) with generalised seizures."( Zonisamide. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in epilepsy.
Peters, DH; Sorkin, EM, 1993
)
2.45
"Zonisamide has been proven to have a pharmacological profile that is very similar to that of carbamazepine."( The first open study of zonisamide, a novel anticonvulsant, shows efficacy in mania.
Arata, E; Kamijima, K; Kanba, S; Kinoshita, N; Koshikawa, H; Nibuya, M; Otaki, J; Suzuki, T; Tajima, O; Yagi, G, 1994
)
1.32
"Zonisamide, which has been commercially available in Japan for some years, also has a multifactorial mode of action, possibly involving the blockade of sodium channels, T-type calcium channels and inhibition of carbonic anhydrase."( The clinical pharmacokinetics of the newer antiepileptic drugs. Focus on topiramate, zonisamide and tiagabine.
Bialer, M; Perucca, E, 1996
)
1.24
"Zonisamide has previously been reported to be effective in two patients with PME."( Zonisamide for progressive myoclonus epilepsy: long-term observations in seven patients.
Ben-Menachem, E; Kyllerman, M, 1998
)
2.46
"Zonisamide has efficacy as an add-on treatment in patients with drug-resistant partial epilepsy. "( Zonisamide for drug-resistant partial epilepsy.
Chadwick, DW; Marson, AG, 2000
)
3.19
"Zonisamide has been approved for use in Japan for ten years prior to approval in USA and Europe."( An assessment of zonisamide as an anti-epileptic drug.
Jain, KK, 2000
)
1.37
"Zonisamide has efficacy as an add-on treatment in people with drug-resistant partial epilepsy. "( Zonisamide add-on for drug-resistant partial epilepsy.
Chadwick, DW; Marson, AG, 2002
)
3.2
"Zonisamide has a broader therapeutic range than other antiepileptic drugs."( Neuropharmacology of zonisamide, a new antiepileptic drug.
Hammond, EJ; McLean, JR; Perchalski, RJ; Wilder, BJ, 1987
)
1.31

Actions

Zonisamide displays predictable, dose-dependent pharmacokinetics and has a half-life of ~60 h. It can cause an idiosyncratic reaction leading to choroidal effusion with or without acute angle closure.

ExcerptReferenceRelevance
"Zonisamide can cause an idiosyncratic reaction leading to choroidal effusion with or without acute angle closure. "( Zonisamide-induced Choroidal Effusion: A Case Report.
Baradad Jurjo, MC; Caminal Mitjana, JM; Lillo Sopena, J; Moix Gil, E; Sanz Moreno, S, 2020
)
3.44
"Zonisamide displays predictable, dose-dependent pharmacokinetics and has a half-life of ~60 h, allowing once- or twice-daily administration."( Zonisamide: its pharmacology, efficacy and safety in clinical trials.
Ben-Menachem, E; Brodie, MJ; Chouette, I; Giorgi, L, 2012
)
2.54

Treatment

Zonisamide treatment alone did not produce any lasting effects on ex vivo MAO-B activity, indicating that it is a reversible inhibitor of the enzyme. Pretreatment with zonisamide (100 μM) alleviated the DRG neuronal death caused by OHP.

ExcerptReferenceRelevance
"Zonisamide treatment was discontinued."( Zonisamide-induced Choroidal Effusion: A Case Report.
Baradad Jurjo, MC; Caminal Mitjana, JM; Lillo Sopena, J; Moix Gil, E; Sanz Moreno, S, 2020
)
2.72
"The zonisamide-treated group received an intraperitoneal injection of zonisamide."( Zonisamide attenuates hyperoxia-induced apoptosis in the developing rat brain.
Bayram, E; Karaoğlu, P; Kumral, A; Kurul, SH; Ozbal, S; Topçu, Y; Tuğyan, K; Yılmaz, O; Yiş, U, 2014
)
2.33
"Zonisamide treatment was associated with a maintained reduction in seizure frequency, with some patients achieving prolonged periods of seizure freedom."( Long-term safety and efficacy of zonisamide in patients with refractory partial-onset epilepsy.
Marshall, A; Wroe, SJ; Yeates, AB, 2008
)
1.35
"Zonisamide treatment alone did not produce any lasting effects on ex vivo MAO-B activity, indicating that it is a reversible inhibitor of the enzyme."( The antiepileptic drug zonisamide inhibits MAO-B and attenuates MPTP toxicity in mice: clinical relevance.
Buckley, B; Sonsalla, PK; Winnik, B; Wong, LY, 2010
)
1.39
"Zonisamide treatment was started at 100 mg/day and increased by 100 mg every 2 weeks to a maximum of 300 mg/day in divided doses (b.i.d."( A preliminary open-label study of zonisamide treatment for bipolar depression in 10 patients.
Anand, A; Bukhari, L; Jennings, SA; Kamat, M; Lee, C; Lightfoot, J; Nurnberger, JI; Shekhar, A, 2005
)
1.33
"Zonisamide treatment was generally well tolerated and was associated with significant reductions in seizure frequency in this pediatric population with a variety of both partial and generalized medically refractory epilepsy syndromes."( Open-label, long-term safety study of zonisamide administered to children and adolescents with epilepsy.
Conry, JA; Pellock, JM; Shinnar, S, 2009
)
2.07
"Pretreatment with zonisamide (100 μM) alleviated the DRG neuronal death caused by OHP (75 μM) and the protective effects were attenuated by a co-incubation with 25 μM of the mitogen-activated protein kinase (MAPK; MEK/ERK) inhibitor, U0126, or the phosphatidyl inositol-3'-phosphate-kinase (PI3K) inhibitor, LY294002."( Pretreatment with Zonisamide Mitigates Oxaliplatin-Induced Toxicity in Rat DRG Neurons and DRG Neuron-Schwann Cell Co-Cultures.
Sango, K; Takaku, S, 2022
)
1.38
"Treatment with zonisamide is well tolerated and is not known to be associated with clinically significant drug-drug interactions, including with oral contraceptives or other antiepileptic drugs."( Zonisamide: Review of Recent Clinical Evidence for Treatment of Epilepsy.
Chen, TC; Chuang, YC; Dash, A; Huang, CW; Jou, SB; Kwan, SY, 2015
)
2.2
"Treatment with zonisamide was well-tolerated and no participants dropped out prematurely."( Effects of zonisamide on tardive dyskinesia: a preliminary open-label trial.
Irie, S; Iwashita, S; Iwata, Y; Mimura, M; Suzuki, T; Uchida, H; Watanabe, K, 2012
)
1.11
"Treatment with zonisamide at a dose of 80 mg/kg increased serum pyridinoline level, a marker of bone resorption, while it does not affect the serum intact osteocalcin level, a marker of bone formation."( Effects of chronic administration of zonisamide, an antiepileptic drug, on bone mineral density and their prevention with alfacalcidol in growing rats.
Kamei, J; Mayanagi, H; Miyazaki, S; Onodera, K; Saito, T; Sakurada, S; Shinoda, H; Takahashi, A, 2003
)
0.93

Toxicity

Zonisamide has several CNS dose-dependent, metabolic and idiosyncratic adverse effects. The most frequent adverse event was fatigue, reported in 23% of the patients. Open-label extension studies suggest continued efficacy of zonisamide in long-term treatment.

ExcerptReferenceRelevance
" Adverse effects involved principally the CNS and were similar to those seen with other antiepileptic drugs."( Efficacy and safety of zonisamide: results of a multicenter study.
Fromm, G; Homan, RW; Leppik, IE; Lesser, RP; Oommen, KJ; Penry, JK; Sackellares, JC; Smith, DB; Wallace, JD; Willmore, LJ, 1993
)
0.6
"At the study's conclusion, information regarding adverse events (AEs) and body weight was recorded."( Safety of 25- and 50-mg capsules in the initiation of zonisamide therapy in patients with epilepsy: an uncontrolled, open-label study.
Anthony, S; James, SP; Miller, GS; Montouris, G; Uthman, BM, 2004
)
0.57
" A total of 1089 adverse events occurred in 476 (31."( Safety of zonisamide therapy: prospective follow-up survey.
Ohtahara, S; Yamatogi, Y, 2004
)
0.73
" The most common adverse events were somnolence, headache, dizziness, and nausea during the titration phase and headache and pharyngitis during the fixed-dose assessment phase."( Dose-dependent safety and efficacy of zonisamide: a randomized, double-blind, placebo-controlled study in patients with refractory partial seizures.
Bitenskyy, V; Brodie, MJ; Duncan, R; Lucas, C; Solyom, A; Vespignani, H, 2005
)
0.6
" Open-label extension studies in the United States and Europe suggest continued efficacy of zonisamide in long-term treatment without development of adverse events further to those seen in registration studies."( Practical prescribing and long-term efficacy and safety of zonisamide.
Leppik, IE, 2006
)
0.8
" Thirty of 112 patients (27%) reported mild to moderate adverse events, such as weight loss (5."( Long-term efficacy and safety of monotherapy and adjunctive therapy with zonisamide.
Tisdell, J; Tosches, WA, 2006
)
0.57
" Seizure count and side effect profile were maintained during therapy."( Efficacy and safety of zonisamide monotherapy in a cohort of children with epilepsy.
Hobdell, E; Kaleyias, J; Khurana, DS; Kothare, SV; Legido, A; Melvin, JJ; Mostofi, N; Valencia, I, 2006
)
0.64
" A total of 1089 adverse events occurred in 476 (31."( Erratum to "Safety of zonisamide therapy: prospective follow-up survey.".
Ohtahara, S; Yamatogi, Y, 2007
)
0.65
" Zonisamide is well tolerated with the majority of adverse events being mild-to-moderate and generally manageable."( Efficacy and safety of adjunctive zonisamide therapy for refractory partial seizures.
Baulac, M; Leppik, IE, 2007
)
1.53
" The occurrence of adverse events (AEs) was the primary safety measure."( Open-label, long-term safety study of zonisamide administered to children and adolescents with epilepsy.
Conry, JA; Pellock, JM; Shinnar, S, 2009
)
0.62
" However, half of the cats that were administered 20mg/kg/day daily showed adverse reactions such as anorexia, diarrhoea, vomiting, somnolence and locomotor ataxia."( Pharmacokinetics and toxicity of zonisamide in cats.
Fujita, M; Hasegawa, D; Kobayashi, M; Kuwabara, T; Ohmura, T; Orima, H, 2008
)
0.63
"A review of the pharmacokinetics, pharmacodynamics, evidence for efficacy in different seizure types and non-seizure conditions, adverse effects, and tolerability of ZNS is presented."( Zonisamide: review of pharmacology, clinical efficacy, tolerability, and safety.
Kaleyias, J; Kothare, SV, 2008
)
1.79
"Zonisamide (ZNS) is an antiepileptic drug (AED) that has been associated with psychiatric adverse events (PAE) and cognitive adverse events (CAE); controlled studies evaluating these adverse events are limited."( Zonisamide discontinuation due to psychiatric and cognitive adverse events: a case-control study.
Beniak, TE; Birnbaum, AK; Leppik, IE; Marino, SE; Walczak, TS; White, JR, 2010
)
3.25
" Our findings support the concept that selected patients are relatively more vulnerable to CNS adverse events when exposed to ZNS."( Zonisamide discontinuation due to psychiatric and cognitive adverse events: a case-control study.
Beniak, TE; Birnbaum, AK; Leppik, IE; Marino, SE; Walczak, TS; White, JR, 2010
)
1.8
" Seizure frequency and adverse effects were documented."( Efficacy and safety of adjunctive zonisamide in adult patients with refractory partial-onset epilepsy: a randomized, double-blind, placebo-controlled trial.
Chen, Y; Hu, Y; Lu, Y; Wang, X; Xiao, F; Xiao, Z; Yu, W, 2011
)
0.65
" There was no difference in the incidence of adverse effects between zonisamide and placebo."( Efficacy and safety of adjunctive zonisamide in adult patients with refractory partial-onset epilepsy: a randomized, double-blind, placebo-controlled trial.
Chen, Y; Hu, Y; Lu, Y; Wang, X; Xiao, F; Xiao, Z; Yu, W, 2011
)
0.88
" Concurrent treatment of mice with zonisamide and MPTP did not show any inhibition of the toxic effect of MPTP towards dopamine contents at 1 week after treatment but it increased the number and area of TH-positive neurons compared to the MPTP-treated group."( Zonisamide-induced long-lasting recovery of dopaminergic neurons from MPTP-toxicity.
Choudhury, ME; Kubo, M; Kyaw, WT; Matsuda, S; Moritoyo, T; Nagai, M; Nishikawa, N; Nomoto, M; Yabe, H, 2011
)
2.09
" The most common reported adverse effects are somnolence, anorexia, dizziness, and headache."( Moderate toxic effects following acute zonisamide overdose.
Ceschi, A; Hofer, KE; Kullak-Ublick, GA; Kupferschmidt, H; Rauber-Lüthy, C; Trachsel, C, 2011
)
0.64
"The adverse effect profile of this drug from controlled, randomized studies and open and long-term studies and case reports is described herein."( Drug safety evaluation of zonisamide for the treatment of epilepsy.
Cincotta, M; Tramacere, L; Zaccara, G, 2011
)
0.67
"Zonisamide has several CNS dose-dependent, metabolic and idiosyncratic adverse effects."( Drug safety evaluation of zonisamide for the treatment of epilepsy.
Cincotta, M; Tramacere, L; Zaccara, G, 2011
)
2.11
" Treatment-emergent adverse events (AEs) were reported in 80 patients."( Short-term efficacy and safety of zonisamide as adjunctive treatment for refractory partial seizures: a multicenter open-label single-arm trial in Korean patients.
Cho, YW; Heo, K; Kim, KS; Kim, OJ; Kim, SE; Kim, SH; Lee, BI; Lee, JH; Lee, SJ; Park, SP; Shin, DJ; Song, HK; Yi, SD, 2012
)
0.66
"Drug-induced weight alteration can be a serious side effect that applies to several therapeutic agents and must be referred to in the respective approved labeling texts."( Weight-reducing side effects of the antiepileptic agents topiramate and zonisamide.
Antel, J; Hebebrand, J, 2012
)
0.61
" In all four trials, zonisamide 300-600 mg/day resulted in significant reductions in median total seizure rates vs placebo, and zonisamide was generally well tolerated; the most frequently reported adverse events being somnolence, dizziness and anorexia/weight loss."( Zonisamide: its pharmacology, efficacy and safety in clinical trials.
Ben-Menachem, E; Brodie, MJ; Chouette, I; Giorgi, L, 2012
)
2.14
"The first aim of our study was to analyze the adverse events statistically significantly associated with zonisamide, through a systematic review and meta-analysis of available randomized placebo-controlled trials (RCTs)."( The adverse event profile of zonisamide: a meta-analysis.
Di Sabatino, F; Loiacono, G; Verrotti, A; Zaccara, G, 2013
)
0.9
" Assessments included treatment-emergent adverse events (TEAEs), clinical laboratory parameters and weight change."( Safety and tolerability of zonisamide in elderly patients with epilepsy.
Giorgi, L; Patten, A; Segieth, J; Trinka, E, 2013
)
0.69
" Since psychiatric adverse effects, including mania, psychosis, and suicidal ideation, have been associated with its use, it was suggested that the presence of antecedent psychiatric disorders is an important factor associated with the discontinuation of zonisamide therapy in patients with epilepsy."( Psychiatric adverse effects of zonisamide in patients with epilepsy and mental disorder comorbidities.
Cavanna, AE; Seri, S, 2013
)
0.86
" Safety assessments included treatment-emergent adverse events (TEAEs) and clinical laboratory parameters."( Long-term safety and efficacy of zonisamide versus carbamazepine monotherapy for treatment of partial seizures in adults with newly diagnosed epilepsy: results of a phase III, randomized, double-blind study.
Baulac, M; Giorgi, L; Patten, A, 2014
)
0.68
" There were no reports of Stevens-Johnson syndrome or toxic epidermal necrolysis in either group."( Long-term safety and efficacy of zonisamide versus carbamazepine monotherapy for treatment of partial seizures in adults with newly diagnosed epilepsy: results of a phase III, randomized, double-blind study.
Baulac, M; Giorgi, L; Patten, A, 2014
)
0.68
" Assessments included treatment-emergent adverse events (TEAEs), clinical laboratory parameters, vital signs and electrocardiography."( Safety and tolerability of zonisamide in paediatric patients with epilepsy.
Auvin, S; Cross, JH; Giorgi, L; Patten, A, 2014
)
0.7
" In addition, data on the efficacy of zonisamide to reduce seizures and reported adverse events were extracted from the medical records and analyzed."( Zonisamide: pharmacokinetics, efficacy, and adverse events in children with epilepsy.
Dahlin, M; Ohman, I; Wallander, KM, 2014
)
2.12
" The overall efficacy of zonisamide for reducing seizure frequency ≥ 50% was 35% and the most frequent adverse event was fatigue, reported in 23% of the patients."( Zonisamide: pharmacokinetics, efficacy, and adverse events in children with epilepsy.
Dahlin, M; Ohman, I; Wallander, KM, 2014
)
2.15
" The underlying illness, etiology of epilepsy, seizure types, previous and concomitant antiepileptic drugs, dosage, and adverse effects of the drug were collected."( Efficacy and safety of zonisamide in Thai children and adolescents with intractable seizures.
Khongkhatithum, C; Thampratankul, L; Visudtibhan, A, 2015
)
0.73
" Adverse effects include somnolence and weight decrease, but data suggest that long-term treatment with ZNS is safe with only rare newly occurring adverse effects, and good long-term tolerability also regarding mood, behavior, cognition and bone maturation."( The safety and long-term efficacy of zonisamide as adjunctive therapy for focal epilepsy.
Schulze-Bonhage, A, 2015
)
0.69
" The open phase did not reveal new adverse effects."( [Zonisamid in additional treatment of pediatric partial epilepsy: a review of efficacy and safety in randomized double blind pacebo-controlled III phase study].
Belousova, E, 2015
)
0.42
"There are a limited number of anticonvulsant medications that can be administered with an oral loading dose in order to rapidly achieve an effective serum level, and most of these have associated adverse effects."( Safety and tolerability of an oral zonisamide loading dose.
Bazil, CW; Jongeling, AC; Richins, RJ, 2015
)
0.69
"This report is the first to suggest a method of rapidly initiating zonisamide therapy, achieving therapeutic serum levels in a shorter time frame, with an adverse effect profile similar to the recommended titration schedule."( Safety and tolerability of an oral zonisamide loading dose.
Bazil, CW; Jongeling, AC; Richins, RJ, 2015
)
0.93
" However, oral zonisamide appeared to be safe and tolerable in the study."( Safety, tolerability, and effectiveness of oral zonisamide therapy in comparison with intramuscular adrenocorticotropic hormone therapy in infants with West syndrome.
Angappan, D; Malhi, P; Sahu, JK; Singhi, P, 2019
)
1.12
" CONCLUSIONS AND CLINICAL RELEVANCE Twice-daily oral administration of zonisamide to Hispaniolan Amazon parrots resulted in plasma concentrations known to be therapeutic in dogs without evidence of adverse effects on body weight, attitude, and urofeces or clinically relevant changes to hematologic and biochemical variables."( Pharmacokinetics and safety of zonisamide after oral administration of single and multiple doses to Hispaniolan Amazon parrots (Amazona ventralis).
Boothe, DM; de Matos, RE; Guzman, DS; Kass, PH; Keller, KA; Paul-Murphy, JR; Petritz, OA; Visser, M, 2019
)
1.03
" After the exposure period, sperm concentration, motility, morphology, and DNA damage, as biomarkers of reproductive toxic effects, were determined, and histopathological examination of testis was performed."( Reproductive toxic effects and possible mechanisms of zonisamide in male rats.
Atli-Eklioglu, O; Aydogan-Kılıc, G; Baysal, M; Ilgin, S; Karaduman, AB; Kilic, V; Ucarcan, S, 2019
)
0.76
" Other outcomes included the changes in Mini-Mental State Examination (MMSE) and Neuropsychiatric Inventory-10 (NPI-10) scores, and the incidence of adverse events."( Efficacy and Safety of Zonisamide in Dementia with Lewy Bodies Patients with Parkinsonism: A Post Hoc Analysis of Two Randomized, Double-Blind, Placebo-Controlled Trials.
Hasegawa, K; Kochi, K; Konishi, O; Maruyama, H; Odawara, T; Toya, S, 2021
)
0.93
" There was no difference in the incidence of adverse events between the zonisamide and placebo groups except for decreased appetite, which had an increased frequency in the zonisamide 50 mg group compared with placebo."( Efficacy and Safety of Zonisamide in Dementia with Lewy Bodies Patients with Parkinsonism: A Post Hoc Analysis of Two Randomized, Double-Blind, Placebo-Controlled Trials.
Hasegawa, K; Kochi, K; Konishi, O; Maruyama, H; Odawara, T; Toya, S, 2021
)
1.16
" The primary objective was to determine efficacy in terms of proportion with complete spasm resolution, we also intended to determine proportion with at least 50% spasm reduction, hypsarrhythmia resolution, and nature/frequency of adverse effects."( Efficacy, tolerability, and safety of zonisamide in children with epileptic spasms: A systematic review and meta-analysis.
Dawman, L; Panda, P; Panda, PK; Sharawat, IK, 2021
)
0.89
"9-35 mg/kg/day dose with only mild adverse effects in a few patients."( Efficacy, tolerability, and safety of zonisamide in children with epileptic spasms: A systematic review and meta-analysis.
Dawman, L; Panda, P; Panda, PK; Sharawat, IK, 2021
)
0.89
"Zonisamide can reduce spasms in 21% of children with epileptic spasms, without major adverse effects."( Efficacy, tolerability, and safety of zonisamide in children with epileptic spasms: A systematic review and meta-analysis.
Dawman, L; Panda, P; Panda, PK; Sharawat, IK, 2021
)
2.34
" No unexpected neurological or psychiatric adverse events occurred, and no adverse events increased in incidence in the open-label period."( Long-Term Efficacy and Safety of Zonisamide for Treatment of Parkinsonism in Patients With Dementia With Lewy Bodies: An Open-Label Extension of a Phase three Randomized Controlled Trial.
Hasegawa, K; Kajiwara, R; Kosaka, K; Murata, M; Odawara, T; Tagawa, M; Takeuchi, H, 2022
)
1
"Oxaliplatin (OHP) is a platinum-based agent that can cause peripheral neuropathy, an adverse effect in which the dorsal root ganglion (DRG) neurons are targeted."( Pretreatment with Zonisamide Mitigates Oxaliplatin-Induced Toxicity in Rat DRG Neurons and DRG Neuron-Schwann Cell Co-Cultures.
Sango, K; Takaku, S, 2022
)
1.06
" Adverse events reported in the RCTs will be considered in the final safety analysis."( Zonisamide's Efficacy and Safety on Parkinson's Disease and Dementia with Lewy Bodies: A Meta-Analysis and Systematic Review.
Jiang, Z; Kong, L; Liu, H; Wang, Z; Xi, J; Yu, X, 2022
)
2.16
" The mainstay of treatment is with multiple anti-seizure medications (ASMs); however, the ASMs themselves can be associated with psychobehavioural adverse events, and effects (negative or positive) on cognition and sleep."( Psychobehavioural and Cognitive Adverse Events of Anti-Seizure Medications for the Treatment of Developmental and Epileptic Encephalopathies.
Schubert-Bast, S; Strzelczyk, A, 2022
)
0.72
" For safety outcomes, rasagiline was associated with a higher incidence of adverse events than placebo and safinamide."( Comparative efficacy and safety of monoamine oxidase type B inhibitors plus channel blockers and monoamine oxidase type B inhibitors as adjuvant therapy to levodopa in the treatment of Parkinson's disease: a network meta-analysis of randomized controlled
Cai, G; Cai, H; Cui, Y; Feng, T; Lin, F; Su, D; Yan, R, 2023
)
0.91
" Therefore, knowledge about the typical adverse events (AEs) for ASMs and other coadministered drugs (CDs) is essential for practitioners and patients."( Adverse Event Profiles of Antiseizure Medications and the Impact of Coadministration on Drug Tolerability in Adults with Epilepsy.
Knake, S; Kovac, S; Rosenow, F; Strzelczyk, A; van der Goten, M; von Podewils, F; Willems, LM; Zöllner, JP, 2023
)
0.91
" Primary outcomes were the change from baseline in Unified Parkinson's Disease Rating Scale section III (UPDRS-III) and serious adverse events."( Efficacy and Safety of MAO-B Inhibitors Safinamide and Zonisamide in Parkinson's Disease: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.
Abou-Setta, A; Aboulatta, L; Askin, N; Eltonsy, S; Haidar, L; Lavu, A; Peymani, P; Rabbani, R; Zarychanski, R, 2023
)
1.16
" The meta-analysis showed that both medications have a similar safety profile to placebo with regard to serious adverse events."( Efficacy and Safety of MAO-B Inhibitors Safinamide and Zonisamide in Parkinson's Disease: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.
Abou-Setta, A; Aboulatta, L; Askin, N; Eltonsy, S; Haidar, L; Lavu, A; Peymani, P; Rabbani, R; Zarychanski, R, 2023
)
1.16

Pharmacokinetics

Zonisamide has a pharmacokinetic profile favorable for clinical use. There was no pharmacodynamic evidence that zonisamide is likely to reduce the contraceptive effectiveness of OCs containing EE and NOR.

ExcerptReferenceRelevance
" The effects of other antiepileptics on the serum protein binding, erythrocyte distribution and metabolism of ZNS were also studied in vitro to elucidate the mechanism of pharmacokinetic interaction of ZNS."( Pharmacokinetic interaction of zonisamide in rats. Effect of other antiepileptics on zonisamide.
Fukuchi, H; Kimura, M; Kimura, Y; Kitaura, T; Miyake, K; Tanaka, N, 1992
)
0.57
" Additional pharmacokinetic studies will help to establish the change in pharmacokinetic profile that occurs with dosage titration in patients outside Japan."( Zonisamide. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in epilepsy.
Peters, DH; Sorkin, EM, 1993
)
1.73
" The 266 serum concentration data at steady-state after repetitive oral administration were analyzed using the nonlinear mixed effects model (NONMEM) program designed for estimation of population pharmacokinetic parameters."( Population analysis of the dose-dependent pharmacokinetics of zonisamide in epileptic patients.
Hashimoto, Y; Hori, R; Odani, A; Okuno, T; Tanigawara, Y; Yasuhara, M, 1994
)
0.53
" These results suggest that ZNS has little effect on the pharmacokinetic behaviors of other antiepileptic drugs."( Pharmacokinetic interaction of zonisamide in rats. Effect of zonisamide on other antiepileptics.
Fukuchi, H; Kimura, M; Kimura, Y; Kitaura, T; Miyake, K; Tanaka, N, 1993
)
0.57
" When used as a monotherapy, topiramate is eliminated primarily in the urine in an unchanged form with a half-life of 20 to 30 hours; elimination is faster in patients receiving concurrent medication with enzyme-inducing anticonvulsants, in whom the extent of biotransformation becomes more prominent."( The clinical pharmacokinetics of the newer antiepileptic drugs. Focus on topiramate, zonisamide and tiagabine.
Bialer, M; Perucca, E, 1996
)
0.52
"A 56-day pharmacokinetic study of zonisamide was conducted in 24 healthy volunteers."( Steady-state pharmacokinetics of zonisamide, an antiepileptic agent for treatment of refractory complex partial seizures.
Buchanan, RA; Kochak, GM; Padgett, CS; Page, JG; Peters, R, 1998
)
0.86
" For all drugs that are metabolized, half-life is shortened and clearance is increased when patients receive concomitant enzyme-inducing agents such as barbiturates, phenytoin, and carbamazepine."( The clinical pharmacokinetics of the new antiepileptic drugs.
Perucca, E, 1999
)
0.3
"The pharmacokinetic properties of a drug are the primary deter-minant of the extent and duration of drug action, and influence susceptibility to clinically important drug interactions."( The ideal pharmacokinetic properties of an antiepileptic drug: how close does levetiracetam come?
Johannessen, SI; Perucca, E, 2003
)
0.32
" Three pharmacokinetic profiles were performed: on days -7 and -1, to assess pharmacokinetic parameters of oral phenytoin administered alone, and on day 35, after 14 days of zonisamide treatment, to evaluate the effect of zonisamide on phenytoin pharmacokinetics and to characterize zonisamide pharmacokinetics in the presence of phenytoin."( Lack of a clinically significant effect of zonisamide on phenytoin steady-state pharmacokinetics in patients with epilepsy.
Garnett, WR; Levy, RH; Pan, WJ; Ragueneau-Majlessi, I; Rosenfeld, W; Schmerler, M; Shah, J, 2004
)
0.78
" Zonisamide has a pharmacokinetic profile favorable for clinical use."( Zonisamide: chemistry, mechanism of action, and pharmacokinetics.
Leppik, IE, 2004
)
2.68
"Several antiepileptic drugs have clinically significant pharmacokinetic interactions with oral contraceptives (OCs) that may result in contraceptive failure."( Effect of zonisamide on the pharmacokinetics and pharmacodynamics of a combination ethinyl estradiol-norethindrone oral contraceptive in healthy women.
Dai, Y; Griffith, SG, 2004
)
0.73
"035 mg and norethindrone [NOR] 1 mg) and on pharmacodynamic variables that may be increased in the event of reduced contraceptive efficacy (concentrations of serum luteinizing hormone [LH], follicle-stimulating hormone [FSH], and progesterone)."( Effect of zonisamide on the pharmacokinetics and pharmacodynamics of a combination ethinyl estradiol-norethindrone oral contraceptive in healthy women.
Dai, Y; Griffith, SG, 2004
)
0.73
" There was no pharmacodynamic evidence that zonisamide is likely to reduce the contraceptive effectiveness of OCs containing EE and NOR."( Effect of zonisamide on the pharmacokinetics and pharmacodynamics of a combination ethinyl estradiol-norethindrone oral contraceptive in healthy women.
Dai, Y; Griffith, SG, 2004
)
0.99
" Three pharmacokinetic profiles were obtained: on days -7 and -1, to assess pharmacokinetic parameters of oral valproic acid administered alone, and on day 35, after 14 days of zonisamide treatment at the maximal tolerated dose, to evaluate the effect of zonisamide on valproic acid pharmacokinetics and to characterise zonisamide pharmacokinetics in the presence of valproic acid."( Lack of pharmacokinetic interactions between steady-state zonisamide and valproic acid in patients with epilepsy.
Brodie, M; Grundy, JS; Levy, RH; Ragueneau-Majlessi, I; Shah, J; Smith, D, 2005
)
0.77
"Seventeen patients completed the study, with 16 patients contributing to the pharmacokinetic analyses."( Lack of pharmacokinetic interactions between steady-state zonisamide and valproic acid in patients with epilepsy.
Brodie, M; Grundy, JS; Levy, RH; Ragueneau-Majlessi, I; Shah, J; Smith, D, 2005
)
0.57
" For drugs that are eliminated renally completely unchanged (gabapentin, pregabalin and vigabatrin) or mainly unchanged (levetiracetam and topiramate), the pharmacokinetic variability is less pronounced and more predictable."( Pharmacokinetic variability of newer antiepileptic drugs: when is monitoring needed?
Johannessen, SI; Tomson, T, 2006
)
0.33
" The pharmacokinetics of the 260 PB concentrations at a steady-state obtained from 79 patients was described with a one-compartment open pharmacokinetic model with first-order elimination."( Population estimation of the effects of cytochrome P450 2C9 and 2C19 polymorphisms on phenobarbital clearance in Japanese.
Goto, S; Ishitsu, T; Murata, T; Nakada, N; Nakagawa, K; Seo, T; Ueda, N, 2007
)
0.34
" Older-generation antiepileptic drugs (AEDs) are well known for their pharmacokinetic interaction potential, which generally results from alterations in the metabolism of concomitant drugs due to effects on the cytochrome P450 (CYP) and uridine glucuronyl transferase enzyme systems."( Pharmacokinetics and drug interactions with zonisamide.
Brodie, M; Sills, G, 2007
)
0.6
" Pharmacokinetic parameters obtained with a single administration of ZNS at 10mg/day were as follows: Cmax=13."( Pharmacokinetics and toxicity of zonisamide in cats.
Fujita, M; Hasegawa, D; Kobayashi, M; Kuwabara, T; Ohmura, T; Orima, H, 2008
)
0.63
" The pharmacokinetics of the 282 ZNS concentrations at a steady state obtained from 99 Japanese epileptic patients was performed with a nonlinear mixed-effect modeling program, using a one-compartment open pharmacokinetic model with first-order elimination."( Population estimation regarding the effects of cytochrome P450 2C19 and 3A5 polymorphisms on zonisamide clearance.
Hashimoto, N; Higa, Y; Ishitsu, T; Nakagawa, K; Okada, Y; Seo, T; Wanibuchi, A, 2008
)
0.57
" The developed assay method was applied to a pharmacokinetic study in human volunteers."( Simultaneous estimation of four proton pump inhibitors--lansoprazole, omeprazole, pantoprazole and rabeprazole: development of a novel generic HPLC-UV method and its application to clinical pharmacokinetic study.
Bharathi, DV; Chatki, PK; Hotha, KK; Jagadeesh, B; Mullangi, R; Naidu, A; Thriveni, K, 2009
)
0.35
" The present study was aimed to investigate the potential effects of pregnancy on the pharmacokinetic profile of zonisamide (ZNM) in the rabbit."( Impact of pregnancy on zonisamide pharmacokinetics in rabbits.
Matar, KM, 2013
)
0.91
" The developed method was successfully applied for a pharmacokinetic study by measuring ZNM in rabbit plasma samples."( A simple and accurate liquid chromatography-tandem mass spectrometry method for quantification of zonisamide in plasma and its application to a pharmacokinetic study.
Matar, KM, 2014
)
0.62
" Children have a different pharmacokinetic profile than adults and an adult dose regimen cannot be directly translated into pediatric use."( Zonisamide: pharmacokinetics, efficacy, and adverse events in children with epilepsy.
Dahlin, M; Ohman, I; Wallander, KM, 2014
)
1.85
" The shortage of pharmacokinetic studies of zonisamide in children highlights the need for research of this kind."( Zonisamide: pharmacokinetics, efficacy, and adverse events in children with epilepsy.
Dahlin, M; Ohman, I; Wallander, KM, 2014
)
2.11
" Disappearance half-life (hours) and mean time to maximum concentration (hours) were not significantly different between methods of administration."( Pharmacokinetics of single-dose rectal zonisamide administration in normal dogs.
Boothe, D; Brewer, DM; Cerda-Gonzalez, S; Dewey, CW; Van Horne, K,
)
0.4
"To develop a population-based pharmacokinetic model for the oral antiepileptic drug zonisamide using a cohort of healthy (nonepileptic) subjects and evaluate the effect of individual factors on the pharmacokinetics of zonisamide."( Population pharmacokinetics of zonisamide after oral administration in healthy Chinese volunteers.
Bi, S; Chen, Y; Dai, Q; Liu, Y; Lu, W; Qiu, X; Sun, F; Xia, P; Xiang, R; Xiong, L; Yang, B; Yu, M, 2016
)
0.94
" RESULTS Mean maximum plasma concentration, time to maximum plasma concentration, mean residence time, and elimination half-life did not differ significantly among the 4 treatments."( Pharmacokinetics of zonisamide following rectal administration to healthy dogs.
Boothe, DM; Hodshon, AJ; Michaels, JR; Thomas, WB; Williams, L, 2016
)
0.76
" A population pharmacokinetic approach and nonlinear mixed effects modeling were used to analyze the data."( Population pharmacokinetics of extended-release levetiracetam in epileptic dogs when administered alone, with phenobarbital or zonisamide.
Muñana, KR; Nettifee, JA; Otamendi, AJ; Papich, MG, 2018
)
0.69
" Mean plasma elimination half-life for the single- and multiple-dose trials was 13."( Pharmacokinetics and safety of zonisamide after oral administration of single and multiple doses to Hispaniolan Amazon parrots (Amazona ventralis).
Boothe, DM; de Matos, RE; Guzman, DS; Kass, PH; Keller, KA; Paul-Murphy, JR; Petritz, OA; Visser, M, 2019
)
0.8
"To our knowledge, this is the only research study to date that has attempted to link basal metabolomic status with pharmacokinetic parameters of zonisamide."( Pharmacometabolomics applied to zonisamide pharmacokinetic parameter prediction.
Borobia, AM; Carcás Sansuan, AJ; Dapía, I; Díaz, L; Frías, J; García Bartolomé, A; García, I; Guerra, P; Martínez-Ávila, JC; Tong, HY, 2018
)
0.96

Compound-Compound Interactions

Zonisamide is metabolized by recombinant CYP3A4 and CYP2C19. The metabolism is inhibited to a variable extent by known CYP 3A4/5 substrates and/or inhibitors in human liver microsomes. In vitro-in vivo predictive calculations suggest that several compounds demonstrating CYP1A4-affinity might cause in vivo drug-drug interactions with zonisamide.

ExcerptReferenceRelevance
"Ten expressed human CYPs and human liver microsomes were used in the experiments for the identification of enzymes responsible for zonisamide metabolism and for the prediction of drug-drug interactions of zonisamide metabolism in humans from in vitro data, respectively."( Prediction of drug-drug interactions of zonisamide metabolism in humans from in vitro data.
Kitada, M; Kiuchi, M; Nakamura, H; Nakasa, H; Ohmori, S; Ono, S; Tsutsui, M, 1998
)
0.77
"We demonstrated that: (1) zonisamide is metabolized by recombinant CYP3A4, CYP2C19 and CYP3A5, (2) the metabolism is inhibited to a variable extent by known CYP3A4/5 substrates and/or inhibitors in human liver microsomes, and (3) in vitro-in vivo predictive calculations suggest that several compounds demonstrating CYP3A4-affinity might cause in vivo drug-drug interactions with zonisamide."( Prediction of drug-drug interactions of zonisamide metabolism in humans from in vitro data.
Kitada, M; Kiuchi, M; Nakamura, H; Nakasa, H; Ohmori, S; Ono, S; Tsutsui, M, 1998
)
0.87
" Caution may be necessary when zonisamide is given with phenobarbital and when antiepileptic therapy is changed from phenobarbital to zonisamide."( Pharmacokinetics of zonisamide and drug interaction with phenobarbital in dogs.
Egashira, N; Fujiwara, M; Fukunaga, K; Matsuo, E; Mishima, K; Muto, M; Orito, K; Saito, M; Takikawa, S, 2008
)
0.96
"The multiple drug interactions in which CAIs are involved should be carefully considered when such drugs are used in combination with the drug classes mentioned above, as the risks of developing toxicity and serious side effects if the dosages are not adjusted are high."( Drug interaction considerations in the therapeutic use of carbonic anhydrase inhibitors.
Supuran, CT, 2016
)
0.43

Bioavailability

Zonisamide well absorbed with maximum concentration achieved in 2 to 5 h. Oral bioavailability of zonisamide is excellent in healthy human volunteers.

ExcerptReferenceRelevance
"27 l/kg in a typical 33-kg patient, assuming that the bioavailability of orally administered zonisamide is 100%."( Population analysis of the dose-dependent pharmacokinetics of zonisamide in epileptic patients.
Hashimoto, Y; Hori, R; Odani, A; Okuno, T; Tanigawara, Y; Yasuhara, M, 1994
)
0.75
" It is well absorbed from the gastrointestinal tract and negligibly bound to plasma proteins."( The clinical pharmacokinetics of the newer antiepileptic drugs. Focus on topiramate, zonisamide and tiagabine.
Bialer, M; Perucca, E, 1996
)
0.52
" However, the bioavailability of the three preparations was approximately 100%."( Utility of a rectal suppository containing the antiepileptic drug zonisamide.
Higuchi, S; Mishima, M; Nagatomi, A; Ohdo, S; Tsuzuki, O, 1997
)
0.53
" Oral bioavailability of zonisamide is excellent in healthy human volunteers."( Clinical pharmacology and therapeutic drug monitoring of zonisamide.
Mimaki, T, 1998
)
0.85
" After oral administration, absorption is rapid and relatively efficient for the new AEDs, the most notable exception being gabapentin, whose bioavailability decreases with increasing dosage."( The clinical pharmacokinetics of the new antiepileptic drugs.
Perucca, E, 1999
)
0.3
" time curve, apparent elimination half-life, and bioavailability of zonisamide."( Pharmacokinetics of zonisamide and drug interaction with phenobarbital in dogs.
Egashira, N; Fujiwara, M; Fukunaga, K; Matsuo, E; Mishima, K; Muto, M; Orito, K; Saito, M; Takikawa, S, 2008
)
0.9
" Oral bioavailability was 68 +/- 12%; fraction of unbound drug approximated 60%."( Disposition and safety of zonisamide after intravenous and oral single dose and oral multiple dosing in normal hound dogs.
Boothe, DM; Perkins, J, 2008
)
0.65
" Mean relative bioavailability of PEG-R (85 ± 69%) was significantly higher than that of H2O-R (53 ± 37%) (P = ."( Pharmacokinetics of single-dose rectal zonisamide administration in normal dogs.
Boothe, D; Brewer, DM; Cerda-Gonzalez, S; Dewey, CW; Van Horne, K,
)
0.4
" The most widely used MAO-B inhibitor to maintain the bioavailability of dopamine in the brain of PD patients is L-deprenyl, despite of its potential side-effects."( Garcinol, an effective monoamine oxidase-B inhibitor for the treatment of Parkinson's disease.
Bhattacharya, P; Borah, A; Chakrabarty, J; Dutta, A; Mazumder, MK; Paul, R; Phukan, BC, 2018
)
0.48
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51
" Since zonisamide is marketed as oral formulations, the present study aimed at exploring the potential of the intranasal route to centrally administer zonisamide, evaluating the systemic bioavailability of zonisamide and comparing its brain, lung and kidney pharmacokinetics after intranasal, oral and intravenous administrations."( Pre-Clinical Assessment of the Nose-to-Brain Delivery of Zonisamide After Intranasal Administration.
Alves, G; Bicker, J; Carona, A; Falcão, A; Fortuna, A; Gonçalves, J; Vitorino, C, 2020
)
1.26
"Intranasal route revealed a low absolute bioavailability (54."( Pre-Clinical Assessment of the Nose-to-Brain Delivery of Zonisamide After Intranasal Administration.
Alves, G; Bicker, J; Carona, A; Falcão, A; Fortuna, A; Gonçalves, J; Vitorino, C, 2020
)
0.8

Dosage Studied

The patients have had no other physical or mental problems and decreasing the dosage of zonisamide reduced the problems. There is no apparent clinically significant effect of steady-state dosing of Zonisamide on valproic acid pharmacokinetics.

ExcerptRelevanceReference
" These results suggest that dosage regimens on the basis of body surface area would be more accurate than those on a body weight basis and that there is little effect of other antiepileptics on the serum protein binding of ZNS."( Factors influencing serum concentration of zonisamide in epileptic patients.
Fukuchi, H; Harada, Y; Kimura, M; Kimura, Y; Kitaura, T; Miyake, K; Tanaka, N, 1992
)
0.55
" In rats dosed with [14C]zonisamide (100 mg/kg, ip) 86."( Metabolism of the anticonvulsant agent zonisamide in the rat.
Stiff, DD; Zemaitis, MA,
)
0.7
" These findings suggest that the dosage of zonisamide in epileptic patients might need to be varied depending on the comedication."( Comparative pharmacokinetics of zonisamide (CI-912) in epileptic patients on carbamazepine or phenytoin monotherapy.
Buchanan, RA; Friel, PN; Levy, RH; McLean, JR; Ojemann, LM; Shastri, RA; Wilensky, AJ, 1986
)
0.82
" [14C]AD-810 was found to be completely absorbed from digestive tracts in animals, since urinary and biliary excretion accounted for virtually total recovery of dosed radioactivity."( Absorption, distribution and excretion of 3-(sulfamoyl[14C]methyl)-1,2-benziosoxazole (AD-810) in Rats, Dogs and Monkeys and of AD-810 in Men.
Fujii, T; Hashimoto, M; Kagemoto, A; Maeda, T; Matsumoto, K; Miyazaki, H, 1983
)
0.27
" Plasma and whole blood concentrations were measured by a high-performance liquid chromatograph method after a single dose and up to and at steady state with one or two dosage regimens."( Nonlinear pharmacokinetics of CI-912 in adult epileptic patients.
Berent, S; Donofrio, PD; Sackellares, JC; Sakmar, E; Wagner, JG, 1984
)
0.27
" Additional pharmacokinetic studies will help to establish the change in pharmacokinetic profile that occurs with dosage titration in patients outside Japan."( Zonisamide. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in epilepsy.
Peters, DH; Sorkin, EM, 1993
)
1.73
" ZNS daily dosage is 400-600 mg."( Antiepileptic drugs in development: prospects for the near future.
Leppik, IE, 1994
)
0.29
" The population pharmacokinetic parameters of zonisamide will be useful for designing dosage regimens in epileptic patients."( Population analysis of the dose-dependent pharmacokinetics of zonisamide in epileptic patients.
Hashimoto, Y; Hori, R; Odani, A; Okuno, T; Tanigawara, Y; Yasuhara, M, 1994
)
0.79
" The t 1/2 and AUC values of PB were significantly increased by ZNS coadministration, and a significant decrease in the Vd/F value of PHT was observed after multiple dosing of ZNS."( Pharmacokinetic interaction of zonisamide in rats. Effect of zonisamide on other antiepileptics.
Fukuchi, H; Kimura, M; Kimura, Y; Kitaura, T; Miyake, K; Tanaka, N, 1993
)
0.57
" After trial and error, we found that a reduction of the dosage after long-term anesthesia with high-dose administrations of barbiturate should be made very slowly."( [Experience in managing refractory status epilepticus caused by viral encephalitis under long-term anesthesia with barbiturate: a case report].
Fujioka, Y; Ohori, N; Ohta, M, 1998
)
0.3
" The dosage was initially 2-4 mg/kg per day, and then was increased by 2-5 mg/kg every 2-4 days until the seizures disappeared."( Treatment of infantile spasms with zonisamide.
Hanai, T; Narazaki, O; Yanai, S, 1999
)
0.58
" Recommended initial adult dosage in Japan is 100-200 mg/d, increased if necessary to 200-400 mg/d, up to a maximum of 600 mg/d."( Zonisamide: a new antiepileptic drug.
Mathews, S; Oommen, KJ,
)
1.57
" A dosage of 100 mg/d produced a 20."( Randomized controlled trial of zonisamide for the treatment of refractory partial-onset seizures.
Ayala, R; Faught, E; Leppik, IE; Montouris, GG, 2001
)
0.6
" The minimal effective dosage was 100 mg/d, but 400 mg/d was the most effective dosage."( Randomized controlled trial of zonisamide for the treatment of refractory partial-onset seizures.
Ayala, R; Faught, E; Leppik, IE; Montouris, GG, 2001
)
0.6
" The patients have had no other physical or mental problems and decreasing the dosage of zonisamide reduced the problems."( Selective mutism and obsessive compulsive disorders associated with zonisamide.
Hirai, K; Jozaki, K; Kimiya, S; Kumagai, N; Seki, T; Tabata, K, 2002
)
0.77
" Placebo dosing was identical."( Zonisamide for weight loss in obese adults: a randomized controlled trial.
Franciscy, DM; Gadde, KM; Krishnan, KR; Wagner, HR, 2003
)
1.76
" Although its half-life is relatively short (6 to 8 hours), its duration of action is longer than anticipated from its pharmacokinetics in plasma, and a twice-daily dosing regimen is adequate to produce the desired response."( The ideal pharmacokinetic properties of an antiepileptic drug: how close does levetiracetam come?
Johannessen, SI; Perucca, E, 2003
)
0.32
"This study was designed to assess the safety of 25- and 50-mg dosage strengths of zonisamide for initial titration in patients with epilepsy."( Safety of 25- and 50-mg capsules in the initiation of zonisamide therapy in patients with epilepsy: an uncontrolled, open-label study.
Anthony, S; James, SP; Miller, GS; Montouris, G; Uthman, BM, 2004
)
0.8
" After a screening visit, subjects began zonisamide therapy at a dosage depending on their body weight."( Safety of 25- and 50-mg capsules in the initiation of zonisamide therapy in patients with epilepsy: an uncontrolled, open-label study.
Anthony, S; James, SP; Miller, GS; Montouris, G; Uthman, BM, 2004
)
0.84
" Of these subjects, 125 reached at least the 100-mg dosage before terminating the study."( Safety of 25- and 50-mg capsules in the initiation of zonisamide therapy in patients with epilepsy: an uncontrolled, open-label study.
Anthony, S; James, SP; Miller, GS; Montouris, G; Uthman, BM, 2004
)
0.57
" Despite these limitations, the 25- and 50-mg zonisamide dosage formulations were well tolerated in this study."( Safety of 25- and 50-mg capsules in the initiation of zonisamide therapy in patients with epilepsy: an uncontrolled, open-label study.
Anthony, S; James, SP; Miller, GS; Montouris, G; Uthman, BM, 2004
)
0.83
" Oral zonisamide was administered as an additional therapy at a dosage adequate to achieve serum drug concentrations of 10 to 40 microg/mL."( Zonisamide therapy for refractory idiopathic epilepsy in dogs.
Berg, JM; Boothe, DM; Budsberg, SC; Dewey, CW; Guiliano, R; Joseph, RJ; Kortz, GD,
)
2.05
" Dosage was gradually increased up to 200 to 500 mg/day, and the seizures were controlled satisfactorily."( Dialyzability of the antiepileptic drug zonisamide in patients undergoing hemodialysis.
Fukuda, F; Ijiri, Y; Inoue, T; Kobayashi, T; Shibahara, N; Suzuki, K; Takenaka, H; Tanaka, K, 2004
)
0.59
" For patients undergoing daytime hemodialysis sessions every 2 or 3 days, the usual dosage of ZNS (4-8 mg/kg/day) may be prescribed once a day in the evening."( Dialyzability of the antiepileptic drug zonisamide in patients undergoing hemodialysis.
Fukuda, F; Ijiri, Y; Inoue, T; Kobayashi, T; Shibahara, N; Suzuki, K; Takenaka, H; Tanaka, K, 2004
)
0.59
" Patients received a mean (+/- SD) zonisamide dosage of 236 (+/- 68) mg/day."( Acute treatment of bipolar depression with adjunctive zonisamide: a retrospective chart review.
Baldassano, CF; Chang, A; Ghaemi, SN; Lipari, M; Lyman, A, 2004
)
0.85
" ZNS was initiated at 2mg/kg; daily dosage was doubled at weekly intervals to achieve maintenance dosage (8."( Zonisamide monotherapy with once-daily dosing in children with cryptogenic localization-related epilepsies: clinical effects and pharmacokinetic studies.
Miura, H, 2004
)
1.77
" However, since zonisamide is metabolized by cytochrome P450, liver enzyme-inducing AEDs will increase zonisamide clearance, and dosage adjustments may be necessary when it is used in combination with certain AEDs."( Zonisamide: chemistry, mechanism of action, and pharmacokinetics.
Leppik, IE, 2004
)
2.11
" Median zonisamide maintenance dosage was 400mg/day, and the average therapeutic blood level was 16."( Zonisamide clinical trials: European experience.
Brodie, MJ, 2004
)
2.2
" Based on the lack of clinically relevant in vitro and in vivo effects, adjustment of carbamazepine dosing should not be required with concomitant zonisamide administration."( Carbamazepine pharmacokinetics are not affected by zonisamide: in vitro mechanistic study and in vivo clinical study in epileptic patients.
Bergen, D; Garnett, W; Grundy, JS; Levy, RH; Mather, G; Ragueneau-Majlessi, I; Rosenfeld, W; Shah, J, 2004
)
0.78
"This article reviews preclinical and clinical data on the efficacy and tolerability of these 4 AEDs in the management of neuropathic pain, as well as the pharmacokinetics, drug-interaction potential, adverse effects, and dosing of these agents, with an emphasis on their use in older individuals."( Oxcarbazepine, topiramate, zonisamide, and levetiracetam: potential use in neuropathic pain.
Guay, DR, 2003
)
0.62
" For EE, the mean (SD) AUC over a 24-hour dosing interval (AUC(tau)) was 1139 (317) pg."( Effect of zonisamide on the pharmacokinetics and pharmacodynamics of a combination ethinyl estradiol-norethindrone oral contraceptive in healthy women.
Dai, Y; Griffith, SG, 2004
)
0.73
"In these healthy volunteers, steady-state zonisamide dosing had no clinically significant effect on the pharmacokinetics of EE or NOR."( Effect of zonisamide on the pharmacokinetics and pharmacodynamics of a combination ethinyl estradiol-norethindrone oral contraceptive in healthy women.
Dai, Y; Griffith, SG, 2004
)
0.99
" The latter were mostly associated with dosage alterations in concomitant antiepileptic drugs."( Clinical experience with zonisamide monotherapy and adjunctive therapy in children with epilepsy at a tertiary care referral center.
Aldridge, J; Kim, HL; Rho, JM, 2005
)
0.63
" We designed three protocols to raise the serum ZNS concentration (SZC): (1) increase the dose in three steps, from 3 to 10 mg/kg every 3 days, (2) increase the dose from 5 to 10 mg/kg over 3-7 days, and (3) start with 10 mg/kg and maintain this dosage for 2 weeks."( Zonisamide for West syndrome: a comparison of clinical responses among different titration rate.
Funatsuka, M; Hayashi, K; Imai, K; Oguni, H; Osawa, M; Yanagaki, S; Yoshii, K, 2005
)
1.77
" Physicians were advised to initiate zonisamide at 100 mg/day and titrate either to a clinical response or a maximum dosage of 600 mg/day."( Zonisamide: physician and patient experiences.
Marmarou, A; Pellock, JM,
)
1.85
" Steady-state dosing of zonisamide (200mg twice daily) had no statistically significant effect on the mean (+/- SD) maximum observed plasma concentration (C(max)) [70."( Lack of pharmacokinetic interactions between steady-state zonisamide and valproic acid in patients with epilepsy.
Brodie, M; Grundy, JS; Levy, RH; Ragueneau-Majlessi, I; Shah, J; Smith, D, 2005
)
0.88
"There is no apparent clinically significant effect of steady-state dosing of zonisamide on valproic acid pharmacokinetics, and valproic acid did not appear to affect the pharmacokinetics of zonisamide, indicating that no dosage adjustment of either drug should be required when they are used in combination in patients with epilepsy."( Lack of pharmacokinetic interactions between steady-state zonisamide and valproic acid in patients with epilepsy.
Brodie, M; Grundy, JS; Levy, RH; Ragueneau-Majlessi, I; Shah, J; Smith, D, 2005
)
0.8
" This chart-review study was conducted to evaluate the efficacy, safety, and appropriate dosage of zonisamide for treating seizures in pediatric and adolescent patients."( Use of zonisamide in pediatric patients.
Brotherton, T; Santos, CC, 2005
)
1
" The study drug was titrated over a 6-week period and continued at a fixed dosage for a 6-week maintenance period."( Zonisamide in the treatment of painful diabetic neuropathy: a randomized, double-blind, placebo-controlled pilot study.
Atli, A; Dogra, S,
)
1.57
" Effective control of partial seizures (up to 51% decrease in seizure frequency) is attained at doses of >or=300 mg/day, and optimal titration and maintenance dosing schedules have been established."( Introduction to zonisamide.
Baulac, M, 2006
)
0.68
"3 months (range, 3-46 months), and the average zonisamide dosage was 324 mg/day (range, 100-1000 mg/day)."( Long-term efficacy and safety of monotherapy and adjunctive therapy with zonisamide.
Tisdell, J; Tosches, WA, 2006
)
0.82
" Demographic data, zonisamide dosage and duration of treatment were collected and analysed."( Zonisamide for migraine prophylaxis in refractory patients.
Ashkenazi, A; Benlifer, A; Korenblit, J; Silberstein, SD, 2006
)
2.1
" For these older drugs it has been common practice to adjust the dosage to achieve a serum drug concentration within a predefined 'therapeutic range', representing an interval where most patients are expected to show an optimal response."( Pharmacokinetic variability of newer antiepileptic drugs: when is monitoring needed?
Johannessen, SI; Tomson, T, 2006
)
0.33
" ZNS was initiated at a dosage of 100 mg/day and escalated to 200 mg/day at day 14."( A double-blind placebo-controlled trial of zonisamide (zonegran) in the treatment of essential tremor.
Hauser, RA; Sanchez-Ramos, J; Staffetti, JF; Sullivan, KL; Ward, CL; Zesiewicz, TA, 2007
)
0.6
" Consequently, carbamazepine, phenytoin, and phenobarbital all increase its clearance, an interaction that may necessitate a dosage increase, but which will also permit more rapid attainment of steady-state zonisamide concentrations."( Pharmacokinetics and drug interactions with zonisamide.
Brodie, M; Sills, G, 2007
)
0.79
" It included (1) the drugs used for the treatment, (2) their dosage, and (3) the dosage and the schedule of adrenocorticotropic hormone therapy."( Current treatment of West syndrome in Japan.
Ito, M; Okumura, A; Ozawa, H; Tsuji, T; Watanabe, K, 2007
)
0.34
" At that point in time the mean ZNS dosage was 344 mg and mean TPM dosage was 398 mg."( [Anticonvulsant treatment with zonisamide added to topiramate. A preliminary treatment analysis in 19 patients].
Bauer, J; Bös, M, 2007
)
0.63
" Average zonisamide dosage was 215 mg/day and average duration of the treatment was 121 days."( [Zonisamide in refractory essential tremor].
Anciones, B; Bermejo, PE; Dorado, R; Ruiz-Huete, C,
)
1.46
"To investigate whether zonisamide remains effective and well tolerated in the treatment of refractory partial epilepsy during long-term treatment and with flexible dosing in clinical practice."( Long-term safety and efficacy of zonisamide in patients with refractory partial-onset epilepsy.
Marshall, A; Wroe, SJ; Yeates, AB, 2008
)
0.94
"Patients with refractory partial epilepsy who completed a fixed-dose, randomized, double-blind clinical trial were recruited in an open-label extension study with adjustment of zonisamide and other antiepileptic drug dosage according to the treating physician's usual clinical practice."( Long-term safety and efficacy of zonisamide in patients with refractory partial-onset epilepsy.
Marshall, A; Wroe, SJ; Yeates, AB, 2008
)
0.82
"Flexible dosing with zonisamide demonstrated a good safety profile and sustained efficacy in the long-term adjunctive treatment of refractory partial epilepsy."( Long-term safety and efficacy of zonisamide in patients with refractory partial-onset epilepsy.
Marshall, A; Wroe, SJ; Yeates, AB, 2008
)
0.95
"The ZNS daily dosage varied between 100 mg and 500 mg (mean 368 mg)."( [Zonisamide as add-on treatment for focal epilepsies. An outcome analysis of 74 patients].
Bauer, J; Wellmer, J; Wellmer, S, 2008
)
1.26
"The purpose of this study was to determine an oral dosing regimen of zonisamide in healthy dogs such that therapeutic concentrations would be safely reached and maintained at steady-state."( Disposition and safety of zonisamide after intravenous and oral single dose and oral multiple dosing in normal hound dogs.
Boothe, DM; Perkins, J, 2008
)
0.88
" ZNS mean dosage was of 283."( Efficacy and tolerability of zonisamide as add-on in brain tumor-related epilepsy: preliminary report.
Carapella, CM; Dinapoli, L; Jandolo, B; Maschio, M; Pompili, A; Saveriano, F; Vidiri, A, 2009
)
0.64
"To assess the efficacy and tolerability of zonisamide in a study allowing flexible dosing in a more diverse and less refractory population than assessed in randomized controlled trials."( Flexible dosing of adjunctive zonisamide in the treatment of adult partial-onset seizures: a non-comparative, open-label study (ZEUS).
Baker, G; Dupont, S; Ellis, S; Giallonardo, AT; Smith, P; Springub, J; Striano, S; Trinka, E; Yeates, A, 2010
)
0.91
" The final dosage of zonisamide was 50-200 mg/day, with the 100 mg/day being the most frequently administered dose."( [Zonisamide in the preventive treatment of refractory migraine].
Alvaro-González, LC; Arias, M; Blanco, M; Bueno, V; Caminero, A; Díaz-González, M; Forcea, N; García-Moncó, JC; Gracia-Naya, M; Guerrero-Peral, AL; Hernando, I; Iglesias--Díez, F; Leira, R; Maciñeiras-Montero, JL; Mateos, V; Mederer-Hengstl, S; Ortega, F; Oterino, A; Pascual-Gómez, J; Pato-Pato, A; Pego-Reigosa, R; Pérez, C; Rodríguez, R; Sánchez-Herrero, J; Santos-García, D,
)
1.36
" Zonisamide was initiated at a dosage of 100 mg/d, which was increased by 100 mg/d every 2 weeks for 8 weeks to a maximum dosage of 500 mg/d."( Placebo-controlled trial of zonisamide for the treatment of alcohol dependence.
Arias, AJ; Covault, J; Feinn, R; Kranzler, HR; Oncken, C, 2010
)
1.56
" Zonisamide was titrated to a target dosage of 300 or 400 mg/day."( Efficacy and safety of adjunctive zonisamide in adult patients with refractory partial-onset epilepsy: a randomized, double-blind, placebo-controlled trial.
Chen, Y; Hu, Y; Lu, Y; Wang, X; Xiao, F; Xiao, Z; Yu, W, 2011
)
1.56
" Zonisamide is a second-generation antiepileptic drug (AED) that has broad-spectrum efficacy, a favorable side-effect profile and simpler dosing than earlier drugs."( Zonisamide in the treatment of epilepsy.
Holder, JL; Wilfong, AA, 2011
)
2.72
"008), but was not correlated with patients' age, results of lipid profile, and dosage of zonisamide."( Low serum leptin level is associated with zonisamide-induced weight loss in overweight female epilepsy patients.
Kim, DW; Park, KS; Yoo, MW, 2012
)
0.86
" Because clinical trials are conducted under tightly controlled conditions, using rigid dosing schedules and employing strict exclusion/exclusion criteria, there is a need for 'real-world' evidence of an antiepileptic drug's effectiveness and tolerability in clinical practice, where patients are much more diverse in terms of clinical characteristics and treatment is tailored to the individual's specific needs."( Zonisamide in clinical practice.
Dupont, S; Stefan, H, 2012
)
1.82
") Interventions were daily dosing with placebo (n = 74), 200 mg of zonisamide (n = 76), or 400 mg of zonisamide (n = 75), in addition to diet and lifestyle counseling by a dietitian for 1 year."( Zonisamide for weight reduction in obese adults: a 1-year randomized controlled trial.
Allison, DB; Bray, GA; Gadde, KM; Kopping, MF; Wagner, HR; Yonish, GM, 2012
)
2.06
" Once-daily dosing is indicated, considering the long plasma half-life and linear pharmacokinetics of the drug."( Profile of once-daily zonisamide as monotherapy for treatment of partial seizures in adults.
Mula, M, 2013
)
0.7
" During the subsequent open-label period (45-57 weeks), zonisamide dosing could be adjusted according to tolerability/response."( Adjunctive zonisamide therapy in the long-term treatment of children with partial epilepsy: results of an open-label extension study of a phase III, randomized, double-blind, placebo-controlled trial.
Bradshaw, K; Giorgi, L; Guerrini, R; Rosati, A, 2014
)
1.04
" The mean dosage of ZNS was 388 mg."( Zonisamide for refractory juvenile absence epilepsy.
Crespel, A; Gelisse, P; Genton, P; Serafini, A; Velizarova, R, 2014
)
1.85
" Patients continued their randomized treatment, with dosing adjusted according to tolerability/response (zonisamide 200-500 mg/day; carbamazepine 400-1,200 mg/day)."( Long-term safety and efficacy of zonisamide versus carbamazepine monotherapy for treatment of partial seizures in adults with newly diagnosed epilepsy: results of a phase III, randomized, double-blind study.
Baulac, M; Giorgi, L; Patten, A, 2014
)
0.9
" The patients were given ZNS as add-on treatment, and the ZNS dosing and the visit frequency were governed by the treating physician."( Retention rate of zonisamide in intractable epilepsy.
Andersen, H; Lindstrøm, P; Nakken, KO, 2015
)
0.75
" Dogs tolerated all dosing forms with no evidence of adverse effects."( Pharmacokinetics of single-dose rectal zonisamide administration in normal dogs.
Boothe, D; Brewer, DM; Cerda-Gonzalez, S; Dewey, CW; Van Horne, K,
)
0.4
" Pronounced threshold increases were observed following administration of a constant zonisamide dosage combined with different doses of perampanel."( Synergism of perampanel and zonisamide in the rat amygdala kindling model of temporal lobe epilepsy.
Komori, T; Potschka, H; Rettenbeck, ML; Russmann, V; Salvamoser, JD, 2016
)
0.95
" An additional 9 subjects (22-24 years) were administered once daily zonisamide at 300 mg for 14 days, and comprised the multiple dosing group."( Population pharmacokinetics of zonisamide after oral administration in healthy Chinese volunteers.
Bi, S; Chen, Y; Dai, Q; Liu, Y; Lu, W; Qiu, X; Sun, F; Xia, P; Xiang, R; Xiong, L; Yang, B; Yu, M, 2016
)
0.95
"The lack of commercially available liquid dosage forms for pediatric patients prompted this study."( Long-term Stability of Zonisamide, Amitriptyline, and Glycopyrrolate in Extemporaneously Prepared Liquid-dosage Forms at Two Temperatures.
Nahata, MC,
)
0.44
"The aim of this review was to evaluate current literature for dosing recommendations for the use of antiepileptic medications in patients receiving renal replacement therapy (RRT)."( Antiepileptic dosing for critically ill adult patients receiving renal replacement therapy.
Bastin, ML; Cook, AM; Oyler, DR; Smetana, KS, 2016
)
0.43
" Micromedex® DRUGDEX as well as package inserts were used to obtain known pharmacokinetic properties and dosage adjustment recommendations in RRT if known."( Antiepileptic dosing for critically ill adult patients receiving renal replacement therapy.
Bastin, ML; Cook, AM; Oyler, DR; Smetana, KS, 2016
)
0.43
"Data regarding antiepileptic drug use in RRT are limited and mostly consist of case reports limiting our proposed dosing recommendations."( Antiepileptic dosing for critically ill adult patients receiving renal replacement therapy.
Bastin, ML; Cook, AM; Oyler, DR; Smetana, KS, 2016
)
0.43
"Additional studies are necessary before specific dosing recommendations can be made for most antiepileptic drugs in critically ill patients receiving RRT, specifically with newer agents."( Antiepileptic dosing for critically ill adult patients receiving renal replacement therapy.
Bastin, ML; Cook, AM; Oyler, DR; Smetana, KS, 2016
)
0.43
"Hydrophilic matrix systems are currently some of the most widely used drug delivery systems for controlled-release oral dosage forms."( Evaluation of the drug solubility and rush ageing on drug release performance of various model drugs from the modified release polyethylene oxide matrix tablets.
Maniruzzaman, M; Nokhodchi, A; Shojaee, S, 2017
)
0.46
" Mean dosage of ZNS at final follow-up was 300 mg/d."( Zonisamide in Brain Tumor-Related Epilepsy: An Observational Pilot Study.
Cantelmi, T; Dinapoli, L; Fabi, A; Giannarelli, D; Maialetti, A; Maschio, M; Vidiri, A; Zarabla, A,
)
1.57
" Therefore, drug monitoring is necessary for appropriate dosage adjustments."( Chromatographic determination of zonisamide, topiramate and sulpiride in plasma by a fluorescent 'turn-on' chemosensor.
Barary, MA; El-Yazbi, AF; Ibrahim, FA; Wagih, MM, 2017
)
0.74
" The dosage of zonisamide was therefore decreased."( Suspected zonisamide-related anticonvulsant hypersensitivity syndrome in a cat.
Collinet, A; Sammut, V, 2017
)
1.21
" To reduce the daily dosing of L-DOPA in patients, inhibitors of dopamine catabolizing enzymes, particularly monoamine oxidase-B (MAO-B), are prescribed."( Garcinol, an effective monoamine oxidase-B inhibitor for the treatment of Parkinson's disease.
Bhattacharya, P; Borah, A; Chakrabarty, J; Dutta, A; Mazumder, MK; Paul, R; Phukan, BC, 2018
)
0.48
" Two trials provided evidence of a dose-response relationship for this outcome."( Zonisamide add-on therapy for focal epilepsy.
Behzadifar, M; Bragazzi, NL; Brigo, F; Igwe, SC; Lattanzi, S, 2018
)
1.92
" Responder status, side effects, and dosage were recorded."( Zonisamide for Cluster Headache Prophylaxis: A Case Series.
Holland, LC; Limmer, AL; Loftus, BD, 2019
)
1.96
" The levetiracetam dosage was increased (150 mg/kg [68 mg/lb], PO, q 8 h), and zonisamide (20 mg/kg [9."( Diagnosis and long-term management of post-traumatic seizures in a white-crowned pionus (
Beaufrère, H; Brouwer, E; James, F; Kabakchiev, C; Laniesse, D; Zur Linden, A, 2020
)
0.79
" Two trials provided evidence of a dose-response relationship for this outcome."( Zonisamide add-on therapy for focal epilepsy.
Behzadifar, M; Bragazzi, NL; Brigo, F; Igwe, SC; Lattanzi, S, 2020
)
2
" Age, sex, treatment duration, and ZNS dosage were included as covariates for adjustment in the ANCOVA model."( Effects of zonisamide monotherapy on bone health in drug-naive epileptic patients.
Koo, DL; Nam, H, 2020
)
0.95
" Exposure to certain newer ASMs, such as lamotrigine and levetiracetam, does not thus far appear to impact certain aspects of neurodevelopment, but further delineation across the different neurodevelopmental domains and dosage levels is required."( Neurodevelopmental outcomes in children exposed to newer antiseizure medications: A systematic review.
Bromley, RL; Knight, R; Wittkowski, A, 2021
)
0.62
" In the subsequent open-label 40 week period, all patients initially received zonisamide 25 mg/day for at least 2 weeks followed by optional flexible dosing with zonisamide 25 or 50 mg/day for the remaining period."( Long-Term Efficacy and Safety of Zonisamide for Treatment of Parkinsonism in Patients With Dementia With Lewy Bodies: An Open-Label Extension of a Phase three Randomized Controlled Trial.
Hasegawa, K; Kajiwara, R; Kosaka, K; Murata, M; Odawara, T; Tagawa, M; Takeuchi, H, 2022
)
1.23
" The present study aimed to model the effect sizes obtained from different doses in multiple studies using a two-stage dose-response meta-analytic approach while taking dose variations into account."( Investigation of the Utility of Multivariate Meta-Analysis Methods in Estimating the Summary Dose Response Curve.
Deepthy, MS; Harichandrakumar, KT; Karun, KM; Nair, NS, 2022
)
0.72
"Different dose-response meta-analysis models using linear, quadratic, and restricted cubic spline (RCS) functions were fitted."( Investigation of the Utility of Multivariate Meta-Analysis Methods in Estimating the Summary Dose Response Curve.
Deepthy, MS; Harichandrakumar, KT; Karun, KM; Nair, NS, 2022
)
0.72
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (5)

RoleDescription
anticonvulsantA drug used to prevent seizures or reduce their severity.
antioxidantA substance that opposes oxidation or inhibits reactions brought about by dioxygen or peroxides.
central nervous system drugA class of drugs producing both physiological and psychological effects through a variety of mechanisms involving the central nervous system.
protective agentSynthetic or natural substance which is given to prevent a disease or disorder or are used in the process of treating a disease or injury due to a poisonous agent.
T-type calcium channel blockerAny agent that interferes with the activity of T-type calcium channels.
[role 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]

Drug Classes (2)

ClassDescription
1,2-benzoxazolesCompounds based on a fused 1,2-oxazole and benzene bicyclic ring skeleton, with the O atom positioned adjacent to one of the positions of ring fusion.
sulfonamideAn amide of a sulfonic acid RS(=O)2NR'2.
[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]

Protein Targets (54)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, MAJOR APURINIC/APYRIMIDINIC ENDONUCLEASEHomo sapiens (human)Potency5.62340.003245.467312,589.2998AID2517
gemininHomo sapiens (human)Potency1.41250.004611.374133.4983AID624297
lamin isoform A-delta10Homo sapiens (human)Potency0.89130.891312.067628.1838AID1487
Interferon betaHomo sapiens (human)Potency0.33290.00339.158239.8107AID1347407
Cellular tumor antigen p53Homo sapiens (human)Potency33.49150.002319.595674.0614AID651631
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Carbonic anhydrase Astrosclera willeyanaKi0.16500.03201.51729.6000AID644379
Carbonic anhydrase Sulfurihydrogenibium sp. YO3AOP1Ki0.14000.00450.16240.8760AID1268964
Carbonic anhydrase Stylophora pistillataKi0.25900.00000.686710.0000AID436565; AID552130
Carbonic anhydraseStylophora pistillataKi0.64500.00000.50715.7100AID552131
ATP-binding cassette sub-family C member 3Homo sapiens (human)IC50 (µMol)133.00000.63154.45319.3000AID1473740
Multidrug resistance-associated protein 4Homo sapiens (human)IC50 (µMol)133.00000.20005.677410.0000AID1473741
Carbonic anhydraseHelicobacter pylori 26695Ki0.22450.02000.54864.3600AID261581; AID263638
Carbonic anhydrase 12Homo sapiens (human)IC50 (µMol)1.86000.00571.39908.5700AID1165421
Carbonic anhydrase 12Homo sapiens (human)Ki120.92780.00021.10439.9000AID1067227; AID1766625; AID1799588; AID239126; AID441209; AID441714; AID770582
Prolyl endopeptidaseRattus norvegicus (Norway rat)Ki0.02000.00000.10840.6300AID578223
Bile salt export pumpHomo sapiens (human)IC50 (µMol)134.00000.11007.190310.0000AID1443980; AID1473738
Carbonic anhydrase 1Homo sapiens (human)IC50 (µMol)1.86000.00582.14107.9000AID1165421
Carbonic anhydrase 1Homo sapiens (human)Ki30.71490.00001.372610.0000AID1067230; AID1142833; AID1188134; AID1190063; AID1194024; AID1195369; AID1262263; AID1268962; AID1275913; AID1287517; AID1434427; AID1453412; AID1628036; AID1766622; AID1796552; AID1796595; AID1798769; AID1799588; AID1803138; AID1803139; AID1803140; AID261579; AID263636; AID271172; AID349605; AID366657; AID367820; AID369271; AID371554; AID414955; AID427125; AID436563; AID436746; AID441206; AID441705; AID497127; AID552127; AID577526; AID578221; AID587130; AID588186; AID599953; AID601813; AID612725; AID633370; AID644037; AID644084; AID644380; AID669320; AID725955; AID743515; AID764719; AID770586
Carbonic anhydrase 2Homo sapiens (human)IC50 (µMol)1.86000.00021.10608.3000AID1165421
Carbonic anhydrase 2Homo sapiens (human)Ki26.14290.00000.72369.9200AID1061069; AID1067229; AID1142834; AID1188135; AID1190064; AID1194025; AID1195370; AID1240217; AID1262264; AID1268963; AID1275912; AID1278409; AID1287518; AID1434428; AID1453413; AID1628037; AID1766623; AID1796552; AID1796595; AID1798769; AID1799586; AID1799588; AID1803138; AID1803139; AID1803140; AID238852; AID239286; AID261580; AID263637; AID271173; AID328195; AID349606; AID366658; AID367821; AID369272; AID371555; AID414956; AID427124; AID436564; AID436747; AID437749; AID441207; AID441706; AID47905; AID497129; AID552128; AID577527; AID578222; AID587131; AID588187; AID599954; AID601814; AID612726; AID633371; AID644035; AID644085; AID644381; AID648179; AID648180; AID669115; AID669321; AID725956; AID743514; AID764718; AID770585
Carbonic anhydrase 2Bos taurus (cattle)IC50 (µMol)1.86000.00200.72891.8600AID1802607
Carbonic anhydrase 3Homo sapiens (human)IC50 (µMol)1.86000.02001.66866.5000AID1165421
Carbonic anhydrase 3Homo sapiens (human)Ki442.84170.00022.010210.0000AID1799588; AID301578; AID441707
Polyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)Ki0.11700.00010.03040.1570AID669485
Translocator proteinRattus norvegicus (Norway rat)Ki38.45000.00010.65108.9300AID644036
Amine oxidase [flavin-containing] BRattus norvegicus (Norway rat)Ki2.90000.00081.09276.0000AID570286
Arachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)Ki0.11700.00090.04010.1170AID669485
Carbonic anhydrase 4Homo sapiens (human)IC50 (µMol)1.86000.00320.31712.0000AID1165421
Carbonic anhydrase 4Homo sapiens (human)Ki98.24980.00021.97209.9200AID1799588; AID1803139; AID1803140; AID371556; AID441708; AID644036; AID644086
Carbonic anhydrase 6Homo sapiens (human)IC50 (µMol)1.86000.02001.33175.7900AID1165421
Carbonic anhydrase 6Homo sapiens (human)Ki88.66550.00011.47109.9200AID1798769; AID1799588; AID1803138; AID1803139; AID369273; AID441711; AID644034; AID644087
Sodium-dependent dopamine transporterRattus norvegicus (Norway rat)Ki0.03520.00030.37088.1600AID239286
Amine oxidase [flavin-containing] BHomo sapiens (human)Ki3.10000.00061.777110.0000AID570284
Delta-type opioid receptorMus musculus (house mouse)Ki0.04550.00000.53939.4000AID1188134; AID1188135
Delta-type opioid receptorRattus norvegicus (Norway rat)Ki0.02780.00000.60689.2330AID1188135; AID239287
Mu-type opioid receptorRattus norvegicus (Norway rat)Ki0.05600.00000.38458.6000AID1188134
Carbonic anhydrase 5A, mitochondrialHomo sapiens (human)IC50 (µMol)1.86000.02003.10819.4000AID1165421
Carbonic anhydrase 5A, mitochondrialHomo sapiens (human)Ki119.09080.00001.27259.9000AID1799588; AID239287; AID366659; AID371557; AID436748; AID441709; AID578223
Carbonic anhydrase 7Homo sapiens (human)IC50 (µMol)1.86000.02001.21363.4400AID1165421
Carbonic anhydrase 7Homo sapiens (human)Ki97.54770.00021.37379.9000AID1060765; AID1766624; AID1799586; AID1799588; AID441712; AID600082; AID601815; AID669485; AID764717; AID770584
Carbonic anhydraseSaccharomyces cerevisiae S288CKi0.10600.08200.56098.7000AID367822
D(2) dopamine receptorRattus norvegicus (Norway rat)Ki6.03300.00000.437510.0000AID436749
Carbonic anhydrase Mycobacterium tuberculosis H37RvKi0.21000.01202.72389.1200AID588182
Mu-type opioid receptorCavia porcellus (domestic guinea pig)Ki0.03500.00000.27869.0000AID1188135
Beta-carbonic anhydrase 1Mycobacterium tuberculosis H37RvKi114.72000.00483.38419.8400AID1798985; AID349607; AID588183
Carbonic anhydrase 2Mycobacterium tuberculosis H37RvKi0.87600.00902.20969.8400AID437750
Carbonic anhydrase 9Homo sapiens (human)IC50 (µMol)1.86000.00030.63029.3900AID1165421
Carbonic anhydrase 9Homo sapiens (human)Ki83.09220.00010.78749.9000AID1067228; AID1796595; AID1798769; AID1799588; AID239102; AID271174; AID369274; AID441208; AID441713; AID633372; AID669486; AID770583
Carbonic anhydrase, alpha family Hydrogenovibrio crunogenus XCL-2Ki0.41100.00250.32341.1000AID1268965
Carbonic anhydrase Cryptococcus neoformans var. grubiiKi0.97050.01000.73648.3470AID588185; AID669116
Carbonic anhydrase 3Bos taurus (cattle)Ki14.26200.11303.88159.7100AID1803140; AID644088
Carbonic anhydraseCandida albicans SC5314Ki0.94740.01051.44448.3470AID1799266; AID427122; AID588184; AID669117
Carbonic anhydrase Anopheles gambiae (African malaria mosquito)Ki0.26300.00980.51174.3600AID1195371
Delta carbonic anhydraseConticribra weissflogiiKi0.40400.04960.99789.2000AID1061066
Carbonic anhydrase Nakaseomyces glabratus CBS 138Ki0.11400.00701.21749.1700AID744415
Carbonic anhydrase 13Homo sapiens (human)IC50 (µMol)1.86000.02000.86802.0000AID1165421
Carbonic anhydrase 13Homo sapiens (human)Ki160.21820.00031.23099.8000AID1799588; AID441715
Canalicular multispecific organic anion transporter 1Homo sapiens (human)IC50 (µMol)133.00002.41006.343310.0000AID1473739
Carbonic anhydrase 15Mus musculus (house mouse)Ki0.49780.00091.884610.0000AID1798769; AID369275; AID441717
Carbonic anhydrase 14Homo sapiens (human)IC50 (µMol)1.86000.02000.53292.0000AID1165421
Carbonic anhydrase 14Homo sapiens (human)Ki126.04860.00021.50999.9000AID1799588; AID239703; AID441716; AID601816; AID633373; AID669487
Carbonic anhydrase 5B, mitochondrialHomo sapiens (human)IC50 (µMol)1.86000.02000.86802.0000AID1165421
Carbonic anhydrase 5B, mitochondrialHomo sapiens (human)Ki436.83040.00001.34129.9700AID1799588; AID239287; AID366660; AID371558; AID436749; AID441710; AID578224
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Activation Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Carbonic anhydrase 2Homo sapiens (human)Kd0.04760.00000.41575.5500AID295948
Carbonic anhydrase 5A, mitochondrialHomo sapiens (human)Kd0.02060.00700.38641.0000AID295949
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Other Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Carbonic anhydrase Brucella suis 1330Kinact1.85000.01700.86285.8700AID459696
Carbonic anhydrase 12Homo sapiens (human)Kinact11.00000.00300.66749.6000AID320314
Carbonic anhydrase 1Homo sapiens (human)Kinact0.05180.01000.93878.6000AID293811; AID299242; AID320305; AID456398; AID464118
Carbonic anhydrase 2Homo sapiens (human)Kinact0.02900.00300.794610.0000AID293812; AID299243; AID320306; AID456397; AID464119
Carbonic anhydrase 4Homo sapiens (human)Kinact8.59000.07402.39348.5900AID300467; AID320308
Carbonic anhydrase 6Homo sapiens (human)Kinact0.08900.00090.72615.3000AID300470; AID320311
Carbonic anhydrase 5A, mitochondrialHomo sapiens (human)Kinact0.02000.02000.85809.4000AID320309; AID456399
Carbonic anhydrase 7Homo sapiens (human)Kinact0.11700.00020.28525.7300AID300471; AID320312
Carbonic anhydrase 9Homo sapiens (human)Kinact1.75340.00500.31976.6700AID293813; AID320313; AID464120
Carbonic anhydrase 13Mus musculus (house mouse)Kinact0.43000.01300.56698.2300AID300474; AID320315
Carbonic anhydrase 14Homo sapiens (human)Kinact3.50230.00021.44958.5900AID300475; AID320316; AID464121
Carbonic anhydrase 5B, mitochondrialHomo sapiens (human)Kinact6.03300.00900.92319.0400AID300469; AID320310; AID456400
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (257)

Processvia Protein(s)Taxonomy
xenobiotic metabolic processATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
bile acid and bile salt transportATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transportATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
leukotriene transportATP-binding cassette sub-family C member 3Homo sapiens (human)
monoatomic anion transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transport across blood-brain barrierATP-binding cassette sub-family C member 3Homo sapiens (human)
prostaglandin secretionMultidrug resistance-associated protein 4Homo sapiens (human)
cilium assemblyMultidrug resistance-associated protein 4Homo sapiens (human)
platelet degranulationMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic metabolic processMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
bile acid and bile salt transportMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transportMultidrug resistance-associated protein 4Homo sapiens (human)
urate transportMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
cAMP transportMultidrug resistance-associated protein 4Homo sapiens (human)
leukotriene transportMultidrug resistance-associated protein 4Homo sapiens (human)
monoatomic anion transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
export across plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
transport across blood-brain barrierMultidrug resistance-associated protein 4Homo sapiens (human)
guanine nucleotide transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
estrous cycleCarbonic anhydrase 12Homo sapiens (human)
chloride ion homeostasisCarbonic anhydrase 12Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 12Homo sapiens (human)
fatty acid metabolic processBile salt export pumpHomo sapiens (human)
bile acid biosynthetic processBile salt export pumpHomo sapiens (human)
xenobiotic metabolic processBile salt export pumpHomo sapiens (human)
xenobiotic transmembrane transportBile salt export pumpHomo sapiens (human)
response to oxidative stressBile salt export pumpHomo sapiens (human)
bile acid metabolic processBile salt export pumpHomo sapiens (human)
response to organic cyclic compoundBile salt export pumpHomo sapiens (human)
bile acid and bile salt transportBile salt export pumpHomo sapiens (human)
canalicular bile acid transportBile salt export pumpHomo sapiens (human)
protein ubiquitinationBile salt export pumpHomo sapiens (human)
regulation of fatty acid beta-oxidationBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transportBile salt export pumpHomo sapiens (human)
bile acid signaling pathwayBile salt export pumpHomo sapiens (human)
cholesterol homeostasisBile salt export pumpHomo sapiens (human)
response to estrogenBile salt export pumpHomo sapiens (human)
response to ethanolBile salt export pumpHomo sapiens (human)
xenobiotic export from cellBile salt export pumpHomo sapiens (human)
lipid homeostasisBile salt export pumpHomo sapiens (human)
phospholipid homeostasisBile salt export pumpHomo sapiens (human)
positive regulation of bile acid secretionBile salt export pumpHomo sapiens (human)
regulation of bile acid metabolic processBile salt export pumpHomo sapiens (human)
transmembrane transportBile salt export pumpHomo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 1Homo sapiens (human)
morphogenesis of an epitheliumCarbonic anhydrase 2Homo sapiens (human)
positive regulation of synaptic transmission, GABAergicCarbonic anhydrase 2Homo sapiens (human)
positive regulation of cellular pH reductionCarbonic anhydrase 2Homo sapiens (human)
angiotensin-activated signaling pathwayCarbonic anhydrase 2Homo sapiens (human)
regulation of monoatomic anion transportCarbonic anhydrase 2Homo sapiens (human)
secretionCarbonic anhydrase 2Homo sapiens (human)
regulation of intracellular pHCarbonic anhydrase 2Homo sapiens (human)
neuron cellular homeostasisCarbonic anhydrase 2Homo sapiens (human)
positive regulation of dipeptide transmembrane transportCarbonic anhydrase 2Homo sapiens (human)
regulation of chloride transportCarbonic anhydrase 2Homo sapiens (human)
carbon dioxide transportCarbonic anhydrase 2Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 2Homo sapiens (human)
angiotensin-activated signaling pathwayCarbonic anhydrase 2Bos taurus (cattle)
regulation of monoatomic anion transportCarbonic anhydrase 2Bos taurus (cattle)
regulation of intracellular pHCarbonic anhydrase 2Bos taurus (cattle)
positive regulation of dipeptide transmembrane transportCarbonic anhydrase 2Bos taurus (cattle)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell activation involved in immune responseInterferon betaHomo sapiens (human)
cell surface receptor signaling pathwayInterferon betaHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to virusInterferon betaHomo sapiens (human)
positive regulation of autophagyInterferon betaHomo sapiens (human)
cytokine-mediated signaling pathwayInterferon betaHomo sapiens (human)
natural killer cell activationInterferon betaHomo sapiens (human)
positive regulation of peptidyl-serine phosphorylation of STAT proteinInterferon betaHomo sapiens (human)
cellular response to interferon-betaInterferon betaHomo sapiens (human)
B cell proliferationInterferon betaHomo sapiens (human)
negative regulation of viral genome replicationInterferon betaHomo sapiens (human)
innate immune responseInterferon betaHomo sapiens (human)
positive regulation of innate immune responseInterferon betaHomo sapiens (human)
regulation of MHC class I biosynthetic processInterferon betaHomo sapiens (human)
negative regulation of T cell differentiationInterferon betaHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIInterferon betaHomo sapiens (human)
defense response to virusInterferon betaHomo sapiens (human)
type I interferon-mediated signaling pathwayInterferon betaHomo sapiens (human)
neuron cellular homeostasisInterferon betaHomo sapiens (human)
cellular response to exogenous dsRNAInterferon betaHomo sapiens (human)
cellular response to virusInterferon betaHomo sapiens (human)
negative regulation of Lewy body formationInterferon betaHomo sapiens (human)
negative regulation of T-helper 2 cell cytokine productionInterferon betaHomo sapiens (human)
positive regulation of apoptotic signaling pathwayInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell differentiationInterferon betaHomo sapiens (human)
natural killer cell activation involved in immune responseInterferon betaHomo sapiens (human)
adaptive immune responseInterferon betaHomo sapiens (human)
T cell activation involved in immune responseInterferon betaHomo sapiens (human)
humoral immune responseInterferon betaHomo sapiens (human)
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycle G2/M phase transitionCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
ER overload responseCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
mitophagyCellular tumor antigen p53Homo sapiens (human)
in utero embryonic developmentCellular tumor antigen p53Homo sapiens (human)
somitogenesisCellular tumor antigen p53Homo sapiens (human)
release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
hematopoietic progenitor cell differentiationCellular tumor antigen p53Homo sapiens (human)
T cell proliferation involved in immune responseCellular tumor antigen p53Homo sapiens (human)
B cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
T cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
response to ischemiaCellular tumor antigen p53Homo sapiens (human)
nucleotide-excision repairCellular tumor antigen p53Homo sapiens (human)
double-strand break repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
protein import into nucleusCellular tumor antigen p53Homo sapiens (human)
autophagyCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrestCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediatorCellular tumor antigen p53Homo sapiens (human)
transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
Ras protein signal transductionCellular tumor antigen p53Homo sapiens (human)
gastrulationCellular tumor antigen p53Homo sapiens (human)
neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
protein localizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA replicationCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
determination of adult lifespanCellular tumor antigen p53Homo sapiens (human)
mRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
rRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
response to salt stressCellular tumor antigen p53Homo sapiens (human)
response to inorganic substanceCellular tumor antigen p53Homo sapiens (human)
response to X-rayCellular tumor antigen p53Homo sapiens (human)
response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
positive regulation of gene expressionCellular tumor antigen p53Homo sapiens (human)
cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
viral processCellular tumor antigen p53Homo sapiens (human)
glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
cerebellum developmentCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell growthCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
mitotic G1 DNA damage checkpoint signalingCellular tumor antigen p53Homo sapiens (human)
negative regulation of telomere maintenance via telomeraseCellular tumor antigen p53Homo sapiens (human)
T cell differentiation in thymusCellular tumor antigen p53Homo sapiens (human)
tumor necrosis factor-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
regulation of tissue remodelingCellular tumor antigen p53Homo sapiens (human)
cellular response to UVCellular tumor antigen p53Homo sapiens (human)
multicellular organism growthCellular tumor antigen p53Homo sapiens (human)
positive regulation of mitochondrial membrane permeabilityCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
entrainment of circadian clock by photoperiodCellular tumor antigen p53Homo sapiens (human)
mitochondrial DNA repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
transcription initiation-coupled chromatin remodelingCellular tumor antigen p53Homo sapiens (human)
negative regulation of proteolysisCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of RNA polymerase II transcription preinitiation complex assemblyCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
response to antibioticCellular tumor antigen p53Homo sapiens (human)
fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
circadian behaviorCellular tumor antigen p53Homo sapiens (human)
bone marrow developmentCellular tumor antigen p53Homo sapiens (human)
embryonic organ developmentCellular tumor antigen p53Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylationCellular tumor antigen p53Homo sapiens (human)
protein stabilizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of helicase activityCellular tumor antigen p53Homo sapiens (human)
protein tetramerizationCellular tumor antigen p53Homo sapiens (human)
chromosome organizationCellular tumor antigen p53Homo sapiens (human)
neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
hematopoietic stem cell differentiationCellular tumor antigen p53Homo sapiens (human)
negative regulation of glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
type II interferon-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
cardiac septum morphogenesisCellular tumor antigen p53Homo sapiens (human)
positive regulation of programmed necrotic cell deathCellular tumor antigen p53Homo sapiens (human)
protein-containing complex assemblyCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stressCellular tumor antigen p53Homo sapiens (human)
thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
necroptotic processCellular tumor antigen p53Homo sapiens (human)
cellular response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
cellular response to xenobiotic stimulusCellular tumor antigen p53Homo sapiens (human)
cellular response to ionizing radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to UV-CCellular tumor antigen p53Homo sapiens (human)
stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
cellular response to actinomycin DCellular tumor antigen p53Homo sapiens (human)
positive regulation of release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
cellular senescenceCellular tumor antigen p53Homo sapiens (human)
replicative senescenceCellular tumor antigen p53Homo sapiens (human)
oxidative stress-induced premature senescenceCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
oligodendrocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of execution phase of apoptosisCellular tumor antigen p53Homo sapiens (human)
negative regulation of mitophagyCellular tumor antigen p53Homo sapiens (human)
regulation of mitochondrial membrane permeability involved in apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of G1 to G0 transitionCellular tumor antigen p53Homo sapiens (human)
negative regulation of miRNA processingCellular tumor antigen p53Homo sapiens (human)
negative regulation of glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
negative regulation of pentose-phosphate shuntCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
regulation of fibroblast apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
positive regulation of cellular senescenceCellular tumor antigen p53Homo sapiens (human)
positive regulation of intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
response to bacteriumCarbonic anhydrase 3Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 3Homo sapiens (human)
negative regulation of endothelial cell proliferationPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
leukocyte chemotaxis involved in inflammatory responsePolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
leukocyte migration involved in inflammatory responsePolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
leukotriene production involved in inflammatory responsePolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
leukotriene metabolic processPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
humoral immune responsePolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
negative regulation of angiogenesisPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
leukotriene biosynthetic processPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
lipoxygenase pathwayPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
positive regulation of bone mineralizationPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
dendritic cell migrationPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
glucose homeostasisPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
long-chain fatty acid biosynthetic processPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
regulation of fat cell differentiationPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
regulation of inflammatory responsePolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
negative regulation of inflammatory responsePolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
regulation of insulin secretionPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
negative regulation of vascular wound healingPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
negative regulation of wound healingPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
regulation of inflammatory response to woundingPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
regulation of cytokine production involved in inflammatory responsePolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
regulation of cellular response to oxidative stressPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
leukotriene A4 biosynthetic processPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
regulation of reactive oxygen species biosynthetic processPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
negative regulation of response to endoplasmic reticulum stressPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
negative regulation of sprouting angiogenesisPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
positive regulation of leukocyte adhesion to arterial endothelial cellPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
lipoxin biosynthetic processPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
arachidonic acid metabolic processPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
lipid oxidationPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
leukotriene production involved in inflammatory responseArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
positive regulation of acute inflammatory responseArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
leukotriene biosynthetic processArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
lipoxygenase pathwayArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
protein homotrimerizationArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
cellular response to calcium ionArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
cellular oxidant detoxificationArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
bicarbonate transportCarbonic anhydrase 4Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 4Homo sapiens (human)
detection of chemical stimulus involved in sensory perception of bitter tasteCarbonic anhydrase 6Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 6Homo sapiens (human)
response to xenobiotic stimulusAmine oxidase [flavin-containing] BHomo sapiens (human)
response to toxic substanceAmine oxidase [flavin-containing] BHomo sapiens (human)
response to aluminum ionAmine oxidase [flavin-containing] BHomo sapiens (human)
response to selenium ionAmine oxidase [flavin-containing] BHomo sapiens (human)
negative regulation of serotonin secretionAmine oxidase [flavin-containing] BHomo sapiens (human)
phenylethylamine catabolic processAmine oxidase [flavin-containing] BHomo sapiens (human)
substantia nigra developmentAmine oxidase [flavin-containing] BHomo sapiens (human)
response to lipopolysaccharideAmine oxidase [flavin-containing] BHomo sapiens (human)
dopamine catabolic processAmine oxidase [flavin-containing] BHomo sapiens (human)
response to ethanolAmine oxidase [flavin-containing] BHomo sapiens (human)
positive regulation of dopamine metabolic processAmine oxidase [flavin-containing] BHomo sapiens (human)
hydrogen peroxide biosynthetic processAmine oxidase [flavin-containing] BHomo sapiens (human)
response to corticosteroneAmine oxidase [flavin-containing] BHomo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 5A, mitochondrialHomo sapiens (human)
positive regulation of synaptic transmission, GABAergicCarbonic anhydrase 7Homo sapiens (human)
positive regulation of cellular pH reductionCarbonic anhydrase 7Homo sapiens (human)
neuron cellular homeostasisCarbonic anhydrase 7Homo sapiens (human)
regulation of chloride transportCarbonic anhydrase 7Homo sapiens (human)
regulation of intracellular pHCarbonic anhydrase 7Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 7Homo sapiens (human)
response to hypoxiaCarbonic anhydrase 9Homo sapiens (human)
morphogenesis of an epitheliumCarbonic anhydrase 9Homo sapiens (human)
response to xenobiotic stimulusCarbonic anhydrase 9Homo sapiens (human)
response to testosteroneCarbonic anhydrase 9Homo sapiens (human)
secretionCarbonic anhydrase 9Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 9Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 13Homo sapiens (human)
xenobiotic metabolic processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
negative regulation of gene expressionCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bile acid and bile salt transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
heme catabolic processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic export from cellCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transepithelial transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
leukotriene transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
monoatomic anion transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 14Homo sapiens (human)
response to bacteriumCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (82)

Processvia Protein(s)Taxonomy
ATP bindingATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type xenobiotic transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type bile acid transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATP hydrolysis activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
icosanoid transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
guanine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
protein bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ATP bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type xenobiotic transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
urate transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
purine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type bile acid transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
efflux transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
15-hydroxyprostaglandin dehydrogenase (NAD+) activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATP hydrolysis activityMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 12Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 12Homo sapiens (human)
protein bindingBile salt export pumpHomo sapiens (human)
ATP bindingBile salt export pumpHomo sapiens (human)
ABC-type xenobiotic transporter activityBile salt export pumpHomo sapiens (human)
bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
canalicular bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transporter activityBile salt export pumpHomo sapiens (human)
ABC-type bile acid transporter activityBile salt export pumpHomo sapiens (human)
ATP hydrolysis activityBile salt export pumpHomo sapiens (human)
arylesterase activityCarbonic anhydrase 1Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 1Homo sapiens (human)
protein bindingCarbonic anhydrase 1Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 1Homo sapiens (human)
hydro-lyase activityCarbonic anhydrase 1Homo sapiens (human)
cyanamide hydratase activityCarbonic anhydrase 1Homo sapiens (human)
arylesterase activityCarbonic anhydrase 2Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 2Homo sapiens (human)
protein bindingCarbonic anhydrase 2Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 2Homo sapiens (human)
cyanamide hydratase activityCarbonic anhydrase 2Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 2Bos taurus (cattle)
cyanamide hydratase activityCarbonic anhydrase 2Bos taurus (cattle)
cytokine activityInterferon betaHomo sapiens (human)
cytokine receptor bindingInterferon betaHomo sapiens (human)
type I interferon receptor bindingInterferon betaHomo sapiens (human)
protein bindingInterferon betaHomo sapiens (human)
chloramphenicol O-acetyltransferase activityInterferon betaHomo sapiens (human)
transcription cis-regulatory region bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
core promoter sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
TFIID-class transcription factor complex bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
protease bindingCellular tumor antigen p53Homo sapiens (human)
p53 bindingCellular tumor antigen p53Homo sapiens (human)
DNA bindingCellular tumor antigen p53Homo sapiens (human)
chromatin bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activityCellular tumor antigen p53Homo sapiens (human)
mRNA 3'-UTR bindingCellular tumor antigen p53Homo sapiens (human)
copper ion bindingCellular tumor antigen p53Homo sapiens (human)
protein bindingCellular tumor antigen p53Homo sapiens (human)
zinc ion bindingCellular tumor antigen p53Homo sapiens (human)
enzyme bindingCellular tumor antigen p53Homo sapiens (human)
receptor tyrosine kinase bindingCellular tumor antigen p53Homo sapiens (human)
ubiquitin protein ligase bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase regulator activityCellular tumor antigen p53Homo sapiens (human)
ATP-dependent DNA/DNA annealing activityCellular tumor antigen p53Homo sapiens (human)
identical protein bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase bindingCellular tumor antigen p53Homo sapiens (human)
protein heterodimerization activityCellular tumor antigen p53Homo sapiens (human)
protein-folding chaperone bindingCellular tumor antigen p53Homo sapiens (human)
protein phosphatase 2A bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor bindingCellular tumor antigen p53Homo sapiens (human)
14-3-3 protein bindingCellular tumor antigen p53Homo sapiens (human)
MDM2/MDM4 family protein bindingCellular tumor antigen p53Homo sapiens (human)
disordered domain specific bindingCellular tumor antigen p53Homo sapiens (human)
general transcription initiation factor bindingCellular tumor antigen p53Homo sapiens (human)
molecular function activator activityCellular tumor antigen p53Homo sapiens (human)
promoter-specific chromatin bindingCellular tumor antigen p53Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 3Homo sapiens (human)
protein bindingCarbonic anhydrase 3Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 3Homo sapiens (human)
nickel cation bindingCarbonic anhydrase 3Homo sapiens (human)
arachidonate 5-lipoxygenase activityPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
arachidonate 12(S)-lipoxygenase activityPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
iron ion bindingPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
protein bindingPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
hydrolase activityPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
arachidonate 8(S)-lipoxygenase activityPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
arachidonate 5-lipoxygenase activityArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
protein bindingArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
enzyme activator activityArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
enzyme bindingArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
identical protein bindingArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
protein-containing complex bindingArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
arachidonic acid bindingArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
glutathione transferase activityArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
glutathione peroxidase activityArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
leukotriene-C4 synthase activityArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
protein bindingCarbonic anhydrase 4Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 4Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 4Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 6Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 6Homo sapiens (human)
protein bindingAmine oxidase [flavin-containing] BHomo sapiens (human)
primary amine oxidase activityAmine oxidase [flavin-containing] BHomo sapiens (human)
electron transfer activityAmine oxidase [flavin-containing] BHomo sapiens (human)
identical protein bindingAmine oxidase [flavin-containing] BHomo sapiens (human)
aliphatic amine oxidase activityAmine oxidase [flavin-containing] BHomo sapiens (human)
monoamine oxidase activityAmine oxidase [flavin-containing] BHomo sapiens (human)
flavin adenine dinucleotide bindingAmine oxidase [flavin-containing] BHomo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 5A, mitochondrialHomo sapiens (human)
zinc ion bindingCarbonic anhydrase 5A, mitochondrialHomo sapiens (human)
zinc ion bindingCarbonic anhydrase 7Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 7Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 9Homo sapiens (human)
protein bindingCarbonic anhydrase 9Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 9Homo sapiens (human)
molecular function activator activityCarbonic anhydrase 9Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 3Bos taurus (cattle)
protein bindingCarbonic anhydrase 13Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 13Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 13Homo sapiens (human)
protein bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
organic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type xenobiotic transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP hydrolysis activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 14Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 14Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
zinc ion bindingCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (59)

Processvia Protein(s)Taxonomy
plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basal plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basolateral plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
nucleolusMultidrug resistance-associated protein 4Homo sapiens (human)
Golgi apparatusMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
membraneMultidrug resistance-associated protein 4Homo sapiens (human)
basolateral plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
platelet dense granule membraneMultidrug resistance-associated protein 4Homo sapiens (human)
external side of apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneCarbonic anhydrase 12Homo sapiens (human)
membraneCarbonic anhydrase 12Homo sapiens (human)
basolateral plasma membraneCarbonic anhydrase 12Homo sapiens (human)
apical plasma membraneCarbonic anhydrase 12Homo sapiens (human)
plasma membraneCarbonic anhydrase 12Homo sapiens (human)
basolateral plasma membraneBile salt export pumpHomo sapiens (human)
Golgi membraneBile salt export pumpHomo sapiens (human)
endosomeBile salt export pumpHomo sapiens (human)
plasma membraneBile salt export pumpHomo sapiens (human)
cell surfaceBile salt export pumpHomo sapiens (human)
apical plasma membraneBile salt export pumpHomo sapiens (human)
intercellular canaliculusBile salt export pumpHomo sapiens (human)
intracellular canaliculusBile salt export pumpHomo sapiens (human)
recycling endosomeBile salt export pumpHomo sapiens (human)
recycling endosome membraneBile salt export pumpHomo sapiens (human)
extracellular exosomeBile salt export pumpHomo sapiens (human)
membraneBile salt export pumpHomo sapiens (human)
cytosolCarbonic anhydrase 1Homo sapiens (human)
extracellular exosomeCarbonic anhydrase 1Homo sapiens (human)
cytoplasmCarbonic anhydrase 2Homo sapiens (human)
cytosolCarbonic anhydrase 2Homo sapiens (human)
plasma membraneCarbonic anhydrase 2Homo sapiens (human)
myelin sheathCarbonic anhydrase 2Homo sapiens (human)
apical part of cellCarbonic anhydrase 2Homo sapiens (human)
extracellular exosomeCarbonic anhydrase 2Homo sapiens (human)
cytoplasmCarbonic anhydrase 2Homo sapiens (human)
plasma membraneCarbonic anhydrase 2Homo sapiens (human)
apical part of cellCarbonic anhydrase 2Homo sapiens (human)
cytoplasmCarbonic anhydrase 2Bos taurus (cattle)
plasma membraneCarbonic anhydrase 2Bos taurus (cattle)
extracellular spaceInterferon betaHomo sapiens (human)
extracellular regionInterferon betaHomo sapiens (human)
nuclear bodyCellular tumor antigen p53Homo sapiens (human)
nucleusCellular tumor antigen p53Homo sapiens (human)
nucleoplasmCellular tumor antigen p53Homo sapiens (human)
replication forkCellular tumor antigen p53Homo sapiens (human)
nucleolusCellular tumor antigen p53Homo sapiens (human)
cytoplasmCellular tumor antigen p53Homo sapiens (human)
mitochondrionCellular tumor antigen p53Homo sapiens (human)
mitochondrial matrixCellular tumor antigen p53Homo sapiens (human)
endoplasmic reticulumCellular tumor antigen p53Homo sapiens (human)
centrosomeCellular tumor antigen p53Homo sapiens (human)
cytosolCellular tumor antigen p53Homo sapiens (human)
nuclear matrixCellular tumor antigen p53Homo sapiens (human)
PML bodyCellular tumor antigen p53Homo sapiens (human)
transcription repressor complexCellular tumor antigen p53Homo sapiens (human)
site of double-strand breakCellular tumor antigen p53Homo sapiens (human)
germ cell nucleusCellular tumor antigen p53Homo sapiens (human)
chromatinCellular tumor antigen p53Homo sapiens (human)
transcription regulator complexCellular tumor antigen p53Homo sapiens (human)
protein-containing complexCellular tumor antigen p53Homo sapiens (human)
cytosolCarbonic anhydrase 3Homo sapiens (human)
cytosolCarbonic anhydrase 3Homo sapiens (human)
cytoplasmCarbonic anhydrase 3Homo sapiens (human)
extracellular regionPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
extracellular spacePolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
nuclear envelopePolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
nuclear envelope lumenPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
nucleoplasmPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
cytosolPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
nuclear matrixPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
nuclear membranePolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
secretory granule lumenPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
perinuclear region of cytoplasmPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
ficolin-1-rich granule lumenPolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
nuclear envelopePolyunsaturated fatty acid 5-lipoxygenaseHomo sapiens (human)
nuclear envelopeArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
endoplasmic reticulumArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
endoplasmic reticulum membraneArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
membraneArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
nuclear membraneArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
nuclear envelopeArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
endoplasmic reticulumArachidonate 5-lipoxygenase-activating proteinHomo sapiens (human)
basolateral plasma membraneCarbonic anhydrase 4Homo sapiens (human)
rough endoplasmic reticulumCarbonic anhydrase 4Homo sapiens (human)
endoplasmic reticulum-Golgi intermediate compartmentCarbonic anhydrase 4Homo sapiens (human)
Golgi apparatusCarbonic anhydrase 4Homo sapiens (human)
trans-Golgi networkCarbonic anhydrase 4Homo sapiens (human)
plasma membraneCarbonic anhydrase 4Homo sapiens (human)
external side of plasma membraneCarbonic anhydrase 4Homo sapiens (human)
cell surfaceCarbonic anhydrase 4Homo sapiens (human)
membraneCarbonic anhydrase 4Homo sapiens (human)
apical plasma membraneCarbonic anhydrase 4Homo sapiens (human)
transport vesicle membraneCarbonic anhydrase 4Homo sapiens (human)
secretory granule membraneCarbonic anhydrase 4Homo sapiens (human)
brush border membraneCarbonic anhydrase 4Homo sapiens (human)
perinuclear region of cytoplasmCarbonic anhydrase 4Homo sapiens (human)
extracellular exosomeCarbonic anhydrase 4Homo sapiens (human)
plasma membraneCarbonic anhydrase 4Homo sapiens (human)
extracellular regionCarbonic anhydrase 6Homo sapiens (human)
extracellular spaceCarbonic anhydrase 6Homo sapiens (human)
cytosolCarbonic anhydrase 6Homo sapiens (human)
extracellular exosomeCarbonic anhydrase 6Homo sapiens (human)
extracellular spaceCarbonic anhydrase 6Homo sapiens (human)
mitochondrionAmine oxidase [flavin-containing] BHomo sapiens (human)
mitochondrial envelopeAmine oxidase [flavin-containing] BHomo sapiens (human)
mitochondrial outer membraneAmine oxidase [flavin-containing] BHomo sapiens (human)
dendriteAmine oxidase [flavin-containing] BHomo sapiens (human)
neuronal cell bodyAmine oxidase [flavin-containing] BHomo sapiens (human)
mitochondrionAmine oxidase [flavin-containing] BHomo sapiens (human)
mitochondrial matrixCarbonic anhydrase 5A, mitochondrialHomo sapiens (human)
mitochondrionCarbonic anhydrase 5A, mitochondrialHomo sapiens (human)
cytoplasmCarbonic anhydrase 5A, mitochondrialHomo sapiens (human)
mitochondrionCarbonic anhydrase 5A, mitochondrialHomo sapiens (human)
cytosolCarbonic anhydrase 7Homo sapiens (human)
cytoplasmCarbonic anhydrase 7Homo sapiens (human)
nucleolusCarbonic anhydrase 9Homo sapiens (human)
plasma membraneCarbonic anhydrase 9Homo sapiens (human)
membraneCarbonic anhydrase 9Homo sapiens (human)
basolateral plasma membraneCarbonic anhydrase 9Homo sapiens (human)
microvillus membraneCarbonic anhydrase 9Homo sapiens (human)
plasma membraneCarbonic anhydrase 9Homo sapiens (human)
cytosolCarbonic anhydrase 13Homo sapiens (human)
myelin sheathCarbonic anhydrase 13Homo sapiens (human)
intracellular membrane-bounded organelleCarbonic anhydrase 13Homo sapiens (human)
cytoplasmCarbonic anhydrase 13Homo sapiens (human)
cytosolCarbonic anhydrase 13Homo sapiens (human)
plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
cell surfaceCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
intercellular canaliculusCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
plasma membraneCarbonic anhydrase 14Homo sapiens (human)
membraneCarbonic anhydrase 14Homo sapiens (human)
basolateral plasma membraneCarbonic anhydrase 14Homo sapiens (human)
apical plasma membraneCarbonic anhydrase 14Homo sapiens (human)
plasma membraneCarbonic anhydrase 14Homo sapiens (human)
mitochondrionCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
mitochondrial matrixCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
mitochondrionCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
cytoplasmCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (467)

Assay IDTitleYearJournalArticle
AID504749qHTS profiling for inhibitors of Plasmodium falciparum proliferation2011Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043
Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347425Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347424RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347407qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection2020ACS 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.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1262264Inhibition of human CA2 incubated for 15 mins prior to testing by stopped flow CO2 hydrase assay2015Bioorganic & medicinal chemistry letters, Dec-01, Volume: 25, Issue:23
Anion and sulfonamide inhibition studies of an α-carbonic anhydrase from the Antarctic hemoglobinless fish Chionodraco hamatus.
AID669115Inhibition of human carbonic anhydrase 2 preincubated for 15 mins measured for 10 to 100 sec by stopped-flow method2012Journal of medicinal chemistry, Apr-12, Volume: 55, Issue:7
Molecular cloning, characterization, and inhibition studies of a β-carbonic anhydrase from Malassezia globosa, a potential antidandruff target.
AID441208Inhibition of human cloned CA9 catalytic domain by stopped flow CO2 hydration assay2009Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20
S-glycosyl primary sulfonamides--a new structural class for selective inhibition of cancer-associated carbonic anhydrases.
AID644379Inhibition of GST-tagged astrosclera willeyana Astrosclerin-3 expressed in Escherichia coli after 15 mins preincubation by stopped flow CO2 hydration assay2012Bioorganic & medicinal chemistry, Feb-15, Volume: 20, Issue:4
Cloning, characterization and sulfonamide inhibition studies of an α-carbonic anhydrase from the living fossil sponge Astrosclera willeyana.
AID459696Inhibition of Brucella suis CA1 expressed in Escherichia coli BL21(DE3) by stopped-flow CO2-hydration assay2010Journal of medicinal chemistry, Mar-11, Volume: 53, Issue:5
Cloning, characterization, and inhibition studies of a beta-carbonic anhydrase from Brucella suis.
AID644087Inhibition of human carbonic anhydrase 6 using 4-nitrophenylacetate as substrate after 3 mins using spectrophotometry by Lineweaver-Burk plot analysis2012European journal of medicinal chemistry, Mar, Volume: 49Structure-activity relationships for the interaction of 5,10-dihydroindeno[1,2-b]indole derivatives with human and bovine carbonic anhydrase isoforms I, II, III, IV and VI.
AID770585Inhibition of human cytosolic carbonic anhydrase 2 preincubated for 15 mins at room temperature followed by 72 hrs at 4 degC by stopped flow CO2 hydration assay2013Bioorganic & medicinal chemistry, Oct-01, Volume: 21, Issue:19
Carbonic anhydrase inhibitors: synthesis and inhibition of the human carbonic anhydrase isoforms I, II, VII, IX and XII with benzene sulfonamides incorporating 4,5,6,7-tetrabromophthalimide moiety.
AID1067225Selectivity ratio of Ki for human transmembrane carbonic anhydrase 2 to Ki for human cytosolic carbonic anhydrase 122014Bioorganic & medicinal chemistry, Mar-01, Volume: 22, Issue:5
Carbonic anhydrase inhibitors: synthesis and inhibition of the human carbonic anhydrase isoforms I, II, IX and XII with benzene sulfonamides incorporating 4- and 3-nitrophthalimide moieties.
AID408763Anticonvulsant activity against maximal electroshock-induced seizures in orally dosed rat model2008Bioorganic & medicinal chemistry, Jun-01, Volume: 16, Issue:11
Synthesis and anticonvulsant activity of aromatic tetramethylcyclopropanecarboxamide derivatives.
AID1278413Inhibition of recombinant Colwellia psychrerythraea gamma carbonic anhydrase preincubated for 15 mins by stopped flow CO2 hydration assay2016Bioorganic & medicinal chemistry letters, Feb-15, Volume: 26, Issue:4
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the Antarctic bacterium Colwellia psychrerythraea.
AID441715Inhibition of human recombinant CA13 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID295951Selectivity for human CA5A to human CA22007Bioorganic & medicinal chemistry, Jun-15, Volume: 15, Issue:12
Molecular modeling study for the binding of zonisamide and topiramate to the human mitochondrial carbonic anhydrase isoform VA.
AID1240216Inhibition of Methanosarcina thermophila recombinant gamma carbonic anhydrase by stopped flow CO2 hydrase assay method2015Bioorganic & medicinal chemistry letters, Sep-01, Volume: 25, Issue:17
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the Antarctic bacterium Pseudoalteromonas haloplanktis.
AID436748Inhibition of human recombinant full length mitochondrial carbonic anhydrase 5A by stopped-flow CO2 hydration assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Carbonic anhydrase inhibitors. Aromatic/heterocyclic sulfonamides incorporating phenacetyl, pyridylacetyl and thienylacetyl tails act as potent inhibitors of human mitochondrial isoforms VA and VB.
AID441211Selectivity for human cloned CA9 over human cloned CA22009Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20
S-glycosyl primary sulfonamides--a new structural class for selective inhibition of cancer-associated carbonic anhydrases.
AID552131Inhibition of Stylophora pistillata carbonic anhydrase 2 by stopped-flow CO2 hydration assay2011Bioorganic & medicinal chemistry letters, Jan-15, Volume: 21, Issue:2
Carbonic anhydrase inhibitors. Inhibition studies with anions and sulfonamides of a new cytosolic enzyme from the scleractinian coral Stylophora pistillata.
AID1194025Inhibition of human recombinant carbonic anhydrase 2 by stopped flow CO2 hydrase assay2015Bioorganic & medicinal chemistry, Apr-15, Volume: 23, Issue:8
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the Antarctic cyanobacterium Nostoc commune.
AID441206Inhibition of human cloned CA1 by stopped flow CO2 hydration assay2009Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20
S-glycosyl primary sulfonamides--a new structural class for selective inhibition of cancer-associated carbonic anhydrases.
AID23922Lipophilicity of the compound2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Carbonic anhydrase inhibitors: anticonvulsant sulfonamides incorporating valproyl and other lipophilic moieties.
AID588184Inhibition of Candida albicans recombinant Nce103 beta-carbonic anhydrase after 15 mins by stopped flow CO2 hydration assay2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Natural product-based phenols as novel probes for mycobacterial and fungal carbonic anhydrases.
AID261580Inhibition of human recombinant carbonic anhydrase 2 by stopped-flow CO2 hydrase assay2006Journal of medicinal chemistry, Mar-23, Volume: 49, Issue:6
Carbonic anhydrase inhibitors: DNA cloning and inhibition studies of the alpha-carbonic anhydrase from Helicobacter pylori, a new target for developing sulfonamide and sulfamate gastric drugs.
AID1766625Inhibition of recombinant human CA12 pre-incubated for 15 mins measured by stopped flow CO2 hydration assay2021Journal of medicinal chemistry, 03-25, Volume: 64, Issue:6
Discovery of Potent Carbonic Anhydrase Inhibitors as Effective Anticonvulsant Agents: Drug Design, Synthesis, and In Vitro and In Vivo Investigations.
AID633373Inhibition of human recombinant full length carbonic anhydrase 14 preincubated for 15 mins by stopped flow CO2 hydration assay2011Bioorganic & medicinal chemistry, Dec-01, Volume: 19, Issue:23
Synthesis and biological profile of new 1,2,3,4-tetrahydroisoquinolines as selective carbonic anhydrase inhibitors.
AID588183Inhibition of Mycobacterium tuberculosis recombinant Rv1284 beta-carbonic anhydrase after 15 mins by stopped flow CO2 hydration assay2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Natural product-based phenols as novel probes for mycobacterial and fungal carbonic anhydrases.
AID464120Inhibition of human recombinant CA9 by stopped-flow CO2 hydration assay2010Journal of medicinal chemistry, Mar-25, Volume: 53, Issue:6
Identification of 3,4-Dihydroisoquinoline-2(1H)-sulfonamides as potent carbonic anhydrase inhibitors: synthesis, biological evaluation, and enzyme--ligand X-ray studies.
AID669487Inhibition of human recombinant full length CA14-mediated CO2 hydration preincubated for 15 mins by stopped-flow assay2012Journal of medicinal chemistry, Apr-26, Volume: 55, Issue:8
Synthesis, structure-activity relationship studies, and X-ray crystallographic analysis of arylsulfonamides as potent carbonic anhydrase inhibitors.
AID271172Inhibition of human recombinant carbonic anhydrase 1 by stopped-flow CO2 hydrase assay2006Journal of medicinal chemistry, Sep-07, Volume: 49, Issue:18
Carbonic anhydrase inhibitors: Hypoxia-activatable sulfonamides incorporating disulfide bonds that target the tumor-associated isoform IX.
AID261579Inhibition of human recombinant carbonic anhydrase 1 by stopped-flow CO2 hydrase assay2006Journal of medicinal chemistry, Mar-23, Volume: 49, Issue:6
Carbonic anhydrase inhibitors: DNA cloning and inhibition studies of the alpha-carbonic anhydrase from Helicobacter pylori, a new target for developing sulfonamide and sulfamate gastric drugs.
AID1240215Inhibition of Pseudoalteromonas haloplanktis gamma carbonic anhydrase by CO2 hydration assay2015Bioorganic & medicinal chemistry letters, Sep-01, Volume: 25, Issue:17
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the Antarctic bacterium Pseudoalteromonas haloplanktis.
AID1291363Inhibition of recombinant Vibrio cholerae gamma-carbonic anhydrase preincubated for 15 mins by stopped-flow CO2 hydration assay2016Bioorganic & medicinal chemistry letters, Apr-15, Volume: 26, Issue:8
Comparison of the sulfonamide inhibition profiles of the α-, β- and γ-carbonic anhydrases from the pathogenic bacterium Vibrio cholerae.
AID1194024Inhibition of human recombinant carbonic anhydrase 1 by stopped flow CO2 hydrase assay2015Bioorganic & medicinal chemistry, Apr-15, Volume: 23, Issue:8
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the Antarctic cyanobacterium Nostoc commune.
AID644085Inhibition of human carbonic anhydrase 2 using 4-nitrophenylacetate as substrate after 3 mins using spectrophotometry by Lineweaver-Burk plot analysis2012European journal of medicinal chemistry, Mar, Volume: 49Structure-activity relationships for the interaction of 5,10-dihydroindeno[1,2-b]indole derivatives with human and bovine carbonic anhydrase isoforms I, II, III, IV and VI.
AID441711Inhibition of human recombinant CA6 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID552129Inhibition of human recombinant CA6 by stopped-flow CO2 hydration assay2011Bioorganic & medicinal chemistry letters, Jan-15, Volume: 21, Issue:2
Carbonic anhydrase inhibitors. Inhibition studies with anions and sulfonamides of a new cytosolic enzyme from the scleractinian coral Stylophora pistillata.
AID436751Selectivity ratio of Ki for human recombinant cytosolic carbonic anhydrase 2 to Ki for human recombinant full length mitochondrial carbonic anhydrase 5B2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Carbonic anhydrase inhibitors. Aromatic/heterocyclic sulfonamides incorporating phenacetyl, pyridylacetyl and thienylacetyl tails act as potent inhibitors of human mitochondrial isoforms VA and VB.
AID320314Inhibition of human catalytic domain carbonic hydrase 12 by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Carbonic anhydrase inhibitors. Interaction of 2-N,N-dimethylamino-1,3,4-thiadiazole-5-methanesulfonamide with 12 mammalian isoforms: kinetic and X-ray crystallographic studies.
AID1434427Inhibition of recombinant human carbonic anhydrase 1 assessed as reduction in CO2 hydration preincubated for 15 mins followed by CO2 addition measured for 10 to 100 sec by Line-Weaver Burk plot analysis
AID263636Inhibition of human recombinant CA12006Bioorganic & medicinal chemistry letters, Apr-15, Volume: 16, Issue:8
Carbonic anhydrase inhibitors: cloning and sulfonamide inhibition studies of a carboxyterminal truncated alpha-carbonic anhydrase from Helicobacter pylori.
AID441707Inhibition of human recombinant CA3 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID436746Inhibition of human recombinant cytosolic carbonic anhydrase 1 by stopped-flow CO2 hydration assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Carbonic anhydrase inhibitors. Aromatic/heterocyclic sulfonamides incorporating phenacetyl, pyridylacetyl and thienylacetyl tails act as potent inhibitors of human mitochondrial isoforms VA and VB.
AID371556Inhibition of truncated human cloned membrane-associated carbonic anhydrase 4 preincubated for 15 mins by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Dec-15, Volume: 18, Issue:24
Carbonic anhydrase inhibitors: 2-substituted-1,3,4-thiadiazole-5-sulfamides act as powerful and selective inhibitors of the mitochondrial isozymes VA and VB over the cytosolic and membrane-associated carbonic anhydrases I, II and IV.
AID409601Inhibition of human aquaporin 4 M23 isoform expressed in Xenopus laevis oocytes2009Bioorganic & medicinal chemistry, Jan-01, Volume: 17, Issue:1
Inhibition of aquaporin 4 by antiepileptic drugs.
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).
AID540233Dose normalised AUC in human after po administration2005Xenobiotica; the fate of foreign compounds in biological systems, Feb, Volume: 35, Issue:2
Comparative evaluation of oral systemic exposure of 56 xenobiotics in rat, dog, monkey and human.
AID648180Inhibition of human wild type carbonic anhydrase 2 Gln92Val mutant expressed in Escherichia coli after 15 mins preincubation by stopped flow CO2 hydration assay2012Bioorganic & medicinal chemistry, Apr-01, Volume: 20, Issue:7
Mutation of active site residues Asn67 to Ile, Gln92 to Val and Leu204 to Ser in human carbonic anhydrase II: influences on the catalytic activity and affinity for inhibitors.
AID1473740Inhibition of human MRP3 overexpressed in Sf9 insect cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 10 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID539464Solubility of the compound in 0.1 M phosphate buffer at 600 uM at pH 7.4 after 24 hrs by LC/MS/MS analysis2010Bioorganic & medicinal chemistry letters, Dec-15, Volume: 20, Issue:24
Experimental solubility profiling of marketed CNS drugs, exploring solubility limit of CNS discovery candidate.
AID1188134Inhibition of human recombinant Carbonic anhydrase 1 compound preincubated for 15 mins by stopped flow CO2 hydrase assay method2014Bioorganic & medicinal chemistry, Sep-01, Volume: 22, Issue:17
Sulfonamide inhibition study of the carbonic anhydrases from the bacterial pathogen Porphyromonas gingivalis: the β-class (PgiCAb) versus the γ-class (PgiCA) enzymes.
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID588195Selectivity ratio of Ki for human recombinant alpha-carbonic anhydrase 2 to Ki for Mycobacterium tuberculosis recombinant Rv1284 beta-carbonic anhydrase2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Natural product-based phenols as novel probes for mycobacterial and fungal carbonic anhydrases.
AID644035Inhibition of human carbonic anhydrase 2 esterase activity using 4-nitrophenylacetate as substrate2012Bioorganic & medicinal chemistry letters, Feb-01, Volume: 22, Issue:3
Synthesis and carbonic anhydrase inhibitory properties of novel cyclohexanonyl bromophenol derivatives.
AID1275913Inhibition of human Carbonic anhydrase1 using CO2 as substrate preincubated for 15 mins by stopped-flow CO2 hydration assay2016Bioorganic & medicinal chemistry, Mar-01, Volume: 24, Issue:5
Sulfonamide inhibition studies of the β-carbonic anhydrase from the pathogenic bacterium Vibrio cholerae.
AID293812Inhibition of human recombinant CA2 by stopped flow CO2 hydrase assay2007Bioorganic & medicinal chemistry letters, Mar-15, Volume: 17, Issue:6
Carbonic anhydrase inhibitors: inhibition of cytosolic/tumor-associated isoforms I, II, and IX with iminodiacetic carboxylates/hydroxamates also incorporating benzenesulfonamide moieties.
AID1653809Substrate activity at human mARC2 expressed in Escherichia coli assessed as turnover rates at 1 mM pre-incubated for 3 mins followed by NADH addition and measured after 15 mins by LC-MS analysis based assay2020Journal of medicinal chemistry, 06-25, Volume: 63, Issue:12
Drug Metabolism by the Mitochondrial Amidoxime Reducing Component (mARC): Rapid Assay and Identification of New Substrates.
AID123884Percentage block of the hind-limb tonic-extensor seizure was determined after application of an electric shock to mice for 60 min followed by 40 mg/kg peroral dose1987Journal of medicinal chemistry, May, Volume: 30, Issue:5
Anticonvulsant O-alkyl sulfamates. 2,3:4,5-Bis-O-(1-methylethylidene)-beta-D-fructopyranose sulfamate and related compounds.
AID497127Inhibition of wild type human recombinant carbonic anhydrase 1 expressed in Escherichia coli BL21 (DE3) after 15 mins by CO2 hydration method2010Bioorganic & medicinal chemistry, Aug-01, Volume: 18, Issue:15
Mutation of Phe91 to Asn in human carbonic anhydrase I unexpectedly enhanced both catalytic activity and affinity for sulfonamide inhibitors.
AID743513Inhibition of Helicobacter pylori recombinant alpha carbonic anhydrase preincubated for 15 mins by CO2 hydration stopped-flow assay2013Bioorganic & medicinal chemistry, Mar-15, Volume: 21, Issue:6
The alpha-carbonic anhydrase from the thermophilic bacterium Sulfurihydrogenibium yellowstonense YO3AOP1 is highly susceptible to inhibition by sulfonamides.
AID743515Inhibition of human recombinant carbonic anhydrase 1 preincubated for 15 mins by CO2 hydration stopped-flow assay2013Bioorganic & medicinal chemistry, Mar-15, Volume: 21, Issue:6
The alpha-carbonic anhydrase from the thermophilic bacterium Sulfurihydrogenibium yellowstonense YO3AOP1 is highly susceptible to inhibition by sulfonamides.
AID1061069Inhibition of human recombinant carbonic anhydrase 2 preincubated for 15 mins by stopped flow CO2 hydration assay2014Bioorganic & medicinal chemistry letters, Jan-01, Volume: 24, Issue:1
Sulfonamide inhibition studies of the δ-carbonic anhydrase from the diatom Thalassiosira weissflogii.
AID441713Inhibition of human recombinant CA9 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID1262263Inhibition of human CA1 incubated for 15 mins prior to testing by stopped flow CO2 hydrase assay2015Bioorganic & medicinal chemistry letters, Dec-01, Volume: 25, Issue:23
Anion and sulfonamide inhibition studies of an α-carbonic anhydrase from the Antarctic hemoglobinless fish Chionodraco hamatus.
AID588185Inhibition of Cryptococcus neoformans recombinant Can2 beta-carbonic anhydrase after 15 mins by stopped flow CO2 hydration assay2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Natural product-based phenols as novel probes for mycobacterial and fungal carbonic anhydrases.
AID239126Inhibitory constant against catalytic domain of human carbonic anhydrase XII2005Bioorganic & medicinal chemistry letters, Sep-01, Volume: 15, Issue:17
Carbonic anhydrase inhibitors: inhibition of the transmembrane isozyme XIV with sulfonamides.
AID238852Mean inhibitory constant towards human carbonic anhydrase II determined by stopped-flow method2005Bioorganic & medicinal chemistry letters, May-02, Volume: 15, Issue:9
Carbonic anhydrase inhibitors. Zonisamide is an effective inhibitor of the cytosolic isozyme II and mitochondrial isozyme V: solution and X-ray crystallographic studies.
AID644380Inhibition of human recombinant carbonic anhydrase 1 after 15 mins by stopped flow CO2 hydration assay2012Bioorganic & medicinal chemistry, Feb-15, Volume: 20, Issue:4
Cloning, characterization and sulfonamide inhibition studies of an α-carbonic anhydrase from the living fossil sponge Astrosclera willeyana.
AID644084Inhibition of human carbonic anhydrase 1 using 4-nitrophenylacetate as substrate after 3 mins using spectrophotometry by Lineweaver-Burk plot analysis2012European journal of medicinal chemistry, Mar, Volume: 49Structure-activity relationships for the interaction of 5,10-dihydroindeno[1,2-b]indole derivatives with human and bovine carbonic anhydrase isoforms I, II, III, IV and VI.
AID1278409Inhibition of human carbonic anhydrase 2 preincubated for 15 mins by CO2 hydrase stopped flow assay2016Bioorganic & medicinal chemistry letters, Feb-15, Volume: 26, Issue:4
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the Antarctic bacterium Colwellia psychrerythraea.
AID588196Selectivity ratio of Ki for human recombinant alpha-carbonic anhydrase 2 to Ki for Candida albicans recombinant Nce103 beta-carbonic anhydrase2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Natural product-based phenols as novel probes for mycobacterial and fungal carbonic anhydrases.
AID1278412Inhibition of Pseudoalteromonas haloplanktis gamma carbonic anhydrase preincubated for 15 mins by stopped flow CO2 hydration assay2016Bioorganic & medicinal chemistry letters, Feb-15, Volume: 26, Issue:4
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the Antarctic bacterium Colwellia psychrerythraea.
AID669116Inhibition of Cryptococcus neoformans Can2 preincubated for 15 mins measured for 10 to 100 sec by stopped-flow method2012Journal of medicinal chemistry, Apr-12, Volume: 55, Issue:7
Molecular cloning, characterization, and inhibition studies of a β-carbonic anhydrase from Malassezia globosa, a potential antidandruff target.
AID644381Inhibition of human recombinant carbonic anhydrase 2 after 15 mins by stopped flow CO2 hydration assay2012Bioorganic & medicinal chemistry, Feb-15, Volume: 20, Issue:4
Cloning, characterization and sulfonamide inhibition studies of an α-carbonic anhydrase from the living fossil sponge Astrosclera willeyana.
AID320306Inhibition of human recombinant full length carbonic hydrase 2 by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Carbonic anhydrase inhibitors. Interaction of 2-N,N-dimethylamino-1,3,4-thiadiazole-5-methanesulfonamide with 12 mammalian isoforms: kinetic and X-ray crystallographic studies.
AID456400Inhibition of human recombinant carbonic anhydrase 5B by stopped flow CO2 hydration method2010Bioorganic & medicinal chemistry, Jan-01, Volume: 18, Issue:1
Carbonic anhydrase inhibitors. Identification of selective inhibitors of the human mitochondrial isozymes VA and VB over the cytosolic isozymes I and II from a natural product-based phenolic library.
AID570292Competitive inhibition of zebrafish MAO by spectrophotometry2011Journal of medicinal chemistry, Feb-10, Volume: 54, Issue:3
Interactions of monoamine oxidases with the antiepileptic drug zonisamide: specificity of inhibition and structure of the human monoamine oxidase B complex.
AID349607Inhibition of Mycobacterium tuberculosis recombinant carbonic anhydrase 1 encoded by Rv1284 by stopped flow CO2 hydration assay2009Journal of medicinal chemistry, May-14, Volume: 52, Issue:9
Carbonic anhydrase inhibitors. Cloning, characterization, and inhibition studies of a new beta-carbonic anhydrase from Mycobacterium tuberculosis.
AID300475Inhibition of human recombinant full length CA14 by stopped-flow technique2007Bioorganic & medicinal chemistry letters, Sep-01, Volume: 17, Issue:17
Carbonic anhydrase inhibitors. Interaction of the antiepileptic drug sulthiame with twelve mammalian isoforms: kinetic and X-ray crystallographic studies.
AID1262266Inhibition of weddell seal alphaCA incubated for 15 mins prior to testing by stopped flow CO2 hydrase assay2015Bioorganic & medicinal chemistry letters, Dec-01, Volume: 25, Issue:23
Anion and sulfonamide inhibition studies of an α-carbonic anhydrase from the Antarctic hemoglobinless fish Chionodraco hamatus.
AID577530Inhibition of Brucella suis carbonic anhydrase II by spectrophotometry at pH 8.32011Bioorganic & medicinal chemistry, Feb-01, Volume: 19, Issue:3
A new β-carbonic anhydrase from Brucella suis, its cloning, characterization, and inhibition with sulfonamides and sulfamates, leading to impaired pathogen growth.
AID414961Inhibition of Mycobacterium tuberculosis H37Rv recombinant beta-carbonic anhydrase 1 expressed in Escherichia coli BL21 by stopped flow CO2 hydration method2009Journal of medicinal chemistry, Apr-23, Volume: 52, Issue:8
Molecular cloning, characterization, and inhibition studies of the Rv1284 beta-carbonic anhydrase from Mycobacterium tuberculosis with sulfonamides and a sulfamate.
AID123725Percentage block of the hind-limb tonic-extensor seizure was determined after application of an electric shock to mice for 120 min followed by 100 mg/kg intraperitoneal dose; ND means no data1987Journal of medicinal chemistry, May, Volume: 30, Issue:5
Anticonvulsant O-alkyl sulfamates. 2,3:4,5-Bis-O-(1-methylethylidene)-beta-D-fructopyranose sulfamate and related compounds.
AID711212Inhibition of recombinant Vibrio cholerae carbonic anhydrase expressed in Escherichia coli (DE3) preincubated for 15 mins by stopped-flow CO2 hydrase assay2012Journal of medicinal chemistry, Dec-13, Volume: 55, Issue:23
DNA cloning, characterization, and inhibition studies of an α-carbonic anhydrase from the pathogenic bacterium Vibrio cholerae.
AID342472Inhibition of AQP4 in mouse erythrocytes assessed as inhibition of osmotic water permeability at 100 uM after 15 mins by stopped-flow light scattering method2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Lack of aquaporin-4 water transport inhibition by antiepileptics and arylsulfonamides.
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).
AID299242Inhibition of human carbonic anhydrase 1 by stopped-flow CO2 hydrase assay2007Bioorganic & medicinal chemistry letters, Jul-01, Volume: 17, Issue:13
Carbonic anhydrase inhibitors: the beta-carbonic anhydrase from Helicobacter pylori is a new target for sulfonamide and sulfamate inhibitors.
AID725956Inhibition of human recombinant carbonic anhydrase 2 by stopped flow CO2 hydration assay2013Journal of medicinal chemistry, Feb-28, Volume: 56, Issue:4
Cloning, characterization, and sulfonamide and thiol inhibition studies of an α-carbonic anhydrase from Trypanosoma cruzi, the causative agent of Chagas disease.
AID1123816Neurotoxicity in po dosed STD-dd mouse assessed as muscle incoordination administered via gavage by rotarod test1979Journal of medicinal chemistry, Feb, Volume: 22, Issue:2
Studies on 3-substituted 1,2-benzisoxazole derivatives. 6. Syntheses of 3-(sulfamoylmethyl)-1,2-benzisoxazole derivatives and their anticonvulsant activities.
AID47905Inhibitory effect on human Carbonic anhydrase II2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Carbonic anhydrase inhibitors: anticonvulsant sulfonamides incorporating valproyl and other lipophilic moieties.
AID263637Inhibition of human recombinant CA22006Bioorganic & medicinal chemistry letters, Apr-15, Volume: 16, Issue:8
Carbonic anhydrase inhibitors: cloning and sulfonamide inhibition studies of a carboxyterminal truncated alpha-carbonic anhydrase from Helicobacter pylori.
AID1489015Anticonvulsant activity in amygdala kindling rat model assessed as change in after discharge duration at 100 mg/kg, po (Rvb = -5.5%)2017Bioorganic & medicinal chemistry letters, 09-01, Volume: 27, Issue:17
N-alkyl-[1,1'-biphenyl]-2-sulfonamide derivatives as novel broad spectrum anti-epileptic drugs with efficacy equivalent to that of sodium valproate.
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID1194028Inhibition of recombinant Nostoc commune gamma-carbonic anhydrase preincubated for 15 mins by stopped flow CO2 hydrase assay2015Bioorganic & medicinal chemistry, Apr-15, Volume: 23, Issue:8
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the Antarctic cyanobacterium Nostoc commune.
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.
AID1287519Inhibition of Vibrio cholerae beta carbonic anhydrase incubated for 15 mins by stopped-flow CO2 hydration assay2016Bioorganic & medicinal chemistry letters, Apr-01, Volume: 26, Issue:7
Sulfonamide inhibition studies of the β-carbonic anhydrase from the newly discovered bacterium Enterobacter sp. B13.
AID342470Inhibition of AQP4 in wild type mouse brain gilial cells assessed as osmotic water permeability at 10 to 100 uM after 15 mins by calcein quenching assay2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Lack of aquaporin-4 water transport inhibition by antiepileptics and arylsulfonamides.
AID185053Neuroprotective activity was determined in the rat middle cerebral artery occlusion (MCAO) model of focal stroke2001Journal of medicinal chemistry, Jan-18, Volume: 44, Issue:2
Medicinal chemistry of neuronal voltage-gated sodium channel blockers.
AID414955Inhibition of human recombinant carbonic anhydrase 1 by stopped flow CO2 hydration method2009Journal of medicinal chemistry, Apr-23, Volume: 52, Issue:8
Molecular cloning, characterization, and inhibition studies of the Rv1284 beta-carbonic anhydrase from Mycobacterium tuberculosis with sulfonamides and a sulfamate.
AID1453411Inhibition of Burkholderia pseudomallei beta-carbonic anhydrase assessed as reduction in CO2 hydration preincubated for 15 mins followed by CO2 addition measured for 10 to 100 secs by stopped-flow assay
AID1142834Inhibition of human carbonic anhydrase-2 by stopped-flow CO2 hydration assay2014Bioorganic & medicinal chemistry, Jun-01, Volume: 22, Issue:11
Sulfonamide inhibition studies of two β-carbonic anhydrases from the bacterial pathogen Legionella pneumophila.
AID1067228Inhibition of human transmembrane carbonic anhydrase 9 by stopped-flow CO2 hydration assay2014Bioorganic & medicinal chemistry, Mar-01, Volume: 22, Issue:5
Carbonic anhydrase inhibitors: synthesis and inhibition of the human carbonic anhydrase isoforms I, II, IX and XII with benzene sulfonamides incorporating 4- and 3-nitrophthalimide moieties.
AID369273Inhibition of human full length recombinant carbonic anhydrase 6 by stopped flow CO2 hydrase assay2009Journal of medicinal chemistry, Feb-12, Volume: 52, Issue:3
Cloning, expression, post-translational modifications and inhibition studies on the latest mammalian carbonic anhydrase isoform, CA XV.
AID1190065Inhibition of Plasmodium falciparum Eta-carbonic anhydrase pre-incubated for 15 mins before CO2 substrate addition by stopped-flow CO2 hydration assay2015Bioorganic & medicinal chemistry, Feb-01, Volume: 23, Issue:3
Sulfonamide inhibition studies of the η-class carbonic anhydrase from the malaria pathogen Plasmodium falciparum.
AID441709Inhibition of human recombinant CA5A by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID468443Inhibition of human FAAH at 1 uM2009Bioorganic & medicinal chemistry letters, Dec-01, Volume: 19, Issue:23
Mining biologically-active molecules for inhibitors of fatty acid amide hydrolase (FAAH): identification of phenmedipham and amperozide as FAAH inhibitors.
AID1268962Inhibition of recombinant human carbonic anhydrase-1 by stopped flow CO2 hydrase assay2016Bioorganic & medicinal chemistry letters, Jan-15, Volume: 26, Issue:2
Sulfonamide inhibition studies of the α-carbonic anhydrase from the gammaproteobacterium Thiomicrospira crunogena XCL-2, TcruCA.
AID1251246Anticonvulsant activity in rat amygdala kindling model assessed as change in after-discharge duration at 100 mg/kg, po2015Bioorganic & medicinal chemistry letters, Oct-15, Volume: 25, Issue:20
Discovery of benzothiazine derivatives as novel, orally-active anti-epileptic drug candidates with broad anticonvulsant effect.
AID588194Selectivity ratio of Ki for human recombinant alpha-carbonic anhydrase 2 to Ki for Mycobacterium tuberculosis recombinant Rv3273 beta-carbonic anhydrase2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Natural product-based phenols as novel probes for mycobacterial and fungal carbonic anhydrases.
AID320308Inhibition of human recombinant full length carbonic hydrase 4 by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Carbonic anhydrase inhibitors. Interaction of 2-N,N-dimethylamino-1,3,4-thiadiazole-5-methanesulfonamide with 12 mammalian isoforms: kinetic and X-ray crystallographic studies.
AID239286Mean inhibitory constant towards human carbonic anhydrase II determined by stopped-flow method after 1 hr of incubation2005Bioorganic & medicinal chemistry letters, May-02, Volume: 15, Issue:9
Carbonic anhydrase inhibitors. Zonisamide is an effective inhibitor of the cytosolic isozyme II and mitochondrial isozyme V: solution and X-ray crystallographic studies.
AID436565Inhibition of cloned Stylophora pistillata alpha-CA expressed in human HEK293 cells by stopped-flow CO2 assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Carbonic anhydrase inhibitors. Inhibition studies of a coral secretory isoform by sulfonamides.
AID633370Inhibition of human recombinant full length CA1 preincubated for 15 mins by stopped flow CO2 hydration assay2011Bioorganic & medicinal chemistry, Dec-01, Volume: 19, Issue:23
Synthesis and biological profile of new 1,2,3,4-tetrahydroisoquinolines as selective carbonic anhydrase inhibitors.
AID552130Inhibition of Stylophora pistillata carbonic anhydrase by stopped-flow CO2 hydration assay2011Bioorganic & medicinal chemistry letters, Jan-15, Volume: 21, Issue:2
Carbonic anhydrase inhibitors. Inhibition studies with anions and sulfonamides of a new cytosolic enzyme from the scleractinian coral Stylophora pistillata.
AID570284Competitive inhibition of human MAO B by spectrophotometry2011Journal of medicinal chemistry, Feb-10, Volume: 54, Issue:3
Interactions of monoamine oxidases with the antiepileptic drug zonisamide: specificity of inhibition and structure of the human monoamine oxidase B complex.
AID464122Selectivity ratio of Ki for human CA2 to Ki for human CA92010Journal of medicinal chemistry, Mar-25, Volume: 53, Issue:6
Identification of 3,4-Dihydroisoquinoline-2(1H)-sulfonamides as potent carbonic anhydrase inhibitors: synthesis, biological evaluation, and enzyme--ligand X-ray studies.
AID1251244Anticonvulsant activity in rat amygdala kindling model assessed as change in after-discharge threshold at 100 mg/kg, po2015Bioorganic & medicinal chemistry letters, Oct-15, Volume: 25, Issue:20
Discovery of benzothiazine derivatives as novel, orally-active anti-epileptic drug candidates with broad anticonvulsant effect.
AID1434430Inhibition of Vibrio cholerae Gamma-carbonic anhydrase assessed as reduction in CO2 hydration preincubated for 15 mins followed by CO2 addition measured for 10 to 100 sec by Line-Weaver Burk plot analysis
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).
AID300474Inhibition of mouse recombinant full length CA13 by stopped-flow technique2007Bioorganic & medicinal chemistry letters, Sep-01, Volume: 17, Issue:17
Carbonic anhydrase inhibitors. Interaction of the antiepileptic drug sulthiame with twelve mammalian isoforms: kinetic and X-ray crystallographic studies.
AID669320Inhibition of human recombinant full length CA1-mediated CO2 hydration preincubated for 15 mins by stopped-flow assay2012Journal of medicinal chemistry, Apr-26, Volume: 55, Issue:8
Synthesis, structure-activity relationship studies, and X-ray crystallographic analysis of arylsulfonamides as potent carbonic anhydrase inhibitors.
AID1251243Anticonvulsant activity in rat amygdala kindling model assessed as change in after-discharge threshold at 30 mg/kg, po2015Bioorganic & medicinal chemistry letters, Oct-15, Volume: 25, Issue:20
Discovery of benzothiazine derivatives as novel, orally-active anti-epileptic drug candidates with broad anticonvulsant effect.
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).
AID1067229Inhibition of human cytosolic carbonic anhydrase 2 by stopped-flow CO2 hydration assay2014Bioorganic & medicinal chemistry, Mar-01, Volume: 22, Issue:5
Carbonic anhydrase inhibitors: synthesis and inhibition of the human carbonic anhydrase isoforms I, II, IX and XII with benzene sulfonamides incorporating 4- and 3-nitrophthalimide moieties.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID123753Percentage block of the hind-limb tonic-extensor seizure was determined after application of an electric shock to mice for 30 min followed by 40 mg/kg peroral dose1987Journal of medicinal chemistry, May, Volume: 30, Issue:5
Anticonvulsant O-alkyl sulfamates. 2,3:4,5-Bis-O-(1-methylethylidene)-beta-D-fructopyranose sulfamate and related compounds.
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID577531Inhibition of Brucella suis carbonic anhydrase I by spectrophotometry at pH 8.32011Bioorganic & medicinal chemistry, Feb-01, Volume: 19, Issue:3
A new β-carbonic anhydrase from Brucella suis, its cloning, characterization, and inhibition with sulfonamides and sulfamates, leading to impaired pathogen growth.
AID271174Inhibition of human recombinant carbonic anhydrase 9 by stopped-flow CO2 hydrase assay2006Journal of medicinal chemistry, Sep-07, Volume: 49, Issue:18
Carbonic anhydrase inhibitors: Hypoxia-activatable sulfonamides incorporating disulfide bonds that target the tumor-associated isoform IX.
AID342467Inhibition of AQP4 expressed in rat FRT cells assessed as osmotic water permeability at 100 uM after 15 mins by stopped-flow light scattering method2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Lack of aquaporin-4 water transport inhibition by antiepileptics and arylsulfonamides.
AID552127Inhibition of human recombinant CA1 by stopped-flow CO2 hydration assay2011Bioorganic & medicinal chemistry letters, Jan-15, Volume: 21, Issue:2
Carbonic anhydrase inhibitors. Inhibition studies with anions and sulfonamides of a new cytosolic enzyme from the scleractinian coral Stylophora pistillata.
AID669119Inhibition of GST-tagged Malassezia globosa ATCC 96807/CBS 7966 MG-CA expressed in Escherichia coli BL21(DE3) cells preincubated for 15 mins measured for 10 to 100 sec by stopped-flow method2012Journal of medicinal chemistry, Apr-12, Volume: 55, Issue:7
Molecular cloning, characterization, and inhibition studies of a β-carbonic anhydrase from Malassezia globosa, a potential antidandruff target.
AID1194026Inhibition of recombinant Methanosarcina thermophila gamma-carbonic anhydrase by stopped flow CO2 hydrase assay2015Bioorganic & medicinal chemistry, Apr-15, Volume: 23, Issue:8
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the Antarctic cyanobacterium Nostoc commune.
AID1190064Inhibition of human recombinant carbonic anhydrase 2 by stopped-flow CO2 hydration assay2015Bioorganic & medicinal chemistry, Feb-01, Volume: 23, Issue:3
Sulfonamide inhibition studies of the η-class carbonic anhydrase from the malaria pathogen Plasmodium falciparum.
AID578222Inhibition of human recombinant CA2 cytosolic isoform by stopped-flow CO2 hydration assay2011Bioorganic & medicinal chemistry letters, Mar-01, Volume: 21, Issue:5
(R)-/(S)-10-camphorsulfonyl-substituted aromatic/heterocyclic sulfonamides selectively inhibit mitochondrial over cytosolic carbonic anhydrases.
AID669486Inhibition of human recombinant CA9 catalytic domain-mediated CO2 hydration preincubated for 15 mins by stopped-flow assay2012Journal of medicinal chemistry, Apr-26, Volume: 55, Issue:8
Synthesis, structure-activity relationship studies, and X-ray crystallographic analysis of arylsulfonamides as potent carbonic anhydrase inhibitors.
AID1165421Inhibition of carbonic anhydrase (unknown origin)2014Bioorganic & medicinal chemistry, Dec-01, Volume: 22, Issue:23
Substituted thieno[2,3-b]thiophenes and related congeners: Synthesis, β-glucuronidase inhibition activity, crystal structure, and POM analyses.
AID648179Inhibition of human wild type carbonic anhydrase 2 Asn67Ile mutant expressed in Escherichia coli after 15 mins preincubation by stopped flow CO2 hydration assay2012Bioorganic & medicinal chemistry, Apr-01, Volume: 20, Issue:7
Mutation of active site residues Asn67 to Ile, Gln92 to Val and Leu204 to Ser in human carbonic anhydrase II: influences on the catalytic activity and affinity for inhibitors.
AID299243Inhibition of human carbonic anhydrase 2 by stopped-flow CO2 hydrase assay2007Bioorganic & medicinal chemistry letters, Jul-01, Volume: 17, Issue:13
Carbonic anhydrase inhibitors: the beta-carbonic anhydrase from Helicobacter pylori is a new target for sulfonamide and sulfamate inhibitors.
AID1195371Inhibition of Anopheles gambiae carbonic anhydrase pre-incubated for 15 mins by stopped-flow CO2 hydration assay2015Bioorganic & medicinal chemistry, May-15, Volume: 23, Issue:10
The β-carbonic anhydrase from the malaria mosquito Anopheles gambiae is highly inhibited by sulfonamides.
AID123735Percentage block of the hind-limb tonic-extensor seizure was determined after application of an electric shock to mice for 240 min followed by 100 mg/kg intraperitoneal dose; ND means no data1987Journal of medicinal chemistry, May, Volume: 30, Issue:5
Anticonvulsant O-alkyl sulfamates. 2,3:4,5-Bis-O-(1-methylethylidene)-beta-D-fructopyranose sulfamate and related compounds.
AID436563Inhibition of human recombinant CA1 by stopped-flow CO2 assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Carbonic anhydrase inhibitors. Inhibition studies of a coral secretory isoform by sulfonamides.
AID770582Inhibition of human membrane bound carbonic anhydrase 12 preincubated for 15 mins at room temperature followed by 72 hrs at 4 degC by stopped flow CO2 hydration assay2013Bioorganic & medicinal chemistry, Oct-01, Volume: 21, Issue:19
Carbonic anhydrase inhibitors: synthesis and inhibition of the human carbonic anhydrase isoforms I, II, VII, IX and XII with benzene sulfonamides incorporating 4,5,6,7-tetrabromophthalimide moiety.
AID1333089Inhibition of voltage dependent T-type Ca2+ channel in mouse N1E-115 cells assessed as reduction in transient inward Ca2+ current at 50 uM by whole-cell patch clamp method relative to control2016European journal of medicinal chemistry, Nov-10, Volume: 123Synthesis and T-type calcium channel-blocking effects of aryl(1,5-disubstituted-pyrazol-3-yl)methyl sulfonamides for neuropathic pain treatment.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID743512Inhibition of Sulfurihydrogenibium yellowstonense YO3AOP1 recombinant carbonic anhydrase preincubated for 15 mins by CO2 hydration stopped-flow assay2013Bioorganic & medicinal chemistry, Mar-15, Volume: 21, Issue:6
The alpha-carbonic anhydrase from the thermophilic bacterium Sulfurihydrogenibium yellowstonense YO3AOP1 is highly susceptible to inhibition by sulfonamides.
AID644088Inhibition of bovine carbonic anhydrase 3 using 4-nitrophenylacetate as substrate after 3 mins using spectrophotometry by Lineweaver-Burk plot analysis2012European journal of medicinal chemistry, Mar, Volume: 49Structure-activity relationships for the interaction of 5,10-dihydroindeno[1,2-b]indole derivatives with human and bovine carbonic anhydrase isoforms I, II, III, IV and VI.
AID570287Drug level in parkinson's disease patient serum at 25 mg/day2011Journal of medicinal chemistry, Feb-10, Volume: 54, Issue:3
Interactions of monoamine oxidases with the antiepileptic drug zonisamide: specificity of inhibition and structure of the human monoamine oxidase B complex.
AID1067226Selectivity ratio of Ki for human transmembrane carbonic anhydrase 2 to Ki for human cytosolic carbonic anhydrase 92014Bioorganic & medicinal chemistry, Mar-01, Volume: 22, Issue:5
Carbonic anhydrase inhibitors: synthesis and inhibition of the human carbonic anhydrase isoforms I, II, IX and XII with benzene sulfonamides incorporating 4- and 3-nitrophthalimide moieties.
AID1489019Anticonvulsant activity in amygdala kindling rat model assessed as change in after discharge threshold at 100 mg/kg, po relative to control2017Bioorganic & medicinal chemistry letters, 09-01, Volume: 27, Issue:17
N-alkyl-[1,1'-biphenyl]-2-sulfonamide derivatives as novel broad spectrum anti-epileptic drugs with efficacy equivalent to that of sodium valproate.
AID669321Inhibition of human recombinant full length CA2-mediated CO2 hydration preincubated for 15 mins by stopped-flow assay2012Journal of medicinal chemistry, Apr-26, Volume: 55, Issue:8
Synthesis, structure-activity relationship studies, and X-ray crystallographic analysis of arylsulfonamides as potent carbonic anhydrase inhibitors.
AID540231Dose normalised AUC in dog after po administration2005Xenobiotica; the fate of foreign compounds in biological systems, Feb, Volume: 35, Issue:2
Comparative evaluation of oral systemic exposure of 56 xenobiotics in rat, dog, monkey and human.
AID441716Inhibition of human recombinant CA14 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID1142833Inhibition of human carbonic anhydrase-1 by stopped-flow CO2 hydration assay2014Bioorganic & medicinal chemistry, Jun-01, Volume: 22, Issue:11
Sulfonamide inhibition studies of two β-carbonic anhydrases from the bacterial pathogen Legionella pneumophila.
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.
AID1489018Anticonvulsant activity in amygdala kindling rat model assessed as change in after discharge threshold at 30 mg/kg, po relative to control2017Bioorganic & medicinal chemistry letters, 09-01, Volume: 27, Issue:17
N-alkyl-[1,1'-biphenyl]-2-sulfonamide derivatives as novel broad spectrum anti-epileptic drugs with efficacy equivalent to that of sodium valproate.
AID587132Inhibition of Leptonychotes weddellii alpha-carbonic anhydrase after 15 mins by CO2 hydrase assay at pH 7.52011Bioorganic & medicinal chemistry, Mar-15, Volume: 19, Issue:6
Purification and inhibition studies with anions and sulfonamides of an α-carbonic anhydrase from the Antarctic seal Leptonychotes weddellii.
AID271175Selectivity for human recombinant carbonic anhydrase 9 over carbonic anhydrase 22006Journal of medicinal chemistry, Sep-07, Volume: 49, Issue:18
Carbonic anhydrase inhibitors: Hypoxia-activatable sulfonamides incorporating disulfide bonds that target the tumor-associated isoform IX.
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.
AID263639Selectivity for Helicobacter pylori recombinant CA over human recombinant CA22006Bioorganic & medicinal chemistry letters, Apr-15, Volume: 16, Issue:8
Carbonic anhydrase inhibitors: cloning and sulfonamide inhibition studies of a carboxyterminal truncated alpha-carbonic anhydrase from Helicobacter pylori.
AID577527Inhibition of human carbonic anhydrase II by spectrophotometry at pH 7.52011Bioorganic & medicinal chemistry, Feb-01, Volume: 19, Issue:3
A new β-carbonic anhydrase from Brucella suis, its cloning, characterization, and inhibition with sulfonamides and sulfamates, leading to impaired pathogen growth.
AID1453410Inhibition of Francisella tularensis beta-carbonic anhydrase assessed as reduction in CO2 hydration preincubated for 15 mins followed by CO2 addition measured for 10 to 100 secs by stopped-flow assay
AID1060765Inhibition of human recombinant carbonic anhydrase 7 preincubated for 15 mins by stopped flow CO2 hydration assay2014European journal of medicinal chemistry, Jan, Volume: 71Structure-based screening for the discovery of new carbonic anhydrase VII inhibitors.
AID600083Selectivity ratio of Ki for human recombinant carbonic anhydrase 2 to Ki for human recombinant carbonic anhydrase 72009Bioorganic & medicinal chemistry letters, Jun-15, Volume: 19, Issue:12
Carbonic anhydrase inhibitors. Phenacetyl-, pyridylacetyl- and thienylacetyl-substituted aromatic sulfonamides act as potent and selective isoform VII inhibitors.
AID300470Inhibition of human recombinant full length CA6 by stopped-flow technique2007Bioorganic & medicinal chemistry letters, Sep-01, Volume: 17, Issue:17
Carbonic anhydrase inhibitors. Interaction of the antiepileptic drug sulthiame with twelve mammalian isoforms: kinetic and X-ray crystallographic studies.
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.
AID320311Inhibition of human recombinant full length carbonic hydrase 6 by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Carbonic anhydrase inhibitors. Interaction of 2-N,N-dimethylamino-1,3,4-thiadiazole-5-methanesulfonamide with 12 mammalian isoforms: kinetic and X-ray crystallographic studies.
AID1188138Inhibition of Porphyromonas gingivalis Gamma-carbonic anhydrase compound preincubated for 15 mins by stopped flow CO2 hydrase assay method2014Bioorganic & medicinal chemistry, Sep-01, Volume: 22, Issue:17
Sulfonamide inhibition study of the carbonic anhydrases from the bacterial pathogen Porphyromonas gingivalis: the β-class (PgiCAb) versus the γ-class (PgiCA) enzymes.
AID1061066Inhibition of Thalassiosira weissflogii delta carbonic anhydrase preincubated for 15 mins by stopped flow CO2 hydration assay2014Bioorganic & medicinal chemistry letters, Jan-01, Volume: 24, Issue:1
Sulfonamide inhibition studies of the δ-carbonic anhydrase from the diatom Thalassiosira weissflogii.
AID369272Inhibition of human recombinant carbonic anhydrase 2 by stopped flow CO2 hydrase assay2009Journal of medicinal chemistry, Feb-12, Volume: 52, Issue:3
Cloning, expression, post-translational modifications and inhibition studies on the latest mammalian carbonic anhydrase isoform, CA XV.
AID371554Inhibition of human recombinant cytosolic carbonic anhydrase 1 pre-incubated for 15 mins by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Dec-15, Volume: 18, Issue:24
Carbonic anhydrase inhibitors: 2-substituted-1,3,4-thiadiazole-5-sulfamides act as powerful and selective inhibitors of the mitochondrial isozymes VA and VB over the cytosolic and membrane-associated carbonic anhydrases I, II and IV.
AID644034Inhibition of human carbonic anhydrase 6 esterase activity using 4-nitrophenylacetate as substrate2012Bioorganic & medicinal chemistry letters, Feb-01, Volume: 22, Issue:3
Synthesis and carbonic anhydrase inhibitory properties of novel cyclohexanonyl bromophenol derivatives.
AID1473738Inhibition of human BSEP overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-taurocholate in presence of ATP measured after 15 to 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID408764Anticonvulsant activity against scMet-induced seizures in orally dosed rat model2008Bioorganic & medicinal chemistry, Jun-01, Volume: 16, Issue:11
Synthesis and anticonvulsant activity of aromatic tetramethylcyclopropanecarboxamide derivatives.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID1204106Inhibition of recombinant Streptococcus mutans UA159 beta-carbonic anhydrase expressed in Escherichia coli Arctic cells preincubated for 15 mins by stopped flow CO2 hydrase assay2015Bioorganic & medicinal chemistry letters, Jun-01, Volume: 25, Issue:11
Sulfonamide inhibition study of the β-class carbonic anhydrase from the caries producing pathogen Streptococcus mutans.
AID300469Inhibition of human recombinant full length CA5B by stopped-flow technique2007Bioorganic & medicinal chemistry letters, Sep-01, Volume: 17, Issue:17
Carbonic anhydrase inhibitors. Interaction of the antiepileptic drug sulthiame with twelve mammalian isoforms: kinetic and X-ray crystallographic studies.
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID464123Selectivity ratio of Ki for human CA2 to Ki for human CA142010Journal of medicinal chemistry, Mar-25, Volume: 53, Issue:6
Identification of 3,4-Dihydroisoquinoline-2(1H)-sulfonamides as potent carbonic anhydrase inhibitors: synthesis, biological evaluation, and enzyme--ligand X-ray studies.
AID1489023Anticonvulsant activity in po dosed subcutaneous pentylenetetrazole-induced seizure mouse model assessed as reduction in convulsions2017Bioorganic & medicinal chemistry letters, 09-01, Volume: 27, Issue:17
N-alkyl-[1,1'-biphenyl]-2-sulfonamide derivatives as novel broad spectrum anti-epileptic drugs with efficacy equivalent to that of sodium valproate.
AID570288Selectivity ratio of Ki for soluble human MAO B to IC50 for membrane-bound mouse MAO B2011Journal of medicinal chemistry, Feb-10, Volume: 54, Issue:3
Interactions of monoamine oxidases with the antiepileptic drug zonisamide: specificity of inhibition and structure of the human monoamine oxidase B complex.
AID1628036Inhibition of full length human cytosolic carbonic anhydrase 1 preincubated for 15 mins by stop flow CO2 hydrase assay2016Bioorganic & medicinal chemistry letters, 09-01, Volume: 26, Issue:17
Cloning, expression, purification and sulfonamide inhibition profile of the complete domain of the η-carbonic anhydrase from Plasmodium falciparum.
AID570283Competitive inhibition of human MAOA by spectrophotometry2011Journal of medicinal chemistry, Feb-10, Volume: 54, Issue:3
Interactions of monoamine oxidases with the antiepileptic drug zonisamide: specificity of inhibition and structure of the human monoamine oxidase B complex.
AID299250Inhibition of Helicobacter pylori beta carbonic anhydrase by stopped-flow CO2 hydrase assay2007Bioorganic & medicinal chemistry letters, Jul-01, Volume: 17, Issue:13
Carbonic anhydrase inhibitors: the beta-carbonic anhydrase from Helicobacter pylori is a new target for sulfonamide and sulfamate inhibitors.
AID1268964Inhibition of recombinant Sulfurihydrogenibium yellowstonense YO3AOP1 carbonic anhydrase by stopped flow CO2 hydrase assay2016Bioorganic & medicinal chemistry letters, Jan-15, Volume: 26, Issue:2
Sulfonamide inhibition studies of the α-carbonic anhydrase from the gammaproteobacterium Thiomicrospira crunogena XCL-2, TcruCA.
AID1434429Inhibition of Burkholderia pseudomallei Gamma-carbonic anhydrase assessed as reduction in CO2 hydration preincubated for 15 mins followed by CO2 addition measured for 10 to 100 sec by Line-Weaver Burk plot analysis
AID320315Inhibition of mouse recombinant full length carbonic hydrase 13 by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Carbonic anhydrase inhibitors. Interaction of 2-N,N-dimethylamino-1,3,4-thiadiazole-5-methanesulfonamide with 12 mammalian isoforms: kinetic and X-ray crystallographic studies.
AID300471Inhibition of human recombinant full length CA7 by stopped-flow technique2007Bioorganic & medicinal chemistry letters, Sep-01, Volume: 17, Issue:17
Carbonic anhydrase inhibitors. Interaction of the antiepileptic drug sulthiame with twelve mammalian isoforms: kinetic and X-ray crystallographic studies.
AID328196Binding affinity to human carbonic anhydrase 2 in presence of 10 mM HEPES and 100 uM Na2SO4 at pH 7.5 by ThermoFluor method2008Journal of medicinal chemistry, Apr-24, Volume: 51, Issue:8
Carbonic anhydrase-II inhibition. what are the true enzyme-inhibitory properties of the sulfamide cognate of topiramate?
AID1251236Anticonvulsant activity in ip-dosed mouse assessed as protection against subcutaneous pentylenetetrazol-induced seizure2015Bioorganic & medicinal chemistry letters, Oct-15, Volume: 25, Issue:20
Discovery of benzothiazine derivatives as novel, orally-active anti-epileptic drug candidates with broad anticonvulsant effect.
AID456398Inhibition of human recombinant carbonic anhydrase 1 by stopped flow CO2 hydration method2010Bioorganic & medicinal chemistry, Jan-01, Volume: 18, Issue:1
Carbonic anhydrase inhibitors. Identification of selective inhibitors of the human mitochondrial isozymes VA and VB over the cytosolic isozymes I and II from a natural product-based phenolic library.
AID1766624Inhibition of recombinant human CA7 pre-incubated for 15 mins measured by stopped flow CO2 hydration assay2021Journal of medicinal chemistry, 03-25, Volume: 64, Issue:6
Discovery of Potent Carbonic Anhydrase Inhibitors as Effective Anticonvulsant Agents: Drug Design, Synthesis, and In Vitro and In Vivo Investigations.
AID427123Inhibition of Cryptococcus neoformans recombinant Can2 by stopped-flow CO2 hydration assay2009Bioorganic & medicinal chemistry, Jul-01, Volume: 17, Issue:13
Carbonic anhydrase inhibitors. Inhibition and homology modeling studies of the fungal beta-carbonic anhydrase from Candida albicans with sulfonamides.
AID441717Inhibition of mouse recombinant CA15 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID441706Inhibition of human recombinant CA2 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID293811Inhibition of human recombinant CA1 by stopped flow CO2 hydrase assay2007Bioorganic & medicinal chemistry letters, Mar-15, Volume: 17, Issue:6
Carbonic anhydrase inhibitors: inhibition of cytosolic/tumor-associated isoforms I, II, and IX with iminodiacetic carboxylates/hydroxamates also incorporating benzenesulfonamide moieties.
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID770586Inhibition of human cytosolic carbonic anhydrase 1 preincubated for 15 mins at room temperature followed by 72 hrs at 4 degC by stopped flow CO2 hydration assay2013Bioorganic & medicinal chemistry, Oct-01, Volume: 21, Issue:19
Carbonic anhydrase inhibitors: synthesis and inhibition of the human carbonic anhydrase isoforms I, II, VII, IX and XII with benzene sulfonamides incorporating 4,5,6,7-tetrabromophthalimide moiety.
AID1766623Inhibition of recombinant human CA2 pre-incubated for 15 mins measured by stopped flow CO2 hydration assay2021Journal of medicinal chemistry, 03-25, Volume: 64, Issue:6
Discovery of Potent Carbonic Anhydrase Inhibitors as Effective Anticonvulsant Agents: Drug Design, Synthesis, and In Vitro and In Vivo Investigations.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID1142837Inhibition of Legionella pneumophilia subsp. Pneumophila strain Philadelphia-1 carbonic anhydrase-2 assessed as CO2 hydrase activity by stopped-flow assay2014Bioorganic & medicinal chemistry, Jun-01, Volume: 22, Issue:11
Sulfonamide inhibition studies of two β-carbonic anhydrases from the bacterial pathogen Legionella pneumophila.
AID1195370Inhibition of human carbonic anhydrase 2 pre-incubated for 15 mins by stopped-flow CO2 hydration assay2015Bioorganic & medicinal chemistry, May-15, Volume: 23, Issue:10
The β-carbonic anhydrase from the malaria mosquito Anopheles gambiae is highly inhibited by sulfonamides.
AID436747Inhibition of human recombinant cytosolic carbonic anhydrase 2 by stopped-flow CO2 hydration assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Carbonic anhydrase inhibitors. Aromatic/heterocyclic sulfonamides incorporating phenacetyl, pyridylacetyl and thienylacetyl tails act as potent inhibitors of human mitochondrial isoforms VA and VB.
AID587130Inhibition of human carbonic anhydrase 1 after 15 mins by CO2 hydrase assay at pH 7.52011Bioorganic & medicinal chemistry, Mar-15, Volume: 19, Issue:6
Purification and inhibition studies with anions and sulfonamides of an α-carbonic anhydrase from the Antarctic seal Leptonychotes weddellii.
AID540232Dose normalised AUC in monkey after po administration2005Xenobiotica; the fate of foreign compounds in biological systems, Feb, Volume: 35, Issue:2
Comparative evaluation of oral systemic exposure of 56 xenobiotics in rat, dog, monkey and human.
AID601815Inhibition of human carbonic anhydrase 7 preincubated with compound for 15 mins by carbon dioxide hydration assay2011Journal of medicinal chemistry, Jun-09, Volume: 54, Issue:11
Anticonvulsant 4-aminobenzenesulfonamide derivatives with branched-alkylamide moieties: X-ray crystallography and inhibition studies of human carbonic anhydrase isoforms I, II, VII, and XIV.
AID1453413Inhibition of human carbonic anhydrase-2 assessed as reduction in CO2 hydration preincubated for 15 mins followed by CO2 addition measured for 10 to 100 secs by stopped-flow assay
AID588193Selectivity ratio of Ki for human recombinant alpha-carbonic anhydrase 1 to Ki for Cryptococcus neoformans recombinant Can2 beta-carbonic anhydrase2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Natural product-based phenols as novel probes for mycobacterial and fungal carbonic anhydrases.
AID427124Inhibition of Helicobacter pylori beta-carbonic anhydrase by stopped-flow CO2 hydration assay2009Bioorganic & medicinal chemistry, Jul-01, Volume: 17, Issue:13
Carbonic anhydrase inhibitors. Inhibition and homology modeling studies of the fungal beta-carbonic anhydrase from Candida albicans with sulfonamides.
AID441705Inhibition of human recombinant CA1 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID227699Virtual screen for compounds with anticonvulsant activity2003Bioorganic & medicinal chemistry letters, Aug-18, Volume: 13, Issue:16
Topological virtual screening: a way to find new anticonvulsant drugs from chemical diversity.
AID764719Inhibition of human cytosolic carbonic anhydrase 1 preincubated for 15 mins by stopped flow CO2 hydration assay2013Bioorganic & medicinal chemistry, Sep-01, Volume: 21, Issue:17
Carbonic anhydrase inhibitors: Synthesis and inhibition of the cytosolic mammalian carbonic anhydrase isoforms I, II and VII with benzene sulfonamides incorporating 4,5,6,7-tetrachlorophthalimide moiety.
AID1489026Anticonvulsant activity in po dosed maximal electroshock induced seizure mouse model assessed as reduction in convulsions2017Bioorganic & medicinal chemistry letters, 09-01, Volume: 27, Issue:17
N-alkyl-[1,1'-biphenyl]-2-sulfonamide derivatives as novel broad spectrum anti-epileptic drugs with efficacy equivalent to that of sodium valproate.
AID599954Inhibition of human recombinant carbonic anhydrase 2 by stopped flow CO2 hydration method2009Bioorganic & medicinal chemistry letters, Jun-15, Volume: 19, Issue:12
Carbonic anhydrase inhibitors. Phenacetyl-, pyridylacetyl- and thienylacetyl-substituted aromatic sulfonamides act as potent and selective isoform VII inhibitors.
AID770584Inhibition of human cytosolic carbonic anhydrase 7 preincubated for 15 mins at room temperature followed by 72 hrs at 4 degC by stopped flow CO2 hydration assay2013Bioorganic & medicinal chemistry, Oct-01, Volume: 21, Issue:19
Carbonic anhydrase inhibitors: synthesis and inhibition of the human carbonic anhydrase isoforms I, II, VII, IX and XII with benzene sulfonamides incorporating 4,5,6,7-tetrabromophthalimide moiety.
AID436564Inhibition of human recombinant CA2 by stopped-flow CO2 assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Carbonic anhydrase inhibitors. Inhibition studies of a coral secretory isoform by sulfonamides.
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.
AID408766Protective index, ratio of TD50 for rat by rotarod test to ED50 for rat by scMet test2008Bioorganic & medicinal chemistry, Jun-01, Volume: 16, Issue:11
Synthesis and anticonvulsant activity of aromatic tetramethylcyclopropanecarboxamide derivatives.
AID349608Inhibition of full length Mycobacterium tuberculosis H37Rv recombinant carbonic anhydrase 3 expressed in Escherichia coli BL21 by stopped flow CO2 hydration assay2009Journal of medicinal chemistry, May-14, Volume: 52, Issue:9
Carbonic anhydrase inhibitors. Cloning, characterization, and inhibition studies of a new beta-carbonic anhydrase from Mycobacterium tuberculosis.
AID570289Selectivity ratio of Ki for soluble rat MAO B to IC50 for membrane-bound mouse MAO B2011Journal of medicinal chemistry, Feb-10, Volume: 54, Issue:3
Interactions of monoamine oxidases with the antiepileptic drug zonisamide: specificity of inhibition and structure of the human monoamine oxidase B complex.
AID464118Inhibition of human recombinant CA1 by stopped-flow CO2 hydration assay2010Journal of medicinal chemistry, Mar-25, Volume: 53, Issue:6
Identification of 3,4-Dihydroisoquinoline-2(1H)-sulfonamides as potent carbonic anhydrase inhibitors: synthesis, biological evaluation, and enzyme--ligand X-ray studies.
AID600082Inhibition of human recombinant carbonic anhydrase 7 by stopped flow CO2 hydration method2009Bioorganic & medicinal chemistry letters, Jun-15, Volume: 19, Issue:12
Carbonic anhydrase inhibitors. Phenacetyl-, pyridylacetyl- and thienylacetyl-substituted aromatic sulfonamides act as potent and selective isoform VII inhibitors.
AID371557Inhibition of full length human recombinant mitochondrial carbonic anhydrase 5A pre-incubated for 15 mins by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Dec-15, Volume: 18, Issue:24
Carbonic anhydrase inhibitors: 2-substituted-1,3,4-thiadiazole-5-sulfamides act as powerful and selective inhibitors of the mitochondrial isozymes VA and VB over the cytosolic and membrane-associated carbonic anhydrases I, II and IV.
AID441210Selectivity for human cloned CA9 over human cloned CA12009Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20
S-glycosyl primary sulfonamides--a new structural class for selective inhibition of cancer-associated carbonic anhydrases.
AID599955Selectivity ratio of Ki for human recombinant carbonic anhydrase 1 to Ki for human recombinant carbonic anhydrase 72009Bioorganic & medicinal chemistry letters, Jun-15, Volume: 19, Issue:12
Carbonic anhydrase inhibitors. Phenacetyl-, pyridylacetyl- and thienylacetyl-substituted aromatic sulfonamides act as potent and selective isoform VII inhibitors.
AID408765Toxicity in orally dosed rat by rotarod test2008Bioorganic & medicinal chemistry, Jun-01, Volume: 16, Issue:11
Synthesis and anticonvulsant activity of aromatic tetramethylcyclopropanecarboxamide derivatives.
AID342471Inhibition of AQP4 in wild type mouse brain gilial cells assessed as reduction of osmotic equilibrium rate at 10 to 100 uM after 15 mins by calcein quenching assay relative to water permeability2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Lack of aquaporin-4 water transport inhibition by antiepileptics and arylsulfonamides.
AID1195369Inhibition of human carbonic anhydrase 1 pre-incubated for 15 mins by stopped-flow CO2 hydration assay2015Bioorganic & medicinal chemistry, May-15, Volume: 23, Issue:10
The β-carbonic anhydrase from the malaria mosquito Anopheles gambiae is highly inhibited by sulfonamides.
AID633372Inhibition of human CA9 catalytic domain preincubated for 15 mins by stopped flow CO2 hydration assay2011Bioorganic & medicinal chemistry, Dec-01, Volume: 19, Issue:23
Synthesis and biological profile of new 1,2,3,4-tetrahydroisoquinolines as selective carbonic anhydrase inhibitors.
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).
AID320309Inhibition of human recombinant full length carbonic hydrase 5A by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Carbonic anhydrase inhibitors. Interaction of 2-N,N-dimethylamino-1,3,4-thiadiazole-5-methanesulfonamide with 12 mammalian isoforms: kinetic and X-ray crystallographic studies.
AID1142836Inhibition of Legionella pneumophilia subsp. Pneumophila strain Philadelphia-1 carbonic anhydrase-1 assessed as CO2 hydrase activity by stopped-flow assay2014Bioorganic & medicinal chemistry, Jun-01, Volume: 22, Issue:11
Sulfonamide inhibition studies of two β-carbonic anhydrases from the bacterial pathogen Legionella pneumophila.
AID369271Inhibition of human recombinant carbonic anhydrase 1 by stopped flow CO2 hydrase assay2009Journal of medicinal chemistry, Feb-12, Volume: 52, Issue:3
Cloning, expression, post-translational modifications and inhibition studies on the latest mammalian carbonic anhydrase isoform, CA XV.
AID123746Percentage block of the hind-limb tonic-extensor seizure was determined after application of an electric shock to mice for 30 min followed by 100 mg/kg intraperitoneal dose; ND means no data1987Journal of medicinal chemistry, May, Volume: 30, Issue:5
Anticonvulsant O-alkyl sulfamates. 2,3:4,5-Bis-O-(1-methylethylidene)-beta-D-fructopyranose sulfamate and related compounds.
AID295949Inhibition of human carbonic anhydrase 5A2007Bioorganic & medicinal chemistry, Jun-15, Volume: 15, Issue:12
Molecular modeling study for the binding of zonisamide and topiramate to the human mitochondrial carbonic anhydrase isoform VA.
AID503304Antiproliferative activity against human PC3 cells at 5 uM after 120 hrs by MTT assay relative to DMSO2006Nature chemical biology, Jun, Volume: 2, Issue:6
Identifying off-target effects and hidden phenotypes of drugs in human cells.
AID1287517Inhibition of human carbonic anhydrase 1 incubated for 15 mins by stopped-flow CO2 hydration assay2016Bioorganic & medicinal chemistry letters, Apr-01, Volume: 26, Issue:7
Sulfonamide inhibition studies of the β-carbonic anhydrase from the newly discovered bacterium Enterobacter sp. B13.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID1188136Inhibition of Helicobacter pylori Beta-carbonic anhydrase compound preincubated for 15 mins by stopped flow CO2 hydrase assay method2014Bioorganic & medicinal chemistry, Sep-01, Volume: 22, Issue:17
Sulfonamide inhibition study of the carbonic anhydrases from the bacterial pathogen Porphyromonas gingivalis: the β-class (PgiCAb) versus the γ-class (PgiCA) enzymes.
AID1262267Inhibition of Chionodraco hamatus alphaCA incubated for 15 mins prior to testing by stopped flow CO2 hydrase assay2015Bioorganic & medicinal chemistry letters, Dec-01, Volume: 25, Issue:23
Anion and sulfonamide inhibition studies of an α-carbonic anhydrase from the Antarctic hemoglobinless fish Chionodraco hamatus.
AID669485Inhibition of human recombinant full length CA7-mediated CO2 hydration preincubated for 15 mins by stopped-flow assay2012Journal of medicinal chemistry, Apr-26, Volume: 55, Issue:8
Synthesis, structure-activity relationship studies, and X-ray crystallographic analysis of arylsulfonamides as potent carbonic anhydrase inhibitors.
AID320316Inhibition of human recombinant full length carbonic hydrase 14 by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Carbonic anhydrase inhibitors. Interaction of 2-N,N-dimethylamino-1,3,4-thiadiazole-5-methanesulfonamide with 12 mammalian isoforms: kinetic and X-ray crystallographic studies.
AID570286Competitive inhibition of rat MAO B by spectrophotometry2011Journal of medicinal chemistry, Feb-10, Volume: 54, Issue:3
Interactions of monoamine oxidases with the antiepileptic drug zonisamide: specificity of inhibition and structure of the human monoamine oxidase B complex.
AID601816Inhibition of human carbonic anhydrase 14 preincubated with compound for 15 mins by carbon dioxide hydration assay2011Journal of medicinal chemistry, Jun-09, Volume: 54, Issue:11
Anticonvulsant 4-aminobenzenesulfonamide derivatives with branched-alkylamide moieties: X-ray crystallography and inhibition studies of human carbonic anhydrase isoforms I, II, VII, and XIV.
AID367822Inhibition of Saccharomyces cerevisiae recombinant CA expressed in Escherichia coli by stopped-flow CO2 hydrase assay2009Bioorganic & medicinal chemistry, Feb-01, Volume: 17, Issue:3
Carbonic anhydrase inhibitors: inhibition of the beta-class enzyme from the yeast Saccharomyces cerevisiae with sulfonamides and sulfamates.
AID369274Inhibition of human recombinant carbonic anhydrase 9 catalytic domain by stopped flow CO2 hydrase assay2009Journal of medicinal chemistry, Feb-12, Volume: 52, Issue:3
Cloning, expression, post-translational modifications and inhibition studies on the latest mammalian carbonic anhydrase isoform, CA XV.
AID239703Inhibitory constant against human carbonic anhydrase XIV in CO2 hydrase assay2005Bioorganic & medicinal chemistry letters, Sep-01, Volume: 15, Issue:17
Carbonic anhydrase inhibitors: inhibition of the transmembrane isozyme XIV with sulfonamides.
AID1653804Substrate activity at human mARC1 expressed in Escherichia coli assessed as turnover rates at 1 mM pre-incubated for 3 mins followed by NADH addition and measured after 15 mins by LC-MS analysis based assay2020Journal of medicinal chemistry, 06-25, Volume: 63, Issue:12
Drug Metabolism by the Mitochondrial Amidoxime Reducing Component (mARC): Rapid Assay and Identification of New Substrates.
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1061067Inhibition of Porphyromonas gingivalis recombinant gamma-carbonic anhydrase preincubated for 15 mins by stopped flow CO2 hydration assay2014Bioorganic & medicinal chemistry letters, Jan-01, Volume: 24, Issue:1
Sulfonamide inhibition studies of the δ-carbonic anhydrase from the diatom Thalassiosira weissflogii.
AID1653799Substrate activity at human mARC2 expressed in Escherichia coli assessed as turnover rates at 1 mM pre-incubated for 3 mins followed by NADH addition and measured after 15 mins by UV-Visible spectroscopy based NADH assay2020Journal of medicinal chemistry, 06-25, Volume: 63, Issue:12
Drug Metabolism by the Mitochondrial Amidoxime Reducing Component (mARC): Rapid Assay and Identification of New Substrates.
AID1067230Inhibition of human cytosolic carbonic anhydrase 1 by stopped-flow CO2 hydration assay2014Bioorganic & medicinal chemistry, Mar-01, Volume: 22, Issue:5
Carbonic anhydrase inhibitors: synthesis and inhibition of the human carbonic anhydrase isoforms I, II, IX and XII with benzene sulfonamides incorporating 4- and 3-nitrophthalimide moieties.
AID300467Inhibition of human recombinant full length CA4 by stopped-flow technique2007Bioorganic & medicinal chemistry letters, Sep-01, Volume: 17, Issue:17
Carbonic anhydrase inhibitors. Interaction of the antiepileptic drug sulthiame with twelve mammalian isoforms: kinetic and X-ray crystallographic studies.
AID441710Inhibition of human recombinant CA5B by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID1278410Inhibition of Porphyromonas gingivalis gamma carbonic anhydrase preincubated for 15 mins by stopped flow CO2 hydration assay2016Bioorganic & medicinal chemistry letters, Feb-15, Volume: 26, Issue:4
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the Antarctic bacterium Colwellia psychrerythraea.
AID456399Inhibition of human recombinant carbonic anhydrase 5A by stopped flow CO2 hydration method2010Bioorganic & medicinal chemistry, Jan-01, Volume: 18, Issue:1
Carbonic anhydrase inhibitors. Identification of selective inhibitors of the human mitochondrial isozymes VA and VB over the cytosolic isozymes I and II from a natural product-based phenolic library.
AID1190066Selectivity index, ratio of Ki for Trypanosoma cruzi carbonic anhydrase to Ki for Plasmodium falciparum Eta-carbonic anhydrase2015Bioorganic & medicinal chemistry, Feb-01, Volume: 23, Issue:3
Sulfonamide inhibition studies of the η-class carbonic anhydrase from the malaria pathogen Plasmodium falciparum.
AID1142838Inhibition of Helicobacter pylori carbonic anhydrase by stopped-flow CO2 hydration assay2014Bioorganic & medicinal chemistry, Jun-01, Volume: 22, Issue:11
Sulfonamide inhibition studies of two β-carbonic anhydrases from the bacterial pathogen Legionella pneumophila.
AID1061170Inhibition of Porphyromonas gingivalis gamma-carbonic anhydrase expressed in Escherichia coli preincubated for 15 mins by stopped flow CO2 hydration assay2014Bioorganic & medicinal chemistry letters, Jan-01, Volume: 24, Issue:1
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the oral pathogen Porphyromonas gingivalis.
AID367821Inhibition of human recombinant CA2 by stopped-flow CO2 hydrase assay2009Bioorganic & medicinal chemistry, Feb-01, Volume: 17, Issue:3
Carbonic anhydrase inhibitors: inhibition of the beta-class enzyme from the yeast Saccharomyces cerevisiae with sulfonamides and sulfamates.
AID1434428Inhibition of human carbonic anhydrase 2 assessed as reduction in CO2 hydration preincubated for 15 mins followed by CO2 addition measured for 10 to 100 sec by Line-Weaver Burk plot analysis
AID633371Inhibition of human recombinant full length CA2 preincubated for 15 mins by stopped flow CO2 hydration assay2011Bioorganic & medicinal chemistry, Dec-01, Volume: 19, Issue:23
Synthesis and biological profile of new 1,2,3,4-tetrahydroisoquinolines as selective carbonic anhydrase inhibitors.
AID578224Inhibition of human recombinant CA5B mitochondrial isoform by stopped-flow CO2 hydration assay2011Bioorganic & medicinal chemistry letters, Mar-01, Volume: 21, Issue:5
(R)-/(S)-10-camphorsulfonyl-substituted aromatic/heterocyclic sulfonamides selectively inhibit mitochondrial over cytosolic carbonic anhydrases.
AID578223Inhibition of human recombinant CA5A mitochondrial isoform by stopped-flow CO2 hydration assay2011Bioorganic & medicinal chemistry letters, Mar-01, Volume: 21, Issue:5
(R)-/(S)-10-camphorsulfonyl-substituted aromatic/heterocyclic sulfonamides selectively inhibit mitochondrial over cytosolic carbonic anhydrases.
AID427122Inhibition of Candida albicans recombinant Nce103 by stopped-flow CO2 hydration assay2009Bioorganic & medicinal chemistry, Jul-01, Volume: 17, Issue:13
Carbonic anhydrase inhibitors. Inhibition and homology modeling studies of the fungal beta-carbonic anhydrase from Candida albicans with sulfonamides.
AID263638Inhibition of Helicobacter pylori recombinant CA2006Bioorganic & medicinal chemistry letters, Apr-15, Volume: 16, Issue:8
Carbonic anhydrase inhibitors: cloning and sulfonamide inhibition studies of a carboxyterminal truncated alpha-carbonic anhydrase from Helicobacter pylori.
AID601813Inhibition of human carbonic anhydrase 1 preincubated with compound for 15 mins by carbon dioxide hydration assay2011Journal of medicinal chemistry, Jun-09, Volume: 54, Issue:11
Anticonvulsant 4-aminobenzenesulfonamide derivatives with branched-alkylamide moieties: X-ray crystallography and inhibition studies of human carbonic anhydrase isoforms I, II, VII, and XIV.
AID464119Inhibition of human recombinant CA2 by stopped-flow CO2 hydration assay2010Journal of medicinal chemistry, Mar-25, Volume: 53, Issue:6
Identification of 3,4-Dihydroisoquinoline-2(1H)-sulfonamides as potent carbonic anhydrase inhibitors: synthesis, biological evaluation, and enzyme--ligand X-ray studies.
AID1061169Inhibition of recombinant Methanosarcina thermophila gamma-CA CAM by stopped flow CO2 hydration assay2014Bioorganic & medicinal chemistry letters, Jan-01, Volume: 24, Issue:1
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the oral pathogen Porphyromonas gingivalis.
AID1766622Inhibition of recombinant human CA1 pre-incubated for 15 mins measured by stopped flow CO2 hydration assay2021Journal of medicinal chemistry, 03-25, Volume: 64, Issue:6
Discovery of Potent Carbonic Anhydrase Inhibitors as Effective Anticonvulsant Agents: Drug Design, Synthesis, and In Vitro and In Vivo Investigations.
AID1251235Anticonvulsant activity in mouse assessed as protection against maximal electroshock-induced seizure2015Bioorganic & medicinal chemistry letters, Oct-15, Volume: 25, Issue:20
Discovery of benzothiazine derivatives as novel, orally-active anti-epileptic drug candidates with broad anticonvulsant effect.
AID342469Inhibition of AQP4 expressed in rat FRT cells assessed as transepithelial osmotic water permeability at 100 uM by dye dilution method2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Lack of aquaporin-4 water transport inhibition by antiepileptics and arylsulfonamides.
AID612725Inhibition of human recombinant carbonic anhydrase 1 at pH 7.5 by stopped flow CO2 hydration assay2011Bioorganic & medicinal chemistry, Aug-15, Volume: 19, Issue:16
Inhibition studies of the β-carbonic anhydrases from the bacterial pathogen Salmonella enterica serovar Typhimurium with sulfonamides and sulfamates.
AID320307Inhibition of human recombinant full length carbonic hydrase 3 by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Carbonic anhydrase inhibitors. Interaction of 2-N,N-dimethylamino-1,3,4-thiadiazole-5-methanesulfonamide with 12 mammalian isoforms: kinetic and X-ray crystallographic studies.
AID261582Selectivity ratio for human carbonic anhydrase 2 over Helicobacter pylori carbonic anhydrase2006Journal of medicinal chemistry, Mar-23, Volume: 49, Issue:6
Carbonic anhydrase inhibitors: DNA cloning and inhibition studies of the alpha-carbonic anhydrase from Helicobacter pylori, a new target for developing sulfonamide and sulfamate gastric drugs.
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).
AID570291Selectivity ratio of Ki for rat MAO B to ratio of Ki for zebrafish MAO2011Journal of medicinal chemistry, Feb-10, Volume: 54, Issue:3
Interactions of monoamine oxidases with the antiepileptic drug zonisamide: specificity of inhibition and structure of the human monoamine oxidase B complex.
AID1275912Inhibition of human Carbonic anhydrase2 using CO2 as substrate preincubated for 15 mins by stopped-flow CO2 hydration assay2016Bioorganic & medicinal chemistry, Mar-01, Volume: 24, Issue:5
Sulfonamide inhibition studies of the β-carbonic anhydrase from the pathogenic bacterium Vibrio cholerae.
AID1512065Inhibition of MAO-B in mouse brain assessed as reduction in H2O2 production incubated for 30 mins using benzylamine as substrate by Amplex red reagent based fluorescence assay2019Bioorganic & medicinal chemistry letters, 11-01, Volume: 29, Issue:21
1,3,4-Oxadiazol-2-ylbenzenesulfonamides as privileged structures for the inhibition of monoamine oxidase B.
AID409600Inhibition of human aquaporin 4 M23 isoform expressed in Xenopus laevis oocytes at 20 uM2009Bioorganic & medicinal chemistry, Jan-01, Volume: 17, Issue:1
Inhibition of aquaporin 4 by antiepileptic drugs.
AID123743Percentage block of the hind-limb tonic-extensor seizure was determined after application of an electric shock to mice for 240 min followed by 40 mg/kg peroral dose1987Journal of medicinal chemistry, May, Volume: 30, Issue:5
Anticonvulsant O-alkyl sulfamates. 2,3:4,5-Bis-O-(1-methylethylidene)-beta-D-fructopyranose sulfamate and related compounds.
AID648181Inhibition of human wild type carbonic anhydrase 2 Leu204Ser mutant expressed in Escherichia coli after 15 mins preincubation by stopped flow CO2 hydration assay2012Bioorganic & medicinal chemistry, Apr-01, Volume: 20, Issue:7
Mutation of active site residues Asn67 to Ile, Gln92 to Val and Leu204 to Ser in human carbonic anhydrase II: influences on the catalytic activity and affinity for inhibitors.
AID366658Inhibition of human cloned CA2 by CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Aug-15, Volume: 18, Issue:16
Inhibition of human mitochondrial carbonic anhydrases VA and VB with para-(4-phenyltriazole-1-yl)-benzenesulfonamide derivatives.
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).
AID441714Inhibition of human recombinant CA12 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID644086Inhibition of human carbonic anhydrase 4 using 4-nitrophenylacetate as substrate after 3 mins using spectrophotometry by Lineweaver-Burk plot analysis2012European journal of medicinal chemistry, Mar, Volume: 49Structure-activity relationships for the interaction of 5,10-dihydroindeno[1,2-b]indole derivatives with human and bovine carbonic anhydrase isoforms I, II, III, IV and VI.
AID577526Inhibition of human carbonic anhydrase I by spectrophotometry at pH 7.52011Bioorganic & medicinal chemistry, Feb-01, Volume: 19, Issue:3
A new β-carbonic anhydrase from Brucella suis, its cloning, characterization, and inhibition with sulfonamides and sulfamates, leading to impaired pathogen growth.
AID599953Inhibition of human recombinant carbonic anhydrase 1 by stopped flow CO2 hydration method2009Bioorganic & medicinal chemistry letters, Jun-15, Volume: 19, Issue:12
Carbonic anhydrase inhibitors. Phenacetyl-, pyridylacetyl- and thienylacetyl-substituted aromatic sulfonamides act as potent and selective isoform VII inhibitors.
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.
AID744415Inhibition of recombinant full length Candida glabrata NCE103 expressed in Escherichia coli BL21 preincubated for 15 mins by stopped-flow CO2 hydrase assay2013Bioorganic & medicinal chemistry letters, May-01, Volume: 23, Issue:9
Carbonic anhydrase inhibitors: inhibition of the β-class enzyme from the pathogenic yeast Candida glabrata with sulfonamides, sulfamates and sulfamides.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID437749Inhibition of human recombinant CA2 by stopped-flow hydration assay2009Bioorganic & medicinal chemistry letters, Dec-01, Volume: 19, Issue:23
Carbonic anhydrase inhibitors. Characterization and inhibition studies of the most active beta-carbonic anhydrase from Mycobacterium tuberculosis, Rv3588c.
AID1473739Inhibition of human MRP2 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID612726Inhibition of human recombinant carbonic anhydrase 2 at pH 7.5 by stopped flow CO2 hydration assay2011Bioorganic & medicinal chemistry, Aug-15, Volume: 19, Issue:16
Inhibition studies of the β-carbonic anhydrases from the bacterial pathogen Salmonella enterica serovar Typhimurium with sulfonamides and sulfamates.
AID239287Mean inhibitory constant towards human carbonic anhydrase V determined by spectrophotometric dansylamide binding assay2005Bioorganic & medicinal chemistry letters, May-02, Volume: 15, Issue:9
Carbonic anhydrase inhibitors. Zonisamide is an effective inhibitor of the cytosolic isozyme II and mitochondrial isozyme V: solution and X-ray crystallographic studies.
AID271173Inhibition of human recombinant carbonic anhydrase 2 by stopped-flow CO2 hydrase assay2006Journal of medicinal chemistry, Sep-07, Volume: 49, Issue:18
Carbonic anhydrase inhibitors: Hypoxia-activatable sulfonamides incorporating disulfide bonds that target the tumor-associated isoform IX.
AID1188135Inhibition of human recombinant Carbonic anhydrase 2 compound preincubated for 15 mins by stopped flow CO2 hydrase assay method2014Bioorganic & medicinal chemistry, Sep-01, Volume: 22, Issue:17
Sulfonamide inhibition study of the carbonic anhydrases from the bacterial pathogen Porphyromonas gingivalis: the β-class (PgiCAb) versus the γ-class (PgiCA) enzymes.
AID437750Inhibition of full length Mycobacterium tuberculosis H37Rv recombinant carbonic anhydrase 2 encoded by RV3588c by stopped flow CO2 hydration assay2009Bioorganic & medicinal chemistry letters, Dec-01, Volume: 19, Issue:23
Carbonic anhydrase inhibitors. Characterization and inhibition studies of the most active beta-carbonic anhydrase from Mycobacterium tuberculosis, Rv3588c.
AID1287518Inhibition of human carbonic anhydrase 2 incubated for 15 mins by stopped-flow CO2 hydration assay2016Bioorganic & medicinal chemistry letters, Apr-01, Volume: 26, Issue:7
Sulfonamide inhibition studies of the β-carbonic anhydrase from the newly discovered bacterium Enterobacter sp. B13.
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.
AID371558Inhibition of full length human recombinant mitochondrial carbonic anhydrase 5B preincubated for 15 mins by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Dec-15, Volume: 18, Issue:24
Carbonic anhydrase inhibitors: 2-substituted-1,3,4-thiadiazole-5-sulfamides act as powerful and selective inhibitors of the mitochondrial isozymes VA and VB over the cytosolic and membrane-associated carbonic anhydrases I, II and IV.
AID1067227Inhibition of human transmembrane carbonic anhydrase 12 by stopped-flow CO2 hydration assay2014Bioorganic & medicinal chemistry, Mar-01, Volume: 22, Issue:5
Carbonic anhydrase inhibitors: synthesis and inhibition of the human carbonic anhydrase isoforms I, II, IX and XII with benzene sulfonamides incorporating 4- and 3-nitrophthalimide moieties.
AID320305Inhibition of human recombinant full length carbonic hydrase 1 by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Carbonic anhydrase inhibitors. Interaction of 2-N,N-dimethylamino-1,3,4-thiadiazole-5-methanesulfonamide with 12 mammalian isoforms: kinetic and X-ray crystallographic studies.
AID1275910Inhibition of Vibrio cholerae beta-carbonic anhydrase using CO2 as substrate preincubated for 15 mins by stopped-flow CO2 hydration assay2016Bioorganic & medicinal chemistry, Mar-01, Volume: 24, Issue:5
Sulfonamide inhibition studies of the β-carbonic anhydrase from the pathogenic bacterium Vibrio cholerae.
AID1061068Inhibition of Leishmania donovani chagasi recombinant beta-carbonic anhydrase preincubated for 15 mins by stopped flow CO2 hydration assay2014Bioorganic & medicinal chemistry letters, Jan-01, Volume: 24, Issue:1
Sulfonamide inhibition studies of the δ-carbonic anhydrase from the diatom Thalassiosira weissflogii.
AID320310Inhibition of human recombinant full length carbonic hydrase 5B by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Carbonic anhydrase inhibitors. Interaction of 2-N,N-dimethylamino-1,3,4-thiadiazole-5-methanesulfonamide with 12 mammalian isoforms: kinetic and X-ray crystallographic studies.
AID588191Selectivity ratio of Ki for human recombinant alpha-carbonic anhydrase 1 to Ki for Mycobacterium tuberculosis recombinant Rv1284 beta-carbonic anhydrase2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Natural product-based phenols as novel probes for mycobacterial and fungal carbonic anhydrases.
AID261581Inhibition of Helicobacter pylori recombinant carbonic anhydrase by stopped-flow CO2 hydrase assay2006Journal of medicinal chemistry, Mar-23, Volume: 49, Issue:6
Carbonic anhydrase inhibitors: DNA cloning and inhibition studies of the alpha-carbonic anhydrase from Helicobacter pylori, a new target for developing sulfonamide and sulfamate gastric drugs.
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID1443980Inhibition of human BSEP expressed in fall armyworm sf9 cell plasma membrane vesicles assessed as reduction in vesicle-associated [3H]-taurocholate transport preincubated for 10 mins prior to ATP addition measured after 15 mins in presence of [3H]-tauroch2010Toxicological sciences : an official journal of the Society of Toxicology, Dec, Volume: 118, Issue:2
Interference with bile salt export pump function is a susceptibility factor for human liver injury in drug development.
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.
AID436749Inhibition of human recombinant full length mitochondrial carbonic anhydrase 5B by stopped-flow CO2 hydration assay2009Bioorganic & medicinal chemistry, Jul-15, Volume: 17, Issue:14
Carbonic anhydrase inhibitors. Aromatic/heterocyclic sulfonamides incorporating phenacetyl, pyridylacetyl and thienylacetyl tails act as potent inhibitors of human mitochondrial isoforms VA and VB.
AID578221Inhibition of human recombinant CA1 cytosolic isoform by stopped-flow CO2 hydration assay2011Bioorganic & medicinal chemistry letters, Mar-01, Volume: 21, Issue:5
(R)-/(S)-10-camphorsulfonyl-substituted aromatic/heterocyclic sulfonamides selectively inhibit mitochondrial over cytosolic carbonic anhydrases.
AID1188137Inhibition of Porphyromonas gingivalis Beta-carbonic anhydrase compound preincubated for 15 mins by stopped flow CO2 hydrase assay method2014Bioorganic & medicinal chemistry, Sep-01, Volume: 22, Issue:17
Sulfonamide inhibition study of the carbonic anhydrases from the bacterial pathogen Porphyromonas gingivalis: the β-class (PgiCAb) versus the γ-class (PgiCA) enzymes.
AID320312Inhibition of human recombinant full length carbonic hydrase 7 by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Carbonic anhydrase inhibitors. Interaction of 2-N,N-dimethylamino-1,3,4-thiadiazole-5-methanesulfonamide with 12 mammalian isoforms: kinetic and X-ray crystallographic studies.
AID1268963Inhibition of recombinant human carbonic anhydrase-2 by stopped flow CO2 hydrase assay2016Bioorganic & medicinal chemistry letters, Jan-15, Volume: 26, Issue:2
Sulfonamide inhibition studies of the α-carbonic anhydrase from the gammaproteobacterium Thiomicrospira crunogena XCL-2, TcruCA.
AID644036Inhibition of human carbonic anhydrase 4 esterase activity using 4-nitrophenylacetate as substrate2012Bioorganic & medicinal chemistry letters, Feb-01, Volume: 22, Issue:3
Synthesis and carbonic anhydrase inhibitory properties of novel cyclohexanonyl bromophenol derivatives.
AID1333764Anticonvulsant activity in ip dosed Carworth Farm1 mouse assessed as protection against maximal electroshock-induced seizures administered 30 mins prior to 60-Hz current induction2017Bioorganic & medicinal chemistry letters, 01-01, Volume: 27, Issue:1
Simple N,N-dimethyl phenylsulfonamides show potent anticonvulsant effect in two standard epilepsy models.
AID367820Inhibition of human recombinant CA1 by stopped-flow CO2 hydrase assay2009Bioorganic & medicinal chemistry, Feb-01, Volume: 17, Issue:3
Carbonic anhydrase inhibitors: inhibition of the beta-class enzyme from the yeast Saccharomyces cerevisiae with sulfonamides and sulfamates.
AID587131Inhibition of human carbonic anhydrase 2 after 15 mins by CO2 hydrase assay at pH 7.52011Bioorganic & medicinal chemistry, Mar-15, Volume: 19, Issue:6
Purification and inhibition studies with anions and sulfonamides of an α-carbonic anhydrase from the Antarctic seal Leptonychotes weddellii.
AID1333767Anticonvulsant activity in ip dosed Carworth Farm1 mouse assessed as protection against subcutaneous pentylenetetrazole-induced seizures after 30 mins2017Bioorganic & medicinal chemistry letters, 01-01, Volume: 27, Issue:1
Simple N,N-dimethyl phenylsulfonamides show potent anticonvulsant effect in two standard epilepsy models.
AID601814Inhibition of human carbonic anhydrase 2 preincubated with compound for 15 mins by carbon dioxide hydration assay2011Journal of medicinal chemistry, Jun-09, Volume: 54, Issue:11
Anticonvulsant 4-aminobenzenesulfonamide derivatives with branched-alkylamide moieties: X-ray crystallography and inhibition studies of human carbonic anhydrase isoforms I, II, VII, and XIV.
AID1194027Inhibition of recombinant Porphyromonas gingivalis gamma-carbonic anhydrase by stopped flow CO2 hydrase assay2015Bioorganic & medicinal chemistry, Apr-15, Volume: 23, Issue:8
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the Antarctic cyanobacterium Nostoc commune.
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.
AID366659Inhibition of human recombinant CA5A by CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Aug-15, Volume: 18, Issue:16
Inhibition of human mitochondrial carbonic anhydrases VA and VB with para-(4-phenyltriazole-1-yl)-benzenesulfonamide derivatives.
AID726232Inhibition of Trypanosoma cruzi CL Brener recombinant alpha-carbonic anhydrase expressed in insect Sf9 cell Baculovirus system by stopped flow CO2 hydration assay2013Journal of medicinal chemistry, Feb-28, Volume: 56, Issue:4
Cloning, characterization, and sulfonamide and thiol inhibition studies of an α-carbonic anhydrase from Trypanosoma cruzi, the causative agent of Chagas disease.
AID441209Inhibition of human cloned CA12 catalytic domain by stopped flow CO2 hydration assay2009Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20
S-glycosyl primary sulfonamides--a new structural class for selective inhibition of cancer-associated carbonic anhydrases.
AID441207Inhibition of human cloned CA2 by stopped flow CO2 hydration assay2009Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20
S-glycosyl primary sulfonamides--a new structural class for selective inhibition of cancer-associated carbonic anhydrases.
AID1123815Anticonvulsant activity in po dosed STD-dd mouse assessed as protection against hind-limb extensor component of maximal electroshock seizure administered via gavage measured 2 hrs after drug dosing1979Journal of medicinal chemistry, Feb, Volume: 22, Issue:2
Studies on 3-substituted 1,2-benzisoxazole derivatives. 6. Syntheses of 3-(sulfamoylmethyl)-1,2-benzisoxazole derivatives and their anticonvulsant activities.
AID293813Inhibition of human recombinant CA9 by stopped flow CO2 hydrase assay2007Bioorganic & medicinal chemistry letters, Mar-15, Volume: 17, Issue:6
Carbonic anhydrase inhibitors: inhibition of cytosolic/tumor-associated isoforms I, II, and IX with iminodiacetic carboxylates/hydroxamates also incorporating benzenesulfonamide moieties.
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).
AID588190Selectivity ratio of Ki for human recombinant alpha-carbonic anhydrase 1 to Ki for Mycobacterium tuberculosis recombinant Rv3273 beta-carbonic anhydrase2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Natural product-based phenols as novel probes for mycobacterial and fungal carbonic anhydrases.
AID644037Inhibition of human carbonic anhydrase 1 esterase activity using 4-nitrophenylacetate as substrate2012Bioorganic & medicinal chemistry letters, Feb-01, Volume: 22, Issue:3
Synthesis and carbonic anhydrase inhibitory properties of novel cyclohexanonyl bromophenol derivatives.
AID612732Inhibition of Salmonella Typhimurium recombinant carbonic anhydrase 2 at pH 8.3 by stopped flow CO2 hydration assay2011Bioorganic & medicinal chemistry, Aug-15, Volume: 19, Issue:16
Inhibition studies of the β-carbonic anhydrases from the bacterial pathogen Salmonella enterica serovar Typhimurium with sulfonamides and sulfamates.
AID669117Inhibition of Candida albicans CaNce103 preincubated for 15 mins measured for 10 to 100 sec by stopped-flow method2012Journal of medicinal chemistry, Apr-12, Volume: 55, Issue:7
Molecular cloning, characterization, and inhibition studies of a β-carbonic anhydrase from Malassezia globosa, a potential antidandruff target.
AID293814Selectivity for human recombinant CA9 over human recombinant CA22007Bioorganic & medicinal chemistry letters, Mar-15, Volume: 17, Issue:6
Carbonic anhydrase inhibitors: inhibition of cytosolic/tumor-associated isoforms I, II, and IX with iminodiacetic carboxylates/hydroxamates also incorporating benzenesulfonamide moieties.
AID1653794Substrate activity at human mARC1 expressed in Escherichia coli assessed as turnover rates at 1 mM pre-incubated for 3 mins followed by NADH addition and measured after 15 mins by UV-Visible spectroscopy based NADH assay2020Journal of medicinal chemistry, 06-25, Volume: 63, Issue:12
Drug Metabolism by the Mitochondrial Amidoxime Reducing Component (mARC): Rapid Assay and Identification of New Substrates.
AID366660Inhibition of human recombinant CA5B by CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Aug-15, Volume: 18, Issue:16
Inhibition of human mitochondrial carbonic anhydrases VA and VB with para-(4-phenyltriazole-1-yl)-benzenesulfonamide derivatives.
AID441708Inhibition of human recombinant CA4 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID320313Inhibition of human catalytic domain carbonic hydrase 9 by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Carbonic anhydrase inhibitors. Interaction of 2-N,N-dimethylamino-1,3,4-thiadiazole-5-methanesulfonamide with 12 mammalian isoforms: kinetic and X-ray crystallographic studies.
AID497130Selectivity ratio of Ki for wild type human recombinant carbonic anhydrase 1 to Ki for human recombinant carbonic anhydrase 1 Phe91Asn mutant2010Bioorganic & medicinal chemistry, Aug-01, Volume: 18, Issue:15
Mutation of Phe91 to Asn in human carbonic anhydrase I unexpectedly enhanced both catalytic activity and affinity for sulfonamide inhibitors.
AID349606Inhibition of human recombinant carbonic anhydrase 2 by stopped flow CO2 hydration assay2009Journal of medicinal chemistry, May-14, Volume: 52, Issue:9
Carbonic anhydrase inhibitors. Cloning, characterization, and inhibition studies of a new beta-carbonic anhydrase from Mycobacterium tuberculosis.
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).
AID770581Selectivity ratio of Ki for human carbonic anhydrase 2 to Ki for human carbonic anhydrase 92013Bioorganic & medicinal chemistry, Oct-01, Volume: 21, Issue:19
Carbonic anhydrase inhibitors: synthesis and inhibition of the human carbonic anhydrase isoforms I, II, VII, IX and XII with benzene sulfonamides incorporating 4,5,6,7-tetrabromophthalimide moiety.
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).
AID366657Inhibition of human cloned CA1 by CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Aug-15, Volume: 18, Issue:16
Inhibition of human mitochondrial carbonic anhydrases VA and VB with para-(4-phenyltriazole-1-yl)-benzenesulfonamide derivatives.
AID552128Inhibition of human recombinant CA2 by stopped-flow CO2 hydration assay2011Bioorganic & medicinal chemistry letters, Jan-15, Volume: 21, Issue:2
Carbonic anhydrase inhibitors. Inhibition studies with anions and sulfonamides of a new cytosolic enzyme from the scleractinian coral Stylophora pistillata.
AID540230Dose normalised AUC in rat after po administration2005Xenobiotica; the fate of foreign compounds in biological systems, Feb, Volume: 35, Issue:2
Comparative evaluation of oral systemic exposure of 56 xenobiotics in rat, dog, monkey and human.
AID612731Inhibition of Salmonella Typhimurium recombinant carbonic anhydrase 1 at pH 8.3 by stopped flow CO2 hydration assay2011Bioorganic & medicinal chemistry, Aug-15, Volume: 19, Issue:16
Inhibition studies of the β-carbonic anhydrases from the bacterial pathogen Salmonella enterica serovar Typhimurium with sulfonamides and sulfamates.
AID497128Inhibition of human recombinant carbonic anhydrase 1 Phe91Asn mutant expressed in Escherichia coli BL21 (DE3) after 15 mins by CO2 hydration method2010Bioorganic & medicinal chemistry, Aug-01, Volume: 18, Issue:15
Mutation of Phe91 to Asn in human carbonic anhydrase I unexpectedly enhanced both catalytic activity and affinity for sulfonamide inhibitors.
AID588186Inhibition of human recombinant alpha-carbonic anhydrase 1 after 15 mins by stopped flow CO2 hydration assay2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Natural product-based phenols as novel probes for mycobacterial and fungal carbonic anhydrases.
AID464121Inhibition of human recombinant CA14 by stopped-flow CO2 hydration assay2010Journal of medicinal chemistry, Mar-25, Volume: 53, Issue:6
Identification of 3,4-Dihydroisoquinoline-2(1H)-sulfonamides as potent carbonic anhydrase inhibitors: synthesis, biological evaluation, and enzyme--ligand X-ray studies.
AID1287520Inhibition of recombinant Enterobacter sp. B13 beta carbonic anhydrase incubated for 15 mins by stopped-flow CO2 hydration assay2016Bioorganic & medicinal chemistry letters, Apr-01, Volume: 26, Issue:7
Sulfonamide inhibition studies of the β-carbonic anhydrase from the newly discovered bacterium Enterobacter sp. B13.
AID349605Inhibition of human recombinant carbonic anhydrase 1 by stopped flow CO2 hydration assay2009Journal of medicinal chemistry, May-14, Volume: 52, Issue:9
Carbonic anhydrase inhibitors. Cloning, characterization, and inhibition studies of a new beta-carbonic anhydrase from Mycobacterium tuberculosis.
AID588192Selectivity ratio of Ki for human recombinant alpha-carbonic anhydrase 1 to Ki for Candida albicans recombinant Nce103 beta-carbonic anhydrase2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Natural product-based phenols as novel probes for mycobacterial and fungal carbonic anhydrases.
AID1251245Anticonvulsant activity in rat amygdala kindling model assessed as change in after-discharge duration at 30 mg/kg, po2015Bioorganic & medicinal chemistry letters, Oct-15, Volume: 25, Issue:20
Discovery of benzothiazine derivatives as novel, orally-active anti-epileptic drug candidates with broad anticonvulsant effect.
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID743514Inhibition of human recombinant carbonic anhydrase 2 preincubated for 15 mins by CO2 hydration stopped-flow assay2013Bioorganic & medicinal chemistry, Mar-15, Volume: 21, Issue:6
The alpha-carbonic anhydrase from the thermophilic bacterium Sulfurihydrogenibium yellowstonense YO3AOP1 is highly susceptible to inhibition by sulfonamides.
AID123757Percentage block of the hind-limb tonic-extensor seizure was determined after application of an electric shock to mice for 60 min followed by 100 mg/kg intraperitoneal dose; ND means no data1987Journal of medicinal chemistry, May, Volume: 30, Issue:5
Anticonvulsant O-alkyl sulfamates. 2,3:4,5-Bis-O-(1-methylethylidene)-beta-D-fructopyranose sulfamate and related compounds.
AID1275911Inhibition of Vibrio cholerae alpha-carbonic anhydrase using CO2 as substrate preincubated for 15 mins by stopped-flow CO2 hydration assay2016Bioorganic & medicinal chemistry, Mar-01, Volume: 24, Issue:5
Sulfonamide inhibition studies of the β-carbonic anhydrase from the pathogenic bacterium Vibrio cholerae.
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1489013Anticonvulsant activity in amygdala kindling rat model assessed as change in after discharge duration at 30 mg/kg, po (Rvb = -5.5%)2017Bioorganic & medicinal chemistry letters, 09-01, Volume: 27, Issue:17
N-alkyl-[1,1'-biphenyl]-2-sulfonamide derivatives as novel broad spectrum anti-epileptic drugs with efficacy equivalent to that of sodium valproate.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID1473741Inhibition of human MRP4 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID778725Inhibition of recombinant Leishmania donovani chagasi beta-carbonic anhydrase expressed in baculovirus infected insect Sf9 cells incubated for 15 mins prior to testing by stopped flow CO2 hydrase assay2013Journal of medicinal chemistry, Sep-26, Volume: 56, Issue:18
Cloning, characterization, and inhibition studies of a β-carbonic anhydrase from Leishmania donovani chagasi, the protozoan parasite responsible for leishmaniasis.
AID456397Inhibition of human recombinant carbonic anhydrase 2 by stopped flow CO2 hydration method2010Bioorganic & medicinal chemistry, Jan-01, Volume: 18, Issue:1
Carbonic anhydrase inhibitors. Identification of selective inhibitors of the human mitochondrial isozymes VA and VB over the cytosolic isozymes I and II from a natural product-based phenolic library.
AID427125Inhibition of human recombinant carbonic anhydrase 1 by stopped-flow CO2 hydrase method2009Bioorganic & medicinal chemistry, Jul-01, Volume: 17, Issue:13
Carbonic anhydrase inhibitors. Inhibition and homology modeling studies of the fungal beta-carbonic anhydrase from Candida albicans with sulfonamides.
AID764717Inhibition of human cytosolic carbonic anhydrase 7 preincubated for 15 mins by stopped flow CO2 hydration assay2013Bioorganic & medicinal chemistry, Sep-01, Volume: 21, Issue:17
Carbonic anhydrase inhibitors: Synthesis and inhibition of the cytosolic mammalian carbonic anhydrase isoforms I, II and VII with benzene sulfonamides incorporating 4,5,6,7-tetrachlorophthalimide moiety.
AID123732Percentage block of the hind-limb tonic-extensor seizure was determined after application of an electric shock to mice for 120 min followed by 40 mg/kg peroral dose1987Journal of medicinal chemistry, May, Volume: 30, Issue:5
Anticonvulsant O-alkyl sulfamates. 2,3:4,5-Bis-O-(1-methylethylidene)-beta-D-fructopyranose sulfamate and related compounds.
AID1333088Inhibition of voltage dependent T-type Ca2+ channel in Wistar rat cerebral cortex assessed as reduction in transient inward Ca2+ current at -60 mV holding potential at 500 uM by whole-cell patch clamp method relative to control2016European journal of medicinal chemistry, Nov-10, Volume: 123Synthesis and T-type calcium channel-blocking effects of aryl(1,5-disubstituted-pyrazol-3-yl)methyl sulfonamides for neuropathic pain treatment.
AID570285Competitive inhibition of rat MAOA by spectrophotometry2011Journal of medicinal chemistry, Feb-10, Volume: 54, Issue:3
Interactions of monoamine oxidases with the antiepileptic drug zonisamide: specificity of inhibition and structure of the human monoamine oxidase B complex.
AID764718Inhibition of human cytosolic carbonic anhydrase 2 preincubated for 15 mins by stopped flow CO2 hydration assay2013Bioorganic & medicinal chemistry, Sep-01, Volume: 21, Issue:17
Carbonic anhydrase inhibitors: Synthesis and inhibition of the cytosolic mammalian carbonic anhydrase isoforms I, II and VII with benzene sulfonamides incorporating 4,5,6,7-tetrachlorophthalimide moiety.
AID588197Selectivity ratio of Ki for human recombinant alpha-carbonic anhydrase 2 to Ki for Cryptococcus neoformans recombinant Can2 beta-carbonic anhydrase2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Natural product-based phenols as novel probes for mycobacterial and fungal carbonic anhydrases.
AID588182Inhibition of Mycobacterium tuberculosis recombinant Rv3273 beta-carbonic anhydrase after 15 mins by stopped flow CO2 hydration assay2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Natural product-based phenols as novel probes for mycobacterial and fungal carbonic anhydrases.
AID725955Inhibition of human recombinant carbonic anhydrase 1 by stopped flow CO2 hydration assay2013Journal of medicinal chemistry, Feb-28, Volume: 56, Issue:4
Cloning, characterization, and sulfonamide and thiol inhibition studies of an α-carbonic anhydrase from Trypanosoma cruzi, the causative agent of Chagas disease.
AID342466Inhibition of AQP4 expressed in rat FRT cells assessed as osmotic water permeability at 10 uM by stopped-flow light scattering method2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Lack of aquaporin-4 water transport inhibition by antiepileptics and arylsulfonamides.
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).
AID414956Inhibition of human recombinant carbonic anhydrase 2 by stopped flow CO2 hydration method2009Journal of medicinal chemistry, Apr-23, Volume: 52, Issue:8
Molecular cloning, characterization, and inhibition studies of the Rv1284 beta-carbonic anhydrase from Mycobacterium tuberculosis with sulfonamides and a sulfamate.
AID371555Inhibition of human recombinant cytosolic carbonic anhydrase 2 pre-incubated for 15 mins by stopped-flow CO2 hydration assay2008Bioorganic & medicinal chemistry letters, Dec-15, Volume: 18, Issue:24
Carbonic anhydrase inhibitors: 2-substituted-1,3,4-thiadiazole-5-sulfamides act as powerful and selective inhibitors of the mitochondrial isozymes VA and VB over the cytosolic and membrane-associated carbonic anhydrases I, II and IV.
AID588187Inhibition of human recombinant alpha-carbonic anhydrase 2 after 15 mins by stopped flow CO2 hydration assay2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Natural product-based phenols as novel probes for mycobacterial and fungal carbonic anhydrases.
AID369275Inhibition of mouse recombinant carbonic anhydrase 15 by stopped flow CO2 hydrase assay2009Journal of medicinal chemistry, Feb-12, Volume: 52, Issue:3
Cloning, expression, post-translational modifications and inhibition studies on the latest mammalian carbonic anhydrase isoform, CA XV.
AID441712Inhibition of human recombinant CA7 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID497129Inhibition of human recombinant carbonic anhydrase 2 after 15 mins by CO2 hydration method2010Bioorganic & medicinal chemistry, Aug-01, Volume: 18, Issue:15
Mutation of Phe91 to Asn in human carbonic anhydrase I unexpectedly enhanced both catalytic activity and affinity for sulfonamide inhibitors.
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).
AID239102Inhibitory constant against catalytic domain of human carbonic anhydrase IX2005Bioorganic & medicinal chemistry letters, Sep-01, Volume: 15, Issue:17
Carbonic anhydrase inhibitors: inhibition of the transmembrane isozyme XIV with sulfonamides.
AID588189Inhibition of Candida albicans recombinant Nce103 after 15 mins by stopped flow CO2 hydration assay relative to phenol2011Journal of medicinal chemistry, Mar-24, Volume: 54, Issue:6
Natural product-based phenols as novel probes for mycobacterial and fungal carbonic anhydrases.
AID342468Inhibition of AQP4 expressed in rat FRT cells assessed as osmotic water permeability at 100 uM after 60 mins by stopped-flow light scattering method2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Lack of aquaporin-4 water transport inhibition by antiepileptics and arylsulfonamides.
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).
AID770583Inhibition of human membrane bound carbonic anhydrase 9 preincubated for 15 mins at room temperature followed by 72 hrs at 4 degC by stopped flow CO2 hydration assay2013Bioorganic & medicinal chemistry, Oct-01, Volume: 21, Issue:19
Carbonic anhydrase inhibitors: synthesis and inhibition of the human carbonic anhydrase isoforms I, II, VII, IX and XII with benzene sulfonamides incorporating 4,5,6,7-tetrabromophthalimide moiety.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID47716Inhibitory effect on human Carbonic anhydrase I (hCA-I); NT is Not tested2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Carbonic anhydrase inhibitors: anticonvulsant sulfonamides incorporating valproyl and other lipophilic moieties.
AID1453412Inhibition of human carbonic anhydrase-1 assessed as reduction in CO2 hydration preincubated for 15 mins followed by CO2 addition measured for 10 to 100 secs by stopped-flow assay
AID570290Selectivity ratio of Ki for human MAO B to ratio of Ki for zebrafish MAO2011Journal of medicinal chemistry, Feb-10, Volume: 54, Issue:3
Interactions of monoamine oxidases with the antiepileptic drug zonisamide: specificity of inhibition and structure of the human monoamine oxidase B complex.
AID1628037Inhibition of human cytosolic carbonic anhydrase 2 preincubated for 15 mins by stop flow CO2 hydrase assay2016Bioorganic & medicinal chemistry letters, 09-01, Volume: 26, Issue:17
Cloning, expression, purification and sulfonamide inhibition profile of the complete domain of the η-carbonic anhydrase from Plasmodium falciparum.
AID1268965Inhibition of recombinant Thiomicrospira crunogena XCL-2 carbonic anhydrase by stopped flow CO2 hydrase assay2016Bioorganic & medicinal chemistry letters, Jan-15, Volume: 26, Issue:2
Sulfonamide inhibition studies of the α-carbonic anhydrase from the gammaproteobacterium Thiomicrospira crunogena XCL-2, TcruCA.
AID301578Inhibition of human recombinant CA 3 assessed as CO2 hydration by stopped flow kinetic assay2007Bioorganic & medicinal chemistry, Dec-01, Volume: 15, Issue:23
Carbonic anhydrase inhibitors: cloning, characterization, and inhibition studies of the cytosolic isozyme III with sulfonamides.
AID328195Inhibition of human carbonic anhydrase 2 by 4-NPA hydrolysis assay2008Journal of medicinal chemistry, Apr-24, Volume: 51, Issue:8
Carbonic anhydrase-II inhibition. what are the true enzyme-inhibitory properties of the sulfamide cognate of topiramate?
AID1628038Inhibition of recombinant Plasmodium falciparum eta-carbonic anhydrase (181 to 538 residues) expressed in Escherichia coli artic express (DE3) preincubated for 15 mins by stop flow CO2 hydrase assay2016Bioorganic & medicinal chemistry letters, 09-01, Volume: 26, Issue:17
Cloning, expression, purification and sulfonamide inhibition profile of the complete domain of the η-carbonic anhydrase from Plasmodium falciparum.
AID1190063Inhibition of human recombinant carbonic anhydrase 1 by stopped-flow CO2 hydration assay2015Bioorganic & medicinal chemistry, Feb-01, Volume: 23, Issue:3
Sulfonamide inhibition studies of the η-class carbonic anhydrase from the malaria pathogen Plasmodium falciparum.
AID295948Inhibition of human carbonic anhydrase 22007Bioorganic & medicinal chemistry, Jun-15, Volume: 15, Issue:12
Molecular modeling study for the binding of zonisamide and topiramate to the human mitochondrial carbonic anhydrase isoform VA.
AID1240217Inhibition of human recombinant carbonic anhydrase-2 by stopped flow CO2 hydrase assay method2015Bioorganic & medicinal chemistry letters, Sep-01, Volume: 25, Issue:17
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the Antarctic bacterium Pseudoalteromonas haloplanktis.
AID1240214Inhibition of Nostoc commune gamma carbonic anhydrase by CO2 hydration assay2015Bioorganic & medicinal chemistry letters, Sep-01, Volume: 25, Issue:17
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the Antarctic bacterium Pseudoalteromonas haloplanktis.
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).
AID1278411Inhibition of Nostoc commune gamma carbonic anhydrase preincubated for 15 mins by stopped flow CO2 hydration assay2016Bioorganic & medicinal chemistry letters, Feb-15, Volume: 26, Issue:4
Sulfonamide inhibition studies of the γ-carbonic anhydrase from the Antarctic bacterium Colwellia psychrerythraea.
AID601817Anticonvulsant activity against maximal electroshock-induced seizures in po dosed rat2011Journal of medicinal chemistry, Jun-09, Volume: 54, Issue:11
Anticonvulsant 4-aminobenzenesulfonamide derivatives with branched-alkylamide moieties: X-ray crystallography and inhibition studies of human carbonic anhydrase isoforms I, II, VII, and XIV.
AID299249Inhibition of Helicobacter pylori alpha carbonic anhydrase by stopped-flow CO2 hydrase assay2007Bioorganic & medicinal chemistry letters, Jul-01, Volume: 17, Issue:13
Carbonic anhydrase inhibitors: the beta-carbonic anhydrase from Helicobacter pylori is a new target for sulfonamide and sulfamate inhibitors.
AID48290Inhibitory effect on bovine Carbonic anhydrase IV; NT is Not tested2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Carbonic anhydrase inhibitors: anticonvulsant sulfonamides incorporating valproyl and other lipophilic moieties.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504812Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504810Antagonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID1799588Inhibition Assay from Article 10.1111/j.1747-0285.2009.00857.x: \\Which carbonic anhydrases are targeted by the antiepileptic sulfonamides and sulfamates?\\2009Chemical biology & drug design, Sep, Volume: 74, Issue:3
Which carbonic anhydrases are targeted by the antiepileptic sulfonamides and sulfamates?
AID1803140Esterase Activity Assay from Article 10.3109/14756366.2011.643303: \\Carbonic anhydrase inhibitors: in vitro inhibition of a isoforms (hCA I, hCA II, bCA III, hCA IV) by flavonoids.\\2013Journal of enzyme inhibition and medicinal chemistry, Apr, Volume: 28, Issue:2
Carbonic anhydrase inhibitors: in vitro inhibition of α isoforms (hCA I, hCA II, bCA III, hCA IV) by flavonoids.
AID1803139Esterase Activity Assay from Article 10.3109/14756366.2011.637202: \\Simple methanesulfonates are hydrolyzed by the sulfatase carbonic anhydrase activity.\\2012Journal of enzyme inhibition and medicinal chemistry, Dec, Volume: 27, Issue:6
Simple methanesulfonates are hydrolyzed by the sulfatase carbonic anhydrase activity.
AID1796595CA Inhibition Assay from Article 10.1021/jm060531j: \\Carbonic anhydrase inhibitors: Hypoxia-activatable sulfonamides incorporating disulfide bonds that target the tumor-associated isoform IX.\\2006Journal of medicinal chemistry, Sep-07, Volume: 49, Issue:18
Carbonic anhydrase inhibitors: Hypoxia-activatable sulfonamides incorporating disulfide bonds that target the tumor-associated isoform IX.
AID1802607Carbonic Anhydrase II Inhibition Assay from Article 10.1016/j.bioorg.2017.03.014: \\Carbohydrazones as new class of carbonic anhydrase inhibitors: Synthesis, kinetics, and ligand docking studies.\\2017Bioorganic chemistry, 06, Volume: 72Carbohydrazones as new class of carbonic anhydrase inhibitors: Synthesis, kinetics, and ligand docking studies.
AID1798769CA Inhibition Assay from Article 10.1021/jm801267c: \\Cloning, expression, post-translational modifications and inhibition studies on the latest mammalian carbonic anhydrase isoform, CA XV.\\2009Journal of medicinal chemistry, Feb-12, Volume: 52, Issue:3
Cloning, expression, post-translational modifications and inhibition studies on the latest mammalian carbonic anhydrase isoform, CA XV.
AID1799266CA Inhibition Assay from Article 10.1016/j.bmc.2009.05.002: \\Carbonic anhydrase inhibitors. Inhibition and homology modeling studies of the fungal beta-carbonic anhydrase from Candida albicans with sulfonamides.\\2009Bioorganic & medicinal chemistry, Jul-01, Volume: 17, Issue:13
Carbonic anhydrase inhibitors. Inhibition and homology modeling studies of the fungal beta-carbonic anhydrase from Candida albicans with sulfonamides.
AID1798985CA Inhibition Assay from Article 10.1021/jm9000488: \\Molecular cloning, characterization, and inhibition studies of the Rv1284 beta-carbonic anhydrase from Mycobacterium tuberculosis with sulfonamides and a sulfamate.\\2009Journal of medicinal chemistry, Apr-23, Volume: 52, Issue:8
Molecular cloning, characterization, and inhibition studies of the Rv1284 beta-carbonic anhydrase from Mycobacterium tuberculosis with sulfonamides and a sulfamate.
AID1803138CA Inhibition Assay from Article 10.3109/14756366.2011.637200: \\Inhibition of mammalian carbonic anhydrase isoforms I, II and VI with thiamine and thiamine-like molecules.\\2013Journal of enzyme inhibition and medicinal chemistry, Apr, Volume: 28, Issue:2
Inhibition of mammalian carbonic anhydrase isoforms I, II and VI with thiamine and thiamine-like molecules.
AID1796552CA Inhibition Assay from Article 10.1021/jm0512600: \\Carbonic anhydrase inhibitors: DNA cloning and inhibition studies of the alpha-carbonic anhydrase from Helicobacter pylori, a new target for developing sulfonamide and sulfamate gastric drugs.\\2006Journal of medicinal chemistry, Mar-23, Volume: 49, Issue:6
Carbonic anhydrase inhibitors: DNA cloning and inhibition studies of the alpha-carbonic anhydrase from Helicobacter pylori, a new target for developing sulfonamide and sulfamate gastric drugs.
AID1799586Inhibition Assay from Article 10.1111/j.1747-0285.2009.00842.x: \\Carbonic anhydrase inhibitors: inhibition of cytosolic carbonic anhydrase isozymes II and VII with simple aromatic sulfonamides and some azo dyes.\\2009Chemical biology & drug design, Aug, Volume: 74, Issue:2
Carbonic anhydrase inhibitors: inhibition of cytosolic carbonic anhydrase isozymes II and VII with simple aromatic sulfonamides and some azo dyes.
AID1798982CA Inhibition Assay from Article 10.1021/jm9003126: \\Carbonic anhydrase inhibitors. Cloning, characterization, and inhibition studies of a new beta-carbonic anhydrase from Mycobacterium tuberculosis.\\2009Journal of medicinal chemistry, May-14, Volume: 52, Issue:9
Carbonic anhydrase inhibitors. Cloning, characterization, and inhibition studies of a new beta-carbonic anhydrase from Mycobacterium tuberculosis.
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
AID1346210Human carbonic anhydrase 12 (4.2.1.1 Carbonate dehydratases)2013Bioorganic & medicinal chemistry, Oct-01, Volume: 21, Issue:19
Carbonic anhydrase inhibitors: synthesis and inhibition of the human carbonic anhydrase isoforms I, II, VII, IX and XII with benzene sulfonamides incorporating 4,5,6,7-tetrabromophthalimide moiety.
AID1345928Human carbonic anhydrase 1 (4.2.1.1 Carbonate dehydratases)2013Bioorganic & medicinal chemistry, Oct-01, Volume: 21, Issue:19
Carbonic anhydrase inhibitors: synthesis and inhibition of the human carbonic anhydrase isoforms I, II, VII, IX and XII with benzene sulfonamides incorporating 4,5,6,7-tetrabromophthalimide moiety.
AID1346202Human carbonic anhydrase 7 (4.2.1.1 Carbonate dehydratases)2013Bioorganic & medicinal chemistry, Oct-01, Volume: 21, Issue:19
Carbonic anhydrase inhibitors: synthesis and inhibition of the human carbonic anhydrase isoforms I, II, VII, IX and XII with benzene sulfonamides incorporating 4,5,6,7-tetrabromophthalimide moiety.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (863)

TimeframeStudies, This Drug (%)All Drugs %
pre-199025 (2.90)18.7374
1990's104 (12.05)18.2507
2000's305 (35.34)29.6817
2010's319 (36.96)24.3611
2020's110 (12.75)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 83.01

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 Index83.01 (24.57)
Research Supply Index6.95 (2.92)
Research Growth Index5.21 (4.65)
Search Engine Demand Index155.12 (26.88)
Search Engine Supply Index2.09 (0.95)

This Compound (83.01)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials121 (13.12%)5.53%
Reviews165 (17.90%)6.00%
Case Studies124 (13.45%)4.05%
Observational12 (1.30%)0.25%
Other500 (54.23%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (71)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
A Randomized. Single-Dose, Two-Way Crossover Relative Bioavailability Study of Zonisamide Formulations in Fasted Normal, Healthy Men and Women [NCT01161966]Phase 126 participants (Actual)Interventional2005-01-31Completed
Evaluation of Safety and Efficacy of Zonisamide in Adult Patients With Partial, Generalized and Combined Seizures: An Open Labeled, Non-comparative, Observational Study [NCT01283256]655 participants (Actual)Observational2011-01-31Completed
Efficacy and Tolerability of Low vs. Standard Daily Doses of Antiepileptic Drugs in Newly Diagnosed, Previously Untreated Epilepsy (STANDLOW). A Multicenter, Randomized, Single-blind, Parallel-group Trial [NCT03689114]Phase 4374 participants (Anticipated)Interventional2020-01-07Not yet recruiting
Zonisamide Treatment of Alcohol Use Disorder: an Evaluation of Efficacy and Mechanism of Action [NCT02900352]Phase 3156 participants (Actual)Interventional2016-10-31Completed
Zonisamide/Bupropion Effects on Switching to Electronic Cigarettes [NCT04388319]Phase 326 participants (Actual)Interventional2020-05-27Completed
A Multicenter, Placebo-controlled, Double-blind Study to Evaluate the Efficacy and Safety of Zonisamide in the Treatment of Partial Seizures [NCT00327717]Phase 3240 participants (Actual)Interventional2006-09-30Completed
Pharmaceutical Interventions for Noise-Induced Hearing Loss-Acute Exposure Treatment [NCT04768569]Phase 224 participants (Actual)Interventional2021-10-04Terminated(stopped due to PINIHL Program terminated by DoD)
A Randomized. Single-Dose, Two-Way Crossover Relative Bioavailability Study of Zonisamide Formulations in Normal, Healthy Men and Women Following a Standard Meal [NCT01161979]Phase 126 participants (Actual)Interventional2005-01-31Completed
A Korean Open-label, Multi-center, Community-based Trial Assessing the Efficacy and Safety of Zonisamide as Adjunctive Therapy in Patients With Uncontrolled Partial Epilepsy [NCT01140867]Phase 4121 participants (Actual)Interventional2008-02-29Completed
Comparative Study of Zonisamide and Carbamazepine as an Initial Monotherapy: Efficacy and Safety Evaluation [NCT01127256]Phase 4200 participants (Actual)Interventional2006-05-31Completed
Zonisamide for the Treatment of Alcohol Use Disorder in the Addiction Neuroclinical Assessment Framework [NCT05134857]Phase 2205 participants (Anticipated)Interventional2022-01-07Recruiting
Pharmaceutical Interventions for Noise-Induced Hearing Loss-Acute Exposure Treatment [NCT04774250]Phase 238 participants (Actual)Interventional2021-11-10Terminated(stopped due to Low accrual)
A Randomised Controlled Trial of the Ketogenic Diet in the Treatment of Epilepsy in Children Under the Age of Two Years [NCT02205931]Phase 4160 participants (Anticipated)Interventional2015-01-31Recruiting
An Open-Label Tolerability and Exploratory Efficacy Study of Zonisamide for Dyskinesias in Parkinson's Disease [NCT03034538]Phase 420 participants (Anticipated)Interventional2016-04-08Suspended(stopped due to Site staffing)
Zonisamide and Methylprednisolone to Prevent Noise-induced Temporary Hearing Loss [NCT02049073]Phase 1/Phase 20 participants (Actual)Interventional2017-10-31Withdrawn(stopped due to new data makes this trial unethical)
Characterization of Epilepsy Patients At-risk for Adverse Outcomes Related to Switching Antiepileptic Drug Products: BEEP 2b Study [NCT02707965]Phase 121 participants (Actual)Interventional2017-06-08Completed
A Phase IIB, Multi-Center, Dose-Parallel, Randomized, Double-Blind, Monotherapy and Placebo-Controlled Safety and Efficacy Study of Zonisamide SR Plus Bupropion SR Combination Therapy in Subjects With Obesity [NCT00709371]Phase 2729 participants (Actual)Interventional2008-07-31Completed
A Double-blind, Randomised, Placebo-controlled, Multi-centre Study to Assess the Efficacy and Safety of Adjunctive Zonisamide in Myoclonic Seizures Associated With Idiopathic Generalised Epilepsy [NCT00693017]Phase 310 participants (Actual)Interventional2008-06-30Terminated(stopped due to Sponsor's decision)
A Double-blind, Randomised, Placebo-controlled Multi-centre Study to Assess the Efficacy and Safety of Adjunctive Zonisamide in Primary Generalised Tonic Clonic Seizures [NCT00692003]Phase 321 participants (Actual)Interventional2008-08-01Terminated(stopped due to Sponsor's decision)
Single-Dose Fasting In Vivo Bioequivalence Study of Zonisamide Capsules (100 mg; Mylan) to Zonegran® Capsules (100 mg; Elan) in Healthy Volunteers [NCT00650052]Phase 1107 participants (Actual)Interventional2003-11-30Completed
Post-authorization, Observational and Prospective Follow up Study to Evaluate Effectiveness and Tolerability of Zonisamide as Adjunctive Therapy in Patients With Partial Onset Seizures Treated With Two Antiepileptic Drugs [NCT00659958]Phase 432 participants (Actual)Interventional2008-04-30Completed
The Assessment of the Safety, Efficacy, and Practicality of an Algorithm Including Amantadine, Metformin and Zonisamide for the Prevention of Olanzapine-Associated Weight Gain in Outpatients With Schizophrenia [NCT00401973]Phase 3199 participants (Actual)Interventional2006-11-30Completed
A Randomized, Double-Blind Extension Study To Assess The Long-Term Safety And To Explore The Long-Term Efficacy Of Zonisamide As Monotherapy In Newly Diagnosed Partial Seizures [NCT00848549]Phase 3295 participants (Actual)Interventional2008-10-31Completed
Interdisciplinary Study of Two Novel Anticonvulsants in Alcoholism [NCT02901041]Phase 381 participants (Actual)Interventional2017-09-21Completed
A Multicentre, Randomised, Active Comparator, Parallel Group Study To Compare The Effect On Cognition Of Adjunctive Therapy With Zonisamide Versus Sodium Valproate [NCT00713622]Phase 42 participants (Actual)Interventional2008-06-30Completed
A Double-blind, Randomised, Placebo-controlled, Multi-centre Study to Assess the Efficacy and Safety of Adjunctive Zonisamide in Paediatric Partial Onset Seizures [NCT00566254]Phase 3207 participants (Actual)Interventional2008-12-31Completed
A Multi-center Comparative Trial of Low and High Dose Zonisamide in Children as Monotherapy [NCT01127165]Phase 4125 participants (Actual)Interventional2006-03-31Completed
An Open-label Extension Study Following a Double-blind, Randomized, Placebo-controlled, Multi-centre Study to Assess the Efficacy and Safety of Adjunctive Zonisamide in Pediatric Partial Onset Seizures [NCT01136954]Phase 3144 participants (Actual)Interventional2008-07-31Completed
Cognitive Side Effects of Commonly Prescribed Medications in Pediatric Migraine [NCT00777218]0 participants (Actual)Interventional2007-08-31Withdrawn(stopped due to Enrollment criteria was too challenging and Investigators changed Institutions)
[NCT00154076]Phase 4140 participants (Anticipated)Interventional2005-09-30Completed
The Effects of Zonisamide on Alcohol Dependence [NCT00406692]Phase 216 participants (Actual)Interventional2006-11-30Completed
A Study for Evaluating the Efficacy and Safety of Zonisamide and Lamotrigine (Lamictal) for Subjects With Refractory Simple Partial, Complex Partial or Partial With Secondary Generalized Seizures [NCT00292461]Phase 364 participants (Actual)Interventional2006-03-31Completed
Novel Therapies for Essential Tremor - Zonisamide Pilot Study [NCT00223743]Phase 225 participants (Actual)Interventional2004-11-30Completed
Zonegran for the Treatment of Weight Gain Associated With Psychotropic Medication Use: A Placebo-Controlled Trial [NCT00203450]Phase 420 participants (Actual)Interventional2003-05-31Completed
Zonisamide for Weight Reduction in Obese Adults [NCT00275834]225 participants (Actual)Interventional2006-01-31Completed
Liceo Study: A Prospective, Observational Study On The Effectiveness Of New Antiepileptic Drugs As First Bitherapy In The Daily Clinical Practice [NCT00855738]Phase 4111 participants (Actual)Interventional2007-05-31Completed
Single-Dose Food In Vivo Bioequivalence Study of Zonisamide Capsules (100 mg; Mylan) to Zonegran® Capsules (100 mg; Elan) in Healthy Volunteers [NCT00649714]Phase 1110 participants (Actual)Interventional2003-12-31Completed
A Relative Bioavailability Study of 100 mg Zonisamide Capsules Under Non-Fasting Conditions [NCT00687167]Phase 134 participants (Actual)Interventional2005-01-31Completed
Comparative Study of the Efficiency of Zonisamide in Myoclonus Dystonia: A Monocentric , Randomized in Cross Over and Double Blind Study Versus Placebo Study [NCT01806805]Phase 324 participants (Actual)Interventional2012-02-29Completed
A Randomized, Multi-centre, Double-blind Study, to Compare the Efficacy and Safety of Zonisamide and Carbamazepine as Monotherapy, in Newly Diagnosed Partial Epilepsy [NCT00477295]Phase 3583 participants (Actual)Interventional2007-05-31Completed
Randomized Trial to Assess Efficacy and Safety of an add-on Treatment With Zonisamide in Adults With Focal Epileptic Seizures With or Without Secondary Generalization [NCT00165828]Phase 4157 participants (Actual)Interventional2005-05-31Terminated
An Open Label Study Of Zonegran (Zonisamide) In Patients With Partial Onset Seizures [NCT00215592]Phase 41,000 participants (Actual)Interventional2005-10-31Completed
Zonisamide vs. Placebo in the Treatment of Alcohol Dependence [NCT00595556]Phase 440 participants (Actual)Interventional2006-07-31Completed
A Double-Blind, Placebo-Controlled, Parallel Group Design Trial of; Levetiracetam, Zonisamide, Topiramate, and Placebo Control for the Treatment of Alcohol Dependent Subjects. [NCT00862563]Phase 285 participants (Actual)Interventional2009-05-31Terminated(stopped due to Recruitment goals could not be met before ending of funding for this project.)
Zonisamide for Fibromyalgia & Migraine [NCT00259636]Phase 40 participants (Actual)Interventional2004-08-31Withdrawn(stopped due to Logistical problems prevented enrollment)
Zonisamide in Addition to Enhanced Cognitive Processing Therapy-C (E-CPT-C) for Veterans With PTSD and Comorbid Alcohol Dependence [NCT01847469]Phase 224 participants (Actual)Interventional2013-06-30Completed
Zonegran in the Treatment of Binge Eating Disorder Associated With Obesity: A Single Center, Double-Blind, Placebo-controlled, Flexible-Dose Study in Outpatients [NCT00221442]Phase 360 participants (Actual)Interventional2005-08-31Completed
A Dose Parallel, Randomized, Placebo-Controlled, Multicenter Study of the Safety and Efficacy of Multiple Regimens of the Combination of Zonisamide CR Plus Bupropion SR in the Treatment of Subjects With Uncomplicated Obesity [NCT00339014]Phase 2611 participants (Actual)Interventional2006-05-31Completed
[NCT00047567]Phase 420 participants Interventional2002-07-31Terminated
A Double-Blind, Randomized, Multicenter, Parallel Dose Study to Evaluate the Safety and Efficacy of Zonisamide 150 mg and 300 mg Per Day and Placebo in Subjects With Migraine Headache [NCT00055484]Phase 2204 participants Interventional2002-03-31Completed
A Double-Blind, Randomized, Multicenter, Parallel Group Study to Establish Dose-Response, Safety, and Efficacy of Zonegran (Zonisamide) as Monotherapy in Patients With Newly Diagnosed Epilepsy [NCT00056576]Phase 3165 participants Interventional2002-02-28Completed
Pilot Study of Zonisamide in the Treatment of Essential Tremor [NCT00616343]9 participants (Actual)Interventional2003-06-30Terminated(stopped due to Principal Investigator left the study site on December 28, 2012.)
Effectiveness of Zonisamide in the Treatment of Alcohol Dependent Veterans [NCT02368431]Phase 392 participants (Actual)Interventional2015-03-01Terminated(stopped due to Funding ended prematurely)
A Proof of Concept, Multi-Center, Randomized, Double-Blind, Parallel, Placebo-Controlled, Study of Zonisamide Sustained Release (SR) 360 mg Versus Placebo in the Prevention of Weight Gain Associated With Olanzapine Therapy for Psychosis [NCT00734435]Phase 226 participants (Actual)Interventional2008-09-30Terminated(stopped due to Sponsor Decision- Financial Considerations)
A Relative Bioavailability Study of 100 mg Zonisamide Capsules Under Fasting Conditions [NCT00685139]Phase 134 participants (Actual)Interventional2005-01-31Completed
An Open-label, Randomized, Multi-centre, Superiority Study to Compare, in Patients With Partial Onset Seizures, the Efficacy and Safety of Adjunctive Zonisamide vs Replacement With Zonisamide of the Last Added Antiepileptic Drug [NCT01630057]Phase 4200 participants (Actual)Interventional2009-09-30Completed
A 1 Month Randomized Placebo Controlled, Double Blind Trial With a 5 Month Open Extension Phase to Explore the Efficacy of Zonisamide on Apnea/Hypopnea Index in Overweight/Obese Sleep Apnea Patients. [NCT01765608]Phase 250 participants (Actual)Interventional2010-03-31Completed
Effect of Zonisamide on Cocaine Reinforcement, Craving, and Relapse [NCT01137890]Phase 1/Phase 219 participants (Actual)Interventional2010-06-30Completed
Role of Zonisamide in Advanced Parkinson's Disease (PD) in Egyptian Population: Pilot Study [NCT04182399]69 participants (Actual)Interventional2020-04-01Completed
Zonisamide Augmentation of Varenicline Treatment for Smoking Cessation [NCT01685996]Phase 1/Phase 274 participants (Actual)Interventional2012-09-30Completed
Zonisamide for Heavy Drinkers With Bipolar Disorder [NCT01566370]Phase 23 participants (Actual)Interventional2012-05-31Terminated(stopped due to recruitment infeasible)
Modification of Epilepsy Screen Questionnaire and Treatment Feasibility Evaluation [NCT04939675]40 participants (Anticipated)Interventional2021-07-01Not yet recruiting
Systematic Review: Retigabine for Adjunctive Therapy in Partial Epilepsy [NCT01587339]6,498 participants (Actual)Observational2010-09-30Completed
A Randomised, Double Blind, Placebo-controlled Study to Evaluate the Safety and Tolerability and to Explore the Efficacy of Zonisamide as add-on Therapy in Elderly Patients With Refractory Partial Seizures [NCT01546688]Phase 441 participants (Actual)Interventional2008-11-30Terminated
A Randomized Controlled Trial to Determine the Effects of Combination Zonisamide and Bupropion on Switching to an Electronic Cigarette [NCT05205811]Phase 3180 participants (Anticipated)Interventional2021-12-14Recruiting
Population Pharmacokinetics of Antiepileptic in Pediatrics [NCT03196466]1,000 participants (Anticipated)Observational2017-06-19Recruiting
An Open-label, Multi-centre, Multi-national Post-marketing Non-interventional Observational Study of the Use of Zonisamide (ZNS) in the Adjunctive Treatment of Adult Patients With Partial Onset Seizures Treated With One Antiepileptic Drug (AED) as Baselin [NCT01830868]104 participants (Actual)Observational2012-03-31Completed
Alcohol Self Administration Laboratory [NCT00398918]10 participants (Actual)Interventional2006-11-30Completed
Randomized Double Blind Placebo-controlled Study of Zonisamide Effectiveness in Early Parkinson Disease [NCT01766128]Phase 2/Phase 30 participants (Actual)Interventional2013-02-28Withdrawn(stopped due to Practical problems)
Zonisamide as a New Treatment for Post-Traumatic Stress Disorder and Co-Occurring Alcohol Use Disorder [NCT03376139]Phase 20 participants (Actual)Interventional2019-03-01Withdrawn(stopped due to Futility)
A Double-Blind, Placebo-Controlled Study of Zonisamide to Prevent Olanzapine-Associated Weight Gain [NCT00363376]Phase 342 participants (Actual)Interventional2008-01-31Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00275834 (8) [back to overview]Quality of Life as Measured by HADS_D
NCT00275834 (8) [back to overview]Proportions of Patients With 5% Weight Loss
NCT00275834 (8) [back to overview]Waist Circumference
NCT00275834 (8) [back to overview]Change in Body Weight
NCT00275834 (8) [back to overview]Change in Blood Pressure
NCT00275834 (8) [back to overview]Change in Lipids
NCT00275834 (8) [back to overview]Inflammatory Markers (CRP)
NCT00275834 (8) [back to overview]Proportions of Patients With 10% Weight Loss
NCT00292461 (4) [back to overview]Response Rate: Defined as the Percentage of Participants With >= 50% Reduction of Monthly Seizure Frequency at the End of 16-week Treatment From Baseline.
NCT00292461 (4) [back to overview]The Percentage Change of Monthly Seizure Frequency at the End of the 16-week Treatment From Baseline
NCT00292461 (4) [back to overview]Global Assessment of Efficacy by Participants at the End of the 16-week Treatment Period
NCT00292461 (4) [back to overview]Global Assessment of Efficacy by Physician at the End of 16-week Treatment Period
NCT00327717 (10) [back to overview]Mean Percentage of Change in Seizure Free Days
NCT00327717 (10) [back to overview]Drop - Out Rate
NCT00327717 (10) [back to overview]Mean Number of Seizure Free Days
NCT00327717 (10) [back to overview]Mean Time to First Seizure (Days)
NCT00327717 (10) [back to overview]Median Percent Change From Baseline in All Partial Seizure Frequency (Complex Partial Seizures (CP)+ Simple Partial Seizures (SP) + Secondary Generalization Seizures (SGS)) During the Fixed-dose Phase
NCT00327717 (10) [back to overview]Percentage of Seizure-free Participants During Fixed-dose Phase
NCT00327717 (10) [back to overview]Responder Rate
NCT00327717 (10) [back to overview]The Mean Percent Change From Baseline in Complex Partial (CP) Seizure Frequency
NCT00327717 (10) [back to overview]The Mean Percent Change From Baseline in Partial Seizures With Secondary Generalization (SGS)
NCT00327717 (10) [back to overview]The Mean Percent Change From Baseline in Simple Partial (SP) Seizure Frequency
NCT00398918 (2) [back to overview]Grams Ethanol Consumed During Second Hour of the Alcohol Self-Administration Sessions
NCT00398918 (2) [back to overview]Score Digit Symbol Modalities Test
NCT00401973 (11) [back to overview]Mean Change From Baseline to Endpoint in Fasting High Density Lipoprotein (HDL) Cholesterol
NCT00401973 (11) [back to overview]Mean Change From Baseline to Endpoint in Fasting Low Density Lipoprotein (LDL) Cholesterol
NCT00401973 (11) [back to overview]Mean Change From Baseline to Endpoint in Fasting Triglycerides
NCT00401973 (11) [back to overview]Mean Change From Baseline to Endpoint in Hemoglobin A1c
NCT00401973 (11) [back to overview]Mean Change From Baseline to Endpoint in Fasting Glucose
NCT00401973 (11) [back to overview]Change From Baseline to Endpoint in Weight
NCT00401973 (11) [back to overview]Change From Baseline to Endpoint in Brief Psychiatric Rating Scale (BPRS) Total Score
NCT00401973 (11) [back to overview]Change From Baseline to Endpoint in Clinical Global Impression - Severity Scale (CGI-S)
NCT00401973 (11) [back to overview]Mean Change From Baseline to Endpoint in Fasting Total Cholesterol
NCT00401973 (11) [back to overview]Change From Baseline to Endpoint in Montgomery-Asberg Depression Rating Scale (MADRS) Total Score
NCT00401973 (11) [back to overview]Correlations Between Weight Changes and Changes in Eating Inventory (EI) and Food Craving Inventory (FCI) at 2 Weeks and 22 Weeks
NCT00406692 (3) [back to overview]Difference in Mean Words for the Phonetic Portion of the Controlled Word Association Test (COWAT).
NCT00406692 (3) [back to overview]Symbol Digit Modalities Test (DSMT)
NCT00406692 (3) [back to overview]The Weekly Mean Number of Standard Drinks Consumed Per Day at Baseline and Treatment Phase
NCT00477295 (11) [back to overview]Change From Baseline in SF-36 Aggregate Mental and Physical Component Score at Maintenance Period Visit 1
NCT00477295 (11) [back to overview]Change From Baseline in Bond and Lader VAS Mood Sub-Scores at Maintenance Period Visit 1
NCT00477295 (11) [back to overview]Time to 6-months Seizure Freedom
NCT00477295 (11) [back to overview]Percentage of Participants Who Experienced Seizure Freedom for 26-weeks During the Maintenance Phase
NCT00477295 (11) [back to overview]Percentage of Participants Who Experienced Seizure Freedom for 12-months During the FDP and Maintenance Period
NCT00477295 (11) [back to overview]Change From Baseline in Total ABNAS Score at Maintenance Period Visit 1
NCT00477295 (11) [back to overview]Change From Baseline in QOLIE-31-P Overall Score at Maintenance Period Visit 1
NCT00477295 (11) [back to overview]Analysis of Time to Drop Out Due to Lack of Efficacy
NCT00477295 (11) [back to overview]Time to 12-months Seizure Freedom
NCT00477295 (11) [back to overview]Analysis of Time to Drop Out Due to an Adverse Event (AE)
NCT00477295 (11) [back to overview]Percentage of Participants With EQ-5D Scores at Maintenance Period Visit 1
NCT00566254 (4) [back to overview]Percent of Participants With =50% to < 75% and = 75% Decrease From Baseline in 28-day Seizure Frequency During the Maintenance Period(LOCF)
NCT00566254 (4) [back to overview]Percent of Participants With =25% and =100% Increase From Baseline in 28-day Seizure Frequency During the Maintenance Period (LOCF)
NCT00566254 (4) [back to overview]Percentage of Participants With a Decrease From Baseline in 28-day Seizure Frequency of =50%(Responder) in the Maintenance Period(LOCF)
NCT00566254 (4) [back to overview]Median Percent Change From Baseline in the 28-day Seizure Frequency During the Maintenance Period (LOCF)
NCT00595556 (5) [back to overview]Change in Gamma-glutamyl Transferase (GGT) Concentration
NCT00595556 (5) [back to overview]Change in Number of Drinks Per Week by Week
NCT00595556 (5) [back to overview]Change in Number of Heavy Drinking Days (i.e., 5 or More Drinks Per Day for Men, and 4 or More Per Day for Women)Per Week, by Week
NCT00595556 (5) [back to overview]Weekly Rate of Change in Abstinent Days
NCT00595556 (5) [back to overview]Change in the Urge to Drink Alcohol as Measured by the Alcohol Urge Questionnaire (AUQ)
NCT00685139 (2) [back to overview]Area Under the Concentration Versus Time Curve From Time 0 to Time t [AUC(0-t)]
NCT00685139 (2) [back to overview]Maximum Plasma Concentration (Cmax)
NCT00687167 (2) [back to overview]Maximum Plasma Concentration (Cmax)
NCT00687167 (2) [back to overview]Area Under the Concentration Versus Time Curve From Time 0 to Time t [AUC(0-t)]
NCT00848549 (5) [back to overview]Percentage of Participants That Are Seizure Free for at Least 24 Month Consecutive Period in the Base Study and Extension Phase
NCT00848549 (5) [back to overview]Time to Drop-out Due to Adverse Event (AE)
NCT00848549 (5) [back to overview]Time to Drop-out Due to Lack of Efficacy
NCT00848549 (5) [back to overview]Change From Baseline in Quality of Life Assessed by Quality of Life in Epilepsy-Problems Questionnaire (QOLIE-31-P) Overall Score at Each Visit
NCT00848549 (5) [back to overview]Percentage of Participants Remaining in the Study at Each Visit
NCT00855738 (17) [back to overview]Percent of Participants With Cessation of Occupation, Requirement of Caregiver, or Admission to Intensive Care Unit
NCT00855738 (17) [back to overview]Percent of Participants That Reduced, Maintained and Increased Their Doses of New Antiepileptic Drugs (AED)
NCT00855738 (17) [back to overview]Change in Sleep Disturbances From Baseline to Month 6: Medical Outcomes Study Sleep Scale (MOS-SS)
NCT00855738 (17) [back to overview]Change From Baseline to Months 3 and 6 in Health Condition: Euro Quality of Life Scale (EQ-5D) Visual Analog Scale (VAS)
NCT00855738 (17) [back to overview]Change From Baseline to Month 6 in Visits to a Specialist or the Emergency Room Because of Epilepsy
NCT00855738 (17) [back to overview]Change From Baseline to Month 6 in the Hospital Anxiety and Depression Scale (HADS)
NCT00855738 (17) [back to overview]Change From Baseline to Month 6 in Quality of Life 10 Domains (QOLIE-10)
NCT00855738 (17) [back to overview]Time to First Seizure
NCT00855738 (17) [back to overview]Percent of Participants Who Continued on Study Medication to Month 6
NCT00855738 (17) [back to overview]Percent Change From Baseline in the Median Number of Seizures During the Last 3 Months of Treatment
NCT00855738 (17) [back to overview]Change From Baseline to Month 6 in Total Number of Days Hospitalized Because of Epilepsy
NCT00855738 (17) [back to overview]Percent of Participants Classified as Responders
NCT00855738 (17) [back to overview]Percent of Seizure-free Participants During the Last 3 Months Before Discontinuation
NCT00855738 (17) [back to overview]Percent of Participants That Reduced, Maintained and Increased the Doses of the Initial Treatment Administered in Monotherapy
NCT00855738 (17) [back to overview]Percent of Participants Reaching Monotherapy
NCT00855738 (17) [back to overview]Percent of Participants With Reduction in Number of Seizures >=25% and >=75% During the Last 3 Months of Treatment
NCT00855738 (17) [back to overview]Percent of Participants Indicating Optimal Sleep on the Optimal Sleep Subscale: Medical Outcomes Study Sleep Scale (MOS-SS)
NCT00862563 (8) [back to overview]COWAT-Category
NCT00862563 (8) [back to overview]Mean Percent Days Heavy Drinking
NCT00862563 (8) [back to overview]Percent Days Drinking
NCT00862563 (8) [back to overview]The Primary Efficacy Measure is the Mean Number of Drinks Consumed Per Day Over the Period From Treatment Weeks 10 Through 12 When All Study Medications Should be at Their Maximum Steady Levels Based on Their Known Pharmacokinetic Properties.
NCT00862563 (8) [back to overview]Wechsler Memory Scale-3rd Ed. Spatial Span
NCT00862563 (8) [back to overview]Wechsler Memory Scales (WMS)-3d Ed Digit Span-Age Adjusted Total
NCT00862563 (8) [back to overview]AB-Neurotoxicity Scale.
NCT00862563 (8) [back to overview]Controlled Word Association Test (COWAT)- Letter Fluency
NCT01127165 (4) [back to overview]Change in Korean-Quality of Life Childhood Epilepsy (K-QOLCE)
NCT01127165 (4) [back to overview]Percentage of Participants Who Were Assessed As Seizure Free
NCT01127165 (4) [back to overview]Change in Cognitive Assessment Korean-Wechsler Intelligence Scale for Children (K-WISC-Ⅲ)
NCT01127165 (4) [back to overview]Change in Behavior Assessment Korea-Child Behavior Checklist (K-CBCL)
NCT01127256 (3) [back to overview]Quality of Life in Epilepsy (QoL-QOLIE31)
NCT01127256 (3) [back to overview]The Percentage of Participants With Seizure Free Rate
NCT01127256 (3) [back to overview]The Percentage of Participants With Retention Rate
NCT01136954 (4) [back to overview]Median Percent Change From Study 312 Baseline in the 28-day Seizure Frequency During the Open Label Period
NCT01136954 (4) [back to overview]Percentage of Participants With a Decrease From Baseline in 28-day Seizure Frequency of =50%(Responder) in the Open Label Period
NCT01136954 (4) [back to overview]Treatment Emergent Non-Serious Adverse Events With Greater Than 5% Frequency
NCT01136954 (4) [back to overview]Median Change From Study 312 Baseline in the 28-day Seizure Frequency During the Open Label Period
NCT01137890 (4) [back to overview]Drug Value Questionnaire
NCT01137890 (4) [back to overview]Change in Visual Analog Questionnaire (VAQ) Score
NCT01137890 (4) [back to overview]Behavioral Choice Measures
NCT01137890 (4) [back to overview]Cocaine Craving
NCT01140867 (4) [back to overview]Seizure Reduction Rate
NCT01140867 (4) [back to overview]Seizure Free Rate
NCT01140867 (4) [back to overview]Responder Rate
NCT01140867 (4) [back to overview]QoL-QOLIE31 (Quality of Life in Epilepsy)
NCT01546688 (4) [back to overview]Percent Change in Seizure Frequency From Baseline to the Last 28 Days of the Maintenance Period
NCT01546688 (4) [back to overview]Change From Baseline in Bond and Lader Visual Analogue Scale (VAS) Mood Sub-Scores for Sedation by Visit During Titration and Maintenance Period
NCT01546688 (4) [back to overview]Change From Baseline in CVST of the FePsy Test (Mean Reaction Time) by Visit During Titration and Maintenance Period
NCT01546688 (4) [back to overview]Percentage of Responders During Last 28 Days of Maintenance Period
NCT01685996 (2) [back to overview]Percent Participants Abstinent From Smoking During Study Weeks 7-10
NCT01685996 (2) [back to overview]Nicotine Withdrawal Symptom Severity
NCT01847469 (3) [back to overview]Number of Drinking Days
NCT01847469 (3) [back to overview]Clinician-Administered PTSD Scale (CAPS) Total Score
NCT01847469 (3) [back to overview]Number of Heavy Drinking Days
NCT02368431 (6) [back to overview]Alcohol Urge Questionnaire Score (AUQ)
NCT02368431 (6) [back to overview]Change in Quality of Life
NCT02368431 (6) [back to overview]Gamma Glutamyl Transferase (GGT)
NCT02368431 (6) [back to overview]Number of Drinks Per Week
NCT02368431 (6) [back to overview]Number of Heavy Drinking Days Per Week
NCT02368431 (6) [back to overview]Level of Alcohol-related Problems (SIP)
NCT02707965 (5) [back to overview]Number of Seizures Reported
NCT02707965 (5) [back to overview]Mean Cmin_ss (Test vs. Reference)
NCT02707965 (5) [back to overview]Number of Adverse Events
NCT02707965 (5) [back to overview]Mean AUC0-last_ss (Test vs. Reference)
NCT02707965 (5) [back to overview]Mean Cmax_ss (Test vs. Reference)
NCT02900352 (7) [back to overview]Level of Alcohol-related Problems
NCT02900352 (7) [back to overview]Gamma Glutamyl Transferase (GGT) Levels
NCT02900352 (7) [back to overview]Change in Quality of Life
NCT02900352 (7) [back to overview]Change in Alcohol Urge Questionnaire Score (AUQ)
NCT02900352 (7) [back to overview]Percentage of Subjects With No Heavy Drinking Days
NCT02900352 (7) [back to overview]Number of Drinks Per Week
NCT02900352 (7) [back to overview]Number of Heavy Drinking Days Per Week
NCT02901041 (26) [back to overview]Percent Heavy Drinking Days
NCT02901041 (26) [back to overview]Percent Heavy Drinking Days
NCT02901041 (26) [back to overview]Cued Go No-Go: Inhibition Error
NCT02901041 (26) [back to overview]Connor's Continuous Performance Task: AX Test Commission Rate
NCT02901041 (26) [back to overview]Connor's Continuous Performance Task (CPT): X Test Omission Rate
NCT02901041 (26) [back to overview]Connor's Continuous Performance Task (CPT): X Test Commission Rate
NCT02901041 (26) [back to overview]Connor's Continuous Performance Task (CPT) - X Test Omission Rate
NCT02901041 (26) [back to overview]Connor's Continous Performance Task: AX Test Commission Rate
NCT02901041 (26) [back to overview]Balloon Analogue Risk Task: Total Pump Count
NCT02901041 (26) [back to overview]Balloon Analogue Risk Task: Total Pump Count
NCT02901041 (26) [back to overview]Average Weekly Standard Drinking Units (SDUs)
NCT02901041 (26) [back to overview]Average Weekly Standard Drinking Units (SDUs)
NCT02901041 (26) [back to overview]Connor's Continuous Performance Task (CPT): X Test Commission Rate
NCT02901041 (26) [back to overview]Connor's Continuous Performance Task (CPT): AX Test Omission Rate
NCT02901041 (26) [back to overview]Average Standard Drinking Units Per Day
NCT02901041 (26) [back to overview]Average Standard Drinking Units Per Day
NCT02901041 (26) [back to overview]Roger's Risk Task: Risk Adjustment
NCT02901041 (26) [back to overview]Roger's Risk Task: Delay Aversion
NCT02901041 (26) [back to overview]Roger's Risk Task: Risk Adjustment
NCT02901041 (26) [back to overview]Roger's Risk Task: Mean Percent Bet
NCT02901041 (26) [back to overview]Roger's Risk Task: Mean Percent Bet
NCT02901041 (26) [back to overview]Roger's Risk Task: Delay Aversion
NCT02901041 (26) [back to overview]Cued Go/No-go Task: Inhibition Error
NCT02901041 (26) [back to overview]Percentage of Drinking Days
NCT02901041 (26) [back to overview]Connor's Continuous Performance Task (CPT): AX Test Omission Rate
NCT02901041 (26) [back to overview]Percentage of Drinking Days
NCT04388319 (3) [back to overview]Change in Rewarding Effects of Smoking Combustible Cigarettes
NCT04388319 (3) [back to overview]Number of Participants That Completely Switched From Combustible Cigarettes to Halo G6 E-Cigarettes
NCT04388319 (3) [back to overview]Point Abstinence From Combustible Cigarettes

Quality of Life as Measured by HADS_D

Hospital Anxiety and Depression Scale - Depression (HADS-D) The HADS is a 14-item self-administered questionnaire that consists of 2 scales, one measuring anxiety (HADS-A), and the other measuring depression (HADS-D). Each subscale consists of 7 statements and the participant responds as to how each item applies to him/her over the past week on 4-point response scale. Separate scores are calculated for anxiety and depression and a score (ranging from 0 to 21) is obtained for each subscale. The higher the score, the more severe the anxiety or depression. (NCT00275834)
Timeframe: 1 year

Interventionunits on a scale (Least Squares Mean)
Placebo2.12
Zonisamide 200 mg2.76
Zonisamide 400 mg1.95

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Proportions of Patients With 5% Weight Loss

These were the proportions of patients losing 5% or more weight at 1-year relative to baseline. The measures were modeled with logistic regressions that included the three-level group proxy and a baseline weight covariate. (NCT00275834)
Timeframe: 1 year

Interventionparticipants (Number)
Placebo23
Zonisamide 200 mg26
Zonisamide 400 mg41

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Waist Circumference

Analyses was based on intent-to-treat ANCOVA. Difference scores from baseline to endpoint (Month-12) for each measure were regressed on the three-level proxy denoting group while controlling for the baseline value of the same measure. Contrasts were subsequently estimated in models, which had a significant overall treatment effect. (NCT00275834)
Timeframe: 1 year

Interventioncm (Mean)
Placebo-4.8
Zonisamide 200 mg-6.1
Zonisamide 400 mg-8.5

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Change in Body Weight

The primary endpoint was weight loss at 1-year, Month-12 weight minus baseline weight, in kilograms. (NCT00275834)
Timeframe: 1 year

Interventionkg (Mean)
Placebo-4.0
Zonisamide 200 mg-4.4
Zonisamide 400 mg-7.3

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Change in Blood Pressure

(NCT00275834)
Timeframe: Baseline, 1 year

,,
Interventionmm Hg (Least Squares Mean)
SystolicDiastolic
Placebo-0.6-1.5
Zonisamide 200 mg-4.4-3.6
Zonisamide 400 mg-1.9-3.9

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Change in Lipids

(NCT00275834)
Timeframe: baseline, 1 year

,,
Interventionmg/dL (Least Squares Mean)
Total CholesterolLDL CholesterolHDL CholesterolTriglycerides
Placebo-1.9-2.02.5-11.3
Zonisamide 200 mg4.11.71.50.7
Zonisamide 400 mg-0.1-0.33.4-11.7

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Inflammatory Markers (CRP)

C reactive Protein (CRP) (NCT00275834)
Timeframe: 1 year

Interventionmg/L (Mean)
Placebo0.523
Zonisamide 200 mg0.536
Zonisamide 400 mg0.443

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Proportions of Patients With 10% Weight Loss

This outcomes measure followed the same principles at measurement of proportions of patients with 5% weight loss described elsewhere. (NCT00275834)
Timeframe: 1 year

Interventionparticipants (Number)
Placebo6
Zonisamide 200 mg17
Zonisamide 400 mg24

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Response Rate: Defined as the Percentage of Participants With >= 50% Reduction of Monthly Seizure Frequency at the End of 16-week Treatment From Baseline.

(NCT00292461)
Timeframe: Baseline and 16 weeks

Interventionpercentage of participants (Number)
Zonegran45.8
Lamotrigine45.8

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The Percentage Change of Monthly Seizure Frequency at the End of the 16-week Treatment From Baseline

Percentage Change of Frequency = (T-B)/B*100% T= Total seizure frequency during maintenance dose period / maintenance dose period (weeks)* 4 B= The monthly seizure frequence with one month prior to enrollment (NCT00292461)
Timeframe: Baseline and 16 weeks

Interventionpercent change (Median)
Zonegran-32.7
Lamotrigine-35.6

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Global Assessment of Efficacy by Participants at the End of the 16-week Treatment Period

(NCT00292461)
Timeframe: Baseline and 16 weeks

,
Interventionparticipants (Number)
Greatly improvedSomewhat improvedNo changeSomewhat worsenedGreatly worsened
Lamotrigine812400
Zonegran314430

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Global Assessment of Efficacy by Physician at the End of 16-week Treatment Period

(NCT00292461)
Timeframe: Baseline and 16 weeks

,
Interventionparticipants (Number)
Greatly improvedSomewhat improvedNo changeSomewhat worsenedGreatly worsened
Lamotrigine415500
Zonegran591000

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Mean Percentage of Change in Seizure Free Days

(NCT00327717)
Timeframe: 16 weeks

InterventionPercent Change (Mean)
Zonisamide 100 mg Tablet79.69
Placebo76.52

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Drop - Out Rate

Number of Participants who dropped out of the study. In the Study drop-out rate is defined as number of participants. (NCT00327717)
Timeframe: 16 weeks

InterventionNumber of Participants (Number)
Zonisamide 100 mg Tablet4
Placebo6

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Mean Number of Seizure Free Days

Mean number of seizure free days per 28 day period during fixed dose phase (NCT00327717)
Timeframe: 12 weeks

InterventionDays (Mean)
Zonisamide 100 mg Tablet22.31
Placebo21.43

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Mean Time to First Seizure (Days)

Mean time to first seizure during fixed dose phase (NCT00327717)
Timeframe: 16 weeks

InterventionDays (Mean)
Zonisamide 100 mg Tablet22.31
Placebo21.43

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Median Percent Change From Baseline in All Partial Seizure Frequency (Complex Partial Seizures (CP)+ Simple Partial Seizures (SP) + Secondary Generalization Seizures (SGS)) During the Fixed-dose Phase

The median percent change in seizure frequency of all partial seizures (CP+SP+SGS) from baseline during the fixed-dose phase. (NCT00327717)
Timeframe: Baseline and 16 weeks

InterventionPercent Change (Median)
Zonisamide 100 mg Tablet-48.42
Placebo-26.58

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Percentage of Seizure-free Participants During Fixed-dose Phase

Percentage of seizure-free participants during fixed-dose phase (NCT00327717)
Timeframe: 16 weeks

InterventionPercentage of Participants (Number)
Zonisamide 100 mg Tablet1.8
Placebo2.8

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Responder Rate

Responder rate is defined as percentage of participants with >=50% reduction in seizure frequency from baseline. (NCT00327717)
Timeframe: Baseline and 16 weeks

InterventionPercentage of Participants (Number)
Zonisamide 100 mg Tablet48.6
Placebo34.9

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The Mean Percent Change From Baseline in Complex Partial (CP) Seizure Frequency

The Mean Percent Change in seizure frequency of CP from baseline during the fixed-dose phase. (NCT00327717)
Timeframe: Baseline and 16 weeks

InterventionPercent Change (Mean)
Zonisamide 100 mg Tablet-31.65
Placebo-25.21

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The Mean Percent Change From Baseline in Partial Seizures With Secondary Generalization (SGS)

The mean percent change in seizure frequency of SGS from baseline during the fixed-dose phase. (NCT00327717)
Timeframe: Baseline and 16 weeks

InterventionPercent Change (Mean)
Zonisamide 100 mg Tablet-53.2
Placebo-4.08

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The Mean Percent Change From Baseline in Simple Partial (SP) Seizure Frequency

The Mean percent change in seizure frequency of SP from baseline during the fixed-dose phase. (NCT00327717)
Timeframe: Baseline and 16 weeks

InterventionPercent Change (Mean)
Zonisamide 100 mg Tablet-49.14
Placebo56.03

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Grams Ethanol Consumed During Second Hour of the Alcohol Self-Administration Sessions

Grams Ethanol Consumed During Second Hour of the Alcohol Self-Administration Sessions for Zonisamide and Placebo Conditions (NCT00398918)
Timeframe: 1 day

InterventionGrams (Mean)
ZonisamidePlacebo
Zonisamide-Placebo Sessions9.018.2

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Score Digit Symbol Modalities Test

Difference score between zonisamide and placebo treatment conditions for the Digit Symbol Modalities Test scores obtained 40 minutes after ingestion of a priming dose of ethanol.This test involves transcribing from a key in which numbers appear below a series of symbols to boxes below symbols matched to those in the key. This task must be completed in 90 nseconds. This test measures visuomotor speed and aspects of attention. Scoring is the total number of correctly transcribed numbers. The maximum score on this test 110 points. (NCT00398918)
Timeframe: 40 minutes post alcohol ingestion

InterventionNumeric Score (Mean)
Zonisamide-Placebo Sessions2.2

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Mean Change From Baseline to Endpoint in Fasting High Density Lipoprotein (HDL) Cholesterol

(NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionmillimole per liter (mmol/L) (Mean)
BaselineChange from Baseline
Olanzapine1.25-0.00
Olanzapine + Amantadine1.26-0.11
Olanzapine + Metformin1.22-0.08

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Mean Change From Baseline to Endpoint in Fasting Low Density Lipoprotein (LDL) Cholesterol

(NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionmillimole per Liter (mmol/L) (Mean)
BaselineChange from Baseline
Olanzapine3.020.16
Olanzapine + Amantadine3.06-0.04
Olanzapine + Metformin2.91-0.02

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Mean Change From Baseline to Endpoint in Fasting Triglycerides

(NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionmillimoles per Liter (mmol/L) (Mean)
BaselineChange from Baseline
Olanzapine1.580.33
Olanzapine + Amantadine1.610.35
Olanzapine + Metformin1.680.06

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Mean Change From Baseline to Endpoint in Hemoglobin A1c

(NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionpercent hemoglobin A1c (Mean)
BaselineChange from Baseline
Olanzapine5.510.09
Olanzapine + Amantadine5.480.10
Olanzapine + Metformin5.53-0.03

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Mean Change From Baseline to Endpoint in Fasting Glucose

(NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionmillimole per Liter (mmol/L) (Mean)
BaselineChange from Baseline
Olanzapine5.320.26
Olanzapine + Amantadine5.250.10
Olanzapine + Metformin5.280.01

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Change From Baseline to Endpoint in Weight

(NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

Interventionkilograms (Least Squares Mean)
Olanzapine2.76
Olanzapine + Amantadine2.40
Olanzapine + Metformin0.65

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Change From Baseline to Endpoint in Brief Psychiatric Rating Scale (BPRS) Total Score

The BPRS is an 18-item clinician-administered scale used to assess the degree of severity of a subject's general psychopathological symptoms. Each item is rated on a scale from 1 (symptom not present) to 7 (symptom extremely severe). The BPRS total score ranges from 18 to 126. (NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionunits on a scale (Mean)
BaselineChange from Baseline
Olanzapine48.24-13.89
Olanzapine + Amantadine45.90-9.90
Olanzapine + Metformin47.00-9.72

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Change From Baseline to Endpoint in Clinical Global Impression - Severity Scale (CGI-S)

Measures severity of illness at the time of assessment compared with start of treatment. Scores range from 1 (normal, not at all ill) to 7 (among the most extremely ill patients). (NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionunits on a scale (Mean)
BaselineChange from Baseline
Olanzapine4.06-0.98
Olanzapine + Amantadine4.03-0.72
Olanzapine + Metformin4.00-0.79

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Mean Change From Baseline to Endpoint in Fasting Total Cholesterol

(NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionmillimole per Liter (mmol/L) (Mean)
BaselineChange from Baseline
Olanzapine5.010.36
Olanzapine + Amantadine5.030.01
Olanzapine + Metformin4.91-0.08

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Change From Baseline to Endpoint in Montgomery-Asberg Depression Rating Scale (MADRS) Total Score

The MADRS is a rating scale for severity of depressive mood symptoms. The MADRS has a 10-item checklist. Items are rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). (NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionunits on a scale (Mean)
BaselineChange from Baseline
Olanzapine12.76-6.39
Olanzapine + Amantadine14.22-4.12
Olanzapine + Metformin15.40-4.36

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Correlations Between Weight Changes and Changes in Eating Inventory (EI) and Food Craving Inventory (FCI) at 2 Weeks and 22 Weeks

To understand the drivers of weight gain as indicated by the correlation between weight changes and changes in the Eating Inventory (EI) and Food Craving Inventory (FCI). The EI is a 51-item inventory that measures dietary restraint, disinhibition, and perceived hunger. The FCI is a 28-item instrument measuring the frequency over the past month of general cravings and cravings for specific types of foods, namely: high fats, sweets, carbohydrates/starches, and fast-food fats. Correlations were computed on the combined treatment groups. (NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,
Interventioncorrelation (Number)
EI: DisinhibitionEI: Cognitive RestraintEI: HungerFCI: Carbohydrates/Starches (N=186, N=141)FCI: Fast Food Fats (N=188, N=140)FCI: High Fats (N=186, N=138)FCI: Sweets (N=187, N=140)FCI: Total Score (N=184, N=137)
2 Weeks-0.034-0.273-0.1500.013-0.0190.0510.0220.039
22 Weeks0.285-0.0380.148-0.0640.0470.043-0.008-0.000

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Difference in Mean Words for the Phonetic Portion of the Controlled Word Association Test (COWAT).

Subjects were asked to generate as many words as possible starting with a particular letter over a 60 second period. Three letters were used for each sessions. Values shown are the differences between values obtained for the baseline and week 12 test session. (NCT00406692)
Timeframe: Week 0- Baseline and Week 12

InterventionNumber of Words (Mean)
Zonisamide-6.4

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Symbol Digit Modalities Test (DSMT)

Number of correct digit substitutions on the DSMT per session with the possible maximum score being 188. The value shown is for difference between mean scores obtained for baseline and week 12 sessions. (NCT00406692)
Timeframe: Baseline, Week 12

InterventionUnits on a scale (Mean)
Zonisamide-1.5

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The Weekly Mean Number of Standard Drinks Consumed Per Day at Baseline and Treatment Phase

The mean daily standard alcoholic drinks were determined for the baseline period and each treatment week as a measure of alcohol intake. One standard drink=14g of alcohol. Mean value is the difference between mean standard drinks for the baseline period and week 12 of the study. (NCT00406692)
Timeframe: Baseline and Week 12

InterventionStandard Drinks (Mean)
Zonisamide-6.7

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Change From Baseline in SF-36 Aggregate Mental and Physical Component Score at Maintenance Period Visit 1

The Short Form 36 Health and Well-Being Questionnaire (SF-36) is a 36-item generic health related QOL instrument covering the following domains: physical functioning, role-physical,bodily pain, general health, social functioning,role-emotional, mental health, and vitality. It yields a profile of eight scores, one for each domain, and physical and mental health summary measures. Each domain is described by a score ranging from 0 to 100, for a range of total possible scoes of 0-400 for physical and 0-400 for mental. An increase represents an improvement, whereas a decrease reflects a worsening. (NCT00477295)
Timeframe: Baseline and Maintenance Period Visit 1 (Week 31 to Week 83)

,
InterventionScores on a Scale (Mean)
Aggregate Mental Component ScoreAggregate Physical Component Score
Carbamazepine2.4952.041
Zonisamide1.0271.895

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Change From Baseline in Bond and Lader VAS Mood Sub-Scores at Maintenance Period Visit 1

"The Bond-Lader Visual Analogue Scale (VAS) is made up of 16 pairs of alternative descriptors of mood and attention at either end of a 10 cm line.~Subjects were asked to rate their feelings at the time of assessment by indicating the point on the line which best represent their mood. Each item was scored by measuring the position relative to the left hand end of the line and levels of anxiety, sedation, and dysphoria were then calculated from the combined scores of selected items. The scores ranged from 0 to 100, with a high score reflecting a high level of anxiety, sedation or dysphoria." (NCT00477295)
Timeframe: Baseline and Maintenance Period Visit 1 (Week 31 to Week 83)

,
InterventionScores on a Scale (Mean)
AnxietySedationDysphoria
Carbamazepine-1.993-1.362-3.833
Zonisamide-2.036-0.475-1.930

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Time to 6-months Seizure Freedom

A subject achieved a 6-months seizure-free period if they were free of all seizures, regardless of seizure type, for 6-months while receiving the same dose. The occurrence of seizures was documented in the seizure diary, which was maintained by the subject and reviewed at each following visit. (NCT00477295)
Timeframe: Week 5 through Week 83

InterventionDays (Mean)
Zonisamide222.7
Carbamazepine220.4

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Percentage of Participants Who Experienced Seizure Freedom for 26-weeks During the Maintenance Phase

A subject achieved a 26-week seizure-free period if they were free of all seizures, regardless of seizure type, for 26 weeks while receiving the same dose. The occurrence of seizures was documented in the seizure diary, which was maintained by the subject and reviewed at each following visit. (NCT00477295)
Timeframe: Week 31 through Week 109

InterventionPercentage of Participants (Number)
Zonisamide79.4
Carbamazepine83.7

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Percentage of Participants Who Experienced Seizure Freedom for 12-months During the FDP and Maintenance Period

A subject achieved a 12-month seizure-free period if they were free of all seizures, regardless of seizure type, for 12 months while receiving the same dose. The occurrence of seizures was documented in the seizure diary, which was maintained by the subject and reviewed at each following visit. (NCT00477295)
Timeframe: Week 5 through Week 109

InterventionPercentage of participants (Number)
Zonisamide67.6
Carbamazepine74.7

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Change From Baseline in Total ABNAS Score at Maintenance Period Visit 1

The Aldenkamp-Baker Neuropsychological Assessment Scale(ABNAS) is a subject based questionnaire to measure subjective perceived drug-related cognitive impairments. The ABNAS measured seven critical domains of cognition(tiredness/fatigue,hyperexcitability, slowing(mental and motor),memory impairment,attention disorders,impairment of motor coordination, and language disorders). The total score ranged from 0 to 72, with a higher score reflecting a high level of problems. (NCT00477295)
Timeframe: Baseline and Maintenance Period Visit 1 (Week 31 to Week 83)

InterventionScores on a Scale (Mean)
Zonisamide1.6
Carbamazepine-0.1

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Change From Baseline in QOLIE-31-P Overall Score at Maintenance Period Visit 1

"The Quality of Life in Epilepsy - Problems(QOLIE-31-P) was completed by the patient and contained 30 items covering seven subscales(seizure worry, overall~Quality of Life (QOL),emotional well-being,energy-fatigue, cognition,medication effects and social function) and one item covering health status. It also included seven items addressing overall distress related to each subscale, an item addressing the relative importance of each subscale topic, and an item addressing perception of overall change in QOL at the end of the study. A high score reflects a good QOL. The following scale range is a sample of 1 of the 7 of the subscales:~10 (Best possible quality of life) - 0 (Worst possible quality of life);~Rand Corporation QOLIE-31 Scoring Manual was used. The QOLIE-31 overall score is calculated by summing the product of each scale score times its weight and summing overall all scales." (NCT00477295)
Timeframe: Baseline and Maintenance Period Visit 1 (Week 31 to Week 83)

InterventionScores on a Scale (Mean)
Zonisamide4.474
Carbamazepine6.090

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Analysis of Time to Drop Out Due to Lack of Efficacy

Lack of efficacy was evaluated by the subject and on the basis of whether zonisamide and carbamazepine gave the subject at least a 26-week seizure free rate. The subject could withdraw at any time due to lack of efficacy. (NCT00477295)
Timeframe: Week 1 through Week 109

InterventionMedian Days (Median)
Zonisamide722
CarbamazepineNA

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Time to 12-months Seizure Freedom

A subject achieved a 12-month seizure-free period if they were free of all seizures, regardless of seizure type, for 12-months while receiving the same dose. The occurrence of seizures was documented in the seizure diary, which was maintained by the subject and reviewed at each following visit. (NCT00477295)
Timeframe: Week 5 through Week 83

InterventionDays (Mean)
Zonisamide399.3
Carbamazepine395.6

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Analysis of Time to Drop Out Due to an Adverse Event (AE)

An AE is defined as any untoward medical occurrence in a subject and does not necessarily have a causal relationship with the medicinal product. Adverse events were identified by: any unfavorable or unintended sign, symptom or disease temporarily associated with the use of a medicinal product; any new disease or exacerbation of an existing disease; any deterioration in nonprotocol-required measurements of laboratory values or other clinical test; and recurrence of an intermittent medical condition not present at Baseline. (NCT00477295)
Timeframe: Week 1 through Week 109

InterventionMedian Days (Median)
ZonisamideNA
CarbamazepineNA

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Percentage of Participants With EQ-5D Scores at Maintenance Period Visit 1

The European Quality of Life Group 5-Dimension Self-Report Questionnaire (EQ-5D) is a preference based generic health related quality of life (HRQoL) instrument which classifies health states across five domains: mobility, self-care, usual activities, pain/discomfort, and anxiety/depression. Each domain has three levels, they are (1) no problems, (2) some problems, (3) extreme problems. The percentages shown are calculated from the number of subjects at that visit with non-missing data for that score. (NCT00477295)
Timeframe: Week 31 through Week 83

,
InterventionPercentage of Participants (Number)
Mobility: No problemsMobility: Some problemsMobility: Confined to BedSelf-Care:No problemsSelf-Care: Some problemsSelf-Care: Unable to wash or dressUsual Activities: No problemsUsual Activities: Some problemsUsual Activities: Unable to performPain/Discomfort: NonePain/Discomfort: ModeratePain/Discomfort: ExtremeAnxiety/Depression: NoneAnxiety/Depression: ModerateAnxiety/Depression: Extreme
Carbamazepine86.712.90.597.62.40.084.815.20.073.225.41.462.934.82.4
Zonisamide90.88.70.596.72.70.589.19.81.175.522.32.264.331.34.4

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Percent of Participants With =50% to < 75% and = 75% Decrease From Baseline in 28-day Seizure Frequency During the Maintenance Period(LOCF)

Participants' parent or guardian maintained a seizure diary recording the date, number, and type of seizures the subject had. Seizure frequency of simple partial, complex partial,and partial seizures with secondary generalization were assessed. (NCT00566254)
Timeframe: Baseline (Week -8 to Week 0) and Week 8 to Week 20

,
InterventionPercentage of Participants (Number)
Greater than or equal to 75% decreaseGreat than or equal to50% to less than75% decrease
Placebo12.019.0
Zonisamide27.123.4

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Percent of Participants With =25% and =100% Increase From Baseline in 28-day Seizure Frequency During the Maintenance Period (LOCF)

Participants' parent or guardian maintained a seizure diary recording the date, number, and type of seizures the subject had. Seizure frequency of simple partial, complex partial, and partial seizures with secondary generalization were assessed. (NCT00566254)
Timeframe: Baseline (Week -8 to Week 0) and Week 8 to Week 20

,
InterventionPercentage of Participants (Number)
Greater than or equal to 25% increaseGreater than or equal to 100% increase
Placebo21.09.0
Zonisamide10.05.0

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Percentage of Participants With a Decrease From Baseline in 28-day Seizure Frequency of =50%(Responder) in the Maintenance Period(LOCF)

A participant with a decrease from baseline in seizure frequency of =50 % was considered a responder. Participants' parent or guardian maintained a seizure diary recording the date, number, and type of seizures the subject had. The primary analysis assessed the percent of responders in the Maintenance Period (28- day seizure frequency in Week 8 to Week 20 compared to Week -8 to Week 0 at Last Observation Carried Forward (LOCF)). Seizure frequency of simple partial, complex partial, and partial seizures with secondary generalization were assessed. (NCT00566254)
Timeframe: Baseline (Week -8 to Week 0), and Week 8 to Week 20

InterventionPercentage of Participants (Number)
Placebo31
Zonisamide50

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Median Percent Change From Baseline in the 28-day Seizure Frequency During the Maintenance Period (LOCF)

Participants' parent or guardian maintained a seizure diary recording the date, number,and type of seizures the subject had. Seizure frequency of simple partial,complex partial,and partial seizures with secondary generalization were assessed. (NCT00566254)
Timeframe: Baseline (Week -8 to Week 0) and Week 8 to Week 20

InterventionPercentage Change in Seizure Frequency (Median)
Placebo-24.5
Zonisamide-50.0

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Change in Gamma-glutamyl Transferase (GGT) Concentration

This outcome measure looks at the change in blood levels of this enzyme assay from baseline, and then after 6 weeks (midpoint), and then at the endpoint (12 weeks). The analysis takes into account all three time points, and reports the average change between each of the three time points. (NCT00595556)
Timeframe: 12 weeks (from initiation to end of treatment)

InterventionUnits/Liter (Mean)
Zonisamide Medication Treatment8.4
Placebo2.9

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Change in Number of Drinks Per Week by Week

This outcome measure represents the change in the total number of standard drinks per week (weekly data) from baseline to the end of week twelve. This was analyzed using weekly measurements from baseline to week 12 week of the study period (thirteen time points, 12 measurements)with a repeated measures analysis (SPSS linear mixed models), by interaction with time (week). (NCT00595556)
Timeframe: baseline to the end of 12 weeks in treatment

Interventiondrinks/week (Mean)
Zonisamide Medication Treatment-2.2
Placebo-1.4

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Change in Number of Heavy Drinking Days (i.e., 5 or More Drinks Per Day for Men, and 4 or More Per Day for Women)Per Week, by Week

This outcome measure represents the change in number of heavy drinking days (i.e., 5 or more drinks per day for men, and 4 or more per day for women)per week, from baseline to the end of week twelve. This was analyzed using weekly measurements over the 12 week study period (thirteen time points, 12 measurements)with a repeated measures analysis (SPSS linear mixed models), by interaction with time (week). (NCT00595556)
Timeframe: baseline to the end of 12 weeks in treatment

InterventionDays/week (Mean)
Zonisamide Medication Treatment-.30
Placebo-.20

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Weekly Rate of Change in Abstinent Days

This outcome measure analyzed the weekly rate of change in number of abstinent days over the twelve weeks of the study from baseline to the end of week twelve. This was analyzed using weekly measurements over the 12 week study period (thirteen time points, 12 measurements)with a repeated measures analysis (SPSS proc mixed), by interaction with time (week). (NCT00595556)
Timeframe: baseline to the end of 12 weeks in treatment

Interventiondays/week (Mean)
Zonisamide Medication Treatment0.17
Placebo0.13

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Change in the Urge to Drink Alcohol as Measured by the Alcohol Urge Questionnaire (AUQ)

This is the change in measured urge to drink alcohol as measured by the Alcohol Urge Questionnaire (AUQ), measured every 2 weeks from baseline until the last week of the study (over twelve weeks, 7 timepoint measurements of AUQ, 6 calculated changes). It is reported in terms of change per visit (every 2 weeks). AUQ measures a feeling state, and uses a 7 point (1-7)Likert scale for each of 8 items (questions). The lowest urge score is 8 (representing less urge to drink), and the highest would be tabulated as 56 (meaning more urge to drink). Repeated measures SPPS linear mixed models used. (NCT00595556)
Timeframe: baseline to the end of 12 weeks in treatment

Interventionunits on a scale/visit (Mean)
Zonisamide Medication Treatment-1.4
Placebo-0.6

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Area Under the Concentration Versus Time Curve From Time 0 to Time t [AUC(0-t)]

The area under the plasma concentration versus time curve, from time 0 to the time of the last measurable concentration (t), as calculated by the linear trapezoidal rule. (NCT00685139)
Timeframe: serial pharmacokinetic plasma concentrations were drawn prior to dose administration (0 hour) and at 1, 1.5, 2, 2.5, 3, 3.5, 4, 4.5, 5, 5.5, 6, 6.5, 7, 8, 10, 12, 16, 24, 36, 48, 60 and 72 hours after drug administration.

Interventionng-hr/mL (Mean)
Zonisamide 100 mg Capsules42,338.31
Zonegran® 100 mg Capsules42,873.95

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Maximum Plasma Concentration (Cmax)

The maximum or peak concentration that the drug reaches in the plasma. (NCT00685139)
Timeframe: serial pharmacokinetic plasma concentrations were drawn prior to dose administration (0 hour) and at 1, 1.5, 2, 2.5, 3, 3.5, 4, 4.5, 5, 5.5, 6, 6.5, 7, 8, 10, 12, 16, 24, 36, 48, 60 and 72 hours after drug administration.

Interventionng/mL (Mean)
Zonisamide 100 mg Capsules1,052.65
Zonegran® 100 mg Capsules1,078.46

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Maximum Plasma Concentration (Cmax)

The maximum or peak concentration that the drug reaches in the plasma. (NCT00687167)
Timeframe: serial pharmacokinetic plasma concentrations were drawn prior to dose administration (0 hour) and at 1, 2, 3, 4, 4.5, 5, 5.5, 6, 6.5, 7, 8, 9, 10, 11, 12, 14, 16, 24, 36, 48, 60 and 72 hours after drug administration.

Interventionng/mL (Mean)
Zonisamide 100 mg Capsules910.95
Zonegran® 100 mg Capsules921.68

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Area Under the Concentration Versus Time Curve From Time 0 to Time t [AUC(0-t)]

The area under the plasma concentration versus time curve, from time 0 to the time of the last measurable concentration (t), as calculated by the linear trapezoidal rule. (NCT00687167)
Timeframe: serial pharmacokinetic plasma concentrations were drawn prior to dose administration (0 hour) and at 1, 2, 3, 4, 4.5, 5, 5.5, 6, 6.5, 7, 8, 9, 10, 11, 12, 14, 16, 24, 36, 48, 60 and 72 hours after drug administration.

Interventionng-hr/mL (Mean)
Zonisamide 100 mg Capsules40,122.78
Zonegran® 100 mg Capsules40,275.57

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Percentage of Participants That Are Seizure Free for at Least 24 Month Consecutive Period in the Base Study and Extension Phase

The number of participants that have remained seizure free for at least a 24 month consecutive period from the start of the Flexible Dosing Period (FDP: the period following the Titration Period and leading into the Maintenance Period) in the base study through the treatment period of this study. Seizure freedom was defined as the absence of all seizure regardless of seizure type. (NCT00848549)
Timeframe: Week 5 to Week 109 (in base study) and Month 1 to Month 27 (in extension phase)

InterventionPercentage of Participants (Number)
Zonisamide32.3
Carbamazepine35.2

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Time to Drop-out Due to Adverse Event (AE)

"Adverse events in study subjects included any change in the subject's condition.~This includes symptoms, physical findings, or clinical syndromes. All AEs that occurred after signing of informed consent through the last visit and for 15 days following study drug discontinuation were captured on the AE Case Report Form (CRF)." (NCT00848549)
Timeframe: Week 1 to Week 109 (in base study) and Month 1 to Month 27 (in extension study)

InterventionDays (Mean)
Zonisamide131.9
Carbamazepine97.2

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Time to Drop-out Due to Lack of Efficacy

Lack of efficacy was if the subject had poor seizure control (defined as experiencing a seizure despite being on the maximum dose for = 2 weeks). The subject could withdraw at any time due to lack of efficacy. (NCT00848549)
Timeframe: Week 1 to Week 109 (in core study) and Month 1 to Month 27 (in extension study)

InterventionDays (Mean)
Zonisamide297.9
Carbamazepine289.0

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Change From Baseline in Quality of Life Assessed by Quality of Life in Epilepsy-Problems Questionnaire (QOLIE-31-P) Overall Score at Each Visit

The QOLIE-31-P is a 31-item questionnaire evaluating a participant's QOL perception in 7 domains: seizure worry,emotional well being,energy/fatigue, cognitive functioning, medication effects, social functioning,overall QOL. The overall score is derived by weighing and then summing the 7 domain scores. Precoded numeric values for some domains are such that a higher number reflects a more favorable health state; others are such that a higher number reflects a less favorable state. Precoded values are converted to 0-100 point scores; higher converted scores always reflect better QOL. (NCT00848549)
Timeframe: Weeks 0, 26, 52, 78 and 117

,
InterventionScore on a scale (Mean)
Week 0Week 26Week 52Week 78Week 117
Carbamazepine7.10110.95611.6871.90215.849
Zonisamide4.6976.1018.6024.287-0.292

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Percentage of Participants Remaining in the Study at Each Visit

The retention rate is defined as the percentage of subjects remaining on the study at each visit, starting from the first dose of study drug in the extension phase. (NCT00848549)
Timeframe: At 3, 6, 9, 12, 15, 18, 21, 24, and 27 months

,
InterventionPercentage of Participants (Number)
3 months6 months9 months12 months15 months18 months21 months24 months27 months
Carbamazepine93.784.275.361.443.727.812.72.50.6
Zonisamide95.687.676.658.438.727.713.15.81.5

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Percent of Participants With Cessation of Occupation, Requirement of Caregiver, or Admission to Intensive Care Unit

Percent of participants with cessation of usual occupation, requirement of an informal caregiver, and who required admission to the intensive care unit (ICU). (NCT00855738)
Timeframe: Month 6

Interventionpercent of participants (Number)
Stopped Usual OccupationRequired Informal CaregiverRequired Admission to ICU
All Antiepileptic Drugs16.26.60.0

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Percent of Participants That Reduced, Maintained and Increased Their Doses of New Antiepileptic Drugs (AED)

(NCT00855738)
Timeframe: Baseline to Month 6 (or end of treatment)

Interventionpercent of participants (Number)
ReducedMaintainedIncreased
All Antiepileptic Drugs0.968.530.6

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Change in Sleep Disturbances From Baseline to Month 6: Medical Outcomes Study Sleep Scale (MOS-SS)

Subject rated instrument to assess key constructs of sleep; assesses sleep quality and quantity. Consists of a 6-item and 9-item overall sleep problems index measuring time to fall asleep and sleep duration in past 4 weeks; 5 subscales rated 1 (all the time) to 6 (none of the time): sleep disturbance, snoring, awaken short of breath, somnolence, and adequacy. Transformed scores range = 0 to 100; higher score indicates greater intensity of attribute. Two additional subscales = sleep quantity (range 0-24 hours) and optimal sleep (number of participants with optimal sleep 7-8 hours per night). (NCT00855738)
Timeframe: Baseline to Month 6

Interventionscores on scale (Mean)
Sleep disturbanceSnoringAwake short of breathQuantityAdequacySomnolenceSleep problems (summary 6)Sleep problems (summary 9)
All Antiepileptic Drugs-1.70.01.10.22.80.6-0.9-0.9

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Change From Baseline to Months 3 and 6 in Health Condition: Euro Quality of Life Scale (EQ-5D) Visual Analog Scale (VAS)

Assessment of the health condition of the subjects using the EQ-5D VAS: subject rated questionnaire to assess health-related quality of life in terms of a single index value. Using the VAS subjects rated current health state on a scale from 0 (worst imaginable health state) to 100 (best imaginable health state); higher scores indicate a better health state. (NCT00855738)
Timeframe: Baseline, Month 3, Month 6

Interventionscores on scale (Mean)
Month 3Month 6
All Antiepileptic Drugs-0.41.2

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Change From Baseline to Month 6 in Visits to a Specialist or the Emergency Room Because of Epilepsy

Numerical assessment of change in the number of visits to a specialist or the emergency room because of epilepsy needed during the study. (NCT00855738)
Timeframe: Baseline to Month 6

Interventionvisits (Mean)
Number of visits to a specialist (n=94)Number of visits to the emergency room (n=79)
All Antiepileptic Drugs-0.6-0.3

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Change From Baseline to Month 6 in the Hospital Anxiety and Depression Scale (HADS)

HADS: subject rated questionnaire with 2 subscales. HADS-A assesses state of generalized anxiety (anxious mood, restlessness, anxious thoughts, panic attacks); HADS-D assesses state of lost interest and diminished pleasure response (lowering of hedonic tone). Each subscale comprised of 7 items with range 0 (no presence of anxiety or depression) to 3 (severe feeling of anxiety or depression). Total score 0 to 21 for each subscale; higher score indicates greater severity of anxiety and depression symptoms. (NCT00855738)
Timeframe: Baseline to Month 6

Interventionscores on scale (Mean)
DepressionAnxiety
All Antiepileptic Drugs-0.5-0.6

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Change From Baseline to Month 6 in Quality of Life 10 Domains (QOLIE-10)

QOLIE-10: 10-item questionnaire evaluates health-related quality of life in individuals with epliepsy. Comprised of 7 components: seizure worry, overall quality of life, emotional well-being, energy, cognitive functioning, medication effects (physical and mental effects), and social function (work, driving, social function). Total score rated 0 to 100; higher score = higher quality of life. (NCT00855738)
Timeframe: Baseline to Month 6

Interventionscores on scale (Mean)
EnergyEmotions (mood)Daily activitiesMental functionMedication effects (physical/ mental)Worry about seizures (impact of seizures)Overall quality of life
All Antiepileptic Drugs0.40.70.61.2-1.19.03.8

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Time to First Seizure

Number of days to first seizure after baseline. (NCT00855738)
Timeframe: Baseline to Month 6 (or end of treatment)

Interventiondays (Mean)
All Antiepileptic Drugs35.9

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Percent of Participants Who Continued on Study Medication to Month 6

Retention rate: percent of participants who continued on study medication throughout the 6 Month period after inclusion in the study. (NCT00855738)
Timeframe: Baseline to Month 6

Interventionpercent of participants (Number)
All Antiepileptic Drugs97.1

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Percent Change From Baseline in the Median Number of Seizures During the Last 3 Months of Treatment

(NCT00855738)
Timeframe: Baseline, Month 3, Month 6 (last 3 months of treatment)

Interventionpercent change (Median)
All Antiepileptic Drugs-75.0

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Change From Baseline to Month 6 in Total Number of Days Hospitalized Because of Epilepsy

Numerical assessment of change in total number of days hospitalized because of epilepsy during the study. (NCT00855738)
Timeframe: Baseline to Month 6

InterventionDays (Mean)
All Antiepileptic Drugs-8.0

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Percent of Participants Classified as Responders

Responder = decrease in number of seizures by >=50 percent (%) during the last 3 months of treatment before discontinuation (assessed at Month 3 and Month 6) versus the number of seizures that occurred during the 3 months before the baseline visit (baseline). (NCT00855738)
Timeframe: Baseline, Month 3, Month 6 (last 3 months of treatment)

Interventionpercent of participants (Number)
Month 3Month 6
All Antiepileptic Drugs76.780.0

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Percent of Seizure-free Participants During the Last 3 Months Before Discontinuation

(NCT00855738)
Timeframe: Baseline, Month 3, Month 6 (last 3 months of treatment)

Interventionpercent of participants (Number)
Month 3Month 6
All Antiepileptic Drugs10.020.0

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Percent of Participants That Reduced, Maintained and Increased the Doses of the Initial Treatment Administered in Monotherapy

(NCT00855738)
Timeframe: Baseline through Month 6 (or end of treatment)

Interventionpercent of participants (Number)
ReducedMaintainedIncreased
All Antiepileptic Drugs0.0100.00.0

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Percent of Participants Reaching Monotherapy

Percent of participants who started on more than one treatment (bitherapy) and reached monotherapy by end of study. (NCT00855738)
Timeframe: Baseline through Month 6 (or end of study)

Interventionpercent of partipants (Number)
All Antiepileptic Drugs2.9

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Percent of Participants With Reduction in Number of Seizures >=25% and >=75% During the Last 3 Months of Treatment

Percent of participants with reduction in number of seizures >=25% and >=75% during the last 3 months of treatment before discontinuation (assessed at Month 3 and Month 6) versus the 3 month period before the baseline visit. (NCT00855738)
Timeframe: Baseline, Month 3, Month 6 (last 3 months of treatment)

Interventionpercent of participants (Number)
Month 3: >=25%Month 3: >=75%Month 6: >= 25%Month 6: >=75%
All Antiepileptic Drugs86.727.886.754.4

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Percent of Participants Indicating Optimal Sleep on the Optimal Sleep Subscale: Medical Outcomes Study Sleep Scale (MOS-SS)

MOS-SS: subject rated instrument used to assess the key constructs of sleep; assesses sleep quantity and quality and is comprised of 12 items yielding 7 subscale scores and 2 composite index scores. Optimal sleep subscale is derived from sleep quantity average hours of sleep over the past 4 weeks; percent of participants with response YES (optimal) if sleep quantilty was 7-8 hours of sleep per night. (NCT00855738)
Timeframe: Baseline, Month 6

Interventionpercent of participants (Number)
BaselineMonth 6
All Antiepileptic Drugs56.565.7

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COWAT-Category

Number of words produced by subjects over 60 seconds for a semantic category (Animals). The COAWAT-Category sub-test provides a measure of verbal fluency. Mean value shown are actual means for the number of words produced. (NCT00862563)
Timeframe: Baseline, Week12

,,,
InterventionNumber of Words Produced (Mean)
BaselineWeek 12
Levetiracetam20.921.2
Sugar Pill21.620.8
Topiramate21.917.0
Zonisamide22.617.4

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Mean Percent Days Heavy Drinking

Mean weekly values for each treatment group for percent days heavy drinking. Heavy drinking was defined as 4 or more drinks per day for women and 5 or more drinks per day for men. (NCT00862563)
Timeframe: Weeks 10, 11, 12

,,,
InterventionPercentage of Days/Week (Mean)
Week 10Week 11Week 12
Levetiracetam49.647.944.5
Sugar Pill65.761.760.9
Topiramate32.129.521.0
Zonisamide38.436.634.3

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Percent Days Drinking

Mean percent days drinking for Weeks 10, 11, 12. A drinking day is considered to be a day in which 1 or more drinks have been consumed. Means are model generated least means squares values obtained from a two-way repeated measures analysis from data obtained from Weeks 1 through 12, with Week as the within subject factor and treatment group as the between group factor. (NCT00862563)
Timeframe: Weeks 10, 11, 12

,,,
InterventionPercentage of Days/ Week (Mean)
Week 10Week 11Week 12
Levetiracetam72.268.973.1
Sugar Pill83.687.278.2
Topiramate51.843.851.4
Zonisamide61.662.161.3

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The Primary Efficacy Measure is the Mean Number of Drinks Consumed Per Day Over the Period From Treatment Weeks 10 Through 12 When All Study Medications Should be at Their Maximum Steady Levels Based on Their Known Pharmacokinetic Properties.

Mean standard drinks consumed per day for each treatment week, weeks 10 thru 12. Actual mean values obtained are shown. Analyses are based on model generated least squares means for a two -way repeated measures mixed models analysis for data obtained for weeks 1 through 12, with baseline values used as covariates. Week (time) was used as the within subject factor and treatment group was the between group factor. (NCT00862563)
Timeframe: Weeks 10, 11, 12

,,,
InterventionStandard Drinks per day (Mean)
Week 10Week 11Week 12
Levetiracetam4.64.34.3
Sugar Pill6.36.86.0
Topiramate3.22.72.5
Zonisamide3.83.42.5

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Wechsler Memory Scale-3rd Ed. Spatial Span

WMS Spatial Span test measures working memory for a spatial sequence of numbers. This assesses visual working memory. Age adjusted scaled scores are presented. Score may range between 1 and 19, with lower scores indicating greater impairment in performance. (NCT00862563)
Timeframe: Baseline, Week 12

,,,
Interventionunits on a scale (Mean)
BaselineWeek 12
Levetiracetam10.510.9
Sugar Pill10.810.4
Topiramate12.08.4
Zonisamide10.87.9

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Wechsler Memory Scales (WMS)-3d Ed Digit Span-Age Adjusted Total

WMS Digit Span is a measure of working memory. Subjects respond by repeating lists of number sequences presented by the test administrator. Age adjusted scores are presented below. Scores may range between 1 and 19, with lower scores indicating poorer performance on the task. (NCT00862563)
Timeframe: Baseline, Week 12

,,,
Interventionunits on a scale (Mean)
BaselineWeek 12
Levetiracetam11.912.2
Sugar Pill12.613.0
Topiramate12.17.7
Zonisamide11.810.0

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AB-Neurotoxicity Scale.

Total Scores AB-Neurotoxicity Scale Week 12. This scale provides subject ratings of anticonvulsant neurotoxic effects. Scores may range 0 to 72, with possibility of an additional 30 points being for complaints not listed in the list of complaints provides. Total scores, therefore, may be as high as 102, with higher scores indicating greater severity of problems. Actual mean scores are shown. Means for the analysis are least means squares values obtained from a two-way repeated measures mixed models analysis, with Week (time) as the the within subject factor and treatment as the between group factor. Baseline values were used as covariates. (NCT00862563)
Timeframe: Week 12

InterventionScale Scores (Mean)
Zonisamide7.1
Levetiracetam11.3
Topiramate15.4
Sugar Pill5.8

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Controlled Word Association Test (COWAT)- Letter Fluency

Number of words generated that start with a set of 3 letters. The COWAT provides a measure of verbal fluency. Actual means for COWAT results are shown. (NCT00862563)
Timeframe: Baseline & Week 12

,,,
InterventionNumber of Words Produced (Mean)
BaselineWeek 12
Levetiracetam46.245.4
Sugar Pill47.450.5
Topiramate43.428.1
Zonisamide46.532.5

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Change in Korean-Quality of Life Childhood Epilepsy (K-QOLCE)

The difference of K-QOLCE between before and after the administration. K-QOLCE is Korean version of the Quality of Life in Childhood Epilepsy Questionnaire. The calculated total score ranges 0-100, with higher scores indicating higher quality of life. (NCT01127165)
Timeframe: Baseline and 24 weeks

InterventionScores on a Scale (Mean)
Zonisamide Low Dose Group4.7931
Zonisamide High Dose Group1.2286

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Percentage of Participants Who Were Assessed As Seizure Free

The percentage of participants who showed no seizure during the maintenance phase. (NCT01127165)
Timeframe: 24 weeks

Interventionpercentage of participants (Number)
Zonisamide Low Dose Group63.1
Zonisamide High Dose Group57.6

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Change in Cognitive Assessment Korean-Wechsler Intelligence Scale for Children (K-WISC-Ⅲ)

Cognitive assessment was performed using K-WISC-III. The total score of K-WISC-III is calculated as Full Scale IQ which ranges from 31 (worst) to 151(best). Higher scores indicate greater intelligence, lower scores indicate less intelligence. Thus a positive change indicated an improvement. (NCT01127165)
Timeframe: Baseline and 24 weeks

InterventionScores on a Scale (Mean)
Zonisamide Low Dose Group-1.3913
Zonisamide High Dose Group0.1071

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Change in Behavior Assessment Korea-Child Behavior Checklist (K-CBCL)

The difference of K-CBCL between before and after the administration. K-CBCL is the Korean version of CBCL which is a standardized form that parents fill out to describe their children's behavioral and emotional problems. The total score ranges 0- 234, with higher scores indicating worse behavioral and emotional problems. (NCT01127165)
Timeframe: Baseline and 24 weeks

InterventionScores on a Scale (Mean)
Zonisamide Low Dose Group-5.259
Zonisamide High Dose Group-1.611

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Quality of Life in Epilepsy (QoL-QOLIE31)

Quality of life assessment tool. Overall scores is calculated by summing subsections, and it ranges from 0 to 100. Higher score presents higher quality of life. (NCT01127256)
Timeframe: 24 weeks

,
InterventionUnits On a Scale (Mean)
Pre-QOLIE 31Post-QOLIE 31
Carbamazepine61.9669.51
Zonisamide60.7267.27

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The Percentage of Participants With Seizure Free Rate

The percentage of participants who had no seizure during the trial. (NCT01127256)
Timeframe: 24 weeks

Interventionpercentage of participants (Number)
Zonisamide73.7
Carbamazepine83.1

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The Percentage of Participants With Retention Rate

The percentage of participants who completed the trial. (NCT01127256)
Timeframe: 24 weeks

Interventionpercentage of participants (Number)
Zonisamide59.4
Carbamazepine62.5

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Median Percent Change From Study 312 Baseline in the 28-day Seizure Frequency During the Open Label Period

Participants' parent or guardian maintained a seizure diary recording the date, number, and type of seizures the subject had. Seizure frequency of simple partial, complex partial, and partial seizures with secondary generalization were assessed from baseline of study 312 through the Open Label Visit Period. Percentage change = 100% x (seizure frequency at period - seizure frequency at Study 312 baseline)/seizure frequency at Study 312 baseline. (NCT01136954)
Timeframe: Baseline of study 312 (Week -8 to Week 0) to Week 59 of study 313

InterventionPercentage Change (Median)
Zonisamide(Placebo During Core Study)-64.6
Zonisamide (Zonisamide During Core Study)-67.9

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Percentage of Participants With a Decrease From Baseline in 28-day Seizure Frequency of =50%(Responder) in the Open Label Period

A participant with a decrease from baseline in seizure frequency of =50 % was considered a responder. Participants'parent or guardian maintained a seizure diary recording the date,number, and type of seizures the subject had. The primary analysis assessed the percent of responders from baseline in the Open Label Visit Period. Seizure frequency of simple partial, complex partial, and partial seizures with secondary generalization were assessed. (NCT01136954)
Timeframe: Baseline through Week 59

InterventionPercentage of Participants (Number)
Zonisamide(Placebo During Core Study)55.6
Zonisamide (Zonisamide During Core Study)56.9

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Treatment Emergent Non-Serious Adverse Events With Greater Than 5% Frequency

Treatment Emergent Adverse Event (TEAE) is defined as an Adverse Event with a start date on or after Day 1 and within 15 days of last dose. For each event, each participant experiencing an event is only counted once even if they had multiple episodes. (NCT01136954)
Timeframe: Week 1 through Week 59

,
InterventionParticipants (Number)
NasopharyngitisBronchitisRespiratory tract infectionHeadacheWeight decreasedAbdominal painDecreased Appetite
Zonisamide (Placebo During Core Study)6424615
Zonisamide (Zonisamide During Core Study)9347644

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Median Change From Study 312 Baseline in the 28-day Seizure Frequency During the Open Label Period

Participants' parent or guardian maintained a seizure diary recording the date, number, and type of seizures the subject had. Seizure frequency of simple partial, complex partial, and partial seizures with secondary generalization were assessed from baseline of study 312 through the Open Label Visit Period. (NCT01136954)
Timeframe: Baseline of study 312 (Week -8 to Week 0) to Week 59 of study 313

InterventionSeizures (Median)
Zonisamide(Placebo During Core Study)-3.8
Zonisamide (Zonisamide During Core Study)-4.7

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Drug Value Questionnaire

"Street Value of Sampled Dose. After co-administration of cocaine-zonisamide, participants were asked to hypothetically estimate the value of the drug they received, if they were to purchase it on the street. The mean value (dollars) across all drug conditions is reported here.~Repeated within-subject measures ANOVA performed to observe the main effects of zonisamide dose (0, 300, and 600mg) and cocaine dose (0, 20, and 40mg), and their interaction. Only participants who received the active zonisamide medication (n=8) were included in this portion of the analysis. Additionally, all 8 subjects who received zonisamide completed both 300mg and 600mg doses.~Within-subject repeated interval during self-administration sessions. Cocaine not administered (only Zon) during Weeks 2 & 4, thus no measures taken at these times" (NCT01137890)
Timeframe: Weeks 1-5; mean of weeks 1, 3 and 5 reported

Interventiondollars (Mean)
1mg-0mg0
1mg-300mg0
1mg-600mg0
20mg-0mg9.29
20mg-300mg8.50
20mg-600mg7.63
40mg-0mg16
40mg-300mg18.13
40mg-600mg9.5

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Change in Visual Analog Questionnaire (VAQ) Score

"VAQ measures the change in effect after dose administration. Participants rate 6 items (Any Drug Effect, Rush, Good Effects, Bad Effects, Liking, & Desire for Cocaine) by pointing an arrow along a 100-point line anchored at either end with none (0) & extremely (100). Each participant's score is equal to the sum of all 6 ratings, & the mean of all participant's scores is reported across each condition. The VAQ is only administered to subjects in the zonisamide (Zon) condition (n=8). Repeated within-subject measures ANOVA performed to observe the main effects of Zon dose (0, 300, & 600mg) & cocaine dose (1, 20, & 40mg), & their interaction. All 8 subjects who received Zon completed both 300mg & 600mg doses. Assessments obtained on Week 1 (0mg Zon), Week 3 (300mg Zon), & Week 5 (600mg Zon), in which all 3 cocaine were co-administered at these times. Cocaine not administered (only Zon) during Weeks 2 & 4, thus no measures taken at these times" (NCT01137890)
Timeframe: Weeks 1-5; mean of weeks 1, 3 and 5 reported

Interventionunits on a scale (Mean)
1mg-0mg0.38
1mg-300mg3.75
1mg-600mg0.38
20mg-0mg40.63
20mg-300mg32.63
20mg-600mg30.00
40mg-0mg37.38
40mg-300mg29.75
40mg-600mg37.25

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Behavioral Choice Measures

"In each condition of cocaine-zonisamide dose, participants were asked to choose whether they would rather have a repeated cocaine dose (same dose as most recent administration) or cash of varying monetary value. The mean number of cocaine choices across each drug condition are reported. This measure only included participants in the zonisamide (Zon) condition (n=8), with each arm representing variation in co-administration of cocaine-Zon.~Repeated within-subject measures ANOVA performed to observe the main effects of zonisamide dose (0, 300, and 600mg) and cocaine dose (1, 20, and 40mg), and their interaction. Only participants who received the active zonisamide medication (n=8) were included in this portion of the analysis.~During self-administration sessions are every 15 min over 1hr45min period. Assessment on Weeks 1 (0mg Zon), 3 (300mg Zon), 5 (600mg Zon), in which varying cocaine doses co-administered. Cocaine not administered (only Zon) during Weeks 2 & 4" (NCT01137890)
Timeframe: Weeks 1-5, mean of weeks 1, 3 and 5 reported

Interventionnumber of cocaine choices (Mean)
1mg-0mg0
1mg-300mg0
1mg-600mg0.25
20mg-0mg2
20mg-300mg2.38
20mg-600mg2.25
40mg-0mg3.5
40mg-300mg3
40mg-600mg3.38

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Cocaine Craving

Cocaine craving measured by Cocaine Selectivity Severity Assessment (CSSA). The CSSA is a reliable and valid tool to measure cocaine withdrawal severity within a 24 hr period, and has been shown to predict treatment response in a treatment setting. Participants are asked to rate 18-items on a Likert scale 0-7, with composite scores ranging 0-126 and higher numbers indicative of more severe withdrawal. Mean scores on CSSA across 39-day time period are reported. (NCT01137890)
Timeframe: Day 1-39

,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,
Interventionunits on a scale (Mean)
ZonisamidePlacebo
Day 127.8842.75
Day 109.6319
Day 1111.7525.33
Day 1214.2525.25
Day 1312.3822.75
Day 1423.6322.75
Day 1526.7524.75
Day 1624.8819.25
Day 1725.3824.00
Day 1824.1322.5
Day 1925.1324.5
Day 227.2541
Day 2012.7526
Day 2125.525.5
Day 2215.2523
Day 2316.8818
Day 2413.8819
Day 258.2515.5
Day 2610.2516.
Day 2710.7514.5
Day 287.6316.5
Day 297.6324
Day 32530.25
Day 306.5716.5
Day 319.5016.5
Day 3211.2519.5
Day 338.518.
Day 3413.517.
Day 3521.3819.
Day 368.1316
Day 3723.2519
Day 388.2520
Day 3919.2516.5
Day 419.1328.25
Day 517.8828.25
Day 613.526.5
Day 712.7529.5
Day 812.1327.25
Day 913.7528.5

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Seizure Reduction Rate

The percentage of the seizure reduction after Zonisamide treatment comparing baseline seizure frequency. (NCT01140867)
Timeframe: Baseline and 16 weeks

InterventionPercentage of Seizure Reduction Rate (Mean)
Zonisamide-16.35

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Seizure Free Rate

The percentage of the participants who experienced no seizure during the trial. (NCT01140867)
Timeframe: 16 weeks

InterventionPercentage of Participants (Number)
Zonisamide24.51

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Responder Rate

The percentage of participants whose median percentage change in seizure frequency after Zonisamide treatment is reduced over 50%. (NCT01140867)
Timeframe: Baseline and 16 weeks

InterventionPercentage of Participants (Number)
Zonisamide61.76

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QoL-QOLIE31 (Quality of Life in Epilepsy)

Quality of life assessment tool. Overall scores is calculated by summing subsections, and it ranges from 0 to 100. Higher score presents higher quality of life. (NCT01140867)
Timeframe: Baseline and 16 weeks

InterventionUnits on a Scale (Mean)
Baseline- Pre-QOLIE 31 total score (N=90)16 weeks - Post- QOLIE 31 total score (N=90)
Zonisamide56.6757.70

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Percent Change in Seizure Frequency From Baseline to the Last 28 Days of the Maintenance Period

Seizure frequency was assessed by a seizure diary, maintained daily from Baseline, in which the subject recorded the occurrence of any seizure. (NCT01546688)
Timeframe: Baseline and Month 4

InterventionPercent Change (Median)
Placebo-100
Zonisamide-100

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Change From Baseline in Bond and Lader Visual Analogue Scale (VAS) Mood Sub-Scores for Sedation by Visit During Titration and Maintenance Period

The Bond-Lader mood rating scale measured sedation, with scores ranging from 0 to 100. A high score reflects a high level of sedation. (NCT01546688)
Timeframe: Baseline, Week 4, Week 8, Week 12, Week 16

,
InterventionScores on a Scale (Mean)
Week 4Week 8Week 12Week 16
Placebo-1.3377.6881.3862.502
Zonisamide1.6541.990-0.6823.943

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Change From Baseline in CVST of the FePsy Test (Mean Reaction Time) by Visit During Titration and Maintenance Period

The Computer Visual Search Task (CVST) of the Ferrum Psyche (FePsy)measured cognition. A decrease from Baseline (negative change value) signifies an improvement in the mean reaction time of CVST. (NCT01546688)
Timeframe: Baseline, Week 4, Week 8, Week 12, Week 16

,
InterventionSeconds (Mean)
Week 4Week 8Week 12Week 16
Placebo-3.448-2.776-7.223-3.324
Zonisamide-3.898-0.650-2.731-5.102

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Percentage of Responders During Last 28 Days of Maintenance Period

Seizure frequency was assessed by a seizure diary, maintained daily from Baseline, in which the subject recorded the occurrence of any seizure. A responder is a subject who had at least a 50 percent or greater reduction in the seizure frequency of all seizures during the last 28 days of the Maintenance Period compared to the Baseline Period seizure frequency. Due to the exploratory nature of the objective for efficacy and the truncated study size, analysis of efficacy was based on observed cases, without imputation for missing data. As a result, there are some variations in sample sizes for efficacy at different visits, depending on if particular efficacy variables were missing for particular visits. (NCT01546688)
Timeframe: Baseline and Month 4

,
InterventionPercentage of Participants (Number)
Responders (Yes)Non-Responders (No)Missing
Placebo62.512.525
Zonisamide7514.310.7

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Percent Participants Abstinent From Smoking During Study Weeks 7-10

Biochemically-verified continuous smoking abstinence during weeks 7-10 of the study. (NCT01685996)
Timeframe: weeks 7-10

InterventionParticipants (Count of Participants)
Zonisamide5
Placebo6

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Nicotine Withdrawal Symptom Severity

Total Score from the Minnesota Nicotine Withdrawal Questionnaire (MNWQ), assessed at weekly visits. The MNWQ is a commonly-used 12-item Likert scale self-report measure of nicotine symptoms. Individual symptoms were rated from 0 (none) to 4 (severe) for each item and the Total score range was 0 - 48. Ratings were collected once weekly during study visits. (NCT01685996)
Timeframe: Past 24 hours

,
Interventionunits on a scale (Mean)
Screening VisitAdmission VisitWeek 1 (pre-quit day)Week 2 (pre-quit day)Week 3 (target quit day)Week 4Week 5Week 6Week 7Week 8Week 9Week 10
Placebo5.67.06.25.76.65.94.74.04.44.04.14.8
Zonisamide4.65.15.34.84.73.83.83.43.82.73.12.6

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Number of Drinking Days

Using a 90 day Timeline Follow Back (TLFB), the total number of drinking days at baseline and at 12 weeks of treatment were used. (NCT01847469)
Timeframe: 12 weeks

,
Interventiondays (Mean)
Baseline12 weeks
Placebo51.0017.33
Zonisamide46.877.44

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Clinician-Administered PTSD Scale (CAPS) Total Score

"The Clinician-Administered PTSD Scale (CAPS) Total Score will be used to measure PTSD symptoms at the end of the 12 week intervention. The CAPS Total Score is a summing of the 17 items that are each scored 0-4- where 0 indicates none. The range of Total Scores can be 0 to 136, where 136 would be the highest amount of scored PTSD symptoms." (NCT01847469)
Timeframe: 12 weeks

,
Interventionunits on a scale (Mean)
Baseline12 weeks
Placebo72.8323.80
Zonisamide67.3330.83

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Number of Heavy Drinking Days

"Timeline Follow Back (TLFB) will be used to document the number of heavy drinking days during 12 weeks of treatment. Heavy drinking is defined as greater than or equal to 5 drinks for men and greater than or equal to 4 drinks for women." (NCT01847469)
Timeframe: 12 weeks

,
Interventiondays (Mean)
Baseline12 weeks
Placebo31.504.16
Zonisamide43.945.50

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Alcohol Urge Questionnaire Score (AUQ)

This is the change in AUQ scores (urge to drink) measured weekly compared between groups using repeated measures. The AUQ is a 8 item participant rated questionnaire. Participants indicate how much they agree or disagree with the statements by selecting one number, 1 strongly disagree through 7 strongly agree. Participants can scores between 8 (lowest) - 56 (highest), the higher the score the more urge to drink. (NCT02368431)
Timeframe: over 16 weeks (weeks 1-16)

,
Interventionunits on a scale (Mean)
BaselineWeek 1Week 2Week 3Week 4Week 5Week 6Week 7Week 8Week 9Week 10Week 11Week 12Week 13Week 14Week 15Week 16
Placebo14.812.711.810.710.710.710.712.111.311.010.710.910.310.39.89.79.8
Zonisamide17.113.314.014.713.513.612.312.712.413.411.910.911.710.311.810.812.0

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Change in Quality of Life

Change in quality of life scores measured by the Quality of Life Enjoyment and Satisfaction Questionnaire (Q-LES-Q). The Q-LES-Q is a 16 item participant rated questionnaire. Participants indicate how they are feeling over the 16 item from Very poor (1), Poor (2), Fair (3), Good (4), and Very Good (5). Participants can scores between 14 (lowest) - 70 (highest) the higher the score more satisfied with quality of life. (NCT02368431)
Timeframe: Over 16 weeks (Baseline and 16 weeks)

,
Interventionunits on a scale (Mean)
BaselineWeek 16
Placebo55.872.9
Zonisamide56.973.3

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Gamma Glutamyl Transferase (GGT)

Difference between groups on change in levels of Gamma glutamyl transferase (GGT) over time from baseline to endpoint, which will include several interim data points. This will analyzed with a mixed models longitudinal analysis (repeated measures). Normal range for GGT levels are 10 U/L - 65 U/L - above 65 U/L above 65 U/L is considered a high GGT level (NCT02368431)
Timeframe: Baseline, Week 4, 8 and 16

,
InterventionUnits/Liter (U/L) (Mean)
BaselineWeek 4Week 8Week 16
Placebo78.250.045.546.4
Zonisamide76.063.461.4062.8

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Number of Drinks Per Week

Difference between groups in the number of total standard drinks per week over 8 weeks (weeks 9-16, the weeks on the target dose) performed using a mixed models longitudinal analysis. (NCT02368431)
Timeframe: over 8 weeks (weeks 9-16)

,
InterventionNumber of total drinks (Mean)
Week 9Week 10Week 11Week 12Week 13Week 14Week 15Week 16
Placebo8.18.83.66.212.54.33.38.7
Zonisamide17.812.215.910.39.49.913.711.1

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Number of Heavy Drinking Days Per Week

The difference in the number of heavy drinking days per week compared between groups (zonisamide and placebo) during the time spent on the target dose of the medication. Performed using a mixed models longitudinal analysis (repeated measures). (NCT02368431)
Timeframe: over 16 weeks (weeks 1-16)

,
InterventionNumber of heavy drinking days (Mean)
Week 1Week 2Week 3Week 4Week 5Week 6Week 7Weel 8Week 9Week 10Week 11Week 12Week 13Week 14Week 15Week 16
Placebo0.60.90.80.30.50.60.60.50.50.50.40.50.30.20.56.5
Zonisamide1.10.90.81.10.80.80.81.01.01.00.80.80.70.90.811.4

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Number of Seizures Reported

Number of seizures reported in all groups (NCT02707965)
Timeframe: Through the approximately 2 week period when the treatment is given.

,,,,,,,,
InterventionNumber of Seizures (Number)
Reference ProductTest (Generic)
Carbamazepine ER Capsule31
Carbamazepine ER Tablet00
Lamotrigine ER Tablet Group4425
Lamotrigine IR Tablet Group00
Levetiracetam ER Tablet Group4272
Levetiracetam IR Tablet Group165
Topiramate Tablet Group95
Valproic Acid ER Tablet Group120
Zonisamide Capsule Group00

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Mean Cmin_ss (Test vs. Reference)

Average minimum drug plasma concentration (Cmin); (NCT02707965)
Timeframe: For all study drugs, time points are: predose, 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4, 5, and 6 hr postdose. For twice-a-day regimen, additional points are:8, 10, and 12 hr postdose. For once-a-day drugs, additional times are:8, 10, 12, 16, and 24 hr postdose.

,,,,,,
Interventionmicrog/mL (Mean)
Test ProductReference Product
Carbamazepine ER Capsule8.567.66
Carbamazepine ER Tablet7.377.97
Lamotrigine ER Tablet4.0533333334.21
Levetiracetam ER Tablet12.60514.395
Levetiracetam IR Tablet15.4533333317.45666667
Topiramate Tablet6.3266.53
Zonisamide Capsule8.468.34

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Number of Adverse Events

summed for each anti-epileptic drug from when taking brand and generic. (NCT02707965)
Timeframe: Through the approximately 2 week period when the treatment is given.

Interventionevents (Number)
Topiramate29
Lamotrigine ER9
Levetiracetam IR17
Levetiracetam ER4
Carbamazepine ER Capsule15
Zonisamide6
Carbamazepine ER Tablet10
Valproic Acid10

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Mean AUC0-last_ss (Test vs. Reference)

Average AUC (area under the drug plasma curve. (NCT02707965)
Timeframe: For all study drugs, time points are: predose, 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4, 5, and 6 hr postdose. For twice-a-day regimen, additional points are:8, 10, and 12 hr postdose. For once-a-day drugs, additional times are:8, 10, 12, 16, and 24 hr postdose.

,,,,,,
Interventionmicro/mL/hr (Mean)
Test ProductReference Product
Carbamazepine ER Capsule114.96106.45
Carbamazepine ER Tablet104.6115.16
Lamotrigine ER Tablet62.7666666767.19333333
Levetiracetam ER Tablet260.3262.305
Levetiracetam IR Tablet419.97445.2
Topiramate Tablet92.88494.456
Zonisamide Capsule233.16226.14

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Mean Cmax_ss (Test vs. Reference)

Average maximum drug plasma concentration; (NCT02707965)
Timeframe: For all study drugs, time points are: predose, 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4, 5, and 6 hr postdose. For twice-a-day regimen, additional points are:8, 10, and 12 hr postdose. For once-a-day drugs, additional times are:8, 10, 12, 16, and 24 hr postdose.

,,,,,,
Interventionmicrog/mL (Mean)
Test ProductReference Product
Carbamazepine ER Capsule10.959.91
Carbamazepine ER Tablet10.0010.6
Lamotrigine ER Tablet6.246.903333333
Levetiracetam ER Tablet31.0528.04
Levetiracetam IR Tablet71.0233333369.29333333
Topiramate Tablet9.8749.646
Zonisamide Capsule12.2911.68

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Gamma Glutamyl Transferase (GGT) Levels

Difference between groups on levels of GGT over time from baseline to endpoint, which will includes two interim data points for a total of four time points. This will analyzed with a mixed models longitudinal analysis (repeated measures). Levels are in Units per Liter. (NCT02900352)
Timeframe: over 16 weeks (weeks 1-16)

,
InterventionInternational Units per Liter (UI/L) (Mean)
Baseline VisitVisit 5 (Week 5)Visit 7 (Week 9)Visit 9 (Week 13)Visit 10 (Week 16)
Placebo71.8864.470.2425.7556.65
Zonisamide78.3552.3359.4916.054.48

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Change in Quality of Life

Change in quality of life scores measured by the Q-LES-Q. ' Min: 16 Max: 80 Higher Scores = Higher Life Enjoyment (NCT02900352)
Timeframe: over 16 weeks (weeks 1-16) and at 2 week and 3 month follow up

,
Interventionscore on a scale (Mean)
Visit 2 (Baseline)Visit 10 (Week 16)Visit 11 (2 Week Follow up)Visit 12 (3 Month Follow up)
Placebo59.8463.260.4864.64
Zonisamide6061.66865.12

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Change in Alcohol Urge Questionnaire Score (AUQ)

"This is the change in AUQ scores (urge to drink) measured weekly compared between groups using repeated measures~Min value: 8 Max value: 42 higher score = worse craving" (NCT02900352)
Timeframe: over 16 weeks (weeks 1-16) and at 2 week and 3 month follow up

,
Interventionscore on a scale (Mean)
Visit 2 (Baseline)Visit 3 (Week 1)Visit 4 (Week 3)Visit 5 (Week 5)Visit 6 (Week 7)Visit 7 (Week 9)Visit 8 (Week 11)Visit 9 (Week 13)Visit 10 (Week 16)Visit 11 (2 Week follow up)Visit 12 (3 Month follow up)
Placebo16.0617.1215.2814.414.7216.2414.5614.413.3614.3213.68
Zonisamide16.214.415.213.8412.814.0813.613.613.3614.5614.16

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Percentage of Subjects With No Heavy Drinking Days

percentage of subjects with no heavy drinking days (PSNHDD) The PSNHDD can be derived from each subject's Timeline Followback (TLFB) data. (NCT02900352)
Timeframe: over the last 8 weeks (weeks 9-16)

InterventionPercentage of participants (Number)
Zonisamide8.97
Placebo5.13

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Number of Drinks Per Week

Difference between groups in the number of total standard drinks per week over 8 weeks (weeks 9-16, the weeks on the target dose) performed using a mixed models longitudinal analysis. (NCT02900352)
Timeframe: over 8 weeks (weeks 9-16)

InterventionNumber of drinks per week (Mean)
Zonisamide19.7
Placebo23.7

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Number of Heavy Drinking Days Per Week

The difference in the number of heavy drinking days per week compared between groups (zonisamide and placebo) for the last 8 weeks of treatment (during the time spent on the target dose of the medication). Performed using a mixed models longitudinal analysis (repeated measures). (NCT02900352)
Timeframe: over the last 8 weeks (weeks 9-16)

InterventionNumber of heavy drinking days/week (Mean)
Zonisamide2.7
Placebo3.3

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Percent Heavy Drinking Days

TLFB was be used to estimate participants' daily drinking. In this assessment, participants are presented with a calendar and asked to provide retrospective estimates of their daily alcohol consumption over a specified time period. TLFB was used to gather information on participants' daily drinking. In this assessment, participants are presented with a calendar and asked to provide retrospective estimates of their daily alcohol consumption over a specified time period. TLFB data from 28 days before BL were used to calculate pre-treatment outcomes. In instances where 28 days of data were not available, 21 days were used instead. Heavy drinking days refers to the percentage of heavy drinking days within that window (4 or more drinks for women, 5 or more for men). (NCT02901041)
Timeframe: Pre-treatment

Interventionpercentage of heavy drinking days (Mean)
Zonisamide & Computerized Psychotherapy46.43
Placebo & Computerized Psychotherapy43.82

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Percent Heavy Drinking Days

TLFB was be used to estimate participants' daily drinking. (See outcome measure 1 for more details description.) In this assessment, participants are presented with a calendar and asked to provide retrospective estimates of their daily alcohol consumption over a specified time period. TLFB data from 28 days before post-treatment were used to calculate post-treatment outcomes. In instances where 28 days of data were not available, 21 days were used instead. Heavy drinking days refers to the percentage of heavy drinking days within that window (4 or more drinks for women, 5 or more for men). (NCT02901041)
Timeframe: Post-treatment (Week 12)

InterventionPercent heavy drinking days (Mean)
Zonisamide & Computerized Psychotherapy19.83
Placebo & Computerized Psychotherapy31.12

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Cued Go No-Go: Inhibition Error

In this online task, participants are first presented with a go or a no-go cue, and are then presented with a go or no-go target. Participants are instructed to respond to a go target by clicking on a button, and not to respond to a no-go target. The cues have a high probability of signaling a correct target (valid cues), and a low probability of signaling an incorrect target (invalid cues). Incorrect responses to the no-go target are used to assess inhibitory control, which reflect impulse control. A test includes 250 trials and takes approximately 15 minutes to complete. Here, inhibition error is reported as the error rate (as a percentage) for trials where a go cue was followed by a no-go target. Larger error rates reflect less inhibitory control. (NCT02901041)
Timeframe: Post-treatment (Week 12)

Interventionpercentage of incorrect responses (Mean)
Zonisamide & Computerized Psychotherapy0.63
Placebo & Computerized Psychotherapy1.05

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Connor's Continuous Performance Task: AX Test Commission Rate

The CPT includes two attention tasks, the second one being more difficult than the first. In the second task (reported on here), participants are presented with a series of letters, and are instructed to click on the button only when the letter X appears directly after the letter A appears (an AX presentation). The letters appear at approximately 0.92s intervals, and responses are scored correctly if the button is clicked within 0.69s after the letter appears. A commission occurs when a participant presses the button at any time other than following an AX presentation (i.e. during a non-AX presentation). The commission rate is calculated by dividing the number of commissions by the number of non-AX presentations and converting that to a percentage. Higher commission rates indicate worse performance on this attentional task. (NCT02901041)
Timeframe: Post-treatment (Week 12)

Interventionpercentage of commission responses (Mean)
Zonisamide & Computerized Psychotherapy0.87
Placebo & Computerized Psychotherapy0.84

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Connor's Continuous Performance Task (CPT): X Test Omission Rate

The CPT includes two attention tasks, the second one being more difficult than the first. In the first task (reported on here), participants are presented a series of letters, one letter by one letter, and are asked to click on a button when the letter X appears. The letters appear at approximately 0.92s intervals, and responses are scored correctly if the button is clicked within 0.69s after the letter appears. An omission occurs when the X appears but the participant does not click the button within 0.69 seconds after it appears. The omission rate is calculated by dividing the number of omissions by the number of X presentations and converting that to a percentage. Higher omission rates indicate worse performance on this attentional task. (NCT02901041)
Timeframe: Post-treatment (Week 12)

Interventionpercentage of omitted responses (Mean)
Zonisamide & Computerized Psychotherapy29.76
Placebo & Computerized Psychotherapy26.42

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Connor's Continuous Performance Task (CPT): X Test Commission Rate

The CPT includes two attention tasks, the second one being more difficult than the first. In the first task (reported on here), participants are presented a series of letters, one letter by one letter, and are asked to click on a button when the letter X appears.The letters appear at approximately 0.92s intervals, and responses are scored correctly if the button is clicked within 0.69s after the letter appears. A commission occurs when a participant clicks a button when something other than the letter X has been presented. The commission rate is calculated by dividing the number of commissions by the total number of non-X presentations and converting that to a percentage. Higher commission rates indicate worse performance on this attentional task. (NCT02901041)
Timeframe: Post-treatment (Week 12)

Interventionpercentage of commission responses (Mean)
Zonisamide & Computerized Psychotherapy0.84
Placebo & Computerized Psychotherapy0.43

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Connor's Continuous Performance Task (CPT) - X Test Omission Rate

The CPT includes two attention tasks, the second one being more difficult than the first. In the first task (reported on here), participants are presented a series of letters, one letter by one letter, and are asked to click on a button when the letter X appears. The letters appear at approximately 0.92s intervals, and responses are scored correctly if the button is clicked within 0.69s after the letter appears. An omission occurs when the X appears but the participant does not click the button within 0.69 seconds after it appears. The omission rate is calculated by dividing the number of omissions by the number of X presentations and converting that to a percentage. Higher omission rates indicate worse performance on this attentional task. (NCT02901041)
Timeframe: Pre-treatment

Interventionpercentage of omitted responses (Mean)
Zonisamide & Computerized Psychotherapy23.51
Placebo & Computerized Psychotherapy23.37

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Connor's Continous Performance Task: AX Test Commission Rate

The CPT includes two attention tasks, the second one being more difficult than the first. In the second task (reported on here), participants are presented with a series of letters, and are instructed to click on the button only when the letter X appears directly after the letter A appears (an AX presentation). The letters appear at approximately 0.92s intervals, and responses are scored correctly if the button is clicked within 0.69s after the letter appears. A commission occurs when a participant presses the button at any time other than following an AX presentation (i.e. during a non-AX presentation). The commission rate is calculated by dividing the number of commissions by the number of non-AX presentations and converting that to a percentage. Higher commission rates indicate worse performance on this attentional task. (NCT02901041)
Timeframe: Pre-treatment

Interventionpercentage of commission responses (Mean)
Zonisamide & Computerized Psychotherapy.80
Placebo & Computerized Psychotherapy0.40

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Balloon Analogue Risk Task: Total Pump Count

In this online task, participants are presented with a balloon. Clicking a button will pump the balloon, causing it to inflate and the participant to be awarded a certain amount of money. This happens until a threshold when a pump will cause the balloon to explode and all money would be lost. At any point in time, participants can choose between pumping the balloon further and risking it exploding, or not pumping the balloon and collecting the money they have already earned. 90 trials are conducted and the average number of pumps delivered are used to measure levels of risk-taking. Higher numbers of balloon pumps are associated with greater risk-taking. (NCT02901041)
Timeframe: Pre-treatment

Interventionpumps (Mean)
Zonisamide & Computerized Psychotherapy709.23
Placebo & Computerized Psychotherapy682.16

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Balloon Analogue Risk Task: Total Pump Count

In this online task, participants are presented with a balloon. Clicking a button will pump the balloon, causing it to inflate and the participant to be awarded a certain amount of money. This happens until a threshold when a pump will cause the balloon to explode and all money would be lost. At any point in time, participants can choose between pumping the balloon further and risking it exploding, or not pumping the balloon and collecting the money they have already earned. 90 trials are conducted and the average number of pumps delivered are used to measure levels of risk-taking. Higher numbers of balloon pumps are associated with greater risk-taking. (NCT02901041)
Timeframe: Post-treatment (Week 12)

Interventionpumps (Mean)
Zonisamide & Computerized Psychotherapy829.09
Placebo & Computerized Psychotherapy730.04

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Average Weekly Standard Drinking Units (SDUs)

"Timeline followback (TLFB) was used to collect information on participant's daily drinking. TLFB is a form of interview used to collect retroactive data related to participant's drinking. Participants are presented with a calendar are asked to report what they drank each day for a specified timeframe (e.g. in the past week). Participants were encouraged to give their best estimate in the absence of total certainty regarding their drinking on a given day. Study assessors then used these responses to identify how many standard drinking units participants drank each day. The National Institute of Alcohol Abuse and Alcoholism (NIAAA) defines one standard drinking unit as containing 14 grams of pure alcohol, and provide guidelines for calculating standard drinking units based on the alcohol content and size of a given drink. TLFB data from 28 days before BL were used to calculate pre-treatment outcomes. In instances where 28 days of data were not available, 21 days were used instead." (NCT02901041)
Timeframe: Post-treatment (Week 12)

Interventionstandard drinking units per week (Mean)
Zonisamide & Computerized Psychotherapy15.64
Placebo & Computerized Psychotherapy21.43

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Average Weekly Standard Drinking Units (SDUs)

"Timeline follow back is a form of interview used to collect retroactive data related to participant's drinking. Participants are presented with a calendar are asked to report what they drank each day for a specified timeframe (e.g. in the past week). Participants were encouraged to give their best estimate in the absence of total certainty regarding their drinking on a given day. Study assessors then used these responses to identify how many standard drinking units participants drank each day. The National Institute of Alcohol Abuse and Alcoholism (NIAAA) defines one standard drinking unit as containing 14 grams of pure alcohol, and provide guidelines for calculating standard drinking units based on the alcohol content and size of a given drink. These standards, which can be found the NIAAA website, were used to calculate participant's average drinking units." (NCT02901041)
Timeframe: Pre-treatment

Interventionstandard drinking units per week (Mean)
Zonisamide & Computerized Psychotherapy31.51
Placebo & Computerized Psychotherapy31.37

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Connor's Continuous Performance Task (CPT): X Test Commission Rate

The CPT includes two attention tasks, the second one being more difficult than the first. In the first task (reported on here), participants are presented a series of letters, one letter by one letter, and are asked to click on a button when the letter X appears. The letters appear at approximately 0.92s intervals, and responses are scored correctly if the button is clicked within 0.69s after the letter appears. A commission occurs when a participant clicks a button when something other than the letter X has been presented. The commission rate is calculated by dividing the number of commissions by the total number of non-X presentations and converting that to a percentage. Higher commission rates indicate worse performance on this attentional task. (NCT02901041)
Timeframe: Pre-treatment

Interventionpercentage of commission responses (Mean)
Zonisamide & Computerized Psychotherapy0.74
Placebo & Computerized Psychotherapy0.42

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Connor's Continuous Performance Task (CPT): AX Test Omission Rate

The CPT includes two attention tasks, the second one being more difficult than the first. In the second task (reported on here), participants are presented with a series of letters, and are instructed to click on the button only when the letter X appears directly after the letter A appears (an AX presentation). The letters appear at approximately 0.92s intervals, and responses are scored correctly if the button is clicked within 0.69s after the letter appears. An omission occurs when a participant does not click the button when the letter X appears directly after the letter A. The omission rate is calculated by dividing the number of omissions by the total number of AX presentations and converting that to a percentage. Higher omission rates indicate worse performance on this attentional task. (NCT02901041)
Timeframe: Pre-treatment

Interventionpercentage of omission responses (Mean)
Zonisamide & Computerized Psychotherapy6.40
Placebo & Computerized Psychotherapy3.33

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Average Standard Drinking Units Per Day

"Timeline followback (TLFB) was used to collect information on participant's daily drinking. TLFB is a form of interview used to collect retroactive data related to participant's drinking. Participants are presented with a calendar are asked to report what they drank each day for a specified timeframe (e.g. in the past week). Participants were encouraged to give their best estimate in the absence of total certainty regarding their drinking on a given day. Study assessors then used these responses to identify how many standard drinking units participants drank each day. The National Institute of Alcohol Abuse and Alcoholism (NIAAA) defines one standard drinking unit as containing 14 grams of pure alcohol, and provide guidelines for calculating standard drinking units based on the alcohol content and size of a given drink. TLFB data from 28 days before BL were used to calculate pre-treatment outcomes. In instances where 28 days of data were not available, 21 days were used instead." (NCT02901041)
Timeframe: Pre-treatment

Interventionstandard drinking units per day (Mean)
Zonisamide & Computerized Psychotherapy4.50
Placebo & Computerized Psychotherapy4.48

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Average Standard Drinking Units Per Day

"Timeline followback (TLFB) was used to collect information on participant's daily drinking. TLFB is a form of interview used to collect retroactive data related to participant's drinking. Participants are presented with a calendar are asked to report what they drank each day for a specified timeframe (e.g. in the past week). Participants were encouraged to give their best estimate in the absence of total certainty regarding their drinking on a given day. Study assessors then used these responses to identify how many standard drinking units participants drank each day. The National Institute of Alcohol Abuse and Alcoholism (NIAAA) defines one standard drinking unit as containing 14 grams of pure alcohol, and provide guidelines for calculating standard drinking units based on the alcohol content and size of a given drink. TLFB data from 28 days before BL were used to calculate pre-treatment outcomes. In instances where 28 days of data were not available, 21 days were used instead." (NCT02901041)
Timeframe: Post-treatment (Week 12)

Interventionstandard drinking units per day (Mean)
Zonisamide & Computerized Psychotherapy2.23
Placebo & Computerized Psychotherapy3.06

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Roger's Risk Task: Risk Adjustment

Participants are given 10 boxes. Some of these boxes are red, the others are blue. They are told that a yellow token is hidden under one of these boxes and they have to guess the color of the box under which the yellow token is hidden. Once they decide on the color, they are asked to bet points on this choice: the computer provides the bets in either ascending (bets get bigger) or descending order (bets get smaller) and participants are asked to click on a bet when they want to bet this number of points. If they win, the bet number is added to their total points. If they lose the bet number is taken away from their total points. Risk adjustment is a measure of the difference between their risk taking behavior during ascending versus descending trials, and represents whether the participant changes their bet based on the odds of winning. There are no min or max scores, and a higher score indicates the subject is more likely to change the wager depending on the probability of winning. (NCT02901041)
Timeframe: Pre-treatment

Interventionscore on a scale (Mean)
Zonisamide & Computerized Psychotherapy0.67
Placebo & Computerized Psychotherapy0.94

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Roger's Risk Task: Delay Aversion

Participants are given 10 boxes. Some of these boxes are red, the others are blue. They are told that a yellow token is hidden under one of these boxes and they have to guess the color of the box under which the yellow token is hidden. Once they decide on the color, they are asked to bet points on this choice: the computer provides the bets in either ascending (bets get bigger) or descending order (bets get smaller) and participants are asked to click on a bet when they want to bet this number of points. If they win, the bet number is added to their total points. If they lose the bet number is taken away from their total points. Delay aversion is the difference between the risk-taking score in the descend and ascend conditions. There is no min or max score. Participants who find delays aversive tend to select an amount to bet early in the sequence; i.e., a large bet in the descend condition, and a small bet in the ascend condition. Thus, they will have a higher risk aversion score. (NCT02901041)
Timeframe: Post-treatment (Week 12)

Interventionscore on a scale (Mean)
Zonisamide & Computerized Psychotherapy0.16
Placebo & Computerized Psychotherapy0.30

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Roger's Risk Task: Risk Adjustment

Participants are given 10 boxes. Some of these boxes are red, the others are blue. They are told that a yellow token is hidden under one of these boxes and they have to guess the color of the box under which the yellow token is hidden. Once they decide on the color, they are asked to bet points on this choice: the computer provides the bets in either ascending (bets get bigger) or descending order (bets get smaller) and participants are asked to click on a bet when they want to bet this number of points. If they win, the bet number is added to their total points. If they lose the bet number is taken away from their total points. Risk adjustment is a measure of the difference between their risk taking behavior during ascending versus descending trials, and represents whether the participant changes their bet based on the odds of winning. There are no min or max scores, and a higher score indicates the subject is more likely to change the wager depending on the probability of winning. (NCT02901041)
Timeframe: Post-treatment (Week 12)

Interventionscore on a scale (Mean)
Zonisamide & Computerized Psychotherapy0.55
Placebo & Computerized Psychotherapy0.91

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Roger's Risk Task: Mean Percent Bet

"Participants are given 10 boxes. Some of these boxes are red, the others are blue. They are told that a yellow token is hidden under one of these boxes and they have to guess the color of the box under which the yellow token is hidden. Once they decide on the color, they are asked to bet points on this choice: the computer provides the bets in either ascending (bets get bigger) or descending order (bets get smaller) and participants are asked to click on a bet when they want to bet this number of points. If they win, the bet number is added to their total points. If they lose the bet number is taken away from their total points. Mean percent bet refers to the overall mean percentage of their points participants bet across trials." (NCT02901041)
Timeframe: Pre-treatment

Interventionpercentage of points bet (Mean)
Zonisamide & Computerized Psychotherapy61.51
Placebo & Computerized Psychotherapy59.48

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Roger's Risk Task: Mean Percent Bet

"Participants are given 10 boxes. Some of these boxes are red, the others are blue. They are told that a yellow token is hidden under one of these boxes and they have to guess the color of the box under which the yellow token is hidden. Once they decide on the color, they are asked to bet points on this choice: the computer provides the bets in either ascending (bets get bigger) or descending order (bets get smaller) and participants are asked to click on a bet when they want to bet this number of points. If they win, the bet number is added to their total points. If they lose the bet number is taken away from their total points. Mean percent bet refers to the overall mean percentage of their points participants bet across trials." (NCT02901041)
Timeframe: Post-treatment (Week 12)

Interventionpercentage of points bet (Mean)
Zonisamide & Computerized Psychotherapy56.01
Placebo & Computerized Psychotherapy61.62

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Roger's Risk Task: Delay Aversion

Participants are given 10 boxes. Some of these boxes are red, the others are blue. They are told that a yellow token is hidden under one of these boxes and they have to guess the color of the box under which the yellow token is hidden. Once they decide on the color, they are asked to bet points on this choice: the computer provides the bets in either ascending (bets get bigger) or descending order (bets get smaller) and participants are asked to click on a bet when they want to bet this number of points. If they win, the bet number is added to their total points. If they lose the bet number is taken away from their total points. Delay aversion is the difference between the risk-taking score in the descend and ascend conditions. There is no min or max score. Participants who find delays aversive tend to select an amount to bet early in the sequence; i.e., a large bet in the descend condition, and a small bet in the ascend condition. Thus, they will have a higher risk aversion score. (NCT02901041)
Timeframe: Pre-treatment

Interventionscore on a scale (Mean)
Zonisamide & Computerized Psychotherapy0.32
Placebo & Computerized Psychotherapy0.30

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Cued Go/No-go Task: Inhibition Error

In this online task, participants are first presented with a go or a no-go cue, and are then presented with a go or no-go target. Participants are instructed to respond to a go target by clicking on a button, and not to respond to a no-go target. The cues have a high probability of signaling a correct target (valid cues), and a low probability of signaling an incorrect target (invalid cues). Incorrect responses to the no-go target are used to assess inhibitory control, which reflect impulse control. A test includes 250 trials and takes approximately 15 minutes to complete. Here, inhibition error is reported as the error rate (as a percentage) for trials where a go cue was followed by a no-go target. Larger error rates reflect less inhibitory control. (NCT02901041)
Timeframe: Pre-treatment

Interventionpercentage of incorrect responses (Mean)
Zonisamide & Computerized Psychotherapy2.48
Placebo & Computerized Psychotherapy1.63

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Percentage of Drinking Days

"Timeline followback (TLFB) was used to collect information on participant's daily drinking. TLFB is a form of interview used to collect retroactive data related to participant's drinking. Participants are presented with a calendar are asked to report what they drank each day for a specified timeframe (e.g. in the past week). Participants were encouraged to give their best estimate in the absence of total certainty regarding their drinking on a given day. Study assessors then used these responses to identify how many standard drinking units participants drank each day. The National Institute of Alcohol Abuse and Alcoholism (NIAAA) defines one standard drinking unit as containing 14 grams of pure alcohol, and provide guidelines for calculating standard drinking units based on the alcohol content and size of a given drink. TLFB data from 28 days before BL were used to calculate pre-treatment outcomes. In instances where 28 days of data were not available, 21 days were used instead." (NCT02901041)
Timeframe: Pre-treatment

InterventionPercentage of drinking days (Mean)
Zonisamide & Computerized Psychotherapy72.77
Placebo & Computerized Psychotherapy79.62

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Connor's Continuous Performance Task (CPT): AX Test Omission Rate

The CPT includes two attention tasks, the second one being more difficult than the first. In the first task, participants are presented a series of 31 letters, one letter by one letter, and are asked to click on a button when the letter X appears. In the second task (reported on here), participants are presented with a series of 31 letters, and are instructed to click on the button only when the letter X appears directly after the letter A appears (an AX presentation). The letters appear at approximately 0.92s intervals, and responses are scored correctly if the button is clicked within 0.69s after the letter appears. An omission occurs when a participant does not click the button when the letter X appears directly after the letter A. The omission rate is calculated by dividing the number of omissions by the total number of AX presentations and converting that to a percentage. Higher omission rates indicate worse performance on this attentional task. (NCT02901041)
Timeframe: Post-treatment (Week 12)

Interventionpercentage of omission responses (Mean)
Zonisamide & Computerized Psychotherapy8.76
Placebo & Computerized Psychotherapy5.58

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Percentage of Drinking Days

"Timeline followback (TLFB) was used to collect information on participant's daily drinking. TLFB is a form of interview used to collect retroactive data related to participant's drinking. Participants are presented with a calendar are asked to report what they drank each day for a specified timeframe (e.g. in the past week). Participants were encouraged to give their best estimate in the absence of total certainty regarding their drinking on a given day. Study assessors then used these responses to identify how many standard drinking units participants drank each day. The National Institute of Alcohol Abuse and Alcoholism (NIAAA) defines one standard drinking unit as containing 14 grams of pure alcohol, and provide guidelines for calculating standard drinking units based on the alcohol content and size of a given drink. TLFB data from 28 days before BL were used to calculate pre-treatment outcomes. In instances where 28 days of data were not available, 21 days were used instead." (NCT02901041)
Timeframe: Post-treatment (Week 12)

Interventionpercentage of drinking days (Mean)
Zonisamide & Computerized Psychotherapy51.27
Placebo & Computerized Psychotherapy68.14

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Change in Rewarding Effects of Smoking Combustible Cigarettes

Characterize changes in the two primary scales of the Cigarette Evaluation Questionnaire (mCEQ), assessing smoking satisfaction and psychological reward, compared between cigarettes smoked after meals versus all others smoked during the day, examining how this difference changes after zonisamide/bupropion usage. The mCEQ uses a 7-point scale (0=Not at all; 1=Very little; 2=A little; 3=Moderately; 4=A lot, 5=Quite a lot; 6=Extremely) to measure the following subscales: Satisfaction, Psychological Reward, Enjoyment of Respiratory Tract Sensations, Craving Reduction, Aversion. (NCT04388319)
Timeframe: First week compared to after start of study drugs (Weeks 2-13 post baseline)

Interventionscore on a scale (Mean)
CEQ Satisfaction ScaleCEQ Psych Reward Scale
Combination Zonisamide and Bupropion With E-cigarette00.2

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Number of Participants That Completely Switched From Combustible Cigarettes to Halo G6 E-Cigarettes

Defined as self-report of no cigarette smoking (not even a puff), confirmed by an expired air CO reading of less than 5 ppm. (NCT04388319)
Timeframe: Weeks 8-11 post-quit date (weeks 10-13 post baseline)

InterventionParticipants (Count of Participants)
Combination Zonisamide and Bupropion With E-cigarette8

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Point Abstinence From Combustible Cigarettes

Assessed by self-report utilizing an automated SMS messaging system. (NCT04388319)
Timeframe: Six months post switch day (approximately 6 months post baseline)

InterventionParticipants (Count of Participants)
Combination Zonisamide and Bupropion With E-cigarette15

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