PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32505479-0 2020 KCNT1-positive epilepsy of infancy with migrating focal seizures successfully treated with nonnarcotic antitussive drugs after treatment failure with quinidine: A case report. Quinidine 150-159 potassium sodium-activated channel subfamily T member 1 Homo sapiens 0-5 32505479-3 2020 Since gain of function is the only type of mutation identified in patients with EIMFS, quinidine, a partial antagonist of KCa4.1 channel, is considered as a potential candidate for targeted treatment of EIMFS. Quinidine 87-96 potassium sodium-activated channel subfamily T member 1 Homo sapiens 122-128 31208268-11 2019 Our data suggest that alternative therapies to quinidine should be considered as a therapeutic option for patients with KCNT1-related epilepsy. Quinidine 47-56 potassium sodium-activated channel subfamily T member 1 Homo sapiens 120-125 30782581-0 2019 Quinidine therapy and therapeutic drug monitoring in four patients with KCNT1 mutations. Quinidine 0-9 potassium sodium-activated channel subfamily T member 1 Homo sapiens 72-77 31388363-0 2019 Concurrent Quinidine and Phenobarbital in the Treatment of a Patient with 2 KCNT1 Mutations. Quinidine 11-20 potassium sodium-activated channel subfamily T member 1 Homo sapiens 76-81 31388363-4 2019 We report the case of an infant with 2 KCNT1 mutations who experienced minor relief with quinidine and discuss the drug"s important interaction with phenobarbital. Quinidine 89-98 potassium sodium-activated channel subfamily T member 1 Homo sapiens 39-44 31359944-0 2019 Two South Indian Children with KCNT1-Related Malignant Migrating Focal Seizures of Infancy - Clinical Characteristics and Outcome of Targeted Treatment with Quinidine. Quinidine 157-166 potassium sodium-activated channel subfamily T member 1 Homo sapiens 31-36 31359944-9 2019 A critical review on the current status of targeted treatment of KCNT1-related epileptic encephalopathies with quinidine is attempted. Quinidine 111-120 potassium sodium-activated channel subfamily T member 1 Homo sapiens 65-70 31054119-11 2019 More favorable response to quinidine in patients with KCNT1 variants distal to the NADP domain within the RCK2 domain may suggest a variant-specific response. Quinidine 27-36 potassium sodium-activated channel subfamily T member 1 Homo sapiens 54-59 31072785-0 2019 Corrigendum to "Does age affect response to quinidine in patients with KCNT1 mutations? Quinidine 44-53 potassium sodium-activated channel subfamily T member 1 Homo sapiens 71-76 30804880-0 2019 Quinidine Therapy for Lennox-Gastaut Syndrome With KCNT1 Mutation. Quinidine 0-9 potassium sodium-activated channel subfamily T member 1 Homo sapiens 51-56 30804880-9 2019 Previous studies revealed that quinidine could block the KCNT1 channel. Quinidine 31-40 potassium sodium-activated channel subfamily T member 1 Homo sapiens 57-62 30804880-13 2019 In conclusion, quinidine therapy may offer a new choice for the treatment of Lennox-Gastaut syndrome with KCNT1 mutations. Quinidine 15-24 potassium sodium-activated channel subfamily T member 1 Homo sapiens 106-111 30782581-1 2019 Several recent studies have reported potassium sodium-activated channel subfamily T member 1 (KCNT1) mutations in epilepsy patients on quinidine therapy. Quinidine 135-144 potassium sodium-activated channel subfamily T member 1 Homo sapiens 94-99 30782581-3 2019 We herein report the cases of four patients with KCNT1 mutations treated with quinidine. Quinidine 78-87 potassium sodium-activated channel subfamily T member 1 Homo sapiens 49-54 30782581-10 2019 Based on a review of previous reports and our experience with this case, quinidine should be considered as a promising drug for patients with EIMFS harbouring KCNT1 mutations, however, its efficacy remains controversial due to the limited number of cases, and more information on optimal serum concentrations and appropriate titration methods is required. Quinidine 73-82 potassium sodium-activated channel subfamily T member 1 Homo sapiens 159-164 29037447-0 2018 A quinidine non responsive novel KCNT1 mutation in an Indian infant with epilepsy of infancy with migrating focal seizures. Quinidine 2-11 potassium sodium-activated channel subfamily T member 1 Homo sapiens 33-38 30182418-0 2018 Lack of response to quinidine in KCNT1-related neonatal epilepsy. Quinidine 20-29 potassium sodium-activated channel subfamily T member 1 Homo sapiens 33-38 30182418-1 2018 OBJECTIVE: To evaluate the clinical efficacy and safety of quinidine in patients with KCNT1-related epilepsy of infancy with migrating focal seizures (EIMFS) in the infantile period and to compare with the effect of quinidine on mutant channels in vitro. Quinidine 59-68 potassium sodium-activated channel subfamily T member 1 Homo sapiens 86-91 30112700-0 2018 Early Treatment with Quinidine in 2 Patients with Epilepsy of Infancy with Migrating Focal Seizures (EIMFS) Due to Gain-of-Function KCNT1 Mutations: Functional Studies, Clinical Responses, and Critical Issues for Personalized Therapy. Quinidine 21-30 potassium sodium-activated channel subfamily T member 1 Homo sapiens 132-137 30112700-2 2018 The most common cause for EIMFS is a gain-of-function mutation in the KCNT1 potassium channel gene, and treatment with the KCNT1 blocker quinidine has been suggested as a rational approach for seizure control in EIMFS patients. Quinidine 137-146 potassium sodium-activated channel subfamily T member 1 Homo sapiens 70-75 30112700-2 2018 The most common cause for EIMFS is a gain-of-function mutation in the KCNT1 potassium channel gene, and treatment with the KCNT1 blocker quinidine has been suggested as a rational approach for seizure control in EIMFS patients. Quinidine 137-146 potassium sodium-activated channel subfamily T member 1 Homo sapiens 123-128 30112700-4 2018 In the present study, we provide a detailed description of the clinical, genetic, in vitro, and in vivo electrophysiological profile and pharmacological responses to quinidine of 2 EIMFS unrelated patients with a heterozygous de novo KCNT1 mutation: c.2849G>A (p.R950Q) in patient 1 and c.2677G>A (p.E893K) in patient 2. Quinidine 166-175 potassium sodium-activated channel subfamily T member 1 Homo sapiens 234-239 30112700-8 2018 Based on the present experience, early quinidine intervention associated with heart monitoring and control of blood levels is among the critical factors for therapy effectiveness in EIMFS patients with KCNT1 gain-of-function mutations. Quinidine 39-48 potassium sodium-activated channel subfamily T member 1 Homo sapiens 202-207 29866938-0 2018 Reader response: Quinidine-associated skin discoloration in KCNT1-associated pediatric epilepsy. Quinidine 17-26 potassium sodium-activated channel subfamily T member 1 Homo sapiens 60-65 29866939-0 2018 Author response: Quinidine-associated skin discoloration in KCNT1-associated pediatric epilepsy. Quinidine 17-26 potassium sodium-activated channel subfamily T member 1 Homo sapiens 60-65 29866940-0 2018 Quinidine-associated skin discoloration in KCNT1-associated pediatric epilepsy. Quinidine 0-9 potassium sodium-activated channel subfamily T member 1 Homo sapiens 43-48 29037447-5 2018 Antagonist of KCNT1 coded ion channel like Quinidine has shown promising results in MMPSI. Quinidine 43-52 potassium sodium-activated channel subfamily T member 1 Homo sapiens 14-19 27578169-1 2017 The KCNT1 gene encodes the sodium-dependent potassium channel, with quinidine being a partial antagonist of the KCNT1 channel. Quinidine 68-77 potassium sodium-activated channel subfamily T member 1 Homo sapiens 4-9 29291456-0 2018 Does age affect response to quinidine in patients with KCNT1 mutations? Quinidine 28-37 potassium sodium-activated channel subfamily T member 1 Homo sapiens 55-60 29291456-4 2018 Here we report 3 additional children, with such KCNT1 mutations and refractory seizures, who received quinidine therapy. Quinidine 102-111 potassium sodium-activated channel subfamily T member 1 Homo sapiens 48-53 29291456-11 2018 CONCLUSION: The above-mentioned findings support performance of prospective controlled studies of quinidine efficacy in children with KCNT1 gain-of-function mutations that control for age as a possible variable affecting response. Quinidine 98-107 potassium sodium-activated channel subfamily T member 1 Homo sapiens 134-139 29158296-0 2017 Quinidine-associated skin discoloration in KCNT1-associated pediatric epilepsy. Quinidine 0-9 potassium sodium-activated channel subfamily T member 1 Homo sapiens 43-48 29196578-1 2018 OBJECTIVE: To evaluate quinidine as a precision therapy for severe epilepsy due to gain of function mutations in the potassium channel gene KCNT1. Quinidine 23-32 potassium sodium-activated channel subfamily T member 1 Homo sapiens 140-145 29196578-14 2018 CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that for persons with severe epilepsy due to gain of function mutations in the potassium channel gene KCNT1, quinidine does not significantly reduce seizure frequency. Quinidine 175-184 potassium sodium-activated channel subfamily T member 1 Homo sapiens 168-173 29196579-11 2018 All evaluated KCNT1 variants resulted in marked gain of function with significantly increased channel amplitude and variable blockade by quinidine. Quinidine 137-146 potassium sodium-activated channel subfamily T member 1 Homo sapiens 14-19 27578169-1 2017 The KCNT1 gene encodes the sodium-dependent potassium channel, with quinidine being a partial antagonist of the KCNT1 channel. Quinidine 68-77 potassium sodium-activated channel subfamily T member 1 Homo sapiens 112-117 27578169-13 2017 Thus, quinidine therapy should be attempted in patients with West syndrome caused by KCNT1 mutations, as reported for MPSI. Quinidine 6-15 potassium sodium-activated channel subfamily T member 1 Homo sapiens 85-90 26748457-0 2016 Ineffective quinidine therapy in early onset epileptic encephalopathy with KCNT1 mutation. Quinidine 12-21 potassium sodium-activated channel subfamily T member 1 Homo sapiens 75-80 26784557-6 2016 Interestingly, the KCNT1 blockers quinidine (3-1000muM) and bepridil (0.03-10muM) inhibited both wild-type and mutant KCNT1 currents in a concentration-dependent manner, with mutant channels showing higher sensitivity to blockade. Quinidine 34-43 potassium sodium-activated channel subfamily T member 1 Homo sapiens 19-24 26784557-6 2016 Interestingly, the KCNT1 blockers quinidine (3-1000muM) and bepridil (0.03-10muM) inhibited both wild-type and mutant KCNT1 currents in a concentration-dependent manner, with mutant channels showing higher sensitivity to blockade. Quinidine 34-43 potassium sodium-activated channel subfamily T member 1 Homo sapiens 118-123 26022171-3 2015 Examples of that include the need to avoid specific drugs in Dravet syndrome and the ongoing investigations of the potential use of new directed therapies such as retigabine in KCNQ2-related epilepsies, quinidine in KCNT1-related epilepsies, and memantine in GRIN2A-related epilepsies. Quinidine 203-212 potassium sodium-activated channel subfamily T member 1 Homo sapiens 216-221 26369628-0 2015 Quinidine in the treatment of KCNT1-positive epilepsies. Quinidine 0-9 potassium sodium-activated channel subfamily T member 1 Homo sapiens 30-35 26369628-1 2015 We report 2 patients with drug-resistant epilepsy caused by KCNT1 mutations who were treated with quinidine. Quinidine 98-107 potassium sodium-activated channel subfamily T member 1 Homo sapiens 60-65 25042079-3 2014 The antiarrhythmic drug quinidine is a partial antagonist of KCNT1 and hence may be a candidate drug for treatment of this condition. Quinidine 24-33 potassium sodium-activated channel subfamily T member 1 Homo sapiens 61-66 25042079-4 2014 We report the case of a child with migrating partial seizures of infancy secondary to an activating mutation in KCNT1 treated with quinidine. Quinidine 131-140 potassium sodium-activated channel subfamily T member 1 Homo sapiens 112-117 16876206-4 2006 Two known blockers of KNa channels, bepridil and quinidine, inhibited Slack currents in a concentration-dependent manner and decreased channel activity in excised membrane patches. Quinidine 49-58 potassium sodium-activated channel subfamily T member 1 Homo sapiens 70-75 34122071-0 2021 Case Report of Novel Genetic Variant in KCNT1 Channel and Pharmacological Treatment With Quinidine. Quinidine 89-98 potassium sodium-activated channel subfamily T member 1 Homo sapiens 40-45 34122071-4 2021 Aim: To present the pharmacological response and therapeutic drug monitoring of a paediatric patient with a severe encephalopathy carrying a genetic variant in KCNT1 gene, whose identification led to include quinidine (QND) in the treatment regimen as an antiepileptic drug. Quinidine 208-217 potassium sodium-activated channel subfamily T member 1 Homo sapiens 160-165 35369761-3 2022 Quinidine is an anti-arrhythmic drug that functions as a moderately potent inhibitor of Slack channels; however, quinidine use is limited by its poor selectivity, safety and pharmacokinetic profile. Quinidine 0-9 potassium sodium-activated channel subfamily T member 1 Homo sapiens 88-93 35369761-3 2022 Quinidine is an anti-arrhythmic drug that functions as a moderately potent inhibitor of Slack channels; however, quinidine use is limited by its poor selectivity, safety and pharmacokinetic profile. Quinidine 113-122 potassium sodium-activated channel subfamily T member 1 Homo sapiens 88-93