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quinidine bisulfate (Kiditard)

✓ Approved

Adare Pharma Solutions · SCN5A · Small Molecule

What is quinidine bisulfate?

quinidine bisulfate is a small molecule developed by Adare Pharma Solutions. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesKiditard
CompanyAdare Pharma Solutions
Drug ClassSmall Molecule
Molecular TargetSCN5A
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Adare Pharma Solutions

Mechanism of Action

Molecular Targets

quinidine bisulfate acts on 1 molecular target:

SCN5Asodium voltage-gated channel alpha subunit 5 (CMD1E, SSS1)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

quinidine bisulfate is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Cardiac disordersArrhythmia✓ Approved

Related Research Articles

PubMedInternational journal of pharmaceutical compounding2026-09-17

Development and Chemical Stability Assessment of a Methyl-β-Cyclodextrin-Containing Dextromethorphan/ Quinidine Oral Solution for Extemporaneous Compounding.

Cedric Wernli W, Uli Loesch L

Pseudobulbar affect is a distressing condition frequently observed in patients with amyotrophic lateral sclerosis (ALS), for which a fixed-dose combination of dextromethorphan and quinidine is approved in the United States. In Europe, no commercial product is available, and compounded capsules or suspensions are used; however, capsules may be unsuitable for patients with dysphagia, and suspensions require shaking before administration. The aim of this study was to develop simple fully water-soluble formulation of dextromethorphan hydrobromide and quinidine sulfate using methyl-ß-cyclodextrin as a solubilizing agent and to evaluate its stability under different storage conditions, enabling pharmacies to compound the preparation without complex infrastructure. Preliminary qualitative solubility experiments showed that the dextromethorphan hydrobromide/ quinidine sulfate powder mixture did not dissolve in water without methyl-ß-cyclodextrin. Addition of methyl-ß-cyclodextrin improved dissolution; however, the initial preparation targeting 20 mg/mL dextromethorphan hydrobromide and 10 mg/mL quinidine sulfate in a final volume of 100 mL remained incompletely dissolved. Increasing the final volume to 250 mL yielded a clear formulation containing nominal concentrations of 8.4 mg/mL dextromethorphan hydrobromide and 4.2 mg/mL quinidine sulfate. Three independently prepared batches were stored in amber PET bottles providing light protection and fitted with child-resistant closure at 2-8°C, 15-25°C, and 40°C and analyzed by HPLC for four weeks. HPLC assay values remained within 10% of the corresponding baseline values at each storage condition, and no visible precipitation was observed. The results support the physical clarity and chemical consistency of the tested methyl-ß-cyclodextrin- containing formulation over four weeks under the evaluated storage conditions. Microbiological stability, preservative effectiveness, formal method validation in the author's laboratory, and the extent of cyclodextrin inclusion complexation were not assessed. This formulation may serve as a basis for further pharmaceutical, microbiological, and clinical evaluation of an extemporaneously compounded oral liquid.

PMID 42752431
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PubMedMolecular pharmacology2026-09-11

Molecular basis for state-dependent drug block of Kv11.1 (human ether-à-go-go-related gene) potassium channels.

Zhou Claire Jinmeng CJ, Ma Joanne G JG, Ng Chai-Ann CA, Hunter Mark J MJ et al.

Many structurally and therapeutically diverse drugs block the human ether-à-go-go-related gene (HERG) potassium channel, predisposing patients to an increased risk of arrhythmias and sudden cardiac death. Many of these drugs show state dependence of block, exhibiting a greater preference for block of the inactivated state. Four key residues, ie, T623, S624, Y652, and F656, within the central pore cavity of HERG have been implicated in drug binding. However, whether drugs bind differently to these key residues to dictate preference for binding to the inactivated over the open state is not known. We used the SyncroPatch 384PE, automated patch clamp platform to measure how drug block was impacted by point mutations at these 4 residues when introduced into wild-type (WT) HERG (preferentially occupies the inactivated state) and N588K-HERG (preferentially occupies the open state) channels at depolarized potentials. Mutations to Y652 and F656, which abolished aromatic and hydrophobic characteristics, respectively, reduced drug binding in both WT and N588K backgrounds. The S624A mutation attenuated block by cisapride, astemizole, and quinidine in the WT background but not in the N588K background. We suggest that relative movements between the polar S624 sidechain and the aromatic Y652 sidechains in WT (inactivated) compared with N588K (open) channels can explain preferential binding to the inactivated state. An improved understanding of the structural basis of where and how drugs bind to HERG channels should facilitate efforts to reduce inadvertent HERG drug block during the drug development process. SIGNIFICANCE STATEMENT: A diverse range of drugs block human ether-à-go-go-related gene (HERG) potassium channels, which can have serious side effects, including sudden death. Most problematic drugs bind to the inactivated state of HERG channels. This study shows that the polar side chain of Ser624, at the base of the selectivity filter, is critical for preferential drug block of inactivated compared with open channels. A better understanding of state-dependent drug binding should facilitate efforts to reduce inadvertent HERG drug block.

PMID 42727199
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PubMedThe British journal of cardiology2026-09-10

Management of Brugada storm in a district general hospital.

Coutts Scott R SR, Campbell James J, Stirrat Colin G CG

A 61-year-old man with Brugada syndrome (BrS) (SCN5A mutation) presented with chest pain to a district general hospital (DGH). There was no history of syncope or ventricular arrhythmias. A subcutaneous implantable cardioverter-defibrillator (S-ICD) was in situ for primary prevention following extraction of a previous transvenous ICD due to infection. Investigations suggested a non-ST-elevation myocardial infarction. While awaiting coronary angiography, he developed a ventricular tachycardia (VT) storm with recurrent cardiac arrests over 30 minutes due to polymorphic VT, receiving seven S-ICD shocks. Defibrillation, isoprenaline and quinidine were employed to manage the polymorphic VT storm, permitting transfer to a tertiary centre for further investigations. Coronary angiography demonstrated an occluded marginal artery, which was managed medically. Isoprenaline was weaned following quinidine initiation, the S-ICD reactivated, and he was discharged. A year later, there have been no further ventricular arrhythmias while on quinidine. This case report demonstrates the effectiveness of isoprenaline, which is easily accessible and readily available in DGHs, in stabilising an acute Brugada storm. Quinidine allowed successful weaning from isoprenaline, but lack of availability limits its use. Finally, this case report highlights both the benefits and risks of primary prevention ICDs in BrS.

PMID 42719369
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PubMedCureus2026-09-10

Tachycardia As Therapy: Control of an Electrical Storm Through Mechanism-Directed Treatment After Refractory Ventricular Arrhythmias.

Santos Miguel M, Albuquerque Ana A, Dias Gonçalo G, Henriques Fernando F et al.

Electrical storm (ES) is a life-threatening clinical syndrome defined by recurrent episodes of ventricular tachycardia (VT) or ventricular fibrillation (VF) within a short time frame. Although contemporary management relies on guideline-directed therapies, including antiarrhythmic drugs, deep sedation, sympathetic modulation, and catheter ablation in selected refractory cases, some patients remain unstable and require individualized treatment guided by the suspected electrophysiological substrate. We report the case of a 44-year-old previously healthy woman who presented with out-of-hospital cardiac arrest due to VF. Following successful resuscitation, she developed recurrent polymorphic VT apparently initiated by short-coupled premature ventricular complexes (PVCs). Despite implementation of several conventional and guideline-supported strategies for ES, ventricular arrhythmias continued to recur. The clinical pattern and electrocardiographic/telemetry recordings were considered compatible with a short-coupled ectopy-triggered mechanism, raising suspicion for a Purkinje-mediated substrate. Based on this hypothesis, a therapeutic strategy aimed at increasing the basal heart rate was adopted using continuous isoproterenol infusion. Following isoproterenol titration to achieve sinus tachycardia of approximately 120 beats per minute, no further VT was documented. Quinidine therapy was subsequently introduced, allowing withdrawal of isoproterenol with sustained arrhythmia suppression. This case illustrates how careful interpretation of arrhythmia patterns may guide therapeutic decisions in refractory ES and highlights the potential role of heart rate acceleration in selected patients with suspected short-coupled PVC-triggered ventricular arrhythmias.

PMID 42719472
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PubMedHeart & lung : the journal of critical care2026-09-04

Association of common QT-prolonging medications with arrhythmic risk in patients with bundle branch block: A stratified cohort analysis in left bundle branch block vs. right bundle branch block phenotypes.

Derector Evan E, DO Tirth Patel TP, Watanabe Hiroto H, Solomon Diana D et al.

Bundle branch block (BBB) affects 11-17% of adults over 80 and is associated with mortality and heart failure. Conventional QTc formulae overestimate repolarization in wide QRS complexes, with clinicians holding symptom-management therapies based on inaccurate measurements. This retrospective study utilized the MIMIC-IV database to examine arrhythmogenic risk by drug class and BBB phenotype. Adult ICU admissions with BBB were stratified by drug exposure: amiodarone, high-risk anti-arrhythmics (sotalol, dofetilide, procainamide, ibutilide, quinidine, disopyramide), and common non-cardiac QT-prolonging agents (haloperidol, ondansetron, quetiapine, methadone, levofloxacin, azithromycin). The primary outcome was a composite of ventricular arrhythmia and cardiac arrest; a sensitivity analysis restricted to ventricular arrhythmia was performed. Propensity score matching (1:1) with time-varying Cox regression addressed confounding and immortal time bias. The matched cohort included 1722 admissions (LBBB =1252; RBBB =470). Common non-cardiac agents were not associated with the composite outcome in LBBB (HR 0.96, p = 0.83) or RBBB (HR 0.61, p = 0.24; 28 events, hypothesis-generating). Amiodarone was associated with the composite (LBBB: HR 3.63, p < 0.01; RBBB HR: 3.90, p < 0.01), but not the LBBB sensitivity analysis (HR 1.61, p = 0.19), suggesting confounding by indication. Among patients with QTc >500 ms, common agents remained non-significant. Common non-cardiac QT-prolonging medications were not associated with increased risk in patients with BBB, even with prolonged QTc. The divergence between composite and sensitivity results for amiodarone highlights the influence of confounding by indication. Medication alerts should incorporate stratification by drug class rather than QTc alone.

PMID 42697068
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PubMedJournal of clinical pharmacology2026-09-03

Effect of Food on Balcinrenone/Dapagliflozin Pharmacokinetics and the Pharmacokinetics of Balcinrenone When Dosed with a P-gp Inhibitor.

Eriksson Anna L AL, Karsanji Deeyen D, Shi Amy H AH, Parkinson Joanna J et al.

Balcinrenone (AZD9977) is a novel selective non-steroidal mineralocorticoid receptor antagonist with a distinct mode of action being developed as a fixed-dose combination with the sodium-glucose cotransporter-2 inhibitor dapagliflozin for the treatment of heart failure with impaired kidney function, and chronic kidney disease. In this Phase 1 randomized open-label three-way crossover study we investigated the effect of food on balcinrenone/dapagliflozin pharmacokinetics, and the pharmacokinetics of balcinrenone when dosed with a P-glycoprotein (P-gp) inhibitor. Fourteen healthy participants were administered an oral capsule of balcinrenone/dapagliflozin 40 mg/10 mg in three dosing periods: fasted (reference), fed (high-fat, high-calorie meal) and with a P-gp inhibitor (quinidine 300 mg × 2). Balcinrenone exposure was comparable in the fed and fasted states (geometric mean ratios [GMRs] [90% CI]: maximum plasma concentration [Cmax] 1.05 [0.88, 1.25]; area under the plasma concentration-time curve from time 0 to infinity [AUCinf] 1.12 [1.06, 1.19]). In the fed state, dapagliflozin AUCinf was comparable to the fasted state (GMR [90% CI] 1.05 [1.01, 1.09]), whereas Cmax was decreased (GMR [90% CI] 0.59 [0.51, 0.69]), in line with previous dapagliflozin food interaction studies. Co-administration with quinidine increased balcinrenone exposure: GMRs (90% CI) 1.48 (1.24, 1.76) and 1.24 (1.17, 1.31) for Cmax and AUCinf, respectively, but AUC fold increase was <2, the level used for classification of sensitive P-gp substrates. All interventions were well tolerated. In conclusion, this study supports dosing of balcinrenone/dapagliflozin without regard to food. Balcinrenone is not considered a sensitive P-gp substrate. No P-gp based dosing precautions are warranted based on this study.

PMID 42687606
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