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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

PubMedScience advances2026-10-14

Bisulfate-mediated selective methane oxidation under mild aqueous conditions.

Lu Shike S, Wen Shao-Chun SC, Liu Wenxuan W, Li Haonan H et al.

The selective oxidation of methane under mild conditions remains a formidable challenge because of the inert C─H bond and the ease of over-oxidation. Here we report a facile strategy that enables methane conversion at room temperature and ambient pressure using molecular O2 and commercially available Cu powder in dilute aqueous H2SO4. The reaction is capable of proceeding with only trace CO2 formation, producing methyl bisulfate and methanol as the primary partial oxidation products. In situ Raman spectroscopy indicates that an in situ O2-derived Cu2O surface is the reaction-relevant phase associated with C─H bond activation. The observed selectivity arises from bisulfate adsorption on this Cu2O surface, which suppresses methanol over-oxidation, together with the interception of surface-generated methyl intermediates to form oxidation-resistant methyl bisulfate. This Cu/O2-H2SO4 system demonstrates that methane can be selectively oxidized under mild aqueous conditions and provides mechanistic insight into Cu/O2-mediated oxidation, suggesting a bisulfate-assisted approach to suppressing over-oxidation that may be applicable to other substrates.

PMID 42873888
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PubMedThe Journal of pharmacology and experimental therapeutics2026-10-14

Locomotor stimulant and methamphetamine-like interoceptive effects of putative impurity N-ethyl-methamphetamine in rodents: Role of Phase I metabolism.

Gannon Brenda M BM, Pressley Justin M JM, Fomin Andriy A, Rowe Sierra S et al.

Over the past 20 years, N-ethyl-methamphetamine (NEM) has been identified in seized methamphetamine (METH) samples. Often considered a byproduct or impurity of illicit METH synthesis, its structural similarity to METH suggests that it may have pharmacological actions of its own or be metabolically converted to METH or amphetamine (AMPH) in vivo. These studies assessed the potency and effectiveness of NEM as a locomotor stimulant compared to METH in NIH Swiss mice, and probed the role of cytochrome P450 (CYP) vs non-CYP metabolism in these locomotor effects using pretreatments with the broad spectrum CYP inhibitor 1-aminobenzotriazole (1-ABT) or the selective CYP2D6 inhibitor quinidine. Blood samples taken from mice treated with NEM, with and without pretreatments of 1-ABT or quinidine, were quantitively analyzed for NEM, METH, and AMPH using Quadrupole Time-of-Flight. Additionally, the discriminative stimulus effects of NEM were assayed in Sprague-Dawley rats trained to discriminate METH from saline. NEM produced dose-dependent locomotor stimulant and METH-like interoceptive effects, but with a slower onset and less potently than METH. Locomotor stimulant effects of NEM were abolished by pretreatment with 1-ABT or quinidine, and both pretreatments also decreased conversion of NEM to METH and AMPH in mouse blood. These data demonstrate METH-like biological effects of NEM and suggest that the likely mechanism for these effects is metabolic conversion of NEM to METH and AMPH via CYP2D6. NEM thus functions as a prodrug for METH and AMPH, and would be expected to have METH-like abuse liability in humans. SIGNIFICANCE STATEMENT: N-ethyl-methamphetamine (NEM) has been identified in seized methamphetamine (METH) samples, and is typically considered a byproduct or impurity of illicit METH synthesis. These studies demonstrate METH-like biological effects of NEM and suggest that the likely mechanism for these effects is metabolic conversion of NEM to METH and AMPH via CYP2D6. NEM thus functions as a prodrug for METH and AMPH, and would be expected to have METH-like abuse liability in humans.

PMID 42874276
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PubMedGenes2026-09-26

Drug Repositioning Based on Single-Cell Transcriptomics Data Identifies Quinidine as a Potential Drug for Treating Osteoporosis.

Wang Rong R, Li Jia-Li JL, Liu Kun K, Lu Xuan X et al.

Osteoporosis (OP) is characterized by low bone mass and impaired bone microarchitecture, and the long-term use of current therapies is limited by adverse effects and poor adherence. This study sought to identify drugs that could be repurposed for glucocorticoid-induced osteoporosis. Single-cell RNA-sequencing data from two subjects with osteoporotic fractures and three control subjects were analyzed to identify transcriptional changes in osteoblasts. Candidate drugs were screened using ASGARD and L1000 drug-response signatures. Two-sample Mendelian randomization was used to examine associations between genetically predicted expression of drug-target genes and osteoporosis risk. Quinidine was tested in dexamethasone-treated Tu and Tg(Ola.Sp7:nlsGFP) zebrafish larvae using Alizarin Red staining, fluorescence imaging, and qRT-PCR. Adult zebrafish were assessed by micro-CT. Four candidate drugs were identified, of which quinidine was selected for experimental evaluation. Genetically predicted SCN5A expression was positively associated with osteoporosis risk. Quinidine partially restored cranial mineralization in dexamethasone-treated larvae, with the greatest effect at 10 μmol/L; the 100 μmol/L treatment was less effective. Quinidine also altered the expression of several bone-remodeling-related genes. In adult zebrafish, quinidine treatment was associated with higher bone mineral density and bone volume fraction than dexamethasone treatment alone. Quinidine alleviated several dexamethasone-induced skeletal phenotypes in zebrafish and represents a candidate for further drug-repurposing studies in osteoporosis. Direct validation of its molecular mechanism and safety profile is still required.

PMID 42792954
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PubMedJournal of veterinary pharmacology and therapeutics2026-09-24

Preliminary Comparison of Competitive Efflux and Historical Transwell Assays for Assessing Canine P-Glycoprotein Substrate Status of Eleven Drugs Representing Ten Different Drug Classes.

Mealey K L KL, Burke N S NS

Because P-glycoprotein (P-gp) influences the disposition of substrate drugs, regulatory agencies recommend ascertaining the P-gp substrate status of active pharmaceutical ingredients (API's) intended for humans. Transwell-based assays using P-gp-overexpressing human cell lines are routinely used to predict the API's P-gp substrate status. Although ABCB1-1Δ-mediated P-gp deficiency contributes to serious canine adverse drug reactions, assessment of canine P-gp status is not currently recommended by regulatory agencies for canine API's. We have previously employed a competitive efflux assay to assess drugs as canine P-gp substrates as it affords some advantages over transwell assays. Our objective was to preliminarily compare results generated from these two methods using historical data for transwell assays. Eleven drugs were assessed as canine P-gp substrates by both methods, with two identified as non-P-gp substrates (erythromycin, propranolol) and nine identified as canine P-gp substrates (clarithromycin, daunorubicin, digoxin, etoposide, paclitaxel, quinidine, ritonavir, verapamil, vinblastine). Erythromycin was identified as a canine P-gp substrate by competitive efflux assay at roughly 10-fold higher concentrations than was used for transwell assays. Concordance of these methods assessing canine P-gp substrate status using historical data supports the need for head-to-head studies comparing these two methods for identifying canine P-gp substrates.

PMID 42779004
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PubMedJACC. Case reports2026-09-23

Malignant Early Repolarization Syndrome Unmasked by Acute Respiratory Distress Syndrome in a Young Adult.

Sah Shiva S, Doshi Preet P, Bhandari Jenish J, Chapagain Himal H et al.

Early repolarization syndrome (ERS) is an important cause of idiopathic ventricular fibrillation (VF) in structurally normal hearts and may be exacerbated by systemic stressors. A previously healthy 24-year-old man presented with out-of-hospital VF arrest. Coronary angiography and cardiac magnetic resonance imaging showed no structural disease. His course was complicated by aspiration pneumonia and acute respiratory distress syndrome. He developed recurrent VF triggered by short-coupled premature ventricular complexes during hypoxemia and hypokalemia. An electrocardiogram demonstrated inferolateral J-point elevation >0.2 mV. Quinidine and isoproterenol suppressed further arrhythmias, and a subcutaneous implantable cardioverter-defibrillator was placed for secondary prevention. He remained arrhythmia-free at follow-up. ERS-related repolarization heterogeneity predisposes to VF. Acute respiratory distress syndrome and associated metabolic stress may amplify this arrhythmogenic substrate. ERS should be considered in young patients with unexplained VF. Recognition of triggers, targeted therapy, and implantable cardioverter-defibrillator placement are essential.

PMID 42776113
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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.

Wernli Cedric C, Loesch Uli U

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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