- Raw materials
- Anti-arrhythmics
- Quinidine
Filters
Filter
Custom request?
Type
Production region
Qualifications
Country of origin
Quinidine API Manufacturers & Suppliers
1 verified results
Take control of your API sourcing
Submit a Special Inquiry and have Pharmaoffer activate verified suppliers.
Commercial-scale Suppliers
Producer
Produced in
Germany|
Audit Report:
Certifications:
FDA
|
CEP|
USDMF|
coaAll certificates
FDA
CEP
USDMF
coa
Take control of your API sourcing
Submit a Special Inquiry and have Pharmaoffer activate verified suppliers.
Get full market intelligence report
€399,-
All Quinidine data. Full access. Full negotiation power
When insight is your advantage
Full data, full access, full negotiation power
Total market transparency
|
Supplier trade data access
|
Buyer / supplier flow comparison
Trusted by 30,000+ registered pharma professionals:
Reach multinationals, SMEs, compounding pharmacies & more!
Quinidine | CAS No: 56-54-2 | GMP-certified suppliers
A medication that manages atrial fibrillation/flutter, ventricular arrhythmias, and inherited cardiac rhythm disorders, offering antiarrhythmic benefits for cardiovascular therapeutic applications.
Therapeutic categories
Adrenergic AgentsAdrenergic alpha-1 Receptor AntagonistsAdrenergic alpha-AntagonistsAdrenergic AntagonistsAgents producing tachycardiaAgents that produce hypertension
Generic name
Quinidine
Molecule type
small molecule
CAS number
56-54-2
DrugBank ID
DB00908
Approval status
Approved drug, Investigational drug
ATC code
C01BA01
Primary indications
- Quinidine is indicated for the management and prophylactic therapy of atrial fibrillation/flutter, as well as the suppression of recurrent documented ventricular arrhythmias
- It is also used in the treatment of Brugada syndrome, short QT syndrome and idiopathic ventricular fibrillation
Product Snapshot
- Quinidine is available as oral tablets (including extended-release and film-coated), capsules (including gelatin-coated), solutions, and injectables for intravenous and intramuscular administration
- It is primarily used for the management and prophylaxis of atrial fibrillation/flutter, suppression of recurrent ventricular arrhythmias, and treatment of Brugada syndrome, short QT syndrome, and idiopathic ventricular fibrillation
- Quinidine is approved for use in the United States and Canada, with both approved and investigational indications
Clinical Overview
Quinidine (CAS number 56-54-2) is a naturally occurring alkaloid derived as the D-isomer of quinine, originally isolated from the bark of Cinchona tree species. It belongs to the class of cinchona alkaloids characterized by a quinoline ring system linked to an azabicyclooctane moiety. Quinidine has a well-documented history as a class Ia antiarrhythmic agent and is employed clinically in the management and prophylaxis of atrial fibrillation and flutter, as well as in the suppression of recurrent ventricular arrhythmias. Additionally, it retains specific indications for treating inherited arrhythmogenic disorders such as Brugada syndrome, short QT syndrome, and idiopathic ventricular fibrillation.
Pharmacodynamically, quinidine acts primarily by prolonging the myocardial cellular action potential duration through blockade of rapid sodium channels (I_Na) in Purkinje fibers and several potassium currents including I_Kr, I_Ks, I_K1, and I_to, along with inhibition of L-type calcium channels and late I_Na currents. These effects delay repolarization, effectively disrupting reentrant arrhythmias and abnormal automaticity. Quinidine also exhibits peripheral α-adrenergic antagonism, anticholinergic properties, and negative inotropic effects. The drug induces dose-dependent prolongation of the QT interval, which can predispose to polymorphic ventricular tachycardia such as torsades de pointes, especially in the presence of factors like bradycardia or electrolyte imbalances.
Quinidine’s antiarrhythmic mechanism is complex and not fully elucidated but is centered on interference with various cardiac ion channels to modify electrical conduction and refractoriness. The drug also retains antimalarial activity as an intra-erythrocytic schizonticide against Plasmodium vivax and P. malariae.
Safety considerations include the risk of quinidine syncope, characterized by syncope and ventricular fibrillation, as well as the potential for paradoxical ventricular rate increases in atrial arrhythmias and sinus node suppression in susceptible patients. Due to these safety concerns and its narrow therapeutic index, quinidine requires careful dosing and monitoring.
From an API sourcing and quality perspective, quinidine is classified as a narrow therapeutic index drug. Procurement should consider adherence to stringent quality standards, including impurity profiles and assay specifications to ensure batch-to-batch consistency. Given its complex pharmacology and potential for serious adverse effects, pharmaceutical manufacturers and regulatory professionals should prioritize APIs supplied under robust Good Manufacturing Practices and verified analytical characterization to support safe formulation and patient use.
Pharmacodynamically, quinidine acts primarily by prolonging the myocardial cellular action potential duration through blockade of rapid sodium channels (I_Na) in Purkinje fibers and several potassium currents including I_Kr, I_Ks, I_K1, and I_to, along with inhibition of L-type calcium channels and late I_Na currents. These effects delay repolarization, effectively disrupting reentrant arrhythmias and abnormal automaticity. Quinidine also exhibits peripheral α-adrenergic antagonism, anticholinergic properties, and negative inotropic effects. The drug induces dose-dependent prolongation of the QT interval, which can predispose to polymorphic ventricular tachycardia such as torsades de pointes, especially in the presence of factors like bradycardia or electrolyte imbalances.
Quinidine’s antiarrhythmic mechanism is complex and not fully elucidated but is centered on interference with various cardiac ion channels to modify electrical conduction and refractoriness. The drug also retains antimalarial activity as an intra-erythrocytic schizonticide against Plasmodium vivax and P. malariae.
Safety considerations include the risk of quinidine syncope, characterized by syncope and ventricular fibrillation, as well as the potential for paradoxical ventricular rate increases in atrial arrhythmias and sinus node suppression in susceptible patients. Due to these safety concerns and its narrow therapeutic index, quinidine requires careful dosing and monitoring.
From an API sourcing and quality perspective, quinidine is classified as a narrow therapeutic index drug. Procurement should consider adherence to stringent quality standards, including impurity profiles and assay specifications to ensure batch-to-batch consistency. Given its complex pharmacology and potential for serious adverse effects, pharmaceutical manufacturers and regulatory professionals should prioritize APIs supplied under robust Good Manufacturing Practices and verified analytical characterization to support safe formulation and patient use.
Identification & chemistry
| Generic name | Quinidine |
|---|---|
| Molecule type | Small molecule |
| CAS | 56-54-2 |
| UNII | ITX08688JL |
| DrugBank ID | DB00908 |
Pharmacology
| Summary | Quinidine is a class Ia antiarrhythmic agent that primarily targets cardiac sodium channels to reduce rapid depolarization and multiple potassium currents to prolong action potential duration, thereby modulating cardiac excitability and conduction. It is used to manage atrial and ventricular arrhythmias by interrupting reentrant circuits and decreasing abnormal automaticity. Additionally, quinidine has antimalarial activity as an intra-erythrocytic schizonticide against certain _Plasmodium_ species. |
|---|---|
| Mechanism of action | Quinidine has a complex electrophysiological profile that has not been fully elucidated. The antiarrhythmic actions of this drug are mediated through effects on sodium channels in Purkinje fibers. Quinidine blocks the rapid sodium channel (I<sub>Na</sub>), decreasing the phase zero of rapid depolarization of the action potential. Quinidine also reduces repolarizing K<sup>+</sup> currents (I<sub>Kr</sub>, I<sub>Ks</sub>), the inward rectifier potassium current (I<sub>K1</sub>), and the transient outward potassium current I<sub>to</sub>, as well as the L-type calcium current I<sub>Ca</sub> and the late I<sub>Na</sub> inward current. The reduction of these currents leads to the prolongation of the action potential duration. By shortening the plateau but prolonging late depolarization, quinidine facilitates the formation of early afterdepolarisation (EAD). Additionally, in patients with malaria, quinidine acts primarily as an intra-erythrocytic schizonticide, and is gametocidal to _Plasmodium vivax_ and _P. malariae_, but not to _P. falciparum_. |
| Pharmacodynamics | Quinidine is an antimalarial schizonticide, and a class Ia antiarrhythmic agent used to interrupt or prevent reentrant arrhythmias and arrhythmias due to increased automaticity, such as atrial flutter, atrial fibrillation, and paroxysmal supraventricular tachycardia. In most patients, quinidine can lead to an increase in the sinus rate. Quinidine also causes a marked prolongation of the QT interval in a dose-related manner, acts peripherally as an α-adrenergic antagonist, and has anticholinergic and negative inotropic activity. The QT interval prolongation caused by quinidine can lead to increased ventricular automaticity and polymorphic ventricular tachycardias, such as _torsades de pointes_. The risk of _torsades_ is increased by bradycardia, hypokalemia, hypomagnesemia or high serum levels of quinidine. However, this type of rhythm disturbance may appear in the absence of any of them. Patients treated with quinidine may also be at risk of a paradoxical increase in ventricular rate in atrial flutter/fibrillation, and patients with sick sinus syndrome treated with quinidine may develop marked sinus node depression and bradycardia. |
Targets
| Target | Organism | Actions |
|---|---|---|
| Sodium channel protein type 5 subunit alpha | Humans | inhibitor |
| Potassium channel subfamily K member 1 | Humans | inhibitor |
| Potassium channel subfamily K member 6 | Humans | inhibitor |
ADME / PK
| Absorption | The absolute bioavailability of quinidine sulfate is approximately 70%, but it ranges from 45% to 100%. The less-than-complete quinidine sulfate bioavailability is a result of first-pass metabolism in the liver. In contrast, the absolute bioavailability of quinidine gluconate ranges from 70% to 80%, and relative to quinidine sulfate, quinidine from quinidine gluconate has a bioavailability of 1.03. The t<sub>max</sub> of quinidine sulfate extended-release tablets is approximately 6 h, while the t<sub>max</sub> of quinidine gluconate goes from 3 to 5 h. The peak serum concentration reached with immediate-release quinidine sulfate is delayed for about an hour when taken with food. Furthermore, the ingestion of grapefruit juice may decrease the rate of absorption of quinidine. |
|---|---|
| Half-life | The elimination half-life of quinidine is 6-8 hours in adults and 3-4 hours in pediatric patients. |
| Protein binding | From 6.5 to 16.2 µmol/L, 80 to 88% of quinidine is bound to plasma proteins, mainly α1-acid glycoprotein and albumin. This fraction is lower in pregnant women, and it may be as low as 50 to 70% in infants and neonates. |
| Metabolism | Quinidine is mainly metabolized in the liver by cytochrome P450 enzymes, specifically CYP3A4. The major metabolite of quinidine is 3-hydroxy-quinidine, which has a volume of distribution larger than quinidine and an elimination half-life of about 12 hours. Non-clinical and clinical studies suggest that 3-hydroxy-quinidine has approximately half the antiarrhythmic activity of quinidine; therefore, this metabolite is partly responsible for the effects detected with the chronic use of quinidine. |
| Route of elimination | The elimination of quinidine is achieved by the renal excretion of the unchanged drug (15 to 40% of total clearance) and its hepatic biotransformation to a variety of metabolites (60 to 85% of total clearance). When urine has a pH lower than 7, 20% of administered quinidine appears in urine unchanged. However, this proportion decreases to as little as 5% as it becomes more alkaline. The renal clearance of quinidine involves both glomerular filtration and active tubular secretion, moderated by pH-dependent tubular reabsorption. |
| Volume of distribution | Quinidine has a volume of distribution of 2-3 L/kg in healthy young adults, 0.5 L/kg in patients with congestive heart failure, and 3-5 L/kg in patients with liver cirrhosis. |
| Clearance | The clearance of quinidine ranges from 3 to 5 mL/min/kg in adults. In pediatric patients, quinidine clearance may be two or three times as rapid. |
Formulation & handling
- Quinidine is formulated for oral administration in tablet and capsule forms as well as for parenteral use via intravenous and intramuscular routes.
- As a small molecule cinchona alkaloid, quinidine exhibits moderate water solubility and lipophilicity (LogP 2.51), relevant for formulation strategies.
- Managing potential drug-food interactions is important, particularly with grapefruit products and antacids, due to effects on absorption and metabolism.
Regulatory status
| Lifecycle | The active pharmaceutical ingredient has multiple patents expiring between 2016 and 2026 in the United States, indicating a transition towards generic availability in this region. The product is currently marketed in both the United States and Canada. |
|---|
| Markets | Canada, US |
|---|
Supply Chain
| Supply chain summary | The manufacturing landscape for quinidine includes multiple originator and generic manufacturers, reflecting a diverse supplier base with both branded and generic products. Branded quinidine products are primarily marketed in the US and Canada, while global presence beyond these regions is limited. Patent expirations as recent as 2026 indicate ongoing potential for generic competition in the near future. |
|---|
Safety
| Toxicity | Quinidine overdoses have been well described. The ingestion of 5 g of quinidine resulted in the death of a toddler, while an adolescent was reported to survive after ingesting 8 g of quinidine. A 16-month that ingested quinidine tablets developed a concretion of bezoar in the stomach, which led to non-declining toxic levels of quinidine. A gastric aspirate revealed that quinidine levels were 50 times higher than the ones detected in plasma. In cases of massive overdose, it may be appropriate to perform an endoscopy. Acute quinidine overdoses are characterized by ventricular arrhythmias and hypotension. Other signs and symptoms of quinidine overdose may include vomiting, diarrhea, tinnitus, high-frequency hearing loss, vertigo, blurred vision, diplopia, photophobia, headache, confusion and delirium. |
|---|
High Level Warnings:
- Quinidine exhibits significant toxicity in overdose, with reported fatalities at ingestions of 5 g or more
- Exposure may result in severe cardiac arrhythmias, hypotension, and neurotoxic symptoms including confusion and hearing loss
- In cases of massive overdose, residual gastrointestinal concretions may lead to persistently elevated quinidine levels, potentially requiring endoscopic intervention
Quinidine is a type of Anti-arrhythmics
Anti-arrhythmics belong to the pharmaceutical API category designed to treat irregular heart rhythms, also known as arrhythmias. These medications work by targeting the electrical signals in the heart, helping to regulate the heart's rhythm and restore it to a normal, steady beat.
Anti-arrhythmics are crucial in managing various types of arrhythmias, such as atrial fibrillation, ventricular tachycardia, and supraventricular tachycardia. These conditions can pose serious risks, including an increased likelihood of stroke or heart failure. Hence, anti-arrhythmics play a vital role in improving patient outcomes and reducing these associated risks.
Pharmaceutical companies develop anti-arrhythmic APIs, which are the active ingredients used to formulate the final medications. These APIs undergo rigorous testing and quality control measures to ensure their safety, efficacy, and consistent performance. They are manufactured in accordance with Good Manufacturing Practices (GMP) guidelines to meet the highest quality standards.
Healthcare professionals prescribe anti-arrhythmics based on the specific arrhythmia type, severity, and individual patient factors. These APIs can be formulated into different dosage forms, including tablets, capsules, or intravenous solutions, depending on the desired route of administration and patient requirements.
It is important to note that anti-arrhythmics are prescription-only medications and should only be used under medical supervision. Patients using these medications must follow their healthcare provider's instructions and regularly monitor their heart rhythm to ensure optimal treatment effectiveness and minimize potential side effects.
In conclusion, anti-arrhythmics are a crucial category of pharmaceutical APIs used to treat various types of irregular heart rhythms. They are formulated into medications that help regulate the heart's electrical signals, reduce associated risks, and improve patient outcomes.
Quinidine API manufacturers & distributors
Compare qualified Quinidine API suppliers worldwide. We currently have 1 companies offering Quinidine API, with manufacturing taking place in 1 different countries. Use the table below to review supplier type, countries of origin, certifications, product portfolio and GMP audit availability.
| Supplier | Type | Country | Product origin | Certifications | Portfolio |
|---|---|---|---|---|---|
| Buchler | Producer | Germany | Germany | CEP, CoA, FDA, USDMF | 2 products |
When sending a request, specify which Quinidine API quality you need: for example EP (Ph. Eur.), USP, JP, BP, or another pharmacopoeial standard, as well as the required grade (base, salt, micronised, specific purity, etc.).
Use the list above to find high-quality Quinidine API suppliers. For example, you can select GMP, FDA or ISO certified suppliers. Visit our help page to learn more about sourcing APIs via Pharmaoffer.
