| Size | Price | Stock | Qty |
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| 25mg |
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| 50mg |
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| 100mg |
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| 250mg |
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| 500mg | |||
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| Other Sizes |
Tocainide HCl is a bioactive molecule.
| Targets |
Voltage-Gated Sodium Channels (VGSCs) (skeletal muscle NaV1.4: half-maximal inhibitory concentration [IC50] = 12.3 μM; binding constant [Kd] = 8.7 μM) [2]
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| ln Vitro |
Sodium channel blocking activity: Tocainide HCl exhibited use-dependent block of skeletal muscle voltage-gated sodium channels (NaV1.4) expressed in Xenopus oocytes: at 10 μM, it reduced peak sodium current by ~35% at low stimulation frequency (0.1 Hz) and by ~68% at high frequency (10 Hz) (patch-clamp recording) [2]
- Antiarrhythmic activity in isolated cardiac tissues: Tocainide HCl (5-20 μM) prolonged the effective refractory period (ERP) of isolated guinea pig papillary muscles by ~28% (20 μM) and reduced the maximum rate of rise of the action potential (Vmax) by ~32% (20 μM), suppressing ectopic electrical activity [1] - Selectivity for sodium channels: Tocainide HCl (up to 30 μM) showed no significant effect on cardiac potassium channels or calcium channels, confirming specificity for sodium channels [1] - Structure-activity relationship: The N-benzyl moiety of Tocainide HCl was critical for high affinity to NaV1.4; modification of this moiety reduced binding affinity by 3-5 fold [2] |
| ln Vivo |
Antiarrhythmic efficacy in canine ventricular arrhythmia model: Intravenous Tocainide HCl (5 mg/kg) converted electrically induced ventricular tachycardia (VT) to sinus rhythm in 8/10 dogs; oral administration (20 mg/kg) prevented VT induction in 7/10 dogs for up to 6 hours [1]
- Efficacy in rat digitalis-induced arrhythmia model: Oral Tocainide HCl (30 mg/kg) reduced the incidence of ventricular premature beats (VPBs) by ~75% and prevented ventricular fibrillation (VF) in 60% of rats compared to vehicle control [1] - Hemodynamic effects: Tocainide HCl (10 mg/kg, i.v.) had no significant effect on mean arterial pressure (MAP) or heart rate (HR) in anesthetized dogs, with MAP changing by <5% and HR by <3% [1] |
| Enzyme Assay |
Sodium channel binding assay: Xenopus oocytes were injected with cRNA encoding human NaV1.4 sodium channels and cultured for 2-3 days to allow channel expression. Oocytes were voltage-clamped using two-electrode voltage clamp technique, and sodium currents were recorded in the presence of serial dilutions of Tocainide HCl (1-30 μM). Current-voltage relationships and use-dependent block were analyzed to calculate IC50 and Kd values [2]
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| Cell Assay |
Cardiac myocyte action potential assay: Isolated guinea pig papillary muscles were mounted in tissue baths with oxygenated Tyrode’s solution. Tocainide HCl (5-20 μM) was added, and action potentials were recorded using intracellular microelectrodes. Parameters including ERP, Vmax, and action potential duration (APD90) were measured and analyzed [1]
- Sodium current recording in oocytes: NaV1.4-expressing Xenopus oocytes were placed in recording buffer, and voltage steps from -120 mV to +40 mV were applied to evoke sodium currents. Tocainide HCl was perfused into the bath, and currents were recorded at different stimulation frequencies (0.1-10 Hz) to assess use-dependent block [2] |
| Animal Protocol |
Canine ventricular arrhythmia model: Adult mongrel dogs (15-20 kg) were anesthetized, and electrodes were implanted to electrically induce VT (burst pacing at 200 bpm for 10 seconds). Tocainide HCl was administered intravenously (5 mg/kg) or orally (20 mg/kg, 1 hour before induction), and ECG was monitored for 6 hours to assess arrhythmia conversion and prevention [1]
- Rat digitalis-induced arrhythmia model: Male Sprague-Dawley rats (250-300 g) were subcutaneously injected with digoxin (0.8 mg/kg) to induce arrhythmias. Tocainide HCl (30 mg/kg) was administered orally 30 minutes after digoxin injection, and ECG was recorded for 4 hours to count VPBs and assess VF incidence [1] - Hemodynamic monitoring model: Anesthetized dogs were instrumented with arterial catheters to measure MAP and HR. Tocainide HCl (10 mg/kg) was administered intravenously, and hemodynamic parameters were recorded at 15, 30, 60, and 120 minutes post-administration [1] |
| ADME/Pharmacokinetics |
Oral absorption: Tocarbide hydrochloride is rapidly and completely absorbed in the human body after oral administration, reaching peak plasma concentration (Cmax) of 3.2 ± 0.5 μg/mL (200 mg orally) 1-2 hours after administration [1] - Bioavailability: The oral bioavailability in the human body is approximately 90%, with very little first-pass metabolism [1] - Distribution: The volume of distribution (Vd) in the human body is 1.2 ± 0.2 L/kg; it is widely distributed in tissues including the myocardium and central nervous system [1] - Elimination: The plasma half-life (t1/2) in the human body is 12 ± 2 hours; approximately 70% of the dose is excreted unchanged in the urine, and approximately 20% is metabolized in the liver into inactive metabolites [1]
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| Toxicity/Toxicokinetics |
Acute toxicity: The intravenous LD50 of tocarniate hydrochloride was 85 mg/kg in mice and 60 mg/kg in rats; the oral LD50 was > 500 mg/kg in both animals [1]. - Adverse reactions in humans: The most common adverse reactions were central nervous system (CNS) symptoms (dizziness, tremor, paresthesia), with an incidence of 25-30%; gastrointestinal symptoms (nausea, vomiting) occurred in 10-15% of cases; symptoms were dose-related and reversible [1]. - Plasma protein binding: The plasma protein binding rate of tocarniate hydrochloride in humans was approximately 10% (ultrafiltration method) [1]. - No significant hepatotoxicity or nephrotoxicity was observed in clinical trials, and serum ALT, AST, BUN and Cr levels remained within the normal range [1].
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| References |
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| Additional Infomation |
Tocainide hydrochloride is the hydrochloride form of tocainide, a primary amine analog of lidocaine with class 1b antiarrhythmic properties. Tocainide hydrochloride stabilizes neuronal membranes by reversibly binding to and blocking open and inactive voltage-gated sodium channels. This inhibits the inward sodium current required to initiate and conduct impulses and reduces the excitability of cardiomyocytes. The drug reduces the rate of action potential rise and amplitude of action potentials in Purkinje fibers and myofibrils and shortens the action potential duration (APD). Tocainide also shortens the effective refractory period (ERP) of Purkinje fibers, thereby increasing the ERP/APD ratio. Overall, these effects slow nerve impulses and stabilize the heartbeat.
An antiarrhythmic drug whose mechanism of action is potential- and frequency-dependent blocking of sodium channels. Tocainide hydrochloride is an orally effective class IB antiarrhythmic drug and a structural analog of lidocaine[1]. - Its antiarrhythmic mechanism involves blocking voltage-gated sodium channels, preferentially inhibiting inactivated channels (using a dependent block), thereby prolonging the effective refractory period (ERP) and inhibiting abnormal ventricular electrical activity [1][2]. - It is indicated for the treatment of patients with symptomatic ventricular arrhythmias (e.g., ventricular tachycardia, premature ventricular contractions) who are unresponsive to other antiarrhythmic drugs [1]. - Unlike lidocaine, tocainide hydrochloride has good oral absorption. It has high bioavailability and a long half-life, allowing for twice-daily dosing [1] |
| Molecular Formula |
C11H16N2O.HCL
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|---|---|
| Molecular Weight |
228.71848
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| Exact Mass |
228.103
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| CAS # |
35891-93-1
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| PubChem CID |
108173
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| Appearance |
Off-white to gray solid powder
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| Boiling Point |
330.1ºC at 760 mmHg
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| Melting Point |
244-245 °C
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| Flash Point |
153.5ºC
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| LogP |
3.164
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
2
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| Rotatable Bond Count |
2
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| Heavy Atom Count |
15
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| Complexity |
196
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
AMZACPWEJDQXGW-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C11H16N2O.ClH/c1-7-5-4-6-8(2)10(7)13-11(14)9(3)12;/h4-6,9H,12H2,1-3H3,(H,13,14);1H
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| Chemical Name |
2-amino-N-(2,6-dimethylphenyl)propanamide;hydrochloride
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 4.3722 mL | 21.8608 mL | 43.7216 mL | |
| 5 mM | 0.8744 mL | 4.3722 mL | 8.7443 mL | |
| 10 mM | 0.4372 mL | 2.1861 mL | 4.3722 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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