| Systematic (IUPAC) name | |
|---|---|
| (RS)-N-{4-[1-hydroxy-2-(propan-2-ylamino)ethyl]phenyl}methanesulfonamide | |
| Clinical data | |
| Trade names | Betapace |
| AHFS/Drugs.com | monograph |
| MedlinePlus | a693010 |
| Pregnancy cat. | B(US) |
| Legal status | ℞ Prescription only |
| Routes | oral |
| Pharmacokinetic data | |
| Bioavailability | >95% |
| Metabolism | Not metabolized |
| Half-life | 12 hours |
| Excretion | Renal Lactic (In lactating females) |
| Identifiers | |
| CAS number | 3930-20-9 |
| ATC code | C07AA07 |
| PubChem | CID 5253 |
| DrugBank | DB00489 |
| ChemSpider | 5063 |
| UNII | A6D97U294I |
| KEGG | D08525 |
| ChEMBL | CHEMBL471 |
| Chemical data | |
| Formula | C12H20N2O3S |
| Mol. mass | 272.3624 g/mol |
| SMILES | eMolecules & PubChem |
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Sotalol is a drug used in individuals with rhythm disturbances (cardiac arrhythmias) of the heart, and to treat hypertension in some individuals. It is a non-selective competitive β-adrenergic receptor blocker that also exhibits Class III antiarrhythmic properties by its inhibition of potassium channels.[1][2] Because of this dual action, Sotalol prolongs both the PR interval and the QT interval. Originally discovered around 1960, sotalol became widely used first as a β-blocker in the 1980s, and its function as an antiarrhythmic drug was discovered soon after.[3] Due to the dual action of sotalol, it is often used preferentially to other β-blockers as treatment for both ventricular fibrillation and ventricular tachycardia.[1][4]
Trade names for Sotalol include Betapace and Betapace AF (Berlex Laboratories), and Sotalex and Sotacor (Bristol-Myers Squibb).
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Sotalol is used to treat ventricular tachycardias[5] as well as atrial fibrillation.[6] Betapace AF is specifically labeled for atrial fibrillation.
Some evidence suggests that sotalol should be avoided in the setting of decreased ejection fraction due to an increased risk of death.[7]
It has also been suggested that it be used in the prevention of atrial fibrillation.[8]
Ventricular fibrillation is an uncontrolled and asynchronous series of contractions of the ventricles resulting in poor cardiac output. It is often associated with factors that affect the electrical signal for contraction and trigger a premature contraction before complete relaxation.[9] Ventricular tachycardia is closely associated with ventricular fibrillation and is an abnormally high rate of contraction from the ventricles often resulting from increased intracellular calcium levels. This increase in cytosolic calcium leads to an increase in calcium release from the sarcoplasmic reticulum, which increases rate of contraction by providing more calcium for interaction with force-generating filaments in the muscle cell for a prolonged period of time.[10]
Sotalol non-selectively binds to both β1- and β2-adrenergic receptors preventing activation of the receptors by their stimulatory ligand1. Without the binding of this ligand to the receptor, the G-protein complex associated with the receptor cannot activate production of cyclic AMP, which is responsible for turning on calcium inflow channels.[11] A decrease in activation of calcium channels will therefore result in a decrease in intracellular calcium. In cardiac cells, calcium is important in generating electrical signals for contraction, as well as generating force for contraction.[12] In consideration of these important properties of calcium, two conclusions can be drawn. Firstly, with less calcium in the cell, there is a decrease in electrical signals for contraction, thus allowing time for the heart’s natural pacemaker to rectify arrhythmic contractions3. Secondly, lower calcium means a decrease in strength and rate of the contractions, which can be helpful in treatment of abnormally high heart rates in patients with tachycardia3.
Sotalol also acts on potassium channels and causes a delay in relaxation of the ventricles2. By blocking these potassium channels, sotalol inhibits efflux of K+ ions, which results in an increase in the time before another electrical signal can be generated in ventricular myocytes8. This increase in the period before a new signal for contraction is generated, helps to correct arrhythmias by reducing the potential for premature or abnormal contraction of the ventricles but also prolongs the frequency of ventricular contraction to help treat tachycardia.
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