Chemical formula: C₂₃H₁₆O₁₁ Molecular mass: 468.367 g/mol PubChem compound: 2882
Sodium cromoglicate inhibits the activation of many of the cell types involved in the development and progression of asthma. Thus, sodium cromoglicate inhibits the release of inflammatory mediators including cytokines from mast cells and reduces the chemotactic activity of eosinophils and neutrophils. Activation of and mediator release from monocytes and macrophages in vitro is also reduced by sodium cromoglicate.
The diverse range of activities of the drug may be explained by the ability of sodium cromoglicate to block chloride channels in different cell types which are important in cell activation.
In acute bronchial provocation tests in humans, sodium cromoglicate has been shown to inhibit or diminish the asthmatic reaction to antigen, exercise and to a range of non-specific triggers including cold air, sulphur dioxide, hypertonic saline and bradykinin. Antigen-induced increased bronchial hyperactivity to histamine is prevented and a reduction in bronchial mucus eosinophils and antigen-specific IgE occurs after 4 weeks treatment of asthmatic subjects with sodium cromoglicate.
The solution exerts its effect locally in the eye.
In vitro and in vivo animal studies have shown that sodium cromoglicate inhibits the degranulation of sensitised mast cells which occurs after exposure to specific antigens. Sodium cromoglicate acts by inhibiting the release of histamine and various membrane derived mediators from the mast cell.
Sodium cromoglicate has demonstrated the activity in vitro to inhibit the degranulation of non-sensitised rat mast cells by phospholipase A and subsequent release of chemical mediators. Sodium cromoglicate did not inhibit the enzymatic activity of released phospholipase A on its specific substrate.
Sodium cromoglicate has no intrinsic vasoconstrictor or antihistamine activity.
Sodium cromoglicate is poorly absorbed. When multiple doses of sodium cromoglicate ophthalmic solution are instilled into normal rabbit eyes, less than 0.07% of the administered dose of sodium cromoglicate is absorbed into the systemic circulation (presumably by way of the eye, nasal passages, buccal cavity and gastrointestinal tract). Trace amounts (less than 0.01%) of the sodium cromoglicate does penetrate into the aqueous humour and clearance from this chamber is virtually complete within 24 hours after treatment is stopped.
In normal volunteers, analysis of drug excretion indicates that approximately 0.03% of sodium cromoglicate is absorbed following administration to the eye.
After inhalation in man via a metered dose inhaler approximately 10% of a dose of sodium cromoglicate is absorbed from the respiratory tract. The remainder is either exhaled or deposited in the oropharynx, or swallowed and eliminated via the alimentary tract, as only a small amount (1%) of the dose is absorbed from the gastrointestinal tract. The rate of absorption of sodium cromoglicate from the respiratory tract is slower than the elimination rate (t½ of 1.5-2h). Hence, the drug remains effectively in the lungs to produce its local therapeutic effect and is then cleared rapidly from the systemic circulation. No substantial increase in plasma concentration occurs during repeated dose therapy.
Sodium cromoglicate is moderately and reversibly bound to plasma proteins (≈65%) and is not metabolised in humans. It is excreted unchanged in both urine and bile in approximately equal proportions.
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