ACTEIN Effervescent Tablet

Reduce the viscosity of the secretion from respirectory tract.

Antidotes for acute poisoning: Acetaminophen overdosage.

Dosage and administration

Adults and children over 6 years of aged:

Dissolve effervescent tablets 600mg in about half a glass of water, 1-2 times daily, avoid the addition of drugs to the solution, take it before or after meals.

No unusual severe type of toxicity has been reported from the prescription experience of Actein oral: slight gastrointestinal disturbances (nausea, dyspepsia, pyrosis) have occurred occasionally.

The sulfur odour on opening the sachets does not indicate deterioration of the product, but is due to the active ingredient.

Actein can be administered concurrently with such antibiotics as amoxycillin, doxycillin, doxycyclin, thiamphenicol.

When other oral antibiotics or drugs are required, they should be administered1-2 hours apart from Actein in order to avoid possible interaction with thiol group.

The N-acetylcysteine (NAC) is the N-acetyl derivative of the naturally occurring amino acid L-cysteine. NAC has an intense fluidifying action, through its free sulfydryl group, on the mucoid or mucopurulent secretions by cleaving the intramolecular and intermolecular disulfide bonds in glycoprotein aggregates.

NAC is stable in simulated gastric and intestinal fluid, is rapidly absorbed after oral administration, and distributed to body tissues including the lung.

Acute toxicity, chronic toxicity, teratology and reproduction studies support oral NAC safety. Coagulation parameters, platelet aggregation, immunoglobulins (serum and sputum IgA), hematological, hepatic and renal laboratory indices remained unchanged after oral NAC administration.

Acetylcysteine is considered to reduce the hepatic toxicity, the highly reactive intermediate metabolite following ingestion of a high dose of paracetamol, by at least two mechanisms. First, acetylcysteine acts as a precursor for the synthesis of glutathione and, therefore, maintains cellular glutathione at a level sufficient to inactivate NAPQI. This is thought to be the main mechanism by which acetylcysteine acts in the early stages of paracetamol toxicity.