RINOFLUIMUCIL 1% + 0.5% Nasal Spray
N-Acetylcysteine, Tuaminoheptane sulphate
(1% + 0.5%)
ZAMBON SpA
| Pack size | 1 Amber-Glass bottle (10ml) |
|---|---|
| Dispensing mode | POM |
| Source | ITALY |
| Agent | New Country Healthcare L.L.C. |
| Retail Price | 22.00 AED |
Indications
RINOFLUIMUCIL 1% + 0.5% Nasal Spray is used for:
Acetylcysteine
Acetylcysteine is used mainly as a mucolytic and in the management of paracetamol (acetaminophen) overdose.
Acetylcysteine is used mainly as a mucolytic and in the management of paracetamol (acetaminophen) overdose.
Adult Dose
Child Dose
Renal Dose
Administration
Contra Indications
Precautions
Pregnancy-Lactation
Interactions
Adverse Effects
Side effects of N-Acetylcysteine, Tuaminoheptane sulphate :
Mechanism of Action
Acetylcysteine
Acetylcysteine protects against acetaminophen overdose-induced hepatotoxicity by maintaining or restoring hepatic concentrations of glutathione. It does this by producing the glutathione precursor L-cysteine. Glutathione is required to inactivate an intermediate metabolite (N-acetyl-p-benzoquinoneimine or NAPQI) of acetaminophen that is thought to be hepatotoxic. In acetaminophen overdose cases, excessive quantities of this metabolite are formed because the primary metabolic (glucuronide and sulfate conjugation) pathways become saturated. Acetylcysteine may act by reducing the metabolite to the parent compound and/or by providing sulfhydryl for conjugation of the metabolite. Experimental evidence also suggests that a sulfhydryl-containing compound such as acetylcysteine may also directly inactivate the metabolite. The mechanisms of action for acetylcysteineFs well-known mucolytic effects are different. In particular, when inhaled, acetylcysteine (and its metabolic byproduct cysteine) exerts its mucolytic action through its free sulfhydryl group, which reduces the disulfide bonds in the mucus matrix and lowers mucus viscosity. This action increases with increasing pH and is most significant at pH 7 to 9. The mucolytic action of acetylcysteine is not affected by the presence of DNA. Acetylcysteine is also an antioxidant and reduces oxidative stress. Acetylcysteine serves as a prodrug to L-cysteine which is a precursor to the biologic antioxidant, glutathione and hence administration of acetylcysteine replenishes glutathione stores. L-cysteine also serves as a precursor to cystine which in turn serves as a substrate for the cystine-glutamate antiporter on astrocytes hence increasing glutamate release into the extracellular space. This glutamate in turn acts on mGluR2/3 receptors, and at higher doses of acetylcysteine, mGluR5. Glutathione also modulates the NMDA receptor by acting at the redox site. These effects on glutamate and NMDA signaling appear to explain some of the positive neuropsychotropic effects associated with NAC. Acetylcysteine also possesses some anti-inflammatory effects possibly via inhibiting NF-?B through redox activation of the nuclear factor kappa kinases thereby modulating cytokine synthesis.
Acetylcysteine protects against acetaminophen overdose-induced hepatotoxicity by maintaining or restoring hepatic concentrations of glutathione. It does this by producing the glutathione precursor L-cysteine. Glutathione is required to inactivate an intermediate metabolite (N-acetyl-p-benzoquinoneimine or NAPQI) of acetaminophen that is thought to be hepatotoxic. In acetaminophen overdose cases, excessive quantities of this metabolite are formed because the primary metabolic (glucuronide and sulfate conjugation) pathways become saturated. Acetylcysteine may act by reducing the metabolite to the parent compound and/or by providing sulfhydryl for conjugation of the metabolite. Experimental evidence also suggests that a sulfhydryl-containing compound such as acetylcysteine may also directly inactivate the metabolite. The mechanisms of action for acetylcysteineFs well-known mucolytic effects are different. In particular, when inhaled, acetylcysteine (and its metabolic byproduct cysteine) exerts its mucolytic action through its free sulfhydryl group, which reduces the disulfide bonds in the mucus matrix and lowers mucus viscosity. This action increases with increasing pH and is most significant at pH 7 to 9. The mucolytic action of acetylcysteine is not affected by the presence of DNA. Acetylcysteine is also an antioxidant and reduces oxidative stress. Acetylcysteine serves as a prodrug to L-cysteine which is a precursor to the biologic antioxidant, glutathione and hence administration of acetylcysteine replenishes glutathione stores. L-cysteine also serves as a precursor to cystine which in turn serves as a substrate for the cystine-glutamate antiporter on astrocytes hence increasing glutamate release into the extracellular space. This glutamate in turn acts on mGluR2/3 receptors, and at higher doses of acetylcysteine, mGluR5. Glutathione also modulates the NMDA receptor by acting at the redox site. These effects on glutamate and NMDA signaling appear to explain some of the positive neuropsychotropic effects associated with NAC. Acetylcysteine also possesses some anti-inflammatory effects possibly via inhibiting NF-?B through redox activation of the nuclear factor kappa kinases thereby modulating cytokine synthesis.
Note
RINOFLUIMUCIL 1% + 0.5% (1% + 0.5%) Nasal Spray manufactured by ZAMBON SpA. Its generic name is N-Acetylcysteine, Tuaminoheptane sulphate. RINOFLUIMUCIL 1% + 0.5% is availble in United Arab Emirates.
Farmaco UAE drug index information on RINOFLUIMUCIL 1% + 0.5% Nasal Spray is not intended for diagnosis, medical advice or treatment; neither intended to be a substitute for the exercise of professional judgment.