mechanisms ofaction and resistance Zanamivir inhibits viral neuraminidase and thus causes viral aggregation at the cell surface and reduced spread of virus within the respiratory tract.

In vitro resistance to zanamivir results from mutations in the viral hemagglutinin and/or neu-raminidase. Hemagglutinin variants generally have mutations in or near the receptor binding site that make them less dependent on neuraminidase for release from cells, although they typically retain some drug susceptibility. Hemagglutinin variants are cross-resistant to other neuraminidase inhibitors. Neuraminidase variants contain mutations in the enzyme active site that diminish binding of zanamivir, but the altered enzymes show reduced activity or stability. Zanamivir resistance has not emerged in immunocompetent hosts but has been seen in immunocompromised patients.


The oral bioavailability of zanamivir is low (<5%) (Table 49—3), and the drug is delivered by oral inhalation. After inhalation, ~15% is deposited in the lower respiratory tract and ~80% in the oropharynx. Overall bioavailability is <20%. The plasma t/2 of zanamivir averages 2.5—5 hours after inhalation but only 1.7 hours following intravenous dosing. Over 90% is eliminated in the urine unmetabolized.

Blood Pressure Health

Blood Pressure Health

Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...

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