| Ημερομηνία | barcode | code | περιεχομενο | τιμή παραγωγός | χονδρική | λιανική |
|---|---|---|---|---|---|---|
| 05/2018 | 2802534001014 | 253400101 | VIREAD F.C.TAB 245MG/TAB ΒΤΧ30 | 135.85 | 142.51 | 175.23 |
For use, in combination with other antiretroviral agents, for the treatment of HIV-1 infection.
Tenofovir inhibits the activity of HIV reverse transcriptase by competing with the natural substrate deoxyadenosine 5’-triphosphate and, after incorporation into DNA, by DNA chain termination. Specifically, the drugs are analogues of the naturally occurring deoxynucleotides needed to synthesize the viral DNA and they compete with the natural deoxynucleotides for incorporation into the growing viral DNA chain. However, unlike the natural deoxynucleotides substrates, NRTIs and NtRTIs (nucleoside/tide reverse transcriptase inhibitors) lack a 3'-hydroxyl group on the deoxyribose moiety. As a result, following incorporation of an NRTI or an NtRTI, the next incoming deoxynucleotide cannot form the next 5'-3' phosphodiester bond needed to extend the DNA chain. Thus, when an NRTI or NtRTI is incorporated, viral DNA synthesis is halted, a process known as chain termination. All NRTIs and NtRTIs are classified as competitive substrate inhibitors.
Limited clinical experience at doses higher than the therapeutic dose of tenofovir 300 mg is available. In Study 901 tenofovir disoproxil fumarate 600 mg was administered to 8 patients orally for 28 days. No severe adverse reactions were reported. The effects of higher doses are not known.
The oral bioavailability in fasted patients is approximately 25%. Administration of food (high fat meal containing 40 to 50% fat) increases the oral bioavailability, with an increase in the AUC of approximately 40%.
Approximately 17 hours.
* 1.3 ± 0.6 L/kg [tenofovir 1.0 mg/kg] * 1.2 ± 0.4 L/kg [tenofovir 3.0 mg/kg]