| Ημερομηνία | barcode | code | περιεχομενο | τιμή παραγωγός | χονδρική | λιανική |
|---|---|---|---|---|---|---|
| 05/2018 | 2802911001019 | 291100101 | VALOMED F.C.TAB 500MG/TAB BTx10 TABS | 4.54 | 4.76 | 6.56 |
| 05/2018 | 2802911001026 | 291100102 | VALOMED F.C.TAB 500MG/TAB BTx42 TABS | 18.87 | 19.79 | 27.27 |
| 05/2018 | 2802911002016 | 291100201 | VALOMED F.C.TAB 1000MG/TAB BTx21 TABS | 18.97 | 19.90 | 27.42 |
For the treatment and management of herpes zoster (shingles), genital herpes, and chickenpox
Viral (HSV-1, HSV-2 and VZV) thymidine kinase converts aciclovir to the aciclovir monophosphate, which is then converted to the diphosphate by cellular guanylate kinase, and finally to the triphosphate by phosphoglycerate kinase, phosphoenolpyruvate carboxykinase, and pyruvate kinase. Aciclovir triphosphate competitively inhibits viral DNA polymerase and competes with the natural deoxyguanosine triphosphate, for incorporation into viral DNA. Once incorporated, aciclovir triphosphate inhibits DNA synthesis by acting as a chain terminator.
Aciclovir may cause nephrotoxicity (crystallization of aciclovir within renal tubules, elevation of serum creatinine, transient), and neurotoxicity (coma, hallucinations, lethargy, seizures, tremors). Nephrotoxicity and neurotoxicity usually resolve after cessation of aciclovir therapy. However, there is no well-defined relationship between aciclovir concentrations in the blood and these adverse effects.
Oral: bioavailability 10 to 20%
2.5-3.3 hours
Acyclovir is cleared renally.
For the treatment or suppression of cold sores (herpes labialis), herpes zoster (shingles), genital herpes in immunocompetent individuals, and recurrent genital herpes in HIV-infected individuals.
Valaciclovir is phosphorylated by viral thymidine kinase to acyclovir triphosphate (the active metabolite) which then inhibits herpes viral DNA replication by competitive inhibition of viral DNA polymerase, and by incorporation into and termination of the growing viral DNA chain. When used as a substrate for viral DNA polymerase, acyclovir triphosphate competitively inhibits dATP leading to the formation of 'faulty' DNA. This is where acyclovir triphosphate is incorporated into the DNA strand replacing many of the adenosine bases. This results in the prevention of DNA synthesis, as phosphodiester bridges can longer to be built, destabilizing the strand.
Adverse effects of overexposure might include headache and nausea.
After oral administration, valaciclovir hydrochloride is rapidly absorbed from the gastrointestinal tract. The absolute bioavailability of acyclovir after administration of valaciclovir is 54.5% ± 9.1%.
2.5-3.3 hours
Acyclovir accounted for 89% of the radioactivity excreted in the urine.
* Renal cl=255 +/- 86 mL/min [healthy] * apparent cl=86.3 +/- 21.3 mL/min/1.73 m2 [dialysis patients] * apparent cl=679.16 +/- 162.76 mL/min/1.73 m2 [healthy]