| Customization: | Available |
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| Quality Standard: | USP, Bp |
| Package: | 10 Tablets |
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| Generic Name | Vacyclovir Hydrochloride Tablets |
| Strength | 500mg |
| Packing | 10 Tablets/box |
| Origin | China |
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Product name:
Vacyclovir Hydrochloride Tablets
Character:
This product is a film coating, after removing the film coating will appear white to almost white.
Indications:
This product is suitable for the treatment of shingles.
This product is suitable for the treatment of herpes simplex virus infection.
This product is used to prevent (inhibit) recurrence of herpes simplex virus infection.
Drug overdose:
Data on overdose of this product is limited. However, there have been patients with a single dose of acyclovir up to 20g that has been partially absorbed through the gastrointestinal tract without common toxic reactions.
Several days after accidental oral repeated overdoses of acyclovir, associated gastrointestinal reactions (such as nausea and vomiting) and neurological reactions (headache and confusion) were observed.
Excessive intravenous administration of acyclovir can cause an increase in plasma creatinine, which can lead to kidney failure. There have also been neurological reactions associated with intravenous acyclovir overdose, including confusion, hallucinations, excitement, convulsions, and coma.
Patients should be closely observed for symptoms of poisoning. Hemodialysis can significantly increase the clearance of acyclovir from the blood and, therefore, can be used as a treatment option after overdose.
Pharmacology and toxicology:
Pharmacological action
Pharmacotherapeutics Group:
Valaciclovir, an antiviral agent, is the L-valine ester of acyclovir. Acyclovir is a nucleoside analogue of purine (guanine).
Valaciclovir is almost entirely rapidly converted to acyclovir and valine in the human body by the action of valaciclovir hydrolase.
Acyclovir is a specific inhibitor of herpes virus and has in vitro inhibitory effects on herpes simplex virus (HSV) types 1 and 2, varicella-zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human herpesvirus 6(HHV-6). Acyclovir is phosphorylated and converted to the active triphosphate form, which can inhibit viral DNA synthesis.
The first step of phosphorylation requires the activity of virus-specific enzymes. For HSV, VZV, and EBV, the enzyme is viral thymine kinase (TK), which is present only in virus-infected cells. This selectivity persists in phosphorylated CMV and is mediated, at least in part, by the gene product of UL97 phosphotransferase. Acyclovir activation requires virus-specific enzymes, a condition that explains the selectivity of its action.
Phosphorylation is accomplished by the action of cell kinases (conversion from monophosphate to triphosphate). Acyclovir triphosphates competitively inhibit viral DNA polymerase, and binding to this nucleoside analogue results in termination of the required chain, interrupting viral DNA synthesis and thus blocking viral replication.
In clinical trials for the treatment of shingles, this product has been shown to reduce the pain associated with shingles, including acute pain and post-herpetic neuralgia, while also reducing the time to form new lesions.
Extensive clinical monitoring of patients treated or prophylaxis with acyclovir has shown that reduced sensitivity to acyclovir is rare in immunorobust patients, and is occasionally seen in patients with severe immunodeficiency, such as patients with solid organ or bone marrow transplants, patients with malignant tumors undergoing chemotherapy, and people infected with human immunodeficiency virus (HIV).
Drug resistance is generally caused by a thymine kinase defective phenotype that puts the virus at a significant disadvantage in its natural host. In rare cases, reduced sensitivity to acyclovir may be caused by mutations in viral thymine kinase or DNA polymerase. The virulence of these variants is similar to that of the wild-type virus strains.
Toxicity study
Mutagenicity: Results of in vivo and in vitro mutagenicity tests indicate that valaciclovir is not genetically dangerous for humans.
Carcinogenic effect: Bioassays in rats and mice showed no carcinogenic effect of valaciclovir.
Teratogenicity: Valaciclovir has no teratogenic effect on rats and rabbits, and almost all of them are metabolized to acyclovir.
In internationally recognized experiments, subcutaneous acyclovir injection in rats and rabbits did not show teratogenic effects. In another rat study, fetal abnormalities were observed at subcutaneous plasma concentrations up to 100 μg/ml, resulting in maternal poisoning.
Fecundity: Oral administration of valaciclovir did not affect fecundity in male and female rats.
Storage:
Store below 30ºC
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