U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

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Showing 21 - 28 of 28 results

Status:
Possibly Marketed Outside US

Class (Stereo):
CHEMICAL (ABSOLUTE)

Buciclovir is an acyclic guanosine analog with activity against herpes simplex virus (HSV). Buciclovir is phosphorylated to its triphosphate form by HSV thymidine kinase in infected cells and acts as a specific inhibitor of the viral DNA polymerase. Buciclovir inhibited DNA synthesis, not RNA synthesis, and prevented an increase in the size of newly synthesized DNA. Topical treatment initiated early after infection was efficacious, in contrast to topical treatment delayed 24 h or more. Systemic treatment of infected mice could not prevent the spread of the virus to the brain and mortality. Systemically administered buciclovir had an effect in guinea pigs, even after the delayed onset of treatment, but this effect required high doses of the drug. Buciclovir has only a limited effect against herpesvirus infections once the virus is present in the nervous systems of infected
mixture
Status:
Possibly Marketed Outside US
Source:
Octaplasma by Octapharma Pharmazeutika Produktionsges M B H [Canada]
Source URL:

Class:
MIXTURE

structurally diverse
Status:
Investigational
Source:
NCT04222985: Phase 1 Interventional Terminated Genital Herpes
(2020)
Source URL:

Class:
STRUCTURALLY DIVERSE

structurally diverse
Status:
Other

Class:
STRUCTURALLY DIVERSE

Acyclovir is a synthetic antiviral nucleoside analogue. A screening program for antiviral drugs begun at Burroughs Wellcome in the 1960s resulted in the discovery of acyclovir in 1974. Preclinical investigation brought the drug to clinical trials in 1977 and the first form of the drug (topical) was available to physicians in 1982. Activity of acyclovir is greatest against herpes 1 and herpes 2, less against varicella zoster, still less against Epstein-Barr, and very little against cytomegalovirus. Acyclovir is an antiviral agent only after it is phosphorylated in infected cells by a viral-induced thymidine kinase. Acyclovir monophosphate is phosphorylated to diphosphate and triphosphate forms by cellular enzymes in the infected host cell where the drug is concentrated. Acyclovir triphosphate inactivates viral deoxyribonucleic acid polymerase.