Arasena-A
Arasena-A Uses, Dosage, Side Effects, Food Interaction and all others data.
A nucleoside antibiotic isolated from Streptomyces antibioticus. It has some antineoplastic properties and has broad spectrum activity against DNA viruses in cell cultures and significant antiviral activity against infections caused by a variety of viruses such as the herpes viruses, the vaccinia VIRUS and varicella zoster virus.
Arasena-A is a synthetic purine nucleoside analogue with in vitro and in vivo inhibitory activity against herpes simplex virus types 1 (HSV-1), 2 (HSV-2), and varicella-zoster virus (VZV). The inhibitory activity of Arasena-A is highly selective due to its affinity for the enzyme thymidine kinase (TK) encoded by HSV and VZV. This viral enzyme converts Arasena-A into Arasena-A monophosphate, a nucleotide analogue. The monophosphate is further converted into diphosphate by cellular guanylate kinase and into triphosphate by a number of cellular enzymes. In vitro, Arasena-A triphosphate stops the DNA replication of herpes virus by being incorporated into the DNA strand and preventing the formation of phosphodiester bridges between bases. This ultimately leads to destabilization of the viral DNA strands.
| Trade Name | Arasena-A |
| Generic | Vidarabine |
| Vidarabine Other Names | Spongoadenosine, Vidarabine, Vidarabinum |
| Type | |
| Formula | C10H13N5O4 |
| Weight | Average: 267.2413 Monoisotopic: 267.096753929 |
| Protein binding | 24-38% |
| Groups | Approved, Investigational |
| Therapeutic Class | |
| Manufacturer | |
| Available Country | |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Arasena-A is an antiviral agent used to treat various viral infections.
For treatment of chickenpox - varicella, herpes zoster and herpes simplex
How Arasena-A works
Arasena-A stops replication of herpes viral DNA in 2 ways: 1) competitive inhibition of viral DNA polymerase, and consequently 2) incorporation into and termination of the growing viral DNA chain. Arasena-A is sequentially phosphorylated by kinases to the triphosphate ara-ATP, which is the active form of vidarabine that acts as both an inhibitor and a substrate of viral DNA polymerase. By acting as a substrate for viral DNA polymerase, ara-ATP competitively inhibits dATP leading to the formation of ‘faulty’ DNA. Ara-ATP can also be incorporated into the DNA strand to replace many of the adenosine bases, resulting in the disruption of DNA synthesis.
Toxicity
Acute massive overdosage by oral ingestion of the ophthalmic ointment has not occurred. However, the rapid deamination to arabinosylhypoxanthine should preclude any difficulty. The oral LD50 for vidarabine is greater than 5020 mg/kg in mice and rats. No untoward effects should result from ingestion of the entire contents of the tube. Overdosage by ocular instillation is unlikely because any excess should be quickly expelled from the conjunctival sac.
Elimination Route
Systemetic absorption of vidarabine should not be expected to occur following ocular administration and swallowing lacrimal secretions.
Innovators Monograph
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