For use in keratoconjunctivitis and keratitis caused by herpes simplex virus.
In chemical structure idoxuridine closely approximates the configuration of thymidine, one of the four building blocks of DNA (the genetic material of the Herpes virus). As a result, idoxuridine is able to replace thymidine in the enzymatic step of viral replication or "growth". The consequent production of faulty DNA results in a pseudostructure which cannot infect or destroy tissue. In short, by pre-empting a vital building block in the genetic material of the Herpes simplex virus, Herplex-D topical solution destroys the infective and destructive capacity of the viral material. The virus infected cell may only be attacked during the period of active synthesis of DNA. This occurs early in the development of the Herpes simplex lesion, but at different times in different cells. Therefore, ideally, the affected area should remain saturated with the antiviral agent.
Mode of Action:
Idoxuridine acts as an antiviral agent by inhibiting viral replication by substituting itself for thymidine in viral DNA. This in turn inhibits thymidylate phosphorylase and viral DNA polymerases from properly functioning. The effect of Idoxuridine results in the inability of the virus to reproduce or to infect/destroy tissue.
Idoxuridine is rapidly inactivated by deaminases or nucleotidases.
Hypersensitivity or increased sensitivity of eyes to light. LD50=3080 mg/kg (orally in mice).
Seth AK, Misra A, Umrigar D: Topical liposomal gel of idoxuridine for the treatment of herpes simplex: pharmaceutical and clinical implications. Pharm Dev Technol. 2004 Aug;9(3):277-89. Pubmed Otto SE: Radiopharmaceuticals (Strontium 89) and radiosensitizers (idoxuridine). J Intraven Nurs. 1998 Nov-Dec;21(6):335-7. Pubmed Fauth E, Zankl H: Comparison of spontaneous and idoxuridine-induced micronuclei by chromosome painting. Mutat Res. 1999 Apr 6;440(2):147-56. Pubmed
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