indication

For the treatment of psoriasis and vitiligo

pharmacology

Methoxsalen selectively inhibits the synthesis of deoxyribonucleic acid (DNA). The guanine and cytosine content correlates with the degree of Methoxsalen-induced cross-linking. At high concentrations of the drug, cellular RNA and protein synthesis are also suppressed.

mechanism of action

After activation it binds preferentially to the guanine and cytosine moieties of DNA, leading to cross-linking of DNA, thus inhibiting DNA synthesis and function.

half life

Approximately 2 hours

route of elimination

In both mice and man, methoxsalen is rapidly metabolized. Approximately 95% of the drug is excreted as a series of metabolites in the urine within 24 hours (Pathak et al. 1977).

drug interactions

Ethotoin: The hydantoin decreases the effect of psoralene

Fosphenytoin: The hydantoin decreases the effect of psoralene

Mephenytoin: The hydantoin decreases the effect of psoralene

Phenytoin: The hydantoin decreases the effect of psoralene

Tacrine: The metabolism of Tacrine, a CYP1A2 substrate, may be reduced by strong CYP1A2 inhibitors such as Methoxsalen. Consider modifying therapy to avoid Tacrine toxicity. Monitor the efficacy and toxicity of Tacrine if Methoxsalen is initiated, discontinued or if the dose is changed.

Thiothixene: The strong CYP1A2 inhibitor, Methoxsalen, may decrease the metabolism and clearance of Thiothixene, a CYP1A2 substrate. Consider alternate therapy or monitor for changes in Thiothixene therapeutic and adverse effects if Methoxsalen is initiated, discontinued or dose changed.

Tizanidine: Methoxsalen may decrease the metabolism and clearance of Tizanidine. Consider alternate therapy or use caution during co-administration.