Home / Drugs / Starting with M /
indicationFor the treatment of psoriasis and vitiligo
pharmacologyMethoxsalen 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 actionAfter 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 lifeApproximately 2 hours
route of eliminationIn 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 interactionsEthotoin: 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.