Oral<unk>  is rapidly absorbed and then converted by mixed-function oxidase enzymes <unk> tochrome P450 system) in the liver to active metabolites. The main active metabolite is 4-hydroxycyclophosphamide, which exists in equilibrium with its tautomer, aldophosphamide. Most of the aldophosphamide is then oxidised by the enzyme aldehyde dehydrogenase (ALDH) to make carboxycyclophosphamide. A small proportion of aldophosphamide freely diffuses into cells, where it is decomposed into two compounds, phosphoramide mustard and acrolein. The active metabolites of<unk>  are highly protein bound and distributed to all tissues, are assumed to cross the placenta and are known to be present in breast milk. It is specifically in the oxazaphosphorine group of medications.<unk>  metabolites are primarily excreted in the urine unchanged, and drug dosing should be appropriately adjusted in the setting of renal dysfunction. Drugs altering hepatic microsomal enzyme activity (e.g., alcohol, barbiturates, rifampicin, or phenytoin) may result in accelerated metabolism of<unk>  into its active metabolites, increasing both pharmacologic and toxic effects of the drug; alternatively, drugs that inhibit hepatic microsomal enzymes (e.g. corticosteroids, tricyclic antidepressants, or allopurinol) result in slower conversion of<unk>  into its metabolites and consequently reduced therapeutic and toxic effects.<unk>  reduces plasma pseudocholinesterase activity and may result in prolonged neuromuscular blockade when administered concurrently with succinylcholine. Tricyclic antidepressants and other anticholinergic agents can result in delayed bladder emptying and prolonged bladder exposure to acrolein.
Cyclophosphamide
Ifosfamide
Vincristine
Lenalidomide
Mitoxantrone
Cytarabine
Cladribine
Phototrexate