Multiple sclerosis (MS) is an acquired inflammatory immune-mediated disorder of the central nervous system, characterized by inflammation, demyelination, and primary or secondary axonal degeneration. It clinically manifests with signs of multiple neurological dysfunctions, followed by recovery or increasing disability. Cyclophosphamide (cy) (the generic name for Endoxan, Cytoxan, Neosar, Procytox, and Revimmune), also known as cytophosphane, is a nitrogen mustard alkylating agent from the oxazophorine group (Figure 1). An alkylating agent adds an alkyl group (CnH2n + 1) to DNA. It attaches the alkyl group to the guanine base of DNA, at number 7 nitrogen atom of the imidazole ring. This leads to the synthesis of aberrant couples of cytosin-tymine. The DNA reparation system of the cells removes the modified guanine, triggering cell apoptosis. Cy is converted by mixed function oxidase enzymes 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 oxidised by the enzyme aldehyde dehydrogenase (ALDH) to make carboxyphosphamide. The intracellular level of this enzyme has been shown to be directly related to cellular resistance to activated cy and is believed to be important in the survival of cells capable of repopulating marrow in autologous bone marrow transplant procedures [1]. Both hematopoietic progenitors and intestinal crypt stem cells display high levels of cytosolic ALDH and are accordingly relatively resistant to cy. Tumor cell resistance to cy may also result from high cytosolic ALDH levels [2]. A small proportion of aldophosphamide is converted into phosphoramide mustard and acrolein. Acrolein is toxic to the bladder epithelium and can lead to hemorrhagic cystitis [3].