S-Adenosylmethionine (SAMe), first discovered in 1952 (1), is formed from the essential amino acid methionine and adenosine triphosphate (ATP). SAMe is found in every living cell, where it functions as a donor of methyl groups in over 100 different reactions catalyzed by methlytransferase enzymes, which act on substrates such as DNA, proteins, phospholipids, monoamine neurotransmitters, and many other low molecular weight compounds (2,3). In its native form SAMe is labile and degrades rapidly. However, several patents on SAMe stable salts have been granted. Among them, SAMe-1, 4butanedisulfonate has been chosen for pharmaceutical development because of its high stability and tolerability, allowing preclinical and clinical studies to be performed. Numerous studies over the last two decades have shown SAMe to be effective in the treatment of depression (4-6), osteoarthritis (7,8), and liver disease (9-11). Moreover, SAMe has a very low side effect profile, comparable to that of placebo, affording considerable advantages as an alternative to standard antidepressant and antiinflammatory prescription medications that have unwanted and, in many cases, intolerable side effects.