It is also an important therapy and steroid-sparing agent for inflammatory bowel disease (such as Crohns disease and ulcerative colitis) and for multiple sclerosis.In the United States, it is approved by the Food and Drug Administration  for use in kidney transplantation from human donors, and for rheumatoid arthritis. Transplantation
Azathioprine is used to prevent rejections of kidney or liver allografts, usually in conjunction with other therapies including corticosteroids, other immunosuppressants, and local radiation therapy. The administration protocol starts either at the time of transplantation or within the following two days. Rheumatoid arthritis
Being a disease-modifying antirheumatic drug (DMARD), azathioprine has been used for the management of the signs and symptoms of adult rheumatoid arthritis. Nonsteroidal anti-inflammatory drugs  and corticosteroids may be combined or continued (if they were already in use) with azathioprine, but the combination with other DMARDs is not recommended. Inflammatory bowel disease
Azathioprine has been used in the management of moderate to severe chronically active Crohns disease, to maintain clinical remission (absence of disease activity) in corticosteroid-dependent patients, and to provide benefit in people with fistulizing Crohns disease. The onset of action is slow, and it may require several months to achieve clinical response.Azathioprine treatment is associated with an increased risk of lymphoma, but if this is due to the drug or a predisposition related to Crohns disease is unclear. Lower doses of azathioprine are used as a therapy in children with refractory or corticosteroid-dependent Crohns disease, without causing many side effects. It may also be used to prevent flares in those with ulcerative colitis.
6-MP is metabolized analogously to natural purines, giving thioguanosine triphosphate (TGTP) and thiodeoxyguanosine triphosphate (TdGTP) via thioinosine monophosphate (TIMP) and several further intermediates. On a second path, the sulfur atom of 6-MP and TIMP is methylated. The end products of azathioprine metabolism are thiouric acid (38%) and various methylated and hydroxylated purines, which are excreted via the urine. Mechanism of action
Azathioprine inhibits purine synthesis. Purines are needed to produce DNA and RNA. By inhibiting purine synthesis, less DNA and RNA are produced for the synthesis of white blood cells, thus causing immunosuppression. Azathioprine is converted within tissues to 6-MP, some of which is converted, in turn, to 6-thioguanine by the addition of an amino group. Both 6-MP and 6-thioguanine are conjugated with ribose, and then phosphorylated to form the nucleotides  thioinosinic acid and thioguanylic acid, respectively. These nucleotides masquerade, respectively, as inosinic acid and guanylic acid; the former is the starting point for purine nucleotide biosynthesis, while the latter is one of the building blocks of DNA and RNA. The nucleotides are  incorporated into newly synthesized (but nonfunctional) DNA, halting replication. The nucleotides act to inhibit glutamine-phosphoribosyl pyrophosphate amidotransferase (GPAT), one of the enzymes involved in purine biosynthesis, one of the earlier steps in the synthesis of DNA and RNA. They achieve GPAT inhibition through a form of negative feedback called product inhibition.