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 Methotrexate

Description of Methotrexate: Methotrexate is an antimetabolite and antifolate agent with antineoplastic and immunosuppressant activities. Methotrexate binds to and inhibits the enzyme dihydrofolate reductase, resulting in inhibition of purine nucleotide and thymidylate synthesis and, subsequently, inhibition of DNA and RNA syntheses. Methotrexate also exhibits potent immunosuppressant activity although the mechanism(s) of actions is unclear. Check for active clinical trials or closed clinical trials using this agent. (NCI Thesaurus)

Trexall™ (methotrexate tablets), for oral administration, are available in 5 mg, 7.5 mg, 10 mg and 15 mg strengths. Each tablet contains methotrexate sodium in an amount equivalent to the labeled amount of methotrexate, and contains the following inactive ingredients: anhydrous lactose, crospovidone, hydroxypropyl methylcellulose, magnesium stearate, microcrystalline cellulose, polyethylene glycol, polysorbate 80, pregelatinized starch, sodium carbonate monohydrate, talc and titanium dioxide. The 5 mg also contains: D&C yellow no. 10 aluminum lake, FD&C blue no. 1 aluminum lake and FD&C yellow no. 6 aluminum lake. The 7.5 mg also contains: FD&C blue no.1 aluminum lake. The 10 mg also contains: FD&C red no. 40 aluminum lake. The 15 mg also contains: FD&C blue no. 2 aluminum lake and FD&C red no. 40 aluminum lake.

Accordinng to http://en.wikipedia.org/wiki/Methotrexate, In 1947, a team of researchers led by Sidney Farber showed that aminopterin, a chemical analogue of folic acid developed by Yellapragada Subbarao Lederle, could induce remission in children with acute lymphoblastic leukemia. The development of folic acid analogues had been prompted by the discovery that the administration of folic acid worsened leukemia, and that a diet deficient in folic acid could, conversely, produce improvement; the mechanism of action behind these effects was still unknown at the time. Other analogues of folic acid were in development, and by 1950, methotrexate (then known as amethopterin) was being proposed as a treatment for leukemia. Animal studies published in 1956 showed that the therapeutic index of methotrexate was better than that of aminopterin, and clinical use of aminopterin was thus abandoned in favor of methotrexate. In that same year, methotrexate was found to be a curative treatment for choriocarcinoma—a solid tumor, unlike leukemia, which is a cancer of the blood. The drug was then investigated as a treatment for many other cancers, alone or in combination with other drugs, and was studied for other, non-cancer indications in the 1970s. In 1988, it was approved by the U.S. Food and Drug Administration (FDA) to treat rheumatoid arthritis.

Methotrexate was originally used as part of combination chemotherapy regimens to treat many kinds of cancers. It is still the mainstay for the treatment of many neoplastic disorders including acute lymphoblastic leukemia.

Methotrexate is commonly used (generally in combination with misoprostol) to terminate early pregnancies (i.e. as an abortifacient). It is also used to treat ectopic pregnancies.[6] In the case of early missed miscarriage (particularly a blighted ovum), in which fetal demise has occurred but the body has not expelled the fetus, methotrexate may be used to help the body begin the miscarriage process.
[edit] Other uses

It has come into use as a treatment for some autoimmune diseases, including Myasthenia Gravis, polymyositis, dermatomyositis, inclusion body myositis, ankylosing spondylitis, Crohn's disease, psoriasis, pustular psoriasis, psoriatic arthritis, rheumatoid arthritis, Wegener's granulomatosis, Adult-Onset Still's Disease, and scleroderma (see disease-modifying antirheumatic drugs). A parallel use with TNFα blockers, such as adalimumab, infliximab, or etanercept, has been shown to markedly improve symptoms.

It is also sometimes used to treat a rare condition called Behçet's disease where it is taken weekly, along with folic acid daily. In the case of immune disorders, such as Behçet's disease and rheumatoid disorders, it is believed that the clinical goal of the low dose methotrexate regimen is to inhibit AICAR transformylase, which leads to increased AICA ribose (AICAR transformylase's substrate). The AICA ribose inhibits adenosine deaminase, resulting in a build-up of extracellular adenosine. Extracellular adenosine inhibits the expression of IL-2 receptors on circulating T-lymphocytes, causing a suppression of the immune system, and thus ameliorating the effects of the immune disorder.