What is the mechanism of action of methotrexate (disease-modifying antirheumatic drug (DMARD)) in a patient with rheumatoid arthritis (RA)?

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Methotrexate Mechanism of Action in Rheumatoid Arthritis

Methotrexate inhibits dihydrofolate reductase, blocking DNA synthesis and cellular replication, but its precise mechanism in rheumatoid arthritis remains unknown and likely involves immunomodulatory and anti-inflammatory effects rather than direct cytotoxic action. 1

Primary Pharmacologic Mechanism

  • Methotrexate inhibits dihydrofolate reductase, the enzyme that reduces dihydrofolates to tetrahydrofolates, which are essential carriers of one-carbon groups needed for synthesis of purine nucleotides and thymidylate. 1

  • This inhibition interferes with DNA synthesis, repair, and cellular replication, particularly affecting actively proliferating tissues such as malignant cells, bone marrow, fetal cells, and mucosal cells. 1

  • Polyglutamated derivatives of methotrexate are potent inhibitors of various enzymes including dihydrofolate reductase and 5-aminoimidazole-4-carboxamide ribonucleotide transformylase, and these metabolites are selectively retained in cells. 2

Mechanism Specific to Rheumatoid Arthritis

  • The mechanism of action in rheumatoid arthritis is unknown and may affect immune function, as explicitly stated by the FDA. 1

  • Methotrexate appears to act as an anti-inflammatory agent with subtle immunomodulating properties rather than as a direct cytotoxic agent in RA. 2

  • In vitro studies show methotrexate inhibits DNA precursor uptake by stimulated mononuclear cells, and animal studies demonstrate partial correction of spleen cell hyporesponsiveness and suppressed IL-2 production in polyarthritis. 1

  • However, other laboratories have been unable to demonstrate similar immunologic effects, and clarification of methotrexate's effect on immune activity and its relation to rheumatoid immunopathogenesis awaits further studies. 1

Additional Proposed Mechanisms

  • Inhibitory effects on cytokines, particularly interleukin-1, and on arachidonic acid metabolism have been reported, some of which may be linked to the antifolate properties. 2

  • Effects on proteolytic enzymes have been documented. 2

  • Direct inhibitory effects on rapidly proliferating cells in the synovium have been suggested as a potential mechanism. 2

Clinical Effects and Timeline

  • Effects on articular swelling and tenderness can be seen as early as 3 to 6 weeks in patients with rheumatoid arthritis. 1

  • Methotrexate clearly ameliorates symptoms of inflammation (pain, swelling, stiffness), but there is no evidence that it induces remission of rheumatoid arthritis. 1

  • No beneficial effect has been demonstrated on bone erosions and other radiologic changes that result in impaired joint use, functional disability, and deformity, according to FDA labeling. 1

Important Clinical Caveat

The disconnect between methotrexate's well-established clinical efficacy in RA and the lack of a clearly defined mechanism of action represents a significant knowledge gap. The drug's effectiveness appears to rely more on immunomodulatory and anti-inflammatory properties than on its classic antifolate cytotoxic effects, distinguishing its use in RA from its use in malignancy where the antiproliferative mechanism is primary. 2

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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