methotrexate (oncologic)

Brand: Trexall, Otrexup, Rasuvo

⚠ BBW ISMP High Alert TDM Required Prototype Drug
Drug Class: antimetabolite antineoplastic
Drug Family: antineoplastic
Subclass: folate antagonist
Organ Systems: hematology-oncologyimmunologymusculoskeletal

Mechanism of Action

Competitively inhibits DHFR, blocking tetrahydrofolate production; depletes pools of folate cofactors required for purine and thymidylate synthesis; also polyglutamated intracellularly to forms that inhibit thymidylate synthase; S-phase specific.

dihydrofolate reductase (DHFR)thymidylate synthase

Indications

  • acute lymphoblastic leukemia (ALL) — cornerstone
  • osteosarcoma
  • non-Hodgkin lymphoma
  • choriocarcinoma
  • breast cancer
  • CNS prophylaxis (intrathecal)
  • rheumatoid arthritis (low dose)
  • psoriasis (low dose)
  • ectopic pregnancy (intramuscular)

Contraindications

  • methotrexate hypersensitivity
  • severe renal impairment (high-dose)
  • immunodeficiency syndromes (live vaccines)
  • pleural effusion or ascites (third-space sequestration)
  • pregnancy (teratogenic)
  • breastfeeding

Adverse Effects

Common

  • mucositis/stomatitis
  • nausea/vomiting
  • myelosuppression
  • hepatotoxicity

Serious

  • severe myelosuppression
  • mucositis
  • nephrotoxicity (at high doses)
  • pulmonary toxicity (methotrexate pneumonitis)
  • hepatic fibrosis/cirrhosis (chronic low-dose)
  • neurotoxicity (intrathecal)
  • teratogenicity

Pharmacokinetics (ADME)

Absorption 50–90% oral at low doses; IV at high doses for oncology
Distribution widely distributed; 50% protein-bound; intrathecal distribution limited to CSF
Metabolism partial hepatic metabolism; polyglutamation in cells (active, retained intracellularly)
Excretion primarily renal (90% unchanged at high doses); dose adjustment essential in renal impairment
Half-life 3–10 hours (low dose); up to 24 hours (high dose)
Onset hours
Peak 1–4 hours (oral)
Duration varies by indication
Protein Binding 50%
Vd moderate

Drug Interactions

Drug / Agent Mechanism Severity
NSAIDs/aspirin reduce renal tubular secretion of methotrexate; increase levels to toxic; deaths reported — avoid with high-dose MTX major
trimethoprim/sulfonamides additive folate antagonism; severe myelosuppression major
proton pump inhibitors reduce renal tubular secretion of MTX at high doses; delay elimination major
leucovorin (folinic acid) rescues normal cells after high-dose MTX — must be administered on schedule; delays require additional leucovorin rescue beneficial

Nursing Considerations

  1. High-dose methotrexate requires mandatory leucovorin rescue — verify leucovorin is prescribed and the first dose is given at the correct time relative to methotrexate infusion (typically 24 hours after MTX start).
  2. Maintain urinary pH >7 with sodium bicarbonate during and after high-dose MTX infusion — alkaline urine prevents methotrexate precipitation in renal tubules.
  3. Monitor methotrexate levels at 24, 48, and 72 hours; if levels are above the nomogram thresholds, increase leucovorin rescue dose.
  4. NSAIDs (including OTC ibuprofen, naproxen, aspirin) must be held before and during high-dose MTX — these can cause fatal toxicity by blocking renal elimination.

Clinical Pearls

  • Leucovorin rescue (folinic acid) after high-dose methotrexate is a clinically elegant strategy: leucovorin bypasses DHFR to restore folate pools in normal cells, while entering cancer cells poorly due to lower affinity for the folate carrier — providing differential rescue.
  • Methotrexate polyglutamates are the active intracellular forms with long retention times — this explains the persistent antiproliferative effects of even weekly low-dose MTX for RA and psoriasis, where circulating drug levels are undetectable between doses.

Safety Profile

Pregnancy contraindicated
Lactation avoid
Renal Adjustment Required
Hepatic Adjustment Required
TDM Required