Antimetabolites
Folate antagonists, fluoropyrimidines, cytidine analogs, purine analogs, and hypomethylating agents
5-FU = 5-fluorouracil · ALL = acute lymphoblastic leukemia · AML = acute myeloid leukemia · ara-C = cytarabine · CLL = chronic lymphocytic leukemia · DHF = dihydrofolate · DHFR = dihydrofolate reductase · DPD = dihydropyrimidine dehydrogenase · FCR = fludarabine, cyclophosphamide, rituximab · FdUMP = fluorodeoxyuridine monophosphate · HMA = hypomethylating agent · MDS = myelodysplastic syndrome · MTX = methotrexate · THF = tetrahydrofolate · TPMT = thiopurine methyltransferase · TS = thymidylate synthase · XO = xanthine oxidase
Methotrexate: Mechanism and Rescue
- MTX blocks DHFR: DHF cannot be reduced to THF
- THF depletion → halts thymidylate and purine synthesis
- Polyglutamation by FPGS traps MTX intracellularly for weeks
- Polyglutamates also directly inhibit TS and purine synthesis enzymes
- S-phase specific; cycle-dependent exposure required
- NSAIDs + PPIs: reduce renal MTX clearance → 2–10× higher levels
- Third-space fluids (ascites, effusions): drain before high-dose MTX
- Leucovorin rescue: begins 24–42 h after MTX; continue until MTX < 0.1 μmol/L
- Glucarpidase: reserved for severe toxicity or failed leucovorin rescue
- Pemetrexed: requires folic acid + vitamin B12 pre-supplementation
5-Fluorouracil: Schedule-Dependent Toxicity
| Feature |
Bolus 5-FU |
Continuous Infusion 5-FU |
| Dominant mechanism |
RNA disruption (FUTP incorporation) |
TS inhibition (FdUMP ternary complex) |
| Dose-limiting toxicity |
Myelosuppression |
Mucositis, hand-foot syndrome |
| Leucovorin benefit |
Less pronounced |
Stabilizes ternary complex; ~2× response rate |
| DPD role |
DPD catabolizes >85% of 5-FU; deficiency → life-threatening toxicity at standard doses |
Cytidine Analogs and Purine Analogs: Key Points
- S-phase specific: 7-day continuous infusion in AML induction
- Activated by deoxycytidine kinase; resistance = loss of deoxycytidine kinase
- High-dose ara-C: cerebellar toxicity (ataxia) — check neuro before each cycle
- Indication: AML induction and consolidation
- Self-potentiating: diphosphate inhibits ribonucleotide reductase → less competition for DNA polymerase
- Indications: pancreatic cancer, NSCLC, bladder, ovarian
- Toxicity: thrombocytopenia, pulmonary toxicity, rare hemolytic uremic syndrome
- Fludarabine: CLL (FCR regimen); profound CD4 depletion months to years
- Cladribine: hairy cell leukemia; single 7-day course → >90% complete remission
- Both require PCP and herpesvirus prophylaxis throughout and after therapy
- Fludarabine: stop immediately if autoimmune hemolytic anemia develops
Pharmacogenomics: Two Mandatory Pre-Treatment Screens
- Low TPMT (~0.3%): 10–20% of standard dose; standard dose = fatal aplasia
- Intermediate TPMT (~10%): 30–50% dose reduction
- Allopurinol (XO inhibitor) + 6-mercaptopurine: fourfold level rise → aplasia; reduce to 25%
- Complete DPD deficiency: fatal toxicity within days of first dose
- Partial deficiency (~3–5%): severe grade 3–4 toxicity in ~25–30%
- DPYD genotyping or plasma uracil level recommended before first dose
- Capecitabine + warfarin: inhibits CYP2C9 → INR rises; monitor weekly