Study aid only. Verify against current guidelines before clinical use.

Antitumor antibiotics

Pharmacology
Antitumor antibiotics

Mechanism and Class Overview

  • Class mechanism: Mechanisms vary by drug: anthracyclines intercalate DNA and inhibit topo II (cell-cycle independent); bleomycin causes free-radical DNA breaks (G2-specific); mitomycin cross-links DNA; dactinomycin blocks transcription.
  • Resistance: ↑ P170 (MDR) glycoprotein and ↑ P190 (MRP) drug efflux, altered topoisomerase II, and ↑ sulfhydryl proteins.

Anthracyclines

Ruler of cumulative doxorubicin dose: low cardiotoxicity risk below 350 mg/m2, about 10% at 450 to 500, lifetime maximum 450 to 550 (400 with prior mediastinal RT or other cardiotoxic therapy), dexrazoxane above 300, with panels on acute versus chronic cardiotoxicity and why the heart is vulnerable.
Doxorubicin cumulative dose and cardiotoxicity risk, with acute versus chronic patterns. Tap to enlarge.
  • Class mechanism: Form iron-dependent free radicals causing DNA strand breaks, inhibit topoisomerase II, and intercalate directly into DNA. Metabolized ~50% in the liver, so dose reduce with hepatic dysfunction. Phenobarbital and phenytoin ↑ doxorubicin clearance; cyclophosphamide, mitomycin C, trastuzumab, taxanes, and bevacizumab ↑ toxicity.
  • Cardiotoxicity mechanism: The heart is iron-rich and poor in free-radical detoxification. Risk is low below a total dose of 350 mg/m2 and rises to ~10% at a cumulative 450 to 500 mg/m2. Obtain a baseline TTE in all patients.
    • Acute: within 2 to 3 days, dose-independent, arrhythmias, pericarditis, myocarditis.
    • Chronic: dose-dependent dilated cardiomyopathy. Risk ↑ with older age, CAD, HTN, and prior mediastinal radiotherapy.
  • Dexrazoxane: An iron chelator that reduces anthracycline cardiotoxicity, added once cumulative dose thresholds are reached (typically dosed at a 10:1 ratio to the anthracycline). It is also the antidote for anthracycline extravasation.
Anthracyclines: cumulative dose limitsEstablished dexrazoxane thresholds only for doxorubicin ≥ 300 mg/m2 (US Zinecard) and epirubicin ≥ 540 mg/m2 (EU Cardioxane); no validated daunorubicin or idarubicin thresholds; consider dexrazoxane from the start in high cardiovascular-risk patients.
DrugLifetime maxDexrazoxane above
Doxorubicin450 to 550 mg/m2 (400 if prior mediastinal RT or other cardiotoxic therapy)300 mg/m2
Daunorubicin550 mg/m2No validated threshold
Epirubicin900 mg/m2540 mg/m2
Idarubicin150 mg/m2 (label: ↑ CHF above 90 mg/m2)No validated threshold

Doxorubicin (Adriamycin)

  • Indications: Breast, lymphoma, sarcoma, AML, and other solid tumors.
  • Toxicities: Myelosuppression, GI toxicity, vesicant (treat extravasation with dexrazoxane started within 6 h, removing cold packs at least 15 min before the infusion; do not combine with topical DMSO), radiation-recall skin reaction, alopecia, red/orange urine discoloration on days 1 to 2, infertility, and cumulative cardiotoxicity. Highly emetogenic at doses ≥60 mg/m2 (anthracycline plus cyclophosphamide combos always high-risk).
  • Liposomal doxorubicin: ↓ nausea/vomiting, ↓ cardiotoxicity, and ↓ myelosuppression, but causes hand-foot syndrome and acute infusion reactions.

Daunorubicin (Cerubidine)

  • Indications: AML, ALL.
  • Toxicities: Cumulative cardiotoxicity, myelosuppression, alopecia, GI toxicity.

Idarubicin (Idamycin)

  • Indications: AML, ALL (enhanced intracellular uptake).
  • Toxicities: Cardiotoxicity, myelosuppression, GI toxicity, alopecia.

Epirubicin (Ellence)

  • Indications: Breast cancer (higher cumulative dose ceiling than doxorubicin). Highly emetogenic at doses > 90 mg/m2.
  • Toxicities: Cardiotoxicity, myelosuppression, alopecia.

Other Intercalators

Mitoxantrone (Novantrone)

  • Mechanism: Anthracenedione that intercalates DNA and inhibits topoisomerase II; structurally distinct from the anthracyclines.
  • Indications: AML, lymphoma, multiple sclerosis.
  • Toxicities: Cardiotoxicity: cumulative, dose-related cardiac dysfunction/CHF (anthracycline-like); monitor LVEF, myelosuppression, blue-green discoloration of urine and sclera, GI toxicity.

Others

Dactinomycin (Actinomycin D)

  • Mechanism: Intercalates into DNA (G-C pairs) and blocks DNA-dependent RNA polymerase (↓ RNA synthesis); also inhibits topoisomerase II, causing DNA breaks.
  • Indications: Wilms tumor, rhabdomyosarcoma, germ cell tumors, choriocarcinoma.
  • Toxicities: Myelosuppression, nausea/vomiting, alopecia, radiation recall, and hepatic veno-occlusive disease (↑ mortality in children). Vesicant.

Bleomycin (Blenoxane)

  • Mechanism: Binds DNA and generates single- and double-strand breaks, ↓ DNA synthesis.
  • Indications: Testicular cancer (BEP), Hodgkin lymphoma (ABVD), head and neck and ovarian cancers.
  • Pulmonary toxicity: dose-limiting; presents as pneumonitis (cough, dyspnea, interstitial changes), can progress to fibrosis. Risk ↑ with concurrent growth-factor use, prior lung disease, prior chest radiotherapy, age > 65, and a cumulative dose > 400 units. Follow PFTs (DLCO).
  • Other toxicities: Hyperpigmentation, skin peeling, mucositis, and hypersensitivity/fever reactions.

Mitomycin C

  • Mechanism: Alkylates DNA to produce cross-links, ↓ DNA synthesis.
  • Indications: Anal, gastric, and bladder cancers (intravesical).
  • Toxicities: Delayed myelosuppression with very late count recovery (~2 months), mucositis, hemolytic-uremic syndrome (a classic dose-related cause, along with gemcitabine and cyclosporine), and pneumonitis.
Veli Bakalov MD, Board Review Notes 2026