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Home / Drugs / Starting with E / Etoposide

A semisynthetic derivative of podophyllotoxin that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle. [PubChem]
Vepesid J
CategoriesNucleic Acid Synthesis Inhibitors
Antineoplastic Agents, Phytogenic
ManufacturersMylan pharmaceuticals inc
Bristol myers squibb co
Accord healthcare inc usa
App pharmaceuticals llc
Bedford laboratories div ben venue laboratories inc
Hospira inc
Marsam pharmaceuticals llc
Pharmachemie bv
Pierre fabre medicament
Teva parenteral medicines inc
Watson laboratories inc
PackagersAPP Pharmaceuticals
Baxter International Inc.
Bedford Labs
Ben Venue Laboratories Inc.
Bristol-Myers Squibb Co.
Hospira Inc.
Mead Johnson and Co.
Pfizer Inc.
Pharmachemie BV
Pharmacia Inc.
R.P. Scherer GmbH and Co. KG
RP Scherer Canada Inc.
Sicor Pharmaceuticals
Teva Pharmaceutical Industries Ltd.
UDL Laboratories
Wyeth Pharmaceuticals
Etoposidum [INN-Latin]


For use in combination with other chemotherapeutic agents in the treatment of refractory testicular tumors and as first line treatment in patients with small cell lung cancer. Also used to treat other malignancies such as lymphoma, non-lymphocytic leukemia, and glioblastoma multiforme.


Etoposide is an antineoplastic agent and an epipodophyllotoxin (a semisynthetic derivative of the podophyllotoxins). It inhibits DNA topoisomerase II, thereby ultimately inhibiting DNA synthesis. Etoposide is cell cycle dependent and phase specific, affecting mainly the S and G2 phases. Two different dose-dependent responses are seen. At high concentrations (10 µg/mL or more), lysis of cells entering mitosis is observed. At low concentrations (0.3 to 10 µg/mL), cells are inhibited from entering prophase. It does not interfere with microtubular assembly. The predominant macromolecular effect of etoposide appears to be the induction of DNA strand breaks by an interaction with DNA-topoisomerase II or the formation of free radicals.

mechanism of action

Etoposide inhibits DNA topoisomerase II, thereby inhibiting DNA re-ligation. This causes critical errors in DNA synthesis at the premitotic stage of cell division and can lead to apoptosis of the cancer cell.. Etoposide is cell cycle dependent and phase specific, affecting mainly the S and G2 phases of cell division.


Side effects include alopecia, constipation, diarrhea, nausea and vomiting and secondary malignancies (leukemia).


Primarily hepatic (through O-demethylation via the CYP450 3A4 isoenzyme pathway) with 40% excreted unchanged in the urine.


Absorbed well, time to peak plasma concentration is 1-1.5 hrs. Mean bioavailability is 50%.

half life

4-12 hours

route of elimination

Etoposide is cleared by both renal and nonrenal processes, i.e., metabolism and biliary excretion. Glucuronide and/or sulfate conjugates of etoposide are also excreted in human urine. Biliary excretion of unchanged drug and/or metabolites is an important route of etoposide elimination as fecal recovery of radioactivity is 44% of the intravenous dose. Only 8% or less of an intravenous dose is excreted in the urine as radiolabeled metabolites of 14C-etoposide.

drug interactions

Aprepitant: Aprepitant may change levels of the chemotherapy agent, etoposide.

Cyclosporine: Cyclosporine may increase the therapeutic and adverse effects of etoposide.

Quinupristin: This combination presents an increased risk of toxicity

Telithromycin: Telithromycin may reduce clearance of Etoposide. Consider alternate therapy or monitor for changes in the therapeutic/adverse effects of Etoposide if Telithromycin is initiated, discontinued or dose changed.

Trastuzumab: Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events.

Voriconazole: Voriconazole, a strong CYP3A4 inhibitor, may increase the serum concentration of etoposide by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of etoposide if voriconazole is initiated, discontinued or dose changed.