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Systematic (IUPAC) name
Clinical data
Trade names Vumon
AHFS/Drugs.com monograph
MedlinePlus a692045
  • AU: D
  • US: D (Evidence of risk)
Legal status
Routes of
Pharmacokinetic data
Bioavailability N/A
Protein binding >99%
Metabolism Hepatic (CYP2C19-mediated)
Biological half-life 5 hours
Excretion Renal and fecal
CAS Number 29767-20-2 YesY
ATC code L01CB02
PubChem CID 34698
DrugBank DB00444 N
ChemSpider 31930 N
UNII 957E6438QA N
KEGG D02698 YesY
Synonyms VM-26
Chemical data
Formula C32H32O13S
Molar mass 656.655 g/mol
 NYesY (what is this?)  (verify)

Teniposide (trade name Vumon) is a chemotherapeutic medication[1] used in the treatment of childhood acute lymphocytic leukemia (ALL), Hodgkin's lymphoma, certain brain tumours, and other types of cancer.[2] It is in a class of drugs known as podophyllotoxin derivatives and slows the growth of cancer cells in the body.[3]

Medical uses[edit]

Teniposide is used for the treatment of a number of cancer types in children. In the US, it is approved for the second-line therapy of acute lymphocytic leukemia (ALL) in combination with other antineoplastic drugs.[3] In Europe, it is also approved for the treatment of Hodgkin's lymphoma, generalized malignant lymphoma, reticulocyte sarcoma, acute leukaemia, primary brain tumours (glioblastoma, ependymoma, astrocytoma), bladder cancer, neuroblastoma and other solid tumours in children.[2]


The medication is injected though a vein and burns if it leaks under the skin. It can be used in combination with other anticancer drugs.[2]


The drug is contraindicated during pregnancy and lactation, in patients with severe liver or kidney impairment or severely impaired haematopoiesis.[2]

Side effects[edit]

Teniposide, when used with other chemotherapeutic agents for the treatment of ALL, results in severe bone marrow suppression. Other common side effects include gastrointestinal toxicity, hypersensitivity reactions, and reversible alopecia.[2]


No systematic interaction studies are available. The enzyme inducers phenobarbital and phenytoin have been found to lower its blood plasma concentrations.[4] Theoretically possible interactions include increased plasma concentrations when combined with sodium salicylate, sulfamethizole or tolbutamide, which displace teniposide from plasma protein binding, at least in vitro.[2][3]


Mechanism of action[edit]

Teniposide causes dose-dependent single- and double-stranded breaks in DNA and DNA-protein cross-links.[2] The substance has been found to act as an inhibitor of topoisomerase II (an enzyme that aids in DNA unwinding),[4][5] since it does not intercalate into DNA or bind strongly to DNA. The cytotoxic effects of teniposide are related to the relative number of double-stranded DNA breaks produced in cells, which are a reflection of the stabilization of a topoisomerase II-DNA intermediate.[citation needed]

Physical and chemical properties[edit]

An illustration of the wild mandrake, showing part of the rhizome (at bottom)

Teniposide is a semisynthetic derivative of podophyllotoxin[2] from the rhizome of the wild mandrake (Podophyllum peltatum). More specifically, it is a glycoside of podophyllotoxin with a D-glucose derivative. It is chemically similar to the anti-cancer drug etoposide, being distinguished only by a thienyl rest where etoposide has a methyl.[4] Both these compounds have been developed with the aim of creating less toxic derivatives of podophyllotoxin.[6]


  1. ^ Cragg, Gordon M.; Newman, David J. (2005). "Plants as a source of anti-cancer agents". Journal of Ethnopharmacology 100 (1–2): 72–9. doi:10.1016/j.jep.2005.05.011. PMID 16009521. 
  2. ^ a b c d e f g h Jasek, W, ed. (2007). Austria-Codex (in German) (62nd ed.). Vienna: Österreichischer Apothekerverlag. pp. 8855–6. ISBN 978-3-85200-181-4. 
  3. ^ a b c Drugs.com: Teniposide monograph.
  4. ^ a b c Mutschler, Ernst; Schäfer-Korting, Monika (2001). Arzneimittelwirkungen (in German) (8 ed.). Stuttgart: Wissenschaftliche Verlagsgesellschaft. pp. 894–5. ISBN 3-8047-1763-2. 
  5. ^ De Jong, S; Kooistra, A. J.; De Vries, E. G.; Mulder, N. H.; Zijlstra, J. G. (1993). "Topoisomerase II as a target of VM-26 and 4'-(9-acridinylamino)methanesulfon-m-aniside in atypical multidrug resistant human small cell lung carcinoma cells". Cancer research 53 (5): 1064–71. PMID 8382551. 
  6. ^ Dinnendahl, V, Fricke, U, ed. (2015). Arzneistoff-Profile (in German) 4 (28 ed.). Eschborn, Germany: Govi Pharmazeutischer Verlag. ISBN 978-3-7741-9846-3.