From Wikipedia, the free encyclopedia
Clinical data
Trade namesVumon
Other namesVM-26
  • AU: D
Routes of
ATC code
Legal status
Legal status
Pharmacokinetic data
Protein binding>99%
MetabolismHepatic (CYP2C19-mediated)
Elimination half-life5 hours
ExcretionRenal and fecal
  • (5R,5aR,8aR,9S)-5,8,8a,9-Tetrahydro-5-(4-hydroxy-3,5-dimethoxyphenyl)-9-({4,6-O-[(R)-2-thienylmethylene]-β-D-glucopyranosyl}oxy)furo[3',4':6,7]naphtho[2,3-d]-1,3-dioxol-6(5aH)-one
CAS Number
PubChem CID
CompTox Dashboard (EPA)
ECHA InfoCard100.045.286 Edit this at Wikidata
Chemical and physical data
Molar mass656.66 g·mol−1
3D model (JSmol)
  • COc1cc(cc(c1O)OC)[C@@H]2c3cc4c(cc3[C@H]([C@@H]5[C@@H]2C(=O)OC5)O[C@H]6[C@@H]([C@H]([C@H]7[C@H](O6)COC(O7)c8cccs8)O)O)OCO4
  • InChI=1S/C32H32O13S/c1-37-19-6-13(7-20(38-2)25(19)33)23-14-8-17-18(42-12-41-17)9-15(14)28(16-10-39-30(36)24(16)23)44-32-27(35)26(34)29-21(43-32)11-40-31(45-29)22-4-3-5-46-22/h3-9,16,21,23-24,26-29,31-35H,10-12H2,1-2H3/t16-,21+,23+,24-,26+,27+,28+,29+,31?,32-/m0/s1 ☒N
 ☒NcheckY (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]


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 GM, Newman DJ (August 2005). "Plants as a source of anti-cancer agents". Journal of Ethnopharmacology. 100 (1–2): 72–79. 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 E, Schäfer-Korting M (2001). Arzneimittelwirkungen (in German) (8th ed.). Stuttgart: Wissenschaftliche Verlagsgesellschaft. pp. 894–5. ISBN 3-8047-1763-2.
  5. ^ de Jong S, Kooistra AJ, de Vries EG, Mulder NH, Zijlstra JG (March 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): 1064–1071. PMID 8382551.
  6. ^ Dinnendahl V, Fricke U, eds. (2015). Arzneistoff-Profile (in German). Vol. 4 (28th ed.). Eschborn, Germany: Govi Pharmazeutischer Verlag. ISBN 978-3-7741-9846-3.