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Clinical data
ATC code
Legal status
Legal status
  • US: a
Pharmacokinetic data
Protein binding96 to 98%
Elimination half-life8–9 hours
  • N-(4-(acridin-9-ylamino)-3-methoxyphenyl)methanesulfonamide
CAS Number
PubChem CID
CompTox Dashboard (EPA)
ECHA InfoCard100.051.887 Edit this at Wikidata
Chemical and physical data
Molar mass393.46 g·mol−1
3D model (JSmol)
  • O=S(=O)(Nc1ccc(c(OC)c1)Nc2c4c(nc3c2cccc3)cccc4)C
  • InChI=1S/C21H19N3O3S/c1-27-20-13-14(24-28(2,25)26)11-12-19(20)23-21-15-7-3-5-9-17(15)22-18-10-6-4-8-16(18)21/h3-13,24H,1-2H3,(H,22,23) checkY

Amsacrine (synonyms: m-AMSA, acridinyl anisidide) is an antineoplastic agent.

It has been used in acute lymphoblastic leukemia.[1]


Its planar fused ring system can intercalate into the DNA of tumor cells, thereby altering the major and minor groove proportions. These alterations to DNA structure inhibit both DNA replication and transcription by reducing association between the affected DNA and: DNA polymerase, RNA polymerase and transcription factors.

Amsacrine also expresses topoisomerase inhibitor activity, specifically inhibiting topoisomerase II.[2] In contrast, the structurally similar o-AMSA differing in the position of the methoxy substituent group on the anilino-ring have little ability to poison topoisomerase II despite its intercalative behavior, suggesting that intercalation of the molecule in itself is insufficient to trap topoisomerase II as a covalent complex on DNA.[3][4][5]


  1. ^ Horstmann MA, Hassenpflug WA, zur Stadt U, Escherich G, Janka G, Kabisch H (December 2005). "Amsacrine combined with etoposide and high-dose methylprednisolone as salvage therapy in acute lymphoblastic leukemia in children". Haematologica. 90 (12): 1701–3. PMID 16330449.
  2. ^ Ketron AC, Denny WA, Graves DE, Osheroff N (February 2012). "Amsacrine as a Topoisomerase II Poison: Importance of Drug-DNA Interactions". Biochemistry. 51 (8): 1730–1739. doi:10.1021/bi201159b. PMC 3289736. PMID 22304499.
  3. ^ Wadkins RM, Graves DE (December 1989). "Thermodynamics of the interactions of m-AMSA and o-AMSA with nucleic acids: influence of ionic strength and DNA base composition". Nucleic Acids Research. 17 (23): 9933–46. doi:10.1093/nar/17.23.9933. PMC 335223. PMID 2602146.
  4. ^ DeMarini DM, Doerr CL, Meyer MK, Brock KH, Hozier J, Moore MM (September 1987). "Mutagenicity of m-AMSA and o-AMSA in mammalian cells due to clastogenic mechanism: possible role of topoisomerase". Mutagenesis. 2 (5): 349–55. doi:10.1093/mutage/2.5.349. PMID 2830452.
  5. ^ Nitiss JL (May 2009). "Targeting DNA topoisomerase II in cancer chemotherapy". Nature Reviews. Cancer. 9 (5): 338–50. doi:10.1038/nrc2607. PMC 2748742. PMID 19377506.