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Clinical data
Trade namesDacogen, Demylocan
Other names5-aza-2'-deoxycytidine
License data
Routes of
ATC code
Legal status
Legal status
Pharmacokinetic data
Protein binding<1%
Elimination half-life30 minutes
  • 4-Amino-1-(2-deoxy-β-D-erythro-pentofuranosyl)-1,3,5-triazin-2(1H)-one
CAS Number
PubChem CID
CompTox Dashboard (EPA)
ECHA InfoCard100.017.355 Edit this at Wikidata
Chemical and physical data
Molar mass228.208 g·mol−1
3D model (JSmol)
  • O=C1/N=C(\N=C/N1[C@@H]2O[C@@H]([C@@H](O)C2)CO)N
  • InChI=1S/C8H12N4O4/c9-7-10-3-12(8(15)11-7)6-1-4(14)5(2-13)16-6/h3-6,13-14H,1-2H2,(H2,9,11,15)/t4-,5+,6+/m0/s1 checkY
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Decitabine, sold under the brand name Dacogen among others, acts as a nucleic acid synthesis inhibitor.[3] It is a medication for the treatment of myelodysplastic syndromes, a class of conditions where certain blood cells are dysfunctional, and for acute myeloid leukemia (AML).[4] Chemically, it is a cytidine analog.

Medical uses[edit]

Decitabine is used to treat myelodysplastic syndromes (MDS) including previously treated and untreated, de novo and secondary MDS of all French-American-British subtypes (refractory anemia, refractory anemia with ringed sideroblasts, refractory anemia with excess blasts, refractory anemia with excess blasts in transformation, and chronic myelomonocytic leukemia) and Intermediate-1, Intermediate-2, and High-Risk International Prognostic Scoring System groups. In patients with chronic kidney disease, Batty and colleagues reported the first case series on the feasibility of therapy with hypomethylating agents in patients with chronic kidney disease.[5]

It also has EU approval for acute myeloid leukemia (AML).[4]


Decitabine is a hypomethylating agent.[6][7] It hypomethylates DNA by inhibiting DNA methyltransferase.

It functions in a similar manner to azacitidine, although decitabine can only be incorporated into DNA strands while azacitidine can be incorporated into both DNA and RNA chains.

It incorporates into DNA strands upon replication, and then when DNA methyltransferases (DNMTs) such as DNMT1, are engaged to bind the DNA and to replicate the methylation to the daughter strand, DNMTs are bound to decitabine irreversibly and cannot disengage. Therefore, the action of decitabine is division-dependent, meaning the cells have to divide in order for the pharmaceutical to act. Therefore, cancer cells which divide much more rapidly than most other cells in the body will be more severely affected by decitabine just because they replicate more. In cancer cells, and more specifically in haematological malignancies, it seems that DNA hypermethylation is really critical for their development. Methylation of CpG islands upstream of tumor suppressor genes in order to silence them seems to be critical for these type of cancers. Thus at optimal doses, decitabine blocks this type of methylation and has an anti-neoplastic effect.



A number of investigators have shown a relationship between atherosclerosis and disturbed blood flow. This upregulates DNA methyltransferase expression, which leads to genome-wide DNA methylation alterations and global gene expression changes. These studies have revealed several mechanosensitive genes, such as HoxA5, Klf3, and Klf4, whose promoters were hypermethylated by disturbed blood flow, but rescued by DNA methyltransferases inhibitors such as 5-aza-2'-deoxycytidine. It has been found that use of this DNA methyltranferase inhibitor prevents atherosclerosis lesion formation and reduces the production of inflammatory cytokines by macrophages.[8]


  1. ^ "Summary Basis of Decision (SBD) for Dacogen". Health Canada. 23 October 2014. Retrieved 29 May 2022.
  2. ^ "Summary Basis of Decision (SBD) for Demylocan". Health Canada. 23 October 2014. Retrieved 29 May 2022.
  3. ^ "Decitabine". National Center for Biotechnology Information. Retrieved September 24, 2016.
  4. ^ a b "EC Approves Marketing Authorization Of DACOGEN For Acute Myeloid Leukemia". 2012-09-28. Retrieved 28 September 2012.
  5. ^ Batty GN, Kantarjian H, Issa JP, Jabbour E, Santos FP, McCue D, et al. (June 2010). "Feasibility of therapy with hypomethylating agents in patients with renal insufficiency". Clinical Lymphoma, Myeloma & Leukemia. 10 (3): 205–210. doi:10.3816/CLML.2010.n.032. PMC 3726276. PMID 20511166.
  6. ^ Kantarjian H, Issa JP, Rosenfeld CS, Bennett JM, Albitar M, DiPersio J, et al. (April 2006). "Decitabine improves patient outcomes in myelodysplastic syndromes: results of a phase III randomized study". Cancer. 106 (8): 1794–1803. doi:10.1002/cncr.21792. PMID 16532500. S2CID 9556660.
  7. ^ Kantarjian HM, O'Brien S, Cortes J, Giles FJ, Faderl S, Issa JP, et al. (August 2003). "Results of decitabine (5-aza-2'deoxycytidine) therapy in 130 patients with chronic myelogenous leukemia". Cancer. 98 (3): 522–528. doi:10.1002/cncr.11543. PMID 12879469. S2CID 1149318.
  8. ^ Dunn J, Thabet S, Jo H (July 2015). "Flow-Dependent Epigenetic DNA Methylation in Endothelial Gene Expression and Atherosclerosis". Arteriosclerosis, Thrombosis, and Vascular Biology. 35 (7): 1562–1569. doi:10.1161/atvbaha.115.305042. PMC 4754957. PMID 25953647.

Further reading[edit]

  • Moon C, Kim SH, Park KS, Choi BK, Lee HS, Park JB, et al. (June 2009). "Use of epigenetic modification to induce FOXP3 expression in naïve T cells". Transplantation Proceedings. 41 (5): 1848–1854. doi:10.1016/j.transproceed.2009.02.101. PMID 19545742.

External links[edit]

  • "Decitabine". Drug Information Portal. U.S. National Library of Medicine.