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Trade namesDacogen
Other names5-aza-2'-deoxycytidine
  • 4-Amino-1-(2-deoxy-β-D-erythro-pentofuranosyl)-1,3,5-triazin-2(1H)-one
Clinical data
Drug classPyrimidine analog[1]
Main usesMyelodysplastic syndromes, acute myeloid leukemia (AML)[2][3]
Side effectsFever, low red blood cells, low platelets, pneumonia[3]
  • US: N (Not classified yet)
Routes of
External links
License data
Legal status
  • US: ℞-only
  • In general: ℞ (Prescription only)
Protein binding<1%
Elimination half-life30 minutes
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

Decitabine, sold under the brand name Dacogen, is a medication used to treat myelodysplastic syndromes and acute myeloid leukemia (AML).[2][3] In AML it is used for older people who do not qualify for typical induction chemotherapy.[1] It is given by injection into a vein.[2]

Common side effects include fever, low red blood cells, and low platelets.[3] Other side effects may include pneumonia.[3] Use in pregnancy may harm the baby.[2] It is a pyrimidine analog and works by blocking DNA methyltransferase.[1][3]

Decitabine was approved for medical use in the United States in 2006 and Europe in 2012.[2][3] In the United Kingdom 50 mg costs the NHS about £970 as of 2021.[1] In the United States this amount costs about 214 USD.[4]

Medical uses

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).[6]


Decitabine monotherapy in acute myeloid leukemia.[7]

Decitabine is a hypomethylating agent.[8][9] 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.[10]


  1. 1.0 1.1 1.2 1.3 BNF 81: March-September 2021. BMJ Group and the Pharmaceutical Press. 2021. p. 954. ISBN 978-0857114105.
  2. 2.0 2.1 2.2 2.3 2.4 "Decitabine Monograph for Professionals". Archived from the original on 17 August 2019. Retrieved 21 December 2021.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 "Dacogen". Archived from the original on 18 November 2021. Retrieved 21 December 2021.
  4. "Decitabine Prices, Coupons & Patient Assistance Programs". Retrieved 21 December 2021.
  5. Ravandi, F.; Kantarjian, J. E.; Issa, S.; Jabbour, S.; Santos, G.; McCue, D.; Garcia-Manero, F. P. S.; Pierce, E.; O'Brien, J. P.; Cortés, J. E.; Ravandi, F. (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. "EC Approves Marketing Authorization Of DACOGEN For Acute Myeloid Leukemia". 2012-09-28. Archived from the original on 2017-09-14. Retrieved 28 September 2012.
  7. Santini, Valeria; Lübbert, Michael; Wierzbowska, Agnieszka; Ossenkoppele, Gert J. (April 2022). "The Clinical Value of Decitabine Monotherapy in Patients with Acute Myeloid Leukemia". Advances in Therapy. 39 (4): 1474–1488. doi:10.1007/s12325-021-01948-8. ISSN 1865-8652. Retrieved 5 December 2023.
  8. Kantarjian H, Issa JP, Rosenfeld CS, 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.
  9. Kantarjian HM, O'Brien S, Cortes J, 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.
  10. 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): 1562–9. doi:10.1161/atvbaha.115.305042. PMC 4754957. PMID 25953647.

Further reading

External links

External sites: