Decitabine 50mg powder for solution for infusion vials
Requires a prescription from a doctor or prescriber
Myelodysplastic syndromes (MDS) are a heterogeneous group of hematopoietic neoplasms with variable underlying etiology and presentation, including neutropenia and thrombocytopenia.
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Dacogen 50mg powder for concentrate for solution for infusion vials
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(3)
Decitabine for untreated acute myeloid leukaemia (terminated appraisal) (TA548)
Decitabine for the treatment of acute myeloid leukaemia (terminated appraisal) (TA270)
Decitabine–cedazuridine for untreated acute myeloid leukaemia when intensive chemotherapy is unsuitable (terminated appraisal) (TA932)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 10 · Randomised trials: 8 · 2002–2026
Showing the 50 most relevant studies, sorted by most relevant.
Hagop M. Kantarjian, Xavier Thomas, Anna Dmoszyńska, et al.
Journal of Clinical Oncology, 2012
- Choice Behavior
- Decitabine
- Antimetabolites, Antineoplastic
Pin-fang He, Jing‐dong Zhou, Dong‐ming Yao, et al.
Oncotarget, 2017
- Decitabine
- Antimetabolites, Antineoplastic
- Azacitidine
Lei Gao, Yanqi Zhang, Sanbin Wang, et al.
Journal of Clinical Oncology, 2020
Nicholas J. Short, Hagop M. Kantarjian, Sanam Loghavi, et al.
The Lancet Haematology, 2018
- Decitabine
- Antimetabolites, Antineoplastic
- Leukemia, Myeloid, Acute
Riyas Mohamed FR, Aldubaisi S, Akbar A, et al.
2025
Background/Objectives: Triple-negative breast cancer (TNBC) is an aggressive subtype lacking ER, PR, and HER2 expression, with limited targeted therapies and poor outcomes. Epigenetic dysregulation, particularly aberrant DNA methylation, is a key driver. Decitabine, a DNA methyltransferase inhibitor (DNMTi), shows promise by reactivating silenced tumor suppressor genes and modulating immune responses. This systematic review evaluates preclinical and clinical evidence on decitabine's efficacy, mechanisms, and translational potential in TNBC. Methods: A PRISMA-2020 compliant search of PubMed, EBSCO, Web of Science, and Semantic Scholar was conducted up to April 2025. Included studies assessed decitabine alone or in combination in TNBC preclinical or clinical settings. Risk of bias was assessed using QUIPS and RoB 2.0 tools. Results: Twenty-five studies were included. In vitro, decitabine-induced growth inhibition, apoptosis, and re-expression of silenced genes (such as BRCA1 and CDH1). In vivo, it reduced tumor burden and enhanced anti-tumor immunity through MHC-I, PD-L1, and STING pathway upregulation. Synergy was noted with anti-PD-1, HDAC inhibitors, and chemotherapy. Resistance mechanisms included persistent DNMT activity, low DCK, and miRNA-driven escape (miR-155-TSPAN5). Conclusions: Decitabine demonstrates strong preclinical and early clinical potential in TNBC via epigenetic reprogramming and immune activation. Future strategies should focus on biomarker-based selection and resistance mitigation.
Abstract licence: CC BY
Perrone S, De Fazio L, Monachetti S, et al.
2026
- Sulfonamides
- Antineoplastic Combined Chemotherapy Protocols
- Leukemia, Myeloid, Acute
BackgroundIn younger, fit patients with acute myeloid leukemia (AML), intensive chemotherapy (IC) followed by consolidation or allogeneic hematopoietic stem cell transplantation (HSCT) is the standard approach. The authors performed a systematic review and meta-analysis to evaluate younger patients with AML treated with hypomethylating agents (HMA) plus venetoclax.MethodsThis systematic review and meta-analysis was conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. MEDLINE and the Cochrane Library were systematically searched through February 2026. Studies included AML patients with a median age ResultsEight studies (two randomized controlled trials, two phase 2 trials, and four real-world studies), comprising 429 patients with a mean age of 54 years, were included. The pooled CR/CRi rate was 66% (95% confidence interval [CI], 48%-85%), with an MRD-negative rate of 69% (95% CI, 49%-90%). The pooled 1-year OS was 75% (95% CI, 63%-86%), exceeding Surveillance, Epidemiology, and End Results database cohorts (62%). The 1-year EFS was 59% (95% CI, 53%-65%), with low between-study heterogeneity. Overall, 66% of patients successfully proceeded to HSCT. Meta-regression analyses suggested a trend toward improved EFS and OS in studies using decitabine than azacitidine.ConclusionsIn younger patients with AML, HMA plus venetoclax yielded high response rates, MRD negativity, and a substantial proportion of patients proceeding to HSCT. These findings support HMA/venetoclax as an effective induction strategy in selected younger patients and provide a rationale for prospective randomized trials comparing this approach with IC-based regimens.
Abstract licence: CC BY
Luo C, Zhang J, Huang X, et al.
2025
- Myelodysplastic Syndromes
- Antimetabolites, Antineoplastic
- Transplantation Conditioning
Ellen J. B. Derissen, Jos H. Beijnen, Jan H.M. Schellens
The Oncologist, 2013
- Clinical Trials, Phase III as Topic
- Decitabine
- Antimetabolites, Antineoplastic
Sharma A, Sharma A, Daid SS, et al.
2026
He Y, Zhang L, Liu M, et al.
2026
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
0.62 hours
Mechanism
Myelodysplastic syndromes (MDS) are a group of hematopoietic neoplasms that mani…
Food interactions
None known
Human targets
5 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
15 mg/m
Half-life
0.62 hours
Protein binding
1%
[A2265][L14962]
Volume of distribution
1.42 L/kg
[A2264]
Metabolism
Elimination
1%
[A2264]
Clearance
125 L/h
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Decitabine was developed by MGI Pharma/SuperGen Inc. and was approved by the FDA for the treatment of MDS on February 5, 2006. It was first marketed under the name Dacogen®.[L14962] It is also available as an oral combination product together with the cytidine deaminase inhibitor [cedazuridine].
[L14962]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 532 interactions
Adult male mice administered with between 0.3 and 1% of the recommended daily dose of decitabine three times a week for seven weeks had smaller testes with abnormal histology, decreased sperm count, and decreased fertility.
[L14962]
There is no known antidote for decitabine overdose. Patients experiencing an overdose are at an increased risk of severe adverse effects such as myelosuppression, including prolonged and severe neutropenia and thrombocytopenia. Symptomatic and supportive measures are recommended.
[L14962]
Decitabine is considered a prodrug, as it requires transport into cells and subsequent phosphorylation by distinct kinases to generate the active molecule 5-aza-2'-deoxycytidine-triphosphate, which is incorporated by DNA polymerase during DNA replication.[A2263][A2265][A2266][A2267][A215317][L14962] Once incorporated into DNA, decitabine is recognized as a substrate by DNA methyltransferase enzymes (DNMTs), specifically DNMT1, but due to the presence of an N5 rather than C5 atom, traps the DNMT through the irreversible formation of a covalent bond.[A2266][A2267] At low concentrations, this mode of action depletes DNMTs and results in global DNA hypomethylation while at high concentrations, it additionally results in double-strand breaks and cell death.[A2264][A2267][A215317]
The general hypothesis regarding decitabine's therapeutic efficacy is that the global hypomethylation it induces results in the expression of previously silent tumour suppressor genes.[A2261][A2262][A2263][A2264][A2265][A2266][A2267][A215317][L14962] However, there are other putative mechanisms also related to this change in DNA methylation, including indirect alteration of transcription through effects on transcription factors, indirectly altering histone modifications and chromatin structure, and activating pathways involved in DNA damage response.[A2263][A2265][A2267][A215317] The overall effect of decitabine is a decrease in neoplastic cell proliferation and an increase in the expression of tumour suppressor genes.
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L14962]
Similarly, decitabine at 20 mg/m2 for one hour once daily over five days resulted in a Cmax of 147 ng/mL (49% CV), an AUC0-∞ of 115 ng\*h/mL (43% CV), and a cumulative AUC of 570 ng\*h/mL (95% CI of 470-700).
[L14962]
[L14962]
[A2265][L14962]
[A2264]
[A2263][A2266][A2267][A215317]
Decitabine not incorporated into cellular DNA undergoes deamination by cytidine deaminase followed by additional degradation prior to excretion.
[A2263][A2266][A215317]
[A2264]
[L14962]
Proteins and enzymes this drug interacts with in the body
Associates with chromatin during G2 and M phases to maintain DNA methylation independently of replication. It is responsible for maintaining methylation patterns established in development. DNA methylation is coordinated with methylation of histones.
Mediates transcriptional repression by direct binding to HDAC2. In association with DNMT3B and via the recruitment of CTCFL/BORIS, involved in activation of BAG1 gene expression by modulating dimethylation of promoter histone H3 at H3K4 and H3K9. Probably forms a corepressor complex required for activated KRAS-mediated promoter hypermethylation and transcriptional silencing of tumor suppressor genes (TSGs) or other tumor-related genes in colorectal cancer (CRC) cells .
PMID:24623306
Also required to maintain a transcriptionally repressive state of genes in undifferentiated embryonic stem cells (ESCs) .
PMID:24623306
Associates at promoter regions of tumor suppressor genes (TSGs) leading to their gene silencing .
PMID:24623306
Promotes tumor growth PMID:24623306
PMID:12138111 PMID:16357870 PMID:30478443
DNA methylation is coordinated with methylation of histones .
PMID:12138111 PMID:16357870 PMID:30478443
It modifies DNA in a non-processive manner and also methylates non-CpG sites .
PMID:12138111 PMID:16357870 PMID:30478443
May preferentially methylate DNA linker between 2 nucleosomal cores and is inhibited by histone H1 (By similarity). Plays a role in paternal and maternal imprinting (By similarity). Required for methylation of most imprinted loci in germ cells (By similarity).
Acts as a transcriptional corepressor for ZBTB18 (By similarity). Recruited to trimethylated 'Lys-36' of histone H3 (H3K36me3) sites (By similarity). Can actively repress transcription through the recruitment of HDAC activity (By similarity).
Also has weak auto-methylation activity on Cys-710 in absence of DNA (By similarity)
May function as transcriptional co-repressor by associating with CBX4 and independently of DNA methylation. Seems to be involved in gene silencing (By similarity). In association with DNMT1 and via the recruitment of CTCFL/BORIS, involved in activation of BAG1 gene expression by modulating dimethylation of promoter histone H3 at H3K4 and H3K9.
Isoforms 4 and 5 are probably not functional due to the deletion of two conserved methyltransferase motifs. Functions as a transcriptional corepressor by associating with ZHX1. Required for DUX4 silencing in somatic cells PMID:27153398
PMID:12024216 PMID:18606987 PMID:20308065 PMID:24882211 PMID:26246421 PMID:30538141 PMID:31857589 PMID:30770470 PMID:38534334 PMID:39567688
Plays a central role in microtubule-dependent cell motility by mediating deacetylation of tubulin .
PMID:12024216 PMID:20308065 PMID:26246421
Required for cilia disassembly via deacetylation of alpha-tubulin .
PMID:17604723 PMID:26246421
Alpha-tubulin deacetylation results in destabilization of dynamic microtubules (By similarity). Promotes deacetylation of CTTN, leading to actin polymerization, promotion of autophagosome-lysosome fusion and completion of autophagy .
PMID:30538141
Deacetylates SQSTM1 .
PMID:31857589
Deacetylates peroxiredoxins PRDX1 and PRDX2, decreasing their reducing activity .
PMID:18606987
Deacetylates antiviral protein RIGI in the presence of viral mRNAs which is required for viral RNA detection by RIGI (By similarity). Sequentially deacetylates and polyubiquitinates DNA mismatch repair protein MSH2 which leads to MSH2 degradation, reducing cellular sensitivity to DNA-damaging agents and decreasing cellular DNA mismatch repair activities .
PMID:24882211
Deacetylates DNA mismatch repair protein MLH1 which prevents recruitment of the MutL alpha complex (formed by the MLH1-PMS2 heterodimer) to the MutS alpha complex (formed by the MSH2-MSH6 heterodimer), leading to tolerance of DNA damage .
PMID:30770470
Deacetylates RHOT1/MIRO1 which blocks mitochondrial transport and mediates axon growth inhibition (By similarity).
Deacetylates transcription factor SP1 which leads to increased expression of ENG, positively regulating angiogenesis .
PMID:38534334
Deacetylates KHDRBS1/SAM68 which regulates alternative splicing by inhibiting the inclusion of CD44 alternate exons .
PMID:26080397
Acts as a valine sensor by binding to valine through the primate-specific SE14 repeat region .
PMID:39567688
In valine deprivation conditions, translocates from the cytoplasm to the nucleus where it deacetylates TET2 which promotes TET2-dependent DNA demethylation, leading to DNA damage .
PMID:39567688
Promotes odontoblast differentiation following IPO7-mediated nuclear import and subsequent repression of RUNX2 expression (By similarity). In addition to its protein deacetylase activity, plays a key role in the degradation of misfolded proteins: when misfolded proteins are too abundant to be degraded by the chaperone refolding system and the ubiquitin-proteasome, mediates the transport of misfolded proteins to a cytoplasmic juxtanuclear structure called aggresome .
PMID:17846173
Probably acts as an adapter that recognizes polyubiquitinated misfolded proteins and targets them to the aggresome, facilitating their clearance by autophagy .
PMID:17846173
Involved in the MTA1-mediated epigenetic regulation of ESR1 expression in breast cancer PMID:24413532
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:10455109 PMID:14701834 PMID:15194733 PMID:21795683 PMID:21998139 PMID:30658162 PMID:32126230 PMID:9124315
Involved in renal nucleoside (re)absorption PMID:30658162
ATC L01BC58
ATC L01BC08
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Decitabine
Additional database identifiers
Drugs Product Database (DPD)
23041
ChemSpider
397844
BindingDB
96274
ZINC
ZINC000016929327
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2976
GenAtlas
DNMT1
GeneCards
DNMT1
GenBank Gene Database
X63692
GenBank Protein Database
1632819
Guide to Pharmacology
2605
UniProt Accession
DNMT1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2978
GeneCards
DNMT3A
UniProt Accession
DNM3A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2979
GeneCards
DNMT3B
UniProt Accession
DNM3B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4852
GenAtlas
HDAC1
GeneCards
HDAC1
GenBank Gene Database
U50079
GenBank Protein Database
1277084
Guide to Pharmacology
2658
UniProt Accession
HDAC1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:19086
GeneCards
HDAC11
Guide to Pharmacology
2615
UniProt Accession
HDA11_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4853
GenAtlas
HDAC2
GeneCards
HDAC2
GenBank Gene Database
U31814
GenBank Protein Database
1667394
Guide to Pharmacology
2616
UniProt Accession
HDAC2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4854
GenAtlas
HDAC3
GeneCards
HDAC3
GenBank Gene Database
U66914
GenBank Protein Database
2326173
Guide to Pharmacology
2617
UniProt Accession
HDAC3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:14063
GenAtlas
HDAC4
GeneCards
HDAC4
GenBank Gene Database
AF132607
Guide to Pharmacology
2659
UniProt Accession
HDAC4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:14068
GenAtlas
HDAC5
GeneCards
HDAC5
GenBank Gene Database
BK000028
Guide to Pharmacology
2660
UniProt Accession
HDAC5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:14067
GenAtlas
HDAC7
GeneCards
HDAC7
GenBank Gene Database
BC020505
Guide to Pharmacology
2661
UniProt Accession
HDAC7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:13315
GenAtlas
HDAC8
GeneCards
HDAC8
GenBank Gene Database
AF230097
GenBank Protein Database
8118721
Guide to Pharmacology
2619
UniProt Accession
HDAC8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:14065
GenAtlas
HDAC9
GeneCards
HDAC9
GenBank Gene Database
AY032737
GenBank Protein Database
15590680
Guide to Pharmacology
2620
UniProt Accession
HDAC9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18128
GenAtlas
HDAC10
GeneCards
HDAC10
GenBank Gene Database
AL512711
Guide to Pharmacology
2614
UniProt Accession
HDA10_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:14064
GenAtlas
HDAC6
GeneCards
HDAC6
GenBank Gene Database
AF132609
GenBank Protein Database
4754911
Guide to Pharmacology
2618
UniProt Accession
HDAC6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18170
GenAtlas
CMPK
GeneCards
CMPK1
GenBank Gene Database
AF070416
GenBank Protein Database
6578133
UniProt Accession
KCY_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7849
GenAtlas
NME1
GeneCards
NME1
GenBank Gene Database
X75598
UniProt Accession
NDKA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7850
GenAtlas
NME2
GeneCards
NME2
GenBank Gene Database
X58965
UniProt Accession
NDKB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2704
GenAtlas
DCK
GeneCards
DCK
GenBank Gene Database
M60527
UniProt Accession
DCK_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1712
GenAtlas
CDA
GeneCards
CDA
GenBank Gene Database
L27943
Guide to Pharmacology
3133
UniProt Accession
CDD_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11001
GeneCards
SLC28A1
UniProt Accession
S28A1_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q1181878), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.