Azacitidine 150mg powder for suspension for injection vials
Prescription only
Requires a prescription from a doctor or prescriber
Azacitidine is a pyrimidine nucleoside analogue with anti-neoplastic activity.
Active ingredients:
Azacitidine
No active safety alerts
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Official medicine documents
Source: MHRA Products DatabaseOGL 3.0
Updated 3 months ago(16 Jan 2026)Safety monitoring data
Yellow Card reports
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Suspected adverse reactions reported for Azacitidine
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
2 branded products available
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2 products
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Azacitidine 150mg powder for suspension for injection vials
Azacitidine 150mg powder for suspension for injection vials
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Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Clinical guidelines and formulary information
British National Formulary
Azacitidine
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(9)
Ivosidenib with azacitidine for untreated acute myeloid leukaemia with an IDH1 R132 mutation (TA979)
TA979
Technology appraisal
Updated Jun 2024Venetoclax with azacitidine for untreated acute myeloid leukaemia when intensive chemotherapy is unsuitable (TA765)
TA765
Technology appraisal
Updated Feb 2022Azacitidine for the treatment of myelodysplastic syndromes, chronic myelomonocytic leukaemia and acute myeloid leukaemia (TA218)
TA218
Technology appraisal
Updated Mar 2011Oral azacitidine for maintenance treatment of acute myeloid leukaemia after induction therapy (TA827)
TA827
Technology appraisal
Updated Oct 2022Azacitidine for treating acute myeloid leukaemia with more than 30% bone marrow blasts (TA399)
TA399
Technology appraisal
Updated Jul 2016Venetoclax with low dose cytarabine for untreated acute myeloid leukaemia when intensive chemotherapy is unsuitable (TA787)
TA787
Technology appraisal
Updated Apr 2022Midostaurin for untreated acute myeloid leukaemia (TA523)
TA523
Technology appraisal
Updated Jun 2018Midostaurin for treating advanced systemic mastocytosis (TA728)
TA728
Technology appraisal
Updated Sept 2021Liposomal cytarabine–daunorubicin for untreated acute myeloid leukaemia (TA552)
TA552
Technology appraisal
Updated Dec 2018Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Supply & product information
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Codes for healthcare professionals and prescribing systems
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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 codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
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Searching UK clinical trials...
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.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
41 minutes
Mechanism
Azacitidine (5-azacytidine) is a chemical analogue of the cytosine nucleoside present in DNA and RNA.
Food interactions
None known
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
75 mg/m
Azacitidine is rapidly absorbed after subcutaneous administration.
[A1414][L46861]…
[A1414][L46861]…
Half-life
41 minutes
The mean half-life of azacitidine after subcutaneous administration is 41 minutes.…
Protein binding
Not available.
Volume of distribution
76 L
In patients given an intravenous dose of azacitidine, the volume of distribution is 76 L.
[L46861]
[L46861]
Metabolism
An in vitro study of azacitidine incubation in human liver fractions indicated that cytochrome P450 (CYP) enzymes do not participate in the metabolism of azacitidine.…
Elimination
85%
Azacitidine and its metabolites are mainly excreted through urine.
[A1414][L46861]…
[A1414][L46861]…
Clearance
167 L/h
Azacitidine has an apparent subcutaneous clearance of 167 L/hour in adults.…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Azacitidine is a pyrimidine nucleoside analogue with anti-neoplastic activity. It differs from cytosine by the presence of nitrogen in the C5-position, key in its hypomethylating activity.[A1406][A1413][A1415] Two main mechanisms of action have been proposed for azacitidine. One of them is the induction of cytotoxicity. As an analogue of cytidine, it is able to incorporate into RNA and DNA, disrupting RNA metabolism and inhibiting protein and DNA synthesis. The other one is through the inhibition of DNA methyltransferase, impairing DNA methylation.[A1407] Due to its anti-neoplastic activity and its ability to inhibit methylation in replicating DNA, azacytidine has been used mainly used in the treatment of myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML), two types of cancer characterized by the presence of aberrant DNA methylation.[A1407][A1410][A1411][A1416][A1417]
In May 2004, the FDA approved the use of azacitidine administered subcutaneously for the treatment of MDS of all French-American-British (FAB) subtypes. In January 2007, the FDA approved the intravenous administration of azacitidine.[A1415] The use of oral azacitidine for the treatment of AML in patients in complete remission was approved by the FDA in September 2020.[L35335]
In May 2004, the FDA approved the use of azacitidine administered subcutaneously for the treatment of MDS of all French-American-British (FAB) subtypes. In January 2007, the FDA approved the intravenous administration of azacitidine.[A1415] The use of oral azacitidine for the treatment of AML in patients in complete remission was approved by the FDA in September 2020.[L35335]
Properties:
solid
Avg. mass: 244.20 Da
DrugBank indication
Azacitidine (for subcutaneous or intravenous use) is indicated for the treatment of adult patients with the following French-American-British (FAB) myelodysplastic syndrome (MDS) subtypes: refractory anemia (RA) or refractory anemia with ringed sideroblasts (RARS) (if accompanied by neutropenia or thrombocytopenia or requiring transfusions), refractory anemia with excess blasts (RAEB), refractory anemia with excess blasts in transformation (RAEB-T), and chronic myelomonocytic leukemia (CMMoL). Azacitidine is also indicated for the treatment of pediatric patients aged 1 month and older with newly diagnosed Juvenile Myelomonocytic Leukemia (JMML).
[L41910][L46861]
Azacitidine (for oral use) is indicated for continued treatment of adult patients with acute myeloid leukemia (AML) who achieved first complete remission or complete remission with incomplete blood count recovery following intensive induction chemotherapy and are not able to complete intensive curative therapy.
[L35335]
[L41910][L46861]
Azacitidine (for oral use) is indicated for continued treatment of adult patients with acute myeloid leukemia (AML) who achieved first complete remission or complete remission with incomplete blood count recovery following intensive induction chemotherapy and are not able to complete intensive curative therapy.
[L35335]
Also known as(31)
4-amino-1-beta-D-ribofuranosyl-s-triazin-2(1H)-one
5-Azacitidine
5-azacytidine
Azacitidina
Azacitidine
Azacitidinum
Azacytidine
2.1.1.37
Dosage forms(42)
Injection, powder, for suspension (Subcutaneous)
Injection, powder, lyophilized, for suspension (Subcutaneous) — 100 mg/ml
Injection, powder, for suspension (Parenteral) — 25 mg/ml
Powder (Subcutaneous) — 25 MG/ML
Powder — 25 MG/ML
Powder (Parenteral) — 25 MG/ML
Injection, powder, lyophilized, for solution (Intravenous; Subcutaneous) — 100 mg/1
Injection, powder, lyophilized, for solution (Intravenous; Subcutaneous) — 100 mg/50mL
Molecular properties(19)
Drug interactions(1179)
Known interactions with other medications. Always consult a healthcare professional.
The risk or severity of adverse effects can be increased when Denosumab is combined with Azacitidine.
Etanercept
Unknown severity
The risk or severity of adverse effects can be increased when Etanercept is combined with Azacitidine.
Peginterferon alfa-2a
Unknown severity
The risk or severity of adverse effects can be increased when Peginterferon alfa-2a is combined with Azacitidine.
Interferon alfa-n1
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfa-n1 is combined with Azacitidine.
Interferon alfa-n3
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfa-n3 is combined with Azacitidine.
Peginterferon alfa-2b
Unknown severity
The risk or severity of adverse effects can be increased when Peginterferon alfa-2b is combined with Azacitidine.
The risk or severity of adverse effects can be increased when Anakinra is combined with Azacitidine.
Interferon gamma-1b
Unknown severity
The risk or severity of adverse effects can be increased when Interferon gamma-1b is combined with Azacitidine.
Interferon alfa-2a
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfa-2a is combined with Azacitidine.
Aldesleukin
Unknown severity
The risk or severity of adverse effects can be increased when Aldesleukin is combined with Azacitidine.
Adalimumab
Unknown severity
The risk or severity of adverse effects can be increased when Adalimumab is combined with Azacitidine.
Gemtuzumab ozogamicin
Unknown severity
The risk or severity of adverse effects can be increased when Gemtuzumab ozogamicin is combined with Azacitidine.
Pegaspargase
Unknown severity
The risk or severity of adverse effects can be increased when Pegaspargase is combined with Azacitidine.
Infliximab
Unknown severity
The risk or severity of adverse effects can be increased when Infliximab is combined with Azacitidine.
Interferon beta-1b
Unknown severity
The risk or severity of adverse effects can be increased when Interferon beta-1b is combined with Azacitidine.
Interferon alfacon-1
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfacon-1 is combined with Azacitidine.
The risk or severity of adverse effects can be increased when Rituximab is combined with Azacitidine.
Basiliximab
Unknown severity
The risk or severity of adverse effects can be increased when Basiliximab is combined with Azacitidine.
The risk or severity of adverse effects can be increased when Muromonab is combined with Azacitidine.
Ibritumomab tiuxetan
Unknown severity
The risk or severity of adverse effects can be increased when Ibritumomab tiuxetan is combined with Azacitidine.
Tositumomab
Unknown severity
The risk or severity of adverse effects can be increased when Tositumomab is combined with Azacitidine.
Alemtuzumab
Unknown severity
The risk or severity of adverse effects can be increased when Alemtuzumab is combined with Azacitidine.
The risk or severity of adverse effects can be increased when Alefacept is combined with Azacitidine.
Efalizumab
Unknown severity
The risk or severity of adverse effects can be increased when Efalizumab is combined with Azacitidine.
Antithymocyte immunoglobulin (rabbit)
Unknown severity
The risk or severity of adverse effects can be increased when Antithymocyte immunoglobulin (rabbit) is combined with Azacitidine.
Interferon alfa-2b
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfa-2b is combined with Azacitidine.
Daclizumab
Unknown severity
The risk or severity of adverse effects can be increased when Daclizumab is combined with Azacitidine.
Phenylalanine
Unknown severity
The risk or severity of adverse effects can be increased when Phenylalanine is combined with Azacitidine.
Flunisolide
Unknown severity
The risk or severity of adverse effects can be increased when Flunisolide is combined with Azacitidine.
Bortezomib
Unknown severity
The risk or severity of adverse effects can be increased when Bortezomib is combined with Azacitidine.
Cladribine
Moderate
Azacitidine may increase the immunosuppressive activities of Cladribine.
Carmustine
Unknown severity
The risk or severity of adverse effects can be increased when Carmustine is combined with Azacitidine.
The risk or severity of adverse effects can be increased when Amsacrine is combined with Azacitidine.
The risk or severity of adverse effects can be increased when Bleomycin is combined with Azacitidine.
Chlorambucil
Unknown severity
The risk or severity of adverse effects can be increased when Chlorambucil is combined with Azacitidine.
Raltitrexed
Unknown severity
The risk or severity of adverse effects can be increased when Raltitrexed is combined with Azacitidine.
The risk or severity of adverse effects can be increased when Mitomycin is combined with Azacitidine.
Bexarotene
Unknown severity
The risk or severity of adverse effects can be increased when Bexarotene is combined with Azacitidine.
The risk or severity of adverse effects can be increased when Vindesine is combined with Azacitidine.
Floxuridine
Unknown severity
The risk or severity of adverse effects can be increased when Floxuridine is combined with Azacitidine.
Indomethacin
Unknown severity
The risk or severity of adverse effects can be increased when Indomethacin is combined with Azacitidine.
Tioguanine
Unknown severity
The risk or severity of adverse effects can be increased when Tioguanine is combined with Azacitidine.
Vinorelbine
Unknown severity
The risk or severity of adverse effects can be increased when Vinorelbine is combined with Azacitidine.
Dexrazoxane
Unknown severity
The risk or severity of adverse effects can be increased when Dexrazoxane is combined with Azacitidine.
Beclomethasone dipropionate
Unknown severity
The risk or severity of adverse effects can be increased when Beclomethasone dipropionate is combined with Azacitidine.
The risk or severity of adverse effects can be increased when Sorafenib is combined with Azacitidine.
Streptozocin
Unknown severity
The risk or severity of adverse effects can be increased when Streptozocin is combined with Azacitidine.
Trifluridine
Unknown severity
The risk or severity of adverse effects can be increased when Trifluridine is combined with Azacitidine.
Gemcitabine
Unknown severity
The risk or severity of adverse effects can be increased when Gemcitabine is combined with Azacitidine.
Betamethasone
Unknown severity
The risk or severity of adverse effects can be increased when Betamethasone is combined with Azacitidine.
Showing 50 of 1179 interactions
Toxicity & overdose
One case of overdose with azacitidine was reported during clinical trials. After receiving a single dose of 290 mg/m2 of azacitidine intravenously (almost 4 times the recommended starting dose), a patient experienced diarrhea, nausea, and vomiting. These adverse events resolved without sequelae, and the correct dose was resumed the following day.
In case of overdose, patients should be monitored with appropriate blood counts and receive supportive treatment as necessary. There is no known specific antidote for azacitidine overdosage.
[L46861]
In mice, the oral LD50 of azacitidine is 572 mg/kg, while the intravenous LD50 is approximately 117 mg/kg.
[L46871]
In case of overdose, patients should be monitored with appropriate blood counts and receive supportive treatment as necessary. There is no known specific antidote for azacitidine overdosage.
[L46861]
In mice, the oral LD50 of azacitidine is 572 mg/kg, while the intravenous LD50 is approximately 117 mg/kg.
[L46871]
How it works
Mechanism of action
Azacitidine (5-azacytidine) is a chemical analogue of the cytosine nucleoside present in DNA and RNA.[A1406][A1407] It induces antineoplastic activity by inhibiting DNA methyltransferase at low doses and inducing cytotoxicity by incorporating itself into RNA and DNA at high doses.[A1408][A1409][A1412]
Covalent binding to DNA methyltransferase results in DNA hypomethylation and prevents DNA synthesis.[A1412] On the other hand, the incorporation of azacitidine into RNA and DNA leads to cytotoxicity as follows: Following cellular uptake, azacitidine is phosphorylated by uridine-cytidine kinase to form 5-azacytidine monophosphate. Afterwards, pyrimidine monophosphate and diphosphate kinases phosphorylate 5-azacytidine monophosphate to form 5-azacytidine diphosphate and triphosphate, respectively. Azacitidine triphosphate is able to incorporate into RNA, disrupting RNA metabolism and protein synthesis. The reduction of azacytidine diphosphate leads to the formation of 5-aza-deoxycytidine diphosphate, which is then phosphorylated to form 5-azadeoxycitidine triphosphate, a compound able to incorporate into DNA and inhibit DNA synthesis.[A1407]
As a ribonucleoside, azacitidine incorporates into RNA to a larger extent than into DNA. Incorporating into RNA leads to the disassembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and the inhibition of protein production, resulting in cell death. During the S-phase of the cell cycle, azacitidine exhibits the highest toxicity; however, the predominant mechanism of cytotoxicity has not been elucidated.[A1407]
The cytotoxic effects of azacitidine cause the death of rapidly dividing cells, including cancer cells that are no longer responsive to normal growth control mechanisms. Non-proliferating cells are relatively insensitive to azacitidine. It is believed that azacitidine exerts its antineoplastic effects through direct cytotoxicity on abnormal hematopoietic cells in the bone marrow.[L46861]
Covalent binding to DNA methyltransferase results in DNA hypomethylation and prevents DNA synthesis.[A1412] On the other hand, the incorporation of azacitidine into RNA and DNA leads to cytotoxicity as follows: Following cellular uptake, azacitidine is phosphorylated by uridine-cytidine kinase to form 5-azacytidine monophosphate. Afterwards, pyrimidine monophosphate and diphosphate kinases phosphorylate 5-azacytidine monophosphate to form 5-azacytidine diphosphate and triphosphate, respectively. Azacitidine triphosphate is able to incorporate into RNA, disrupting RNA metabolism and protein synthesis. The reduction of azacytidine diphosphate leads to the formation of 5-aza-deoxycytidine diphosphate, which is then phosphorylated to form 5-azadeoxycitidine triphosphate, a compound able to incorporate into DNA and inhibit DNA synthesis.[A1407]
As a ribonucleoside, azacitidine incorporates into RNA to a larger extent than into DNA. Incorporating into RNA leads to the disassembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and the inhibition of protein production, resulting in cell death. During the S-phase of the cell cycle, azacitidine exhibits the highest toxicity; however, the predominant mechanism of cytotoxicity has not been elucidated.[A1407]
The cytotoxic effects of azacitidine cause the death of rapidly dividing cells, including cancer cells that are no longer responsive to normal growth control mechanisms. Non-proliferating cells are relatively insensitive to azacitidine. It is believed that azacitidine exerts its antineoplastic effects through direct cytotoxicity on abnormal hematopoietic cells in the bone marrow.[L46861]
Pharmacodynamics
The concentration of azacitidine required for maximum inhibition of DNA methylation in vitro does not cause major suppression of DNA synthesis, and hypomethylation may restore normal function to genes critical for differentiation and proliferation.[L46861] Genome-wide DNA methylation levels in bone marrow granulocytes were reduced in patients with juvenile myelomonocytic leukemia after the first treatment cycle of azacitidine (75 mg/m2 or 2.5 mg/kg), confirming the DNA-hypomethylating activity of azacitidine.[L46861]
The use of azacitidine causes anemia, neutropenia and thrombocytopenia in adult patients with myelodysplastic syndrome and pediatric patients with juvenile myelomonocytic leukemia. Azacitidine may cause renal toxicity, tumor lysis syndrome and embryo-fetal toxicity. It may also lead to the development of hepatotoxicity in patients with severe pre-existing hepatic impairment.[L46861]
The use of azacitidine causes anemia, neutropenia and thrombocytopenia in adult patients with myelodysplastic syndrome and pediatric patients with juvenile myelomonocytic leukemia. Azacitidine may cause renal toxicity, tumor lysis syndrome and embryo-fetal toxicity. It may also lead to the development of hepatotoxicity in patients with severe pre-existing hepatic impairment.[L46861]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Azacitidine is rapidly absorbed after subcutaneous administration.
[A1414][L46861]
In adult patients with myelodysplastic syndrome given a single subcutaneous dose of 75 mg/m2 of azacitidine, the Cmax and Tmax were 750 ng/ml and 0.5 hours, respectively. Based on the area under the curve, the bioavailability of subcutaneous azacitidine relative to intravenous azacitidine is approximately 89%. In 21 patients with cancer given subcutaneous azacitidine, the AUC and Cmax were approximately dose-proportional between 25 and 100 mg/m2.
Multiple subcutaneous or intravenous doses of azacitidine are not expected to result in drug accumulation.
[L46861]
[A1414][L46861]
In adult patients with myelodysplastic syndrome given a single subcutaneous dose of 75 mg/m2 of azacitidine, the Cmax and Tmax were 750 ng/ml and 0.5 hours, respectively. Based on the area under the curve, the bioavailability of subcutaneous azacitidine relative to intravenous azacitidine is approximately 89%. In 21 patients with cancer given subcutaneous azacitidine, the AUC and Cmax were approximately dose-proportional between 25 and 100 mg/m2.
Multiple subcutaneous or intravenous doses of azacitidine are not expected to result in drug accumulation.
[L46861]
Half-life
The mean half-life of azacitidine after subcutaneous administration is 41 minutes. The mean elimination half-life of azacitidine and its metabolites was about 4 hours for intravenous and subcutaneous administrations.
[L46861]
[L46861]
Protein binding
Not available.
Volume of distribution
In patients given an intravenous dose of azacitidine, the volume of distribution is 76 L.
[L46861]
[L46861]
Metabolism
An in vitro study of azacitidine incubation in human liver fractions indicated that cytochrome P450 (CYP) enzymes do not participate in the metabolism of azacitidine. Azacitidine is metabolized through spontaneous hydrolysis and deamination mediated by cytidine deaminase.
[L46861]
[L46861]
Route of elimination
Azacitidine and its metabolites are mainly excreted through urine.
[A1414][L46861]
In five cancer patients given radioactive azacitidine intravenously, the cumulative urinary excretion was 85% of the radioactive dose. Fecal excretion accounted for less than 1% of administered radioactivity over three days. Following the subcutaneous administration of 14C-azacitidine, the mean excretion of radioactivity in urine was 50%.
[L46861]
[A1414][L46861]
In five cancer patients given radioactive azacitidine intravenously, the cumulative urinary excretion was 85% of the radioactive dose. Fecal excretion accounted for less than 1% of administered radioactivity over three days. Following the subcutaneous administration of 14C-azacitidine, the mean excretion of radioactivity in urine was 50%.
[L46861]
Clearance
Azacitidine has an apparent subcutaneous clearance of 167 L/hour in adults. In pediatric patients, the geometric mean clearance was 21.8 L/hour.
[L46861]
[L46861]
Drug targets(4)
Proteins and enzymes this drug interacts with in the body
DNA (cytosine-5)-methyltransferase 1
DNMT1
inhibitor
Specific functionDNA (cytosine-5-)-methyltransferase activity
Cellular location
Nucleus
General function & pharmacology
Methylates CpG residues. Preferentially methylates hemimethylated DNA. Associates with DNA replication sites in S phase maintaining the methylation pattern in the newly synthesized strand, that is essential for epigenetic inheritance.
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
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
RNA
other
DNA
other
Poly [ADP-ribose] polymerase 1
PARP1
inhibitor
Specific functionchromatin binding
Cellular location
Chromosome
General function & pharmacology
Poly-ADP-ribosyltransferase that mediates poly-ADP-ribosylation of proteins and plays a key role in DNA repair .
PMID:17177976 PMID:18055453 PMID:18172500 PMID:19344625 PMID:19661379 PMID:20388712 PMID:21680843 PMID:22582261 PMID:23230272 PMID:25043379 PMID:26344098 PMID:26626479 PMID:26626480 PMID:30104678 PMID:31796734 PMID:32028527 PMID:32241924 PMID:32358582 PMID:33186521 PMID:34465625 PMID:34737271
Mediates glutamate, aspartate, serine, histidine or tyrosine ADP-ribosylation of proteins: the ADP-D-ribosyl group of NAD(+) is transferred to the acceptor carboxyl group of target residues and further ADP-ribosyl groups are transferred to the 2'-position of the terminal adenosine moiety, building up a polymer with an average chain length of 20-30 units .
PMID:19764761 PMID:25043379 PMID:28190768 PMID:29954836 PMID:35393539 PMID:7852410 PMID:9315851
Serine ADP-ribosylation of proteins constitutes the primary form of ADP-ribosylation of proteins in response to DNA damage .
PMID:33186521 PMID:34874266
Specificity for the different amino acids is conferred by interacting factors, such as HPF1 and NMNAT1 .
PMID:28190768 PMID:29954836 PMID:32028527 PMID:33186521 PMID:33589610 PMID:34625544 PMID:34874266
Following interaction with HPF1, catalyzes serine ADP-ribosylation of target proteins; HPF1 confers serine specificity by completing the PARP1 active site .
PMID:28190768 PMID:29954836 PMID:32028527 PMID:33186521 PMID:33589610 PMID:34625544 PMID:34874266
Also catalyzes tyrosine ADP-ribosylation of target proteins following interaction with HPF1 .
PMID:29954836 PMID:30257210
Following interaction with NMNAT1, catalyzes glutamate and aspartate ADP-ribosylation of target proteins; NMNAT1 confers glutamate and aspartate specificity (By similarity). PARP1 initiates the repair of DNA breaks: recognizes and binds DNA breaks within chromatin and recruits HPF1, licensing serine ADP-ribosylation of target proteins, such as histones (H2BS6ADPr and H3S10ADPr), thereby promoting decompaction of chromatin and the recruitment of repair factors leading to the reparation of DNA strand breaks .
PMID:17177976 PMID:18172500 PMID:19344625 PMID:19661379 PMID:23230272 PMID:27067600 PMID:34465625 PMID:34874266
HPF1 initiates serine ADP-ribosylation but restricts the polymerase activity of PARP1 in order to limit the length of poly-ADP-ribose chains .
PMID:33683197 PMID:34732825 PMID:34795260
In addition to base excision repair (BER) pathway, also involved in double-strand breaks (DSBs) repair: together with TIMELESS, accumulates at DNA damage sites and promotes homologous recombination repair by mediating poly-ADP-ribosylation .
PMID:26344098 PMID:30356214
Mediates the poly-ADP-ribosylation of a number of proteins, including itself, APLF, CHFR, RPA1 and NFAT5 .
PMID:17396150 PMID:19764761 PMID:24906880 PMID:34049076
In addition to proteins, also able to ADP-ribosylate DNA: catalyzes ADP-ribosylation of DNA strand break termini containing terminal phosphates and a 2'-OH group in single- and double-stranded DNA, respectively .
PMID:27471034
Required for PARP9 and DTX3L recruitment to DNA damage sites .
PMID:23230272
PARP1-dependent PARP9-DTX3L-mediated ubiquitination promotes the rapid and specific recruitment of 53BP1/TP53BP1, UIMC1/RAP80, and BRCA1 to DNA damage sites .
PMID:23230272
PARP1-mediated DNA repair in neurons plays a role in sleep: senses DNA damage in neurons and promotes sleep, facilitating efficient DNA repair (By similarity). In addition to DNA repair, also involved in other processes, such as transcription regulation, programmed cell death, membrane repair, adipogenesis and innate immunity .
PMID:15607977 PMID:17177976 PMID:19344625 PMID:27256882 PMID:32315358 PMID:32844745 PMID:35124853 PMID:35393539 PMID:35460603
Acts as a repressor of transcription: binds to nucleosomes and modulates chromatin structure in a manner similar to histone H1, thereby altering RNA polymerase II .
PMID:15607977 PMID:22464733
Acts both as a positive and negative regulator of transcription elongation, depending on the context .
PMID:27256882 PMID:35393539
Acts as a positive regulator of transcription elongation by mediating poly-ADP-ribosylation of NELFE, preventing RNA-binding activity of NELFE and relieving transcription pausing .
PMID:27256882
Acts as a negative regulator of transcription elongation in response to DNA damage by catalyzing poly-ADP-ribosylation of CCNT1, disrupting the phase separation activity of CCNT1 and subsequent activation of CDK9 .
PMID:35393539
Involved in replication fork progression following interaction with CARM1: mediates poly-ADP-ribosylation at replication forks, slowing fork progression .
PMID:33412112
Poly-ADP-ribose chains generated by PARP1 also play a role in poly-ADP-ribose-dependent cell death, a process named parthanatos (By similarity).
Also acts as a negative regulator of the cGAS-STING pathway .
PMID:32315358 PMID:32844745 PMID:35460603
Acts by mediating poly-ADP-ribosylation of CGAS: PARP1 translocates into the cytosol following phosphorylation by PRKDC and catalyzes poly-ADP-ribosylation and inactivation of CGAS .
PMID:35460603
Acts as a negative regulator of adipogenesis: catalyzes poly-ADP-ribosylation of histone H2B on 'Glu-35' (H2BE35ADPr) following interaction with NMNAT1, inhibiting phosphorylation of H2B at 'Ser-36' (H2BS36ph), thereby blocking expression of pro-adipogenetic genes (By similarity). Involved in the synthesis of ATP in the nucleus, together with NMNAT1, PARG and NUDT5 .
PMID:27257257
Nuclear ATP generation is required for extensive chromatin remodeling events that are energy-consuming PMID:27257257
PMID:17177976 PMID:18055453 PMID:18172500 PMID:19344625 PMID:19661379 PMID:20388712 PMID:21680843 PMID:22582261 PMID:23230272 PMID:25043379 PMID:26344098 PMID:26626479 PMID:26626480 PMID:30104678 PMID:31796734 PMID:32028527 PMID:32241924 PMID:32358582 PMID:33186521 PMID:34465625 PMID:34737271
Mediates glutamate, aspartate, serine, histidine or tyrosine ADP-ribosylation of proteins: the ADP-D-ribosyl group of NAD(+) is transferred to the acceptor carboxyl group of target residues and further ADP-ribosyl groups are transferred to the 2'-position of the terminal adenosine moiety, building up a polymer with an average chain length of 20-30 units .
PMID:19764761 PMID:25043379 PMID:28190768 PMID:29954836 PMID:35393539 PMID:7852410 PMID:9315851
Serine ADP-ribosylation of proteins constitutes the primary form of ADP-ribosylation of proteins in response to DNA damage .
PMID:33186521 PMID:34874266
Specificity for the different amino acids is conferred by interacting factors, such as HPF1 and NMNAT1 .
PMID:28190768 PMID:29954836 PMID:32028527 PMID:33186521 PMID:33589610 PMID:34625544 PMID:34874266
Following interaction with HPF1, catalyzes serine ADP-ribosylation of target proteins; HPF1 confers serine specificity by completing the PARP1 active site .
PMID:28190768 PMID:29954836 PMID:32028527 PMID:33186521 PMID:33589610 PMID:34625544 PMID:34874266
Also catalyzes tyrosine ADP-ribosylation of target proteins following interaction with HPF1 .
PMID:29954836 PMID:30257210
Following interaction with NMNAT1, catalyzes glutamate and aspartate ADP-ribosylation of target proteins; NMNAT1 confers glutamate and aspartate specificity (By similarity). PARP1 initiates the repair of DNA breaks: recognizes and binds DNA breaks within chromatin and recruits HPF1, licensing serine ADP-ribosylation of target proteins, such as histones (H2BS6ADPr and H3S10ADPr), thereby promoting decompaction of chromatin and the recruitment of repair factors leading to the reparation of DNA strand breaks .
PMID:17177976 PMID:18172500 PMID:19344625 PMID:19661379 PMID:23230272 PMID:27067600 PMID:34465625 PMID:34874266
HPF1 initiates serine ADP-ribosylation but restricts the polymerase activity of PARP1 in order to limit the length of poly-ADP-ribose chains .
PMID:33683197 PMID:34732825 PMID:34795260
In addition to base excision repair (BER) pathway, also involved in double-strand breaks (DSBs) repair: together with TIMELESS, accumulates at DNA damage sites and promotes homologous recombination repair by mediating poly-ADP-ribosylation .
PMID:26344098 PMID:30356214
Mediates the poly-ADP-ribosylation of a number of proteins, including itself, APLF, CHFR, RPA1 and NFAT5 .
PMID:17396150 PMID:19764761 PMID:24906880 PMID:34049076
In addition to proteins, also able to ADP-ribosylate DNA: catalyzes ADP-ribosylation of DNA strand break termini containing terminal phosphates and a 2'-OH group in single- and double-stranded DNA, respectively .
PMID:27471034
Required for PARP9 and DTX3L recruitment to DNA damage sites .
PMID:23230272
PARP1-dependent PARP9-DTX3L-mediated ubiquitination promotes the rapid and specific recruitment of 53BP1/TP53BP1, UIMC1/RAP80, and BRCA1 to DNA damage sites .
PMID:23230272
PARP1-mediated DNA repair in neurons plays a role in sleep: senses DNA damage in neurons and promotes sleep, facilitating efficient DNA repair (By similarity). In addition to DNA repair, also involved in other processes, such as transcription regulation, programmed cell death, membrane repair, adipogenesis and innate immunity .
PMID:15607977 PMID:17177976 PMID:19344625 PMID:27256882 PMID:32315358 PMID:32844745 PMID:35124853 PMID:35393539 PMID:35460603
Acts as a repressor of transcription: binds to nucleosomes and modulates chromatin structure in a manner similar to histone H1, thereby altering RNA polymerase II .
PMID:15607977 PMID:22464733
Acts both as a positive and negative regulator of transcription elongation, depending on the context .
PMID:27256882 PMID:35393539
Acts as a positive regulator of transcription elongation by mediating poly-ADP-ribosylation of NELFE, preventing RNA-binding activity of NELFE and relieving transcription pausing .
PMID:27256882
Acts as a negative regulator of transcription elongation in response to DNA damage by catalyzing poly-ADP-ribosylation of CCNT1, disrupting the phase separation activity of CCNT1 and subsequent activation of CDK9 .
PMID:35393539
Involved in replication fork progression following interaction with CARM1: mediates poly-ADP-ribosylation at replication forks, slowing fork progression .
PMID:33412112
Poly-ADP-ribose chains generated by PARP1 also play a role in poly-ADP-ribose-dependent cell death, a process named parthanatos (By similarity).
Also acts as a negative regulator of the cGAS-STING pathway .
PMID:32315358 PMID:32844745 PMID:35460603
Acts by mediating poly-ADP-ribosylation of CGAS: PARP1 translocates into the cytosol following phosphorylation by PRKDC and catalyzes poly-ADP-ribosylation and inactivation of CGAS .
PMID:35460603
Acts as a negative regulator of adipogenesis: catalyzes poly-ADP-ribosylation of histone H2B on 'Glu-35' (H2BE35ADPr) following interaction with NMNAT1, inhibiting phosphorylation of H2B at 'Ser-36' (H2BS36ph), thereby blocking expression of pro-adipogenetic genes (By similarity). Involved in the synthesis of ATP in the nucleus, together with NMNAT1, PARG and NUDT5 .
PMID:27257257
Nuclear ATP generation is required for extensive chromatin remodeling events that are energy-consuming PMID:27257257
Metabolizing enzymes(1)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
CDACytidine deaminase
substrate
Scientific references(12)
Cihak A.
Biological Effects of 5-Azacytidine in Eukaryotes.
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FDA Drug Approval Summary: Azacitidine (5-azacytidine, Vidaza™) for Injectable Suspension.
The Oncologist
200510(3):176-182. doi: 10.1634/theoncologist.10-3-176
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Inhibitors of DNA methylation in the treatment of hematological malignancies and MDS.
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DNA methyltransferase as targets for cancer therapy.
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Randomized Controlled Trial of Azacitidine in Patients With the Myelodysplastic Syndrome: A Study of the Cancer and Leukemia Group B.
Journal of Clinical Oncology
200220(10):2429-2440. doi: 10.1200/jco.2002.04.117
Silverman L.R.
Targeting Hypomethylation of DNA to Achieve Cellular Differentiation in Myelodysplastic Syndromes (MDS).
The Oncologist
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Issa J.P., Kantarjian H.
Azacitidine.
Nature Reviews Drug Discovery
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Azacitidine and the beginnings of therapeutic epigenetic modulation.
Expert Opinion on Pharmacotherapy
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Siddiqui M.A., Scott L.J.
Azacitidine.
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The role of azacitidine in the treatment of myelodysplastic syndromes.
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Keating G.M.
Azacitidine: a review of its use in higher-risk myelodysplastic syndromes/acute myeloid leukaemia.
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Sullivan M., Hahn K., Kolesar J.M.
Azacitidine: A novel agent for myelodysplastic syndromes.
American Journal of Health-System Pharmacy
200562(15):1567-1573. doi: 10.2146/ajhp040385
ATC classification(1 code)
ATC L01BC07
Affected organisms(1)
Humans and other mammals
International brands(2)
Experimental properties(3)
Protein Data Bank entries(1)
Commercial products(72)
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Azacitidine
Additional database identifiers
Drugs Product Database (DPD)
20554
ChemSpider
9072
BindingDB
50424715
PDB
5AE
ZINC
ZINC000003861768
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:270
GenAtlas
PARP1
GeneCards
PARP1
GenBank Gene Database
X16674
GenBank Protein Database
1017423
Guide to Pharmacology
2771
UniProt Accession
PARP1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1712
GenAtlas
CDA
GeneCards
CDA
GenBank Gene Database
L27943
Guide to Pharmacology
3133
UniProt Accession
CDD_HUMAN
International reference pricing
1 formulations
Reference pricing from DrugBank. Prices are indicative and may not reflect current UK costs.
Vidaza 100 mg vial
$588.23/vial
Source: DrugBank. Used under CC BY-NC 4.0 academic licence for non-commercial purposes.
Patent information
3 active patents
8846628
United States
Approved 30 Sept 2014 · Expires 3 Jun 2030
4y 2m
11571436
United States
Approved 7 Feb 2023 · Expires 14 May 2029
3y 1m
12053482
United States
Approved 6 Aug 2024 · Expires 14 May 2029
3y 1m
Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated 26 days ago(8 Mar 2026)