Azacitidine
Identification
- Name
- Azacitidine
- Accession Number
- DB00928
- Description
A pyrimidine nucleoside analogue that inhibits DNA methyltransferase, impairing DNA methylation. It is also an antimetabolite of cytidine, incorporated primarily into RNA. Azacytidine has been used as an antineoplastic agent.
- Type
- Small Molecule
- Groups
- Approved, Investigational
- Structure
Structure for Azacitidine (DB00928)
- Weight
- Average: 244.2047
Monoisotopic: 244.080769514 - Chemical Formula
- C8H12N4O5
- Synonyms
- 4-amino-1-beta-D-ribofuranosyl-s-triazin-2(1H)-one
- 5-azacytidine
- Azacitidina
- Azacitidine
- Azacitidinum
- Azacytidine
- External IDs
- NSC-102816
- U-18,496
- U-18496
Pharmacology
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For treatment of patients with the following French-American-British myelodysplastic syndrome subtypes: refractory anemia or refractory anemia with ringed sideroblasts (if accompanied by neutropenia or thrombocytopenia or requiring transfusions), refractory anemia with excess blasts, refractory anemia with excess blasts in transformation (now classified as acute myelogenous leukemia with multilineage dysplasia), and chronic myelomonocytic leukemia.
- Associated Conditions
- Contraindications & Blackbox Warnings
Contraindications & Blackbox WarningsWith our commercial data, access important information on dangerous risks, contraindications, and adverse effects.Our Blackbox Warnings cover Risks, Contraindications, and Adverse Effects- Pharmacodynamics
Azacitidine is believed to exert its antineoplastic effects by causing hypomethylation of DNA and direct cytotoxicity on abnormal hematopoietic cells in the bone marrow. The concentration of azacitidine required for maximum inhibition of DNA methylation in vitro does not cause major suppression of DNA synthesis. Hypomethylation may restore normal function to genes that are critical for differentiation and proliferation. 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. Upon uptake into cells, azacitidine is phosphorylated to 5-azacytidine monophosphate by uridine-cytidine kinase, then to diphosphate by pyrimidine monophosphate kinases and triphosphate by diphosphate kinases. 5-Azacitidine triphosphate is incorporated into RNA, leading to the disruption of nuclear and cytoplasmic RNA metabolism and inhibition of protein synthesis. 5-Azacytidine diphosphate is reduced to 5-aza-deoxycytidine diphosphate by ribonucleotide reductase. The resultant metabolite is phosphorylated to 5-azadeoxycitidine triphosphate by nucleoside diphosphate kinases. 5-azadeoxycitidine triphosphate is then incoporated into DNA, leading to inhibition of DNA synthesis. Azacitidine is most toxic during the S-phase of the cell cycle.
- Mechanism of action
Azacitidine (5-azacytidine) is a chemical analogue of the cytosine nucleoside used in DNA and RNA. Azacitidine may induce antineoplastic activity by inhibition of DNA methyltransferase at low doses and cytotoxicity through incorporation into RNA and DNA at high doses. Covalent binding to DNA methyltransferase results in hypomethylation of DNA and prevents DNA synthesis. As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.
Target Actions Organism ADNA (cytosine-5)-methyltransferase 1 inhibitorHumans ARNA otherHumans ADNA otherHumans - Absorption
Azacitidine is rapidly absorbed after subcutaneous administration. The bioavailability of subcutaneous azacitidine relative to IV azacitidine is approximately 89%, based on area under the curve.
- Volume of distribution
- 76 ± 26 L
- Protein binding
- Not Available
- Metabolism
An in vitro study of azacitidine incubation in human liver fractions indicated that azacitidine may be metabolized by the liver. The potential of azacitidine to inhibit cytochrome P450 (CYP) enzymes is not known.
- Route of elimination
Following IV administration of radioactive azacitidine to 5 cancer patients, the cumulative urinary excretion was 85% of the radioactive dose. Fecal excretion accounted for <1% of administered radioactivity over three days. Mean excretion of radioactivity in urine following SC administration of 14C-azacitidine was 50%.
- Half-life
Mean elimination half-life is approximately 4 hours.
- Clearance
- 167 +/- 49 L/h
- Adverse Effects
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One case of overdose with azacitidine was reported during clinical trials. A patient experienced diarrhea, nausea, and vomiting after receiving a single IV dose of approximately 290 mg/m2, almost 4 times the recommended starting dose.
- Affected organisms
- Humans and other mammals
- Pathways
- Not Available
- Pharmacogenomic Effects/ADRs
- Not Available
Interactions
- Drug Interactions
- This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.
Drug Interaction Integrate drug-drug
interactions in your softwareAbacavir Azacitidine may decrease the excretion rate of Abacavir which could result in a higher serum level. Abatacept The risk or severity of adverse effects can be increased when Azacitidine is combined with Abatacept. Abciximab The risk or severity of bleeding can be increased when Abciximab is combined with Azacitidine. Aceclofenac Aceclofenac may decrease the excretion rate of Azacitidine which could result in a higher serum level. Acemetacin Acemetacin may decrease the excretion rate of Azacitidine which could result in a higher serum level. Acenocoumarol The risk or severity of bleeding can be increased when Acenocoumarol is combined with Azacitidine. Acetaminophen Acetaminophen may decrease the excretion rate of Azacitidine which could result in a higher serum level. Acetazolamide Acetazolamide may increase the excretion rate of Azacitidine which could result in a lower serum level and potentially a reduction in efficacy. Acetylsalicylic acid Acetylsalicylic acid may decrease the excretion rate of Azacitidine which could result in a higher serum level. Aclidinium Azacitidine may decrease the excretion rate of Aclidinium which could result in a higher serum level. 
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- No interactions found.
Products
Comprehensive & structured drug product infoFrom application numbers to product codes, connect different identifiers through our commercial datasets.Easily connect various identifiers back to our datasets- Product Images
- International/Other Brands
- Ladakamycin / Mylosar
- Brand Name Prescription Products
Name Dosage Strength Route Labeller Marketing Start Marketing End Region Image Azacitidine Injection, powder, lyophilized, for solution 100 mg/1 Intravenous; Subcutaneous Actavis Pharma, Inc. 2016-09-22 2019-04-30 US 
Azacitidine Injection, powder, lyophilized, for solution 100 mg/1 Intravenous; Subcutaneous BluePoint Laboratories 2017-07-01 Not applicable US Azacitidine Accord 25 mg/ml Subcutaneous Accord Healthcare S.L.U. 2020-12-16 Not applicable EU 
Azacitidine Betapharm 25 mg/mL Subcutaneous Betapharm Arzneimittel Gmb H 2020-12-23 Not applicable EU Azacitidine Celgene 25 mg/ml Subcutaneous Celgene Europe Bv 2020-12-16 Not applicable EU Azacitidine for Injection Powder, for suspension Subcutaneous Fresenius Kabi Not applicable Not applicable Canada 
Azacitidine for Injection Powder, for suspension Subcutaneous Jamp Pharma Corporation Not applicable Not applicable Canada Azacitidine for Injection Powder, for suspension Subcutaneous Hikma Canada Limited Not applicable Not applicable Canada Azacitidine for Injection Powder, for suspension Subcutaneous Dr Reddy's Laboratories 2017-10-25 Not applicable Canada Azacitidine Mylan 25 mg/ml Subcutaneous Mylan Ireland Limited 2020-12-23 Not applicable EU - Generic Prescription Products
Name Dosage Strength Route Labeller Marketing Start Marketing End Region Image Azacitidine Injection, powder, lyophilized, for solution 100 mg/50mL Subcutaneous Panacea Biotec Limited 2019-05-06 Not applicable US Azacitidine Injection, powder, lyophilized, for solution 100 mg/1 Intravenous; Subcutaneous Armas Pharmaceuticals Inc. 2018-09-10 Not applicable US Azacitidine Injection, powder, lyophilized, for solution 100 mg/1 Intravenous; Subcutaneous Sandoz Inc 2014-03-27 Not applicable US Azacitidine Injection, powder, lyophilized, for solution 100 mg/1 Intravenous; Subcutaneous Cipla USA Inc. 2018-05-04 Not applicable US Azacitidine Injection, powder, lyophilized, for solution 100 mg/1 Intravenous; Subcutaneous Mylan Institutional LLC 2016-05-23 Not applicable US Azacitidine Injection, powder, lyophilized, for solution 100 mg/1 Intravenous; Subcutaneous Wockhardt USA LLC. 2016-09-29 Not applicable US 
Azacitidine Injection, powder, lyophilized, for solution 100 mg/1 Intravenous; Subcutaneous Seton Pharmaceuticals 2017-05-17 2018-02-13 US Azacitidine Injection, powder, lyophilized, for solution 100 mg/50mL Subcutaneous Breckenridge Pharmaceutical, Inc. 2017-06-23 Not applicable US Azacitidine Injection, powder, lyophilized, for solution 100 mg/1 Intravenous; Subcutaneous Meitheal Pharmaceuticals Inc. 2020-11-02 Not applicable US Azacitidine Injection, powder, lyophilized, for solution 100 mg/1 Intravenous; Subcutaneous Sandoz Inc 2013-09-16 Not applicable US
Categories
- ATC Codes
- L01BC07 — Azacitidine
- Drug Categories
- Antimetabolites
- Antineoplastic Agents
- Antineoplastic and Immunomodulating Agents
- Aza Compounds
- Carbohydrates
- Cytidine Deaminase Substrates
- Drugs that are Mainly Renally Excreted
- Enzyme Inhibitors
- Glycosides
- Immunosuppressive Agents
- Myelosuppressive Agents
- Narrow Therapeutic Index Drugs
- Noxae
- Nucleic Acid Synthesis Inhibitors
- Nucleic Acids, Nucleotides, and Nucleosides
- Nucleoside Metabolic Inhibitor
- Nucleosides
- Pyrimidine Analogues
- Pyrimidine Nucleosides
- Pyrimidines
- Ribonucleosides
- Toxic Actions
- Chemical TaxonomyProvided by Classyfire
- Description
- This compound belongs to the class of organic compounds known as glycosylamines. These are compounds consisting of an amine with a beta-N-glycosidic bond to a carbohydrate, thus forming a cyclic hemiaminal ether bond (alpha-amino ether).
- Kingdom
- Organic compounds
- Super Class
- Organic oxygen compounds
- Class
- Organooxygen compounds
- Sub Class
- Carbohydrates and carbohydrate conjugates
- Direct Parent
- Glycosylamines
- Alternative Parents
- Pentoses / Triazinones / Aminotriazines / 1,3,5-triazines / Tetrahydrofurans / Heteroaromatic compounds / Secondary alcohols / Oxacyclic compounds / Azacyclic compounds / Primary amines show 4 more
- Substituents
- 1,3,5-triazine / Alcohol / Amine / Amino-1,3,5-triazine / Aminotriazine / Aromatic heteromonocyclic compound / Azacycle / Heteroaromatic compound / Hydrocarbon derivative / Monosaccharide show 14 more
- Molecular Framework
- Aromatic heteromonocyclic compounds
- External Descriptors
- nucleoside analogue, N-glycosyl-1,3,5-triazine (CHEBI:2038)
Chemical Identifiers
- UNII
- M801H13NRU
- CAS number
- 320-67-2
- InChI Key
- NMUSYJAQQFHJEW-KVTDHHQDSA-N
- InChI
- InChI=1S/C8H12N4O5/c9-7-10-2-12(8(16)11-7)6-5(15)4(14)3(1-13)17-6/h2-6,13-15H,1H2,(H2,9,11,16)/t3-,4-,5-,6-/m1/s1
- IUPAC Name
- 4-amino-1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]-1,2-dihydro-1,3,5-triazin-2-one
- SMILES
- NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O
References
- Synthesis Reference
Lorenzo DE FERRA, Maurizio ZENONI, Stefano TURCHETTA, Mauro ANIBALDI, Ettore AMMIRATI, Paolo BRANDI, Giorgio BERARDI, "PROCESS FOR THE SYNTHESIS OF AZACITIDINE AND DECITABINE." U.S. Patent US20110245485, issued October 06, 2011.
US20110245485- General References
- Cihak A: Biological effects of 5-azacytidine in eukaryotes. Oncology. 1974;30(5):405-22. [PubMed:4142650]
- Kaminskas E, Farrell AT, Wang YC, Sridhara R, Pazdur R: FDA drug approval summary: azacitidine (5-azacytidine, Vidaza) for injectable suspension. Oncologist. 2005 Mar;10(3):176-82. [PubMed:15793220]
- Leone G, Voso MT, Teofili L, Lubbert M: Inhibitors of DNA methylation in the treatment of hematological malignancies and MDS. Clin Immunol. 2003 Oct;109(1):89-102. [PubMed:14585280]
- Ghoshal K, Bai S: DNA methyltransferases as targets for cancer therapy. Drugs Today (Barc). 2007 Jun;43(6):395-422. [PubMed:17612710]
- Silverman LR, Demakos EP, Peterson BL, Kornblith AB, Holland JC, Odchimar-Reissig R, Stone RM, Nelson D, Powell BL, DeCastro CM, Ellerton J, Larson RA, Schiffer CA, Holland JF: Randomized controlled trial of azacitidine in patients with the myelodysplastic syndrome: a study of the cancer and leukemia group B. J Clin Oncol. 2002 May 15;20(10):2429-40. [PubMed:12011120]
- Silverman LR: Targeting hypomethylation of DNA to achieve cellular differentiation in myelodysplastic syndromes (MDS). Oncologist. 2001;6 Suppl 5:8-14. [PubMed:11700387]
- Issa JP, Kantarjian H: Azacitidine. Nat Rev Drug Discov. 2005 May;Suppl:S6-7. [PubMed:15962522]
- O'Dwyer K, Maslak P: Azacitidine and the beginnings of therapeutic epigenetic modulation. Expert Opin Pharmacother. 2008 Aug;9(11):1981-6. doi: 10.1517/14656566.9.11.1981 . [PubMed:18627335]
- Siddiqui MA, Scott LJ: Azacitidine: in myelodysplastic syndromes. Drugs. 2005;65(13):1781-9; discussion 1790-1. [PubMed:16114977]
- Abdulhaq H, Rossetti JM: The role of azacitidine in the treatment of myelodysplastic syndromes. Expert Opin Investig Drugs. 2007 Dec;16(12):1967-75. [PubMed:18042004]
- Keating GM: Azacitidine: a review of its use in higher-risk myelodysplastic syndromes/acute myeloid leukaemia. Drugs. 2009;69(17):2501-18. doi: 10.2165/11202840-000000000-00000. [PubMed:19911860]
- Sullivan M, Hahn K, Kolesar JM: Azacitidine: a novel agent for myelodysplastic syndromes. Am J Health Syst Pharm. 2005 Aug 1;62(15):1567-73. [PubMed:16030365]
- Dapp MJ, Clouser CL, Patterson S, Mansky LM: 5-Azacytidine can induce lethal mutagenesis in human immunodeficiency virus type 1. J Virol. 2009 Nov;83(22):11950-8. doi: 10.1128/JVI.01406-09. Epub 2009 Sep 2. [PubMed:19726509]
- External Links
- Human Metabolome Database
- HMDB0015063
- KEGG Drug
- D03021
- KEGG Compound
- C11262
- PubChem Compound
- 9444
- PubChem Substance
- 46509032
- ChemSpider
- 9072
- BindingDB
- 50424715
- 1251
- ChEBI
- 2038
- ChEMBL
- CHEMBL1489
- ZINC
- ZINC000003861768
- Therapeutic Targets Database
- DAP000640
- PharmGKB
- PA451996
- PDBe Ligand
- 5AE
- RxList
- RxList Drug Page
- Drugs.com
- Drugs.com Drug Page
- Wikipedia
- Azacitidine
- AHFS Codes
- 10:00.00 — Antineoplastic Agents
- PDB Entries
- 4qd3
- FDA label
- Download (194 KB)
- MSDS
- Download (68.8 KB)
Clinical Trials
- Clinical Trials
Phase Status Purpose Conditions Count 4 Completed Treatment Myelodysplastic Syndromes (MDS) 1 4 Recruiting Treatment Acute Myeloid Leukaemia; Myelodysplastic Syndromes;Chronic Myelomonocytic Leukemia 1 4 Terminated Treatment Myelodysplastic Syndromes (MDS) 1 3 Active Not Recruiting Treatment Acute Myeloid Leukemia (AML) 4 3 Active Not Recruiting Treatment Acute Myeloid Leukemia (AML) / Acute Myeloid Leukemia With FMS-like Tyrosine Kinase (FLT3) Mutation 1 3 Active Not Recruiting Treatment Acute Myeloid Leukemia (AML) / Coronavirus Disease 2019 (COVID‑19) / Leukemia, Myelomonocytic, Chronic / Myelodysplastic Syndrome 1 3 Active Not Recruiting Treatment Isocitrate Dehydrogenase / Myeloid Leukemias 1 3 Active Not Recruiting Treatment MDS 1 3 Active Not Recruiting Treatment Myelodysplastic Syndrome 1 3 Active Not Recruiting Treatment Refractory Angioimmunoblastic T-cell Lymphoma / Relapsed Angioimmunoblastic T-Cell Lymphoma 1
Pharmacoeconomics
- Manufacturers
- Celgene corp
- Packagers
- Baxter International Inc.
- Ben Venue Laboratories Inc.
- Celgene
- Pharmion LLC
- Dosage Forms
Form Route Strength Injection, powder, for suspension Subcutaneous Injection, powder, for suspension Injection, powder, lyophilized, for solution Intravenous; Subcutaneous Powder Subcutaneous Injection, powder, lyophilized, for solution Intravenous; Subcutaneous 100 mg/30mL Injection, powder, lyophilized, for solution Intravenous; Subcutaneous 100 mg/1 Injection, powder, lyophilized, for solution Subcutaneous 100 mg/50mL Powder, for suspension Subcutaneous Powder Intravenous; Subcutaneous 100 mg Injection, powder, for solution Injection Subcutaneous Injection, powder, lyophilized, for suspension Subcutaneous 100 mg/1vial Injection, powder, for suspension Intravenous; Subcutaneous Powder Intravenous Tablet Oral 200 mg Tablet Oral 300 mg Tablet, film coated Oral 200 mg/1 Tablet, film coated Oral 300 mg/1 Injection, powder, lyophilized, for solution Subcutaneous Injection, powder, lyophilized, for suspension Subcutaneous 100 mg/4mL Powder Parenteral; Subcutaneous Powder, for suspension Subcutaneous 100 mg Injection, powder, lyophilized, for suspension Subcutaneous Injection, powder, for suspension Intravenous; Subcutaneous 100 mg Powder Intravenous; Subcutaneous Powder - Prices
Unit description Cost Unit Vidaza 100 mg vial 588.23USD vial DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.- Patents
Patent Number Pediatric Extension Approved Expires (estimated) Region US8846628 No 2010-06-03 2030-06-03 US
Properties
- State
- Solid
- Experimental Properties
Property Value Source melting point (°C) 229 °C PhysProp water solubility 8.9E+004 mg/L Not Available logP -3.5 Not Available - Predicted Properties
Property Value Source Water Solubility 12.1 mg/mL ALOGPS logP -2.4 ALOGPS logP -3.1 ChemAxon logS -1.3 ALOGPS pKa (Strongest Acidic) 12.55 ChemAxon pKa (Strongest Basic) -0.38 ChemAxon Physiological Charge 0 ChemAxon Hydrogen Acceptor Count 8 ChemAxon Hydrogen Donor Count 4 ChemAxon Polar Surface Area 140.97 Å2 ChemAxon Rotatable Bond Count 2 ChemAxon Refractivity 52.19 m3·mol-1 ChemAxon Polarizability 21.5 Å3 ChemAxon Number of Rings 2 ChemAxon Bioavailability 1 ChemAxon Rule of Five Yes ChemAxon Ghose Filter No ChemAxon Veber's Rule No ChemAxon MDDR-like Rule No ChemAxon - Predicted ADMET Features
Property Value Probability Human Intestinal Absorption + 0.9509 Blood Brain Barrier + 0.8753 Caco-2 permeable - 0.8715 P-glycoprotein substrate Non-substrate 0.7879 P-glycoprotein inhibitor I Non-inhibitor 0.9591 P-glycoprotein inhibitor II Non-inhibitor 0.9671 Renal organic cation transporter Non-inhibitor 0.9355 CYP450 2C9 substrate Non-substrate 0.8103 CYP450 2D6 substrate Non-substrate 0.8572 CYP450 3A4 substrate Non-substrate 0.6067 CYP450 1A2 substrate Non-inhibitor 0.9045 CYP450 2C9 inhibitor Non-inhibitor 0.9436 CYP450 2D6 inhibitor Non-inhibitor 0.9438 CYP450 2C19 inhibitor Non-inhibitor 0.9329 CYP450 3A4 inhibitor Non-inhibitor 0.9617 CYP450 inhibitory promiscuity Low CYP Inhibitory Promiscuity 0.9839 Ames test AMES toxic 0.8058 Carcinogenicity Non-carcinogens 0.9182 Biodegradation Not ready biodegradable 0.8432 Rat acute toxicity 1.7991 LD50, mol/kg Not applicable hERG inhibition (predictor I) Weak inhibitor 0.9794 hERG inhibition (predictor II) Non-inhibitor 0.8996
Spectra
- Mass Spec (NIST)
- Not Available
- Spectra
Spectrum Spectrum Type Splash Key Predicted GC-MS Spectrum - GC-MS Predicted GC-MS Not Available Predicted MS/MS Spectrum - 10V, Positive (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 20V, Positive (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 40V, Positive (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 10V, Negative (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 20V, Negative (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 40V, Negative (Annotated) Predicted LC-MS/MS Not Available 1H NMR Spectrum 1D NMR Not Applicable 13C NMR Spectrum 1D NMR Not Applicable
Targets
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- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Inhibitor
- General Function
- Zinc ion binding
- Specific Function
- 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 ...
- Gene Name
- DNMT1
- Uniprot ID
- P26358
- Uniprot Name
- DNA (cytosine-5)-methyltransferase 1
- Molecular Weight
- 183163.635 Da
References
- Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [PubMed:11752352]
- Kaminskas E, Farrell AT, Wang YC, Sridhara R, Pazdur R: FDA drug approval summary: azacitidine (5-azacytidine, Vidaza) for injectable suspension. Oncologist. 2005 Mar;10(3):176-82. [PubMed:15793220]
- Cataldo VD, Cortes J, Quintas-Cardama A: Azacitidine for the treatment of myelodysplastic syndrome. Expert Rev Anticancer Ther. 2009 Jul;9(7):875-84. doi: 10.1586/era.09.61. [PubMed:19589026]
- Leone G, Voso MT, Teofili L, Lubbert M: Inhibitors of DNA methylation in the treatment of hematological malignancies and MDS. Clin Immunol. 2003 Oct;109(1):89-102. [PubMed:14585280]
- Ghoshal K, Bai S: DNA methyltransferases as targets for cancer therapy. Drugs Today (Barc). 2007 Jun;43(6):395-422. [PubMed:17612710]
- Silverman LR, Demakos EP, Peterson BL, Kornblith AB, Holland JC, Odchimar-Reissig R, Stone RM, Nelson D, Powell BL, DeCastro CM, Ellerton J, Larson RA, Schiffer CA, Holland JF: Randomized controlled trial of azacitidine in patients with the myelodysplastic syndrome: a study of the cancer and leukemia group B. J Clin Oncol. 2002 May 15;20(10):2429-40. [PubMed:12011120]
- Fenaux P: Inhibitors of DNA methylation: beyond myelodysplastic syndromes. Nat Clin Pract Oncol. 2005 Dec;2 Suppl 1:S36-44. [PubMed:16341239]
- Silverman LR: Targeting hypomethylation of DNA to achieve cellular differentiation in myelodysplastic syndromes (MDS). Oncologist. 2001;6 Suppl 5:8-14. [PubMed:11700387]
- O'Dwyer K, Maslak P: Azacitidine and the beginnings of therapeutic epigenetic modulation. Expert Opin Pharmacother. 2008 Aug;9(11):1981-6. doi: 10.1517/14656566.9.11.1981 . [PubMed:18627335]
- Hollenbach PW, Nguyen AN, Brady H, Williams M, Ning Y, Richard N, Krushel L, Aukerman SL, Heise C, MacBeth KJ: A comparison of azacitidine and decitabine activities in acute myeloid leukemia cell lines. PLoS One. 2010 Feb 2;5(2):e9001. doi: 10.1371/journal.pone.0009001. [PubMed:20126405]
- Glover AB, Leyland-Jones B: Biochemistry of azacitidine: a review. Cancer Treat Rep. 1987 Oct;71(10):959-64. [PubMed:2443243]
Yes
Other
References
- Muller A, Florek M: 5-Azacytidine/Azacitidine. Recent Results Cancer Res. 2010;184:159-70. doi: 10.1007/978-3-642-01222-8_11. [PubMed:20072837]
- Kaminskas E, Farrell AT, Wang YC, Sridhara R, Pazdur R: FDA drug approval summary: azacitidine (5-azacytidine, Vidaza) for injectable suspension. Oncologist. 2005 Mar;10(3):176-82. [PubMed:15793220]
- Hollenbach PW, Nguyen AN, Brady H, Williams M, Ning Y, Richard N, Krushel L, Aukerman SL, Heise C, MacBeth KJ: A comparison of azacitidine and decitabine activities in acute myeloid leukemia cell lines. PLoS One. 2010 Feb 2;5(2):e9001. doi: 10.1371/journal.pone.0009001. [PubMed:20126405]
- Glover AB, Leyland-Jones B: Biochemistry of azacitidine: a review. Cancer Treat Rep. 1987 Oct;71(10):959-64. [PubMed:2443243]
- Cihak A, Vesely J, Skoda J: Azapyrimidine nucleosides: metabolism and inhibitory mechanisms. Adv Enzyme Regul. 1985;24:335-54. [PubMed:2424284]
- Dapp MJ, Clouser CL, Patterson S, Mansky LM: 5-Azacytidine can induce lethal mutagenesis in human immunodeficiency virus type 1. J Virol. 2009 Nov;83(22):11950-8. doi: 10.1128/JVI.01406-09. Epub 2009 Sep 2. [PubMed:19726509]
Yes
Other
References
- Overington JP, Al-Lazikani B, Hopkins AL: How many drug targets are there? Nat Rev Drug Discov. 2006 Dec;5(12):993-6. [PubMed:17139284]
- Imming P, Sinning C, Meyer A: Drugs, their targets and the nature and number of drug targets. Nat Rev Drug Discov. 2006 Oct;5(10):821-34. [PubMed:17016423]
- Allen A: Epigenetic alterations and cancer: new targets for therapy. IDrugs. 2007 Oct;10(10):709-12. [PubMed:17899489]
- Kaminskas E, Farrell AT, Wang YC, Sridhara R, Pazdur R: FDA drug approval summary: azacitidine (5-azacytidine, Vidaza) for injectable suspension. Oncologist. 2005 Mar;10(3):176-82. [PubMed:15793220]
- O'Dwyer K, Maslak P: Azacitidine and the beginnings of therapeutic epigenetic modulation. Expert Opin Pharmacother. 2008 Aug;9(11):1981-6. doi: 10.1517/14656566.9.11.1981 . [PubMed:18627335]
- Muller A, Florek M: 5-Azacytidine/Azacitidine. Recent Results Cancer Res. 2010;184:159-70. doi: 10.1007/978-3-642-01222-8_11. [PubMed:20072837]
- Hollenbach PW, Nguyen AN, Brady H, Williams M, Ning Y, Richard N, Krushel L, Aukerman SL, Heise C, MacBeth KJ: A comparison of azacitidine and decitabine activities in acute myeloid leukemia cell lines. PLoS One. 2010 Feb 2;5(2):e9001. doi: 10.1371/journal.pone.0009001. [PubMed:20126405]
- Glover AB, Leyland-Jones B: Biochemistry of azacitidine: a review. Cancer Treat Rep. 1987 Oct;71(10):959-64. [PubMed:2443243]
- Cihak A, Vesely J, Skoda J: Azapyrimidine nucleosides: metabolism and inhibitory mechanisms. Adv Enzyme Regul. 1985;24:335-54. [PubMed:2424284]
- Dapp MJ, Clouser CL, Patterson S, Mansky LM: 5-Azacytidine can induce lethal mutagenesis in human immunodeficiency virus type 1. J Virol. 2009 Nov;83(22):11950-8. doi: 10.1128/JVI.01406-09. Epub 2009 Sep 2. [PubMed:19726509]
Enzymes
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Substrate
- General Function
- Zinc ion binding
- Specific Function
- This enzyme scavenges exogenous and endogenous cytidine and 2'-deoxycytidine for UMP synthesis.
- Gene Name
- CDA
- Uniprot ID
- P32320
- Uniprot Name
- Cytidine deaminase
- Molecular Weight
- 16184.545 Da
References
- Garcia-Manero G, Stoltz ML, Ward MR, Kantarjian H, Sharma S: A pilot pharmacokinetic study of oral azacitidine. Leukemia. 2008 Sep;22(9):1680-4. doi: 10.1038/leu.2008.145. Epub 2008 Jun 12. [PubMed:18548103]
Drug created on June 13, 2005 13:24 / Updated on April 12, 2021 12:00