Azacitidine

Identification

Summary

Azacitidine is a pyrimidine nucleoside analogue used to treat certain subtypes of myelodysplastic syndrome.

Brand Names

Onureg, Vidaza

Generic Name

Azacitidine

DrugBank Accession Number

DB00928

Background

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.^1,8,10 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.² 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.^2,5,6,11,12

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.¹⁰ The use of oral azacitidine for the treatment of AML in patients in complete remission was approved by the FDA in September 2020.¹³

Type

Small Molecule

Groups

Approved, Investigational

Structure

Similar Structures

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

CC-486
NSC-102816
U-18,496
U-18496

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Pharmacology

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).^15,16

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.¹³

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Associated Conditions

Indication Type	Indication	Approval Level	Age Group	Patient Characteristics	Dose Form
Treatment of	Acute myeloid leukemia	••••••••••••	•••••		•••••••••
Treatment of	Acute myeloid leukemia (aml)	••••••••••••	•••••	••••••••• ••••••••••••	••••••
Treatment of	Acute myeloid leukemia (aml)	••••••••••••	•••••		••••••
Treatment of	Chronic myelomonocytic leukemia	••••••••••••			•••••••••
Treatment of	Refractory anemia	••••••••••••			•••••••••

Contraindications & Blackbox Warnings

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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.¹⁶ 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.¹⁶

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.¹⁶

Mechanism of action

Azacitidine (5-azacytidine) is a chemical analogue of the cytosine nucleoside present in DNA and RNA.^1,2 It induces antineoplastic activity by inhibiting DNA methyltransferase at low doses and inducing cytotoxicity by incorporating itself into RNA and DNA at high doses.^3,4,7

Covalent binding to DNA methyltransferase results in DNA hypomethylation and prevents DNA synthesis.⁷ 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.²

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.²

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.¹⁶

Target	Actions	Organism
ADNA (cytosine-5)-methyltransferase 1	inhibitor	Humans
ARNA	other	Humans
ADNA	other	Humans

Absorption

Azacitidine is rapidly absorbed after subcutaneous administration.^9,16 In adult patients with myelodysplastic syndrome given a single subcutaneous dose of 75 mg/m² of azacitidine, the C_max and T_max 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 C_max 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.¹⁶

Volume of distribution

In patients given an intravenous dose of azacitidine, the volume of distribution is 76 L.¹⁶

Protein binding

Not available.

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.¹⁶

Route of elimination

Azacitidine and its metabolites are mainly excreted through urine.^9,16 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%.¹⁶

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.¹⁶

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.¹⁶

Adverse Effects

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Toxicity

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.¹⁶ In mice, the oral LD₅₀ of azacitidine is 572 mg/kg, while the intravenous LD₅₀ is approximately 117 mg/kg.¹⁷

Pathways

Not Available

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Not Available

Interactions

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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
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Abacavir	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.

Food Interactions

No interactions found.

Products

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Product Images

International/Other Brands

Ladakamycin / Mylosar

Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End
Azacitidine	Injection, powder, lyophilized, for solution	100 mg/1	Intravenous; Subcutaneous	BluePoint Laboratories	2017-07-01	Not applicable
Azacitidine	Injection, powder, lyophilized, for solution	100 mg/1	Intravenous; Subcutaneous	Actavis Pharma, Inc.	2016-09-22	2019-04-30
Azacitidine Betapharm		25 mg/mL	Subcutaneous	Betapharm Arzneimittel Gmb H	2020-12-23	Not applicable
Azacitidine Celgene		25 mg/ml	Subcutaneous	Celgene Europe Bv	2020-12-16	2021-08-04
Azacitidine for Injection	Powder, for suspension	100 mg / vial	Subcutaneous	Sterimax Inc	Not applicable	Not applicable

Generic Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End
Azacitidine	Injection, powder, lyophilized, for solution	100 mg/50mL	Subcutaneous	Breckenridge Pharmaceutical, Inc.	2017-06-23	2024-01-31
Azacitidine	Injection, powder, lyophilized, for solution	100 mg/1	Intravenous; Subcutaneous	Dr. Reddy's Laboratories Inc.	2015-06-19	Not applicable
Azacitidine	Injection, powder, lyophilized, for solution	100 mg/1	Intravenous; Subcutaneous	Apotex Corp	2024-01-23	Not applicable
Azacitidine	Injection, powder, lyophilized, for solution	100 mg/1	Intravenous; Subcutaneous	Shilpa Medicare Limited	2016-12-05	Not applicable
Azacitidine	Injection, powder, lyophilized, for solution	100 mg/30mL	Intravenous; Subcutaneous	Fresenius Kabi USA, LLC	2017-03-16	Not applicable

Mixture Products

Name	Ingredients	Route	Labeller	Marketing Start	Marketing End
Azacitidine Accord	Azacitidine (100 mg) + Azacitidine (125 mg)	Subcutaneous	Accord Healthcare S.L.U.	2022-06-06	Not applicable
Azacitidine Accord	Azacitidine (100 mg) + Azacitidine (125 mg)	Subcutaneous	Accord Healthcare S.L.U.	2020-12-16	Not applicable
Azacitidine Accord	Azacitidine (100 mg) + Azacitidine (125 mg)	Subcutaneous	Accord Healthcare S.L.U.	2022-06-06	Not applicable
Azacitidine Accord	Azacitidine (100 mg) + Azacitidine (125 mg)	Subcutaneous	Accord Healthcare S.L.U.	2020-12-16	Not applicable

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. [Article]
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. [Article]
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. [Article]
Ghoshal K, Bai S: DNA methyltransferases as targets for cancer therapy. Drugs Today (Barc). 2007 Jun;43(6):395-422. [Article]
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. [Article]
Silverman LR: Targeting hypomethylation of DNA to achieve cellular differentiation in myelodysplastic syndromes (MDS). Oncologist. 2001;6 Suppl 5:8-14. [Article]
Issa JP, Kantarjian H: Azacitidine. Nat Rev Drug Discov. 2005 May;Suppl:S6-7. [Article]
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 . [Article]
Siddiqui MA, Scott LJ: Azacitidine: in myelodysplastic syndromes. Drugs. 2005;65(13):1781-9; discussion 1790-1. [Article]
Abdulhaq H, Rossetti JM: The role of azacitidine in the treatment of myelodysplastic syndromes. Expert Opin Investig Drugs. 2007 Dec;16(12):1967-75. [Article]
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. [Article]
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. [Article]
FDA Approved Drug Products: ONUREG (azacitidine) tablets [Link]
Health Canada Product Monograph: VIDAZA (azacitidine) injection [Link]
FDA Approved Drug Products: VIDAZA (azacitidine) injection, subcutaneous or intravenous use [Link]
FDA Approved Drug Products: VIDAZA (azacitidine) injection, subcutaneous or intravenous use (September 2022) [Link]
Celgene: Azacitidine SDS [Link]

External Links

Human Metabolome Database: HMDB0015063
KEGG Drug: D03021
KEGG Compound: C11262
PubChem Compound: 9444
PubChem Substance: 46509032
ChemSpider: 9072
BindingDB: 50424715
RxNav: 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

PDB Entries

4qd3

Clinical Trials

Clinical Trials Learn More" title="About Clinical Trials" id="clinical-trials-info" class="drug-info-popup" href="javascript:void(0);">

Phase	Status	Purpose	Conditions	Count
4	Active Not Recruiting	Treatment	Acute Myeloid Leukemia	1
4	Completed	Treatment	Myelodysplastic Syndrome	1
4	Not Yet Recruiting	Treatment	Myelodysplastic Syndrome	1
4	Recruiting	Treatment	Acute Myeloid Leukaemia; Myelodysplastic Syndromes;Chronic Myelomonocytic Leukemia	1
4	Terminated	Treatment	Myelodysplastic Syndrome	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, lyophilized, for suspension	Subcutaneous	100 mg/ml
Injection, powder, for suspension		25 mg/ml
Powder	Subcutaneous	25 MG/ML
Powder
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
Injection, powder, lyophilized, for solution	Intravenous; Subcutaneous	100 mg/4mL
Injection, powder, lyophilized, for solution	Intravenous; Subcutaneous	100 mg/30mL
Injection, powder, lyophilized, for solution	Subcutaneous	100 mg/50mL
Powder, for suspension	Subcutaneous	150 mg / vial
Powder	Intravenous; Subcutaneous	100 mg
Injection, powder, for solution		100 mg/1vial
Injection, powder, lyophilized, for suspension	Subcutaneous	100 mg/1vial
Injection, powder, for suspension	Intravenous; Subcutaneous
Injection, powder, lyophilized, for suspension	Subcutaneous	100 mg
Injection	Subcutaneous
Suspension	Subcutaneous	100.00 mg
Powder	Intravenous	100 mg
Tablet	Oral	200 mg
Tablet	Oral	300 mg
Tablet, film coated	Oral	200 MG
Tablet, film coated	Oral	200 mg/1
Tablet, film coated	Oral	300 MG
Tablet, film coated	Oral	300 mg/1
Injection, powder, lyophilized, for solution	Intravenous; Subcutaneous	100 mg
Solution	Subcutaneous	100.000 mg
Solution	Subcutaneous	100.00 mg
Injection, powder, lyophilized, for suspension	Subcutaneous	100 mg/4mL
Powder	Parenteral; Subcutaneous	25 MG/ML
Powder, for suspension	Subcutaneous	100 mg / vial
Suspension	Subcutaneous	100.000 mg
Injection, powder, lyophilized, for suspension	Subcutaneous
Injection, powder, for suspension	Subcutaneous	100 mg
Injection, powder, for suspension	Intravenous; Subcutaneous	100 mg
Injection	Subcutaneous	100 mg
Powder		100 mg/1vial

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	2014-09-30	2030-06-03
US11571436	No	2009-05-14	2029-05-14

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)	1.96	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

ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397)

Spectra

Mass Spec (NIST)

Not Available

Spectra

Spectrum	Spectrum Type	Splash Key
Predicted GC-MS Spectrum - GC-MS	Predicted GC-MS	splash10-08nc-9420000000-deb4c3c2e01ce611d805
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	splash10-03di-0900000000-0926f2f5f469326aa30b
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0hfx-9450000000-50b1083709142293ee8a
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	splash10-03di-2900000000-0ba55a50b07145eb1ddd
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	splash10-014i-9100000000-d40e54e58e9eb978a5a6
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	splash10-00kf-9000000000-76d796b375338cbb893a
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	splash10-022a-9400000000-466015d5596da2aaa07d
1H NMR Spectrum	1D NMR	Not Applicable
13C NMR Spectrum	1D NMR	Not Applicable
Predicted 1H NMR Spectrum	1D NMR	Not Applicable
Predicted 13C NMR Spectrum	1D NMR	Not Applicable

Chromatographic Properties

Collision Cross Sections (CCS)

Adduct	CCS Value (Å²)	Source type	Source
[M-H]-	161.3006852	predicted	DarkChem Lite v0.1.0
[M-H]-	161.0279852	predicted	DarkChem Lite v0.1.0
[M-H]-	160.6494852	predicted	DarkChem Lite v0.1.0
[M-H]-	149.57274	predicted	DeepCCS 1.0 (2019)
[M+H]+	161.2781852	predicted	DarkChem Lite v0.1.0
[M+H]+	162.0811852	predicted	DarkChem Lite v0.1.0
[M+H]+	161.4730852	predicted	DarkChem Lite v0.1.0
[M+H]+	151.9683	predicted	DeepCCS 1.0 (2019)
[M+Na]+	160.7080852	predicted	DarkChem Lite v0.1.0
[M+Na]+	161.2826852	predicted	DarkChem Lite v0.1.0
[M+Na]+	158.94322	predicted	DeepCCS 1.0 (2019)

Targets

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Details1. DNA (cytosine-5)-methyltransferase 1

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. [Article]
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. [Article]
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. [Article]
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. [Article]
Ghoshal K, Bai S: DNA methyltransferases as targets for cancer therapy. Drugs Today (Barc). 2007 Jun;43(6):395-422. [Article]
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. [Article]
Fenaux P: Inhibitors of DNA methylation: beyond myelodysplastic syndromes. Nat Clin Pract Oncol. 2005 Dec;2 Suppl 1:S36-44. [Article]
Silverman LR: Targeting hypomethylation of DNA to achieve cellular differentiation in myelodysplastic syndromes (MDS). Oncologist. 2001;6 Suppl 5:8-14. [Article]
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 . [Article]
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. [Article]
Glover AB, Leyland-Jones B: Biochemistry of azacitidine: a review. Cancer Treat Rep. 1987 Oct;71(10):959-64. [Article]

Details2. RNA

Kind

Nucleotide

Organism

Humans

Pharmacological action

Yes

Actions

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. [Article]
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. [Article]
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. [Article]
Glover AB, Leyland-Jones B: Biochemistry of azacitidine: a review. Cancer Treat Rep. 1987 Oct;71(10):959-64. [Article]
Cihak A, Vesely J, Skoda J: Azapyrimidine nucleosides: metabolism and inhibitory mechanisms. Adv Enzyme Regul. 1985;24:335-54. [Article]
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. [Article]

Details3. DNA

Kind

Nucleotide

Organism

Humans

Pharmacological action

Yes

Actions

Other

DNA is the molecule of heredity, as it is responsible for the genetic propagation of most inherited traits. It is a polynucleic acid that carries genetic information on cell growth, division, and function. DNA consists of two long strands of nucleotides twisted into a double helix and held together by hydrogen bonds. The sequence of nucleotides determines hereditary characteristics. Each strand serves as the template for subsequent DNA replication and as a template for mRNA production, leading to protein synthesis via ribosomes.

References

Overington JP, Al-Lazikani B, Hopkins AL: How many drug targets are there? Nat Rev Drug Discov. 2006 Dec;5(12):993-6. [Article]
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. [Article]
Allen A: Epigenetic alterations and cancer: new targets for therapy. IDrugs. 2007 Oct;10(10):709-12. [Article]
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. [Article]
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 . [Article]
Muller A, Florek M: 5-Azacytidine/Azacitidine. Recent Results Cancer Res. 2010;184:159-70. doi: 10.1007/978-3-642-01222-8_11. [Article]
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. [Article]
Glover AB, Leyland-Jones B: Biochemistry of azacitidine: a review. Cancer Treat Rep. 1987 Oct;71(10):959-64. [Article]
Cihak A, Vesely J, Skoda J: Azapyrimidine nucleosides: metabolism and inhibitory mechanisms. Adv Enzyme Regul. 1985;24:335-54. [Article]
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. [Article]

Enzymes

Details1. Cytidine deaminase

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. [Article]

Drug created at June 13, 2005 13:24 / Updated at February 20, 2024 23:54

Azacitidine

Identification

Structure for Azacitidine (DB00928)

Pharmacology

Interactions

Products

Categories

Chemical Identifiers

References

Clinical Trials

Pharmacoeconomics

Properties

Spectra

Collision Cross Sections (CCS)

Targets

References

References

References

Enzymes

References