WARNING: This product is for research use only, not for human or veterinary use.

MedKoo CAT#: 100070

CAS#: 320-67-2

Description: Azacitidine is a pyrimidine nucleoside analogue of cytidine with antineoplastic activity. Azacitidine is incorporated into DNA, where it reversibly inhibits DNA methyltransferase, thereby blocking DNA methylation. Hypomethylation of DNA by azacitidine may activate tumor suppressor genes silenced by hypermethylation, resulting in an antitumor effect. This agent is also incorporated into RNA, thereby disrupting normal RNA function and impairing tRNA cytosine-5-methyltransferase activity.

Chemical Structure

CAS# 320-67-2

Theoretical Analysis

MedKoo Cat#: 100070
Name: Azacitidine
CAS#: 320-67-2
Chemical Formula: C8H12N4O5
Exact Mass: 244.08077
Molecular Weight: 244.2
Elemental Analysis: C, 39.35; H, 4.95; N, 22.94; O, 32.76

Price and Availability

Size Price Availability Quantity
500.0mg USD 90.0 Same Day
1.0g USD 150.0 Same Day
2.0g USD 250.0 Same Day
5.0g USD 450.0 Same Day
10.0g USD 650.0 Same Day
20.0g USD 950.0 2 Weeks
Bulk inquiry

Synonym: U18496; U-18496; U 18496; Abbreviations: 5AC; 5AZC. 5-azacytidine; azacytidine; ladakamycin. US brand names: Mylosar; Vidaza.

IUPAC/Chemical Name: 4-amino-1-((2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)tetrahydrofuran-2-yl)-1,3,5-triazin-2(1H)-one


InChi Code: 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

SMILES Code: O=C1N([C@@H]2O[C@H](CO)[C@@H](O)[C@H]2O)C=NC(N)=N1

Appearance: white solid powder

Purity: >98% (or refer to the Certificate of Analysis)

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.

Storage Condition: Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).

Solubility: Soluble in DMSO, not in water

Shelf Life: >10 years if stored properly

Drug Formulation: This drug may be formulated in DMSO

Stock Solution Storage: 0 - 4 C for short term (days to weeks), or -20 C for long term (months).

HS Tariff Code: 2934.99.9001

Biological target: Azacitidine (5-Azacytidine, 5-AzaC, Ladakamycin, AZA, 5-Aza, CC-486) is a nucleoside analogue of cytidine that specifically inhibits DNA methylation by trapping DNA methyltransferases.
In vitro activity: To test whether efficient DNA demethylation is indeed critical for the induction of stable Foxp3 expression in vitro, DNA-hypomethylating Aza (azacitidine, 5-azacytidine or 5-aza-deoxycytidine) was used to interfere with de novo DNA methylation. During replication these nucleoside analogs are integrated into DNA (and RNA for 5-azacytidine) and subsequently interfere with the function of DNMT1 (DNA methyltransferase 1) leading to rapid passive DNA demethylation. To test the impact of DNA methylation on the stability of Foxp3 expression, Treg was first indued in vitro by activation of Foxp3–CD25–CD4+ T cells in the presence of TGF-β. After sorting of Foxp3+ iTreg to high purity (97%), cells were restimulated either alone or in the presence of TGF-β or Aza. As depicted in Fig. 2, Aza significantly increased the proportion of cells expressing Foxp3 compared to restimulation cultures without exogenous TGF-β and Aza, which rapidly lost Foxp3 expression over time (Fig. 2B). On day 4 of restimulation, the percentage of Foxp3+ cells in Aza-treated cultures was more than 4-fold increased (Fig. 2A, 47% and 9.3% cells maintained Foxp3 expression in Aza-treated and non-treated cultures, respectively). TGF-β-containing control cultures maintained high Foxp3 expression with 91% Foxp3+ cells on day 4 (Fig. 2A). These results strengthen the idea of an essential role for DNA (de)methylation in the regulation of Foxp3 stability. Reference: Eur J Immunol. 2008 Jun;38(6):1654-63.
In vivo activity: Immunocompetent C57BL/6 mice were injected intraperitoneally (i.p.) with 250,000 VDID8 syngeneic MOSE cells. Mice were treated IP with azacitidine (AZA) (0.5 mg/kg). Hemorrhagic ascites fluid consistently develops at approximately 4–5 weeks post VDID8 injection and is an accurate measurement of tumor burden in mice, allowing observation of tumor growth in real time. After draining hemorrhagic ascites fluid from mice for the second time (typically week 5 post tumor injection), mice treated with single agent AZA demonstrated significantly lower tumor burdens (Fig 1b). Mice treated with AZA had an increase in median survival of 44 days (Fig 1c). Total numbers of lymphocytes are significantly increased by single agent AZA (Fig 1d,,ee). AZA led to significant increases in T cell, NK cell, and IFNγ+ lymphocyte populations examined in the tumor microenvironment (Fig 2a–g). Reference: Cancer Res. 2019 Jul 1;79(13):3445-3454.

Solubility Data

Solvent Max Conc. mg/mL Max Conc. mM
DMSO 31.0 126.95
Water 33.33 136.49

Preparing Stock Solutions

The following data is based on the product molecular weight 244.2 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

Recalculate based on batch purity %
Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 1.15 mL 5.76 mL 11.51 mL
5 mM 0.23 mL 1.15 mL 2.3 mL
10 mM 0.12 mL 0.58 mL 1.15 mL
50 mM 0.02 mL 0.12 mL 0.23 mL
In vitro protocol: 1. Polansky JK, Kretschmer K, Freyer J, Floess S, Garbe A, Baron U, Olek S, Hamann A, von Boehmer H, Huehn J. DNA methylation controls Foxp3 gene expression. Eur J Immunol. 2008 Jun;38(6):1654-63. doi: 10.1002/eji.200838105. PMID: 18493985. 2. Osorio-Montalvo P, Sáenz-Carbonell L, De-la-Peña C. 5-Azacytidine: A Promoter of Epigenetic Changes in the Quest to Improve Plant Somatic Embryogenesis. Int J Mol Sci. 2018 Oct 16;19(10):3182. doi: 10.3390/ijms19103182. PMID: 30332727; PMCID: PMC6214027.
In vivo protocol: 1. Travers M, Brown SM, Dunworth M, Holbert CE, Wiehagen KR, Bachman KE, Foley JR, Stone ML, Baylin SB, Casero RA Jr, Zahnow CA. DFMO and 5-Azacytidine Increase M1 Macrophages in the Tumor Microenvironment of Murine Ovarian Cancer. Cancer Res. 2019 Jul 1;79(13):3445-3454. doi: 10.1158/0008-5472.CAN-18-4018. Epub 2019 May 14. PMID: 31088836; PMCID: PMC6606334.

Molarity Calculator

Calculate the mass, volume, or concentration required for a solution.

*When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and SDS / CoA (available online).

Reconstitution Calculator

The reconstitution calculator allows you to quickly calculate the volume of a reagent to reconstitute your vial. Simply enter the mass of reagent and the target concentration and the calculator will determine the rest.


Dilution Calculator

Calculate the dilution required to prepare a stock solution.

1: Ritchie EK. Safety and efficacy of azacitidine in the treatment of elderly patients with myelodysplastic syndrome. Clin Interv Aging. 2012;7:165-73. doi: 10.2147/CIA.S24659. Epub 2012 Jun 19. Review. PubMed PMID: 22791989; PubMed Central PMCID: PMC3393359.

2: Thorpe M, Montalvão A, Pierdomenico F, Moita F, Almeida A. Treatment of chronic myelomonocytic leukemia with 5-Azacitidine: a case series and literature review. Leuk Res. 2012 Aug;36(8):1071-3. doi: 10.1016/j.leukres.2012.04.024. Epub 2012 May 17. Review. PubMed PMID: 22607959.

3: Keating GM. Azacitidine: a review of its use in the management of myelodysplastic syndromes/acute myeloid leukaemia. Drugs. 2012 May 28;72(8):1111-36. doi: 10.2165/11209430-000000000-00000. Review. Erratum in: Drugs. 2012 Jul 30;72(11):1578. PubMed PMID: 22571445.

4: Forghieri F, Morselli M, Leonardi G, Potenza L, Bonacorsi G, Coluccio V, Paolini A, Maccaferri M, Colaci E, Fantuzzi V, Bigliardi S, Zaldini P, Riva G, Barozzi P, Leonardi L, Rossi A, Marasca R, Narni F, Luppi M. Atraumatic splenic rupture in patients with myelodysplastic syndromes: report of a case occurred during treatment with 5-azacitidine and review of the literature. Leuk Res. 2012 Mar;36(3):e52-6. doi: 10.1016/j.leukres.2011.10.031. Epub 2011 Dec 14. Review. PubMed PMID: 22172466.

5: San Miguel Amigo L, Franco Osorio R, Mercadal Vilchez S, Martínez-Francés A. Azacitidine adverse effects in patients with myelodysplastic syndromes. Adv Ther. 2011 Jun;28 Suppl 4:6-11. doi: 10.1007/s12325-011-0024-2. Epub 2011 May 12. Review. PubMed PMID: 21688207.

6: Martínez-Francés A. Adverse effects of azacitidine: onset, duration, and treatment. Adv Ther. 2011 Jun;28 Suppl 4:1-5. doi: 10.1007/s12325-011-0021-5. Epub 2011 Jun 8. Review. PubMed PMID: 21688206.

7: Font P. Azacitidine for the treatment of patients with acute myeloid leukemia with 20%-30% blasts and multilineage dysplasia. Adv Ther. 2011 Mar;28 Suppl 3:1-9. doi: 10.1007/s12325-011-0002-8. Epub 2011 Mar 9. Review. PubMed PMID: 21431628.

8: Vigil CE, Martin-Santos T, Garcia-Manero G. Safety and efficacy of azacitidine in myelodysplastic syndromes. Drug Des Devel Ther. 2010 Sep 24;4:221-9. Review. PubMed PMID: 20957213; PubMed Central PMCID: PMC2948932.

9: Fenaux P, Bowen D, Gattermann N, Hellström-Lindberg E, Hofmann WK, Pfeilstöcker M, Sanz G, Santini V. Practical use of azacitidine in higher-risk myelodysplastic syndromes: an expert panel opinion. Leuk Res. 2010 Nov;34(11):1410-6. doi: 10.1016/j.leukres.2010.05.021. Epub 2010 Jul 6. Review. PubMed PMID: 20609474.

10: Götze K, Platzbecker U, Giagounidis A, Haase D, Lübbert M, Aul C, Ganser A, Germing U, Hofmann WK. Azacitidine for treatment of patients with myelodysplastic syndromes (MDS): practical recommendations of the German MDS Study Group. Ann Hematol. 2010 Sep;89(9):841-50. doi: 10.1007/s00277-010-1015-0. Epub 2010 Jun 22. Review. PubMed PMID: 20567826.

Additional Information

According to, Azacitidine is mainly used in the treatment of myelodysplastic syndrome (MDS), for which it received approval by the U.S. Food and Drug Administration on May 19, 2004; it is marketed as Vidaza. In a randomized controlled trial comparing azacitidine to supportive treatment of MDS, around 16% of people receiving the drug had a complete or partial response—blood cell counts and bone marrow morphology returning to normal—and 2/3 patients who required blood transfusions before the study no longer needed them after receiving azacitidine. It can also be used in vitro to remove methyl groups from DNA. This may weaken the effects of gene silencing mechanisms that occurred prior to the methylation. Methylation events are therefore believed to secure the DNA in a silenced state. Demethylation may reduce the stability of silencing signals and thus confer relative gene activation.
VIDAZA (azacitidine for injection) contains azacitidine, which is a pyrimidine nucleoside analog of cytidine. Azacitidine is 4-amino-1-β-D-ribofuranosyl-s-triazin-2(1H)-one.  The empirical formula is C8H12N4O5. The molecular weight is 244. Azacitidine is a white to off- white solid. Azacitidine was found to be insoluble in acetone, ethanol, and methyl ethyl ketone; slightly soluble in ethanol/water (50/50), propylene glycol, and polyethylene glycol; sparingly soluble in water, water saturated octanol, 5% dextrose in water, N-methyl-2-pyrrolidone, normal saline and 5% Tween 80 in water; and soluble in dimethylsulfoxide (DMSO). The finished product is supplied in a sterile form for reconstitution as a suspension for subcutaneous injection or reconstitution as a solution with further dilution for intravenous infusion. Vials of VIDAZA contain 100 mg of azacitidine and 100 mg mannitol as a sterile lyophilized powder.
Mechanism of Action
VIDAZA is a pyrimidine nucleoside analog of cytidine. VIDAZA 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 methylationin 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.