1. 5 Azacytidine
2. 5-azacytidine
3. Azacytidine
4. Nsc 102816
5. Nsc-102816
6. Nsc102816
7. Vidaza
1. 5-azacytidine
2. 320-67-2
3. Azacytidine
4. Ladakamycin
5. Vidaza
6. Mylosar
7. 5-azacitidine
8. Azacitidinum
9. Azacitidina
10. Azacitidinum [inn-latin]
11. 5-azac
12. Azacitidina [inn-spanish]
13. Nsc-102816
14. U-18496
15. Onureg
16. Nsc 102816
17. 4-amino-1-beta-d-ribofuranosyl-1,3,5-triazin-2(1h)-one
18. 4-amino-1-beta-d-ribofuranosyl-s-triazin-2(1h)-one
19. Nsc102816
20. 5azac
21. Antibiotic U 18496
22. 4-amino-1-((2r,3r,4s,5r)-3,4-dihydroxy-5-(hydroxymethyl)tetrahydrofuran-2-yl)-1,3,5-triazin-2(1h)-one
23. Chebi:2038
24. M801h13nru
25. 4-amino-1-(beta-d-ribofuranosyl)-1,3,5-triazin-2(1h)-one
26. U-18,496
27. 4-amino-1-[(2r,3r,4s,5r)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]-1,3,5-triazin-2-one
28. 4-amino-1-[(2r,3r,4s,5r)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]-1,2-dihydro-1,3,5-triazin-2-one
29. Wr-183027
30. Ncgc00090851-04
31. Dsstox_cid_116
32. U 18496
33. Dsstox_rid_75378
34. Dsstox_gsid_20116
35. C8h12n4o5
36. 1,3,5-triazin-2(1h)-one, 4-amino-1-.beta.-d-ribofuranosyl-
37. Mfcd00006539
38. Ccris 60
39. Smr000857239
40. Vidaza (tn)
41. Hsdb 6879
42. 5-aza-cr
43. Sr-01000075662
44. Einecs 206-280-2
45. Brn 0620461
46. Unii-m801h13nru
47. Azacitidine (jan/usan/inn)
48. Azacitidine [usan:inn:ban]
49. 4-amino-1-beta-d-ribofuranosyl-1,3,5-traizin-2(1h)-one
50. Ns-17
51. 4-amino-1-[(2r,3r,4s,5r)-3,4-dihydroxy-5-(hydroxymethyl)tetrahydrofuran-2-yl]-1,3,5-triazin-2-one
52. Cas-320-67-2
53. Azacitidine (vidaza)
54. 2-(beta-d-ribofuranosyl)-4-amino-1,3,5-triazin-2-one
55. Antibiotic U18496
56. U18496
57. Spectrum_001262
58. 4-amino-1-beta-d-ribofuranosyl-1,3,5-triazine-2(1h)-one
59. Azacitidine [mi]
60. Spectrum2_000786
61. Spectrum3_001509
62. Spectrum4_000922
63. Spectrum5_001166
64. Azacitidine [inn]
65. Azacitidine [jan]
66. Azacitidine [hsdb]
67. Azacitidine [iarc]
68. Azacitidine [usan]
69. Molmap_000062
70. 4-amino-1-.beta.-d-ribofuranosyl-s-triazin-2(1h)-one
71. A 2385
72. Azacitidine [vandf]
73. Schembl3741
74. Azacitidine [mart.]
75. Chembl1489
76. Azacitidine (5-azacytidine)
77. Lopac0_000035
78. Azacitidine [usp-rs]
79. Azacitidine [who-dd]
80. Bspbio_003157
81. Kbiogr_001444
82. Kbiogr_002556
83. Kbioss_001742
84. Kbioss_002565
85. Mls001333121
86. Mls001333122
87. Mls002153249
88. Mls002548894
89. Divk1c_000125
90. Spectrum1502111
91. Spbio_000892
92. Azacitidine [ema Epar]
93. Gtpl6796
94. Dtxsid9020116
95. S-triazin-2(1h)-one, 4-amino-1-beta-d-ribofuranosyl-
96. Bcbcmap01_000083
97. Hms500g07
98. Kbio1_000125
99. Kbio2_001742
100. Kbio2_002556
101. Kbio2_004310
102. Kbio2_005124
103. Kbio2_006878
104. Kbio2_007692
105. Kbio3_002657
106. Kbio3_003034
107. Nmusyjaqqfhjew-kvtdhhqdsa-
108. Azacitidine [orange Book]
109. Pyrimidine Antimetabolite: Inhibits Nucleic Acid Replication
110. Cmap_000082
111. Ninds_000125
112. Hms1921j22
113. Hms2092d08
114. Hms2231f15
115. Hms3259d19
116. Hms3260g11
117. Pharmakon1600-01502111
118. Zinc3861768
119. 5-azacytidine, >=98% (hplc)
120. Tox21_111032
121. Tox21_302985
122. Tox21_500035
123. Bdbm50424715
124. Ccg-39046
125. Nsc758186
126. S1782
127. Onureg (cc-486; Oral Azacitidine)
128. Akos015896938
129. Tox21_111032_1
130. Am83944
131. Cs-1287
132. Db00928
133. Lp00035
134. Nc00672
135. Nsc-758186
136. Nsc103-627
137. 4-amino-1-[(2r,3r,4s,5r)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]-1,3,5-triaz
138. Idi1_000125
139. Ncgc00090851-01
140. Ncgc00090851-02
141. Ncgc00090851-03
142. Ncgc00090851-05
143. Ncgc00090851-06
144. Ncgc00090851-07
145. Ncgc00090851-08
146. Ncgc00090851-10
147. Ncgc00090851-14
148. Ncgc00090851-22
149. Ncgc00178234-01
150. Ncgc00256541-01
151. Ncgc00260720-01
152. As-13697
153. Hy-10586
154. Sri-10756_10
155. Sri-10756_12
156. Wr183027
157. Db-006955
158. Sl-000003
159. Eu-0100035
160. D03021
161. F10504
162. 320a672
163. A821115
164. Q416451
165. J-700085
166. Sr-01000075662-1
167. Sr-01000075662-3
168. Sr-01000075662-7
169. Brd-k03406345-001-02-1
170. Brd-k03406345-001-27-8
171. 4-amino-1-?-d-ribofuranosyl-1,3,5-triazin-2(1h)-one
172. Z1522566611
173. 4-amino-1-(bet.-d-ribofuranosyl)-1,3,5-triazin-2(1h)-one
174. 4-amino-1-beta-d-ribofuranosyl-1,3,5-tr Iazin-2(1h)-one
175. Azacitidine, United States Pharmacopeia (usp) Reference Standard
176. 4-amino-1-(beta-d-ribofuranosyl)-1,3,5-triazin-2(1h)-one; Ladakamycin
177. Azacitidine, Pharmaceutical Secondary Standard; Certified Reference Material
178. 1401238-97-8
179. 5-azacytidine, Hybri-max(tm), Gamma-irradiated, Lyophilized Powder, Bioxtra, Suitable For Hybridoma
180. 5ae
181. 6-amino-3-[(2r,3r,4s,5r)-3,4-dihydroxy-5-(hydroxymethyl)tetrahydrofuran-2-yl]-1h-1,3,5-triazin-3-ium-2-one
| Molecular Weight | 244.20 g/mol |
|---|---|
| Molecular Formula | C8H12N4O5 |
| XLogP3 | -2.2 |
| Hydrogen Bond Donor Count | 4 |
| Hydrogen Bond Acceptor Count | 5 |
| Rotatable Bond Count | 2 |
| Exact Mass | 244.08076950 g/mol |
| Monoisotopic Mass | 244.08076950 g/mol |
| Topological Polar Surface Area | 141 Ų |
| Heavy Atom Count | 17 |
| Formal Charge | 0 |
| Complexity | 384 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 4 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
| 1 of 4 | |
|---|---|
| Drug Name | Azacitidine |
| PubMed Health | Azacitidine (Injection) |
| Drug Classes | Antineoplastic Agent |
| Drug Label | Vidaza (azacitidine for injectable suspension) contains azacitidine, which is a pyrimidine nucleoside analog of cytidine. Azacitidine is 4-amino-1--D-ribofuranosyl-s-triazin-2(1H)-one. The structural formula is as follows:The empirical formula i... |
| Active Ingredient | Azacitidine |
| Dosage Form | Injectable |
| Route | Intravenous, subcutaneous |
| Strength | 100mg/vial |
| Market Status | Prescription |
| Company | Dr Reddys Labs |
| 2 of 4 | |
|---|---|
| Drug Name | Vidaza |
| PubMed Health | Azacitidine (Injection) |
| Drug Classes | Antineoplastic Agent |
| Drug Label | Vidaza (azacitidine for injectable suspension) contains azacitidine, which is a pyrimidine nucleoside analog of cytidine. Azacitidine is 4-amino-1--D-ribofuranosyl-s-triazin-2(1H)-one. The structural formula is as follows:The empirical formula i... |
| Active Ingredient | Azacitidine |
| Dosage Form | Injectable |
| Route | Intravenous, subcutaneous |
| Strength | 100mg/vial |
| Market Status | Prescription |
| Company | Celgene |
| 3 of 4 | |
|---|---|
| Drug Name | Azacitidine |
| PubMed Health | Azacitidine (Injection) |
| Drug Classes | Antineoplastic Agent |
| Drug Label | Vidaza (azacitidine for injectable suspension) contains azacitidine, which is a pyrimidine nucleoside analog of cytidine. Azacitidine is 4-amino-1--D-ribofuranosyl-s-triazin-2(1H)-one. The structural formula is as follows:The empirical formula i... |
| Active Ingredient | Azacitidine |
| Dosage Form | Injectable |
| Route | Intravenous, subcutaneous |
| Strength | 100mg/vial |
| Market Status | Prescription |
| Company | Dr Reddys Labs |
| 4 of 4 | |
|---|---|
| Drug Name | Vidaza |
| PubMed Health | Azacitidine (Injection) |
| Drug Classes | Antineoplastic Agent |
| Drug Label | Vidaza (azacitidine for injectable suspension) contains azacitidine, which is a pyrimidine nucleoside analog of cytidine. Azacitidine is 4-amino-1--D-ribofuranosyl-s-triazin-2(1H)-one. The structural formula is as follows:The empirical formula i... |
| Active Ingredient | Azacitidine |
| Dosage Form | Injectable |
| Route | Intravenous, subcutaneous |
| Strength | 100mg/vial |
| Market Status | Prescription |
| Company | Celgene |
Anticancer agent used to treat acute myclogenous leukemia
Kirk-Othmer Encyclopedia of Chemical Technology. 4th ed. Volumes 1: New York, NY. John Wiley and Sons, 1991-Present., p. V5 (1993) 872
Expl Ther: The ability of phenylacetate to prevent carcinogenesis by the chemotherapeutic hypomethylating drug 5-aza-2'-deoxycytidine (5AzadC) was tested in vitro and in mice. Transient exposure of immortalized, but poorly tumorigenic ras-transformed 4C8 fibroblasts to 5AzadC resulted in neoplastic transformation manifested by loss of contact inhibition of growth, acquired invasiveness, and increased tumorigenicity in athymic mice.
Prasanna P et al; Clin Cancer Res 1 (8): 865-71
5-Azacytidine, an inhibitor of DNA methylation as well as a cytidine antimetabolite, becomes incorporated predominantly into RNA and has antileukemic and differentiating action. A newer analog, 2',2'-difluorodeoxycytidine (gemcitabine), becomes incorporated into DNA and inhibits the elongation of nascent DNA strands. It has promising activity in various human solid tumors, including lung cancer and ovarian cancer ... .
Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1249
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.
FDA Label
Azacitidine Mylan is indicated for the treatment of adult patients who are not eligible for haematopoietic stem cell transplantation (HSCT) with:
- intermediate 2 and high risk myelodysplastic syndromes (MDS) according to the International Prognostic Scoring System (IPSS),
- chronic myelomonocytic leukaemia (CMML) with 10 29% marrow blasts without myeloproliferative disorder,
- acute myeloid leukaemia (AML) with 20 30% blasts and multi lineage dysplasia, according to World Health Organisation (WHO) classification,
- AML with > 30% marrow blasts according to the WHO classification.
Azacitidine betapharm is indicated for the treatment of adult patients who are not eligible for haematopoietic stem cell transplantation (HSCT) with:
- intermediate-2 and high-risk myelodysplastic syndromes (MDS) according to the International Prognostic Scoring System (IPSS),
- chronic myelomonocytic leukaemia (CMML) with 10 % to 29 % marrow blasts without myeloproliferative disorder,
- acute myeloid leukaemia (AML) with 20 % to 30 % blasts and multi-lineage dysplasia, according to World Health Organization (WHO) classification,
- AML with > 30 % marrow blasts according to the WHO classification.
Azacitidine Accord is indicated for the treatment of adult patients who are not eligible for haematopoietic stem cell transplantation (HSCT) with:
- intermediate-2 and high-risk myelodysplastic syndromes (MDS) according to the International Prognostic Scoring System (IPSS),
- chronic myelomonocytic leukaemia (CMML) with 10-29 % marrow blasts without myeloproliferative disorder,
- acute myeloid leukaemia (AML) with 20-30 % blasts and multi-lineage dysplasia, according to World Health Organisation (WHO) classification,
- AML with > 30% marrow blasts according to the WHO classification.
Azacitidine Celgene is indicated for the treatment of adult patients who are not eligible for haematopoietic stem cell transplantation (HSCT) with:
- intermediate 2 and high-risk myelodysplastic syndromes (MDS) according to the International Prognostic Scoring System (IPSS),
- chronic myelomonocytic leukaemia (CMML) with 10 29 % marrow blasts without myeloproliferative disorder,
- acute myeloid leukaemia (AML) with 20 30 % blasts and multi-lineage dysplasia, according to World Health Organisation (WHO) classification,
- AML with > 30% marrow blasts according to the WHO classification.
Vidaza is indicated for the treatment of adult patients who are not eligible for haematopoietic stem cell transplantation (HSCT) with:
- intermediate 2 and high-risk myelodysplastic syndromes (MDS) according to the International Prognostic Scoring System (IPSS),
- chronic myelomonocytic leukaemia (CMML) with 10 29 % marrow blasts without myeloproliferative disorder,
- acute myeloid leukaemia (AML) with 20 30 % blasts and multi-lineage dysplasia, according to World Health Organisation (WHO) classification.
Vidaza is indicated for the treatment of adult patients aged 65 years or older who are not eligible for HSCT with AML with > 30% marrow blasts according to the WHO classification.
Treatment of myelodysplastic syndrome (including juvenile myelomonocytic leukaemia), Treatment of acute myeloid leukaemia
Onureg is indicated as maintenance therapy in adult patients with acute myeloid leukaemia (AML) who achieved complete remission (CR) or complete remission with incomplete blood count recovery (CRi) following induction therapy with or without consolidation treatment and who are not candidates for, including those who choose not to proceed to, hematopoietic stem cell transplantation (HSCT).
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.
Antimetabolites, Antineoplastic
Antimetabolites that are useful in cancer chemotherapy. (See all compounds classified as Antimetabolites, Antineoplastic.)
Enzyme Inhibitors
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. (See all compounds classified as Enzyme Inhibitors.)
L01BC07
L01BC07
L01BC07
L01BC07
L01BC07
L01BC07
L01BC07
S76 | LUXPHARMA | Pharmaceuticals Marketed in Luxembourg | Pharmaceuticals marketed in Luxembourg, as published by d'Gesondheetskeess (CNS, la caisse nationale de sante, www.cns.lu), mapped by name to structures using CompTox by R. Singh et al. (in prep.). List downloaded from https://cns.public.lu/en/legislations/textes-coordonnes/liste-med-comm.html. Dataset DOI:10.5281/zenodo.4587355
L - Antineoplastic and immunomodulating agents
L01 - Antineoplastic agents
L01B - Antimetabolites
L01BC - Pyrimidine analogues
L01BC07 - Azacitidine
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.
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%.
Volume of Distribution
76 26 L
Clearance
167 +/- 49 L/h
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.
Mean elimination half-life is approximately 4 hours.
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.
Telomerase activation is thought to be a critical step in cellular immortality and oncogenesis. Several reagents including differentiation-inducing and antineoplastic agents are known to inhibit telomerase activity, although the molecular mechanisms through which they inhibit telomerase activity remain unclear. Demethylating reagents have recently been used as potential antineoplastic drugs for some types of cancers including those of the prostate. In the present study, we examined the effect of the demethylating reagent 5-azacytidine (5-aza-CR) on telomerase activity using cells of two prostate cancer cell lines, DU-145 and TSU-PR1. 5-aza-CR treatment significantly reduced telomerase activity in TSU-PR1 cells, but not in DU-145 cells, although growth inhibition was observed to a similar extent in both cell lines. Reverse transcription-PCR analyses revealed that inhibition of telomerase activity was accompanied by down-regulation of telomerase catalytic subunit (hTERT) mRNA expression. Transient expression assays showed that 5-aza-CR repressed the transcriptional activity of the hTERT promoter and that the E-box within the core promoter was responsible for this down-regulation. Western blot analyses revealed that 5-aza-CR reactivated p16 expression and repressed c-Myc expression in TSU-PR1 cells but not in DU-145 cells. Overexpression of p16 in TSU-PR1 cells led to significant repression of c-Myc transcription. These findings suggest that 5-aza-CR inhibits telomerase activity via transcriptional repression of hTERT, in which p16 and c-Myc may play a key role.
PMID:10914736 Kitagawa Y et al; Clin cancer Res 6 (7): 2868-75 (2000)
Cellular differentiation is controlled by a variety of factors including gene methylation, which represses particular genes as cell fate is determined. The incorporation of 5-azacytidine (5azaC) into DNA in vitro prevents methylation and thus can alter cellular differentiation pathways. Human bone marrow fibroblasts and MG63 cells treated with 5azaC were used as models of osteogenic progenitors and of a more mature osteoblast phenotype, respectively. The capacity for differentiation of these cells following treatment with glucocorticoids was investigated. 5azaC treatment led to significant expression of the osteoblastic marker alkaline phosphatase in MG63 osteosarcoma cells, which was further augmented by glucocorticoids; however, in human marrow fibroblasts alkaline phosphatase activity was only observed in glucocorticoid-treated cultures. MG63 cells represent a phenotype late in the osteogenic lineage in which demethylation is sufficient to induce alkaline phosphatase activity. Marrow fibroblasts are at an earlier stage of differentiation and require stimulation with glucocorticoids. In contrast, the expression of osteocalcin, an osteoblastic marker, was unaffected by 5azaC treatment, suggesting that regulation of expression of the osteocalcin gene does not involve methylation. These models provide novel approaches to the study of the control of differentiation in the marrow fibroblastic system.
Locklin RM et al; Cell Biol Int 22 (3): 207-15
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