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12 SPI Pharma
1 Faran Shimi Pharmaceutical
2 Pfanstiehl
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3 Gangwal Chemicals
1 Ingredion Pharma Solutions
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2 Microlex e.U
1 Pluviaendo
3 Roquette
1 Shanghai Shenmei Pharmaceutical Technology Co., Ltd
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1 Sigachi Industries

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11 Taste Masking
10 Chewable & Orodispersible Aids
9 Direct Compression
5 Parenteral
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3 Disintegrants & Superdisintegrants
3 Thickeners and Stabilizers
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Canada

101

Australia

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111

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68EXCIPIENTS BY APPLICATIONS

Chemistry

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Also known as: 5-azacytidine, 320-67-2, Azacytidine, Ladakamycin, Vidaza, Mylosar

Molecular Formula

C₈H₁₂N₄O₅

Molecular Weight

244.20 g/mol

InChI Key

NMUSYJAQQFHJEW-KVTDHHQDSA-N

FDA UNII

M801H13NRU

A pyrimidine 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.

Azacitidine is a Nucleoside Metabolic Inhibitor. The mechanism of action of azacitidine is as a Nucleic Acid Synthesis Inhibitor.

1 2D Structure

Azacitidine

2 Identification

2.1 Computed Descriptors

2.1.1 IUPAC Name

4-amino-1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]-1,3,5-triazin-2-one

2.1.2 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

2.1.3 InChI Key

NMUSYJAQQFHJEW-KVTDHHQDSA-N

2.1.4 Canonical SMILES

C1=NC(=NC(=O)N1C2C(C(C(O2)CO)O)O)N

2.1.5 Isomeric SMILES

C1=NC(=NC(=O)N1[C@H]2[C@@H]([C@@H]([C@H](O2)CO)O)O)N

2.2 Other Identifiers

2.2.1 UNII

M801H13NRU

2.3 Synonyms

2.3.1 MeSH Synonyms

1. 5 Azacytidine

2. 5-azacytidine

3. Azacytidine

4. Nsc 102816

5. Nsc-102816

6. Nsc102816

7. Vidaza

2.3.2 Depositor-Supplied Synonyms

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

2.4 Create Date

2004-09-16

3 Chemical and Physical Properties

Molecular Formula	C₈H₁₂N₄O₅
Molecular Weight	244.20 g/mol
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 Å²
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

4 Drug and Medication Information

4.1 Drug Information

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

4.2 Therapeutic Uses

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

4.3 Drug Indication

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).

5 Pharmacology and Biochemistry

5.1 Pharmacology

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.

5.2 MeSH Pharmacological Classification

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.)

5.3 FDA Pharmacological Classification

5.3.1 Active Moiety

AZACITIDINE

5.3.2 FDA UNII

M801H13NRU

5.3.3 Pharmacological Classes

Nucleoside Metabolic Inhibitor [EPC]; Nucleic Acid Synthesis Inhibitors [MoA]

5.4 ATC Code

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

5.5 Absorption, Distribution and Excretion

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

5.6 Metabolism/Metabolites

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.

5.7 Biological Half-Life

Mean elimination half-life is approximately 4 hours.

5.8 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.

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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