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Chemistry

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Also known as: Hydroxycarbamide, 127-07-1, N-hydroxyurea, Hydrea, 1-hydroxyurea, Oxyurea

Molecular Formula

CH₄N₂O₂

Molecular Weight

76.055 g/mol

InChI Key

VSNHCAURESNICA-UHFFFAOYSA-N

FDA UNII

X6Q56QN5QC

An antineoplastic agent that inhibits DNA synthesis through the inhibition of ribonucleoside diphosphate reductase.

Hydroxyurea is an Antimetabolite.

1 2D Structure

Hydroxyurea

2 Identification

2.1 Computed Descriptors

2.1.1 IUPAC Name

hydroxyurea

2.1.2 InChI

InChI=1S/CH4N2O2/c2-1(4)3-5/h5H,(H3,2,3,4)

2.1.3 InChI Key

VSNHCAURESNICA-UHFFFAOYSA-N

2.1.4 Canonical SMILES

C(=O)(N)NO

2.2 Other Identifiers

2.2.1 UNII

X6Q56QN5QC

2.3 Synonyms

2.3.1 MeSH Synonyms

1. Hydrea

2. Hydroxycarbamid

3. Oncocarbide

2.3.2 Depositor-Supplied Synonyms

1. Hydroxycarbamide

2. 127-07-1

3. N-hydroxyurea

4. Hydrea

5. 1-hydroxyurea

6. Oxyurea

7. Carbamoyl Oxime

8. Biosupressin

9. Hydroxycarbamine

10. Urea, Hydroxy-

11. Onco-carbide

12. Carbamohydroxamic Acid

13. Carbamohydroximic Acid

14. Carbamyl Hydroxamate

15. Droxia

16. Hydura

17. Litalir

18. Hydurea

19. N-carbamoylhydroxylamine

20. Hidrix

21. Siklos

22. Hydroxicarbamidum

23. Hydroxylurea

24. Hydreia

25. Litaler

26. Idrossicarbamide [dcit]

27. Hidroxicarbamida

28. Hydroxyharnstoff

29. Sq 1089

30. Hydroxycarbamidum

31. Carbamohydroxyamic Acid

32. N-hydroxymocovina

33. Hydroxylamine, N-carbamoyl-

34. Hydroxyharnstoff [german]

35. N-hydroxymocovina [czech]

36. Hydroxy Urea

37. Nci-c04831

38. Hydroxylamine, N-(aminocarbonyl)-

39. Sk 22591

40. Hydroxycarbamidum [inn-latin]

41. Hidroxicarbamida [inn-spanish]

42. Urea, N-hydroxy-

43. Hu

44. Ccris 958

45. Hydroxy-urea

46. Nsc 32065

47. Nsc32065

48. Sq-1089

49. Ai3-51139

50. Hydroxyurea (cytodrox)

51. Hydroxycarbamide [inn]

52. Nsc-32065

53. Chembl467

54. X6q56qn5qc

55. Chebi:44423

56. Ncgc00015520-03

57. Hydroxycarbamid

58. Oncocarbide

59. Idrossicarbamide

60. Dsstox_cid_5438

61. Dsstox_rid_77787

62. Dsstox_gsid_25438

63. 8029-68-3

64. Nhy

65. Hydroxyurea (d4)

66. N-hydroxy Urea

67. Mylocel

68. Carbamide Oxide

69. Xromi

70. Cas-127-07-1

71. Smr000059149

72. Hydroxyurea (usp)

73. Droxia (tm)

74. Droxia (tn)

75. Hydrea (tm)

76. Hydroxyaminomethanamide

77. Hsdb 6887

78. Sr-01000075919

79. Drg-0253

80. Einecs 204-821-7

81. Hydrea (tn)

82. Mfcd00007943

83. Hydroxyurea [usan:usp]

84. Unii-x6q56qn5qc

85. Brn 1741548

86. Hydroxycarbamide (jan/inn)

87. Hydroxyl Urea

88. N-hydroxy-urea

89. S-phase/g-1 Interface Inhibitor

90. Aminohydroxamic Acid

91. Carbamic Acid Oxime

92. Carbomohydroxamic Acid

93. Spectrum_000909

94. Wln: Zvmq

95. Hydrea (bristol Meyers)

96. Hydroxyurea [mi]

97. Spectrum2_000064

98. Spectrum3_000462

99. Spectrum4_000012

100. Spectrum5_000836

101. Lopac-h-8627

102. Hydroxyurea [hsdb]

103. Hydroxyurea [iarc]

104. Hydroxyurea [usan]

105. Molmap_000029

106. H 8627

107. Hydroxyurea [vandf]

108. Ncimech_000139

109. Hydroxyurea, 98%, Powder

110. Lopac0_000596

111. Bspbio_002164

112. Hydroxyurea [usp-rs]

113. Kbiogr_000383

114. Kbioss_001389

115. 4-03-00-00170 (beilstein Handbook Reference)

116. Hydroxycarbamide (hydroxyurea)

117. Mls001332381

118. Mls001332382

119. Mls002153389

120. Divk1c_000556

121. Hydroxycarbamide [jan]

122. N-(aminocarbonyl)hydroxylamine

123. Spectrum1500344

124. Spbio_000247

125. Gtpl6822

126. Dtxsid6025438

127. Hydroxycarbamide [mart.]

128. Tetratogen: Inhibits Ribonucleoside Diphosphate Reductase

129. Hms501l18

130. Kbio1_000556

131. Kbio2_001389

132. Kbio2_003957

133. Kbio2_006525

134. Kbio3_001384

135. Hydroxycarbamide [who-dd]

136. Hydroxyurea [orange Book]

137. Ninds_000556

138. Bio1_000451

139. Bio1_000940

140. Bio1_001429

141. Hms1920f09

142. Hms2091l17

143. Hms2234i03

144. Hms3261h14

145. Hms3373g18

146. Hms3655k20

147. Hms3869c03

148. Nci C04831

149. Pharmakon1600-01500344

150. Hydroxycarbamide [ema Epar]

151. Hydroxyurea [usp Monograph]

152. Act02611

153. Albb-028465

154. Amy40858

155. Hy-b0313

156. Str02555

157. Zinc8034120

158. Tox21_110168

159. Tox21_300319

160. Tox21_500596

161. Bbl009928

162. Bdbm50017811

163. Ccg-35236

164. Nsc757072

165. S1896

166. Stl145898

167. Akos005716276

168. Akos006222547

169. Tox21_110168_1

170. Zinc100019199

171. Db01005

172. Hydroxycarbamide [ep Monograph]

173. Lp00596

174. Nsc-757072

175. Sdccgsbi-0050578.p006

176. Idi1_000556

177. Ncgc00015520-01

178. Ncgc00015520-02

179. Ncgc00015520-04

180. Ncgc00015520-05

181. Ncgc00015520-06

182. Ncgc00015520-07

183. Ncgc00015520-08

184. Ncgc00015520-09

185. Ncgc00015520-10

186. Ncgc00015520-11

187. Ncgc00015520-20

188. Ncgc00093974-01

189. Ncgc00093974-02

190. Ncgc00093974-03

191. Ncgc00093974-04

192. Ncgc00093974-05

193. Ncgc00254007-01

194. Ncgc00261281-01

195. Ac-22674

196. Nci60_002773

197. Sbi-0050578.p004

198. Db-041849

199. Eu-0100596

200. Ft-0627160

201. Ft-0627175

202. Ft-0670210

203. H0310

204. Sw218071-2

205. C07044

206. D00341

207. Hydroxyurea, Vetec(tm) Reagent Grade, >=98%

208. Ab00052018-09

209. Ab00052018-10

210. Ab00052018_11

211. Ab00052018_12

212. 127h071

213. A805636

214. Q212272

215. J-504798

216. Sr-01000075919-1

217. Sr-01000075919-3

218. Sr-01000075919-8

219. E0723dba-5af3-49d1-b5f6-59420ab87ac9

220. F8880-0905

221. Z1522566612

222. Hydroxycarbamide, European Pharmacopoeia (ep) Reference Standard

223. Hydroxyurea, United States Pharmacopeia (usp) Reference Standard

2.4 Create Date

2004-09-16

3 Chemical and Physical Properties

Molecular Formula	CH₄N₂O₂
Molecular Weight	76.055 g/mol
XLogP3	-1.8
Hydrogen Bond Donor Count	3
Hydrogen Bond Acceptor Count	2
Rotatable Bond Count	0
Exact Mass	76.027277375 g/mol
Monoisotopic Mass	76.027277375 g/mol
Topological Polar Surface Area	75.4 Å²
Heavy Atom Count	5
Formal Charge	0
Complexity	42.9
Isotope Atom Count	0
Defined Atom Stereocenter Count	0
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 6
Drug Name	Droxia
PubMed Health	Hydroxyurea (By mouth)
Drug Classes	Antineoplastic Agent
Drug Label	DROXIA (hydroxyurea capsules, USP) is available for oral use as capsules providing 200 mg, 300 mg, and 400 mg hydroxyurea. Inactive ingredients: citric acid, gelatin, lactose, magnesium stearate, sodium phosphate, titanium dioxide, and capsule colo...
Active Ingredient	Hydroxyurea
Dosage Form	Capsule
Route	Oral
Strength	300mg; 200mg; 400mg
Market Status	Prescription
Company	Bristol Myers Squibb

2 of 6
Drug Name	Hydrea
PubMed Health	Hydroxyurea (By mouth)
Drug Classes	Antineoplastic Agent
Drug Label	HYDREA (hydroxyurea capsules, USP) is an antineoplastic agent available for oral use as capsules providing 500 mg hydroxyurea. Inactive ingredients: citric acid, colorants (D&C Yellow No. 10, FD&C Blue No. 1, FD&C Red No. 40, and D&C Red N
Active Ingredient	Hydroxyurea
Dosage Form	Capsule
Route	Oral
Strength	500mg
Market Status	Prescription
Company	Bristol Myers Squibb

3 of 6
Drug Name	Hydroxyurea
PubMed Health	Hydroxyurea (By mouth)
Drug Classes	Antineoplastic Agent
Drug Label	DROXIA (hydroxyurea capsules, USP) is available for oral use as capsules providing 200 mg, 300 mg, and 400 mg hydroxyurea. Inactive ingredients: citric acid, gelatin, lactose, magnesium stearate, sodium phosphate, titanium dioxide, and capsule colo...
Active Ingredient	Hydroxyurea
Dosage Form	Capsule
Route	Oral
Strength	500mg
Market Status	Prescription
Company	Par Pharm; Barr

4 of 6
Drug Name	Droxia
PubMed Health	Hydroxyurea (By mouth)
Drug Classes	Antineoplastic Agent
Drug Label	DROXIA (hydroxyurea capsules, USP) is available for oral use as capsules providing 200 mg, 300 mg, and 400 mg hydroxyurea. Inactive ingredients: citric acid, gelatin, lactose, magnesium stearate, sodium phosphate, titanium dioxide, and capsule colo...
Active Ingredient	Hydroxyurea
Dosage Form	Capsule
Route	Oral
Strength	300mg; 200mg; 400mg
Market Status	Prescription
Company	Bristol Myers Squibb

5 of 6
Drug Name	Hydrea
PubMed Health	Hydroxyurea (By mouth)
Drug Classes	Antineoplastic Agent
Drug Label	HYDREA (hydroxyurea capsules, USP) is an antineoplastic agent available for oral use as capsules providing 500 mg hydroxyurea. Inactive ingredients: citric acid, colorants (D&C Yellow No. 10, FD&C Blue No. 1, FD&C Red No. 40, and D&C Red N
Active Ingredient	Hydroxyurea
Dosage Form	Capsule
Route	Oral
Strength	500mg
Market Status	Prescription
Company	Bristol Myers Squibb

6 of 6
Drug Name	Hydroxyurea
PubMed Health	Hydroxyurea (By mouth)
Drug Classes	Antineoplastic Agent
Drug Label	DROXIA (hydroxyurea capsules, USP) is available for oral use as capsules providing 200 mg, 300 mg, and 400 mg hydroxyurea. Inactive ingredients: citric acid, gelatin, lactose, magnesium stearate, sodium phosphate, titanium dioxide, and capsule colo...
Active Ingredient	Hydroxyurea
Dosage Form	Capsule
Route	Oral
Strength	500mg
Market Status	Prescription
Company	Par Pharm; Barr

4.2 Therapeutic Uses

Antineoplastic Agents; Antisickling Agents; Enzyme Inhibitors; Nucleic Acid Synthesis Inhibitors

National Library of Medicine's Medical Subject Headings. Hydroxyurea. Online file (MeSH, 2016). Available from, as of January 19, 2016: https://www.nlm.nih.gov/mesh/2016/mesh_browser/MBrowser.html

/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Hydroxyurea is included in the database.

NIH/NLM; ClinicalTrials.Gov. Available from, as of March 17, 2016: https://clinicaltrials.gov/ct2/results?term=hydroxyurea&Search=Search

Hydroxyurea Capsules USP are indicated for the treatment of: Resistant chronic myeloid leukemia. Locally advanced squamous cell carcinomas of the head and neck (excluding the lip) in combination with chemoradiation. /Included in US product label/

NIH; DailyMed. Current Medication Information for Hydroxyurea Capsule (Updated: January 2016). Available from, as of January 21, 2016: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=b9514ae5-79ae-4cc2-9d7f-c8f7806d1694

Hydroxyurea has been used in the treatment of psoriasis and is reportedly beneficial in the treatment of hypereosinophilic syndrome that does not respond to corticosteroid therapy. /NOT included in US product label/

American Society of Health-System Pharmacists 2015; Drug Information 2015. Bethesda, MD. 2015, p. 1061

For more Therapeutic Uses (Complete) data for HYDROXYUREA (12 total), please visit the HSDB record page.

4.3 Drug Warning

Hydroxyurea is a highly toxic drug with a low therapeutic index, and a therapeutic response is not likely to occur without some evidence of toxicity. Hydroxyurea therapy may be complicated by severe, sometimes life-threatening or fatal, adverse effects. The drug must be used only under constant supervision by clinicians experienced in therapy with cytotoxic agents or the use of this agent for sickle cell anemia.

American Society of Health-System Pharmacists 2015; Drug Information 2015. Bethesda, MD. 2015, p. 1063

Hydroxyurea should be admin with caution to patients who have recently received other cytotoxic drugs or irradiation therapy, since bone marrow depression is likely in these patients. In addition, an exacerbation of post-irradiation erythema may occur.

American Society of Health-System Pharmacists 2015; Drug Information 2015. Bethesda, MD. 2015, p. 1063

Hepatotoxicity, in some cases resulting in fatal hepatic failure, has been reported in patients with HIV infection receiving hydroxyurea in combination with antiretroviral agents. Fatal hepatotoxicity occurred most frequently in patients receiving combination therapy with hydroxyurea, didanosine, and stavudine. Elevation of serum concentrations of hepatic enzymes has been reported in patients receiving hydroxyurea.

American Society of Health-System Pharmacists 2015; Drug Information 2015. Bethesda, MD. 2015, p. 1063

Cutaneous vasculitic toxicities, including vasculitic ulcerations and gangrene, have occurred in patients receiving hydroxyurea for myeloproliferative disorders, particularly in patients who have received or who are receiving interferon therapy.

American Society of Health-System Pharmacists 2015; Drug Information 2015. Bethesda, MD. 2015, p. 1063

For more Drug Warnings (Complete) data for HYDROXYUREA (37 total), please visit the HSDB record page.

4.4 Drug Indication

For management of melanoma, resistant chronic myelocytic leukemia, and recurrent, metastatic, or inoperable carcinoma of the ovary and Sickle-cell anemia.

Siklos is indicated for the prevention of recurrent painful vaso-occlusive crises including acute chest syndrome in paediatric and adult patients suffering from symptomatic sickle-cell syndrome.

Prevention of vaso-occlusive complications of sickle cell disease in patients over 2 years of age

5 Pharmacology and Biochemistry

5.1 Pharmacology

Hydroxyurea has dose-dependent synergistic activity with cisplatin in vitro. In vivo Hydroxyurea showed activity in combination with cisplatin against the LX-1 and CALU-6 human lung xenografts, but minimal activity was seen with the NCI-H460 or NCI-H520 xenografts. Hydroxyurea was synergistic with cisplatin in the Lewis lung murine xenograft. Sequential exposure to Hydroxyurea 4 hours before cisplatin produced the greatest interaction.

5.2 MeSH Pharmacological Classification

Antisickling Agents

Agents used to prevent or reverse the pathological events leading to sickling of erythrocytes in sickle cell conditions. (See all compounds classified as Antisickling Agents.)

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.)

Nucleic Acid Synthesis Inhibitors

Compounds that inhibit cell production of DNA or RNA. (See all compounds classified as Nucleic Acid Synthesis Inhibitors.)

Antineoplastic Agents

Substances that inhibit or prevent the proliferation of NEOPLASMS. (See all compounds classified as Antineoplastic Agents.)

5.3 FDA Pharmacological Classification

5.3.1 Active Moiety

HYDROXYUREA

5.3.2 FDA UNII

X6Q56QN5QC

5.3.3 Pharmacological Classes

Urea [CS]; Antimetabolite [EPC]

5.4 ATC Code

L01XX05

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

L01X - Other antineoplastic agents

L01XX - Other antineoplastic agents

L01XX05 - Hydroxycarbamide

5.5 Absorption, Distribution and Excretion

Absorption

Well absorbed from the gastrointestinal tract.

Route of Elimination

Renal excretion is a pathway of elimination.

Hydroxyurea is readily absorbed from the GI tract. Peak serum concentrations are attained within 1-4 hours following oral administration. Blood concentrations decline rapidly and there is no cumulative effect with repeated administration. For this reason, higher blood concentrations are attained if the regular dosage is given in a large, single oral dose than if it is administered in divided doses. Disproportionate increases in peak plasma concentrations and areas under the concentration-time curve (AUCs) result when drug dosage is increased. The effect of food on the absorption of hydroxyurea has not been determined.

American Society of Health-System Pharmacists 2015; Drug Information 2015. Bethesda, MD. 2015, p. 1065

Hydroxyurea distributes rapidly throughout the body and concentrates in leukocytes and erythrocytes. The estimated volume of distribution of the drug approximates total body water. Hydroxyurea crosses the blood-brain barrier; peak hydroxyurea CSF concentrations are attained within 3 hours following oral administration. The drug distributes into ascites fluid, resulting in drug concentrations in ascites fluid of 2-7.5 times less than plasma drug concentrations.

American Society of Health-System Pharmacists 2015; Drug Information 2015. Bethesda, MD. 2015, p. 1065

Studies using(14)C-labeled hydroxyurea indicate that about one-half an orally administered dose is degraded in the liver and is excreted as respiratory carbon dioxide and in urine as urea. The remaining portion of the drug is excreted intact in urine.

American Society of Health-System Pharmacists 2015; Drug Information 2015. Bethesda, MD. 2015, p. 1065

About 30-60% of an orally administered dose of hydroxyurea is excreted unchanged by the kidneys, although about 35% is generally excreted.

IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V76 361 (2000)

For more Absorption, Distribution and Excretion (Complete) data for HYDROXYUREA (7 total), please visit the HSDB record page.

5.6 Metabolism/Metabolites

Hepatic.

Studies indicate that up to 50% of an orally administered dose of hydroxyurea is metabolized in the liver; however, the precise metabolic pathways have not been determined. A minor metabolic pathway may involve degradation of the drug by urease, an enzyme produced by intestinal bacteria. Acetohydroxamic acid, possibly resulting from the breakdown of hydroxyurea by urease, was detected in the serum of 3 patients with leukemia treated with hydroxyurea.

American Society of Health-System Pharmacists 2015; Drug Information 2015. Bethesda, MD. 2015, p. 1065

5.7 Biological Half-Life

3-4 hours

The half-time of hydroxyurea is short, with an initial half-time of 0.63 hr after intravenous administration and 1.78 hr after oral administration and a terminal half-time of 3.32 hr after oral administration and 3.39 hr after intravenous administration /to humans/.

The half-time of hydroxyurea in rats given 137 mg/kg bw per day intraperitoneally on days 9-12 of gestation was 15 min in the dams and 85 min in the embryos. In rhesus monkeys given 100 mg/kg bw per day intravenously on days 23-32 of gestation, the half-time was 120 min after the last injection in the mothers and 265 min in their fetuses.

5.8 Mechanism of Action

Hydroxyurea is converted to a free radical nitroxide (NO) in vivo, and transported by diffusion into cells where it quenches the tyrosyl free radical at the active site of the M2 protein subunit of ribonucleotide reductase, inactivating the enzyme. The entire replicase complex, including ribonucleotide reductase, is inactivated and DNA synthesis is selectively inhibited, producing cell death in S phase and synchronization of the fraction of cells that survive. Repair of DNA damaged by chemicals or irradiation is also inhibited by hydroxyurea, offering potential synergy between hydroxyurea and radiation or alkylating agents. Hydroxyurea also increases the level of fetal hemoglobin, leading to a reduction in the incidence of vasoocclusive crises in sickle cell anemia. Levels of fetal hemoglobin increase in response to activation of soluble guanylyl cyclase (sGC) by hydroxyurea-derived NO.

The exact mechanism of antineoplastic activity of hydroxyurea has not been fully determined. Some studies indicate that hydroxyurea interferes with the synthesis of DNA without interfering with the synthesis of RNA or protein. Although hydroxyurea may have multiple sites of action, it appears likely that the drug inhibits the incorporation of thymidine into DNA; in addition, it may directly damage DNA. Hydroxyurea can destroy the tyrosyl free radical that is formed as the catalytic center of ribonucleoside diphosphate reductase, the enzyme that catalyzes the reductive conversion of ribonucleotides to deoxyribonucleotides; this conversion is a critical and probably rate-limiting step in the synthesis of DNA. The drug is an S-phase inhibitor and may cause cells to arrest at the G1-S border, decrease the rate of cell progression into the S phase, and/or cause cells to accumulate in the S phase as a result of inhibiting DNA synthesis. Animal studies indicate that the cytotoxic effects of hydroxyurea are limited to those tissues with high rates of cellular proliferation and the effects are evident only in those cells that are actively synthesizing DNA.

American Society of Health-System Pharmacists 2015; Drug Information 2015. Bethesda, MD. 2015, p. 1064

Hydroxyurea, a drug widely used in therapy of several human diseases, inhibits deoxynucleotide synthesis and, consequently, DNA synthesis by blocking the cellular enzyme ribonucleotide reductase. Hydroxyurea inhibits human immunodeficiency virus type 1 (HIV-1) DNA synthesis in activated peripheral blood lymphocytes by decreasing the amount of intracellular deoxynucleotides, thus suggesting that this drug has an antiviral effect. Hydroxyurea has now been shown to block HIV-1 replication in acutely infected primary human lymphocytes (quiescent and activated) and macrophages, as well as in blood cells infected in vivo obtained from individuals with acquired immunodeficiency syndrome (AIDS). The antiviral effect was achieved at nontoxic doses of hydroxyurea, lower than those currently used in human therapy. Combination of hydroxyurea with the nucleoside analog didanosine (2'3'-dideoxyinosine, or ddi) generated a synergistic inhibitory effect without increasing toxicity. In some instances, inhibition of HIV-1 by hydroxyurea was irreversible, even several weeks after suspension of drug treatment. The indirect inhibition of HIV-1 by hydroxyurea is not expected to generate high rates of escape mutants. Hydroxyurea therefore appears to be a possible candidate for AIDS therapy.

PMID:7973634 Lori F et al; Science 266 (5186): 801:5 (1994)

Hydroxyurea (HU) is effectively used in the management of beta-hemoglobinopathies by augmenting the production of fetal hemoglobin (HbF). However, the molecular mechanisms underlying HU-mediated HbF regulation remain unclear. We previously reported that overexpression of the HU-induced SAR1 gene closely mimics the known effects of HU on K562 and CD34(+) cells, including gamma-globin induction and cell-cycle regulation. Here, we show that HU stimulated nuclear factor-kB interaction with its cognate-binding site on the SAR1 promoter to regulate transcriptional expression of SAR1 in K562 and CD34(+) cells. Silencing SAR1 expression not only significantly lowered both basal and HU-elicited HbF production in K562 and CD34(+) cells, but also significantly reduced HU-mediated S-phase cell-cycle arrest and apoptosis in K562 cells. Inhibition of c-Jun N-terminal kinase (JNK)/Jun phosphorylation and silencing of Gia expression in SAR1-transfected K562 and CD34(+) cells reduced both gamma-globin expression and HbF level, indicating that activation of Gia/JNK/Jun proteins is required for SAR1-mediated HbF induction. Furthermore, reciprocal coimmunoprecipitation assays revealed an association between forcibly expressed SAR1 and Gia2 or Gia3 proteins in both K562 and nonerythroid cells. These results indicate that HU induces SAR1, which in turn activates gamma-globin expression, predominantly through the Gia/JNK/Jun pathway. Our findings identify SAR1 as an alternative therapeutic target for beta-globin disorders.

PMID:24914133 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133487 Zhu J et al; Blood 124 (7): 1146-56 (2014)

Hydroxyurea is well absorbed after oral administration, converted to a free radical nitroxide in vivo, and transported by diffusion into cells where it quenches the tyrosyl free radical at the active site of the M2 protein subunit of ribonucleotide reductase, inactivating the enzyme. The entire replitase complex, including ribonucleotide reductase, is inactivated and DNA synthesis is selectively inhibited, producing cell death in S phase and synchronization of the fraction of cells that survive. Repair of DNA damaged by chemicals or irradiation is also inhibited by hydroxyurea, offering potential synergy between hydroxyurea and radiation or alkylating agents. Hydroxyurea renders cells sensitive to bleomycin because the quenched tyrosyl free radical no longer stabilizes the adjacent iron center, making it more susceptible to the chelating properties of bleomycin, which then produces active oxygen. Synergy has also been observed between hydroxyurea and a number of other chemotherapeutic agents, including cytarabine and etoposide. Recently, two new effects of hydroxyurea have been observed: hydroxyurea increases the level of fetal hemoglobin, leading to a reduction in the incidence of vasoocclusive crises in sickle cell anemia, and hydroxyurea selectively reduces the level of episomal DNA and thus potentially may reduce drug resistance associated with duplicated genes retained as episomes.

Yarbro JW; Semin Oncol 19 (3 Suppl 9): 1-10 (1992)

Fanconi's anemia (FA) is a recessive disease; 16 genes are currently recognized in FA. FA proteins participate in the FA/BRCA pathway that plays a crucial role in the repair of DNA damage induced by crosslinking compounds. Hydroxyurea (HU) is an agent that induces replicative stress by inhibiting ribonucleotide reductase (RNR), which synthesizes deoxyribonucleotide triphosphates (dNTPs) necessary for DNA replication and repair. HU is known to activate the FA pathway; however, its clastogenic effects are not well characterized. We have investigated the effects of HU treatment alone or in sequential combination with mitomycin-C (MMC) on FA patient-derived lymphoblastoid cell lines from groups FA-A, B, C, D1/BRCA2, and E and on lymphocytes from two unclassified FA patients. All FA cells showed a significant increase (P < 0.05) in chromosomal aberrations following treatment with HU during the last 3 h before mitosis. Furthermore, when FA cells previously exposed to MMC were treated with HU, we observed an increase of MMC-induced DNA damage that was characterized by high occurrence of DNA breaks and a reduction in rejoined chromosomal aberrations. These findings show that exposure to HU during G2 induces chromosomal aberrations by a mechanism that is independent of its well-known role in replication fork stalling during S-phase and that HU interfered mainly with the rejoining process of DNA damage. We suggest that impaired oxidative stress response, lack of an adequate amount of dNTPs for DNA repair due to RNR inhibition, and interference with cell cycle control checkpoints underlie the clastogenic activity of HU in FA cells.

PMID:25663157 Molina B et al; Environ Mol Mutagen. 2015 Feb 6. doi: 10.1002/em.21938. (Epub ahead of print)

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About the Company : Jai Radhe Sales was founded in 1999 as an out-of-the-box distribution firm specializing in the global supply of high-quality pharmaceutical ingredients. The firm provides complete ...

Jai Radhe Sales was founded in 1999 as an out-of-the-box distribution firm specializing in the global supply of high-quality pharmaceutical ingredients. The firm provides complete sourcing solutions for pharmaceutical products from India, including technical and regulatory assistance. It believes in providing its customers with high-quality products at reasonable prices. It has always endeavored to achieve global standards in the field of pharmaceuticals and has carved out a niche for itself through new methods based on current market needs. Today, it has established itself as a truly global company, with exports to almost every continent.

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Number of Transactions

Total Quantity (KGS)

Total Value (USD)

Quantity (KGS) & Unit rate (USD/KGS) over time

API Imports and Exports

Importing Country	Total Quantity (KGS)	Average Price (USD/KGS)	Number of Transactions

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ACTIVE PHARMA INGREDIENTS

17 API Suppliers

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1 Minakem

1 Evonik

1 Rochem International Inc

2 SPI Pharma

9 DKSH

1 Jai Radhe Sales

1 Chynops Pharma

9 Gangwal Healthcare

3 Nanjing Well Pharmaceutical

4 ACG Worldwide

1 Actylis

1 Alcedo Pharmachem

4 Anhui Sunhere Pharmaceutical Excipients Co.,Ltd

8 BASF

2 Corel Pharma Chem

4 DFE Pharma

2 Finar

5 Gangwal Chemicals

1 Ideal Cures Pvt Ltd

19 Kerry

1 Kima Chemical

3 Lonza Capsugel

12 Microlex e.U

1 NEWEDGE Overseas

2 Pharmatrans-Sanaq

3 Pluviaendo

3 Prachin Chemical

1 Qualicaps

10 Roquette

1 Seppic

2 Shanghai Shenmei Pharmaceutical Technology Co., Ltd

9 Sigachi Industries

1 The Dow Chemical Company

2 Valens Pharmachem

2 Vasa Pharmachem

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7 Controlled & Modified Release

6 Solubilizers

6 Topical

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4 Emulsifying Agents

4 Chewable & Orodispersible Aids

3 Coloring Agents

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