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Chemistry

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Also known as: 518-82-1, Emodol, Frangula emodin, Schuttgelb, 1,3,8-trihydroxy-6-methylanthracene-9,10-dione, Rheum emodin
Molecular Formula
C15H10O5
Molecular Weight
270.24  g/mol
InChI Key
RHMXXJGYXNZAPX-UHFFFAOYSA-N
FDA UNII
KA46RNI6HN

Emodin
Purgative anthraquinone found in several plants, especially RHAMNUS PURSHIANA. It was formerly used as a laxative, but is now used mainly as a tool in toxicity studies.
1 2D Structure

Emodin

2 Identification
2.1 Computed Descriptors
2.1.1 IUPAC Name
1,3,8-trihydroxy-6-methylanthracene-9,10-dione
2.1.2 InChI
InChI=1S/C15H10O5/c1-6-2-8-12(10(17)3-6)15(20)13-9(14(8)19)4-7(16)5-11(13)18/h2-5,16-18H,1H3
2.1.3 InChI Key
RHMXXJGYXNZAPX-UHFFFAOYSA-N
2.1.4 Canonical SMILES
CC1=CC2=C(C(=C1)O)C(=O)C3=C(C2=O)C=C(C=C3O)O
2.2 Other Identifiers
2.2.1 UNII
KA46RNI6HN
2.3 Synonyms
2.3.1 MeSH Synonyms

1. Archin

2. Casanthranol

3. Emodin, Frangula

4. Emodin, Rheum

5. Frangula Emodin

6. Frangulic Acid

7. Peristim

8. Rheum Emodin

2.3.2 Depositor-Supplied Synonyms

1. 518-82-1

2. Emodol

3. Frangula Emodin

4. Schuttgelb

5. 1,3,8-trihydroxy-6-methylanthracene-9,10-dione

6. Rheum Emodin

7. Archin

8. Frangulic Acid

9. 3-methyl-1,6,8-trihydroxyanthraquinone

10. Persian Berry Lake

11. 1,3,8-trihydroxy-6-methylanthraquinone

12. 6-methyl-1,3,8-trihydroxyanthraquinone

13. 1,3,8-trihydroxy-6-methyl-9,10-anthraquinone

14. 1,3,8-trihydroxy-6-methyl-9,10-anthracenedione

15. C.i. Natural Yellow 14

16. 9,10-anthracenedione, 1,3,8-trihydroxy-6-methyl-

17. Alatinone

18. Rheum-emodin

19. 4,5,7-trihydroxy-2-methylanthraquinone

20. Frangulinic Acid

21. C.i. 75440

22. Nsc 408120

23. Nsc 622947

24. Anthraquinone, 1,3,8-trihydroxy-6-methyl-

25. Nsc408120

26. Ka46rni6hn

27. Chembl289277

28. Anthraquinone, 6-methyl-1,3,8-trihydroxy-

29. Chebi:42223

30. 1,3,8-trihydroxy-6-methylanthra-9,10-quinone

31. Nsc622947

32. Nsc-408120

33. Nsc-622947

34. Dsstox_cid_5231

35. Dsstox_rid_77709

36. 6-methyl-1,3,8-trihydroxy-9,10-anthracenedione

37. Dsstox_gsid_25231

38. Emo

39. 1,8-trihydroxy-6-methylanthraquinone

40. Cas-518-82-1

41. Smr000326798

42. Ccris 3528

43. Hsdb 7093

44. Sr-01000075615

45. Einecs 208-258-8

46. Unii-ka46rni6hn

47. Brn 1888141

48. Emdoin

49. Ai3-38286

50. 3bqc

51. Emodin,(s)

52. Mfcd00001207

53. Spectrum_001954

54. 1f0q

55. 3ed0

56. Specplus_000332

57. Emodin [hsdb]

58. Emodin [inci]

59. 1,3,8-tri-hydroxy-6-methyl-anthra-quinone

60. Emodin [usp-rs]

61. Spectrum2_000895

62. Spectrum3_000742

63. Spectrum4_001757

64. Spectrum5_000614

65. Emodin [mi]

66. Lopac-e-7881

67. Emodin, Analytical Standard

68. Ncimech_000049

69. Lopac0_000552

70. Bspbio_002324

71. Kbiogr_002234

72. Kbioss_002508

73. 1,3,8-trihydroxy-6-methyl-anthracene-9,10-dione

74. Mls000563068

75. Mls001066370

76. Mls004257392

77. Mls006011712

78. Divk1c_006428

79. Schembl177689

80. Spbio_000710

81. Megxp0_000460

82. Dtxsid5025231

83. Acon1_001939

84. Bdbm11318

85. Kbio1_001372

86. Kbio2_002500

87. Kbio2_005068

88. Kbio2_007636

89. Kbio3_001544

90. Emodin - Cas 518-82-1

91. Hms2230k22

92. Hms3261p05

93. Hms3373b16

94. Hms3655h22

95. 1,3,8-trihydroxy-6-methyl-9,10-dihydroanthracene-9,10-dione

96. Act03256

97. Bcp18372

98. Ex-a6778

99. Tnp00318

100. Zinc3824868

101. 9, 1,3,8-trihydroxy-6-methyl-

102. Tox21_202999

103. Tox21_303218

104. Tox21_500552

105. Ccg-35263

106. Lmpk13040008

107. S2295

108. Stl581876

109. 3-methyl-1,8-trihydroxyanthraquinone

110. 4,7-trihydroxy-2-methylanthraquinone

111. Akos003348641

112. Ac-1004

113. Cs-1412

114. Db07715

115. Ks-5189

116. Lp00552

117. Sdccgsbi-0050535.p004

118. Anthraquinone,3,8-trihydroxy-6-methyl-

119. Smp2_000211

120. Ncgc00015420-01

121. Ncgc00015420-02

122. Ncgc00015420-03

123. Ncgc00015420-04

124. Ncgc00015420-05

125. Ncgc00015420-06

126. Ncgc00015420-07

127. Ncgc00015420-08

128. Ncgc00015420-09

129. Ncgc00015420-22

130. Ncgc00091540-01

131. Ncgc00091540-02

132. Ncgc00091540-03

133. Ncgc00091540-04

134. Ncgc00091540-05

135. Ncgc00257090-01

136. Ncgc00260544-01

137. Ncgc00261237-01

138. 1,3,8-trihydroxy-6-methyl-anthraquinone

139. Hy-14393

140. Nci60_003906

141. E0500

142. Eu-0100552

143. Ft-0606539

144. Ft-0667846

145. N1854

146. Sw219906-1

147. 1,8-trihydroxy-6-methyl-9,10-anthraquinone

148. Emodin, From Frangula Bark, >=90% (hplc)

149. E 7881

150. K00056

151. Emodin; 6-methyl-1,3,8-trihydroxyanthraquinone

152. 1,3, 8-trihydroxy-6-methyl-9,10-anthraquinone

153. 1,3,8-trihydroxy-6-methylanthra-9,10-quinone #

154. 518e821

155. A828825

156. Q-100581

157. Q4348178

158. Sr-01000075615-1

159. Sr-01000075615-6

160. Brd-k58685305-001-03-0

161. 1,3,8-trihydroxy-6-methyl-9,10-anthracenedione, 9ci

162. 9,10-anthracenedione, 1,3,8-trihydroxy-6-methyl- (9ci)

163. Emodin, United States Pharmacopeia (usp) Reference Standard

164. 1,3,8-trihydroxy-6-methyl-anthracene-9,10-dione;3-methyl-1,6,8-trihydroxyanthraquinone

2.4 Create Date
2004-09-16
3 Chemical and Physical Properties
Molecular Weight 270.24 g/mol
Molecular Formula C15H10O5
XLogP32.7
Hydrogen Bond Donor Count3
Hydrogen Bond Acceptor Count5
Rotatable Bond Count0
Exact Mass270.05282342 g/mol
Monoisotopic Mass270.05282342 g/mol
Topological Polar Surface Area94.8 Ų
Heavy Atom Count20
Formal Charge0
Complexity434
Isotope Atom Count0
Defined Atom Stereocenter Count0
Undefined Atom Stereocenter Count0
Defined Bond Stereocenter Count0
Undefined Bond Stereocenter Count0
Covalently Bonded Unit Count1
4 Drug and Medication Information
4.1 Therapeutic Uses

Emodin /is/ a widely available over-the-counter herbal remedy.

George J et al; Toxicologist 72(S-1): 341 (2003)


/EXPL THER:/ ... Emodin and cassiamin B /were examined as cancer chemopreventive agents/ ... These compounds exhibited the remarkable anti-tumor promoting effect on two-stage carcinogenesis test of mouse skin tumors induced by 7,12-dimethylbenz[a]anthracene as an initiator and 12-O-tetradecanoylphorbol-13-acetate (TPA) as a promoter by both topical application. Furthermore, emodin exhibited potent inhibitory activity on two-stage carcinogenesis test of mouse skin tumors induced by nitric oxide donor, (+/-)-(E)-methyl-2-[(E)-hydroxyimino]-5-nitro-6-methoxy-3-hexeneamide as an initiator and TPA as a promoter.

PMID:12048158 Koyama J et al; Cancer Lett 182(2): 135-9 (2002)


/EXPL THER:/ ... Emodin ameliorates the undesirable effects of concentrated glucose on HPMC /human peritoneal mesothelial cells/ via suppression of PKC activation and CREB phosphorylation, and suggest that emodin may have a therapeutic potential in the prevention or treatment of glucose-induced structural and functional abnormalities in the peritoneal membrane.

PMID:12846747 Chan T et al; Kidney Int 64 (2): 519-533 (2003)


5 Pharmacology and Biochemistry
5.1 MeSH Pharmacological Classification

Protein Kinase Inhibitors

Agents that inhibit PROTEIN KINASES. (See all compounds classified as Protein Kinase Inhibitors.)


Cathartics

Agents that are used to stimulate evacuation of the bowels. (See all compounds classified as Cathartics.)


5.2 Absorption, Distribution and Excretion

Absorption, excretion, tissue distribution and metabolism of the anthraquinone [14C]emodin was studied after a single oral administration (approx. 50 mg/kg) to rats. Urinary excretion amounted to 18(+/- 5)% dose in 24 hr and to 22(+/- 6)% in 72 hr. Metabolites found in pooled urine (0-72 hr) were mostly free anthraquinones (emodin and emodic acid, 16% dose); 3% was conjugated and 3% was non-extractable radioactivity. In 24 hr, 48 +/- 11% and in 120 hr, 68 +/- 8% dose was excreted in the faeces, mostly in the free anthraquinone form. In two cannulated rats biliary excretion reached a maximum at approx. 6 hr and amounted to 49% dose within 15 hr; 70% of biliary activity was in the form of conjugated emodin. The content of radioactivity in most organs decreased significantly between 3 and 5 days. In kidneys, however, the 14C activity was still equiv. to 4.33 ppm. emodin after five days. Mesenterium and fat tissue showed increasing 14C activity from 72 to 120 hr.

Bachmann M et al; Xenobiotica 11(3): 217-25 1981


5.3 Metabolism/Metabolites

... The metabolism of emodin (1,3,8-trihydroxy-6-methylanthraquinone) /was studied/... With rat liver microsomes, the formation of two emodin metabolites, omega-hydroxyemodin and 2-hydroxyemodin, was observed. The rates of formation of omega-hydroxyemodin were not different with microsomes from rats that had been pretreated with inducers for different cytochrome P450 enzymes. Thus, the formation of omega-hydroxyemodin seems to be catalyzed by several cytochrome P450 enzymes at low rates. The formation of 2-hydroxyemodin was increased in liver microsomes from 3-methylcholanthrene-pretreated rats and was inhibited by alpha-naphthoflavone, by an anti-rat cytochrome P450 1A1/2 antibody, and, to a lesser degree, by an anti-rat cytochrome P450 1A1 antibody. These data suggest the involvement of cytochrome P450 1A2 in the formation of this metabolite. However, other cytochrome P450 enzymes also seem to catalyze this reaction. The anthraquinone chrysophanol (1,8-dihydroxy-3-methylanthraquinone) is transformed, in a cytochrome P450-dependent oxidation, to aloe-emodin (1, 8-dihydroxy-3-hydroxymethylanthraquinone) as the major product formed.

PMID:9616189 Mueller S et al; Drug Metab Dispos. 26(6): 540-6 (1998)


The hepatic microsomes derived from various animal species transformed emodin (1,3,8-trihydroxy-6-methylanthraquinone), into an unidentified anthraquinone, along with 2-hydroxy-, 4-hydroxy- and 7-hydroxyemodins. ... This major metabolite /was identified/ as omega-hydroxy-emodin (1,3,8-trihydroxy-6-hydroxymethylanthraquinone). Among 7 animal species, the highest activity to produce this omega-hydroxyemodin was observed in the hepatic microsomes of guinea pig and rat, followed by mouse and rabbit. The microsomal activity to convert emodin into omega-hydroxyemodin was accelerated by the pretreatment of animals with phenobarbital, and inhibited by SKF 525A. The microsomal hydroxylation reactions of the methyl residue and the anthraquinoid nucleus of emodin were presumed to be catalyzed regiospecifically by multiple forms of cytochrome P-450.

PMID:3309636 Murakami H et al; Mutat Res 180 (2): 147-53 (1987)


... Emodin was biotransformed by the microsomal enzymes into at least 5 quinonoid metabolites, among which one pigment, identified as 2-hydroxyemodin (1,2,3,8-tetrahydroxy-6-methyl-anthraquinone), was proven to be a direct mutagen to the test strain, and the remaining 4 quinonoid metabolites were negative or far less active than this active principle.

PMID:6366529 Masuda T et al; Mutat Res 125(2): 135-44 (1984)


Emodin has known human metabolites that include Emodin 3-hydroxy-glucuronide.

S73 | METXBIODB | Metabolite Reaction Database from BioTransformer | DOI:10.5281/zenodo.4056560


5.4 Mechanism of Action

The anthraquinone mycotoxins emodin and skyrin were examined for the inhibitory effects on murine leukemia L1210 culture cells, oxidative phosphorylation of rat liver mitochondria, and Na+, K+-activated ATPase activity of rat brain microsomes to find the differences between their modes of toxic action. Skyrin exhibited a stronger inhibitory effect than emodin on the growth of L1210 culture cells. Emodin showed a stronger uncoupling effect than skyrin on mitochondrial respiration. Skyrin inhibited Na+, K+-activated ATPase activity of rat brain microsomes but emodin did not inhibit.

PMID:6320499 Kawai K et al; Toxicol Lett 20 (2): 155-60 (1984)


... Emodin induces apoptotic responses in the human hepatocellular carcinoma cell lines (HCC) Mahlavu, PLC / PRF / 5 and HepG2. The addition of emodin to these three cell lines led to inhibition of growth in a time- and dose-dependent manner. Emodin generated reactive oxygen species (ROS) in these cells which brought about a reduction of the intracellular mitochondrial transmembrane potential (Deltaym), followed by the activation of caspase-9 and caspase-3, leading to DNA fragmentation and apoptosis.

PMID:12716464 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5927105 Jing X et al; Jpn J Cancer Res 93 (8): 874-82 (2002)


Emodin inhibited the activity of TPK and CK2 and the degradation of I-kappaB.

PMID:12703988 Zhu F et al; Ai Zheng 22 (4): 358-362 (2003)


... Emodin-induced apoptosis of CH27 cells does not involve modulation of endogenous Bcl-X(L) protein expression, but appears to be associated with the increased expression of cellular Bak and Bax proteins.

PMID:11522592 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1572914 Lee HZ et al; Br J Pharmacol 134 (1): 11-20 (2001)


For more Mechanism of Action (Complete) data for EMODIN (9 total), please visit the HSDB record page.


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