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1. Acid, Glycyrrhizic
2. Acid, Glycyrrhizinic
3. Diammonium Glycyrrhizinate
4. Dipotassium Glycyrrhizinate
5. Glycyrrhizate, Zinc
6. Glycyrrhizin
7. Glycyrrhizinate, Diammonium
8. Glycyrrhizinate, Dipotassium
9. Glycyrrhizinic Acid
10. Zinc Glycyrrhizate
1. Glycyrrhizin
2. 1405-86-3
3. Glycyrrhizinic Acid
4. Glycyron
5. Glycyrrhetinic Acid Glycoside
6. Glyzyrrhizin
7. Potenlini
8. Glizigen
9. 18-beta-glycyrrhizic Acid
10. Glycyrrhizate
11. Glycyrrhizin [jan]
12. Liquorice
13. .beta.-glycyrrhizin
14. Chebi:15939
15. Nsc-167409
16. Nsc-234419
17. 18.beta.-glycyrrhizic Acid
18. Chembl441687
19. Nsc 2800
20. Beta-glycyrrhizin
21. 6fo62043wk
22. Glycyram
23. Rizinsan K2 A2 (free Acid)
24. Alpha-d-glucopyranosiduronic Acid, (3beta,20beta)-20-carboxy-11-oxo-30-norolean-12-en-3-yl 2-o-beta-d-glucopyranuronosyl-
25. Dsstox_cid_27006
26. Dsstox_rid_82047
27. Dsstox_gsid_47006
28. Glycyrrhitin
29. Glycyrrhizinate
30. Dermacrin
31. (3beta,20beta)-20-carboxy-11-oxo-30-norolean-12-en-3-yl-2-o-beta-d-glucopyranuronosyl-alpha-d-glucopyranosiduronic Acid
32. 30-hydroxy-11,30-dioxoolean-12-en-3beta-yl (2-o-beta-d-glucopyranosyluronic Acid)-alpha-d-glucopyranosiduronic Acid
33. 18beta-glycyrrhizic Acid
34. Neo-umor
35. Cas-1405-86-3
36. Hsdb 496
37. Einecs 215-785-7
38. Nsc 167409
39. Nsc 234419
40. Brn 0077922
41. Unii-6fo62043wk
42. Ccris 8444
43. Mfcd00065194
44. Ncgc00183128-01
45. (2s,3s,4s,5r,6r)-6-[(2s,3r,4s,5s,6s)-2-[[(3s,4ar,6ar,6bs,8as,11s,12ar,14ar,14bs)-11-carboxy-4,4,6a,6b,8a,11,14b-heptamethyl-14-oxo-2,3,4a,5,6,7,8,9,10,12,12a,14a-dodecahydro-1h-picen-3-yl]oxy]-6-carboxy-4,5-dihydroxy-tetrahydropyran-3-yl]oxy-3,4,5-trihydroxy-tetrahydropyran-2-carboxylic Acid
46. Glycyrrhizin, 93%
47. Ammonium-glycyrrhizinate
48. Glycyrrhizic Acid, 2k
49. Beta-glycyrrhizinic Acid
50. 132215-36-2
51. Glycyrrhizin [ii]
52. Glycyrrhizin [hsdb]
53. Glycyrrhizia Uralensis Fisch
54. Schembl17684
55. 20beta-carboxy-11-oxo-30-norolean-12-en-3beta-yl-2-o-beta-d-glucopyranuronosyl-alpha-d-glucopyranosiduronic Acid
56. 4-18-00-05156 (beilstein Handbook Reference)
57. Alpha-d-glucopyranosiduronic Acid, (3beta,20beta)-20-carboxy-11-oxo-30-norolean-12-en-3-yl-2-o-beta-d-glucopyranuron Osyl-
58. Bidd:er0363
59. Glycyrrhizic Acid [mi]
60. Gtpl4688
61. Dtxsid8047006
62. Glycyrrhizic Acid [inci]
63. Glycyrrhizin (glycyrrhizic Acid)
64. Glycyrrhizic Acid [mart.]
65. Glycyrrhizic Acid [usp-rs]
66. Glycyrrhizic Acid [who-dd]
67. Hy-n0184
68. Tox21_111520
69. Tox21_113426
70. Tox21_303493
71. Bdbm50185127
72. Hmdb:0029843
73. S2302
74. Zinc96015174
75. Akos015893086
76. Akos015969345
77. Ccg-270511
78. Cs-7695
79. Db13751
80. Gm-1292
81. Ncgc00257455-01
82. Ncgc00386162-01
83. Ncgc00386162-02
84. (2s,3s,4s,5r,6r)-6-[(2s,3r,4s,5s,6s)-2-[[(3s,4ar,6ar,6bs,8as,11s,12ar,14ar,14bs)-11-carboxy-4,4,6a,6b,8a,11,14b-heptamethyl-14-oxo-2,3,4a,5,6,7,8,9,10,12,12a,14a-dodecahydro-1h-picen-3-yl]oxy]-6-carboxy-4,5-dihydroxyoxan-3-yl]oxy-3,4,5-trihydroxyoxane-2-carboxylic Acid
85. (3beta,20beta)-20-carboxy-11-oxo-30-norlean-12-en-3-yl-2-o-beta-1- 7-glucopyranuronosyl-alpha-d-glucopyranosiduronic Acid
86. (3beta,20beta)-20-carboxy-11-oxo-30-norolean-12-en-3-yl 2-o-beta-d-glucopyranuronosyl-alpha-d-glucopyranosiduronic Acid
87. Alpha-d-glucopyranosiduronic Acid, (3beta,20beta)-20-carboxy-11-oxo-30-norlean-12-en-3-yl-2-o-beta-1- 7-glucopyranuronosyl-
88. As-13001
89. E958
90. G0150
91. N1792
92. Ab01566834_01
93. 405g863
94. Q418705
95. Q-201172
96. Brd-k83486494-318-01-5
97. Glycyrrhizic Acid (glycyrrhizin) (constituent Of Licorice) [dsc]
98. Glycyrrhizic Acid, United States Pharmacopeia (usp) Reference Standard
99. Xy-4,5-dihydroxyoxan-3-yl]oxy-3,4,5-trihydroxyoxane-2-carboxylic Acid
100. Glycyrrhizic Acid, Pharmaceutical Secondary Standard; Certified Reference Material
101. (2s,3s,4s,5r,6r)-6-[(2s,3r,4s,5s,6s)-2-[[(3s,4ar,6ar,6bs,8as,11s,12ar,14ar,14bs)-11-carboxy-4,4,6a,6b,8a,11,14b-heptamethyl-14-oxo-2,3,4a,5,6,7,8,9,10,12,12a,14a-dodecahydro-1h-picen-3-yl]oxy]-6-carbo
102. (2s,3s,4s,5r,6s)-6-{[(3s,4ar,6ar,6bs,8as,11s,12ar,14ar,14bs)-11-carboxy-4,4,6a,6b,8a,11,14b-heptamethyl-14-oxo-1,2,3,4,4a,5,6,6a,6b,7,8,8a,9,10,11,12,12a,14,14a,14b-icosahydropicen-3-yl]oxy}-5-{[(2r,3r,4s,5s,6s)-6-carboxy-3,4,5-trihydroxyoxan-2-yl]oxy}-3,4-dihydroxyoxane-2-carboxylic Acid
103. (3.beta.,20.beta.)-20-carboxy-11-oxo-30-norlean-12-en-3-yl-2-o-.beta.-1- 7-glucopyranuronosyl-.alpha.-d-glucopyranosiduronic Acid
104. (3.beta.,20.beta.)-20-carboxy-11-oxo-30-norolean-12-en-3-yl 2-o-.beta.-d-glucopyranuronosyl-.alpha.-d-glucopyranosiduronic Acid
| Molecular Weight | 822.9 g/mol |
|---|---|
| Molecular Formula | C42H62O16 |
| XLogP3 | 3.7 |
| Hydrogen Bond Donor Count | 8 |
| Hydrogen Bond Acceptor Count | 16 |
| Rotatable Bond Count | 7 |
| Exact Mass | 822.40378589 g/mol |
| Monoisotopic Mass | 822.40378589 g/mol |
| Topological Polar Surface Area | 267 Ų |
| Heavy Atom Count | 58 |
| Formal Charge | 0 |
| Complexity | 1730 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 19 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
DEMULCENT, MILD LAXATIVE; EXPECTORANT; USED TO DISGUISE TASTE OF MEDICATIONS
Arena, J.M. Poisoning: Toxicology-Symptoms Treatments. Third Edition. Springfield, Illinois: Charles C. Thomas, 1974., p. 575
SNMC (stronger Neominophagen C), whose active component is glycyrrhizin (a saponin extracted from licorice) has been utilized to improve the liver function in Japan. To assess the effectiveness of interferon (IFN), stronger Neominophagen C combination therapy in patients, who did not respond to interferon therapy alone, we investigate 28 patients with histology of CAH 2B at 12 weeks after interferon administration. 15 patients received interferon alone continuously (group A), and 13 patients received interferon with stronger Neominophagen C (group B) for 12 weeks thereafter. Normalization of serum ALT level was observed in 33.3% of group A and in 64.3% of group B. Disappearance of serum HVC RNA was 13.3% in group A and 38.5% in group B. But these data were not significant statistically. Histological improvement was not significant, between group A and B by Knodel's HAI score, but reversal of histological grade (Europe classification) was noted more frequently in group B. A case of post transfusion hepatitis type C, exacerbated by interferon therapy is reported. HLA class I antigen was strongly expressed in the liver tissue after administration of interferon. In this case, potentiation of cellular immunity was thought to be the cause of the exacerbation and interferon, stronger Neominophagen C combination therapy was useful in improving liver function.
PMID:7521424 Abe Y et al; Nippon Rinsho 52 (7): 1817-22 (1994)
Licorice (Glycyrrhiza glabra), a Mediterranean plant, has been used as an antidote, demulcent, and elixir folk medicine for generations in China. The main water-soluble constituent of licorice is glycyrrhizin (GL), which has been shown to possess several pharmacological properties. In this study, we show that oral feeding of glycyrrhizin to Sencar mice resulted in substantial protection against skin tumorigenesis caused by 7,12-dimethyl-benz [a]anthracene (DMBA) initiation and 12-O-tetradecanoylphorbol-13-acetate (TPA) promotion. The latent period prior to the onset of tumor development was considerably prolonged in glycyrrhizin-fed animals compared with animals not fed glycyrrhizin and resulted in significant decrease in the number of tumors per mouse, during and at the termination of the experiment. Oral feeding of glycyrrhizin in drinking water also resulted in inhibition in the binding of topically applied [3H]benzo[a]pyrene and [3H]DMBA to epidermal DNA. The possible mechanism(s) of the antitumor-initiating activity may be due to the involvement of glycyrrhizin as inhibitor of the carcinogen metabolism followed by DNA adduct formation. Our results suggest that glycyrrhizin possesses considerable antitumorigenic activity and could prove useful in protecting some forms of human cancer.
PMID:1907733 Agarwal R et al; Nutr Cancer 15 (3-4): 187-93 (1991)
Hepatocellular carcinoma (HCC) occurs in patients with hepatitis C virus-RNA positive chronic liver disease. It is important to prevent Hepatocellular carcinoma with drug administration. METHODS: A retrospective study was undertaken to evaluate the long term preventive effect of Stronger Neo-Minophagen C (SNMC) on Hepatocellular carcinoma development. Stronger Neo-Minophagen C is a Japanese medicine that is commonly administered to patients with chronic hepatitis C to improve the serum alanine aminotransferase (ALT) level. Of 453 patients diagnosed with chronic hepatitis C retrospectively in the study hospital between January 1979 and April 1984, 84 patients (Group A) had been treated with Stronger Neo-Minophagen C; Stronger Neo-Minophagen C was given at a dose of 100 mL daily for 8 weeks, then 2-7 times a week for 2-16 years (median, 10.1 years). Another group of 109 patients (Group B) could not be treated with Stronger Neo-Minophagen C or interferon for a long period of time (median, 9.2 years) and were given other herbal medicine (such as vitamin K). The patients were retrospectively monitored, and the cumulative incidence of Hepatocellular carcinoma and risk factors for Hepatocellular carcinoma were examined. RESULTS: The 10th-year rates of cumulative Hepatocellular carcinoma incidence for Groups A and B were 7% and 12%, respectively, and the 15th-year rates were 12% and 25%. By Cox regression analysis, the relative risk of Hepatocellular carcinoma incidence in patients not treated with Stronger Neo-Minophagen C (Group B) was 2.49 compared with that of patients treated with Stronger Neo-Minophagen C (Group A). CONCLUSIONS: In this study, long term administration of Stronger Neo-Minophagen C in the treatment of chronic hepatitis C was effective in preventing liver carcinogenesis.
PMID:9118029 Arase Y et al; Cancer 79 (8): 1494-500 (1997)
For more Therapeutic Uses (Complete) data for GLYCYRRHIZIN (6 total), please visit the HSDB record page.
Glycyrrhizic acid is widely applied in foods as a natural sweetener. As a therapeutic agent, is has been used in a vast variety of formulations as it is reported to be anti-inflammatory, anti-ulcer, anti-allergic, antioxidant, anti-tumor, anti-diabetic and hepatoprotective. Due to this properties, its indications have been: treatment of premenstrual syndrome, treatment of viral infections, anti-lipidemic and antihyperglycemic. It is also known to be used as a remedy for peptic ulcer and other stomach diseases.
Glycyrrhizic acid was reported to present antiallergic, antiviral and anti-inflammatory activities as well as improvements in glucose tolerance. The effect of glycyrrhizic acid in metabolic syndrome generates a significant decrease in blood glucose, fasting blood glucose and mean serum insulin concentration.
Anti-Inflammatory Agents
Substances that reduce or suppress INFLAMMATION. (See all compounds classified as Anti-Inflammatory Agents.)
A - Alimentary tract and metabolism
A05 - Bile and liver therapy
A05B - Liver therapy, lipotropics
A05BA - Liver therapy
A05BA08 - Glycyrrhizic acid
Absorption
Glycyrrhizic acid is mainly absorbed after presystemic hydrolysis and formation of glycyrrhetinic acid. Therefore, after oral administration of a dose of 100 mg of glycyrrhizic acid, this major metabolite appears in plasma in a concentration of 200 ng/ml while glycyrrhizic acid cannot be found. The finding of a minimal amount of glycyrrhizic acid in urine suggests the existence of a partial absorption in the gastrointestinal tract.
Route of Elimination
Glycyrrhizic acid presents a biphasic elimination from the central compartment with a dose-dependent second elimination phase. The majority of the administered dose is eliminated by the bile in which glycyrrhizic acid can be eliminated unchanged and undergoes enterohepatic cycling. On the other hand, the major metabolite, glycyrrhetinic acid, forms glucuronide and sulfate conjugates. These conjugates are efficiently transported into the bile and duodenum where commensal bacteria hydrolizes the conjugate for the formation of glycyrrhetinic acid and further reabsorption. This reabsorption behavior seems to be related to the activity of 3-alpha-hydroxysteroid dehydrogenase which transports very efficiently the metabolite from the plasma to the bile. About 1.1-2.5% of the administered dose of glycyrrhizic acid can be found in urine which corresponds to the minimal cycling and reabsorption of this compound.
Volume of Distribution
The apparent volume of distribution of glycyrrhizic acid either in the central compartment and in steady-state are in the range of 37-64 ml/kg and 59-98 ml/kg, respectively.
Clearance
The constant reabsorption of glycyrrhetic acid in the duodenum causes a delay in the terminal plasma clearance. The reported total body clearance of glycyrrhizic acid is reported to be in the range of 16-25 ml.kg/h.
GLYCYRRHIZIN WAS ABSORBED IN RAT SMALL INTESTINE; THERE WAS NO DETECTABLE AMT OF GLYCYRRHETINIC ACID IN BLOOD AFTER BOLUS INJECTION OF GLYCYRRHIZIN INTO PORTAL VEIN; GLYCYRRHETINIC ACID WAS PRESENT IN DETECTABLE AMT IN BLOOD AFTER ORAL ADMIN.
SAKIYA ET AL; CHEM PHARM BULL 27(5) 1125 (1979)
Glycyrrhizic acid (GZA) and glycyrrhetinic acid (GRA) can be determined rapidly and precisely by high-performance liquid chromatography (HPLC) in biological fluids and tissues from experimental animals and humans. From plasma and tissues, glycyrrhizic acid and glycyrrhetinic acid are extracted by organic solvents and the extracts can directly be used for HPLC. From bile or urine, extraction and determination of glycyrrhizic acid and glycyrrhetinic acid are more difficult due to interfering endogenous compounds and conjugation of glycyrrhetinic acid with glucuronides or sulfates. Extraction of glycyrrhizic acid and glycyrrhetinic acid from urine or bile can be performed by ion-pairing followed by extraction with organic solvents or by solid phase extraction. Glycyrrhetinic acid conjugates can be determined by chromatographic separation or by pretreatment with beta-glucuronidase. The pharmacokinetics of glycyrrhetinic acid and glycyrrhizic acid can be described by a biphasic elimination from the central compartment with a dose-dependent second elimination phase. Depending on the dose, the second elimination phase in humans has a half-life of 3.5 hours for glycyrrhizic acid and between 10-30 hours for glycyrrhetinic acid. The major part of both glycyrrhetinic acid or glycyrrhizic acid is eliminated by the bile. While glycyrrhizic acid can be eliminated unmetabolized and undergoes enterohepatic cycling, Glycyrrhetinic acid is conjugated to glycyrrhetinic acid glucuronide or sulfate prior to biliary excretion. Orally administered glycyrrhizic acid is almost completely hydrolyzed by intestinal bacteria and reaches the systemic circulation as glycyrrhetinic acid.
PMID:8191540 Krahenbuhl S et al; Steroids 59 (2): 121-6 (1994)
Glycyrrhizic acid is currently of clinical interest for treatment of chronic hepatitis. It is also applied as a sweetener in food products and chewing tobacco. In some highly exposed subgroups of the population, serious side effects such as hypertension and electrolyte disturbances have been reported. In order to analyze the health risks of exposure to this compound, the kinetics of glycyrrhizic acid and its active metabolites were evaluated quantitatively. Glycyrrhizic acid and its metabolites are subject to complex kinetic processes, including enterohepatic cycling and presystemic metabolism. In humans, detailed information on these processes is often difficult to obtain. Therefore, a model was developed that describes the systemic and gastrointestinal tract kinetics of glycyrrhizic acid and its active metabolite glycyrrhetic acid in rats. Due to the physiologically based structure of the model, data from earlier in vitro and in vivo studies on absorption, enterohepatic cycling, and presystemic metabolism could be incorporated directly. The model demonstrates that glycyrrhizic acid and metabolites are transported efficiently from plasma to the bile, possibly by the hepatic transfer protein 3-alpha-hydroxysteroid dehydrogenase. Bacterial hydrolysis of the biliary excreted metabolites following reuptake of glycyrrhetic acid causes the observed delay in the terminal plasma clearance of glycyrrhetic acid. These mechanistic findings, derived from analysis of experimental data through physiologically based pharmacokinetic modeling, can eventually be used for a quantitative health risk assessment of human exposure to glycyrrhizic acid containing products. Copyright 2000 Academic Press.
PMID:10652246 Ploeger BA et al; Toxicol Appl Pharmacol 162 (3): 177-88 (2000)
To assess the multiplicity for the biliary excretion of xenobiotic conjugates, glycyrrhizic acid (glycyrrhizin) was studied in rats after intravenous (IV) injection of 10 mg/kg glycyrrhizic acid and IV infusion of inhibitors, dibromosulfophthalein and indocyanine green. Indocyanine green did not affect the biliary excretion of glycyrrhizic acid, whereas dibromosulfophthalein reduced it significantly. The plasma level of glycyrrhizic acid was increased by dibromosulfophthalein, but not by indocyanine green. In Eisai hyperbilirubinemic rats, the biliary excretion of glycyrrhizic acid was severely impaired, resulting in an increased plasma level. The findings suggested that the biliary excretion of glycyrrhizic acid is mediated by the system shared by liquiritigenin glucuronides and dibromosulfophthalein, but not by indocyanine green, and that the system is hereditarily defective in Eisai hyperbilirubinemic rats.
PMID:8987080 Shimamura H et al; Pharm Res 13 (Dec): 1833-7 (1996)
When orally administered, glycyrrhizic acid is almost completely hydrolyzed by intestinal bacteria for the formation of glycyrrhetinic acid, which is an active metabolite and can enter systemic circulation, and two molecules of glucuronic acid. This metabolite is transported and taken in the liver for its metabolization to form glucuronide and sulfate conjugates.
BOLUS INJECTION OF GLYCYRRHIZIN GIVEN RATS IN PORTAL VEIN, GAVE RISE IN BLOOD LEVEL OF SUBSTANCE WHICH APPEARS TO BE GLUCURONIC ACID CONJUGATE FORMED AS METABOLITE OF GLYCYRRHETINIC ACID.
SAKIYA ET AL; CHEM PHARM BULL 27(5) 1125 (1979)
Depending on the dose, the second elimination phase in humans has a half-life of 3.5 hours.
Glycyrrhizic acid can be found in the alpha and beta forms. The alpha form is predominant in the liver and duodenum and thus, it is thought that the anti-inflammatory liver effect of this drug are mainly due to the action of this isomer. Glycyrrhizic acid anti-inflammatory effect is generated via suppression of TNF alpha and caspase 3. It also inhibits the translocation of NFkB into the nuclei and conjugates free radicals. Some studies have shown a glycyrrhizic-driven inhibition of CD4+ T cell proliferation via JNK, ERK and PI3K/AKT. The antiviral activity of glycyrrhizic acid includes the inhibition of viral replication and immune regulation. The antiviral activity of glycyrrhizic acid seems to be of a broad spectrum and be able to cover several different viral types such as vaccinia virus, herpes simplex virus, Newcastle disease virus and vesicular stomatitis virus. The effect of glycyrrhizic acid on metabolism is thought to be related to its inhibitory activity towards 11-beta-hydroxysteroid dehydrogenase type 1 which in turn decreases the activity of hexose-6-phosphate dehydrogenase. On the other hand, some studies have shown a potential lipoprotein lipase induction in non-hepatic tissues and thus it is suggested to enhance dyslipidemic conditions.
GLYCYRRHIZIC ACID & ITS DERIVATIVES SHOWED PRONOUNCED ANTIINFLAMMATORY ACTION, INHIBITED DEVELOPMENT OF HISTAMINE-, SEROTONIN-, BRADKININ-, & FORMALIN-INDUCED EDEMA, & DECR VASCULAR PERMEABILITY.
NASYROV KM ET AL; FARMAKOL TOKSIKOL (MOSCOW) 43(4) 399 (1980)
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