Glycyrrhizic acid

822.93200

822.93

215-785-7

DTXSID8047006

Crystals from glacial acetic acid|PLATES OR PRISMS FROM ACETIC ACID

A - Alimentary tract and metabolism

1211903600

267.04000

log Kow = 2.80

Solid

1.43g/cm3

220 °C (decomp)

971.4ºC at 760mmHg

288.1ºC

1.621

Freely sol in hot water, alcohol; practically insol in ether

0mmHg at 25°C

Specific optical rotation: +46.2 deg @ 17 °C/D (alcohol, 1.5%)

Intensely sweet taste

ON HYDROLYSIS IT YIELDS GLYCYRRHETIC ACID & 2 MOLES OF GLUCURONIC ACID|STRUCTURALLY & CHEMICALLY SIMILAR TO ALDOSTERONE & DESOXYCORTICOSTERONE|STRUCTURALLY SIMILAR TO MANY CYCLOPENTANOPHENANTHRENE STEROIDS|Needles from 75% aqueous ethanol, decomp 212-217 °C. Specific optical rotation: +46.9 deg @ 20 °C/D (c= 1.5 in 40% ethanol). UV max: 248 nm (e= 11400). Sol in ammonia water, glacial acetic acid. /Ammonium glycycrrhizinate pentahydrate/

NONH for all modes of transport

S22-S24/25

MD2025000

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

Essential oils, oleoresins (solvent-free), and natural extractives (including distillates) that are generally recognized as safe for their intended use within the meaning of section 409 of the act. Licorice is included on this list. /Licorice/|Substance added directly to human food affirmed as generally recognized as safe (GRAS). /Licorice and licorice derivatives/

ADDITION OF 10-6 M GLYCYRRHETINIC ACID IN PRESENCE OF 10-8 M ALDOSTERONE STIMULATED SHORT-CIRCUIT SIGNIFICANTLY AS COMPARED WITH CONTROL SKIN TREATED WITH ALDOSTERONE ALONE.|ADMIN OF GLYCYRRHIZIN DEPRESSED EFFECT OF INJECTED CORTISONE ON GLYCOGEN STORAGE AND ENHANCED IMMUNOSUPPRESSIVE ACTION OF CORTISONE.|The pharmacokinetics of total and free prednisolone (PSL) in six healthy men, with or without pretreatment with oral glycyrrhizin (GL), was investigated to confirm whether oral administration of GL influences the metabolism of prednisolone in man. Each subject received an intravenous administration of 0.096 mg/kg of prednisolone hemisuccinate (PSL-HS) with or without pretreatment with 50 mg of oral glycyrrhizin four times. Blood samples were taken from a peripheral vein at 5, 10, 15, 30, 45 min and 1, 1.5, 2, 3, 4, 6, 8, 10, 12 and 24 hr after the start of prednisolone-HS infusion. The concentrations of total prednisolone in plasma were analyzed by high-performance liquid chromatography, and the free prednisolone was measured by an isocolloidosmolar equilibrium dialysis method. The pharmacokinetic parameters of prednisolone were determined by non-compartment analysis. Oral administration of glycyrrhizin was found to significantly increase the concentrations of total prednisolone at 6, 8 hr, and of free prednisolone at 4, 6 and 8 hr after prednisolone-hemisuccinate infusion. Moreover, oral administration of glycyrrhizin was also found to modify the pharmacokinetics of both total and free prednisolone. After oral administration of glycyrrhizin, the area under the curve (AUC) was significantly increased, the total plasma clearance (CL) was significantly decreased, and the mean residence time (MRT) was significantly prolonged. However, the volume of distribution (Vdss) showed no evident change. This suggests that oral administration of glycyrrhizin increases the plasma prednisolone concentrations and influences its pharmacokinetics by inhibiting its metabolism, but not by affecting its distribution.|To clarify whether glycyrrhizin, the aqueous extract of licorice root and a drug for treatment of chronic active hepatitis, prevents the development of hepatic injury induced by carbon tetrachloride, allyl formate, and endotoxin, the present study was undertaken in rats. The treatment with glycyrrhizin 20 hr before carbon tetrachloride administration protected the development of the pericentral hepatocellular necrosis. Glycyrrhizin treatment 2 hr prior to the administration of allyl formate also inhibited the development of the periportal hepatocellular necrosis. However, glycyrrhizin did not protect the development of endotoxin-induced focal and random hepatocellular necrosis. These experimental results suggest that glycyrrhizin has no protective effect on hepatic injury following sinusoidal circulatory disturbance as seen in the case of endotoxin and that glycyrrhizin can protect against hepatotoxicity induced by the direct action on the hepatocytes due to hepatotoxins, such as carbon tetrachloride and allyl formate.|To investigate the effects of Potenlini on nuclear factor-kappa B (NF-kappa B) binding activity in the livers of animals models with liver cirrhosis, and to delineate the molecular mechanism of the bioactivities of Potenlini. METHODS: Male SD rats were randomly allocated into a normal control group, a model control group, and a Potenlini group. Rats in the latter two groups were treated with CCl4 and Ethanol solution in order to induce chronic liver injury. Rats in Potenlini group were given Potenlini treatment at the same time. All rats were killed at the 9th week after CCl4 administration. Serum and liver specimens were collected, serum ALT activities and histological findings were assessed. Nuclear extracts from liver tissues were prepared and gel retardation assays were performed for the evaluation of NF-kappa B activity. RESULTS: (1) Serum ALT levels were significantly reduced in rats treated with Potenlini compared with those in rats of the model control group, which had dramatically increased ALT levels. (2) Histologically, liver steatosis and fibrosis were severe in the rats of the model group, but were significantly improved in rats of the Potenlini group. (3) NF-kappa B binding activity was markedly increased in the liver specimens taken from the rats of the model control group in comparison with the binding of normal livers, but the binding levels were nearly normal in the livers of the Potenlini group. CONCLUSION: Potenlini can inhibit the NF-kappa B binding activity in CCl4 and ethanol induced chronic liver injury, and that may partially be the mechanism by which Potenlini protects liver from hepatotoxin-induced liver injury and cirrhosis.

DEMULCENT, MILD LAXATIVE; EXPECTORANT; USED TO DISGUISE TASTE OF MEDICATIONS|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.|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.|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.|For more Therapeutic Uses (Complete) data for GLYCYRRHIZIN (6 total), please visit the HSDB record page.

Substances that reduce or suppress INFLAMMATION. (See all compounds classified as Anti-Inflammatory Agents.)

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.|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.|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.|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.

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.

GLYCYRRHIZIC ACID & ITS DERIVATIVES SHOWED PRONOUNCED ANTIINFLAMMATORY ACTION, INHIBITED DEVELOPMENT OF HISTAMINE-, SEROTONIN-, BRADKININ-, & FORMALIN-INDUCED EDEMA, & DECR VASCULAR PERMEABILITY.

14 VOLUNTEERS ATE DAILY DOSES OF 100-200 G LIQUORICE, EQUIV TO O.7-1.4 G GLYCYRRHIZINIC ACID FOR 1-4 WK. PLASMA K CONCN FELL; PLASMA RENIN & URINARY ALDOSTERONE DEPPRESSED IN ALL SUBJECTS.|...TOXICITY OF THIS COMPOUND & ITS DERIVATIVES BY MOUTH IS PRESUMED TO BE LOW. /GLYCYRRHIZA AND ITS DERIVATIVES/|POTENTIAL SERIOUS METABOLIC EFFECTS MAY OCCUR IN SOME PEOPLE WHO EAT MODEST AMT OF LIQUORICE DAILY FOR LESS THAN A WEEK.|GLYCYRRHIZIC ACID COMPLETELY INHIBITED GROWTH & CYTOPATHIC EFFECTS OF VACCINIA, HERPES SIMPLEX TYPE 1, NEWCASTLE DISEASE & VESICULAR STOMATITIS VIRUSES IN CULTURES OF HUMAN ANEUPLOID HEP2 CELLS.|For more Human Toxicity Excerpts (Complete) data for GLYCYRRHIZIN (10 total), please visit the HSDB record page.

3-hydroxy-11 oxoolean-12-en-30-oic acid-3-O-glucuronopyranosyl-(1-2)glucuronopyranoside|Acid, Glycyrrhizic

For improved water solubility, an ammoniated salt is commonly used. ... either ammonium glycyrrhizinate or monoammonium glycyrrhizinate.|...MAIN CONSTITUENT /OF LICORICE/ IS GLYCYRRHIZIN (THE POTASSIUM-CALCIUM-MAGNESIUM SALT OF GLYCYRRHIZIC ACID); COMMERCIAL GLYCYRRHIZIN IS AMMONIUM SALT OF THE ACID.

.alpha.-D-Glucopyranosiduronic acid, (3.beta.,20.beta.)-20-carboxy-11-oxo-30-norolean-12-en-3-yl 2-O-.beta.-D-glucopyranuronosyl-: ACTIVE|THIS WELL KNOWN ROOT /LICORICE/ CONTAINS 5 TO 7% OF THE SWEET PRINCIPLE GLYCYRRHIZIN, OR GLYCYRRHIZIC ACID...|INCOMPATIBILITIES; SWEETENING POWER OF LICORICE CANNOT BE EMPLOYED IN ACID FOODS BECAUSE OF ITS HYDROLYSIS TO THE NON-SWEET CONSTITUENTS OF THE GLYCOSIDE. /GLYCYRRHIZA/|GLYCYRRHIZIC ACID IS A GLUCOSIDE; ON HYDROLYSIS IT YIELDS GLYCYRRHETIC ACID AND 2 MOLES OF GLUCURONIC ACID.|Exerts strong synergistic action with sucrose.|For more General Manufacturing Information (Complete) data for GLYCYRRHIZIN (6 total), please visit the HSDB record page.

GLYCYRRHIZIN, ACTIVE INGREDIENT IN KAMPO (CHINESE MEDICAL PREPN) WAS DETERMINED BY HIGH-SPEED CHROMATOGRAPHY. SEPARATION OCCURS IN LESS THAN 11 MINUTES.|METHOD IS BASED ON COUPLING ACIDIC GENIN, GLYCYRRHETINIC ACID WITH METHYLENE BLUE & MEASURING EXTINCTION OF THE COUPLED COMPD SOLN WITH CHLOROFORM-ETHANOL.|A DUAL-WAVELENGTH THIN-LAYER CHROMATOGRAPHY SCANNER WAS USED FOR THE DETERMINATION OF GLYCYRRHIZIN IN SAMPLES OF LICORICE AND CHINESE DRUGS.|NORMAL GLYCYRRHIZIN CONTENT OF LICORICE ROOT WAS APPROX 5% & EXTRACTS CONTAINED APPROX 20-24% GLYCYRRHIZIN. DETERMINATIVE PROCEDURE IS BY HIGH-SPEED LIQUID CHROMATOGRAPHY.|For more Analytic Laboratory Methods (Complete) data for GLYCYRRHIZIN (7 total), please visit the HSDB record page.

RAPID ESTIMATION OF GLYCYRRHIZIN AND GLYCYRRHETINIC ACID IN PLASMA BY HIGH-SPEED LIQUID CHROMATOGRAPHY.|SIMULTANEOUS DETERMINATION OF GLYCYRRHIZIN AND GLYCYRRHETIC ACID IN PLASMA BY HIGH SPEED LIQUID CHROMATOGRAPHY.

Food additives -> Flavoring Agents|Cosmetics -> Humectant; Skin conditioning

Flavoring Agents