Shaanxi Fujie Pharmaceutical Co.,Ltd

Licorice Active Pharmaceutical Ingredient

1405-86-3 Licorice Glycyrrhizic Acid A

1405-86-3 Licorice Glycyrrhizic Acid A

Product Name: 1405-86-3 Licorice Glycyrrhizic Acid A
· Resource: 100% natural licorice roots
· Certificate: only cGMP in CHINA.
Appearance: White crystalline powder.
· HS Code: 2938.90
Content: No less than 95%(UV)
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1405-86-3 Licorice Glycyrrhizic Acid A

Basic Info

· Product Name: 1405-86-3 Licorice Glycyrrhizic Acid A

· Resource: 100% natural licorice roots

· Certificate: only cGMP in CHINA.

· Shelf Life:24 moths

· Transport Package:  500g*20 aluminium foil bag every Paper Drum

· Origin: Shaanxi , China

· Appearance: White crystalline powder.

· HS Code: 2938.90

Content: No less than 95%(UV)

· Trademark: FUJIE

· Packing Specification: 10KG/drum

· Molecular formula:C42H62O16

· Molecular weight:822.92g/mol

· CAS NO:471-53-4

Therapeutic Categories:Anti-inflammatory agent,Sweetening agent


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structural formula

Solubility:The product should be a white crystalline powder, odorless and sweetly taste.freely soluble in ethanol,very slightly soluble in water and pratically soluble in chloroform and ether.


Advantage 1.we are manufacturer

           2.we have sufficient licorice quota every year.

           3.We are only have1405-86-3 Licorice Glycyrrhizic Acid A GMP certification in china.

           4.1405-86-3 Licorice Glycyrrhizic Acid A is CHINA name,another name is Glycyrrhizic Acid.

What’s the product?

English name: 1405-86-3 licorice Glycyrrhizic acid A

CAS No.: 1405-86-3
Molecular Formula: C42H62O16

Molecular Weight : 822.92 
Active ingredients: glycyrrhizin acid
Appearance: White crystalline powder
Mesh size:80-100 Mesh

How does it work?

(1) Treatment of peptic ulcer

(2) Masks the unpleasant flavor of medicines
(3) Relieves cough
(4) Promotes the ejection of mucus or exudates from the lungs, bronchi and tracheas
(5) anti-inflammatory and co-emulsifier to treat skin disorders and in cosmetics.

What field apply to?

1.1405-86-3 licorice Glycyrrhizic acid A has the efficacy in antianaphylaxis and moist boost;      

2.1405-86-3 licorice Glycyrrhizic acid A has the effect of strong anti-oxidation and antibacterial effect;

3.1405-86-3 licorice Glycyrrhizic acid A has the useage of feature of low-calorie, innocuity and health care;   

4.1405-86-3 licorice Glycyrrhizic acid A  with the function of anti-flammation, antivirus, antimicrobial activity and liver protection.

Depositor-Supplied Synonyms

glycyrrhizin,Glycyrrhizic acid,Glycyrrhizinic acid,1405-86-3,Glycyron,Glycyrrhetinic acid glycoside,glyzyrrhizin,18beta-Glycyrrhizic acid,18-beta-Glycyrrhizic acid,Glycyrrizin,Liquorice,UNII-6FO62043WK,Rizinsan K2 A2 (free acid),HSDB 496,Glycyrrhizin (Glycyrrhizic Acid),einecs 215-785-7,C42H62O16,NSC 167409

,NSC 234419,BRN 0077922,CHEMBL441687,NSC 2800,beta-Glycyrrhizin,CHEBI:15939,(3beta,20beta)-20-carboxy-11-oxo-30-norolean-12-en


(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

Safety and Hazards

Accidental Release Measures

Disposal Methods

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.

Regulatory Information

FDA Requirements

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/


Toxicological Information


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.

Ishikawa s et al; endocrinol jpn 27 (6): 697 (1980)

admin of glycyrrhizin depressed effect of injected cortisone on glycogen storage and enhanced immunosuppressive action of cortisone.

kumagai a; taisha 10 632 (1973)

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.
Abstract: PubMed

Shibayama Y; Exp Mol Pathol 51 (1): 48-55 (1989)

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.


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