Shaanxi Fujie Pharmaceutical Co.,Ltd

Licorice Active Pharmaceutical Ingredient

Glycyrrhizic Acid A
Glycyrrhizic Acid AProduct Name: Glycyrrhizic Acid A
· Resource: 100% licorice roots
· Appearance: White crystalline powder.
· HS Code: 2938909030
Content: NLT 95%(UV)
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Basic Info

· Product Name: Glycyrrhizic Acid A

· Resource: 100% licorice roots

· Certificate: only GMP certification in CHINA.

· Shelf Life:24 moths

· Transport Package:  All Paper Drum

· Origin: Shaanxi , China

· Appearance: White crystalline powder.

· HS Code: 2938909030

Content: NLT 95%(UV)

· Trademark: FUJIE

· Specification: 10KG/drum

· Molecular formula:C42H62O16

· Molecular weight:822.92

· CAS NO:471-53-4

Therapeutic Categories:Anti-inflammatory agent,Drug acting on the gastrointestinal system,Expectorant,Sweetening agent

Grade:Pharmaceutical,Cosmetic,food

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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.

【annual production】The annual production capability of the factory can reach to twenty tons.

Why choose us?

1.we are manufacturer

2.we have sufficient licorice quota every year.

3.We are only have Glycyrrhizic Acid A GMP certification in china.

4.Glycyrrhizic Acid A is CHINA name,another name is Glycyrrhizic Acid.

Human Toxicity Excerpts

14 volunteers ate daily doses of 100-200g 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.

epstein et al; br med j 1(feb 19) 488 (1977)...

toxicity of this compound & its derivatives by mouth is presumed to be low. /glycyrrhiza and its derivatives/gosselin, r.e., h.c. hodge, r.p. smith, and m.n. Gleason. Clinical Toxicology of Commercial Products. 4th ed. Baltimore: Williams and Wilkins, 1976., p. II-166

potential serious metabolic effects may occur in some people who eat modest amt of liquorice daily for less than a week.

epstein et al; br med j 1(feb 19) 488 (1977)

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.

pompei r et al; nature (london) 281 (5733): 689 (1979)

The pathogenesis of pseudohyperaldosteronism from licorice has been evaluated in 6 male volunteers taking daily 7 g of a commercial preparation of licorice for 7 days, corresponding to an intake of 500 mg/day of glycyrrhizic acid. Pseudohyperaldosteronism was evident during the treatment (increase of body weight, suppression of plasma renin activity and plasma aldosterone, reduction of serum potassium). The ratio (tetrahydrocortisol + allo

tetrahydrocortisol)/tetrahydrocortisone in urine increased in 5 cases after 3 days of treatment, without an increase of plasma mineralocorticoid activity (PMA). In the 6th case the urinary ratio was unchanged and plasma mineralocorticoid activity increased from the pretreatment value. After 7 days of therapy the ratio remained high and plasma mineralocorticoid activity was not measurable in 3 cases, while in the other 3 cases the ratio returned to pretreatment and plasma mineralocorticoid activity was higher than pretreatment value. We conclude that the pseudohyperaldosteronism from licorice is initially related to decreased activity of 11 beta-hydroxysteroid-dehydrogenase and afterwards also a direct effect of licorice derivatives on mineralocorticoid receptors becomes evident in some cases. In other cases however the effect on the enzyme is prevailing probably due to individual factors.
Abstract: PubMed

Armanini D et al; J Endocrinol Invest 19 (9): 624-9 (1996)

Licorice can induce a hypermineralocorticoid syndrome. Current literature usually refers to the effects of sweets containing glycyrrhizin, but little is known about the consequences of a prolonged intake of "pure licorice". We administered graded daily doses of dried, aqueous extract of licorice root, containing 108, 217, 380 and 814 mg of glycyrrhizin, to 4 groups of 6 healthy volunteers of both sexes for 4 weeks, No significant effects occurred in groups 1 and 2. After 2 weeks, side effects leading to withdrawal from the protocol occurred in a female in group 3 (headache), a male with a family history of hypertension in group 4 (arterial hypertension), and a female also taking oral contraceptives in group 4 (hypertension, hypokalaemia and peripheral edema). In group 4, transient reduction in kalaemia and increase in body weight were found after 1 and 2 weeks, respectively. A depression of plasma renin activity occurred in groups 3 and 4. In healthy subjects, only the highest doses of licorice led to untoward effects. These and pronounced than what has been reported after the intake of glycyrrhizin taken as such or as a flavoring agent in confectionery products.
Abstract: PubMed

Bernardi M et al; Life Sciences 55 (11): 863-872 (1994)

A 72-year-old man developed acute renal failure (ARF) following severe hypokalemic rhabdomyolysis. The hypokalemia was due to chronic glycyrrhizin (glycyrrhizic acid) administration. Although glycyrrhizin-induced hypokalemic rhabdomyolysis has been occasionally reported, the association of this type of rhabdomyolysis with acute renal failure has not been described. In the present case, there was a sensitivity to glycyrrhizin the preceding renal insufficiency, and dehydration which was thought to have contributed to acute renal failure. It should be recognized that elderly patients with such predisposing factors may be susceptible to a rapid deterioration of renal function after glycyrrhizin-induced hypokalemic rhabdomyolysis.
Abstract: PubMed

Chubachi A et al; Intern Med 31 (5): 708-11 (1992)

Glycyrrhizic acid (GA) was tested for inhibition of arylamine N-acetyltransferase (NAT) activity in a human colon tumour (adenocarcinoma) cell line (colo 205). Two assay systems were performed, one with cellular cytosols (9000g supernatant), the other with intact colon tumour cell cultures. The N-acetyltransferase activity in a human colon tumour cell line was inhibited by glycyrrhizic acid in a dose-dependent manner in both types of systems examined. The data also indicated that glycyrrhizic acid decreased the apparent values of K(m) and V(max) of N-acetyltransferase enzymes from human colon tumour cells in both examined systems. The DNA-2-aminofluorene adduct formation in human colon tumour cells were inhibited by glycyrrhizic acid. This report is the first to demonstrate that glycyrrhizic acid does inhibit human colon tumour cell N-acetyltransferase activity and DNA adduct formation.
Abstract: PubMed

Chung JG et al; Food Chem Toxicol 38 (2-3): 163-72 (2000)

A 78-year-old man was hospitalized because of muscular weakness and acute renal failure. He had been taking glycyrrhizin (280 mg/day) for the last 7 years. Hypertension was noted in his history. Serum potassium was 1.9 mEq/l with metabolic alkalosis. There was hyporeninemic hypoaldosteronism. Serum enzymes, including GOT, LDH and CPK were markedly elevated. In addition, serum myoglobin was as high as 46 micrograms/ml with massive myoglobinuria. Oliguria occurred and blood urea nitrogen and serum creatinine rapidly elevated from 20.9 to 87 mg/dl and from 1.3 to 6.7 mg/dl, respectively. Profound calcium deposition was found in the damaged skeletal muscles, including the quadriceps femoris, axillar, neck, and cardiac muscles. These results indicate that licorice-induced pseudoaldosteronism produces hypokalemic rhabdomyolysis, resulting in acute renal failure and profound deposition of calcium into the damaged skeletal and cardiac muscles.
Abstract: PubMed

Saito T et al; Nippon Jinzo Gakkai Shi 36 (11): 1308-14 (1994)

Fifty-nine cases of glycyrrhizin (licorice)-induced hypokalemic myopathy (GIHM), 2 females treated in our departments (85 and 73 years old) and 57 cases reported in the literature were studied, and conditions leading to the onset, factors, clinical manifestations, laboratory assessments, muscle biopsy findings, treatment and outcome were discussed. The 59 glycyrrhizin (licorice)-induced hypokalemic myopathy cases comprised 32 men, 25 women and 2 patients without record of sex; the average age was 55.2 years. In many cases, conditions leading to the onset of glycyrrhizin (licorice)-induced hypokalemic myopathy were habitual licorice ingestion, ingestion of antituberculosis agents containing licorice and long-term ingestion of licorice-containing agents for chronic gastritis, chronic hepatitis or chronic dermatitis. The combined use of hypotensive diuretic agents increased the risk of glycyrrhizin (licorice)-induced hypokalemic myopathy in an overwhelming number of cases. The main clinical symptom was flaccid quadriplegia in almost all cases, with muscle pain in 32.2% and peripheral dysesthesia in the extremities, manifested mainly by numbness (27.1%). Laboratory findings included a mean serum K+ value of 1.98 mEq/l (56 glycyrrhizin (licorice)-induced hypokalemic myopathy cases), a mean creatine kinase of 5,385.7 IU/l (n = 30), a mean blood aldosterone concentration of 2.92 ng/dl (n = 30; normal: 2.0-13.0 ng/dl) and a mean plasma renin activity of 0.17 ng/ml/hr (n = 27; normal: 0.8-4.4 ng/ml/hr). Muscle biopsy was performed in 17 of the 59 cases with resultant findings of myopathic changes consisting mainly of phagocytosis, necrotic fibers, vacuolar degeneration, together with sporadic neurogenic changes. Complete cure was attained in 57 of the 59 cases of glycyrrhizin (licorice)-induced hypokalemic myopathy by discontinued ingestion of glycyrrhizin (licorice) and potassium supplement.
Abstract: PubMed

Shintani S et al; Eur Neurol 32 (1): 44-51 (1992)

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