Explore a selection of our essential drug information below, or:
Identification
- Generic Name
- Glycyrrhizic acid
- DrugBank Accession Number
- DB13751
- Background
Glycyrrhizic acid is extracted from the root of the licorice plant; Glycyrrhiza glabra.11 It is a triterpene glycoside with glycyrrhetinic acid that possesses a wide range of pharmacological and biological activities. When extracted from the plant, it can be obtained in the form of ammonium glycyrrhizin and mono-ammonium glycyrrhizin.8 Glycyrrhizic acid has been developed in Japan and China as a hepatoprotective drug in cases of chronic hepatitis.1 From January 2014, glycyrrhizic acid as part of the licorice extract was approved by the FDA as an existing food sweetener.12 It was approved by Health Canada to be used in over-the-counter products but all the products are currently on the status canceled post marketed.10
- Type
- Small Molecule
- Groups
- Approved, Experimental
- Structure
Structure for Glycyrrhizic acid (DB13751)
- Weight
- Average: 822.942
Monoisotopic: 822.403785916 - Chemical Formula
- C42H62O16
- Synonyms
- 18-beta-Glycyrrhizic acid
- Glizigen
- Glycyrrhizin
- External IDs
- NSC-167409
- NSC-234419
Pharmacology
- Indication
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.2 It is also known to be used as a remedy for peptic ulcer and other stomach diseases.9
Reduce drug development failure ratesBuild, train, & validate machine-learning modelswith evidence-based and structured datasets.Build, train, & validate predictive machine-learning models with structured datasets.- Associated Conditions
Indication Type Indication Combined Product Details Approval Level Age Group Patient Characteristics Dose Form Treatment of Hyperglycemia ••• ••• Symptomatic treatment of Premenstrual syndrome ••• ••• - Contraindications & Blackbox Warnings
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Glycyrrhizic acid was reported to present antiallergic, antiviral and anti-inflammatory activities as well as improvements in glucose tolerance.1
The effect of glycyrrhizic acid in metabolic syndrome generates a significant decrease in blood glucose, fasting blood glucose and mean serum insulin concentration.2
- Mechanism of action
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.1
The antiviral activity of glycyrrhizic acid includes the inhibition of viral replication and immune regulation.1 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.2
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.2
Target Actions Organism A11-beta-hydroxysteroid dehydrogenase 1 antagonistHumans ATumor necrosis factor antagonistHumans ACaspase-3 antagonistHumans ANuclear factor NF-kappa-B translocation inhibitorHumans ALipoprotein lipase inducerHumans - Absorption
Glycyrrhizic acid is mainly absorbed after presystemic hydrolysis and formation of glycyrrhetinic acid.3 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.5
- 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.5
- Protein binding
Glycyrrhizic acid does not bind to any plasma proteins as it is not absorbed systemically. On the other hand, its main active metabolite, glycyrrhetinic acid presents a very large binding to serum proteins such as albumin.7
- Metabolism
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.11 This metabolite is transported and taken in the liver for its metabolization to form glucuronide and sulfate conjugates.3
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- 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.4 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.3 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.6
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.5
- Half-life
Depending on the dose, the second elimination phase in humans has a half-life of 3.5 hours.4
- Clearance
The constant reabsorption of glycyrrhetic acid in the duodenum causes a delay in the terminal plasma clearance.3 The reported total body clearance of glycyrrhizic acid is reported to be in the range of 16-25 ml.kg/h.5
- Adverse Effects
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Glycyrrhizic acid is thought to generate inhibition of 11-beta-hydroxysteroid dehydrogenase in the kidney which leads to elevated cortisol levels in the kidney. Intravenous administration of the ammoniated form was shown to produce convulsions and hemolysis.11
Preclinical overdose studies have been shown to produce mineralocorticoid excess. The LD50 in preclinical studies was reported to be in the range of 308-12700 mg/kg.11
Glycyrrhizic acid has been proven to not have mutagenic, genotoxic, teratogenic nor carcinogenic effects.11
- Pathways
- Not Available
- Pharmacogenomic Effects/ADRs
- Not Available
Interactions
- Drug Interactions
- This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.
Drug Interaction Integrate drug-drug
interactions in your softwareAstemizole Astemizole may decrease the excretion rate of Glycyrrhizic acid which could result in a higher serum level. Atazanavir Atazanavir may decrease the excretion rate of Glycyrrhizic acid which could result in a higher serum level. Atenolol Atenolol may decrease the excretion rate of Glycyrrhizic acid which could result in a higher serum level. Atorvastatin Atorvastatin may decrease the excretion rate of Glycyrrhizic acid which could result in a higher serum level. Atropine Atropine may decrease the excretion rate of Glycyrrhizic acid which could result in a higher serum level. - Food Interactions
- No interactions found.
Products
Drug product information from 10+ global regionsOur datasets provide approved product information including:dosage, form, labeller, route of administration, and marketing period.Access drug product information from over 10 global regions.- Product Ingredients
Ingredient UNII CAS InChI Key Ammonium glycyrrhizinate trihydrate 78NEL3149I 911217-00-0 RSPXVECNDMCBGQ-YMYWBCTMSA-N Glycyrrhizinate dipotassium CA2Y0FE3FX 68797-35-3 BIVBRWYINDPWKA-VLQRKCJKSA-L - Over the Counter Products
Name Dosage Strength Route Labeller Marketing Start Marketing End Region Image The Skin House Egf Collagen Ampoule Liquid 0.1 g/100mL Topical NOKSIBCHO cosmetic Co., Ltd. 2020-03-14 Not applicable US 
- Mixture Products
Name Ingredients Dosage Route Labeller Marketing Start Marketing End Region Image Anti-Stretch Mark Glycyrrhizic acid (12 mg/60g) + Glycerin (12 mg/60g) + Mineral oil (12 mg/60g) + Tocopherol (12 mg/60g) Cream Cutaneous Shantou Youjia E-Commerce Co., Ltd. 2024-02-01 2024-12-31 US BAMBOO SALT Eunganggo Jook Yeom Glycyrrhizinate dipotassium (0.04 g/100g) + Aminocaproic acid (0.05 g/100g) + Curcuma xanthorrhiza oil (0.025 g/100g) + Sea salt (3 g/100g) + Silicon dioxide (20 g/100g) + Sodium fluoride (0.22 g/100g) + Ursodeoxycholic acid (0.02 g/100g) Paste Dental Lg Household & Health Care Ltd. 2011-03-15 Not applicable US BAMBOO SALT Eunganggo Jook Yeom Toothpaste Glycyrrhizinate dipotassium (0.04 g/100g) + Aminocaproic acid (0.05 g/100g) + Curcuma xanthorrhiza oil (0.025 g/100g) + Sea salt (3 g/100g) + Silicon dioxide (20 g/100g) + Sodium fluoride (0.22 g/100g) + Ursodeoxycholic acid (0.02 g/100g) Paste Dental Lg Household & Health Care Ltd. 2010-05-25 Not applicable US BOP whiteningtoothpaste Glycyrrhizinate dipotassium (0.3 g/100g) + Xylitol (3 g/100g) Gel Topical Shanghai Gemang Trading Co., Ltd. 2022-02-22 Not applicable US Pulmoll Pastilles Glycyrrhizic acid (7.6 mg / loz) + Levomenthol (1.52 mg / loz) Lozenge Oral Le Nigen N. Industries 1994-12-31 1999-07-16 Canada 
- Unapproved/Other Products
Name Ingredients Dosage Route Labeller Marketing Start Marketing End Region Image BOP whiteningtoothpaste Glycyrrhizinate dipotassium (0.3 g/100g) + Xylitol (3 g/100g) Gel Topical Shanghai Gemang Trading Co., Ltd. 2022-02-22 Not applicable US The Skin House Egf Collagen Ampoule Glycyrrhizinate dipotassium (0.1 g/100mL) Liquid Topical NOKSIBCHO cosmetic Co., Ltd. 2020-03-14 Not applicable US Younggaksan Glycyrrhizic acid (8.3 mg/0.3g) + Apricot kernel oil (0.83 mg/0.3g) + Platycodon grandiflorus root (11.7 mg/0.3g) + Polygala senega root (0.5 mg/0.3g) Powder Oral LYDIA Co., Ltd 2019-10-08 Not applicable US Younggaksan Glycyrrhizic acid (8.3 mg/0.3g) + Apricot kernel oil (0.83 mg/0.3g) + Platycodon grandiflorus root (11.7 mg/0.3g) + Polygala senega root (0.5 mg/0.3g) Powder Oral OASIS TRADING 2018-11-22 Not applicable US Younggaksan Glycyrrhizic acid (8.3 mg/0.3g) + Apricot kernel oil (0.83 mg/0.3g) + Platycodon grandiflorus root (11.7 mg/0.3g) + Polygala senega root (0.5 mg/0.3g) Powder Oral I World Pharmaceutical Co., Ltd. 2019-10-08 Not applicable US
Categories
- ATC Codes
- A05BA08 — Glycyrrhizic acid
- Drug Categories
- Chemical TaxonomyProvided by Classyfire
- Description
- This compound belongs to the class of organic compounds known as triterpene saponins. These are glycosylated derivatives of triterpene sapogenins. The sapogenin moiety backbone is usually based on the oleanane, ursane, taraxastane, bauerane, lanostane, lupeol, lupane, dammarane, cycloartane, friedelane, hopane, 9b,19-cyclo-lanostane, cycloartane, or cycloartanol skeleton.
- Kingdom
- Organic compounds
- Super Class
- Lipids and lipid-like molecules
- Class
- Prenol lipids
- Sub Class
- Terpene glycosides
- Direct Parent
- Triterpene saponins
- Alternative Parents
- Triterpenoids / O-glucuronides / Disaccharides / O-glycosyl compounds / Tricarboxylic acids and derivatives / Beta hydroxy acids and derivatives / Cyclohexenones / Pyrans / Oxanes / Secondary alcohols show 6 more
- Substituents
- 1-o-glucuronide / Acetal / Alcohol / Aliphatic heteropolycyclic compound / Beta-hydroxy acid / Carbonyl group / Carboxylic acid / Carboxylic acid derivative / Cyclohexenone / Disaccharide show 19 more
- Molecular Framework
- Aliphatic heteropolycyclic compounds
- External Descriptors
- enone, tricarboxylic acid, glucosiduronic acid, triterpenoid saponin, pentacyclic triterpenoid (CHEBI:15939)
- Affected organisms
- Humans and other mammals
- Herpes simplex virus
- Various viruses
Chemical Identifiers
- UNII
- 6FO62043WK
- CAS number
- 1405-86-3
- InChI Key
- LPLVUJXQOOQHMX-QWBHMCJMSA-N
- InChI
- InChI=1S/C42H62O16/c1-37(2)21-8-11-42(7)31(20(43)16-18-19-17-39(4,36(53)54)13-12-38(19,3)14-15-41(18,42)6)40(21,5)10-9-22(37)55-35-30(26(47)25(46)29(57-35)33(51)52)58-34-27(48)23(44)24(45)28(56-34)32(49)50/h16,19,21-31,34-35,44-48H,8-15,17H2,1-7H3,(H,49,50)(H,51,52)(H,53,54)/t19-,21-,22-,23-,24-,25-,26-,27+,28-,29-,30+,31+,34-,35-,38+,39-,40-,41+,42+/m0/s1
- IUPAC Name
- (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
- SMILES
- [H][C@@]12C[C@](C)(CC[C@]1(C)CC[C@]1(C)C2=CC(=O)[C@]2([H])[C@@]3(C)CC[C@H](O[C@H]4O[C@@H]([C@@H](O)[C@H](O)[C@H]4O[C@@H]4O[C@@H]([C@@H](O)[C@H](O)[C@H]4O)C(O)=O)C(O)=O)C(C)(C)[C@]3([H])CC[C@@]12C)C(O)=O
References
- General References
- Li JY, Cao HY, Liu P, Cheng GH, Sun MY: Glycyrrhizic acid in the treatment of liver diseases: literature review. Biomed Res Int. 2014;2014:872139. doi: 10.1155/2014/872139. Epub 2014 May 13. [Article]
- Ming LJ, Yin AC: Therapeutic effects of glycyrrhizic acid. Nat Prod Commun. 2013 Mar;8(3):415-8. [Article]
- Ploeger B, Mensinga T, Sips A, Seinen W, Meulenbelt J, DeJongh J: The pharmacokinetics of glycyrrhizic acid evaluated by physiologically based pharmacokinetic modeling. Drug Metab Rev. 2001 May;33(2):125-47. doi: 10.1081/DMR-100104400 . [Article]
- Krahenbuhl S, Hasler F, Krapf R: Analysis and pharmacokinetics of glycyrrhizic acid and glycyrrhetinic acid in humans and experimental animals. Steroids. 1994 Feb;59(2):121-6. [Article]
- Yamamura Y, Kawakami J, Santa T, Kotaki H, Uchino K, Sawada Y, Tanaka N, Iga T: Pharmacokinetic profile of glycyrrhizin in healthy volunteers by a new high-performance liquid chromatographic method. J Pharm Sci. 1992 Oct;81(10):1042-6. [Article]
- Ploeger BA, Meulenbelt J, DeJongh J: Physiologically based pharmacokinetic modeling of glycyrrhizic acid, a compound subject to presystemic metabolism and enterohepatic cycling. Toxicol Appl Pharmacol. 2000 Feb 1;162(3):177-88. doi: 10.1006/taap.1999.8843. [Article]
- Ishida S, Ichikawa T, Sakiya Y: Binding of glycyrrhetinic acid to rat plasma, rat serum albumin, human serum, and human serum albumin. Chem Pharm Bull (Tokyo). 1988 Jan;36(1):440-3. [Article]
- Gloria M. (2003). Encyclopedia of food sciences and nutrition (2nd ed.). Academic Press.
- Sharma M., Dwivedi P., Singh A. and Dwivedi A. (2016). Nutraceuticals. Academic Press.
- Health Canada [Link]
- FDA records [File]
- FDA food aditives [File]
- External Links
- KEGG Drug
- D00157
- KEGG Compound
- C02284
- ChemSpider
- 14263
- BindingDB
- 50185127
- 26143
- ChEBI
- 15939
- ChEMBL
- CHEMBL441687
- ZINC
- ZINC000096015174
- Wikipedia
- Glycyrrhizin
- MSDS
- Download (47.6 KB)
Clinical Trials
- Clinical Trials
Clinical Trial & Rare Diseases Add-on Data Package
Explore 4,000+ rare diseases, orphan drugs & condition pairs, clinical trial why stopped data, & more. Preview package Phase Status Purpose Conditions Count Start Date Why Stopped 100+ additional columns Unlock 175K+ rows when you subscribe.View sample data2 Recruiting Treatment Prostate Cancer 1 somestatus stop reason just information to hide 2, 3 Completed Prevention Ventilator Associated Bacterial Pneumonia (VABP) 1 somestatus stop reason just information to hide 1 Completed Treatment Bacterial Viability of Necrotic Pulp With Asymptomatic Apical Periodontitis 1 somestatus stop reason just information to hide Not Available Completed Not Available Hepatic autoimmune disorders 1 somestatus stop reason just information to hide Not Available Completed Prevention Nausea, Postoperative 1 somestatus stop reason just information to hide
Pharmacoeconomics
- Manufacturers
- Not Available
- Packagers
- Not Available
- Dosage Forms
Form Route Strength Cream Cutaneous Paste Dental Gel Topical Lozenge Oral Liquid Cutaneous Liquid Topical 0.1 g/100mL Powder Oral - Prices
- Not Available
- Patents
- Not Available
Properties
- State
- Solid
- Experimental Properties
Property Value Source melting point (°C) 220 ºC (Decomposes at 200 ºC) 'MSDS' boiling point (°C) Decomposes at 200 ºC 'MSDS' water solubility Easily soluble in hot water 'MSDS' logP 2.8 'MSDS' - Predicted Properties
Property Value Source Water Solubility 0.0545 mg/mL ALOGPS logP 2.78 ALOGPS logP 3.13 Chemaxon logS -4.2 ALOGPS pKa (Strongest Acidic) 2.96 Chemaxon pKa (Strongest Basic) -3.7 Chemaxon Physiological Charge -3 Chemaxon Hydrogen Acceptor Count 16 Chemaxon Hydrogen Donor Count 8 Chemaxon Polar Surface Area 267.04 Å2 Chemaxon Rotatable Bond Count 7 Chemaxon Refractivity 198.83 m3·mol-1 Chemaxon Polarizability 86.31 Å3 Chemaxon Number of Rings 7 Chemaxon Bioavailability 0 Chemaxon Rule of Five No Chemaxon Ghose Filter No Chemaxon Veber's Rule No Chemaxon MDDR-like Rule Yes Chemaxon - Predicted ADMET Features
- Not Available
Spectra
- Mass Spec (NIST)
- Not Available
- Spectra
- Chromatographic Properties
Collision Cross Sections (CCS)
Adduct CCS Value (Å2) Source type Source [M-H]- 285.3729438 predictedDarkChem Lite v0.1.0 [M-H]- 257.07364 predictedDeepCCS 1.0 (2019) [M+H]+ 281.1529438 predictedDarkChem Lite v0.1.0 [M+H]+ 258.79733 predictedDeepCCS 1.0 (2019) [M+Na]+ 265.12057 predictedDeepCCS 1.0 (2019)
Targets
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- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Antagonist
- General Function
- Controls the reversible conversion of biologically active glucocorticoids such as cortisone to cortisol, and 11-dehydrocorticosterone to corticosterone in the presence of NADP(H) (PubMed:10497248, PubMed:12460758, PubMed:14973125, PubMed:15152005, PubMed:15280030, PubMed:17593962, PubMed:21453287, PubMed:27927697, PubMed:30902677). Participates in the corticosteroid receptor-mediated anti-inflammatory response, as well as metabolic and homeostatic processes (PubMed:10497248, PubMed:12414862, PubMed:15152005, PubMed:21453287). Plays a role in the secretion of aqueous humor in the eye, maintaining a normotensive, intraocular environment (PubMed:11481269). Bidirectional in vitro, predominantly functions as a reductase in vivo, thereby increasing the concentration of active glucocorticoids (PubMed:10497248, PubMed:11481269, PubMed:12414862, PubMed:12460758). It has broad substrate specificity, besides glucocorticoids, it accepts other steroid and sterol substrates (PubMed:15095019, PubMed:15152005, PubMed:17593962, PubMed:21453287). Interconverts 7-oxo- and 7-hydroxy-neurosteroids such as 7-oxopregnenolone and 7beta-hydroxypregnenolone, 7-oxodehydroepiandrosterone (3beta-hydroxy-5-androstene-7,17-dione) and 7beta-hydroxydehydroepiandrosterone (3beta,7beta-dihydroxyandrost-5-en-17-one), among others (PubMed:17593962). Catalyzes the stereo-specific conversion of the major dietary oxysterol, 7-ketocholesterol (7-oxocholesterol), into the more polar 7-beta-hydroxycholesterol metabolite (PubMed:15095019, PubMed:15152005). 7-oxocholesterol is one of the most important oxysterols, it participates in several events such as induction of apoptosis, accumulation in atherosclerotic lesions, lipid peroxidation, and induction of foam cell formation (PubMed:15095019). Mediates the 7-oxo reduction of 7-oxolithocholate mainly to chenodeoxycholate, and to a lesser extent to ursodeoxycholate, both in its free form and when conjugated to glycine or taurine, providing a link between glucocorticoid activation and bile acid metabolism (PubMed:21453287). Catalyzes the synthesis of 7-beta-25-dihydroxycholesterol from 7-oxo-25-hydroxycholesterol in vitro, which acts as a ligand for the G-protein-coupled receptor (GPCR) Epstein-Barr virus-induced gene 2 (EBI2) and may thereby regulate immune cell migration (PubMed:30902677)
- Specific Function
- 11-beta-hydroxysteroid dehydrogenase (nadp+) activity
- Gene Name
- HSD11B1
- Uniprot ID
- P28845
- Uniprot Name
- 11-beta-hydroxysteroid dehydrogenase 1
- Molecular Weight
- 32400.665 Da
References
- FDA records [File]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Antagonist
- General Function
- Cytokine that binds to TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. It is mainly secreted by macrophages and can induce cell death of certain tumor cell lines. It is potent pyrogen causing fever by direct action or by stimulation of interleukin-1 secretion and is implicated in the induction of cachexia, Under certain conditions it can stimulate cell proliferation and induce cell differentiation. Impairs regulatory T-cells (Treg) function in individuals with rheumatoid arthritis via FOXP3 dephosphorylation. Up-regulates the expression of protein phosphatase 1 (PP1), which dephosphorylates the key 'Ser-418' residue of FOXP3, thereby inactivating FOXP3 and rendering Treg cells functionally defective (PubMed:23396208). Key mediator of cell death in the anticancer action of BCG-stimulated neutrophils in combination with DIABLO/SMAC mimetic in the RT4v6 bladder cancer cell line (PubMed:16829952, PubMed:22517918, PubMed:23396208). Induces insulin resistance in adipocytes via inhibition of insulin-induced IRS1 tyrosine phosphorylation and insulin-induced glucose uptake. Induces GKAP42 protein degradation in adipocytes which is partially responsible for TNF-induced insulin resistance (By similarity). Plays a role in angiogenesis by inducing VEGF production synergistically with IL1B and IL6 (PubMed:12794819). Promotes osteoclastogenesis and therefore mediates bone resorption (By similarity)
- Specific Function
- Cytokine activity
- Gene Name
- TNF
- Uniprot ID
- P01375
- Uniprot Name
- Tumor necrosis factor
- Molecular Weight
- 25644.15 Da
References
- Li JY, Cao HY, Liu P, Cheng GH, Sun MY: Glycyrrhizic acid in the treatment of liver diseases: literature review. Biomed Res Int. 2014;2014:872139. doi: 10.1155/2014/872139. Epub 2014 May 13. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Antagonist
- General Function
- Thiol protease that acts as a major effector caspase involved in the execution phase of apoptosis (PubMed:18723680, PubMed:20566630, PubMed:23650375, PubMed:35338844, PubMed:35446120, PubMed:7596430). Following cleavage and activation by initiator caspases (CASP8, CASP9 and/or CASP10), mediates execution of apoptosis by catalyzing cleavage of many proteins (PubMed:18723680, PubMed:20566630, PubMed:23650375, PubMed:7596430). At the onset of apoptosis, it proteolytically cleaves poly(ADP-ribose) polymerase PARP1 at a '216-Asp-|-Gly-217' bond (PubMed:10497198, PubMed:16374543, PubMed:7596430, PubMed:7774019). Cleaves and activates sterol regulatory element binding proteins (SREBPs) between the basic helix-loop-helix leucine zipper domain and the membrane attachment domain (By similarity). Cleaves and activates caspase-6, -7 and -9 (CASP6, CASP7 and CASP9, respectively) (PubMed:7596430). Cleaves and inactivates interleukin-18 (IL18) (PubMed:37993714, PubMed:9334240). Involved in the cleavage of huntingtin (PubMed:8696339). Triggers cell adhesion in sympathetic neurons through RET cleavage (PubMed:21357690). Cleaves and inhibits serine/threonine-protein kinase AKT1 in response to oxidative stress (PubMed:23152800). Acts as an inhibitor of type I interferon production during virus-induced apoptosis by mediating cleavage of antiviral proteins CGAS, IRF3 and MAVS, thereby preventing cytokine overproduction (PubMed:30878284). Also involved in pyroptosis by mediating cleavage and activation of gasdermin-E (GSDME) (PubMed:35338844, PubMed:35446120). Cleaves XRCC4 and phospholipid scramblase proteins XKR4, XKR8 and XKR9, leading to promote phosphatidylserine exposure on apoptotic cell surface (PubMed:23845944, PubMed:33725486)
- Specific Function
- Aspartic-type endopeptidase activity
- Gene Name
- CASP3
- Uniprot ID
- P42574
- Uniprot Name
- Caspase-3
- Molecular Weight
- 31607.58 Da
References
- Li JY, Cao HY, Liu P, Cheng GH, Sun MY: Glycyrrhizic acid in the treatment of liver diseases: literature review. Biomed Res Int. 2014;2014:872139. doi: 10.1155/2014/872139. Epub 2014 May 13. [Article]
- Kind
- Protein group
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Translocation inhibitor
- General Function
- NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. In a non-canonical activation pathway, the MAP3K14-activated CHUK/IKKA homodimer phosphorylates NFKB2/p100 associated with RelB, inducing its proteolytic processing to NFKB2/p52 and the formation of NF-kappa-B RelB-p52 complexes. The NF-kappa-B heterodimeric RelB-p52 complex is a transcriptional activator. The NF-kappa-B p52-p52 homodimer is a transcriptional repressor. NFKB2 appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins by p100 and generation of p52 by a cotranslational processing. The proteasome-mediated process ensures the production of both p52 and p100 and preserves their independent function. p52 binds to the kappa-B consensus sequence 5'-GGRNNYYCC-3', located in the enhancer region of genes involved in immune response and acute phase reactions. p52 and p100 are respectively the minor and major form; the processing of p100 being relatively poor. Isoform p49 is a subunit of the NF-kappa-B protein complex, which stimulates the HIV enhancer in synergy with p65. In concert with RELB, regulates the circadian clock by repressing the transcriptional activator activity of the CLOCK-BMAL1 heterodimer
- Specific Function
- Dna-binding transcription activator activity, rna polymerase ii-specific
Components:
| Name | UniProt ID |
|---|---|
| Nuclear factor NF-kappa-B p100 subunit | Q00653 |
| Nuclear factor NF-kappa-B p105 subunit | P19838 |
References
- Li JY, Cao HY, Liu P, Cheng GH, Sun MY: Glycyrrhizic acid in the treatment of liver diseases: literature review. Biomed Res Int. 2014;2014:872139. doi: 10.1155/2014/872139. Epub 2014 May 13. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Inducer
- General Function
- Key enzyme in triglyceride metabolism. Catalyzes the hydrolysis of triglycerides from circulating chylomicrons and very low density lipoproteins (VLDL), and thereby plays an important role in lipid clearance from the blood stream, lipid utilization and storage (PubMed:11342582, PubMed:27578112, PubMed:8675619). Although it has both phospholipase and triglyceride lipase activities it is primarily a triglyceride lipase with low but detectable phospholipase activity (PubMed:12032167, PubMed:7592706). Mediates margination of triglyceride-rich lipoprotein particles in capillaries (PubMed:24726386). Recruited to its site of action on the luminal surface of vascular endothelium by binding to GPIHBP1 and cell surface heparan sulfate proteoglycans (PubMed:11342582, PubMed:27811232)
- Specific Function
- 1-acyl-2-lysophosphatidylserine acylhydrolase activity
- Gene Name
- LPL
- Uniprot ID
- P06858
- Uniprot Name
- Lipoprotein lipase
- Molecular Weight
- 53162.07 Da
References
- Ming LJ, Yin AC: Therapeutic effects of glycyrrhizic acid. Nat Prod Commun. 2013 Mar;8(3):415-8. [Article]
Carriers
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- No
- Actions
- Substrate
- General Function
- Cytosolic aldo-keto reductase that catalyzes the NADH and NADPH-dependent reduction of ketosteroids to hydroxysteroids. Liver specific enzyme that acts as an NAD(P)(H)-dependent 3-, 17- and 20-ketosteroid reductase on the steroid nucleus and side chain (PubMed:10634139, PubMed:10998348, PubMed:11158055, PubMed:14672942, PubMed:1530633, PubMed:19218247, PubMed:7650035). Displays the ability to catalyze both oxidation and reduction in vitro, but most probably acts as a reductase in vivo since the oxidase activity measured in vitro is inhibited by physiological concentration of NADPH (PubMed:14672942). Acts preferentially as a 3-alpha-hydroxysteroid dehydrogenase (HSD) with a subsidiary 3-beta-HSD activity (PubMed:14672942). Catalyzes efficiently the transformation of the potent androgen 5-alpha-dihydrotestosterone (5alpha-DHT or 17beta-hydroxy-5alpha-androstan-3-one) into the less active form, 5-alpha-androstan-3-alpha,17-beta-diol (3-alpha-diol) (PubMed:10998348, PubMed:11158055, PubMed:14672942). Catalyzes the reduction of estrone into 17beta-estradiol but with low efficiency (PubMed:14672942). Metabolizes a broad spectrum of natural and synthetic therapeutic steroid and plays an important role in metabolism of androgens, estrogens, progestereone and conjugated steroids (PubMed:10998348, PubMed:14672942, PubMed:19218247). Catalyzes the biotransformation of the pesticide chlordecone (kepone) to its corresponding alcohol leading to increased biliary excretion of the pesticide and concomitant reduction of its neurotoxicity since bile is the major excretory route (PubMed:2427522)
- Specific Function
- 5alpha-androstane-3beta,17beta-diol dehydrogenase activity
- Gene Name
- AKR1C4
- Uniprot ID
- P17516
- Uniprot Name
- Aldo-keto reductase family 1 member C4
- Molecular Weight
- 37066.52 Da
References
- Ploeger BA, Meulenbelt J, DeJongh J: Physiologically based pharmacokinetic modeling of glycyrrhizic acid, a compound subject to presystemic metabolism and enterohepatic cycling. Toxicol Appl Pharmacol. 2000 Feb 1;162(3):177-88. doi: 10.1006/taap.1999.8843. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- No
- Actions
- Substrate
- General Function
- Cytosolic aldo-keto reductase that catalyzes the NADH and NADPH-dependent reduction of ketosteroids to hydroxysteroids. Acts as a NAD(P)(H)-dependent 3-, 17- and 20-ketosteroid reductase on the steroid nucleus and side chain and regulates the metabolism of androgens, estrogens and progesterone (PubMed:10622721, PubMed:11165022, PubMed:7650035, PubMed:9415401, PubMed:9927279). Displays the ability to catalyze both oxidation and reduction in vitro, but most probably acts as a reductase in vivo since the oxidase activity measured in vitro is inhibited by physiological concentration of NADPH (PubMed:11165022, PubMed:14672942). Acts preferentially as a 17-ketosteroid reductase and has the highest catalytic efficiency of the AKR1C enzyme for the reduction of delta4-androstenedione to form testosterone (PubMed:20036328). Reduces prostaglandin (PG) D2 to 11beta-prostaglandin F2, progesterone to 20alpha-hydroxyprogesterone and estrone to 17beta-estradiol (PubMed:10622721, PubMed:10998348, PubMed:11165022, PubMed:15047184, PubMed:19010934, PubMed:20036328). Catalyzes the transformation of the potent androgen dihydrotestosterone (DHT) into the less active form, 5-alpha-androstan-3-alpha,17-beta-diol (3-alpha-diol) (PubMed:10557352, PubMed:10998348, PubMed:11165022, PubMed:14672942, PubMed:7650035, PubMed:9415401). Also displays retinaldehyde reductase activity toward 9-cis-retinal (PubMed:21851338)
- Specific Function
- 15-hydroxyprostaglandin-d dehydrogenase (nadp+) activity
- Gene Name
- AKR1C3
- Uniprot ID
- P42330
- Uniprot Name
- Aldo-keto reductase family 1 member C3
- Molecular Weight
- 36852.89 Da
References
- Ploeger BA, Meulenbelt J, DeJongh J: Physiologically based pharmacokinetic modeling of glycyrrhizic acid, a compound subject to presystemic metabolism and enterohepatic cycling. Toxicol Appl Pharmacol. 2000 Feb 1;162(3):177-88. doi: 10.1006/taap.1999.8843. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- No
- Actions
- Substrate
- General Function
- Cytosolic aldo-keto reductase that catalyzes the NADH and NADPH-dependent reduction of ketosteroids to hydroxysteroids (PubMed:19218247). Most probably acts as a reductase in vivo since the oxidase activity measured in vitro is inhibited by physiological concentrations of NADPH (PubMed:14672942). Displays a broad positional specificity acting on positions 3, 17 and 20 of steroids and regulates the metabolism of hormones like estrogens and androgens (PubMed:10998348). Works in concert with the 5-alpha/5-beta-steroid reductases to convert steroid hormones into the 3-alpha/5-alpha and 3-alpha/5-beta-tetrahydrosteroids. Catalyzes the inactivation of the most potent androgen 5-alpha-dihydrotestosterone (5-alpha-DHT) to 5-alpha-androstane-3-alpha,17-beta-diol (3-alpha-diol) (PubMed:15929998, PubMed:17034817, PubMed:17442338, PubMed:8573067). Also specifically able to produce 17beta-hydroxy-5alpha-androstan-3-one/5alphaDHT (PubMed:10998348). May also reduce conjugated steroids such as 5alpha-dihydrotestosterone sulfate (PubMed:19218247). Displays affinity for bile acids (PubMed:8486699)
- Specific Function
- Aldose reductase (nadph) activity
- Gene Name
- AKR1C2
- Uniprot ID
- P52895
- Uniprot Name
- Aldo-keto reductase family 1 member C2
- Molecular Weight
- 36734.97 Da
References
- Ploeger BA, Meulenbelt J, DeJongh J: Physiologically based pharmacokinetic modeling of glycyrrhizic acid, a compound subject to presystemic metabolism and enterohepatic cycling. Toxicol Appl Pharmacol. 2000 Feb 1;162(3):177-88. doi: 10.1006/taap.1999.8843. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- No
- Actions
- Binder
- General Function
- Binds water, Ca(2+), Na(+), K(+), fatty acids, hormones, bilirubin and drugs (Probable). Its main function is the regulation of the colloidal osmotic pressure of blood (Probable). Major zinc transporter in plasma, typically binds about 80% of all plasma zinc (PubMed:19021548). Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity). Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity). Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli (PubMed:6234017). Does not prevent iron uptake by the bacterial siderophore aerobactin (PubMed:6234017)
- Specific Function
- Antioxidant activity
- Gene Name
- ALB
- Uniprot ID
- P02768
- Uniprot Name
- Albumin
- Molecular Weight
- 69365.94 Da
References
- Ishida S, Ichikawa T, Sakiya Y: Binding of glycyrrhetinic acid to rat plasma, rat serum albumin, human serum, and human serum albumin. Chem Pharm Bull (Tokyo). 1988 Jan;36(1):440-3. [Article]
Transporters
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- No
- Actions
- Substrate
- General Function
- Catalyzes the transport of the major hydrophobic bile salts, such as taurine and glycine-conjugated cholic acid across the canalicular membrane of hepatocytes in an ATP-dependent manner, therefore participates in hepatic bile acid homeostasis and consequently to lipid homeostasis through regulation of biliary lipid secretion in a bile salts dependent manner (PubMed:15791618, PubMed:16332456, PubMed:18985798, PubMed:19228692, PubMed:20010382, PubMed:20398791, PubMed:22262466, PubMed:24711118, PubMed:29507376, PubMed:32203132). Transports taurine-conjugated bile salts more rapidly than glycine-conjugated bile salts (PubMed:16332456). Also transports non-bile acid compounds, such as pravastatin and fexofenadine in an ATP-dependent manner and may be involved in their biliary excretion (PubMed:15901796, PubMed:18245269)
- Specific Function
- Abc-type bile acid transporter activity
- Gene Name
- ABCB11
- Uniprot ID
- O95342
- Uniprot Name
- Bile salt export pump
- Molecular Weight
- 146405.83 Da
References
- Pedersen JM, Matsson P, Bergstrom CA, Hoogstraate J, Noren A, LeCluyse EL, Artursson P: Early identification of clinically relevant drug interactions with the human bile salt export pump (BSEP/ABCB11). Toxicol Sci. 2013 Dec;136(2):328-43. doi: 10.1093/toxsci/kft197. Epub 2013 Sep 6. [Article]
Drug created at June 23, 2017 20:47 / Updated at October 07, 2021 12:09