18α-Licorice-saponin H2
Based on 1 Customer Validation
18α-Glycyrrhizic acid (18α-GA; Isoglycyrrhizinic acid; 18α-Glycyrrhizic acid) is a derivative of glycyrrhizic acid with oral activity. 18α-Glycyrrhizic acid exhibits antioxidant, anti-inflammatory, hepatoprotective and cardioprotective activities. 18α-Glycyrrhizic acid protects against ethanol-induced alcoholic liver disease in rats by upregulating the expression levels of SOD, GSH, PPAR-α and CPT-1. 18α-Glycyrrhizic acid shows cytotoxicity against T lymphocytes and inhibits HIV-1 replication in these cells. 18α-Glycyrrhizic acid alleviates oxidative stress by reducing the levels of ROS, Nrf2, HO-1 and p-P65, and alleviates pyroptosis by downregulating the expression levels of NLRP3, GSDMD-N, P20 and c-IL-1β. 18α-Glycyrrhizic acid inhibits autophagy, colonic fibrosis and myocardial fibrosis, and regulates intestinal barrier integrity. 18α-Glycyrrhizic acid can be used in research related to alcoholic liver disease, HIV-1 infection, hepatotoxicity, acute liver failure, inflammatory bowel disease and myocardial fibrosis.
For research use only. We do not sell to patients.
- Purity: 99.90%
- CAS No.: 83896-44-0
- Formula: C42H62O16
- Molecular Weight:822.93
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Storage:
-20°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
18α-Glycyrrhizic acid (0.1-100 μg/mL; 4 days) exhibits cytotoxicity against MT-4 human T lymphocytes with a CD50 of 132 μg/mL; it also inhibits the replication of HIV-1 (strain HIV/EVK) in these cells with an ID50 of 105 μg/mL, resulting in a final selectivity index of 1.26[2].
18α-Glycyrrhizic acid (0.01-1.0 mg/mL; 60 min-30 h) dose-dependently inhibits CCl4- and GalN-induced cytotoxicity in primary cultured rat hepatocytes in vitro[3].
18α-Glycyrrhizic acid (1 mg/mL; 2 h) Magnesium reduces Alectinib (HY-13011)-induced cytotoxicity, increases the survival rate of AML-12 mouse hepatocytes treated with 10 μM Alectinib, alleviates mitochondrial structural damage, restores mitochondrial membrane potential, and enhances the activities of NADH-CoQ reductase and coenzyme Q-cytochrome C reductase[5].
18α-Glycyrrhizic acid (1 mg/mL; 2 h) Magnesium reduces the elevated intracellular ROS level in AML-12 cells treated with 10 μM Alectinib, downregulates the expression of oxidative stress-related proteins (Nrf2, HO-1, p-P65) to alleviate oxidative stress, and decreases the expression levels of pyroptosis-related proteins (NLRP3, GSDMD-N, P20, c-IL-1β) to mitigate pyroptosis[5].
18α-Glycyrrhizic acid (5-320 μg/mL; 1 h pretreatment, 24 h ConA co-treatment) Magnesium reduces ConA (HY-P2149)-induced in vitro death of primary mouse hepatocytes by inhibiting autophagy, without altering hepatocyte apoptosis[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:AML-12 mouse hepatocytes
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Concentration:1 mg/mL
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Incubation Time:2 h (pre-incubation); 24 h (alectinib treatment)
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Result:Exhibited no toxicity to AML-12 cells.
Significantly improved the survival rate of cells treated with 10 μM Alectinib.
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Cell Line:AML-12 mouse hepatocytes
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Concentration:1 mg/mL
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Incubation Time:2 h (pre-incubation prior to Alectinib treatment)
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Result:Caused a significant reduction in the levels of Nrf2, HO-1, and phosphorylated P65 (p-P65) in AML-12 cells treated with 10 μM Alectinib.\nSignificantly down-regulated the expression levels of NLRP3, GSDMD-N, P20, and cleaved IL-1β (c-IL-1β) in AML-12 cells treated with 10 μM Alectinib.
18α-Glycyrrhizic acid (30 mg/kg; i.p.; single administration) Magnesium significantly ameliorates ConA-induced acute liver failure in male Balb/c mice by inhibiting autophagy, reducing hepatocyte death and inflammatory responses, and improving survival rate[6].
Magnesium isoglycyrrhizinate (1.25-5 mg/kg; i.p.; once daily; for 7 consecutive days) Magnesium dose-dependently ameliorates DSS (HY-116282)-induced acute and chronic colitis in female C57BL/6 mice by reducing inflammation, maintaining intestinal barrier function, inhibiting NF-κB activation, and alleviating colonic fibrosis[7].
18α-Glycyrrhizic acid (25-50 mg/kg/d; i.p.; daily administration; for 14 consecutive days) Magnesium dose-dependently attenuates isoprenaline (HY-B0468)-induced myocardial fibrosis in *Mus musculus* mice[8].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley (SD) (six-week-old male, alcoholic liver disease model via 40% ethanol oral administration once daily for four weeks)[1]
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Dosage:18α-Glycyrrhizic acid combined with 18β-Glycyrrhizic acid at proportions of 10:0, 8:2, 6:4, 5:5, 4:6, 2:8, 0:10
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Administration:p.o.; daily; 28 days
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Result:Significantly reduced ethanol-induced increases in liver index and brown adipose tissue (BAT) index, with the most pronounced reduction in the 4:6 proportion group.
Significantly decreased serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and γ-glutamyl transferase (GGT) compared to the model group, with the strongest reductions observed in the 4:6, 2:8, and 10:0 proportion groups.
Reduced serum, liver, and fecal total cholesterol (TC) and total triglyceride (TG) levels compared to the model group; restored ethanol-altered high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) levels, with the most profound inhibition of TC and TG seen in the 4:6 and 2:8 proportion groups.
Significantly reversed ethanol-induced decreases in serum and hepatic superoxide dismutase (SOD) and glutathione (GSH) levels, and increases in malonaldehyde (MDA) levels, with the strongest protective effect on oxidative stress observed in the 4:6 and 2:8 proportion groups.
Reduced ethanol-induced hepatocyte enlargement, fatty degeneration, and lipid droplet accumulation compared to the model group, with the 4:6 proportion group showing the greatest reduction in steatosis score.
Significantly reversed ethanol-induced increases in hepatic mRNA and protein levels of sterol regulatory element-binding protein-1c (SREBP-1c) and acetyl-coal carboxylase (ACC), and decreases in peroxisome proliferators activated receptor-α (PPAR-α) and carnitine palmitoyl transferase-1 (CPT-1a) levels, with the most pronounced effects seen in the 4:6 proportion group.
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Animal Model:Balb/c (male, 8-10 weeks old, Concanavalin A-induced immune liver injury model)[6]
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Dosage:30 mg/kg
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Administration:i.p.; single dose
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Result:Significantly reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels compared to the ConA-only group.
Increased mouse survival rate.
Reduced liver congestion and necrotic area (assessed via H&E staining).
Decreased hepatocyte apoptosis (measured by TUNEL staining).
Reduced autophagosome count, decreased LC3b gene and protein expression, and increased p62 protein expression, indicating inhibition of ConA-induced liver autophagy.
Reduced serum levels of pro-inflammatory cytokines including IL-1β, IL-6, TNF-α, KC, MIP-2, IP-10, GM-CSF, LIF, and IL-12 (p40).
Lowered liver tissue expression of IL-1β, IL-6, TNF-α, KC, MIP-2, and IP-10 mRNA.
Decreased caspase-3 activity in liver tissue and reduced hepatocyte death.
Activation of autophagy with rapamycin reversed all these protective effects.
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Animal Model:C57BL/6 (female, 6-8 weeks, 20-24 g, acute colitis induced by 2.5% dextran sulfate sodium)[7]
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Dosage:1.25 mg/kg; 2.5 mg/kg; 5 mg/kg
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Administration:i.p.; once daily; 7 days
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Result:Attenuated DSS-induced body weight loss in a dose-dependent manner.
Reduced disease activity index in a dose-dependent manner.
Increased colon length in a dose-dependent manner.
Lowered histological severity scores in a dose-dependent manner.
Decreased abdominal ROS levels in a dose-dependent manner.
Reduced mRNA expression of pro-inflammatory cytokines Il1b, Il6, Il17, Ifng, Tnfa in a dose-dependent manner.
Lowered protein levels of IL-1β, IL-6, TNF-α in a dose-dependent manner.
Suppressed infiltration of CD45+ leukocytes, CD4+ T cells, and F4/80+ macrophages in colon tissue in a dose-dependent manner.
Reversed DSS-induced reductions in mRNA and protein levels of tight junction proteins occludin, ZO-1, claudin-1 and adherens junction protein E-cadherin in a dose-dependent manner.
Decreased serum FITC-dextran levels to reduce intestinal permeability in a dose-dependent manner.
Inhibited NF-κB activation by reducing p-p65 levels in a dose-dependent manner.
Reduced collagen deposition in colon tissue in a dose-dependent manner.
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Animal Model:C57BL/6 (female, 6-8 weeks, 20-24 g, chronic colitis induced by repeated cycles of 2.5% dextran sulfate sodium)[7]
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Dosage:5 mg/kg
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Administration:i.p.; once daily; 7 days during each DSS administration cycle
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Result:Increased body weight compared to DSS-only mice.
Increased colon length compared to DSS-only mice.
Reduced submucosal edema and mucosal ulceration compared to DSS-only mice.
Lowered histological severity scores compared to DSS-only mice.
Decreased abdominal ROS levels compared to DSS-only mice.
Reduced mRNA expression of pro-inflammatory cytokines Il1b, Il6, Il17, Ifng, Tnfa compared to DSS-only mice.
Suppressed infiltration of CD45+ leukocytes, CD4+ T cells, and F4/80+ macrophages compared to DSS-only mice.
Reversed DSS-induced reductions in tight junction proteins ZO-1, occludin and decrease in claudin-2 levels compared to DSS-only mice.
Inhibited NF-κB activation by reducing p-p65 levels compared to DSS-only mice.
Reduced collagen deposition in colon tissue compared to DSS-only mice.
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Animal Model:Kunming mice (4-5 weeks old, weight 22 g)[8]
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Dosage:25 mg/kg/d; 50 mg/kg/d
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Administration:i.p.; daily; 14 days
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Result:Reduced ISO-induced myocardial fiber disorder, interstitial hyperplasia, and fibrotic scarring in a dose-dependent manner.
Reduced ANP mRNA expression by 23.32%, c-fos mRNA expression by 23.32%, c-jun mRNA expression by 23.32%, and α-MHC mRNA expression by 17.66% at low dose; reduced ANP mRNA expression by 49.82%, c-fos mRNA expression by 49.82%, c-jun mRNA expression by 49.82%, and α-MHC mRNA expression by 45.35% at high dose.
Reduced NF-κB (p65) protein expression by 40.1% and TLR4 protein expression by 36.9% at low dose; reduced NF-κB (p65) protein expression by 55.3% and TLR4 protein expression by 54.5% at high dose.
Reduced serum CK activity by 22.7% and serum LDH activity by 16.4% at low dose; reduced serum CK activity by 24.5% and serum LDH activity by 22.9% at high dose.
Chemical Information
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CAS No. 83896-44-0
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Appearance Solid
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Molecular Weight 822.93
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Formula C42H62O16
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Color White to off-white
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SMILES
C[C@]12[C@@](C(C=C3[C@]2(CC[C@@]4([C@]3([H])C[C@](C)(CC4)C(O)=O)C)C)=O)([H])[C@@]5([C@@](C(C)([C@H](CC5)O[C@@H]6[C@@H]([C@H]([C@@H]([C@H](O6)C(O)=O)O)O)O[C@@H]7O[C@@H]([C@H]([C@@H]([C@H]7O)O)O)C(O)=O)C)([H])CC1)C
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Synonyms
18α-GA; Isoglycyrrhizinic acid; 18α-Glycyrrhizic acid
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
-20°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Solvent & Solubility
DMSO : 100 mg/mL (121.52 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.5 mg/mL (3.04 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL. * In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Purity & Documentation
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Data Sheet (299 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[3]. Kiso Y, et al. Mechanism of antihepatotoxic activity of glycyrrhizin. I: Effect on free radical generation and lipid peroxidation. Planta Med. 1984 Aug;50(4):298-302. [Content Brief]
[5]. Chen Y, et al. Magnesium Isoglycyrrhizinate Alleviates Alectinib-Induced Hepatotoxicity by Inhibiting Mitochondrial Damage-Mediated Pyroptosis. Drug design, development and therapy. 2025;19:6219-6233. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
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| DMSO | 1 mM | 1.2152 mL | 6.0759 mL | 12.1517 mL | 30.3793 mL |
| 5 mM | 0.2430 mL | 1.2152 mL | 2.4303 mL | 6.0759 mL | |
| 10 mM | 0.1215 mL | 0.6076 mL | 1.2152 mL | 3.0379 mL | |
| 15 mM | 0.0810 mL | 0.4051 mL | 0.8101 mL | 2.0253 mL | |
| 20 mM | 0.0608 mL | 0.3038 mL | 0.6076 mL | 1.5190 mL | |
| 25 mM | 0.0486 mL | 0.2430 mL | 0.4861 mL | 1.2152 mL | |
| 30 mM | 0.0405 mL | 0.2025 mL | 0.4051 mL | 1.0126 mL | |
| 40 mM | 0.0304 mL | 0.1519 mL | 0.3038 mL | 0.7595 mL | |
| 50 mM | 0.0243 mL | 0.1215 mL | 0.2430 mL | 0.6076 mL | |
| 60 mM | 0.0203 mL | 0.1013 mL | 0.2025 mL | 0.5063 mL | |
| 80 mM | 0.0152 mL | 0.0759 mL | 0.1519 mL | 0.3797 mL | |
| 100 mM | 0.0122 mL | 0.0608 mL | 0.1215 mL | 0.3038 mL |
18α-Licorice-saponin H2 Related Classifications
HY-N6911A Related Classifications
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- 18α-Licorice-saponin H2
- 83896-44-0
- 18α-GA
- Isoglycyrrhizinic acid
- 18α-Glycyrrhizic acid
- SOD
- PPAR
- Carnitine Palmitoyltransferase (CPT)
- HIV
- Reactive Oxygen Species (ROS)
- Keap1-Nrf2
- Heme Oxygenase (HO)
- NOD-like Receptor (NLR)
- Interleukin Related
- Pyroptosis
- Autophagy
- NF-κB
- TNF Receptor
- ACC
- HIV-1 infection
- SREBP-1c
- TLR4
- alcoholic liver disease
- PPAR-α
- NF-κB p65
- MT-4 human T-lymphocytes
- myocardial fibrosis
- AML-12 mouse hepatocytes
- Inhibitor
- inhibitor
- inhibit