Magnesium isoglycyrrhizinate hydrate
Based on 1 Customer Validation
Magnesium isoglycyrrhizinate hydrate (18α-Glycyrrhizic acid Magnesium hydrate; 18α-GA Magnesium hydrate; 18α-Licorice-saponin H2 Magnesium hydrate) is a derivative of glycyrrhizic acid with oral activity. Magnesium isoglycyrrhizinate hydrate exhibits antioxidant, anti-inflammatory, hepatoprotective and cardioprotective activities. Magnesium isoglycyrrhizinate hydrate protects against ethanol-induced alcoholic liver disease in rats by upregulating the expression levels of SOD, GSH, PPAR-α and CPT-1. Magnesium isoglycyrrhizinate hydrate shows cytotoxicity against T lymphocytes and inhibits HIV-1 replication in these cells. Magnesium isoglycyrrhizinate hydrate 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. Magnesium isoglycyrrhizinate hydrate inhibits autophagy, colonic fibrosis and myocardial fibrosis, and regulates intestinal barrier integrity. Magnesium isoglycyrrhizinate hydrate 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: 99.81%
- CAS No.: 658701-67-8
- Formula: C42H68MgO20
- Molecular Weight:917.28
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Storage:
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
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) Magnesium hydrate 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) Magnesium hydrate 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 hydrate 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].
Magnesium isoglycyrrhizinate (1 mg/mL; 2 h) hydrate 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].
Magnesium isoglycyrrhizinate (5-320 μg/mL; 1 h pretreatment, 24 h ConA co-treatment) hydrate 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.
Magnesium isoglycyrrhizinate (30 mg/kg; i.p.; single administration) hydrate 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) hydrate 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].
Magnesium isoglycyrrhizinate (25-50 mg/kg/d; i.p.; daily administration; for 14 consecutive days) hydrate 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. 658701-67-8
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Appearance Solid
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Molecular Weight 917.28
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Formula C42H68MgO20
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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.[Mg+2].O.O.O.O
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Synonyms
18α-Glycyrrhizic acid Magnesium hydrate; 18α-GA Magnesium hydrate; 18α-Licorice-saponin H2 Magnesium hydrate
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Solvent & Solubility
H2O : 33.33 mg/mL (36.34 mM; adjust pH to 9 with NH3·H2O)
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 (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
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 (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Purity & Documentation
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Data Sheet (301 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 (sealed storage, away from moisture). 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 |
|---|---|---|---|---|---|
| H2O | 1 mM | 1.0902 mL | 5.4509 mL | 10.9018 mL | 27.2545 mL |
| 5 mM | 0.2180 mL | 1.0902 mL | 2.1804 mL | 5.4509 mL | |
| 10 mM | 0.1090 mL | 0.5451 mL | 1.0902 mL | 2.7254 mL | |
| 15 mM | 0.0727 mL | 0.3634 mL | 0.7268 mL | 1.8170 mL | |
| 20 mM | 0.0545 mL | 0.2725 mL | 0.5451 mL | 1.3627 mL | |
| 25 mM | 0.0436 mL | 0.2180 mL | 0.4361 mL | 1.0902 mL | |
| 30 mM | 0.0363 mL | 0.1817 mL | 0.3634 mL | 0.9085 mL |
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
Magnesium isoglycyrrhizinate hydrate Related Classifications
HY-154795 Related Classifications
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- Magnesium isoglycyrrhizinate
- 658701-67-8
- 18α-Glycyrrhizic acid Magnesium
- 18α-GA Magnesium
- 18α-Licorice-saponin H2 Magnesium
- 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