Aureusidin
Based on 1 Customer Validation
Aureusidin is a flavonoid compound that is isolated and extracted from Antirrhinum majus and exhibits oral activity. Aureusidin possesses antioxidant, neuroprotective, and anti-inflammatory properties. Aureusidin directly targets and binds MD2 and Caspase-3 with high affinity, synergistically inhibits the TLR4/NF-κB inflammatory pathway and GSDME-mediated pyroptosis, and activates the Nrf2/HO-1 antioxidant axis via the ROS/MAPKs pathway. Aureusidin is a bovine liver arginase inhibitor with an IC50 of 57.1 µM. Aureusidin is used for research on inflammation-related diseases (osteoarthritis), acute liver injury, and endothelial dysfunction.
For research use only. We do not sell to patients.
- Purity : 97.01%
- CAS No.: 38216-54-5
- Formula: C15H10O6
- Molecular Weight:286.24
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Storage:
4°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
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
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NF-κB |
p38 MAP kinase |
Caspase-3 |
TLR4 |
HO-1 |
iNOS |
TNF-α |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| HeLa | IC50 |
18.5 μM
Compound: 36
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Inhibition of HDAC in human HeLa cell extract after 15 mins by fluorescence assay
Inhibition of HDAC in human HeLa cell extract after 15 mins by fluorescence assay
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[PMID: 25455492] |
| HT-22 | EC50 |
11.9 μM
Compound: 2
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Neuroprotective activity against glutamate induced-neurotoxicity in mouse HT-22 cells assessed as cell viability preincubated for 4 hrs followed by glutamate stimulation and measured after 12 hrs by MTT assay
Neuroprotective activity against glutamate induced-neurotoxicity in mouse HT-22 cells assessed as cell viability preincubated for 4 hrs followed by glutamate stimulation and measured after 12 hrs by MTT assay
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[PMID: 36126323] |
In Vitro
Aureusidin (1-60 μM; pretreatment for 1 h + LPS treatment for 24 h) dose-dependently reduces NO release and significantly inhibits PGE2 and TNF-α production as well as iNOS and COX-2 protein expression in LPS (HY-D1056)-induced RAW264.7 cells[3].
Aureusidin (20-60 μM; 1-6 h) promotes Nrf2 nuclear translocation, downregulates Keap1 expression, and upregulates HO-1 and NQO1 expression in RAW264.7 cells.[3]
Aureusidin (1-100 μM; 24 h) inhibits cell proliferation in LPS-induced RAW264.7 macrophages, with a maximum safe concentration of 60 μM[3].
Aureusidin (60 μM; 15-60 min) significantly increases Akt and MAPKs phosphorylation in RAW264.7 cells[3].
Aureusidin (2.5-20 mM; 5 min) directly binds MD2 protein in recombinant MD2 protein solution in a dose-dependent manner[4].
Aureusidin (10-100 µM; 1 h) inhibits purified bovine liver arginase with an IC50 of 57.1 µM[1].
Aureusidin (10 μM; 1 h) directly targets and binds to Caspase-3 protein in cell lysates of primary rat chondrocytes as a biotin-labeled probe via Pull-down assay[2].
Aureusidin (5-20 μM; pretreatment for 6 h + LPS treatment for 12 h) inhibits apoptosis, downregulates pro-inflammatory factors, decreases MDA levels, increases SOD levels, and suppresses TLR4/MD2-NF-κB signaling pathway proteins in LPS-induced KCs cells[4].
Aureusidin (20-60 μM; pretreatment for 1 h + LPS treatment for 1 h) downregulates pro-inflammatory cytokine mRNA expression, inhibits IκBα phosphorylation, and blocks NF-κB (p65) nuclear translocation in RAW264.7 cells[3].
Aureusidin (20-60 μM; 24 h) increases intracellular ROS levels in RAW264.7 cells[3].
Aureusidin (20 μM; 6 h pretreatment + 12 h LPS treatment) loses its anti-apoptotic and anti-inflammatory protective effects in MD2-knockout KC-MD2-/- cells, indicating that MD2 is its direct target[4].
Aureusidin (5-20 μM; 48 h) dose-dependently inhibits extracellular matrix degradation and attenuates Caspase-3/GSDME-mediated pyroptosis in IL-1β (HY-P703969)-stimulated primary rat chondrocytes[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:RAW264.7
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Concentration:1, 10, 20, 40, 60, 80, 100 μM
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Incubation Time:24 h
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Result:Did not inhibit the proliferation of RAW264.7 cells up to 60 μM.
Significantly inhibited the survival rate of RAW264.7 cells at 80 and 100 μM.
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Cell Line:RAW264.7
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Concentration:20, 40, 60 μM
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Incubation Time:1 h (pretreatment); 24 h (co-treatment with LPS)
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Result:Obviously inhibited PGE2 and TNF-α release induced by LPS in a dose-dependent manner.
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Cell Line:RAW264.7
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Concentration:20, 40, 60 μM
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Incubation Time:1 h (pretreatment); 24 h (co-treatment with LPS)
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Result:Obviously inhibited the LPS-induced expression of iNOS and COX-2 proteins.
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Cell Line:RAW264.7
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Concentration:20, 40, 60 μM
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Incubation Time:1 h (pretreatment); 4 h (co-treatment with LPS)
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Result:Significantly inhibited the gene expressions of iNOS, TNF-α, COX-2, IL-1β, and IL-6 in a dose-dependent manner.
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Cell Line:RAW264.7
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Concentration:60 μM
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Incubation Time:1 h (pretreatment); 1 h (co-treatment with LPS)
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Result:NF-κB was mainly concentrated in the cytoplasm after treatment.
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Cell Line:RAW264.7
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Concentration:20, 40, 60 μM
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Incubation Time:1 h (pretreatment)
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Result:Prevented the expression of p-IκBα induced by LPS.
Significantly inhibited the expression of NF-κB in the nucleus.
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Cell Line:Kupffer cells (KCs)
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Concentration:5, 10, 20 mM
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Incubation Time:6 h (pretreatment); 3, 6, 12 h (co-treatment with LPS)
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Result:LPS induction significantly decreased the viability of KCs, which was significantly suppressed by Aur in a dose-dependent pattern.
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Cell Line:Kupffer cells (KCs)
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Concentration:5, 10, 20 mM
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Incubation Time:6 h (pretreatment); 12 h (co-treatment with LPS)
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Result:Inhibited the apoptosis of KCs.
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Cell Line:Kupffer cells (KCs)
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Concentration:5, 10, 20 mM
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Incubation Time:6 h (pretreatment); 12 h (co-treatment with LPS)
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Result:LPS activated the TLR4 signal and upregulated the expression of TLR4, MyD88, MD2, and p-P65, while Aur treatment downregulated these protein levels.
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Cell Line:Primary rat chondrocytes
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Concentration:5, 10, 20 μM
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Incubation Time:48 h
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Result:Dose-dependently reversed IL-1β-induced aberrant expression changes of Col2a1, Acan, Adamts5, Mmp13, and Mmp3.
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Cell Line:Primary rat chondrocytes
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Concentration:5, 10, 20 μM
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Incubation Time:48 h
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Result:Dose-dependently alleviated pyroptotic morphological changes and reduced PI-positive cell numbers.
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Cell Line:Primary rat chondrocytes
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Concentration:5, 10, 20 μM
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Incubation Time:48 h
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Result:Dose-dependently reversed IL-1β-induced increase in LDH release.
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Cell Line:Primary rat chondrocytes
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Concentration:5, 10, 20 μM
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Incubation Time:48 h
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Result:Dose-dependently decreased the IL-1β-elevated PI-positive cell percentage.
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Cell Line:Primary rat chondrocytes
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Concentration:5, 10, 20 μM
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Incubation Time:48 h
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Result:Dose-dependently inhibited IL-1β-induced upregulation of GSDME-N, Caspase-3, and C-Caspase-3 expression.
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Cell Line:Primary rat chondrocytes
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Concentration:20 μM
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Incubation Time:48 h
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Result:Did not further modify the expression of Collagen II, Aggrecan, ADAMTS-5, MMP13, and MMP3 compared to Z-DEVD-FMK treatment alone.\nDid not further alter GSDME-N, Caspase-3, and C-Caspase-3 expression compared to Z-DEVD-FMK treatment alone.
In Vivo
Aureusidin (5-20 mg/kg; i.g.; once daily; 6 weeks) alleviates cartilage damage and ECM degradation, reduces serum CTX-II and COMP, inhibits pyroptosis in cartilage tissue, and decreases IL-1β/IL-18 secretion in the anterior cruciate ligament transection (ACLT)-induced osteoarthritis model in Sprague-Dawley rats[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 mice[4]
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Dosage:20 mg/kg
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Administration:i.g.; once daily; 7 consecutive days
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Result:Attenuated tissue lesions, relieved inflammatory response and tissue edema.
Suppressed expression of MD2.
Significantly downregulated expression of AST and ALT.
Suppressed expression of inflammatory factors including IL-18, IL-1β, and TNF-α in peripheral blood and liver tissues.
Resulted in barely detectable expression levels of TLR4, MyD88, MD2, and p-P65, lower than the LPS/D-GalN group.
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Animal Model:Sprague-Dawley rats (male, 8 weeks old, ACLT-induced osteoarthritis)[2]
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Dosage:5, 10, and 20 mg/kg
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Administration:i.g.; once daily; 6 weeks
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Result:Alleviated cartilage damage and cartilage matrix degradation in a dose-dependent manner.
Reduced OARSI scores in a dose-dependent manner.
Reduced elevated serum CTX-II levels dose-dependently, with 20 mg/kg restoring levels to 38.98 pg/mL.
Reduced elevated serum COMP levels dose-dependently, with 20 mg/kg restoring levels to 3.40 ng/mL.
Reversed ACLT-induced downregulation of Col2a1 and Acan and upregulation of Adamts5, Mmp13, and Mmp3 in cartilage tissue in a dose-dependent manner.
Reduced C-Caspase-3 and GSDME-positive cell numbers in cartilage tissues dose-dependently.
Downregulated GSDME-N, Caspase-3, and C-Caspase-3 protein expression dose-dependently with no effect on GSDME-FL.
Reduced elevated IL-1β and IL-18 levels in cartilage and serum dose-dependently.
Chemical Information
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CAS No. 38216-54-5
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Appearance Solid
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Molecular Weight 286.24
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Formula C15H10O6
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Color Yellow to orange
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SMILES
O=C1C2=C(O)C=C(O)C=C2O/C1=C\C3=CC(O)=C(C=C3)O
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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
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Solvent & Solubility
In Vitro:
DMSO : 62.5 mg/mL (218.35 mM; ultrasonic and warming and heat to 60°C; 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)
In Vivo:
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: ≥ 2.08 mg/mL (7.27 mM); Clear solution
This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 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.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.08 mg/mL (7.27 mM); Clear solution
This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
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.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam
Purity & Documentation
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Data Sheet (303 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2659 KB)
References
[1]. Arraki K, et al. Mammalian Arginase Inhibitory Activity of Methanolic Extracts and Isolated Compounds from Species. Molecules (Basel, Switzerland). 2021 Mar 18;26(6):1694. [Content Brief]
[2]. Feng S, et al. Aureusidin protects against osteoarthritis via Caspase-3/gasdermin E-mediated pyroptosis. Toxicology and applied pharmacology. 2026 Sep;514:117911. [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 |
|---|---|---|---|---|---|
| DMSO | 1 mM | 3.4936 mL | 17.4679 mL | 34.9357 mL | 87.3393 mL |
| 5 mM | 0.6987 mL | 3.4936 mL | 6.9871 mL | 17.4679 mL | |
| 10 mM | 0.3494 mL | 1.7468 mL | 3.4936 mL | 8.7339 mL | |
| 15 mM | 0.2329 mL | 1.1645 mL | 2.3290 mL | 5.8226 mL | |
| 20 mM | 0.1747 mL | 0.8734 mL | 1.7468 mL | 4.3670 mL | |
| 25 mM | 0.1397 mL | 0.6987 mL | 1.3974 mL | 3.4936 mL | |
| 30 mM | 0.1165 mL | 0.5823 mL | 1.1645 mL | 2.9113 mL | |
| 40 mM | 0.0873 mL | 0.4367 mL | 0.8734 mL | 2.1835 mL | |
| 50 mM | 0.0699 mL | 0.3494 mL | 0.6987 mL | 1.7468 mL | |
| 60 mM | 0.0582 mL | 0.2911 mL | 0.5823 mL | 1.4557 mL | |
| 80 mM | 0.0437 mL | 0.2183 mL | 0.4367 mL | 1.0917 mL | |
| 100 mM | 0.0349 mL | 0.1747 mL | 0.3494 mL | 0.8734 mL |
Aureusidin Related Classifications
HY-N9834 Related Classifications
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Keywords
- Aureusidin
- 38216-54-5
- Endogenous Metabolite
- Reactive Oxygen Species (ROS)
- Toll-like Receptor (TLR)
- Caspase
- Pyroptosis
- Apoptosis
- NF-κB
- Arginase
- Keap1-Nrf2
- Heme Oxygenase (HO)
- p38 MAPK
- PGE synthase
- TNF Receptor
- NO Synthase
- COX
- bovine liver arginase
- RAW264.7 cells
- MD2
- Kupffer cells
- TLR4/MD2-NF-κB signaling
- Nrf2 nuclear translocation
- primary rat chondrocytes
- HO-1
- IκBα phosphorylation
- NF-κB nuclear translocation
- Inhibitor
- inhibitor
- inhibit