Norbergenin
Based on 1 publication(s) in Google Scholar
Norbergenin is a polyphenolic isocoumarin derivative. Norbergenin acts as a non-competitive inhibitor of bovine adrenal tyrosine hydroxylase (TH) with a Ki value of 69.6 μM. Norbergenin inhibits lipopolysaccharide-induced inflammatory responses in macrophages by suppressing the activation of NF-κB, MAPK and STAT3, as well as blocking metabolic reprogramming. Norbergenin inhibits aluminum chloride-induced oxidative stress and apoptosis and restores neurocognitive parameters. Norbergenin scavenges ROS through multiple mechanisms and protects cell membranes from lipid peroxidation damage. Norbergenin can be used in research related to Alzheimer's disease, peptic ulcer and arthritis.
For research use only. We do not sell to patients.
- Purity : 98.31%
- CAS No.: 79595-97-4
- Formula: C13H14O9
- Molecular Weight:314.24
-
Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Biological Activity
-
Chemical Information
-
Solvent & Solubility
- Protocols
- Purity & Documentation
- References
-
Help & FAQs
-
HY-121026
DMNQRedox cycling Agent -
HY-107999
CADD522RUNX2-DNA binding inhibitor -
HY-14937
Succinobucol -
HY-111653
CycLuc1Luciferase Substrate -
HY-13619A
Efaproxiral sodiumHemoglobin Allosteric Modifier -
HY-14937R
Succinobucol (Standard)Antioxidant -
HY-13619AR
Efaproxiral sodium (Standard)Hemoglobin Allosteric Modifier -
HY-107999R
CADD522 (Standard)Reference Standard
Publications Citing Use of MedChemExpress (MCE) Norbergenin
More
Biological Activity
Description
In Vitro
Norbergenin (5-50 μM; 25 h) dose-dependently inhibits LPS (HY-D1056)-induced NO production in iBMDMs at 24 h post-stimulation[2].
Norbergenin (5-50 μM; 25 h) dose-dependently inhibits LPS-induced TNFα production in iBMDMs at 24 h post-stimulation[2].
Norbergenin (50 μM; 2-25 h) inhibits LPS-induced mRNA expression of *Il1b*, *Tnfa*, *Il6* and *Nos2* in iBMDM and BMDM[2].
Norbergenin (5-50 μM; 5-9 h) dose-dependently inhibits LPS-induced activation of NF-κB, STAT3 and MAPK (p38, JNK, ERK) signaling pathways, and reduces the protein levels of pro-IL1β, iNOS and TLR2 in stimulated iBMDMs at 4 h or 8 h[2].
Norbergenin (5-50 μM; 9 h) dose-dependently inhibits LPS-induced glycolysis and maintains mitochondrial oxidative phosphorylation (OXPHOS) in iBMDMs at 8 h post-stimulation[2].
Norbergenin (50 μM; 9 h) alters the proteome profile of iBMDMs stimulated with LPS for 8 h, downregulates proteins related to inflammatory pathways and upregulates proteins related to oxidative phosphorylation, thereby restoring its profile to a state similar to that of the unstimulated control group[2].
Norbergenin (50 μM; 9 h) reverses LPS-induced metabolic reprogramming in iBMDMs after 8 hours, restoring normal activity of glycolysis, tricarboxylic acid (TCA) cycle, and arginine metabolism pathways[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
-
Cell Line:murine immortalized bone marrow-derived macrophages (iBMDMs), primary bone marrow-derived macrophages (BMDMs)
-
Concentration:1, 5, 10 and 50 μM
-
Incubation Time:24 h
-
Result:Showed no significant toxic effects on iBMDMs and BMDMs at concentrations between 1 to 50 μM.
-
Cell Line:murine immortalized bone marrow-derived macrophages (iBMDMs)
-
Concentration:5, 10 and 50 μM
-
Incubation Time:1 h preincubation; 24 h LPS stimulation
-
Result:Significantly reduced LPS-induced TNFα production in a dose-dependent manner, with the 50 μM concentration showing the greatest inhibitory effect.
-
Cell Line:murine immortalized bone marrow-derived macrophages (iBMDMs), primary bone marrow-derived macrophages (BMDMs)
-
Concentration:50 μM
-
Incubation Time:1 h preincubation; 1-24 h LPS stimulation
-
Result:Significantly reduced LPS-induced mRNA expression of Il1b, Tnfa, Il6, and Nos2 at multiple time points (8, 16, 24 h) in both iBMDMs and BMDMs, with statistically significant decreases indicated by *p < 0.05**, **p < 0.01**, and ***p < 0.001.
-
Cell Line:murine immortalized bone marrow-derived macrophages (iBMDMs)
-
Concentration:5, 10 and 50 μM
-
Incubation Time:1 h preincubation; 4-8 h LPS stimulation
-
Result:Caused a dose-dependent reduction in LPS-induced pro-IL1β, iNOS, p-NF-κB, p-IκB-α, p-STAT3, p-p38, p-JNK, p-ERK1/2, and TLR2 protein levels.
Had no effect on LPS-induced TLR4 expression.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
-
CAS No. 79595-97-4
-
Appearance Solid
-
Molecular Weight 314.24
-
Formula C13H14O9
-
Color White to yellow
-
SMILES
OC1=C2[C@@]3([H])[C@@](OC(C2=CC(O)=C1O)=O)([H])[C@H]([C@@H]([C@H](O3)CO)O)O
-
Structure Classification
-
Initial Source
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Publications (1)
-
Journal Impact Factor
-
Most Recent
Solvent & Solubility
In Vitro:
DMSO : 125 mg/mL (397.79 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. 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. 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 (6.62 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 (6.62 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:
-
-
-
-
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
-
%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
-
%+
-
+%Tween-80 + +
-
%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.
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
-
Collagen-Induced Arthritis
Collagen-induced arthritis (CIA) is an autoimmune murine model of rheumatoid arthritis in which immunization with type II collagen (CII) emulsified in an adjuvant induces a T cell- and autoantibody-driven inflammatory arthritis characterized by synovial hyperplasia, immune cell infiltration, and joint destruction. The model typically relies on genetically susceptible mouse strains (e. g. , DBA/1) and reproduces key features of human rheumatoid arthritis, including anti-collagen immune responses and progressive joint inflammation. Disease onset generally occurs within ~3-4 weeks after immunization, depending on antigen/adjuvant combinations and protocol variation. The immunopathology is driven by adaptive immune activation against CII, leading to systemic and local joint inflammation mediated by pro-inflammatory cytokines and effector immune cells, making CIA a standard preclinical platform for evaluating immunomodulatory and anti-arthritic interventions.
-
Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
-
TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
-
Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
-
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
-
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
-
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
-
Ferroptosis Solutions
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by lethal lipid peroxidation and sensitivity to suppression by iron chelators or lipophilic radical-trapping antioxidants. The core pathway links cystine uptake through system Xc−, glutathione availability, GPX4-dependent detoxification of phospholipid hydroperoxides, iron-dependent oxidative reactions, and polyunsaturated-phospholipid metabolism into a cell-death program that is biochemically and morphologically distinct from apoptosis, necrosis, and autophagy. The ferroptosis pathway is experimentally linked to phenotype through chemical and genetic perturbation. Erastin induces ferroptosis by inhibiting cystine uptake through system Xc− and weakening antioxidant defenses, while GPX4 inhibition or depletion causes lipid peroxide accumulation and ferroptotic cancer-cell death. ACSL4 and oxidizable arachidonoyl- or adrenoyl-containing phosphatidylethanolamines shape ferroptosis sensitivity by con
-
Alzheimer’s Disease Modeling
Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by a progressive decline in cognitive functions and loss of specific types of neurons and synapses. Alzheimer's symptoms can be simulated in mice by injecting drugs (such as Aβ) or genetically modified.
Purity & Documentation
-
Data Sheet (287 KB)
-
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)
-
Handling Instructions (2659 KB)
References
[1]. Nalla S, et al. Kaempferide and Norbergenin avert aluminium chloride-induced amyloid β accumulation and neurocognitive shutdown via oxidative and apoptotic mechanisms. International journal of immunopathology and pharmacology. 2025;39:3946320251343687. [Content Brief]
[2]. Li W, et al. Norbergenin prevents LPS-induced inflammatory responses in macrophages through inhibiting NFκB, MAPK and STAT3 activation and blocking metabolic reprogramming. Frontiers in immunology. 2023;14:1117638. [Content Brief]
[3]. Zhang YH, et al. In vitro inhibitory effects of bergenin and norbergenin on bovine adrenal tyrosine hydroxylase. Phytotherapy research : PTR. 2003 Sep;17(8):967-9. [Content Brief]
[4].
Haq KU, et al. Elucidation of reactive oxygen species scavenging pathways of norbergenin utilizing DFT approaches. R Soc Open Sci. 2022 Dec 21;9(12):221349.
[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. 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 | 3.1823 mL | 15.9114 mL | 31.8228 mL | 79.5570 mL |
| 5 mM | 0.6365 mL | 3.1823 mL | 6.3646 mL | 15.9114 mL | |
| 10 mM | 0.3182 mL | 1.5911 mL | 3.1823 mL | 7.9557 mL | |
| 15 mM | 0.2122 mL | 1.0608 mL | 2.1215 mL | 5.3038 mL | |
| 20 mM | 0.1591 mL | 0.7956 mL | 1.5911 mL | 3.9779 mL | |
| 25 mM | 0.1273 mL | 0.6365 mL | 1.2729 mL | 3.1823 mL | |
| 30 mM | 0.1061 mL | 0.5304 mL | 1.0608 mL | 2.6519 mL | |
| 40 mM | 0.0796 mL | 0.3978 mL | 0.7956 mL | 1.9889 mL | |
| 50 mM | 0.0636 mL | 0.3182 mL | 0.6365 mL | 1.5911 mL | |
| 60 mM | 0.0530 mL | 0.2652 mL | 0.5304 mL | 1.3260 mL | |
| 80 mM | 0.0398 mL | 0.1989 mL | 0.3978 mL | 0.9945 mL | |
| 100 mM | 0.0318 mL | 0.1591 mL | 0.3182 mL | 0.7956 mL |
Norbergenin Related Classifications
HY-N9447 Related Classifications
Powered by Bioz
Keywords
- Norbergenin
- 79595-97-4
- Free Radical Scavengers
- Tyrosine Hydroxylase
- Reactive Oxygen Species (ROS)
- Apoptosis
- NF-κB
- p38 MAPK
- STAT
- acetylcholinesterase
- Alzheimer’s disease
- BMDMs
- iBMDMs
- peptic ulcer
- oxidative stress
- bovine adrenal tyrosine hydroxylase
- aluminium chloride
- RAW 264.7 macrophages
- male Wistar rats
- Inhibitor
- inhibitor
- inhibit