Wedelolactone NEW
| Price | $30 | $68 | $117 |
| Package | 1mg | 5mg | 10mg |
| Supply Ability: | 10g |
| Update Time: | 2026-07-14 |
Product Details
| Product Name: Wedelolactone | CAS No.: 524-12-9 |
| Purity: 99.35% | Supply Ability: 10g |
| Release date: 2026/07/14 |
Product Introduction
Bioactivity
| Name | Wedelolactone |
| Description | Wedelolactone (IKK Inhibitor II) is a natural product derived from Eclipta prostrata that inhibits NF-κB-mediated gene transcription in cells by blocking the phosphorylation and degradation of IκBα, and exhibits anticancer, anti-inflammatory, and antioxidant activities. Wedelolactone induces caspase-dependent apoptosis in prostate cancer cells by downregulating PKCε, without inhibiting Akt. Wedelolactone inhibits 5-Lox with an IC50 value of 2.5 μM. Wedelolactone can be used in research on inflammation, tumors, liver disease, and immune-related diseases. |
| In vitro | Methods: RAW264.7 mouse macrophages were pretreated with wedelolactone (5, 10, 20 μM) for 1 hour, followed by stimulation with LPS (500 ng/mL) for 24 hours. TNF-α, IL-6, and NO levels were measured by ELISA. Results: Wedelolactone dose-dependently inhibited LPS-induced cytokine release and gene expression. [1] Methods: Wedelolactone (10 μM) was added to chondrogenically differentiated hiPSC-MSC spheroids and treated for 21 days, followed by RNA-seq analysis of gene changes. Results: Omics data indicated that the FOXO signaling pathway was significantly activated and that wedelolactone upregulated FOXO1 mRNA and protein levels. [2] Methods: Mouse bone marrow mesenchymal stem cells (BMSCs) were treated with wedelolactone at different concentrations (0, 0.625, 1.25, 2.5, 5 μg/mL) were applied to mouse bone marrow mesenchymal stem cells (BMSCs). ALP staining and alizarin red/von Kusserau staining were used to assess osteogenic differentiation and mineralization; qPCR was used to detect osteogenic marker genes; and Western blot and kinase assays were performed to analyze the Wnt/GSK3β/β-catenin pathway. Results: 1.25 μg/mL Wedelolactone significantly promoted ALP activity and bone mineralization, and upregulated the expression of Osterix, Osteocalcin, and Runx2; by inhibiting GSK3β and increasing GSK3β phosphorylation levels, it promoted the nuclear translocation of β-catenin and Runx2, and activated the Wnt pathway to enhance osteogenic differentiation. [3] Methods: RANKL-induced RAW264.7 osteoclast precursor cells were treated with different concentrations (0, 0.625, 1.25, 2.5, 5 μg/mL) of wedelolactone. Actin rings were observed using FITC-phalloidin staining, and resorption pits were detected in dentin sections. qPCR was used to detect osteoclast-related genes, and Western blot and immunofluorescence were employed to analyze the NF-κB/c-Fos/NFATc1 pathway. Results: Wedelolactone significantly inhibited osteoclast actin ring formation and bone resorption function, downregulated the expression of c-Src, c-Fos, and cathepsin K; inhibited NF-κB p65 phosphorylation and blocked NFATc1 nuclear translocation, thereby suppressing the NF-κB/c-Fos/NFATc1 pathway to reduce osteoclastogenesis.[3] |
| In vivo | Methods: Male C57BL/6J mice (WT) received Wedelolactone (5, 10, 20 mg/kg) via oral gavage once daily for 7 consecutive days. One hour after the final dose, LPS (5 mg/kg) was administered via tracheal instillation. Tissue samples were collected 24 hours after LPS stimulation. Results: Wedelolactone dose-dependently reduced pulmonary tissue pathological damage, inhibited NF-κB activation in lung tissue, activated the Nrf2 pathway, and improved mitochondrial morphology and related protein expression. [1] Methods: SD rats underwent full-thickness cartilage defect creation (diameter 1.5 mm, depth 1.5 mm) at the mid-trochanteric region of the femur. Rat BMSCs pretreated with Wedelolactone (10 μM) for 3 days were implanted with hydrogel. Specimens were collected 6 weeks post-implantation. Results: The defect area in the Wedelolactone pretreatment group demonstrated superior cartilage repair outcomes.[2] |
| Storage | Keep away from direct sunlight,Keep away from moisture Powder: -20°C for 3 years | In solvent: -80°C for 1 year Shipping with blue ice/Shipping at ambient temperature. |
| Solubility Information | 10% DMSO+40% PEG300+5% Tween 80+45% Saline : 5.7 mg/mL (18.14 mM), Solution. DMSO : 252.5 mg/mL (803.5 mM), Sonication is recommended. Chloroform, Dichloromethane, Ethyl Acetate, Acetone, etc. : Soluble |
| Keywords | Wedelolactone | Wedelia chinensis | prostate | osteoclast | NF-κB | NFκB | NF-kB | NFkB | migration | LOX | Lipoxygenase | Inhibitor | inhibit | Eclipta alba | Caspase | cancer | BMSC | Apoptosis |
| Inhibitors Related | Stavudine | Aceglutamide | Urea | Tamoxifen | Cysteamine hydrochloride | Metronidazole | Ethyl linoleate | D-Psicose | Formamide | Dimethyl phthalate | Alginic acid | Sildenafil citrate |
| Related Compound Libraries | Anti-Tumor Natural Product Library | Polyphenolic Natural Product Library | Traditional Chinese Medicine Monomer Library | Bioactive Compound Library | Selected Plant-Sourced Compound Library | Natural Product Library | Anti-Inflammatory Traditional Chinese Medicine Compound Library | Inhibitor Library | Natural Product Library for HTS | Anti-Aging Compound Library | Bioactive Compounds Library Max | Food as Medicine Compound Library |
Company Profile Introduction
Target Molecule Corp. (TargetMol) is a global high-tech enterprise, headquartered in Boston, MA, specializing in chemical and biological research product and service to meet the research needs of global customers.
TargetMol has evolved into one of the biggest global compound library and small molecule suppliers and a customer based on 40+ countries. TargetMol offers over 80 types of compound libraries and a wide range of high-quality research chemicals including inhibitors, activator, natural compounds, peptides, inhibitory antibodies, and novel life-science kits, for laboratory and scientific use. Besides, virtual screening service is also available for customers who would like to conduct the computer-aided drug discovery.
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United States- Since: 2011-01-07
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