BrusatolCAS# 14907-98-3 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 14907-98-3 | SDF | Download SDF |
PubChem ID | 73432 | Appearance | White crystalline powder |
Formula | C26H32O11 | M.Wt | 520.53 |
Type of Compound | Diterpenoids | Storage | Desiccate at -20°C |
Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
SMILES | CC1=C(C(=O)CC2(C1CC3C45C2C(C(C(C4C(C(=O)O3)OC(=O)C=C(C)C)(OC5)C(=O)OC)O)O)C)O | ||
Standard InChIKey | ZZZYHIMVKOHVIH-VILODJCFSA-N | ||
Standard InChI | InChI=1S/C26H32O11/c1-10(2)6-15(28)37-18-20-25-9-35-26(20,23(33)34-5)21(31)17(30)19(25)24(4)8-13(27)16(29)11(3)12(24)7-14(25)36-22(18)32/h6,12,14,17-21,29-31H,7-9H2,1-5H3/t12-,14+,17+,18+,19+,20+,21-,24-,25+,26-/m0/s1 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | 1. Brusatol, a Nrf2 inhibitor, has dual anti-hepatitis C virus and anticancer effects and can enhance the comparable effects of sorafenib. 2. Brusatol is a new anti-pancreatic cancer adjuvant, 3. Brusatol-mediated inhibition of c-Myc/ROS signaling pathway increases HIF-1α degradation by promoting PHD activity and induces cell death in colorectal cancer under hypoxia. 4. Brusatol inhibits the response of cultured beta-cells to pro-inflammatory cytokines in vitro. 5. Brusatol shows antitrypanosomal activity against trypomastigotes of Trypanosoma evansi. |
Targets | HCV | Nrf2 | HO-1 | ROS | Akt | PI3K | NF-kB | HIF | c-Myc | IFN-γ | IL Receptor | NO | NOS |
Brusatol Dilution Calculator
Brusatol Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 1.9211 mL | 9.6056 mL | 19.2112 mL | 38.4224 mL | 48.028 mL |
5 mM | 0.3842 mL | 1.9211 mL | 3.8422 mL | 7.6845 mL | 9.6056 mL |
10 mM | 0.1921 mL | 0.9606 mL | 1.9211 mL | 3.8422 mL | 4.8028 mL |
50 mM | 0.0384 mL | 0.1921 mL | 0.3842 mL | 0.7684 mL | 0.9606 mL |
100 mM | 0.0192 mL | 0.0961 mL | 0.1921 mL | 0.3842 mL | 0.4803 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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T-2 toxin-induced toxicity in neuroblastoma-2a cells involves the generation of reactive oxygen, mitochondrial dysfunction and inhibition of Nrf2/HO-1 pathway.[Pubmed:29432840]
Food Chem Toxicol. 2018 Apr;114:88-97.
The molecular mechanisms of T-2 mycotoxin induced neurotoxicity remains enigmatic. In the present study we show that T-2 toxin induced neurotoxicity in mouse neuroblastoma2a (N2a) cells is both dose- and time-dependent and is associated with oxidative stress, mitochondrial dysfunction and apoptosis. T-2 toxin treatment of N2a cells at 10, 20, 40 and 80ng/mL for 24h significantly up-regulated the mRNA expression of p53, Bax, and caspase-8 and down-regulated the expression of Nrf2 and HO-1 mRNA and protein expression. Activation of caspases-8, -9 and -3 was also evident in a concentration-dependent manner. Pre-treatment of the cells with the antioxidant N-acetyl-cysteine markedly suppressed T-2 toxin-induced neurotoxicity and caspase activation. Conversely, pre-treatment of the cells with the Nrf2 inhibitor Brusatol or the HO-1 inhibitor zinc protoporphyrin IX, enhanced T-2 toxin induced neurotoxicity and increased the activation of caspase-9 and -3. Taken together, these novel findings suggest that T-2 toxin-induced neurotoxicity in N2a cells involves oxidative stress, mitochondrial dysfunction and apoptosis via the inhibition of the Nrf2/HO-1 and activation of p53 pathway. The present study highlights the potential of developing much needed pharmacological interventions to prevent T-2 toxin neurotoxicity.
Repurposing of the CDK inhibitor PHA-767491 as a NRF2 inhibitor drug candidate for cancer therapy via redox modulation.[Pubmed:29297149]
Invest New Drugs. 2018 Aug;36(4):590-600.
Oxidative stress and cellular response mechanisms such as NRF2-mediated antioxidant responses play differential roles in healthy and diseased cells. Constant generation and elimination of high levels of reactive oxygen species is a hallmark of many cancer cell types; this phenomenon is not observed during steady state of healthy cells. Manipulation of NRF2 transcriptional activity and the cellular redox homeostasis therefore has potential to be therapeutically exploitable for cancer therapy by preferentially targeting cancer cells for induction of oxidative stress. We found that the NRF2 inhibitor Brusatol triggered increased oxidative stress while compromising viability and proliferation of multiple myeloma cells. Using a repurposing approach we discovered that the Cdc7/CDK9 inhibitor PHA-767491 is also a potent inhibitor of NRF2 transcriptional activity. The molecule was identified by high throughput screening of a library of about 5900 drug-like molecules. Screening assays included two cell-based assays using HepG2 hepatocellular carcinoma cells: a) A NRF2 nuclear translocation assay, and b) A NRF2 luciferase reporter assay. Validation assays were performed in multiple myeloma cells and included detection of mitochondrial superoxide levels and MTS assays. We found that PHA-767491 treatment of multiple myeloma cells was associated with inhibition of nuclear translocation of NRF2, increased mitochondrial superoxide levels and inhibition of cell growth. Our findings suggest that PHA-767491 is a promising drug candidate for cancer therapy with NRF2 inhibitory potency contributing to its anti-cancer properties.
Oxidative stress via inhibition of the mitochondrial electron transport and Nrf-2-mediated anti-oxidative response regulate the cytotoxic activity of plumbagin.[Pubmed:29348410]
Sci Rep. 2018 Jan 18;8(1):1073.
Plumbagin, an anti-cancer agent, is toxic to cells of multiple species. We investigated if plumbagin targets conserved biochemical processes. Plumbagin induced DNA damage and apoptosis in cells of diverse mutational background with comparable potency. A 3-5 fold increase in intracellular oxygen radicals occurred in response to plumbagin. Neutralization of the reactive oxygen species by N-acetylcysteine blocked apoptosis, indicating a central role for oxidative stress in plumbagin-mediated cell death. Plumbagin docks in the ubiquinone binding sites (Q0 and Qi) of mitochondrial complexes I-III, the major sites for oxygen radicals. Plumbagin decreased oxygen consumption rate, ATP production and optical redox ratio (NAD(P)H/FAD) indicating interference with electron transport downstream of mitochondrial Complex II. Oxidative stress induced by plumbagin triggered an anti-oxidative response via activation of Nrf2. Plumbagin and the Nrf2 inhibitor, Brusatol, synergized to inhibit cell proliferation. These data indicate that while inhibition of electron transport is the conserved mechanism responsible for plumbagin's chemotoxicity, activation of Nrf2 is the resulting anti-oxidative response that allows plumbagin to serve as a chemopreventive agent. This study provides the basis for designing potent and selective plumbagin analogs that can be coupled with suitable Nrf2 inhibitors for chemotherapy or administered as single agents to induce Nrf2-mediated chemoprevention.
Synergistic antitumor effect of brusatol combined with cisplatin on colorectal cancer cells.[Pubmed:29328398]
Int J Mol Med. 2018 Mar;41(3):1447-1454.
Colorectal cancer (CRC) is a common and lifethreatening type of malignant cancer, which is associated with a high mortality rate. Cisplatin (CDDP) is a commonly used chemotherapy drug with significant side effects. Brusatol (BR) is one of the principal chemical compounds isolated from the Chinese herb Bruceae Fructus, which has been reported to markedly inhibit the proliferation of numerous cancer cell lines. The present study aimed to investigate the possible synergistic anticancer effects of CDDP combined with BR on CT26 cells, and to evaluate the underlying mechanisms of action. The growth inhibitory effects of BR, CDDP, and BR and CDDP cotreatment on CT26 cells were assessed by MTT assay. Cell apoptosis were determined by flow cytometry and western blot analysis. The results indicated that compared with singleagent treatment, cotreatment of CT26 cells with CDDP and BR synergistically inhibited cell proliferation and increased cellular apoptosis. Furthermore, treatment of CT26 cells with CDDP and BR resulted in a marked increase in the release of cytosolic cytochrome c, decreased expression of procaspase3 and procaspase9, and upregulation of the Bcell lymphoma 2 (Bcl2)associated X protein/Bcl2 ratio compared with treatment with BR or CDDP alone. These results strongly suggested that the combination of CDDP and BR was able to produce a synergistic antitumor effect in CRC cells, thus providing a solid foundation for further development of this combination regimen into an effective therapeutic method for CRC.
Dihydromyricetin relieves rheumatoid arthritis symptoms and suppresses expression of pro-inflammatory cytokines via the activation of Nrf2 pathway in rheumatoid arthritis model.[Pubmed:29656207]
Int Immunopharmacol. 2018 Jun;59:174-180.
Rheumatoid arthritis (RA) is a systemic inflammatory and autoimmune disease. In this research, we estimated the protective effects of Dihydromyricetin (DMY) on RA induced by Complete Freund's Adjuvant (CFA). We found that DMY effectively relieved rheumatoid arthritis symptoms, such as body weight change, paw swelling and rheumatoid arthritis scores. In addition, we also observed that DMY significantly lowered the immune organ indexes (including thymus and spleen) and exhibited the anti-inflammatory effect in CFA-induced rheumatoid arthritis. The results demonstrated that the increased expression levels of interleukin-1beta (IL-1beta), interleukin-6(IL-6), tumor necrosis factor-alpha (TNF-alpha) were significantly inhibited by DMY. Furthermore, the key inflammatory mediator, cyclooxygenase-2 (COX-2) was markedly lowered after treatment with DMY. A mechanistic study indicated that DMY could up-regulate the down-regulation levels of the mRNA and protein of Nrf2, HO-1 and NQO1. Moreover, the Nrf2 activation of DMY was abolished by Nrf2 inhibitor Brusatol. Thus, DMY inhibits the expressions of pro-inflammatory cytokines via activating Nrf2 pathway in RA model, which suggests that DMY has potential for further investigation as a candidate anti-arthritic agent in future.