BardoxoloneOnce-a-day treatment for CKD CAS# 218600-44-3 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 218600-44-3 | SDF | Download SDF |
| PubChem ID | 400010 | Appearance | Powder |
| Formula | C31H41NO4 | M.Wt | 491.66 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | CDDO; RTA 401 | ||
| Solubility | DMSO : 100 mg/mL (203.39 mM; Need ultrasonic) | ||
| Chemical Name | (4aS,6aR,6bS,8aR,12aS,14aR,14bS)-11-cyano-2,2,6a,6b,9,9,12a-heptamethyl-10,14-dioxo-1,3,4,5,6,7,8,8a,14a,14b-decahydropicene-4a-carboxylic acid | ||
| SMILES | CC1(CCC2(CCC3(C(C2C1)C(=O)C=C4C3(CCC5C4(C=C(C(=O)C5(C)C)C#N)C)C)C)C(=O)O)C | ||
| Standard InChIKey | TXGZJQLMVSIZEI-UQMAOPSPSA-N | ||
| Standard InChI | InChI=1S/C31H41NO4/c1-26(2)10-12-31(25(35)36)13-11-30(7)23(19(31)16-26)20(33)14-22-28(5)15-18(17-32)24(34)27(3,4)21(28)8-9-29(22,30)6/h14-15,19,21,23H,8-13,16H2,1-7H3,(H,35,36)/t19-,21-,23-,28-,29+,30+,31-/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 | Bardoxolone is a novel nuclear regulator factor (Nrf-2) activator.In Vitro:Bardoxolone methyl, a novel synthetic triterpenoid and antioxidant inflammation modulator, potently induces Nrf2 and inhibits NF-κB and Janus-activated kinase/STAT signaling. Bardoxolone methyl has been shown to induce differentiation, inhibit proliferation, and induce apoptosis in cancer cell lines[2].In Vivo:Kidney sections from Bardoxolone methyl-treated monkeys demonstrates decreased megalin protein expression despite similar mRNA expression across groups. The visualized decrease in megalin protein expression is confirmed by densitometry analyses, which demonstrated that Bardoxolone methyl administration significantly decreased megalin protein expression in the monkey kidney. Bardoxolone methyl administration does not affect the protein expression of cubilin in the kidney or the mRNA expression of cubilin in the kidney. The creatinine clearance in monkeys administered Bardoxolone methyl significantly differed from that at baseline and in vehicle-treated animals on day 28. After 28 days of Bardoxolone methyl administration, urinary albumin-to-creatinine ratios (UACRs), determined from the 24-hour urine collections, are significantly increased compared with those in animals receiving vehicle. Of note, UACRs decreases 53.3% in vehicle-treated animals and increased 27.9% in Bardoxolone methyl-treated monkeys[3]. Male C57BL/6J mice are administered oral BARD during HFD feeding (HFD/BARD), only fed a high-fat diet (HFD), or fed low-fat diet (LFD) for 21 weeks. Compared with LFD mice, HFD mice have a marked increase in the number of F4/80 crown-like structures (+95%; p<0.001), which is effectively prevented by BARD (−50%; p<0.01). Similarly, the number of F4/80 interstitial macrophages is significantly higher in HFD mice by 98% (p<0.001) compared with LFD mice and by 32% (p<0.01) compared with HFD/BARD mice[4]. References: | |||||
Bardoxolone Dilution Calculator
Bardoxolone Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.0339 mL | 10.1696 mL | 20.3393 mL | 40.6785 mL | 50.8481 mL |
| 5 mM | 0.4068 mL | 2.0339 mL | 4.0679 mL | 8.1357 mL | 10.1696 mL |
| 10 mM | 0.2034 mL | 1.017 mL | 2.0339 mL | 4.0679 mL | 5.0848 mL |
| 50 mM | 0.0407 mL | 0.2034 mL | 0.4068 mL | 0.8136 mL | 1.017 mL |
| 100 mM | 0.0203 mL | 0.1017 mL | 0.2034 mL | 0.4068 mL | 0.5085 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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Bardoxolone methyl, previously known as RTA 402, is the lead molecule in Reata's portfolio of Antioxidant Inflammation Modulators (AIMs). The AIMs are potent inducers of the transcription factor Nrf2, an important biological target that controls the production of many of the body's antioxidant and detoxification enzymes. Because oxidative stress and inflammation occur throughout the course of chronic kidney disease (CKD) and are known to contribute to loss of kidney function, agents that activate the Nrf2 pathway in patients with CKD may provide a novel method for preserving or improving kidney function. Bardoxolone methyl is currently being investigated as a potential oral once-a-day treatment for CKD.
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Bardoxolone methyl modulates efflux transporter and detoxifying enzyme expression in cisplatin-induced kidney cell injury.[Pubmed:27480280]
Toxicol Lett. 2016 Sep 30;259:52-59.
Cisplatin is prescribed for the treatment of solid tumors and elicits toxicity to kidney tubules, which limits its clinical use. Nuclear factor erythroid 2-related factor 2 (Nrf2, NFE2L2) is a critical transcription factor that has been shown to protect against kidney injury through activation of antioxidant mechanisms. We aimed to evaluate the ability of short-term treatment with the Nrf2 activator Bardoxolone methyl (CDDO-Me) to protect against cisplatin-induced kidney cell toxicity. Cell viability was assessed in human kidney proximal tubule epithelial cells (hPTCs) exposed to low, intermediate, and high cisplatin concentrations in the presence and absence of CDDO-Me, administered either prior to or after cisplatin. Treatment with cisplatin alone resulted in reductions in hPTC viability, while CDDO-Me administered prior to or after cisplatin exposure yielded significantly higher cell viability (17%-71%). Gene regulation (mRNA expression) studies revealed the ability of CDDO-Me to modify protective pathways including Nrf2 induced detoxifying genes [GCLC (increased 1.9-fold), NQO1 (increased 9.3-fold)], and an efflux transporter [SLC47A1 (increased 4.5-fold)] at 12h. Protein assessments were in agreement with gene expression. Immunofluorescence revealed localization of GCLC and NQO1 to the nucleus and cytosol, respectively, with CDDO-Me administered prior to or after cisplatin exposure. The findings of enhanced cell viability and increased expression of detoxifying enzymes (GCLC and NQO1) and the multidrug and toxin extrusion protein 1 (MATE1) efflux transporter (SLC47A1) in hPTCs exposed to CDDO-Me, suggest that intermittent treatment with CDDO-Me prior to or after cisplatin exposure may be a promising approach to mitigate acute kidney injury.
Bardoxolone Methyl and a Related Triterpenoid Downregulate cMyc Expression in Leukemia Cells.[Pubmed:28275049]
Mol Pharmacol. 2017 May;91(5):438-450.
Structurally related pentacyclic triterpenoids methyl 2-cyano-3,12-dioxoolean-1,9-dien-28-oate [Bardoxolone-methyl (Bar-Me)] and methyl 2-trifluoromethyl-3,11-dioxoolean-1,12-dien-30-oate (CF3DODA-Me) contain 2-cyano-1-en-3-one and 2-trifluoromethyl-1-en-3-one moieties, respectively, in their A-rings and differ in the position of their en-one structures in ring C. Only Bar-Me forms a Michael addition adduct with glutathione (GSH) and inhibits IKKbeta phosphorylation. These differences may be due to steric hindrance by the 11-keto group in CF3DODA-Me, which prevents Michael addition by the conjugated en-one in the A-ring. In contrast, both Bar-Me and CF3DODA-Me induce reactive oxygen species in HL-60 and Jurkat leukemia cells, inhibit cell growth, induce apoptosis and differentiation, and decrease expression of specificity proteins (Sp) 1, 3, and 4, and cMyc, and these effects are significantly attenuated after cotreatment with the antioxidant GSH. In contrast to solid tumor-derived cells, cMyc and Sp transcriptions are regulated independently and cMyc plays a more predominant role than Sp transcription factors in regulating HL-60 or Jurkat cell proliferation and differentiation compared with that observed in cells derived from solid tumors.
Bardoxolone-methyl inhibits migration and metabolism in MCF7 cells.[Pubmed:28277986]
Free Radic Res. 2017 Feb;51(2):211-221.
Bardoxolone-methyl (BAR) is reported to have anti-inflammatory, anti-proliferative and anti-fibrotic effects. BAR activates Nrf2 and may ameliorate oxidative stress through induction of antioxidant genes. However, off-target effects, probably concentration and NFkB-dependent, have limited the clinical use of BAR. Nrf2 regulates expression of antioxidant and mitochondrial genes and has been proposed as a target for both obesity and breast cancer. Therefore, we explored whether BAR can alter migration and proliferation in the MCF7 cell line and whether metabolic function is affected by BAR. Incubation with BAR caused a time-dependent migratory inhibition and an associated decrease in mitochondrial respiration. Both migratory and mitochondrial inhibition by BAR were further enhanced in the presence of fatty acids. In addition to the activation of Nrf2, BAR altered the expression of target mRNA GCLC and UCP1. After 24 h, BAR inhibited both glycolytic capacity, reserve (p < 0.05) and oxidative phosphorylation (p < 0.001) with an associated increase in mitochondrial ROS and loss of intracellular glutathione in MCF7 cells; however, impairment of mitochondrial activity was prevented by N-acetyl cysteine. The fatty acid, palmitate, increased mitochondrial ROS, impaired migration and oxidative phosphorylation but palmitate toxicity towards MCF7 could not be inhibited by N-acetyl cysteine suggesting that they exert effects through different pathways. BAR-activated AKT, induced DNA damage and inhibited cell proliferation. When the proteasome was inhibited, there was loss of BAR-mediated changes in p65 phosphorylation and SOD2 expression suggesting non-canonical NFkB signaling effects. These data suggest that BAR-induced ROS are important in inhibiting MCF7 migration and metabolism by negatively affecting glycolytic capacity and mitochondrial function.
Bardoxolone methyl prevents obesity and hypothalamic dysfunction.[Pubmed:27417254]
Chem Biol Interact. 2016 Aug 25;256:178-87.
High-fat (HF) diet-induced obesity is associated with hypothalamic leptin resistance and low grade chronic inflammation, which largely impairs the neuroregulation of negative energy balance. Neuroregulation of negative energy balance is largely controlled by the mediobasal and paraventricular nuclei regions of the hypothalamus via leptin signal transduction. Recently, a derivative of oleanolic acid, Bardoxolone methyl (BM), has been shown to have anti-inflammatory effects. We tested the hypothesis that BM would prevent HF diet-induced obesity, hypothalamic leptin resistance, and inflammation in mice fed a HF diet. Oral administration of BM via drinking water (10 mg/kg daily) for 21 weeks significantly prevented an increase in body weight, energy intake, hyperleptinemia, and peripheral fat accumulation in mice fed a HF diet. Furthermore, BM treatment prevented HF diet-induced decreases in the anorexigenic effects of peripheral leptin administration. In the mediobasal and paraventricular nuclei regions of the hypothalamus, BM administration prevented HF diet-induced impairments of the downstream protein kinase b (Akt) pathway of hypothalamic leptin signalling. BM treatment also prevented an increase in inflammatory cytokines, tumour necrosis factor alpha (TNFalpha) and interleukin 6 (IL-6) in these two hypothalamic regions. These results identify a potential novel neuropharmacological application for BM in preventing HF diet-induced obesity, hypothalamic leptin resistance, and inflammation.
