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CDDO-dhTFEA Sale

(Synonyms: RTA dh404) 目录号 : GC35629

CDDO-dhTFEA (RTA dh404) 是一种合成的齐墩果烷三萜化合物,有效激活 Nrf2 并抑制促炎转录因子 NF-κB。 CDDO-dhTFEA 可以恢复高血压 (MAP),增加 Nrf2 及其靶基因的表达,减弱 NF-κB 的活化和转化生长因子-β 途径,并减少慢性肾病 (CKD) 大鼠的肾小球硬化,间质纤维化和炎症。

CDDO-dhTFEA Chemical Structure

Cas No.:1191265-33-4

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产品描述

CDDO-dhTFEA (RTA dh404) is a synthetic oleanane triterpenoid compound which potently activates Nrf2 and inhibits the pro-inflammatory transcription factor NF-κB[1]. CDDO-dhTFEA restores hypertension (MAP), increases Nrf2 and expression of its target genes, attenuates activation of NF-κB and transforming growth factor-β pathways, and reduces glomerulosclerosis, interstitial fibrosis and inflammation in the chronic kidney disease (CKD) rats[2]. NF-κB Nrf2

[1]. Aminzadeh MA, et al. The synthetic triterpenoid RTA dh404 (CDDO-dhTFEA) restores endothelial function impaired by reduced Nrf2 activity in chronic kidney disease. Redox Biol. 2013 Oct 31;1:527-31. [2]. Aminzadeh MA, et al. The synthetic triterpenoid RTA dh404 (CDDO-dhTFEA) restores Nrf2 activity and attenuates oxidative stress, inflammation, and fibrosis in rats with chronic kidney disease. Xenobiotica. 2014 Jun;44(6):570-8.

Chemical Properties

Cas No. 1191265-33-4 SDF
别名 RTA dh404
Canonical SMILES CC(C)([C@](CC[C@@]([C@@]1(CC[C@]2(CCC(C)(C[C@]2([C@]13[H])[H])C)C(NCC(F)(F)F)=O)C)4C)5[H])C(C(C#N)=C[C@]5(C)[C@@]4([H])CC3=O)=O
分子式 C33H45F3N2O3 分子量 574.72
溶解度 DMSO: 260 mg/mL (452.39 mM) 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 1.74 mL 8.6999 mL 17.3998 mL
5 mM 0.348 mL 1.74 mL 3.48 mL
10 mM 0.174 mL 0.87 mL 1.74 mL
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Research Update

CDDO-9,11-dihydro-trifluoroethyl amide (CDDO-dhTFEA) induces hepatic cytoprotective genes and increases bile flow in rats

Xenobiotica 2013 Jul;43(7):571-8.PMID:23244591DOI:10.3109/00498254.2012.750022.

1. The transcription factor Nrf2 is important for hepatoprotection against oxidative stress, as it regulates many cytoprotective genes, including several important for glutathione (GSH) homeostasis. In addition to being an important endogenous antioxidant, GSH is also critical for the maintenance of bile acid-independent bile flow. While it has been well-established that synthetic oleanane triterpenoids pharmacologically activate Nrf2, their effects on bile flow and hepatic cytoprotective capacity have not been fully explored. 2. The present studies were conducted to evaluate the effects of a compound in this class, CDDO-9,11-dihydro-trifluoroethyl amide (CDDO-dhTFEA), on these parameters. CDDO-dhTFEA at 3, 10 or 30 mg/kg was orally administered to bile duct-cannulated rats once daily for 7 days, with bile collected 5 h after each dose for 1 h. Livers were harvested after the final bile collection for the evaluation of histology and Nrf2 targets. 3. CDDO-dhTFEA did not affect liver histology. CDDO-dhTFEA markedly and dose-dependently increased bile flow, as well as the biliary excretion of GSH, cholesterol and phospholipids without affecting biliary excretion of bile acids. This was accompanied by dose-dependent increases in mRNA expression and/or enzyme activity of a broad panel of cytoprotective Nrf2 target genes, including NAD(P)H quinone oxidoreductase 1 (Nqo1), thioredoxin reductase (Txnrd), sulfiredoxin 1(Srxn1), glutamate cysteine ligase catalytic and modifier subunits (Gclc and Gclm), glutathione reductase (Gsr), gamma-glutamyl transpeptidase 1 (Ggt1), heme oxygenase-1 (Ho-1) and epoxide hydrolase-1 (Eh-1). 4. These data further demonstrate the important hepatobiliary attributes of oleanane synthetic triterpenoids and support their continued investigation for liver diseases.

Synthetic Triterpenoid RTA dh404 (CDDO-dhTFEA) Ameliorates Acute Pancreatitis

Pancreas 2016 May-Jun;45(5):720-9.PMID:26495793DOI:10.1097/MPA.0000000000000518.

Objectives: Nuclear factor-erythroid-2-related factor (Nrf2) is a ubiquitous transcriptional factor that regulates expression of cellular antioxidant and detoxifying molecules. This study was undertaken to test the hypothesis that administration of the Nrf2 activator (dh404) may attenuate acute pancreatitis. Methods: Rats were treated with dh404 (1 mg/kg) 24 hours before induction of pancreatitis and for 3 days thereafter. Pancreatitis was induced with L-arginine (600 mg/100 g) or cerulein (40 μg/kg). Pancreases were processed for histology and malondialdehyde, whereas serum was analyzed for amylase. Islet extracted human pancreatic tissue from organ donors were used for in vitro studies. The tissues were incubated with dh404 at 0, 250, and 500 nM for 30 minutes, 60 minutes, 12 hours, and 24 hours. Nuclear factor-erythroid-2-related factor nuclear translocation and expression of Nrf2's target genes and inflammatory mediators were determined. Results: The dh404-treated rat pancreases demonstrated significantly less infiltration of inflammatory cells, destruction of acinar architecture, perilobar edema, and necrosis. Serum amylase and pancreatic malondialdehyde in the dh404-treated rats were significantly lower. dh404-treated human pancreatic tissue showed a significantly higher expression of antioxidant enzymes, lower expression of inflammatory mediators, and greater viability against oxidative stress. Conclusion: Administration of dh404 attenuates acute pancreatitis by lowering oxidative stress and reducing proinflammatory mediators.

The synthetic triterpenoid RTA dh404 (CDDO-dhTFEA) restores Nrf2 activity and attenuates oxidative stress, inflammation, and fibrosis in rats with chronic kidney disease

Xenobiotica 2014 Jun;44(6):570-8.PMID:24195589DOI:10.3109/00498254.2013.852705.

1. Chronic oxidative stress and inflammation are major mediators of chronic kidney disease (CKD) and result in impaired activation of the cytoprotective transcription factor Nrf2. Given the role of oxidative stress and inflammation in CKD pathogenesis, strategies aimed at restoring Nrf2 activity may attenuate CKD progression. 2. The present study investigated whether the synthetic triterpenoid RTA dh404 (2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid-9,11-dihydro-trifluoroethyl amide or CDDO-dhTFEA) would afford renal protection in a 5/6 nephrectomized rat model of CKD. RTA dh404 (2 mg/kg/day) was orally administered once daily for 12 weeks after 5/6 nephrectomy surgery. 3. The remnant kidneys from the vehicle-treated CKD rats showed activation of nuclear factor kappaB (NF-κB), upregulation of NAD(P)H oxidase, glomerulosclerosis, interstitial fibrosis and inflammation, as well as marked reductions in Nrf2 and its target gene products (i.e. catalase, heme oxygenase-1, thioredoxin 1, thioredoxin reductase 1 and peroxiredoxin 1). The functional and structural deficits in the kidney were associated with increased (∼30%) mean arterial pressure (MAP). Treatment with RTA dh404 restored MAP, increased Nrf2 and expression of its target genes, attenuated activation of NF-κB and transforming growth factor-β pathways, and reduced glomerulosclerosis, interstitial fibrosis and inflammation in the CKD rats. 4. Thus, chronic treatment with RTA dh404 was effective in restoring Nrf2 activity and slowing CKD progression in rats following 5/6 nephrectomy.

The synthetic triterpenoid RTA dh404 (CDDO-dhTFEA) restores endothelial function impaired by reduced Nrf2 activity in chronic kidney disease

Redox Biol 2013 Oct 31;1(1):527-31.PMID:24363993DOI:10.1016/j.redox.2013.10.007.

Chronic kidney disease (CKD) is associated with endothelial dysfunction and accelerated cardiovascular disease, which are largely driven by systemic oxidative stress and inflammation. Oxidative stress and inflammation in CKD are associated with and, in part, due to impaired activity of the cytoprotective transcription factor Nrf2. RTA dh404 is a synthetic oleanane triterpenoid compound which potently activates Nrf2 and inhibits the pro-inflammatory transcription factor NF-κB. This study was designed to test the effects of RTA dh404 on endothelial function, inflammation, and the Nrf2-mediated antioxidative system in the aorta of rats with CKD induced by 5/6 nephrectomy. Sham-operated rats served as controls. Subgroups of CKD rats were treated orally with RTA dh404 (2 mg/kg/day) or vehicle for 12 weeks. The aortic rings from untreated CKD rats exhibited a significant reduction in the acetylcholine-induced relaxation response which was restored by RTA dh404 administration. Impaired endothelial function in the untreated CKD rats was accompanied by significant reduction of Nrf2 activity (nuclear translocation) and expression of its cytoprotective target genes, as well as accumulation of nitrotyrosine and upregulation of NAD(P)H oxidases, 12-lipoxygenase, MCP-1, and angiotensin II receptors in the aorta. These abnormalities were ameliorated by RTA dh404 administration, as demonstrated by the full or partial restoration of the expression of all the above analytes to sham control levels. Collectively, the data demonstrate that endothelial dysfunction in rats with CKD induced by 5/6 nephrectomy is associated with impaired Nrf2 activity in arterial tissue, which can be reversed with long term administration of RTA dh404.