CAS NO: | 17019-92-0 |
包装 | 价格(元) |
1mg | 询价 |
5mg | 询价 |
10mg | 询价 |
Cas No. | 17019-92-0 |
别名 | 11-酮基-BETA-乳香酸,11-oxo-β-Boswellic acid,KBA |
化学名 | (3α,4β)-3-hydroxy-11-oxo-urs-12-en-23-oic acid |
Canonical SMILES | O=C1C=C2[C@](CC[C@]3(C)C2[C@@H](C)[C@H](C)CC3)(C)[C@]4(C)CCC5[C@@](C)(C(O)=O)[C@H](O)CC[C@]5(C)C41 |
分子式 | C30H46O4 |
分子量 | 470.4 |
溶解度 | ≤5mg/ml in ethanol;25mg/ml in DMSO;25mg/ml in dimethyl formamide |
储存条件 | 4°C, protect from light |
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
Shipping Condition | Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request |
产品描述 | IC50: 35.8 μM: inhibits MCF-7 (human breast adenocarcinoma) [1]. 37.9 μM: blocks A2780 (cis-platin resistant ovarian cancer cells) [1]. 11-keto-β-Boswellic Acid, known as KBA, is a naturally occurring pentacyclic triterpene isolated from the gum resin of the tree Boswellia serrata. KBA is non-redox, specific leukotriene synthesis inhibitors through the inhibition of 5-lipoxygenase (5-LOX) which has anti-arthritic and anti-inflammatory activities. 5-LOX catalyzes essential fatty acids substrates into leukotrienes and a variety of other biologically active products. KBA is a novel activator of nuclear factor erythroid-2-related factor 2 (Nrf2), which protects against cerebral ischemic injury. In vitro: KBA, concentration dependently, decreased the formation of leukotriene B4 and the synthesis of all 5-LOX products from endogenous arachidonic acid in rat peritoneal neutrophils. In contrast, KBA exerted no remarkable effects on the 12-lipoxygenase and cyclooxygenase activities. [2]. In vivo: Adult male Sprague–Dawley rats were injected KAB intraperitoneally at a dose of 25 mg/kg for 48 hours. KAB remarkably decreased infarct volumes as well as apoptotic cells at 1 h, and then increased neurologic scores when applied 48 h. Moreover, posttreatment with KBA induced the decrease of malondialdehyde levels and the increase of protein Nrf2 and heme oxygenase-1 expression in brain tissues, indicating that the Nrf2/HO-1 pathway was involved in the neuroprotection of KBA against oxidative stress-induced ischemic injury [3]. References: |
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