AKBA
产品说明书
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同义名 : | Acetyl-11-keto-β-boswellic acid;3-O-acetyl-11-keto-β-Boswellic acid;Acetylketo-β-boswellic acid;3-acetyl-11-keto-β-Boswellic Acid |
| CAS号 : | 67416-61-9 | |
| 货号 : | A106831 | |
| 分子式 : | C32H48O5 | |
| 纯度 : | 99%+ | |
| 分子量 : | 512.721 | |
| MDL号 : | MFCD03788777 | |
| 存储条件： |
Pure form Sealed in dry,Store in freezer, under -20°C In solvent -20°C:3-6个月-80°C:12个月 |
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| 溶解度 : |
DMSO: 4 mg/mL(7.8 mM)，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO |
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| 动物实验配方： |
| 生物活性 | |||
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| 描述 | Acetyl-11-keto-β-boswellic acid (AKBA), a naturally occurring pentacyclic triterpene isolated from the gum resin exudate from the stem of the tree Boswellia serrata (frankincense), is a Nrf2 activator against a large number of inflammatory diseases, including cancer, arthritis, chronic colitis, ulcerative colitis, Crohn’s disease, and bronchial asthma[3]. AKBA is as a novel, orally active, non-redox and non-competitive 5-lipoxygenase inhibitor that also inhibits topisomerase I and II in vitro[4]. AKBA enhances apoptosis induced by cytokines and chemotherapeutic agents, inhibits invasion, and suppresses osteoclastogenesis through inhibition of NF-κB-regulated gene expression[3]. In tumor cells, AKBA suppressed both inducible and constitutive NF-κB activation examined by DNA binding. AKBA inhibited the TNF-induced activation of IκBα kinase (IKK), IκBα phosphorylation, IκBα ubiquitination, IκBα degradation, p65 phosphorylation, and p65 nuclear translocation[3]. AKBA inhibited the NF-κB-dependent reporter gene expression activated by TNFR type 1, TNFR-associated death domain protein, TNFR-associated factor 2, NF-κB-inducing kinase, and IKK[3]. Induction of apoptosis in HL-60 and CCRF-CEM by AKBA may be due to inhibition of topoisomerase I in these cells[5]. AKBA suppressed tumor growth in the human prostate tumor xenograft mice treated daily (10 mg/kg AKBA), whose inhibitory effect on tumor growth was well correlated with suppression of angiogenesis induced by VEGFR2 signaling pathways[6]. In mice, AKBA significantly inhibited blood vessel formation in the Matrigel plug assay and effectively suppressed vascular endothelial growth factor (VEGF)–induced microvessel sprouting in rat aortic ring assay ex vivo[6]. In vitro, AKBA suppressed VEGF-induced phosphorylation of VEGF receptor 2 (VEGFR2) kinase (KDR/Flk-1) with IC50 of 1.68 μmol/L[6]. At low micromolar concentrations, AKBA rapidly and potently inhibited the phosphorylation of Erk-1/2 and impaired the motility of meningioma cells[7]. AKBA inhibits the motility of meningioma cells showing a potent cytotoxic activity with half-maximal inhibitory concentrations in the range of 2 - 8 μM[7]. | ||
| 实验方案 | |||
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| 1mg | 5mg | 10mg | |
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1 mM 5 mM 10 mM |
1.95mL 0.39mL 0.20mL |
9.75mL 1.95mL 0.98mL |
19.50mL 3.90mL 1.95mL |
| 参考文献 |
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