| 中文名称： | β-淀粉状蛋白25-35 | 中文别名： | β-淀粉状蛋白25-35 |
|---|---|---|---|
| 英文名称： | β-Amyloid(25-35) | CAS： | 131602-53-4 |
| 产品分类： | 小分子化合物 | 纯度： | HPLC≥97% |
| 产品编号 | 品牌 | 纯度 | 规格 | 库存 | 价格 |
|---|---|---|---|---|---|
| IA8650 | 索莱宝 | HPLC≥97% | 1mg | 有现货 | 540.00 元 |
| IA8650 | 索莱宝 | HPLC≥97% | 10mg | 有现货 | 2,550.00 元 |
| IA8650 | 索莱宝 | HPLC≥97% | 5mg | 有现货 | 1,650.00 元 |
| 标准名称: | β-淀粉状蛋白 (25-35) | 英文名称： | β-Amyloid (25-35) |
|---|---|---|---|
| CAS： | 131602-53-4 | 分子式： | C45H81N13O14S |
| 分子量： | 1060.2683 | 颜色与性状： | No data available |
| 密度： | 1.248±0.06 g/cm3 (20 ºC 760 Torr), | 沸点： | 1517.336°C at 760 mmHg |
| 熔点： | No data available | 水溶性： | Soluble in water. |
| CAS | 131602-53-4 |
| 中文名称 | β-淀粉状蛋白25-35 |
| 英文名称 | β-Amyloid(25-35) |
| 分子式 | C45H81N13O14S |
| 分子量 | 1060.27 |
| 规格 | 5mg ; 10mg ; 1mg |
| 溶解性 | Soluble in Water(该产品在溶液状态不稳定，建议您现用现配) |
| 纯度 | HPLC≥97% |
| 级别 | Cell Culture |
| 外观(性状) | White to off-white Solid |
| 储存条件 | Powder:-20℃，1 year |
| 运输条件 | 冷藏运输 |
| MDL | MFCD00133076 |
| SMILES | CC[C@H](C)[C@@H](C(=O)N[C@@H]([C@@H](C)CC)C(=O)NCC(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CCSC)C(=O)O)NC(=O)[C@H](C)NC(=O)CNC(=O)[C@H](CCCCN)NC(=O)[C@H](CC(=O)N)NC(=O)[C@H](CO)NC(=O)CN |
| InChIKey | WIHBNMPFWRHGDF-SLVFWPMISA-N |
| InChI | InChI=1S/C45H81N13O14S/c1-9-24(5)36(43(69)50-21-35(63)52-29(17-23(3)4)40(66)55-28(45(71)72)14-16-73-8)58-44(70)37(25(6)10-2)57-38(64)26(7)51-34(62)20-49-39(65)27(13-11-12-15-46)54-41(67)30(18-32(48)60)56-42(68)31(22-59)53-33(61)19-47/h23-31，36-37，59H，9-22，46-47H2，1-8H3，(H2，48，60)(H，49，65)(H，50，69)(H，51，62)(H，52，63)(H，53，61)(H，54，67)(H，55，66)(H，56，68)(H，57，64)(H，58，70)(H，71，72)/t24-，25-，26-，27-，28-，29-，30-，31-，36-，37-/m0/s1 |
| PubChem CID | 10843733 |
| 靶点 | Amyloid-β |
| 通路 | Neuronal Signaling |
| 背景说明 | β-Amyloid (25-35)是阿尔茨海默氏淀粉样蛋白β肽的Aβ(25-35) 片段。 |
| 生物活性 | β-Amyloid (25-35) (Amyloid beta-peptide (25-35)) is the fragment Aβ(25-35) of the Alzheimer‘s amyloid β-peptide， has shown neurotoxic activities in cultured cells.[1-5] |
| In Vitro | The amino acid sequence of Aβ(25-35) peptide is NH2-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-COOH， where the first Gly represents the amino acid 25 and the last Met represents the amino acid 35. Amyloid beta-peptide(25-35) is also investigated in gel state for the first time. Comparative studies are also carried out using vibrational absorption and ECD. The conformational preference of Aβ(25-35) peptide film is also investigated using vibrational absorption and VCD spectroscopy[1]. Amyloid beta-peptide(25-35) induces apoptotic effects on isolated brain mitochondria and the redox state of methionine-35， plays a key role in the induction of programmed cellular death pathways and toxic events[2].β-Amyloid Aggregation Guidelines (Following is our recommended protocol. This protocol only provides a guideline， and should be modified according to your specific needs). 1. Solid Aβ peptide was dissolved in cold hexafluoro-2-propanol (HFIP). The peptide was incubated at room temperature for at least 1h to establish monomerization and randomization of structure.2. The HFIP was removed by evaporation， and the resulting peptide was stored as a film at -20 or -80 ℃.3. The resulting film was dissolved in anhydrous DMSO at 5 mM and then diluted into the appropriate concentration and buffer (serum- and phenol red-free culture medium) with vortexing.4. Next， the solution was age 48h at 4-8 ℃. The sample was then centrifuged at 14000g for 10 min at 4-8 ℃; the soluble oligomers were in the supernatant. The supernatant was diluted 10-200-fold for experiments.Methods vary depends on the downstream applications.[1-5] |
| In Vivo | β-Amyloid (25-35) 可用于动物建模，构建阿尔茨海默病模型。β-Amyloid (25-35) 可用于动物建模，构建阿尔茨海默病模型[5]。致病原理β-Amyloid 大量沉积，使神经元内的 Ca2+ 浓度升高，而 Ca2+ 又参与调控Tau 蛋白磷酸化，Tau 蛋白的过度磷酸化造成了神经纤维缠结和神经元死亡，最后动物逐渐出现认知症状，并发展为阿尔茨海默病.造模成功指标分子变化：Aβ1-40蛋白增加； 丙二醛 (MDA) 增加； 海马 CA1 区 AChE 和 Bax 表达减少。认知变化：莫里斯水迷宫测试学习和记忆缺陷。 |
| 细胞实验 | Cell viability is determined by a modified MTS assay， which is based on the conversion of Tetrazolium salt by mitochondrial dehydrogenase to a formazan product spectrophotometrically measurable at 490 nm. PC12 cells are plated in 96-well plates at a density of 10 000 cells/well and maintained for 16 h in complete medium. Cells are then incubated in the absence (control) and presence of 40 μM Aβ(31-35) and Aβ(25-35) with reduced， oxidized and norleucine-substituted methionine-35 staurosporine 10 μM is used as positive control of 100% of cellular death. After 48 h of peptide-incubation， 20 μL of MTS reagent (2.0 mg/mL) is added to each well. The cells are then incubated for 30-45 min at 37 °C in a 5% CO2 incubator. The reaction is stopped by adding 25 μL of 10% SDS. The plates are read with a microplate reader at 490 nm. Each data point is obtained using a triplet-well assay[2]. |
| 动物实验 | Rats[3] Fifty-four Male Sprague-Dawley rats (2 months old， 300-350 g) are used. Amyloid beta-peptide(25-35) is dissolved in sterile distilled water at a concentration of 1 mg/mL as a stocking solution. Animals are infused with 5 μL/side of sterile distilled water (control)， aggregated Aβ25-35 (2 μg/μL)， into bilateral cerebral lateral ventricles at a rate of 1 μL/min; the needle is left in place for 5 min. Then the needles are removed and rats are kept on a warm pad until they are awakened. To determine the neuroprotective effect on AD rats， the Aβ25-35 treated rats are treated with CDS of different doses and Donepezil once daily for 23 days (including duration of behavior test). Experiment is performed to test the effect of CDS on Aβ25-35-induced memory impairment using Morris water-maze and step-through passive avoidance tasks. Specifically， all of the rats are randomly divided into 6 groups for the experiment: (a) Vehicle 1 (for Aβ25-35)+vehicle 2 (for CDS and Donepezil)， (b) Aβ25-35+vehicle 2， (c) Aβ25-35+CDS (130 mg/kg)， (d) Aβ25-35+CDS (260 mg/kg)， (e) Aβ25-35+CDS (520 mg/kg)， (f) Aβ25-35+Donepezil (0.5 mg/kg). One day after cerebroventricular microinfusions of Aβ25-35 (10 μg/side) or its vehicle， rats are treated (i.g.) with CDS or Donepezil or vehicle 2， once daily for 14 days prior to the beginning of Morris water maze， followed by passive avoidance task. |
| 数据来源文献 | [1]. D‘Ursi AM， et al. Solution structure of amyloid beta-peptide (25-35) in different media. J Med Chem. 2004 Aug 12;47(17):4231-8. [2]. Clementi ME， et al. Abeta(31-35) and Abeta(25-35) fragments of amyloid beta-protein induce cellular death throughapoptotic signals: Role of the redox state of methionine-35. FEBS Lett. 2005 May 23;579(13):2913-8. [3]. Liu M， et al. Cognitive improvement of compound danshen in an Aβ25-35 peptide-induced rat model of Alzheimer‘s disease. BMC Complement Altern Med. 2015 Oct 23;15:382. [4]. Patel NS， et al. Potent anti-angiogenic motifs within the Alzheimer beta-amyloid peptide. Amyloid. 2008;15(1):5-19. [5]. Julia Fedotova， et al. Ropren? is a polyprenol preparation from coniferous plants that ameliorates cognitive deficiency in a rat model of beta-amyloid peptide-(25–35)-induced amnesia. Phytomedicine. 2012 Mar 15;19(5):451-6. |
| 单位 | 瓶 |
| 1mM-5mg | 4.7158mL |
| 1mM-1mg | 0.9432mL |
| 1mM-10mg | 9.4316mL |
| 5mM-1mg | 0.1886mL |
| 5mM-5mg | 0.9432mL |
| 5mM-10mg | 1.8863mL |
| 10mM-1mg | 0.0943mL |
| 10mM-5mg | 0.4716mL |
| 10mM-10mg | 0.9432mL |
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| 纯度 | 品牌 | 规格 | 发货地 |
|---|---|---|---|
| - | 索莱宝 | 25mg / 100mg / 1g | 北京 |
