aβ25-35

β-Amyloid (25-35) (Aβ25-35) 是一种阿尔茨海默氏淀粉样蛋白β肽的Aβ(25-35) 片段，在培养细胞中显示出神经毒性作用。

Amyloid-β (25-35) (Aβ (25-35)) is an 11-residue fragment of the Aβ protein that retains the physical and biological characteristics of the full length peptide. It forms fibrils that react to thioflavin T and Congo red and are organized in a cross-β arrangement of β-strands similar to Aβ (1-40) and Aβ (1-42) fibrils. Aggregated Aβ (25-35) decreases the viability of rat adrenal PC12 cells. It also decreases the viability of primary rat cortical neurons at concentrations ranging from 1 nM to 30 μM. In vivo, intracerebral injection of Aβ (25-35) (20 nmol) in rats induces lesions of neuronal and tissue loss. Aggregated Aβ (25-35) administered intracerebroventricularly to rats induces learning and memory impairments in the Y-maze, novel object recognition, and contextual fear conditioning tests.

GSNKGAIIGLM(131602-53-4(free base)) (Amyloid beta-peptide(25-35)) 是阿尔茨海默病淀粉样蛋白 β-肽的片段 Aβ(25-35)。

[Ala28]-β Amyloid(25-35) (β(25-35)KA)为Aβ(25-35)的一种电中性变体，能够促进萤火虫荧光素酶聚集。

L-Clausenamide 是从黄皮 (Clausena lansium (Lour) skeels) 的树叶中提取出来的生物碱，可用于提高认知功能。L-Clausenamide 对β-淀粉样蛋白 (Aβ) 毒性有抑制作用，通过抑制 tau 蛋白磷酸化阻止神经纤维缠结的形成。L-Clausenamide 具有神经保护活性，可用于调节 Aβ25-35 引发的刺激。L-Clausenamide 可用于研究阿尔兹海默症类的神经系统疾病。

Caffeic acid 4-O-glucoside(Linocaffein)是Caffeic acid的糖基化产物，逆转Aβ25-35诱导的轴突萎缩和诱导小鼠皮质神经元轴突再生，可用于阿尔茨海默病研究。

(3R,5R)-Octahydrocurcumin (Compound 7) 是 Curcumin 经肠道菌群代谢后的产物。在 SH-SY5Y 细胞中，(3R,5R)-Octahydrocurcumin 显示出对 Aβ25-35 诱导的细胞损伤的神经保护作用，并在 LPS 刺激的 BV-2 小鼠小胶质细胞中表现出抗炎特性。

Gypenoside XVII (Gynosaponin S) 是一种绞股蓝皂甙类的新型植物雌激素，能够激活雌激素受体。

SAR502250 is a potent, selective, ATP competitive, orally active and brain-penetrant inhibitor of GSK3, with an IC50 of 12 nM for human GSK-3β. SAR502250 displays antidepressant-like activity. SAR502250 can be used for the research of Alzheimer’s disease (AD)[1][2]. SAR502250 (0.01-1 μM; 36 h) attenuates the Aβ25-35-induced cell death in rat embryonic hippocampal neurons[2]. SAR502250 (1-100 mg kg; a single p.o,) attenuates tau hyperphosphorylation in the cortex and spinal cord of transgenic mice expressing P301L tau[2].SAR502250 (10-30 mg kg; p.o. once daily for 7 weeks) improves the cognitive deficit in transgenic APP(SW) Tau(VLW) mice after infusion of Aβ25-35[2].SAR502250 (10-30 mg kg; a single p.o.) significantly increases the percentage of lever-presses in the inter-response time (IRT) bin (49-96 s), with a significant augmentation of the percentage of reinforced responses[2].SAR502250 (30 mg kg; i.p. once daily for 28 d) ameliorates chronic stress-induced degradation of the physical state of the mice coat[2].SAR502250 (10-60 mg kg; a single p.o.) decreases hyperactivity produced by psychostimulantsin mice[2]. [1]. Fukunaga K, et, al. 2-(2-Phenylmorpholin-4-yl)pyrimidin-4(3H)-ones; a new class of potent, selective and orally active glycogen synthase kinase-3β inhibitors. Bioorg Med Chem Lett. 2013 Dec 15;23(24):6933-7.[2]. Griebel G, et, al. The selective GSK3 inhibitor, SAR502250, displays neuroprotective activity and attenuates behavioral impairments in models of neuropsychiatric symptoms of Alzheimer’s disease in rodents. Sci Rep. 2019 Dec 2;9(1):18045.

RAGE SERT-IN-1 是一种 RAGE 和 SERT 抑制剂，口服活性良好，IC50 分别为 8.26 μM 和 31.09 nM。它对 Aβ25-35 诱发的神经元损伤具有显著神经保护效果，并可缓解小鼠抑郁症状。RAGE SERT-IN-1 适用于阿尔茨海默病与抑郁症并发症的研究。

eeAChE eqBuChE-IN-1（compound 3F）是一款可逆的eeAChE eqBuChE双重抑制剂，IC50值为1.3 μM和0.81μM。该化合物不仅展现出抗炎活性，还能对Aβ25-35诱导的PC12细胞损伤提供神经保护。

Neuropeptide Y (29-64), amide, human (TFA) is involved in Alzheimer's disease (AD) and protects rat cortical neurons against β-Amyloid toxicity.It is showed that Neuropeptide Y (29-64), amide, human (TFA) is able to protect cortical neurons from Aβ25-35 t