aβ25-35

β-Amyloid (25-35) is a fragment of the Alzheimer’s amyloid beta peptide Aβ(25-35), exhibiting neurotoxic effects and commonly used to establish both cellular and animal models of Alzheimer’s disease.

β-Amyloid (25-35) acetate is the Aβ(25-35) fragment of amyloid beta peptide, exhibiting neurotoxicity and commonly employed in constructing Alzheimer's disease cell and animal models.

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)) is the fragment Aβ(25-35) of the Alzheimer's amyloid β-peptide.

[Ala28]-β Amyloid(25-35) (β(25-35)KA), an electrically neutral mutant variant of Aβ(25-35), facilitates the accelerated aggregation of Firefly Luciferase [1].

FITC-β-Amyloid (25-35) is a FITC-labeled β-Amyloid (25-35) . FITC is a green fluorescent probe used for labeling biomolecules, while β-Amyloid (25-35) is a neurotoxic amyloid beta peptide fragment associated with Alzheimer's disease.

L-Clausenamide is an alkaloid extracted from the leaves of the yellow bark (Clausena lansium (Lour) skeels) and can be used to improve cognitive function. L-Clausenamide inhibits beta-amyloid (Aβ) toxicity and prevents the formation of neurofibrillary tangles by inhibiting tau phosphorylation. L-Clausenamide has neuroprotective activity and can be used to modulate stimuli triggered by Aβ25-35. L-Clausenamide can be used to study neurological disorders like Alzheimer's disease.

Caffeic acid 4-O-glucoside (Linocaffein), a glycosylation product of Caffeic acid, reverses Aβ25-35-induced axonal atrophy and induces axonal regeneration in mouse cortical neurons, and can be used in Alzheimer's disease research.

(3R,5R)-Octahydrocurcumin (Compound 7) is a metabolite of Curcumin produced by gut microbiota. It exhibits neuroprotective effects against Aβ25-35-induced cell damage in SH-SY5Y cells and possesses anti-inflammatory properties in LPS-stimulated BV-2 mouse microglia.

BChE-IN-22 (compound 5A) is a selective eqBChE inhibitor with an IC50 of 0.53 μM, known for its anti-inflammatory and neuroprotective properties. It can inhibit cell damage induced by Aβ25-35 and improve cognitive impairment caused by Scopolamine.

PROTACGSK-3β Degrader-1 (compound 1) is a degrader targeting GSK-3β with an IC50 of 833 nM. This compound consists of SB-216763 (a GSK-3β inhibitor), a PEG linker, and CRBN (E3 ligase ligand). It reduces neurotoxicity induced by Aβ25-35 peptide and CuSO4 and is applicable in Alzheimer's disease research.

Gypenoside XVII (Gynosaponin S) confers protection against Aβ25-35-induced neurotoxicity through estrogen receptor-dependent activation of PI3K/Akt pathways, activation of Nrf2/ARE/HO-1 and inactivation of GSK-3β pathways.

SAR502250 is a potent, selective, ATP-competitive, orally active, and brain-penetrant GSK3 inhibitor with a human GSK-3β IC50 value of 12 nM, exhibiting antidepressant-like activity and being researched for potential application in Alzheimer's disease (AD) treatment.

RAGE/SERT-IN-1 is a potent, orally active inhibitor of advanced glycation end products (RAGE) and serotonin transporter (SERT), with IC50 values of 8.26 μM and 31.09 nM, respectively. It demonstrates significant neuroprotective effects against Aβ25-35-induced neuronal damage and alleviates depressive behavior in mice. RAGE/SERT-IN-1 is useful for research on the comorbidity of Alzheimer's disease and depression [1].

eeAChE/eqBuChE-IN-1 (compound 3F) serves as a reversible dual inhibitor of eeAChE/eqBuChE, exhibiting IC50 values of 1.3 μM and 0.81 μM, respectively. In addition, this compound demonstrates anti-inflammatory properties and provides neuroprotective effects against Aβ25-35-induced injury in PC12 cells [1].

Gypenoside XVII (Standard) is a reference standard for research and analysis in studies involving Gypenoside XVII. Gypenoside XVII (Gynosaponin S) confers protection against Aβ25-35-induced neurotoxicity through estrogen receptor-dependent activation of PI3K/Akt pathways, activation of Nrf2/ARE/HO-1 and inactivation of GSK-3β pathways.

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