AD-35 free base
AD-35 free base is an orally active, blood-brain barrier-permeable acetylcholinesterase inhibitor with an IC50 of 793 nM. AD-35 free base inhibits metal-induced amyloid-β aggregation and disassembles preformed amyloid-β aggregates. In rat models of cognitive impairment, AD-35 free base attenuates Aβ25-35-induced astrocyte activation, TNF-α and IL-1β release, inhibits ERK phosphorylation, and alleviates learning and memory deficits. AD-35 free base can be used for research on Alzheimer's disease.
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- CAS. Nr.: 1531586-58-9
- Formel: C24H27N3O3
- Molecular Weight:405.50
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
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Biologische Aktivität
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AChE 793 nM (IC50) |
IL-1β |
TNF-α |
AD-35 (pre-incubated for 10 min, incubated with substrate for 15 min) free base moderately inhibits purified acetylcholinesterase (IC50 = 793 nM) and butyrylcholinesterase (IC50 = 31428 nM) in vitro, and exhibits activity preference for acetylcholinesterase[1].
AD-35 (20 μM; 10 min) free base effectively chelates Cu2+ and Fe3+ in vitro, but exhibits extremely weak chelating activity towards Zn2+[1].
AD-35 (6-10 μM; 5 h) free base weakly promotes Cu2+ transport into human neuroblastoma SH-SY5Y cells in vitro[1].
AD-35 (24 h) free base potently inhibits Cu2+-induced Aβ1-42 aggregation in a concentration-dependent manner in vitro, exerts only weak inhibitory effects on the spontaneous aggregation of Aβ1-42, and effectively disassembles preformed Cu2+-induced Aβ1-42 aggregates[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley (SD) (male, 8-10 weeks old, 260-280 g, intracerebroventricular injection of aggregated Aβ25-35 peptide)[1]
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Dosage:0.5 mg/kg; 3 mg/kg; 10 mg/kg
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Administration:p.o.; daily; 28 days
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Result:Prolonged step-down latency and decreased error times dose-dependently in Aβ25-35-injected rats, with complete reversal of Aβ-induced deficits at 10 mg/kg.
Shortened escape latency during 5-day training.
Improved spatial memory in probe trials: 0.5 mg/kg group spent 28.7% of time in target quadrant, 3 mg/kg group spent 38.2%, 10 mg/kg group spent 29.7%, all exceeding 25% chance level.
Normalized time spent in target quadrant (22.91 s) and escape latency to platform (15.43 s) at 3 mg/kg relative to sham controls.
Reduced Aβ-induced TNF-α overexpression in the hippocampus dose-dependently, with significant reduction at 10 mg/kg.
Markedly inhibited Aβ-induced IL-1β overexpression in the hippocampus at all tested doses.
Suppressed Aβ-induced GFAP expression in the cortex and hippocampus.
Inhibited Aβ-induced ERK phosphorylation in the hippocampus dose-dependently.
Chemical Information
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CAS. Nr. 1531586-58-9
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Molecular Weight 405.50
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Formel C24H27N3O3
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SMILES
O=C1C2=CC=3OCOC3C=C2C4(N1CCC5CCN(CC6=NC=CC=C6)CC5)CC4
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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