AD-35
AD-35 is an orally active, blood-brain barrier-permeable acetylcholinesterase inhibitor with an IC50 of 793 nM. AD-35 inhibits metal-induced amyloid-β aggregation and disassembles preformed amyloid-β aggregates. In rat models of cognitive impairment, AD-35 attenuates Aβ25-35-induced astrocyte activation, TNF-α and IL-1β release, inhibits ERK phosphorylation, and alleviates learning and memory deficits. AD-35 can be used for research on Alzheimer's disease.
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- No. CAS: 1531586-64-7
- Fòrmula: C24H30N3O7P
- Peso molecular:503.48
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Almacenamiento:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Actividad biológica
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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) 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) effectively chelates Cu2+ and Fe3+ in vitro, but exhibits extremely weak chelating activity towards Zn2+[1].
AD-35 (6-10 μM; 5 h) weakly promotes Cu2+ transport into human neuroblastoma SH-SY5Y cells in vitro[1].
AD-35 (24 h) 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.
| NCT Number | Sponsor | Condition | Start Date |
Phase
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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No. CAS 1531586-64-7
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Peso molecular 503.48
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Fòrmula C24H30N3O7P
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SMILES
O=C(N(CCC1CCN(CC2=CC=CC=N2)CC1)C34CC4)C(C3=C5)=CC6=C5OCO6.OP(O)(O)=O
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureza y Documentación
Referencias
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
AD-35 Related Classifications
HY-117710B Related Classifications
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