| MDL | - |
|---|---|
| Molecular Weight | 288.18 |
| Molecular Formula | C15H14BrN |
| SMILES | BrC1=CC(CC2=C3C=CC(N(C)C)=C2)=C3C=C1 |
K 01-162 (K162) inhibits the fibril formation of A β peptides and eliminates their neurotoxicity. K 01-162 binds with A β 42 peptide with an EC 50 value of 80 nM. K 01-162 binds directly to AβO with a K D value of 19 μM. K 01-162 is capable of penetrating the brain and can be used for the research of Alzheimer’s disease [1] [2] .
K 01-162 (1 μM; 24 h) reduces the level of intracellular AβO
[2]
.
K 01-162 (0.78-50 μM; 5 min) blocks the synaptic binding activity of AβO in mouse hippocampal neurons
[2]
.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Western Blot Analysis [2]
| Cell Line: | MC65 cell line |
| Concentration: | 1 μM |
| Incubation Time: | 24 hours |
| Result: | Reduced the levels of SDS-stable Aβ trimer and larger aggregates. |
K 01-162 (100 μM; intracerebroventricular infusion 0.25 μL/h for 2 weeks) attenuates amyloid load in vivo [2] .
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
| Animal Model: | 5xFAD mice with cerebral Aβ amyloidosis [2] |
| Dosage: | 100 μM |
| Administration: | Intracerebroventricular infusion; 100 μM 0.25 μL/h; for 2 weeks |
| Result: | Caused no apparent toxicity and significantly reduced the amyloid load in hippocampus to 50% of the mock-treated level. |
Solid
Room temperature in continental US; may vary elsewhere.
| Powder | -20°C | 3 years |
|---|---|---|
| 4°C | 2 years | |
| In solvent | -80°C | 6 months |
| -20°C | 1 month |
DMSO : 14.29 mg/mL ( 49.59 mM ; Need ultrasonic)
| Concentration Solvent Mass | 1 mg | 5 mg | 10 mg |
|---|
| 1 mM | 3.4701 mL | 17.3503 mL | 34.7005 mL |
| 5 mM | 0.6940 mL | 3.4701 mL | 6.9401 mL |
| 10 mM | 0.3470 mL | 1.7350 mL | 3.4701 mL |