| Bioactivity | K 01-162 (K162) inhibits the fibril formation of Aβ peptides and eliminates their neurotoxicity. K 01-162 binds with Aβ42 peptide with an EC50 value of 80 nM. K 01-162 binds directly to AβO with a KD 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]. | ||||||||||||
| Invitro | 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]. Western Blot Analysis[2] Cell Line: | ||||||||||||
| In Vivo | K 01-162 (100 μM; intracerebroventricular infusion 0.25 μL/h for 2 weeks) attenuates amyloid load in vivo[2]. Animal Model: | ||||||||||||
| Name | K 01-162 | ||||||||||||
| CAS | 677746-25-7 | ||||||||||||
| Formula | C15H14BrN | ||||||||||||
| Molar Mass | 288.18 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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| Reference | [1]. Li J, et al. Alzheimer's disease drug candidates stabilize A-β protein native structure by interacting with the hydrophobic core. Biophys J. 2011 Feb 16;100(4):1076-82. [2]. Hong HS, et al. Candidate anti-A beta fluorene compounds selected from analogs of amyloid imaging agents. Neurobiol Aging. 2010 Oct;31(10):1690-9. |