| Size | Price | Stock | Qty |
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| 5mg |
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| Targets |
K 01-162 targets beta-amyloid (Abeta) oligomers and fibrils, which are key pathological aggregates in Alzheimer's disease. The compound binds to and destabilizes AbetaO, inhibiting the formation of Abeta peptide fibrils and eliminating their neurotoxicity. It binds with Abeta42 peptide with an EC50 value of 80 nM and directly binds to AbetaO with a KD value of 19 microM. The compound stabilizes hydrophobic core I of the Abeta42 peptide (residues 17-21) to its alpha-helical conformation by interacting specifically in this region. K 01-162 also targets HDAC6-dependent signaling and is used to evaluate HDAC6 as a potential therapeutic target.
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| ln Vitro |
K 01-162 (1 μM; 24 hours) decreases intracellular AβO levels [2]. K 01-162 (0.78-50 μM; 5 minutes) blocks the synaptic binding activity of AβO in mouse hippocampus neurons [2].
In vitro studies have demonstrated that K 01-162 inhibits the fibril formation of Abeta peptides and eliminates their neurotoxicity. The compound binds with Abeta42 peptide with an EC50 value of 80 nM and binds directly to AbetaO with a KD value of 19 microM. The active drug candidate K162 (EC50 = 0.080 microM) stabilizes hydrophobic core I of the Abeta42 peptide to its alpha-helical conformation by interacting specifically in this region. The compound's ability to inhibit Abeta aggregation and neurotoxicity has been characterized in various cell-based and biochemical assays. |
| ln Vivo |
K 01-162 (100 μM; 0.25 μL/h intracerebroventricular infusion for 2 weeks) can reduce the body's amyloid load [2].
In vivo studies have shown that K 01-162 is capable of penetrating the brain and can reduce the brain amyloid burden that exists in both fibrillar and RIPA-soluble, non-fibrillar forms. The compound binds and destabilizes AbetaO in vivo, with an EC50 of 80 nM. These properties make K 01-162 a valuable tool for studying Alzheimer's disease in animal models. However, detailed in vivo efficacy data, including dose-response relationships and effects on cognitive function, are not widely available in the published literature. |
| Enzyme Assay |
The in vitro binding assays for K 01-162 typically involve measuring the compound's affinity for Abeta42 peptide and Abeta oligomers using techniques such as surface plasmon resonance, fluorescence polarization, or isothermal titration calorimetry. In these assays, the compound is incubated with Abeta42 peptide or AbetaO, and binding affinity is determined. The EC50 for inhibition of Abeta fibril formation is determined using Thioflavin T fluorescence assays, where the compound's ability to inhibit Abeta aggregation is measured. These assays are standard for characterizing Abeta-targeting compounds.
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| Cell Assay |
Western Blot Analysis[2]
Cell Types: MC65 Cell Line Tested Concentrations: 1 μM Incubation Duration: 24 hrs (hours) Experimental Results: diminished levels of SDS-stabilized Aβ trimers and larger aggregates. Cellular assays for K 01-162 are conducted using neuronal cell lines or primary neurons treated with Abeta peptides. Cells are treated with varying concentrations of K 01-162, and Abeta-induced neurotoxicity is assessed by measuring cell viability, apoptosis markers, and neurite degeneration. The compound's ability to eliminate Abeta neurotoxicity is confirmed by comparing cell viability in the presence and absence of the compound. These cell-based assays confirm the compound's neuroprotective activity and provide insights into its mechanism of action in preventing Abeta-induced neuronal damage. |
| Animal Protocol |
Animal/Disease Models: 5xFAD mice with cerebral Aβ amyloidosis [2]
Doses: 100 μM Route of Administration: intracerebroventricular infusion; 100 μM 0.25 μL/h; continued for 2 weeks Experimental Results: No obvious toxicity was caused, and hippocampus The amyloid burden was Dramatically diminished to 50% of simulated treatment levels. In vivo animal studies for K 01-162 are conducted in transgenic mouse models of Alzheimer's disease that express human amyloid precursor protein and develop Abeta plaques. The compound is administered orally or by injection, and its ability to penetrate the brain and reduce amyloid burden is assessed. Brain amyloid burden is measured using biochemical assays and immunohistochemistry. Cognitive function may also be assessed using behavioral tests. These studies confirm the compound's in vivo efficacy and support its potential as a therapeutic agent for Alzheimer's disease. |
| ADME/Pharmacokinetics |
K 01-162 has a molecular weight of 288.18 and a molecular formula of C15H14BrN. The compound is soluble in DMSO at 10 mM. For research use, K 01-162 is typically stored as powder at -20degC for up to 3 years or at 4degC for up to 2 years, and in solvent at -80degC for up to 1 year. The compound is capable of penetrating the brain, which is a critical property for studying central nervous system disorders such as Alzheimer's disease. Detailed pharmacokinetic parameters such as half-life, bioavailability, and tissue distribution have been characterized in preclinical studies.
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| Toxicity/Toxicokinetics |
Toxicological data for K 01-162 are limited. As a research compound, K 01-162 has been evaluated in animal models at doses that produce pharmacological effects without significant toxicity. However, systematic toxicological evaluations have not been published. The compound is for research use only and not for human therapeutic use. Standard safety precautions should be followed when handling the compound, and researchers should consult the Safety Data Sheet (SDS) for specific safety information.
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| References | |
| Additional Infomation |
K 01-162 (K162) is a research compound developed as an inhibitor of beta-amyloid aggregation for the study of Alzheimer's disease. It has a molecular formula of C15H14BrN and a molecular weight of 288.18. The compound binds to Abeta42 peptide with an EC50 of 80 nM and to AbetaO with a KD of 19 microM. K 01-162 inhibits Abeta fibril formation, eliminates neurotoxicity, and is capable of penetrating the brain. The compound is not approved for clinical use and is available only for research purposes in neurodegeneration and Alzheimer's disease research.
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| Molecular Formula |
C15H14NBR
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| Molecular Weight |
288.18236
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| Exact Mass |
287.031
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| CAS # |
677746-25-7
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| PubChem CID |
24858056
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| Appearance |
White to off-white solid powder
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| LogP |
4.086
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| Hydrogen Bond Donor Count |
0
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| Hydrogen Bond Acceptor Count |
1
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| Rotatable Bond Count |
1
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| Heavy Atom Count |
17
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| Complexity |
278
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
KABXKWWJTYSDTD-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C15H14BrN/c1-17(2)13-4-6-15-11(9-13)7-10-8-12(16)3-5-14(10)15/h3-6,8-9H,7H2,1-2H3
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| Chemical Name |
7-bromo-N,N-dimethyl-9H-fluoren-2-amine
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~14.29 mg/mL (~49.59 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: 1.43 mg/mL (4.96 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 14.3 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 1.43 mg/mL (4.96 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 14.3 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 1.43 mg/mL (4.96 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 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 |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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