LY2886721
≥99%
- Product Code: 202272
CAS:
1262036-50-9
Molecular Weight: | 390.41 g./mol | Molecular Formula: | C₁₈H₁₆F₂N₄O₂S |
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Density: | Storage Condition: | -20°C |
Product Description:
LY2886721 is a potent and selective inhibitor of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), which plays a key role in the production of amyloid-beta peptides. These peptides are central to the formation of amyloid plaques found in the brains of Alzheimer’s disease patients. By inhibiting BACE1, LY2886721 reduces the generation of amyloid-beta, making it a candidate for disease-modifying therapy in early-stage Alzheimer’s disease.
The compound was investigated in clinical trials to evaluate its safety, pharmacokinetics, and ability to lower amyloid-beta levels in cerebrospinal fluid. Although development was discontinued due to safety concerns observed in later stages, LY2886721 contributed valuable data on BACE1 inhibition as a therapeutic strategy. It helped validate BACE1 as a pharmacological target and informed the design of future Alzheimer’s treatments aimed at reducing amyloid burden in the brain.
Sizes / Availability / Pricing:
Size | Availability | Price | Quantity |
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5mg | 10-20 days | ฿7,180.00 |
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10mg | 10-20 days | ฿12,220.00 |
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LY2886721
LY2886721 is a potent and selective inhibitor of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), which plays a key role in the production of amyloid-beta peptides. These peptides are central to the formation of amyloid plaques found in the brains of Alzheimer’s disease patients. By inhibiting BACE1, LY2886721 reduces the generation of amyloid-beta, making it a candidate for disease-modifying therapy in early-stage Alzheimer’s disease.
The compound was investigated in clinical trials to evaluate its safety, pharmacokinetics, and ability to lower amyloid-beta levels in cerebrospinal fluid. Although development was discontinued due to safety concerns observed in later stages, LY2886721 contributed valuable data on BACE1 inhibition as a therapeutic strategy. It helped validate BACE1 as a pharmacological target and informed the design of future Alzheimer’s treatments aimed at reducing amyloid burden in the brain.
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