LY2886721

≥99%

  • Product Code: 202272
  CAS:    1262036-50-9
Molecular Weight: 390.41 g./mol Molecular Formula: C₁₈H₁₆F₂N₄O₂S
EC Number: MDL Number:
Melting Point: Boiling Point:
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
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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