339990-02-2

Basic information

• Product Name: AC-LEU-PRO-PHE-PHE-ASP-NH2
• Synonyms: IAB5P PRO18 ASP21;IA-BETA5P;BETA-SHEET BREAKER PEPTIDE IA-BETA5P;AMYLOID BETA42 FIBRILLOGENESIS INHIBITOR III;AC-LPFFD-NH2;AC-LEU-PRO-PHE-PHE-ASP-NH2;A-BETA (1-42) FIBRILLOGENESIS INHIBITOR;A-BETA (1-42) FIBRILLOGENESIS INHIBITOR, IA-BETA5P
• CAS NO: 339990-02-2
• Molecular Formula: C35H46N6O8
• Molecular Weight: 678.78
• Product Categories: peptide
• Mol File: 339990-02-2.mol
• Article Data: 1

Chemical Properties

• Boiling Point: 1107.4±65.0 °C(Predicted)
• Appearance: /
• Density: 1.268±0.06 g/cm3(Predicted)
• PKA: 4.07±0.10(Predicted)
• CAS DataBase Reference: AC-LEU-PRO-PHE-PHE-ASP-NH2(CAS DataBase Reference)
• NIST Chemistry Reference: AC-LEU-PRO-PHE-PHE-ASP-NH2(339990-02-2)
• EPA Substance Registry System: AC-LEU-PRO-PHE-PHE-ASP-NH2(339990-02-2)

Safety Data

• Hazardous Substances Data: 339990-02-2(Hazardous Substances Data)

Usage

General Description

AC-LEU-PRO-PHE-PHE-ASP-NH2 is a synthetic peptide composed of the amino acids leucine, proline, phenylalanine, and aspartic acid, with an amidated carboxyl group at the C-terminus. This peptide is commonly used in research and pharmaceutical applications due to its potential biological activity and role in studying protein-protein interactions. It may also have potential therapeutic applications in the treatment of diseases and conditions related to hormone regulation, neural signaling, and immune response. Additionally, AC-LEU-PRO-PHE-PHE-ASP-NH2 may be used in the development of drug delivery systems and targeted therapies for various medical conditions.

Upstream product

• 35661-60-0 Fmoc-Leu-OH 
• 71989-31-6 Fmoc-Pro-OH 
• 35661-40-6 N-Fmoc L-Phe 
• 71989-14-5 Fmoc-(tBu)Asp-OH 
• 108-24-7 acetic anhydride 

Relevant articles and documents

Protective effects of β-sheet breaker α/β-hybrid peptide against amyloid β-induced neuronal apoptosis in vitro

Alzheimer's disease is most common neurodegenerative disorder and is characterized by increased production of soluble amyloid-β oligomers, the main toxic species predominantly formed from aggregation of monomeric amyloid-β (Aβ). Increased production of Aβ invokes a cascade of oxidative damages to neurons and eventually leads to neuronal death. This study was aimed to investigate the neuroprotective effects of a β-sheet breaker α/β-hybrid peptide (BSBHp) and the underlying mechanisms against Aβ40-induced neurotoxicity in human neuroblastoma SH-SY5Y cells. Cells were pretreated with the peptide Aβ40 to induce neurotoxicity. Assays for cell viability, cell membrane damage, cellular apoptosis, generation of reactive oxygen species (ROS), intracellular free Ca2+, and key apoptotic protein levels were performed in vitro. Our results showed that pretreatment with BSBHp significantly attenuates Aβ40-induced toxicity by retaining cell viability, suppressing generation of ROS, Ca2+ levels, and effectively protects neuronal apoptosis by suppressing pro-apoptotic protein Bax and up-regulating antiapoptotic protein Bcl-2. These results suggest that α/β-hybrid peptide has neuroprotective effects against Aβ40-induced oxidative stress, which might be a potential therapeutic agent for treating or preventing neurodegenerative diseases.