SML1132
Pep2-8 trifluoroacetate salt
≥95% (HPLC), contains 58μL of solution at 10mM in DMSO
Synonym(s):
Ac-TVFTSWEEYLDWV-NH2 trifluoroacetate salt, Ac-TVFTSWEEYLDWV-amide trifluoroacetate salt, Ac-Thr-Val-Phe-Thr-Ser-Trp-Glu-Glu-Tyr-Leu-Asp-Trp-Val-NH2 trifluoroacetate salt
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About This Item
Empirical Formula (Hill Notation):
C83H110N16O24 · xC2HF3O2
Molecular Weight:
1715.85 (free base basis)
UNSPSC Code:
12352200
NACRES:
NA.77
Recommended Products
Assay
≥95% (HPLC)
form
solution
color
colorless to pale yellow
shipped in
wet ice
storage temp.
−20°C
Amino Acid Sequence
Ac-Thr-Val-Phe-Thr-Ser-Trp-Glu-Glu-Tyr-Leu-Asp-Trp-Val-NH2 trifluoroacetate salt
Biochem/physiol Actions
Pep2-8 is a potent PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitor that selectively binds to PCSK9 and interferes with LDL receptor binding to PCSK9. Pep2-8 restores LDL receptor function and LDL uptake of PCSK9-treated HepG2 cells.
Pep2-8, a good mimic of epidermal growth factor precursor homology domain A (EGF-A), serves as a competitive inhibitor of low-density lipoprotein (LDL) receptor binding. It can be used as an anchor peptide in phage-display experiments to bind an extension peptide library to the groove site.
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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Yingnan Zhang et al.
The Journal of biological chemistry, 289(2), 942-955 (2013-11-15)
PCSK9 (proprotein convertase subtilisin/kexin type 9) is a negative regulator of the hepatic LDL receptor, and clinical studies with PCSK9-inhibiting antibodies have demonstrated strong LDL-c-lowering effects. Here we screened phage-displayed peptide libraries and identified the 13-amino acid linear peptide Pep2-8
Yingnan Zhang et al.
Nature structural & molecular biology, 24(10), 848-856 (2017-08-22)
Proprotein convertase subtilisin/kexin type 9 (PCSK9) regulates plasma LDL cholesterol (LDL-c) levels by promoting the degradation of liver LDL receptors (LDLRs). Antibodies that inhibit PCSK9 binding to the EGF(A) domain of the LDLR are effective in lowering LDL-c. However, the
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