pep 2

Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor. Potent inhibitor of PCSK9 binding to LDL receptor (IC50 = 0.8 μM). Restores LDL uptake in HepG2 cells treated with PCSK9.

pep2-EVKI is an inhibitor peptide that selectively disrupts binding of the AMPA receptor subunit GluA2 (at the C-terminal PDZ site) to protein interacting with C kinase (PICK1). Does not affect binding of GluA2 to GRIP or ABP and does not increase AMPA current amplitude or affect long term depression (LTD).

Pep2-EVKI acetate is a cell-permeable peptide. Pep2-EVKI acetate interferes the interaction between protein interacting with C-kinase (PICK1) and GluR2 AMPA receptor subunits.

Pep2-8 is a peptide that has demonstrated enhanced antagonistic activity against proprotein convertase subtilin/kexin type 9 (PCSK9) [1].

Pep2 peptide, a peptide ligand for CD36 (transmembrane glycoprotein or scavenger receptor B2), exhibits selective binding to CD36 over human serum albumin (HSA), IgG, and CD44 in cell-free assays at 1 mM concentration. Pep2 peptide-functionalized micelles, when loaded with the anticancer agent doxorubicin, significantly enhance the cellular uptake and cytotoxicity of doxorubicin in HepG2 hepatocellular carcinoma cells that overexpress CD36, compared to micelles without Pep2 peptide.

Pep 2-8 ammonium salt is Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor. Potent inhibitor of PCSK9 binding to LDL receptor (IC50 = 0.8 μM). Restores LDL uptake in HepG2 cells treated with PCSK9.

pep2-AVKI is an inhibitor peptide that selectively disrupts binding of the AMPA receptor subunit GluA2 (at the C-terminal PDZ site) to protein interacting with C kinase (PICK1). Does not affect binding of GluA2 to GRIP or ABP and does not increase AMPA current amplitude or affect long term depression (LTD).

pep2-AVKI acetate(1315378-69-8 free base) An inhibitor peptide that selectively disrupts binding of the AMPA receptor subunit GluA2 (at the C-terminal PDZ site) to proteins that interact with C-kinase (PICK1). Does not affect GluA2 binding to GRIP or ABP, nor does it increase AMPA current amplitude or affect long-term depression (LTD).

Inhibitor peptide corresponding to last 10 amino acids of the C-terminus of the GluA2 AMPA receptor subunit. Disrupts binding of GluA2 (at the C-terminal PDZ site) with glutamate receptor interacting protein (GRIP), AMPA receptor binding protein (ABP) and

Pep2-SVKI acetate(pep2-SVKI acetate (328944-75-8 free base)) is a synthetic peptide salt that prevents internalization of AMPA-type glutamate receptor.

pep2m aceate is a Peptide inhibitor of the interaction between the C-terminus of the GluR2 subunit and N-ethylmaleimide-sensitive fusion protein

Myristoylated TFA Pep2m (Myr-Pep2m TFA) is a cell-permeable peptide that effectively disrupts the interactions between the protein kinase ζ (PKMζ) downstream targets—N-ethylmaleimide-sensitive factor/glutamate receptor subunit 2 (NSF/GluR2). PKMζ, an autonomously active isozyme of protein kinase C (PKC), plays a crucial role in these interactions [1] [2].

Cell-permeable, myristoylated form of pep2m. Peptide inhibitor of the interaction between the C-terminus of the GluA2 (AMPA receptor) subunit and N-ethylmaleimide-sensitive fusion protein (NSF), a protein that regulates AMPA receptor function. Reduces pos

Pep2m, myristoylated acetate is a Cell-permeable, myristoylated form of pep2m. Peptide inhibitor of the interaction between the C-terminus of the GluA2 (AMPA receptor) subunit and N-ethylmaleimide-sensitive fusion protein (NSF), a protein that regulates A

KRpep-2d, a potent inhibitor of K-Ras, effectively suppresses the proliferation of cancer cells driven by K-Ras. This compound is suitable for use in cancer research [1].

KRpep-2d (TFA) is a potent K-Ras inhibitor that effectively impedes the proliferation of K-Ras-driven cancer cells, making it a valuable asset for cancer research [1].

Angiopep-2 hydrochloride is a brain-targeting peptide vector. Conjugating anticancer agents to Angiopep-2 may enhance their therapeutic effect against brain cancer [1].

DiaPep277, a 24 amino acid peptide sourced from HSP60 positions 437-460, impedes β-cell destruction in NOD mice and modulates diabetogenic T-cell activity in animal diabetes models [1] [2].

KRPEP-2D acetate was identified as a K-Ras(G12D) selective inhibitory peptide against the G12D mutant of K-Ras, which is a key member of the Ras protein family and an attractive cancer therapeutic target.

Pep-20 is a CD47/SIRPα blocking peptide with KD values of 2.91 μM for human CD47 and 3.63 μM for mouse CD47. It inhibits the CD47/SIRPα interaction with IC50 values of 24.56 μM for humans and 12.03 μM for mice. Pep-20 also exhibits antitumor activity.