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|CAT#||Product Name||M.W||Molecular Formula||Inquiry|
|10-101-212||Thymosin β4 (1-4)||487.5||C20H33N5O9||Inquiry|
|10-101-239||Annexin A1 (1-25) (dephosphorylated) (human)||3089.43||C141H210N32O44S||Inquiry|
|10-101-269||C-Reactive Protein (CRP) (77-82)||560.61||C23H40N6O10||Inquiry|
|10-101-270||C-Reactive Protein (CRP) (174-185)||1276.51||C62H93N13O16||Inquiry|
|10-101-280||β-Casomorphin (1-7), bovine||789.92||C41H55N7O9||Inquiry|
|10-101-290||Fibrinopeptide B, human||1552.6||C66H93N19O25||Inquiry|
|10-101-292||Leptin Fragment 116-130 Amide mouse||1560.7||C64H109N19O24S||Inquiry|
Peptide inhibitors have the advantages of high affinity and specificity, low production cost, etc., and have attracted the attention of researchers.
Phage display technology is an efficient biological panning method that uses targets to screen high-affinity peptides and antibodies from libraries. Kotraiah et al. reported that four high-affinity phage clones were screened using recombinant human PD-1 protein, and the peptide sequence displayed on the surface of the phage was chemically synthesized to obtain PD-1 peptide. In vitro experiments proved that PD-1 peptide can bind to human PD-1 receptor and block PD-L1 binding; molecular simulation results showed that PD-1 peptide can bind to specific sites of PD-1 to exert biological activity. In vivo experiments proved that, PD-1 peptide had anti-melanoma metastasis ability similar to PD-1 mAb, increased the survival rate of lethal sepsis in mice, and can also be used as an immune adjuvant to improve the protective efficacy of preventive malaria vaccines. In addition, computer-aided peptide inhibitor design and peptide or peptidomimetic inhibitors designed based on PD1/PD-L1 functional fragments are also in progress.
The role of CCR5 and gp120 has made it an attractive target for anti-HIV-1 drug research. Some polypeptides derived from the extracellular region of CCR5 and some antibodies can selectively interact with the surface glycoprotein of the virus and have the effect of inhibiting the fusion of the virus with cells. Yu Yong et al. designed a series of peptide analogues based on the crystal structure of a monoclonal antibody 17b that directly interacts with gp120, and selected a peptide P20 from them. By testing the ability of the polypeptide to inhibit virus entry, it was found that P20 has a significant ability to inhibit the entry of R5 HIV-1 into human peripheral blood mononuclear cells (PBMC), and had no significant effect on the entry of R4 HIV-1.
L-JNK Peptide Inhibitor competitively blocks the interaction between JNK and c-Jun, thereby inhibiting the signaling events downstream of JNK, like c-Jun, ATF-2 and ELK1 phosphorylation. To convert JIP-1/IB-1 into cell permeable inhibitors of JNK (JNKI1) the minimal 20 amino acids inhibitory sequence of JIP-1/IB1 was covalently linked to the 10 amino acids recognized by TAT transporter. The L-JNKI1 is a potent inhibitor that is specific for JNK and can be used for in vitro applications.
It is worth noting that peptide inhibitors themselves also have disadvantages that need to be improved, such as instability in the body and poor membrane penetration ability. It has been reported in the literature that the combination of configuration transformation and nanotechnology can improve the efficacy of drugs. In addition, polypeptide structure modification, such as introduction of hydrophilic groups, side chain modification, cyclization, etc., can further improve its biological activity and druggability.
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