期刊
INTERNATIONAL JOURNAL OF PEPTIDE RESEARCH AND THERAPEUTICS
卷 14, 期 3, 页码 223-227出版社
SPRINGER
DOI: 10.1007/s10989-008-9136-1
关键词
peptoids; angiogenesis; VEGF receptor; immune response; antigen
资金
- National Heart, Lung, and Blood Institute [NO1-HV-28185]
- Welch Foundation [I-1299]
We have recently reported a peptoid (N-alkyl-oligoglycine) molecule that binds to the Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) with high affinity and specificity. Moreover, this peptoid is capable of inhibiting VEGFR2 function in vivo (Udugamasooriya et al. J Am Chem Soc 130:5744-5745, 2008) and thus is a lead compound for anti-angiogenic agents. Moreover, the assay developed to identify this VEGFR2 inhibitor is likely to be a general route to peptoid antagonists or agonists of integral membrane receptors. Therefore, it is important to determine whether the VEGFR2-targeted peptoid, and indeed peptoids in general, are inherently immunogenic since an anti-peptoid immune response would significantly complicate their development as therapeutic candidates. In this study, the VEGFR2-targeted peptoid as well as other peptoids of varying lengths were injected into mice along with an immunostimulatory agent. We demonstrate that no significant anti-peptoid immune response is induced. It is further shown that this is not a trivial result of the lack of immunogenicity of a particular peptoid sequence, since conjugation of the peptoids to carrier proteins such as KLH prior to injection induces a robust anti-peptoid immune response. We conclude that free peptoid molecules are not immunogenic, probably due to a lack of T cell epitopes and that peptoid-based therapeutics are therefore not likely to be hindered by anti-peptoid antibody production in most cases.
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