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血管内皮细胞生长因子（ＶＥＧＦ）结合酪氨酸激酶受体ＫＤＲ／ＦＬＫ１能促进血管形成．筛选能封闭ＶＥＧＦ与ＫＤＲ相互作用的小肽可以通过阻断血管形成而抑制实体瘤生长．将从噬菌体１２肽库中筛选而获得的能与ＫＤＲ结合的１２肽Ｋ２３７ ＤＮＡ克隆到表达载体ｐＱＥ４２中，在大肠杆菌Ｍ１５中稳定表达二氢叶酸还原酶融合蛋白ＤＨＦＲ－Ｋ２３７，经变性、复性后得到纯度达９０％的可溶性蛋白．体外实验显示，ＤＨＦＲ－ Ｋ２３７能竞争抑制ＶＥＧＦ结合ＫＤＲ，显著抑制由ＶＥＧＦ刺激而引起的人脐静脉内皮细胞增殖；体内实验表明，ＤＨＦＲ－Ｋ２３７能显著抑制鸡胚尿囊膜血管形成和荷瘤裸鼠中肿瘤的生长．结果表明，１２肽Ｋ２３７是ＶＥＧＦ结合ＫＤＲ的有效拮抗剂，具有抗肿瘤生长和转移的潜在应用前景．
Vascular endothelial growth factor (VEGF) binds tyrosine kinase receptor KDR / FLK1 to promote angiogenesis. Screening for small peptides that block the interaction of VEGF with KDR can inhibit the growth of solid tumors by blocking angiogenesis. The 12-mer K237 DNA capable of binding to KDR, obtained from the phage 12 peptide library, was cloned into the expression vector pQE42 and the dihydrofolate reductase fusion protein DHFR-K237 was stably expressed in E. coli M15. The degenerated and refolded After the purity of up to 90% of the soluble protein. In vitro experiments showed that DHFR-K237 could competitively inhibit the binding of VEGF to KDR and significantly inhibit the proliferation of human umbilical vein endothelial cells stimulated by VEGF. In vivo experiments showed that DHFR-K237 could significantly inhibit the formation of chorioallantoic membrane and tumor-bearing nude Tumor growth in mice. The results showed that the 12 peptide K237 is a potent antagonist of VEGF binding to KDR and has the potential application prospect of anti-tumor growth and metastasis.