概要基本信息药物类型合成多肽别名-靶点VEGFR2作用方式拮抗剂作用机制VEGFR2拮抗剂(血管内皮细胞生长因子受体2拮抗剂)治疗领域肿瘤心血管疾病遗传病与畸形+ [3]在研适应症年龄相关性黄斑变性关节炎动脉粥样硬化+ [2]非在研适应症-原研机构Texas A&M University在研机构Texas A&M University非在研机构-权益机构-最高研发阶段临床前首次获批日期-最高研发阶段(中国)-特殊审评-关联100 项与 Peptide Lv 相关的临床结果登录后查看更多信息100 项与 Peptide Lv 相关的转化医学登录后查看更多信息100 项与 Peptide Lv 相关的专利（医药）登录后查看更多信息7 项与 Peptide Lv 相关的文献（医药）2025-05-27·INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCEPeptide Lv Deficiency Adversely Impacts the Structural and Functional Integrity of the Neural RetinaArticle作者: Ko, Gladys Yi-Ping ; Kuo, Lih ; Owusu-Ansah, Kofi ; Ko, Michael Lee ; Strong, Brower C. ; Liberoni, Lora ; Pham, Dylan L. ; Hein, Travis W. Purpose:Peptide Lv (PLv) is a small endogenous secretory peptide expressed in various organs, including the retina and brain. It augments the protein expression and current densities of the L-type voltage-gated calcium channels in photoreceptors, hence the name peptide "Lv." However, its physiological function in the neural retina remains unknown. This study aims to determine the role of PLv in the retina using PLv null (PLv-/-) mice.Methods:Both male and female PLv-/- and age-matched control (PLv+/+) littermates were assessed longitudinally. The retinal light responses were examined using dark-adapted electroretinography (ERG). The thicknesses for whole retinas and various retinal layers were evaluated through spectral-domain optical coherence tomography (SD-OCT) and hematoxylin and eosin staining of retinal sections.Results:Dark-adapted ERG a-wave, b-wave, and oscillatory potentials were compromised in PLv-/- mice, which were more severe in females at younger ages. The whole retina and outer nuclear layer in PLv-/- mice were progressively thinner than the controls, as observed in SD-OCT imaging, which was corroborated by the histologic analyses of retinal sections. The progression of age-related retinal thinning was significantly slower in females than in males in both PLv-/- and PLv+/+ mice.Conclusions:Peptide Lv contributes to the maintenance of the structural and functional integrity of adult retinas, and its deficiency accelerates retinal degeneration. These findings highlight a potential neuroprotective role of peptide Lv in the retina.2019-11-19·Journal of the American Heart Association2区 · 医学Newly Identified Peptide, Peptide Lv, Promotes Pathological Angiogenesis2区 · 医学ArticleOA作者: Bayless, Kayla J. ; Tsai, Shu‐Huai ; Xie, Wankun ; Pham, Dylan ; Kuo, Lih ; Shi, Liheng ; Abbey, Colette A. ; Zhao, Min ; Chapman, Samantha ; Ko, Michael L. ; Ko, Gladys Y.‐P. ; Hein, Travis W. ; Rosa, Robert H. Background:We recently discovered a small endogenous peptide, peptide Lv, with the ability to activate vascular endothelial growth factor receptor 2 and its downstream signaling. As vascular endothelial growth factor through vascular endothelial growth factor receptor 2 contributes to normal development, vasodilation, angiogenesis, and pathogenesis of various diseases, we investigated the role of peptide Lv in vasodilation and developmental and pathological angiogenesis in this study.Methods and Results:The endothelial cell proliferation, migration, and 3‐dimensional sprouting assays were used to test the abilities of peptide Lv in angiogenesis in vitro. The chick chorioallantoic membranes and early postnatal mice were used to examine its impact on developmental angiogenesis. The oxygen‐induced retinopathy and laser‐induced choroidal neovascularization mouse models were used for in vivo pathological angiogenesis. The isolated porcine retinal and coronary arterioles were used for vasodilation assays. Peptide Lv elicited angiogenesis in vitro and in vivo. Peptide Lv and vascular endothelial growth factor acted synergistically in promoting endothelial cell proliferation. Peptide Lv–elicited vasodilation was not completely dependent on nitric oxide, indicating that peptide Lv had vascular endothelial growth factor receptor 2/nitric oxide–independent targets. An antibody against peptide Lv, anti‐Lv, dampened vascular endothelial growth factor–elicited endothelial proliferation and laser‐induced vascular leakage and choroidal neovascularization. While the pathological angiogenesis in mouse eyes with oxygen‐induced retinopathy was enhanced by exogenous peptide Lv, anti‐Lv dampened this process. Furthermore, deletion of peptide Lv in mice significantly decreased pathological neovascularization compared with their wild‐type littermates.Conclusions:These results demonstrate that peptide Lv plays a significant role in pathological angiogenesis but may be less critical during development. Peptide Lv is involved in pathological angiogenesis through vascular endothelial growth factor receptor 2–dependent and –independent pathways. As anti‐Lv dampened the pathological angiogenesis in the eye, anti‐Lv may have a therapeutic potential to treat pathological angiogenesis.2015-05-01·Biochimica et biophysica actaPeptide Lv augments L-type voltage-gated calcium channels through vascular endothelial growth factor receptor 2 (VEGFR2) signalingArticle作者: Ko, Soyoung ; Kim, Andy Jeesu ; Ko, Gladys Y-P ; Ko, Michael L ; Shi, Liheng We previously identified peptide Lv, a novel bioactive peptide that enhances the activity of L-type voltage-gated calcium channels (L-VGCCs) in cone photoreceptors. In this study, we verified that peptide Lv was able to augment L-VGCC currents in cardiomyocytes, as well as promote proliferation of endothelial cells. We used a proteomics approach to determine the specific receptors and binding partners of peptide Lv and found that vascular endothelial growth factor receptor 2 (VEGFR2) interacted with peptide Lv. Peptide Lv treatment in embryonic cardiomyocytes stimulated tyrosine autophosphorylation of VEGFR2 and activated its downstream signaling. Peptide Lv activity was blocked by DMH4, a VEGFR2 specific blocker, but not by SCH202676, an allosteric inhibitor of G protein-coupled receptors, suggesting that the activity of peptide Lv was mediated through VEGFR2 signaling. Inhibition of VEGFR tyrosine kinase or its downstream signaling molecules abolished the augmentation of L-VGCCs elicited by peptide Lv in cardiomyocytes. In addition, peptide Lv promoted cell proliferation of cultured human endothelial cells. Calcium entry through L-VGCCs is essential for excitation-contraction coupling in cardiomyocytes. Since peptide Lv was able to augment L-VGCCs through activation of VEGF signaling in cardiomyocytes and promote proliferation of endothelial cells, peptide Lv may play an important role in regulating the cardiovascular system.100 项与 Peptide Lv 相关的药物交易登录后查看更多信息研发状态10 条进展最快的记录, 登录 后查看更多信息适应症最高研发状态国家/地区公司日期年龄相关性黄斑变性临床前美国 Texas A&M University2022-10-25关节炎临床前美国 Texas A&M University2022-10-25动脉粥样硬化临床前美国 Texas A&M University2022-10-25糖尿病性视网膜病变临床前美国 Texas A&M University2022-10-25肿瘤临床前美国 Texas A&M University2022-10-25登录后查看更多信息临床结果适应症分期评价查看全部结果研究分期人群特征评价人数分组结果评价发布日期 No Data

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