文献

PA007515.m2a：体内实验级重组抗小鼠VEGF单克隆抗体(克隆号G6-31，小鼠IgG2a kappa)

体内实验级重组抗小鼠VEGF单克隆抗体（克隆号G6-31，小鼠IgG2a Kappa）是针对小鼠血管内皮生长因子（VEGF/VEGF-A）的特异性阻断试剂。VEGF作为促血管生成的核心细胞因子，在肿瘤血管生成、血管通透性调节及肿瘤微环境重塑中发挥关键作用。G6-31克隆号抗体能高亲和力结合小鼠及大鼠VEGF，广泛应用于肿瘤生长抑制、眼部血管新生模型、流式细胞术（FC）及体外中和分析，是抗血管生成治疗与肿瘤免疫联合疗法研究的经典工具。

作为高品质的体内实验级重组抗小鼠VEGF单克隆抗体（克隆号G6-31），该产品采用基因工程重组表达与小鼠IgG2a Kappa骨架设计，彻底消除了传统杂交瘤生产中的批次间差异，并具有极高的一致性与特异性。其低内毒素（<1 EU/mg）与无叠氮化钠配方可有效避免非特异性毒性反应，非常适合用于长期动物体内实验（In Vivo）、血管生成机制探究及联合靶向药效评估，为高质量科研数据提供有力保障。

抗小鼠VEGF单抗(G6-31)部分参考文献:

1. Inhibitory effects of anti-VEGF antibody on the growth and angiogenesis of estrogen-induced pituitary prolactinoma in Fischer 344 Rats: animal model of VEGF-targeted therapy for human endocrine tumors.

Katsuhiro Miyajima, et al. Acta Histochem Cytochem. 2010. PMID: 20514290

“To investigate whether tumor development in E2-induced PRLoma is inhibited by anti-VEGF monoclonal antibody (G6-31), we evaluated tumor growth and observed the vascular structures. With simultaneous treatment with G6-31 for the latter three weeks of the 13-week period of E2 stimulation (E2+G6-31 group), the following inhibitory effects on the PRLoma were observed in the E2+G6-31 group as compared with the E2-only group. In the E2+G6-31 group, a tendency to reduction in pituitary weight was observed and significant differences were observed as (1) reductions in the Ki-67-positive anterior cells, (2) increases in TUNEL-positive anterior cells, and (3) repair of the microvessel count by CD34-immunohistochemistry.”

2. Sprouting Angiogenesis in Human Pituitary Adenomas.

Jie Zhou, et al. Front Oncol. 2022. PMID: 35600354

“Anti-VEGF treatment has been demonstrated to successfully treat pituitary tumors in mouse models. Korsisaari et al. used the anti-VEGF antibody G6-31 to treat pituitary tumors in Men1+/- mice (53). After 67 days, they observed that G6-31 treatment reduced the tumor volume by 72% compared to the control group and significantly extended their survival. All pituitary tumors in Men1+/- mice were later identified as prolactinomas (53). The G6-31 antibody was also used to treat Drd2(-/-) mice with hyperplastic pituitary glands by Luque et al. (54).”

3. Antibodies blocking PlGF or VEGF interactions with the NRP1 receptor mediate anti-proliferative effects.

Samuel A Blackman, et al. bioRxiv. 2025. PMID: 41306516

“This can occur via multiple mechanisms, including upregulation of placental growth factor 2 (PlGF-2), an alternative ligand for VEGF receptor 1 (VEGFR1) and neuropilin receptor 1 (NRP1). Activity of both growth factors is mediated by interactions with multiple receptors and extra-cellular matrix components, which complicates efforts to understand their contributions to cancer progression. To complement existing antibodies, we discovered those blocking interactions between PlGF-2 or VEGFA and their shared NRP1 receptor in the presence of heparin. Limiting angiogenesis to promote vascular normalization is one mechanism of anti-VEGF protection; here, anti-VEGFA antibodies blocking interactions with VEGFR1 and NRP1 reduced HUVEC tube formation in a physiological angiogenesis model.”