VEGF Specific Neutra™ Antibody Products

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Vascular endothelial growth factor (VEGF), initially identified as vascular permeability factor (VPF), represents a signaling protein synthesized by cells, exerting a stimulatory influence on blood vessel formation. More precisely, VEGF constitutes a sub-family within the cystine-knot growth factors of the platelet-derived growth factor family, playing pivotal roles as crucial signaling proteins in both vasculogenesis (the embryonic circulatory system's de novo formation) and angiogenesis (the expansion of blood vessels from pre-existing vasculature).

Its Gene ID: 7422, UniProtKB ID: P15692, and OMIM ID: 192240.

VEGF Signaling Pathway

The pivotal involvement of VEGFs and their corresponding receptors in angiogenesis and vasculogenesis underscores their significance in physiological and pathological processes. Angiogenesis, a pivotal mechanism in various biological contexts, intricately governs endothelial cell migration, survival, and proliferation. The orchestration of these cellular events is precisely regulated by the VEGF/VEGFR-2 system. Upon VEGF binding to VEGFR-2, receptor dimerization ensues, initiating a series of intracellular signaling cascades, including SHB-FAK-paxillin, NCK-p38-MAPKAPK2/3, and PLCγ-PKC, contributing to the intricacies of angiogenic processes.

Fig. 1 VEGF/VEGFR activated signaling pathway. (Wang, et al., 2020) Fig.1 VEGF/VEGFR activated signaling pathway.¹

Roles of Anti-VEGF Antibodies in Disease Treatment

Central to this complex network of proangiogenic factors is the pivotal role played by VEGF, which processes the advancement of solid tumors. Intervening in this pathway through VEGF blockade has demonstrated the potential for vascular network regression and inhibition of tumor growth. Presently, the clinical landscape embraces the integration of anti-VEGF monoclonal antibodies as a therapeutic approach for conditions such as colorectal cancer, recurrent high-grade gliomas (HGGs), and breast cancer. Additionally, the use of anti-VEGF antibodies exhibits promising outcomes as a targeted vector for delivering therapeutic and diagnostic agents specifically to brain tumors.

Targeting VEGF in neoplastic angiogenesis for antiangiogenic therapy

The multifaceted functions of VEGF, coupled with its pivotal role in neoplastic angiogenesis, have rendered this molecule an appealing target for antiangiogenic therapy. Inhibitors of VEGF serve to impede the activation of VEGFR receptors, thwarting subsequent intracellular signaling transduction. This, in turn, hampers the proliferation and migration of endothelial cells, thereby preventing the formation of the tumor vascular network. Furthermore, antiangiogenic therapy induces apoptotic death of endothelial cells, leading to the regression of pathological vessels. This multifaceted approach results in a reduction in the number and density of microvessels, decreased permeability, and inhibition of tumor growth. Creative Biolabs provides Recombinant Anti-VEGF Antibody (V3S-0622-YC4041), Anti-VEGF Neutralizing Antibody (V3S-0622-YC2782) for in vivo and in vitro assays

Fig. 2 A schematic overview of illustration of anti-VEGF therapeutic strategy. (Chekhonin, et al., 2013) Fig.2 A schematic overview of illustration of anti-VEGF therapeutic strategy.²

VEGF has the ability of angiogenesis and immunomodulation in NSCLC

Non-small cell lung cancer (NSCLC) stands as the predominant cause of cancer-related mortality worldwide. Elevated expression of VEGF in NSCLC serves as a key mediator, instigating the formation of tumor microvasculature and correlating with the progression, recurrence, and metastasis of NSCLC. Current pharmaceutical interventions targeting the VEGF/VEGFR pathway, encompassing neutralizing antibodies directed at VEGF, have exhibited commendable efficacy in treating NSCLC patients. Beyond its role as a pivotal angiogenic factor, VEGF assumes the additional function of modulating the tumor microenvironment (TME). VEGFs exhibit the capacity to inhibit antigen presentation, activate regulatory T (Treg) cells, and stimulate tumor-associated macrophages, thereby fostering an immune-suppressive microenvironment in NSCLC. Myeloid-derived suppressor cells (MDSCs), a heterogeneous population of immature myeloid cells, experience amplification under the influence of VEGF, playing a crucial role in mediating NSCLC-related immunosuppressive functions and facilitating tumor immune escape.

Fig. 3 The effect of VEGF on MDSC, NK and DC cell. (Zhao, et al., 2022) Fig.3 The effect of VEGF on MDSC, NK and DC cell.³

Creative Biolabs presents a comprehensive selection of intricately engineered anti-VEGF antibody products, tailored to propel research in therapeutic approaches targeting diverse manifestations of solid cancers and neoplastic angiogenesis disorders. Furthermore, we enthusiastically invite inquiries regarding the personalized customization of anti-VEGF bispecific antibodies, emphasizing our commitment to advancing innovative solutions in biomedical research.

REFERENCES

Wang, Xinrong, et al. "Molecular bases of VEGFR-2-mediated physiological function and pathological role." Frontiers in Cell and Developmental Biology 8 (2020): 599281.
Chekhonin, Vladimir P., et al. "VEGF in tumor progression and targeted therapy." Current cancer drug targets 13.4 (2013): 423-443.
Zhao, Yueshui, et al. "VEGF/VEGFR-targeted therapy and immunotherapy in non-small cell lung cancer: targeting the tumor microenvironment." International Journal of Biological Sciences 18.9 (2022): 3845.

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