The upfront payment record for domestic innovative drug license-outs has been broken again. On May 20, 2025, 3SBio announced it had exclusively licensed Pfizer the global (excluding mainland China) rights for development, production, and commercialization of its independently developed PD-1/VEGF bispecific antibody SSGJ-707.
In recent years, PD-(L)1 bispecific products have shown higher objective response rates and more durable efficacy than traditional PD-(L)1 monoclonal antibodies, along with broader market potential. PD-(L)1/VEGF bispecific antibodies are among the star combinations, demonstrating strong effects in clinical trials. Previously, Akeso Biopharma’s AK112 outperformed Keytruda in head-to-head trials, followed by 3SBio’s PD-1/VEGF bispecific SSGJ-707 making headlines with a record-breaking overseas deal, alongside BMS and BioNTech’s strategic collaboration on the PD-L1/VEGF-A bispecific BNT372.
Currently, PD-(L)1/VEGF bispecific therapy is rapidly emerging, with many companies investing in this field.
VEGF (vascular endothelial growth factor) and its receptor VEGFR play central roles in tumor development. On one hand, the VEGF/VEGFR pathway can activate the “switch” for angiogenesis, maintaining abnormal structures of tumor neovasculature, such as distortion and leakage. On the other hand, the VEGF/VEGFR pathway increases vascular permeability, promoting tumor invasion and metastasis. Meanwhile, VEGF inhibits dendritic cell maturation and promotes infiltration of regulatory T cells (Tregs) and tumor-associated macrophages (TAMs), suppressing anti-tumor immunity.
In tumor treatment, drugs targeting the VEGF/VEGFR pathway have become an important strategy. Monoclonal antibodies against VEGF or VEGFR show limited clinical efficacy, while small-molecule TKIs have poor selectivity and generally more side effects. Combination therapy or bispecific antibodies have broader clinical application prospects.
PD-(L)1/VEGF bispecific antibodies simultaneously block immune checkpoints and angiogenesis pathways. Compared with traditional PD-(L)1 monoclonal antibodies, blocking VEGF can suppress PD-L1 upregulation caused by VEGF pathway activation, further delaying the onset of resistance. Studies also report that blocking the VEGF pathway can effectively reduce the tumor tissue barrier to T cells, enhancing PD-1 antibody penetration. Compared with using PD-(L)1 and VEGF antibodies separately, PD-1/VEGF bispecific antibodies can further reduce the risk of capillary leak syndrome caused by free VEGF.
In addition to PD-(L)1/VEGF bispecific antibodies, multiple drugs targeting VEGFR2 (KDR), including monoclonal antibodies, bispecific antibodies, and small-molecule inhibitors, have been approved or are in clinical trials. On June 1, 2025, Hengrui’s small-molecule tyrosine kinase inhibitor (TKI) famitinib malate, targeting multiple pathways including VEGFR, PDGFR-β, and cKIT, was approved. At the 2025 ASCO Annual Meeting, Hengrui also announced results from its Phase II trial of a selective VEGFR2 small-molecule TKI combined with camrelizumab for refractory chordoma. This “double-Ai” combination may provide a new treatment option for advanced chordoma patients.
To support VEGF/VEGFR-related drug development, Kyinno Biotechnology has established VEGF/VEGFR reporter cell lines. These cell lines can be used for antibody and small-molecule inhibitor screening and have been sold to the National Institutes for Food and Drug Control in China, receiving recognition from national institutions. Validation data and additional related cell lists are as follows:
- KC-1840293T-NFAT-Luc2-KDR
- KC-1571Ba/F3-ETV6-KDR
- KC-2007MC38-KDR
Validation Data Examples:
Reporter Cell Activation Function Validation
Antibody Blocking Function Validation
