P1/2, N=215, Recruiting, 4D Molecular Therapeutics | N=150 --> 215 | Trial completion date: Nov 2025 --> Nov 2026 | Trial primary completion date: Nov 2024 --> Nov 2025

P1, N=17, Completed, Innovent Biologics (Suzhou) Co. Ltd. | Active, not recruiting --> Completed

P3, N=990, Active, not recruiting, Opthea Limited | Recruiting --> Active, not recruiting

P1/2, N=15, Active, not recruiting, AsclepiX Therapeutics, Inc. | Recruiting --> Active, not recruiting

P1, N=17, Active, not recruiting, Innovent Biologics (Suzhou) Co. Ltd. | Recruiting --> Active, not recruiting | Trial completion date: Jan 2024 --> Apr 2024

P1/2, N=6, Terminated, AsclepiX Therapeutics, Inc. | Completed --> Terminated; Adverse Events

P1/2, N=3, Terminated, AsclepiX Therapeutics, Inc. | Completed --> Terminated; Adverse Events

P3, N=990, Recruiting, Opthea Limited | Trial completion date: Jul 2025 --> Jul 2026

P3, N=990, Active, not recruiting, Opthea Limited | Recruiting --> Active, not recruiting | Trial completion date: Jul 2025 --> Jul 2026

P3, N=990, Recruiting, Opthea Limited | Trial completion date: Dec 2025 --> Jul 2025 | Trial primary completion date: Dec 2024 --> Jul 2025

P3, N=990, Recruiting, Opthea Limited | Trial completion date: Dec 2024 --> Jul 2025 | Trial primary completion date: Dec 2024 --> Jul 2025

P1/2, N=15, Recruiting, AsclepiX Therapeutics, Inc. | Not yet recruiting --> Recruiting

We investigated novel anti-HCC treatments through either the simultaneous inhibition of glycolysis and gluconeogenesis by "phloretin" and "sodium meta-arsenite", respectively (Combination 1); or the concurrent inhibition of glycolysis and induction of gluconeogenesis by phloretin and dexamethasone, respectively, (combination 2). Biochemically, both combinations caused a significant reduction in ATP levels, ALT, and AST activity compared to the other groups. In conclusion, we propose two novel phloretin-based combinations that can be used in treating HCC through the regulation of glucose metabolism and ATP production.

P3, N=990, Recruiting, Opthea Limited | Trial primary completion date: Dec 2023 --> Dec 2024

P3, N=990, Recruiting, Opthea Limited | Trial completion date: Dec 2024 --> Dec 2025 | Trial primary completion date: Dec 2023 --> Dec 2024

These results suggest that SRC-1 promoted cell metastasis of gastric cancer via VEGFC activator by NF-κB. These novel findings may shed further light on the pathogenesis of gastric cancer and on potential precursor markers.

The VEGFR2 monoclonal antibody could inhibit the angiogenesis and tumor growth of GBM by blocking the signaling pathway mediated by VEGFR2. It may become a new supplementary treatment for GBM.

A marked reduction in tumor mass was recorded (43.25%) with the control, a 41.36% decrease with the nanoparticles and a 61.01% reduction with the LyP-1-modified nanosystem following treatment in mice. The LyP-1-functionalized nanosystem targeted tumor lymphatics, instigated nuclear rupture and mitochondrial distortion, and decreased cell proliferation and migration with inhibition of VEGF-C and MMP2 expression.

Downregulation of OTUD3 and ZFP36 is essential for nicotine-induced VEGF-C production and lymphatic metastasis in esophageal cancer. This study establishes that the OTUD3/ZFP36/VEGF-C axis plays a vital role in nicotine addiction-induced lymphatic metastasis, suggesting that OTUD3 may serve as a prognostic marker, and induction of the VEGF-C mRNA decay might be a potential therapeutic strategy against human esophageal cancer.

Finally, we illustrated in vivo anti-tumor effects of KML001 using an intracranial xenograft mouse model. These results suggest that KML001 could be an effective chemotherapeutic drug for the treatment of glioblastoma cancer patients with higher Akt activity and PTEN loss.

mTOR inhibitor acts on lymphangiogenesis via reducing VEGFC expression in pNET cells and inhibiting tube formation of LECs. In conclusion, mTOR and c-Myc are important for lymphangiogenesis of pNET and are potential therapeutic targets for prevention and treatment of lymph node metastasis in pNET.

A series of domain specific antibodies to NRP2 have been developed and characterized. These antibodies show differential binding to specific domains of NRP2, can inhibit either VEGF-C or Sema3F binding to NRP2, and differentially effect receptor dimerization. The use of these antibodies enabled us to implicate VEGF-C/NRP2 signaling but not SEMA-3F/NRP2 signaling in the function of breast CSCs.

Three different EGFR-TKIs (Gefitinib, Afatinib, and AZD9291) were used to determine the possible biological effects of EGFR-TKIs on lymphangiogenesis in vitro and in vivo. Additional assays confirmed that the JAK/STAT3 signalling pathways play important roles in the anti-lymphangiogenesis process induced by EGFR-TKIs. Inhibition of lymphangiogenesis is another important role that the three EGFR-TKIs play in the treatment of lung cancer and the Janus kinase/signal transducers and activators of transcription 3 (JAK/STAT3) maybe an important signalling pathway regulating lymphangiogenesis, which provides a new idea for clinical therapy of lung cancer.