axitinib

Molecular studies were performed in axitinib (VEGFR inhibitor)-treated human aortic endothelial cells, and vascular studies were undertaken in isolated intact vessels from mice...This was accompanied by increased p53 acetylation; these effects were mitigated by olaparib or the SIRT1 activator SRT1720...In conclusion, inhibition of VEGFR signalling induces oxidative stress and PARP activation, leading to SIRT1 downregulation, endothelial dysfunction and vascular inflammation. Targeting PARP activation or enhancing SIRT1 activity might represent promising strategies to mitigate VEGF inhibitor-induced vascular complications.

P3, N=718, Recruiting, SWOG Cancer Research Network | Not yet recruiting --> Recruiting

Molecular docking revealed that compound BIT (hybrid in which ketone group of isatin clubbed with thiosemicarbazide) exhibited a docking score of -10.2 kcal/mol, surpassing the binding affinities of the reference ligands axitinib and sorafenib, highlighting its promising potential. The BIT compound was evaluated, and the results indicated that it exhibited significant inhibitory activity against MCF-7 cells at a concentration of 30 mM.

P1, N=142, Completed, Merck Sharp & Dohme LLC | Active, not recruiting --> Completed | N=72 --> 142

P1/2, N=40, Not yet recruiting, Cancer Institute and Hospital, Chinese Academy of Medical Sciences

The patient had a history of CML treated with imatinib for 4 years, with loss of complete hematological response for 3 months before being diagnosed with RCC and lung metastases. Due to a T315I mutation in the BCR-ABL1 gene, the treatment regimen included a novel combination of Axitinib, Dasatinib, and low-dose nivolumab. The patient showed a remarkable therapeutic response with a complete metabolic response accompanied by a highly significant reduction in the size of the tumor and complete resolution of the metastatic lung lesions, as well as a major molecular response in terms of CML disease control.

P2, N=62, Active, not recruiting, University of Southern California | Trial completion date: Dec 2026 --> Dec 2027 | Trial primary completion date: Jun 2026 --> Dec 2026

Recent clinical trials (Axi-STS, TAPPAS) demonstrated that single-agent anti-angiogenic inhibitors (axitinib, pazopanib) achieve modest efficacy (median progression-free survival (PFS) 3.0-4.3 months, response rates 5-13%), underscoring angiosarcoma's complex, multipathway-driven pathogenesis. Environmental exposures (vinyl chloride, thorotrast, radiation) drive distinct angiosarcoma subtypes with subtype-specific mutational profiles. We propose that precision-medicine approaches integrating molecular stratification, pathway crosstalk analysis, and biomarker-guided combination therapies represent the rational next steps to overcome therapeutic resistance and improve clinical outcomes in this lethal malignancy.

Patients in the high‑risk group showed improved responses to lapatinib, BI‑2536, OSI‑027, and SB505124, whereas those in the low‑risk subgroup had better sensitivity to axitinib, epirubicin, fulvestrant, and olaparib. Additionally, CD24 overexpression in BC cell lines promoted proliferation and migration, and inhibited apoptosis. These findings contribute to personalized treatment strategies and help elucidate the tumor microenvironment characteristics of BC patients.

This exploratory Bayesian reanalysis complements the interpretation of the JAVELIN Renal 101 trial and offers a probabilistic perspective beyond a dichotomous (i.e., significant/nonsignificant) interpretation.

These results support a role for VEGF signaling and macrophage-mediated microenvironmental changes in edema and cystic growth of NF2-SWN SE. The observed clinical response to AXITINIB in an index patient suggests that new combinations of anti-angiogenic therapies may represent a promising early targeted approach.

P2, N=95, Completed, Jiangsu Alphamab Biopharmaceuticals Co., Ltd | Recruiting --> Completed | N=54 --> 95 | Trial completion date: Dec 2027 --> Dec 2025