sunitinib

P2, N=40, Completed, Asan Medical Center | Recruiting --> Completed

P3, N=450, Recruiting, GlaxoSmithKline

Importantly, treatment with Eeyarestatin I, a small-molecule ER stress agonist, restored sunitinib sensitivity in tumor cells. These findings reveal a novel PABPC1-PGK1 regulatory axis underlying sunitinib resistance and suggest a promising therapeutic strategy for overcoming drug resistance in ccRCC.

P1/2, N=48, Recruiting, Asan Medical Center | Not yet recruiting --> Recruiting

The combination of SNB and FEN represents a promising multi-targeted therapeutic approach against GB. SNB and FEN combination capable of modulating and reprogramming key molecular pathways involved in GB progression and MDR.

In this review, we have evaluated the effects of NET therapies, including somatostatin analogues (SSTAs), molecular targeted therapy (everolimus, sunitinib), Peptide Receptor Radionuclide Therapy (PRRT) and chemotherapy on reproductive and sexual function in patients with NETs. While the effects of PRRT and molecular targeted therapy on fertility are as yet poorly defined, chemotherapy has a proven negative impact on fertility, thus, family and pregnancy planning are strongly recommended before initiation of chemotherapy. Finally, data on the effects of NETs treatment on sexual function are very limited, however neuroendocrine tumour can express Oestrogen Receptors/Progesterone Receptors (ER/PR) or testosterone receptors (TR), thus checking tumour tissue for ER/PR/TR status prior to considering hormonal therapy for sexual dysfunction should be considered but warrants additional studies.

P3, N=338, Recruiting, RayzeBio, Inc. | Trial completion date: Jul 2028 --> Dec 2030

Metabolomic analyses of various TKIs identified convergent signatures along three interconnected axes: (1) mitochondrial bioenergetic dysfunction characterized by impaired long-chain fatty acid oxidation and adenylate depletion; (2) disruption of endothelial nitric oxide signaling with redox imbalance, including increased nitrotyrosine, Nox activation, and eNOS uncoupling; and (3) an inflammatory metabolic profile marked by elevated branched-chain and aromatic amino acids, creatine, and osmolytes. Rodent models of sunitinib and sorafenib replicate these signatures and demonstrate histological injury, contractile dysfunction, and fibrosis. Preclinical intervention data, particularly restoration of myocardial carnitine, AMPK signaling, and fatty acid oxidation by L-carnitine, provide proof of concept for metabolomics-guided cardioprotection. Metabolomics can identify mechanistic biomarkers that facilitate the early detection, risk stratification, and targeted prevention of TKI-induced cardiovascular injury. Translation into precision cardio-oncology requires prospective validation, standardized assays, and biomarker-driven interventional trials.

P2, N=137, Active, not recruiting, Canadian Cancer Trials Group | Trial completion date: Dec 2025 --> Jun 2026

P1/2, N=170, Recruiting, 3D Medicines (Sichuan) Co., Ltd. | Trial primary completion date: Dec 2025 --> Dec 2026

Clinically, ccRCC patients with high DR5 expression show decreased responsiveness to TKI-based therapy. Collectively, these results highlight the importance of the positive feedback loop involving the DR5/NF-κB axis in sunitinib resistance and provide an effective therapeutic strategy for overcoming resistance.

Drug sensitivity analysis indicates that the RORC gene is responsive to agents such as VX-680, MG-132, and Sunitinib. Cell biology experiments have confirmed that RORC overexpression significantly diminishes the proliferation, invasion, and migration capabilities of gastric cancer cells. Integrating bioinformatics and cell biology experiments suggests that RORC, a gene associated with rhythm regulation, acts as a tumor suppressor gene that is underexpressed in gastric cancer, thereby serving as a potential biomarker and therapeutic target for this malignancy.