sunitinib

This tendency was not changed by everolimus (HR = 2.66), but was abrogated slightly by sunitinib (HR = 1.59) and considerably by ICI-based therapies, including nivolumab monotherapy (HR = 1.12), atezolizumab plus bevacizumab (HR = 1.10), and avelumab plus axitinib (HR = 0.69). Overall, our findings suggest that NF1/2 mutations can serve as predictive biomarkers for favorable benefits from ICI-based treatments over VEGFR/mTOR inhibitors in advanced ccRCCs.

P2, N=153, Recruiting, RTOG Foundation, Inc. | Not yet recruiting --> Recruiting

MUC1 expressing ccRCC is a high angiogenic tumor that presents characteristics of increased aggressiveness, and a specific metabolic profile. Serum CA15-3 is a marker of poor survival and predicts response of sunitinib in patients with metastatic disease.

Furthermore, neutralizing NRG1 enhanced the efficacy of sunitinib in RCC models in vivo. Together, these findings highlight targeting the tumor-promoting functions of ApoEhigh CAFs as a promising approach for treating advanced RCC.

After oral administration, the SEDDS formulation increased the ZZP-2 plasma area under the curve (AUC0-∞) by 3.7-fold relative to a suspension formulation in Sprague-Dawley (SD) rats and significantly prolonged survival in MOLM-13-luciferase-bearing NSG mice compared to positive controls sunitinib and gilteritinib, without noticeable toxicity. Our study presents a novel FLT3-ITD inhibitor with high potency and in vivo stability.

We provide novel data on the efficacy of putative and established therapies in patient-derived GEP-NEN primary cultures. Our standardized platform for personalized drug screening and risk assessment in GEP-NEN primary cultures enables prediction of individual tumor treatment response in this orphan disease.

While imatinib revolutionized first-line therapy, resistance and specific mutation profiles necessitate subsequent generations of tyrosine kinase inhibitors (TKIs). Second- and third-generation TKIs have transformed the management of advanced GIST, extending survival and offering mutation-specific precision therapy. Ongoing research into resistance mechanisms, combination strategies, and novel inhibitors promises further optimization of patient-centered care.

P2, N=32, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Jul 2025 --> Jul 2027 | Trial primary completion date: Jul 2025 --> Jul 2027

No significant elevation was obtained with chemotherapy (5-fluorouracil, irinotecan, oxaliplatin, paclitaxel, gemcitabine or temozolomide), tyrosine kinase inhibitors sorafenib and sunitinib, or the immunostimulatory agents polyinosinic:polycytidylic acid, Mycobacterium tuberculosis antigens and diphtheria/pertussis/tetanus vaccine. Combination of the vector and CIKs obtained a strong antitumor effect in the PDAC model, although it was mainly due to vector-mediated recruitment of endogenous immune cells. We conclude that additional barriers beyond chemokine expression should be overcome in order to unleash the full potential of CIKs on solid tumors.

For example, anticancer therapies targeting vascular endothelial growth factor activity have been effective in blocking pro-angiogenic and pro-growth signals, including receptor tyrosine kinase inhibitors (e.g., Sunitinib and Sorafenib) and monoclonal antibodies (e.g., Bevacizumab). The capacity of heparin to promote the association of FGF2 with its cognate receptors (FGFRs) led to the degradation of the entire receptor-ligand complex, thereby reducing the availability of FGFRs at the cancer cell surface, which are necessary for sustained pro-oncogenic signaling. These findings highlight the potential of GLYTACs as an alternative to existing growth factor-blocking anticancer therapies and as a strategy to reshape the extracellular signaling environment of tumors.

Combined with different clinical and pre-clinical anticancer compounds such as V9302, CB839, Sutent, Brigatinib, DRB18 significantly increased death of A549 and Panc1 cells. Mechanistically, DRB18 treatment with paclitaxel elevated the expression of Caspases 3 and 9, suggesting GLUT-inhibiting and apoptosis-inducing anticancer mechanisms of DRB18 with paclitaxel. Collectively, our results demonstrate anticancer efficacy of pan class-I GLUT inhibitor DRB18 in combination with paclitaxel, providing a potentially more efficacious therapeutic strategy for treating advanced NSCLC and other cancers.