sunitinib

Importantly, melatonin works with TKIs like sunitinib and pazopanib to improve mitochondrial homeostasis and increase therapeutic effectiveness. Overall, melatonin provides a multi-targeted, low-toxicity strategy for overcoming metabolic and therapeutic resistance in RCC, emphasizing its translational promise as an adjuvant. Further clinical trials should concentrate on dose optimization, biomarker-guided patient selection, and combination regimens that include immune checkpoint blockade.

Using sunitinib as an internal control, our results show clinically significant antitumour efficacy of [177Lu]Lu-dota-tate in pretreated, progressive, somatostatin receptor-positive, metastatic pancreatic neuroendocrine tumours, and a better quality of life during the treatment phase. Late adverse events were reported in the [177Lu]Lu-dota-tate group that might affect the tolerance of subsequent lines of treatment.

In this study, we investigated the therapeutic potential of combining Sunitinib with copper ionophore Elesclomol as a novel strategy against thyroid carcinoma. Clinically, TCGA analysis reveals SLC31A1 as a vulnerability in advanced thyroid cancer, with expression significantly downregulated in metastatic lesions, a deficit rescued by Sunitinib. Overall, these results demonstrate that Sunitinib and copper ionophores can induce synergistic cytotoxic effect, shedding light on therapeutic strategy for advanced thyroid carcinomas.

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.

miRNA co-regulation distinguished early-stage TNBC through PI3K-AKT-related pathways and advanced-stage TNBC through tumor progression-associated pathways. Docking-based drug repurposing highlighted conventional agents (e.g., doxorubicin) and potential novel candidates (e.g., sunitinib).ConclusionThis study identifies novel stage-specific gene candidates and suggests repurposable drugs for TNBC, supporting progression-specific targeted therapeutic strategies.

Mice were randomized into vehicle control or four sequential treatment groups (Everolimus→Sunitinib [E→S], Sunitinib→Everolimus [S→E], Pazopanib→Sunitinib [P→S], Pazopanib→Everolimus [P→E]). This RCC PDOX platform faithfully preserves patient-specific biology-including metastatic propensity, engraftment efficiency, growth kinetics, and stromal dependency-while enabling real-time evaluation of sequential targeted therapies. Given the limited number of models tested, these findings provide proof-of-concept for individualized treatment exploration in advanced RCC and support future investigation of rational combinations with immune checkpoint blockade in humanized or immunocompetent systems.

Biological evaluation identified compound 15l as a highly potent agent against the HCT116 colon cancer line, outperforming sunitinib and 5-fluorouracil by 3.7-fold and 7.9-fold, respectively...Compound 15h demonstrated VEGFR-2 inhibition comparable to sorafenib, while 15g emerged as a dual MDM2 inhibitor and p53 activator, significantly outperforming doxorubicin...CAM assays supported the anti-angiogenic potential of 15g, 15h, 15j, and 15k. Finally, molecular docking (PDB ID: 5LAW) and dynamic simulations validated the binding stability and mechanism within the MDM2 pocket.

P2, N=153, Suspended, RTOG Foundation, Inc. | Recruiting --> Suspended

P3, N=148, Active, not recruiting, AstraZeneca | Trial completion date: Oct 2025 --> Feb 2027 | Trial primary completion date: Jun 2025 --> Dec 2025

P3, N=482, Active, not recruiting, Cogent Biosciences, Inc. | Trial completion date: Sep 2026 --> Jan 2030

In addition, high-risk patients exhibited significant enrichment in pathways related to TP53 dysfunction, mechanistic target of rapamycin complex 1 (mTORC1) signaling activation, and pro-inflammatory responses, which were closely correlated with NPM1c-FLT3 co-mutations. Decitabine, sunitinib, and MK-1775 were identified as potential therapeutic agents. In summary, we established a 5-ARG prognostic model that may facilitate risk stratification and inform therapeutic decision-making in AML.

PYCR2 promotes HCC progression and Sunitinib resistance via the PPAR signaling pathway, involving regulation of metabolism, immunity, and genomic stability. These findings highlight PYCR2 as a promising therapeutic target for overcoming tyrosine kinase inhibitors resistance in HCC.