tozasertib (MK-0457)

This work set up a prognostic model for LUAD based on 8 MDRGs, pinpointing promising biomarkers and targets for LUAD treatment.

In summary, aurora kinase inhibitor combined with CDDP could suppress the ERK pathway to affect the biological process of esophageal carcinoma cells. Versus a simple drug, a drug combination could effectively inhibit the proliferation and migration of esophageal carcinoma cells, promote apoptosis, reduce angiogenesis, and induce cell cycle arrest.

Everolimus (EVER) and tozasertib (TOZA) encapsulated in NP and targeted with dinutuximab β (DTX-β). DTX-β/EVER-TOZA@PEG-b-PLGA may exert cytotoxic and apoptotic effects in NB. The use of targeted nanocarriers in NB treatment may enhance cytotoxic and apoptotic responses specifically in the tumor region.

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.

To explore therapeutic implications, transcriptomics-guided drug repositioning combined with molecular docking analysis identified five candidate compounds-celastrol, fedratinib, pevonedistat, tozasertib, and withaferin A-predicted to target key network hubs. Overall, this in silico study provides a ceRNA-centered regulatory framework for GC and prioritizes biologically informed biomarkers and repositioned drug candidates with potential applicability across other malignancies to converge precision oncology.

Drug sensitivity prediction indicated that high-risk patients may respond better to agents such as Tozasertib and Navitoclax. This study establishes a robust, demethylation-driven six-gene signature that effectively stratifies HCC patients into distinct prognostic groups. The model integrates multi-omic insights into tumor biology and therapeutic vulnerability, providing a clinically actionable framework for personalized risk assessment and treatment planning in hepatocellular carcinoma.

Selumetinib, entinostat, and erlotinib were identified as candidate drugs for cluster 2, whereas tozasertib, alpelisib, and cediranib showed higher suitability for cluster 1. Ten potential biomarkers, 13 transcription factors, and 2 miRNAs were characterized. This study elucidates the role of UPS in ESCC progression and provides a framework for personalized treatment strategies.

Lastly, MMPBSA showed a higher negative free energy in the presence of Jervine than VX-680 when complexed with AURKB. Finally, our results suggest that Jervine is a potent, dual-targeting kinase inhibitor with favourable pharmacokinetic and therapeutic properties, warranting further experimental validation for anticancer drug development.

High MCMBP expression was ass-ociated with sensitivity to Gemcitabine combined with Paclitaxel, as well as small mo-lecules such as Tozasertib and Motesanib. Overexpression of MCMBP may serve as a prognostic biomarker and p-otential therapeutic target in PAAD. It drives PAAD progression by activating the JAK-STAT3 pathway to upregulate PD-L1.

This validated mitochondrial risk model delivers a clinically actionable biomarker for BLCA prognosis stratification and guides personalized therapeutic selection, enabling precision treatment intensification.

Drug sensitivity analysis identified BX-795 and tozasertib as potential treatments for tumors with high IGSF8 expression. Knockdown of IGSF8 significantly inhibited the proliferation ability of prostate cancer cells. Our findings indicated that IGSF8 might be used as a potential prognostic marker and therapeutic target for various cancers.

Finally, seven repurposed candidate drugs ENTRECTINIB, SORAFENIB, CHEMBL1765740, TOZASERTIB, NERVIANO, AZD-1152-HQPA, and SELICICLIB were proposed through molecular docking analysis. In conclusion, the findings of this study have the potential to significantly impact the early diagnosis, prognosis, and treatment of NSCLC.