Caprelsa (vandetanib)

Selpercatinib conferred significant PFS benefit over SoC in treatment-naïve (1L) patients with RET-mutation-positive MTC, with inconclusive results in the ≥2L setting. Matching retrospective real-world data to prospective trial data is feasible. EC arms to single-arm trials may provide evidence supporting the evaluation of comparative effectiveness.

Our findings uncover a novel mechanism underlying TKI-induced cardiotoxicity, involving calpain-dependent degradation of cardiac myofilament proteins and independent of calcium dysregulation. This study highlights the critical role of sarcomere stability in maintaining cardiac function during TKI therapy and identifies calpain as a promising therapeutic target for cardioprotection, with calpain activation rather than calcium dysregulation being the key driver of vandetanib-induced cardiac dysfunction.

By preserving lysosomal function and calcium homeostasis, this strategy addresses a critical unmet need in precision oncology, enabling prolonged, safer use of vandetanib and related tyrosine kinase inhibitors. The discovery of shared lysosomal injury mechanisms across organs also opens avenues for preventing multi-organ toxicities in broader cancer therapies.

FDA-approved drugs like Gefitinib, Erlotinib, Afatinib, Dacomitinib, and Vandetanib validate the therapeutic significance of the quinazoline framework in modulating different cancer pathways. Structure activity relationship (SAR) analyses reveal that adding halogen, methoxy, or heteroaryl groups at specific ring positions enhance kinase affinity and cytotoxic efficacy. Overall, this review highlights recent progress linking synthetic design, molecular docking, and biological response, establishing quinazoline derivatives as promising multitargeted scaffolds for the design of next-generation anticancer agents.

Repurposed drug candidates were then predicted via signature-based prioritization and evaluated using molecular docking simulations, revealing six promising compounds for GBM (vandetanib, capecitabine, melatonin, agomelatine, ramelteon, and tasimelteon) and one for LGG (ambroxol). This study demonstrates the utility of combining class-balancing, feature selection, and drug repurposing pipelines to uncover clinically relevant glioma biomarkers and therapeutic candidates, thus providing a computational foundation for future experimental and translational validation in these brain cancers and neuro-oncology.

The immunotherapy was well tolerated, but did not have an impact on tumor growth rate at 6 months as measured by calcitonin kinetics.

Grade-based algorithms combining topical corticosteroids/antibiotics, dose interruptions or reductions, and short systemic courses (e.g., doxycycline, antihistamines) enable symptom control while maintaining anticancer intensity... Dermatologic toxicities are predictable, mechanism-linked, and manageable with proactive, multidisciplinary care. Standardized prevention and treatment pathways tailored to specific TKIs-particularly lenvatinib, vandetanib, and cabozantinib-can preserve dose intensity, optimize quality of life, and sustain antineoplastic efficacy.

Drug sensitivity analyses further suggested that vandetanib may have the potential to inhibit recurrence by targeting B2M-related pathways. These findings provide evidence that B2M may contribute to remodeling of the immune microenvironment in recurrent HCC. Our integrative single-cell multi-omics approach highlights a possible mechanism of early recurrence and offers a preliminary predictive tool with therapeutic implications.

The combination of selpercatinib and cemiplimab was possible, with no new safety signals observed.

P1, N=151, Completed, M.D. Anderson Cancer Center | Active, not recruiting --> Completed | Trial completion date: May 2026 --> Oct 2025 | Trial primary completion date: May 2026 --> Oct 2025

Ponatinib, regorafenib, and vandetanib are FDA-approved VEGFR, Tie2, and Ephrin receptor blockers used in the treatment of various malignancies. Other disorders characterized by aberrant angiogenesis include diabetic retinopathies and neovascular age-related macular degeneration.

Moreover, the MTT viability test for compounds 9a, 9b, and 9c demonstrated less cytotoxicity against normal fibroblast cells (WI38), revealing enhanced safety profiles with IC50 values of 28.04, 219.79, and 43.77 μM, respectively, compared to Sorafenib (IC50 = 26 μM). Enzyme inhibition assays revealed that compounds 9a-c effectively inhibited EGFR and VEGFR-2, confirming the multi-targeting potential of this series of compounds.