simvastatin

Moreover, we identified simvastatin as a potent inhibitor of CDT1, effectively inhibiting CDT1-mediated centrosome amplification and PGCC formation. In summary, our findings reveal a critical role for CDT1 in driving centrosome amplification and PGCC formation through activation of the PLK4/SASS6 axis, which subsequently contributes to therapeutic resistance and malignant progression.

Notably, the lipid-lowering drug Simvastatin substantially sensitized Fangchinoline-treated CTCs to undergo apoptosis. Together, these findings identified a novel role of Fangchinoline in inducing CTC senescence and metastasis suppression, provided a mechanistic basis for devising a "One-two punch sequential therapy" using Fangchinoline followed by Simvastatin as a potential strategy to treat melanoma metastasis.

Taken together, these findings establish a mechanistic foundation for a proposed therapeutic optimization strategy: Reducing vismodegib dosing while leveraging its inhibition-driven elevation of simvastatin systemic/tissue exposure, thereby mitigating dose-limiting skeletal toxicity while maintaining anti-tumor efficacy. This mechanism-based strategy provides a clinically actionable framework for pediatric medulloblastoma with urgent unmet therapeutic needs.

P1, N=49, Completed, AstraZeneca | Active, not recruiting --> Completed

Our findings highlights the efficacy of metabolic inhibitors such as Simvastatin, Metformin, and predict compatible partner drugs to enhance their efficacy. Additionally, we predict possible improvements for CRLM treatment using an immunotherapy drug like Pembrolizumab. Overall, this paper suggests potential combinations requiring experimental validation for drug repurposing to improve CRLM treatment outcomes.

Furthermore, in combination with sorafenib (SOR), they inhibited System xc- activity, creating a feedback loop that depleted GSH, synergistically inducing ferroptosis in tumor cells and producing potent antitumor effects. This approach offered a promising strategy for constructing drug self-assembly nanodelivery systems to effectively trigger ferroptosis in cancer therapy.

Functionalized PSLNPs improved the delivery and efficacy of PIO and STAT, overcoming MDR by modulating multiple oncogenic pathways. These results highlight their promise as a multi-targeted nanotherapeutic strategy for HCC treatment.

Non- CSD/ZKD inhibitors, including compounds like C1632 and Simvastatin, have been identified as molecules that can reduce Lin28 activity, though their binding sites remain unknown...Notable examples of these include IPA-3 and FPA124. This review summarizes recent advances in the development of Lin28/let-7 inhibitors and their therapeutic potential, providing an important reference for ongoing research on Lin28 inhibitors in cancer therapy.

P2, N=222, Completed, The Australasian Gastro-Intestinal Trials Group (AGITG) | Recruiting --> Completed

Importantly, we observed that simvastatin synergised with cisplatin in reducing tumour cell proliferation. Collectively, these data suggest that simvastatin is a potential anticancer drug capable of counteracting LCT growth, and it could be proposed as an adjuvant for chemotherapy in LCT treatment.

Importantly, given that many breast cancer patients also suffer from hyperlipidemia, Simvastatin offers dual therapeutic benefits-managing both lipid metabolism and tumor cell proliferation. Thus, Simvastatin holds promise as an adjunctive therapy in the treatment of TNBC and warrants further clinical investigation.