liproxstatin-1

Targeting this pathway with clinically approved statins (atorvastatin, pitavastatin, simvastatin) synergized with PT2385 to suppress CRC cell growth, reduce colony formation, and enhance cell death...These effects are fully reversed by the ferroptosis inhibitor liproxstatin-1...In vivo, co-administration of PT2385 and atorvastatin significantly reduced tumor growth and increased ferroptotic cell death in xenografts, confirming the mechanistic link. Collectively, these findings uncover a metabolic vulnerability of CRC to dual HIF-2α and cholesterol biosynthesis inhibition, supporting a clinically actionable strategy that leverages safe, FDA-approved statins to potentiate HIF-2α-targeted therapy.

Normothermic EVHP combined with Lip-1 treatment can be a promising DCD heart preservation strategy, which can alleviate myocardial IRI, ameliorate endothelial dysfunction, and improve posttransplant cardiac function for DCD hearts via inhibiting myocardial ferroptosis.

Several small-molecule inhibitors-including ferrostatin-1, liproxstatin-1, and iron chelators such as deferoxamine (DFO)-have demonstrated efficacy in animal models by attenuating neuronal damage and improving behavioral outcomes through the suppression of ferroptosis. This review summarizes recent advances in understanding the role of ferroptosis in neurodegenerative disease mechanisms, focusing on its contribution to pathological progression, molecular regulation, and therapeutic interventions. By integrating current findings, we aim to provide theoretical insights into novel pathogenic mechanisms and scientific guidance for the development of targeted therapies that modulate ferroptosis to slow or halt disease progression.

Ferroptosis was induced in B-ALL cells using erastin...PRDX1 knockdown further reduced the viability of B-ALL cells treated with the ferroptosis activator ML210, and treatment with the ferroptosis inhibitor liproxstatin-1 significantly reversed the suppressive effect of PRDX1 knockdown on xenograft tumor growth. Mechanically, PRDX1 deletion triggered ferroptosis in B-ALL cells by inhibiting the cAMP pathway. PRDX1 deficiency modulates ferroptosis in B-ALL cells by blocking the cAMP pathway, which offer a novel perspective on the pathogenesis of B-ALL.

Cytotoxicity and colony formation were evaluated using CyQUANT assays, with pharmacological inhibitors (ZnPP, Liproxstatin-1, Z-VAD-FMK) and HMOX1 siRNA to dissect the roles of ferroptosis and apoptosis...HO-3867 and AKT-100 induce HMOX1-mediated ferroptosis and apoptosis, effectively suppressing endometrial cancer cell growth. These findings support the therapeutic potential of curcumin analogues and provide a foundation for in vivo studies targeting HMOX1 in endometrial cancer.

PRMT1 drives OSCC aggressiveness by methylating and activating STAT3. This axis promotes chemoresistance and oncogenic phenotypes primarily by suppressing ferroptosis through STAT3-mediated transcriptional upregulation of GPX4. Targeting PRMT1 represents a promising strategy to overcome chemoresistance and inhibit progression in OSCC.

This distinction requires the use of lipophilic radical-trapping antioxidants (eg, ferrostatin-1, liproxstatin-1), iron chelators, and evidence implicating glutathione peroxidase 4 (GPX4) or the system Xc- antiporter...Finally, we discuss translational challenges, including tumour microenvironment heterogeneity, NP protein corona dynamics, clearance and off-target effects. We aim to provide a framework that links NP design to ferroptotic mechanisms and clinically relevant outcomes, offering clear criteria and priorities for future research.

Compared with sorafenib treatment alone, additional berberine treatment induced more severe mitochondrial dysfunction and ROS accumulation, following exacerbation of lipid peroxidation, which were abolished by ferroptosis inhibitors liproxstatin-1 and ferrostatin-1. Additionally, we demonstrated NQO1 activation induced by combined treatment was due to SETDB1 inactivation, following ERVs induction and genome instability, which may be another factor for lipid peroxidation and ferroptosis. Collectively, berberine has great potential to be used as a novel chemo-enhancer to improve the efficacy of sorafenib -based therapy.

These findings nominate multi-selenoproteins inhibition as a promising strategy to overcome ferroptosis resistance.

In this study, we observed that the lipid peroxide scavenger Liproxstatin-1 unexpectedly promoted TNF-α-induced apoptosis in HT-29 cells and murine colonic organoids, in contrast to the protective effects previously reported for typical peroxide scavengers in UC...Furthermore, 4-HDHA suppressed NF-κB signaling and apoptosis via PPARγ activation. Collectively, these findings demonstrate that 4-HDHA, identified through targeted lipidomics, attenuates DSS-induced colitis by reducing apoptosis and inflammation through PPARγ activation, highlighting its potential as a promising therapeutic agent for UC.

To assess the role of ferroptosis, ferroptosis inhibitor liproxstatin-1 (Lip-1) was co-administered with FFCT-containing serum...Immunofluorescence analysis of clinical CRC tissue microarrays revealed that NQO1 expression was significantly higher in tumor tissues than in adjacent non-tumor tissues (P < 0.001). FFCT may induce intracellular ferroptosis by downregulating the oncogenic gene NQO1, thereby exerting anti-CRC effects.

The review also discusses therapeutic implications, noting that ferroptosis inhibitors (e.g., liproxstatin-1, deferoxamine) demonstrate protective effects in thrombotic models by restoring endothelial homeostasis and limiting coagulation. However, inducing ferroptosis in oncology may paradoxically elevate thrombotic risk, underscoring the need for balanced therapeutic strategies.