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. 2024 Oct 17;67(21):18981–18992. doi: 10.1021/acs.jmedchem.4c01431

Figure 8.

Figure 8

QCO-105 prevents acute doxorubicin (DXR) toxicity to the heart and attenuates the expression of markers of DXR-induced ferroptosis. QCO-105 (50 mg/kg, ip) attenuated DXR (20 mg/kg)-induced cardiac dysfunction after 7 days, evidenced by preserved ejection fraction (A) and fractional shortening (B); (C) representative echocardiography (LVIDd: left ventricular internal dimension in diastole, LVIDs: left ventricular internal dimension in systole); (D) QCO-105 prevented DXR-induced upregulation of the cardiac dysfunction markers β-MyHC and BNP compared to QCP and Solutol controls (3–7 mice per group); and (E) Gpx4 and HO-1 mRNA expression in the ventricle of mice 7 days after a single DXR injection ± QCO-105 (3–5 mice per group, Solutol was used as the vehicle). Expression was determined by RT-qPCR and normalized to that of Hprt1. Mean ± SEM; ns: no significant difference, n ≥ 3, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.