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Abstract Objective To evaluate the effectiveness, safety, and convenience of in‐class transition (iCT) from intravenous bortezomib‐based induction to ixazomib‐based oral regimens. Methods This retrospective real‐world study was conducted in 16 Chinese hospitals between October 2017 and April 2023 and analyzed newly diagnosed (NDMM) and first‐line relapsed multiple myeloma (FRMM) patients who attained at least a partial response from bortezomib‐based induction therapy, followed by an ixazomib‐based oral regimen for 2 year or until disease progression or intolerable toxicity. Results The study enrolled 199 patients, median age: 63 years old, male 55.4%, 53% as high risk (HR), and 47% as standard risk. Cytogenetic risk stratification by metaphase fluorescence in situ hybridization (M‐FISH), based on the Mayo Clinic risk stratification system. The median duration of total PI therapy was 11 months, with ixazomib‐based treatment spanning 6 months. At the 20‐month median follow‐up, 53% of patients remained on therapy. The 24‐month PFS rate was 84.3% from the initiation of bortezomib‐based induction and 83.4% from the start of ixazomib‐based treatment. Overall response rate (ORR) was 100% post‐bortezomib induction and 90% following 6 cycles of the ixazomib‐based regimen. Based on the Sankey diagrams, 89.51% of patients maintained or improved their disease response after 2 cycles of iCT, 6 cycles (90.14%), and 12 cycles (80%). The HR level of Mayo was found to be a significant independent factor in a worse remission (hazard ratio (HR) 2.55; p = 0.033). Ixazomib's safety profile aligned with previous clinical trial data, with 49% of patients experiencing at least one AE of any grade. The most common AEs included peripheral neuropathy, nausea and vomiting, diarrhea, thrombocytopenia, and granulocytopenia. Conclusion In the real‐world Chinese MM population, NDMM and FRMM patients responded favorably to PI‐based continuous therapy, demonstrating substantial response rates. The ixazomib‐based iCT allows for sustained PI‐based treatment, offering promising efficacy and tolerable AEs.

Patients with diabetes mellitus, particularly those with cardiovascular complications, have increased risk of mortality when subject to anesthetics and surgery, compared with non-diabetic patients. Anesthetics may exert pressure on the cardiovascular system of diabetic patients, directly or by aggravating pre-existing cardiovascular complications. Advanced glycation end products (AGEs) are extremely accumulated in diabetes mellitus, and are confirmed to play an important role in the pathogenesis of diabetic microvascular and macrovascular complications. The purpose of the present study was to investigate the regulatory role of etomidate, which is widely used as intravenous general anesthetics, on the viability and apoptosis of human endothelial Eahy926 cells, in the presence of AGEs. The results demonstrated that etomidate and Glu-BSA (one type of AGE) synergistically reduced the human endothelial Eahy926 cell viability and induced cell apoptosis. In addition, western blot assay of apoptosis-associated molecules indicated that both agents synergistically upregulated the cytochrome c release, activated the apoptosis executor, caspase 3, and promoted the poly-ADP-ribose polymerase (PARP) lysis. Further results confirmed that the two agents synergistically promoted oxidative stress by decreasing mitochon-drial respiratory chain complex IV and mitochondrial membrane potential (MMP), while upregulating reactive oxygen species (ROS) and mitochondrial superoxide. In conclusion, the results presented in this study offer a novel insight into the mechanisms of endothelial cell apoptosis in response to etomidate in the presence of AGEs. These results suggest that oxidative stress has important role in the synergistic promotion of apoptosis by etomidate and AGEs in endothelial Eahy926 cells. [ABSTRACT FROM AUTHOR]