Catalytic Asymmetric Formal C–C Bond Insertion Reaction of Aldehydes via 1,2-Acyl Shift: Construction of All-Carbon Quaternary Stereocenters with Three Carbonyl Groups

The formal C–H bond insertion reaction into aldehydes via 1,2-hydride shift has been well established; however, the formal C–C bond insertion is more challenging. In the presence of chiral oxazaborolidinium ion (COBI) catalyst, the formal C–C bond insertion into glyoxals was developed via an 1,2-acyl shift for the construction of α-alkyl-α-formyl-β-ketoesters in high yield (up to 97%) with high enantioselectivity (up to >99%). Computational evidence indicated that noncovalent interactions (n → π*) between substrates stabilized the transition state, thereby resulting in high enantioselectivity. This method enabled the construction of unique acyclic all-carbon quaternary stereocenters containing three different carbonyl groups

Catalytic Asymmetric Formal C–C Bond Insertion Reaction of Aldehydes via 1,2-Acyl Shift: Construction of All-Carbon Quaternary Stereocenters with Three Carbonyl Groups

The formal C–H bond insertion reaction into aldehydes via 1,2-hydride shift has been well established; however, the formal C–C bond insertion is more challenging. In the presence of chiral oxazaborolidinium ion (COBI) catalyst, the formal C–C bond insertion into glyoxals was developed via an 1,2-acyl shift for the construction of α-alkyl-α-formyl-β-ketoesters in high yield (up to 97%) with high enantioselectivity (up to >99%). Computational evidence indicated that noncovalent interactions (n → π*) between substrates stabilized the transition state, thereby resulting in high enantioselectivity. This method enabled the construction of unique acyclic all-carbon quaternary stereocenters containing three different carbonyl groups

Mitochondria-Targeting Ceria Nanoparticles as Antioxidants for Alzheimer’s Disease

Mitochondrial oxidative stress is a key pathologic factor in neurodegenerative diseases, including Alzheimer’s disease. Abnormal generation of reactive oxygen species (ROS), resulting from mitochondrial dysfunction, can lead to neuronal cell death. Ceria (CeO₂) nanoparticles are known to function as strong and recyclable ROS scavengers by shuttling between Ce³⁺ and Ce⁴⁺ oxidation states. Consequently, targeting ceria nanoparticles selectively to mitochondria might be a promising therapeutic approach for neurodegenerative diseases. Here, we report the design and synthesis of triphenylphosphonium-conjugated ceria nanoparticles that localize to mitochondria and suppress neuronal death in a 5XFAD transgenic Alzheimer’s disease mouse model. The triphenylphosphonium-conjugated ceria nanoparticles mitigate reactive gliosis and morphological mitochondria damage observed in these mice. Altogether, our data indicate that the triphenylphosphonium-conjugated ceria nanoparticles are a potential therapeutic candidate for mitochondrial oxidative stress in Alzheimer’s disease