cu/zn-superoxide

Esomeprazole Magnesium (NEXIUM) is the S-isomer of omeprazole, can reduce gastric acid secretion with selective and irreversible proton pump inhibitor activity.Esomeprazole magnesium acts as an exosome inhibitor by blocking the exosome release via the inhibition of V-H+-ATPases

Esomeprazole Magnesium trihydrate ((S)-Omeprazole magnesium trihydrate) is a proton pump inhibitor indicated for the short-term treatment of gastroesophageal reflux disease in patients with a history of erosive esophagitis.Esomeprazole magnesium trihydrate acts as an exosome inhibitor by blocking the exosome release via the inhibition of V-H+-ATPases

AKV-9 is an inhibitor of mutant Cu Zn superoxide dismutase (SOD1), effectively preventing SOD1-induced protein aggregation and providing protection against SOD1-induced cytotoxicity in PC-12 cells, with an EC50 of 0.3 μM. Additionally, AKV-9 has been shown to improve amyotrophic lateral sclerosis (ALS) in mouse models and extend their lifespan.

The metallo-protein Cu/Zn-superoxide dismutase (SOD1) is a ubiquitous enzyme responsible for scavenging superoxide radicals. Mutations in SOD1, which alter its metal binding capacity and can result in protein misfolding and aggregation, have been linked to familial amyotrophic lateral sclerosis (ALS). Cu-ATSM is an orally bioavailable, blood-brain barrier permeable complex that has traditionally been used in cellular imaging experiments to selectively label hypoxic tissue via its susceptibility to reduction by oxygen-depleted mitochondria. More recently, Cu-ATSM has been reported to improve locomotor function and survival in a transgenic ALS mouse model by delivering copper specifically to cells in the spinal cords of mice producing misfolded SOD1 proteins. Copper chaperone for SOD (CCS) is presumed to utilize the copper from Cu-ATSM to prevent misfolding of the SOD1 protein.

SOD1 (147-153) human, a peptide segment within Cu Zn superoxide dismutase (SOD1), exhibits a high propensity for forming amyloid fibrils. This segment is involved in the formation of aggregates and serves as a common molecular determinant in both familial amyotrophic lateral sclerosis (fALS) and sporadic amyotrophic lateral sclerosis (sALS).