| Description | Ethaselen (BBSKE) is an orally active, selective thioredoxin reductase (TrxR) inhibitor with IC 50 s of 0.5 and 0.35 µM for the wild-type human TrxR1 and rat TrxR1, respectively. Ethaselen specifically binds to the unique selenocysteine-cysteine redox pair in the C-terminal active site of Ethaselen (BBSKE) is an orally active, selective thioredoxin reductase (TrxR) inhibitor with IC 50 s of 0.5 and 0.35 µM for the wild-type human TrxR1 and rat TrxR1, respectively. Ethaselen specifically binds to the unique selenocysteine-cysteine redox pair in the C-terminal active site of mammalian TrxR1. Ethaselen, an organoselenium compound, is a potent antitumor candidate that exerts potent inhibition on non-small cell lung cancer (NSCLC) by targeting TrxRIn VitroEthaselen (2.5-10 µM; 12, 24 hours) suppresses A549 cell viability in a both concentration- and time-dependent manner. H1666, which has considerably lower TrxR1 expression level, is less susceptible to 24 h treatment with Ethaselen. Ethaselen inhibits the intracellular TrxR1 activity in a concentration- and time-dependent manner, with IC 50 values of 4.2 and 2 µM for 12- and 24-h treatments, respectively. Ethaselen (2.5-10 µM; 12, 24 hours) has no effect on the protein amounts of TrxR1 and Trx. The mRNA level of TrxR1 does not show significant alteration in Ethaselen-treated A549 cells. Ethaselen (2.5-50 µM; 1-24 hours) causes intracellular Trx oxidation in A549 cells. Ethaselen (5-10 µM; 12, 24 hours) causes a clear concentration-dependent increase in ROS levels in A549 cells. The inhibition constants for Ethaselen binding to free enzyme (K i ) and the enzyme-substrate complex (K is ) were determined to be 0.022 and 0.087 µM, respectively. Ethaselen also inhibits mammalian TrxR1 in a time-dependent manner possibly by forming a covalent Se-S bond with Cys497 of Trx. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Cell Viability AssayCell Line: A549 cell Concentration: 2.5, 5, 7.5, 10 µM Incubation Time: 12, 24 hours Result: Suppressed A549 cell viability in a both concentration- and time-dependent manner.In VivoEthaselen\t(BBSKE; 36-108 mg/kg/day; PO; for 10 days) shows increased inhibition of tumor growth in a dose-independent manner. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Five-week-old female BALB/c nude mice with A549 cellDosage: 36, 72, 108 mg/kg Administration: PO; daily; for 10 days Result: Showed increased inhibition of tumor growth, and the inhibition levels increased with the dose. The TrxR activity levels of the high dose group (108 mg/kg) decreased more than the middle dose group (72 mg/kg) and low dose group (36 mg/kg).IC50& Target:TrxR... Read More | Biochemical Test:SDS-PAGE (purity > 80%); Western blot with patient sample.Calculated Isoelectric Point:pH 6.10 | Dezamizumab (anti-Serum Amyloid P) is a fully humanized recombinant monoclonal IgG1 anti-serum amyloid P component (SAP) antibody, with potential anti-amyloid activity. Dezamizumab (anti-Serum Amyloid P) triggers immunotherapeutic clearance of amyloid. Dezamizumab (anti-Serum Amyloid P) can be used Dezamizumab (anti-Serum Amyloid P) is a fully humanized recombinant monoclonal IgG1 anti-serum amyloid P component (SAP) antibody, with potential anti-amyloid activity. Dezamizumab (anti-Serum Amyloid P) triggers immunotherapeutic clearance of amyloid. Dezamizumab (anti-Serum Amyloid P) can be used in research of Amyloid light-chain (AL) amyloidosis... Read More | Inquire | Purity:>95%, by SDS-PAGE visualized with Coomassie® Blue Staining.Description：HSPD1, also known as HSP60, is a member of the chaperonin family. HSPD1 may function as a signaling molecule in the innate immune system. This protein is essential for the folding and assembly of newly Purity:>95%, by SDS-PAGE visualized with Coomassie® Blue Staining.Description：HSPD1, also known as HSP60, is a member of the chaperonin family. HSPD1 may function as a signaling molecule in the innate immune system. This protein is essential for the folding and assembly of newly imported proteins in the mitochondria. It may also prevent misfolding and promote the refolding and proper assembly of unfolded polypeptides generated under stress conditions in the mitochondrial matrix. HSPD1 gene is adjacent to a related family member and the region between the 2 genes functions as a bidirectional promoter. Several pseudogenes have been associated with this gene. Mutations associated with this gene cause autosomal recessive spastic paraplegia 13. Defects in HSPD1 are a cause of spastic paraplegia autosomal dominant type 13 (SPG13). Spastic paraplegia is a degenerative spinal cord disorder characterized by a slow, gradual, progressive weakness and spasticity of the lower limbs. Defects in HSPD1 are the cause of leukodystrophy hypomyelinating type 4 (HLD4); also called mitochondrial HSP60 chaperonopathy or MitCHAP-60 disease. HLD4 is a severe autosomal recessive hypomyelinating leukodystrophy. HSPD1 is clinically characterized by infantile-onset rotary nystagmus, progressive spastic paraplegia, neurologic regression, motor impairment, profound mental retardation. Death usually occurs within the first two decades of life... Read More |