| Quantity | 100µl/well, 2×100µl/well | 100mg, 5mg, 2mg, 1mg, 25mg | 100mg, 5mg, 50mg, 10mg, 25mg | 100µg, 10µg, 1mg | 100ml |
| Description | • A unique collection of 827 endogenous bioactive compounds for high-throughput, high content screening• Used for metabolomics and metabolism related research• Research on metabolic diseases in the human body, explore the pathogenesis of diseases such as tumors, and find effective • A unique collection of 827 endogenous bioactive compounds for high-throughput, high content screening• Used for metabolomics and metabolism related research• Research on metabolic diseases in the human body, explore the pathogenesis of diseases such as tumors, and find effective tools for finding new drugs• Diverse structures, significant pharmacological effects, and good cell permeability• Have comprehensive and detailed structural descriptions, target information, IC50 values, and customer feedback data• NMR, HPLC and other detection techniques ensure the correct structure and high purity of the productProduct Details Formulation 713 compounds pre-dissolved in 10mM DMSO，99 compounds pre-dissolved in 10mM H2O,13 compounds pre-dissolved in 2mM DMSO，2 compounds pre-dissolved in 2mM H2O Container 96 Well Format Sample Storage Tube With Screw Cap and Optional 2D Barcode Stability 12 months -20°C in DMSO 24 months -80°C in DMSO Shipping Blue ice or dry ice Human Endogenous Metabolite Compound Library Composition... Read More | Amyloid β-Protein Fragment 25-35 (Aβ25-35) is derived from the amyloid-β protein.amyloid-β protein, which is mapped to human chromosome 21q21.Aβ25-35 lacks the N-terminal domain and the metal binding site and is majorly generated by proteolytic cleavage of Aβ(1−40Amyloid β-Protein Fragment 25-35 (Aβ25-35) is derived from the amyloid-β protein.amyloid-β protein, which is mapped to human chromosome 21q21.Aβ25-35 lacks the N-terminal domain and the metal binding site and is majorly generated by proteolytic cleavage of Aβ(1−40) peptides. It has a β-sheet and β-turn structure. Amino Acid Sequence Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-MetFunctional domain of Aβ required for both neurotrophic and neurotoxic effects... Read More | IRE1α kinase-IN-2 is a potent IRE1α kinase inhibitor, with an EC 50 of 0.82 µM. IRE1α kinase-IN-2 inhibits IRE1α kinase autophosphorylation (IC 50 =3.12 µM). IRE1α kinase-IN-2 inhibits XBP1 mRNA splicing in the WT cell lines.In VitroIRE1α kinase-IN-2 (compoundIRE1α kinase-IN-2 is a potent IRE1α kinase inhibitor, with an EC 50 of 0.82 µM. IRE1α kinase-IN-2 inhibits IRE1α kinase autophosphorylation (IC 50 =3.12 µM). IRE1α kinase-IN-2 inhibits XBP1 mRNA splicing in the WT cell lines.In VitroIRE1α kinase-IN-2 (compound 3) inhibits XBP1 mRNA splicing, even during ER stress. MCE has not independently confirmed the accuracy of these methods. They are for reference only.Form:Solid... Read More | Purity:>90%, by SDS-PAGE visualized with Coomassie® Blue Staining.Description: DCX (doublecortin, N-GST chimera)contains 2 doublecortin domains and belongs to the doublecortin family. It is highly expressed in neuronal cells of fetal brain, but not expressed in other fetal tissues. In the Purity:>90%, by SDS-PAGE visualized with Coomassie® Blue Staining.Description: DCX (doublecortin, N-GST chimera)contains 2 doublecortin domains and belongs to the doublecortin family. It is highly expressed in neuronal cells of fetal brain, but not expressed in other fetal tissues. In the adult, it is highly expressed in the brain frontal lobe, but very low expression in other regions of brain, and not detected in heart, placenta, lung, liver, skeletal muscles, kidney and pancreas. DCX is a microtubule-associated protein required for initial steps of neuronal dispersion and cortex lamination during cerebral cortex development. It may act by competing with the putative neuronal protein kinase DCAMKL1 in binding to a target protein. DCX may in that way participate in a signaling pathway that is crucial for neuronal interaction before and during migration, possibly as part of a calcium ion-dependent signal transduction pathway. It may be part with LIS-1 of a overlapping, but distinct, signaling pathways that promote neuronal migration. Defects in DCX are the cause of lissencephaly X-linked type 1 and subcortical band heterotopia X-linked... Read More | Format:1-ComponentEnzyme:Horseradish peroxidase |