Mouse Anti-SOST Recombinant Antibody (MOB-012LC) (CAT#: MOB-012LC)

De Maré, Annelies, et al. "Sclerostin protects against vascular calcification development in mice." Journal of Bone and Mineral Research 37.4 (2020): 687-699. https://doi.org/10.1002/jbmr.4503

This research investigates the role of sclerostin, a negative regulator of Wnt/β-catenin signaling, in the development of vascular calcification. Using both Sost knockout mice (Sost-/-) and anti-sclerostin antibody treatment in two different mouse models of vascular calcification, the study demonstrates that the absence or inhibition of sclerostin promotes vascular calcification. In the adenine-induced chronic kidney disease model, Sost-/- mice developed more extensive cardiac vessel calcifications compared to wild-type mice. Similarly, in the warfarin-induced calcification model (without kidney disease), mice treated with anti-sclerostin antibody showed significantly increased aortic and renal vessel calcification compared to vehicle-treated controls, accompanied by upregulation of Wnt target genes in the vascular tissue.
Creative Biolabs provided the recombinant anti-SOST therapeutic antibody (MOB-012LC) used in the experimental treatments. This antibody was administered subcutaneously at a dose of 25 mg/kg twice weekly to investigate the effects of sclerostin inhibition on vascular calcification development. The antibody effectively blocked sclerostin function as evidenced by increased bone formation parameters, providing a critical tool that helped establish sclerostin's protective role in vascular calcification. This finding has important implications for therapeutic applications of anti-sclerostin antibodies, suggesting potential cardiovascular risks that should be monitored in patients receiving such treatments, particularly those with chronic kidney disease.