Vascular stress such as hyperlipidemia, oxidized LDL (ox-LDL), and smoking activates NF-κB, MAPKs, and AP-1 signaling in vascular endothelial cells, inducing increased expression of ICAM-1, VCAM-1, and related molecules, along with endothelial inflammation.

As a result, monocyte adhesion and transendothelial migration (TEM) are promoted, while macrophage activation and foam-cell formation accelerate the accumulation and progression of atherosclerotic plaques.

BSP105 is a recombinant protein derived from the AI-powered BSP™ platform, designed to regulate ICAM-1 / VCAM-1-centered endothelial–immune interactions at the upstream level of these vascular inflammatory responses.

BSP105 is designed to stabilize the vascular inflammatory environment by alleviating excessive activation of endothelial inflammatory signaling.

Mechanism-driven therapeutic strategy

• A mechanism-based therapeutic strategy that inhibits vascular inflammatory cell adhesion
  by modulating integrin-mediated inflammatory signaling