BOSON BIOSCIENCE

BOSON BIOSCIENCE

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BSP™ Platform Overview

  • Pipeline

    BSP205

  • Program Target

    FAK-PI3K-AKT

  • Disease indication

    Triple-Negative
    Breast Cancer

  • Development Stage

    Pre-clinical

  • Summary

    Triple-negative breast cancer (TNBC) is an aggressive cancer subtype in which NF-κB and FAK-PI3K-AKT signaling are excessively activated within the tumor microenvironment.

    This signal activation increases inflammatory cytokine secretion and activates EMT, promoting cancer-cell survival, invasion, metastasis, and rapid tumor growth.

    BSP205 is a recombinant protein derived from the AI-powered BSP™ platform, designed to regulate the inflammatory and mechanotransduction signaling axes overactivated in TNBC at an upstream level.

    BSP205 is designed to alleviate the formation of a tumor-promoting microenvironment by regulating the FAK-PI3K-AKT pathway.

  • Structure & Mechanism

    • Mechanism: Regulation of the FAK–PI3K–AKT pathway
    • Response: Reduced inflammatory cytokines and mitigation of EMT-related signaling
  • Preclinical Highlights

    Trend toward inhibition of tumor proliferation

    • Reduced signals associated with tumor growth confirmed in TNBC cells
    • MDA-MB-231 EV
    • MDA-MB-231 BSP205
    • MDA-MB-231
    • MDA-MB-468 EV
    • MDA-MB-468 BSP205
    • MDA-MB-468

    Reduced invasion and migration

    • Reduced EMT-related markers and decreased cell motility

    Mechanism-effect Linkage

    • Confirmed mechanistic association between inflammatory signal regulation and tumor-suppressive responses