PB101 Target Overview

  • Signal 1 (T cell receptor signal), Signal 2 (Co-stimulatory factor), and Signal 3 (cytokine) are required for activation of T cells. It is well known that when only signal 1 is given to T cells without signal 2 (co-stimulatory factor), they become anergic (refractory state).

  • As for co-stimulatory factors, many studies have been conducted on the CD40L-CD40 axis, and blocking this axis has resulted in successful results in various mouse disease models.



    CD40 is expressed on B cells, dendritic cells, macrophages, etc. A typical ligand of CD40 is CD40L (CD154), which is expressed on T cells, platelets, and vascular endothelial cells.

  • Development of a new anti-CD40 antibody by attempting to develop an excellent anti-CD40 antibody that has the same level of CD40 signaling blocking effect as the anti-CD40L antibody and does not cause serious side effects.

MoA & Indication of PB101

Target (MoA) As a humanized monoclonal anti-CD40 antibody that targets CD40 expressed on antigen-presenting cells (B cells, dendritic cells, macrophages), it inhibits T cell activation by blocking CD40L/CD40 binding.
Indication

- Autoimmune disease

  • Multiple sclerosis
  • Sjogren's Syndrome
  • Rheumatoid arthritis

- Organ transplant

  • Cell Transplantation (Islets)
  • Tissue transplant (cornea)

Distinctive advantage of PB101

  • A

    High efficiency in blocking of epitope binding (5-15 times compared to competitors).

  • B

    High affinity (0.45 nM, no further development required)

  • C

    Non-agonistic properties (pure binding blocking antibody)

  • D

    Non- or minimal depleting properties (minimize side effects)

  • E

    Nonhuman primate/human crosslinking (non-clinical/clinical trials possible).

  • F

    Xenograft (porcine)–human signaling blockade (can be specialized for xenotransplantation)

  • G

    Novel epitope binding (broad scope of rights)

  • H

    αCD154 mAb (5C8) counterpart epitope binding (high efficacy expected)

  • I

    Linear form epitope binding (minimum difference in efficacy due to structural change)

    • It meets all the necessary and sufficient conditions for antibody therapeutics.

    • Possibility of Best-In-Class Drug Development