ALTB-268

Therapeutic Area

Product Overview
Inheriting the unique mechanism of action from ALTB-168, ALTB-268 is subtly designed as a multiple-valence molecule to achieve a better efficacy. From preliminary experimental results, ALTB-268 exhibits not only comparable preliminary safety profiles, but also improved potency in eliminating chronic pathogenic T cells. Therefore, a lower dosage to obtain an equal efficacy in clinical is expected.

Indication

Ulcerative Colitis

1

  • PRECLINICAL

    Preclinical

  • PHASE I

  • PHASE IIA

  • PHASE IIB

  • PHASE III

  • MARKET

Introduction

T cells play a key role in immune system, and are particularly important in the chain of events that are believed to lead to the inflammation and autoimmunity.

Based on current structure of ALTB-168, a second generation of the therapeutic antibody with multivalent design that leads to improve potency is being under development. So far, in vitro and in vivo studies with this modified antibody have demonstrated a 10-fold increase at least in activity of abolishing activated T cells (killer immune cells that cause inflammation). The company is dedicated to bring forth this potential candidate for pre-clinical studies.

Solid Organ Transplantation

2

  • PRECLINICAL

    Preclinical

  • PHASE I

  • PHASE IIA

  • PHASE IIB

  • PHASE III

  • MARKET

Introduction

Solid organ transplantation is a potentially life-saving option for patients faced with terminal organ failure. However, immunosuppressive drugs are needed for prevention of rejection of transplanted organs and long-term administration of immunosuppressive medications has potential unfavorable consequences including increased susceptibility to opportunistic infections and malignancies.

Because of the unique MOA of ALTB-168, we believe it has the potential for a durable response allowing patients to avoid long-term administration of immunosuppressive medications. We are currently studying the use of ALTB-168 in preclinical non-human primate renal transplantation models.