The Future of Transplant Care
Veloxis is committed to helping patients discover the possibilities of life after transplant. That’s why we’re leveraging our research and development capabilities in transplant treatments to maintain our focus on improving the lives of patients in need. By working to develop new therapies, we aspire to enhance the current standard of care and increase access to life-changing medication.
Note: Colors in graphic denote different stages of progress.
VEL-101 Clinical Program1
VEL-101 has been evaluated in a first-in-human study to assess the safety, pharmacokinetics, pharmacodynamics, and potency of IV administrations in healthy subjects.
VEL-101 (formerly known as FR104), a pegylated monoclonal antibody fragment CD28 antagonist,
selectively blunts CD28 co-stimulation while sparing the CTLA-4 co-inhibitory signal. The net effect of CD28 antagonism is downregulating effector T cells while potentially promoting regulatory T-cell (Treg) activity.
The CD28/CTLA-4 pathways modulate both effector T-cell activation and regulatory T-cell activity.
The CD28 receptor is expressed on the surface of the majority of naive T cells and is an important costimulatory molecule for T-cell activation.
In contrast, CTLA-4, a CD28 homologue, is expressed on activated T cells, especially Tregs, and has been historically described as an essential component of the regulation of immune self-tolerance.
The CD28-CD80/86 pathway can be inhibited both on the antigen-presenting cell by inhibiting CD80 and CD86, or on the T cell directly by inhibiting CD28. When inhibiting CD80/86, both signaling pathways through CTLA4 and CD28 potentially can be blocked.
Findings from the VEL-101 Phase I clinical study support the continued clinical development of this investigational product in transplantation.
Reference: 1. Poirier N, et al. First-in-human study in healthy subjects with FR104, a pegylated monoclonal antibody fragment antagonist of CD28. J Immunol. 2016;197(12):4593-4602.