FoxP3 Program

FoxP3 Program Overview

FoxP3 homodimerization and interaction with co-activators are required for its transcriptional activity. Disruption of these protein-protein interactions inhibits transcription of genes required for Treg development and function, and results in enhanced anti-tumor immune responses. Our FoxP3 peptide hits target the interaction of FoxP3 homodimers and have demonstrated potent inhibition of FoxP3 gene transcription by reporter assay.

Target Overview – Forkhead Box p3 (FoxP3)

Forkhead box p3 (FoxP3) is a protein involved in regulation of immune system responses. FoxP3 functions as a master regulator for the development and function of regulatory T cells (Tregs), a subpopulation of T cells that modulate immune responses by suppressing induction and proliferation of effector T cells. Depletion or inactivation of FoxP3 results in inhibition of Tregs and improved effector T-cell activity in vitro and in vivo.

Tregs contribute to cancer by suppressing T effector cells, thereby compromising tumor killing and promoting tumor growth. Further, Tregs reduce the number of tumor-infiltrating lymphocytes within the tumor microenvironment, diminishing the efficacy of cancer immunotherapies. In cancer, circulating Tregs are often upregulated compared to healthy individuals. Disruption of FoxP3 regulation of Treg development and function in cancer patients reduces the circulating Treg population, thereby increasing T effector cell activity and improving the anti-tumor activity of immunotherapy.

Source: Biorender