PTX-35 is a First-in-Class Antibody Agonist of TNFRSF25 with the Potential to Promote Anti-Tumor Effector T Cell Responses
How it works:
- TNFRSF25 is a costimulatory molecule expressed on effector T cells that requires antigen engagement to stimulate cellular expansion under primed conditions.
- In the presence of a “danger signal” arising from the presence of cancer antigens, costimulation of TNFRSF25 on T cells promotes the expansion of inflammatory effector T cells, which play a critical role in mediating anti-tumor responses.
- Upon binding to TNFRSF25, PTX-35 induces dose-dependent expansion of inflammatory IFNγ+ Th1 cells, IL17+ Th17, and IFNγ+ CD8+ effector T cells accompanied by an increase in tumor-infiltrating lymphocytes, delayed disease progression, and increased overall survival in solid tumor animal models1,2.

PTX-35 Phase I Clinical Trial in Solid Tumors
PTX-35 is currently being evaluated in an open-label, single arm, Phase I clinical trial evaluating the safety and tolerability of PTX-35 intravenous administration in patients with advanced solid tumors refractory to, or ineligible for, or who refuse available standard of care. This trial is supported by a grant from the Cancer Prevention and Research Institute of Texas (CPRIT).
References
1 Kalim et al. PTX-35, a potential first-in-class TNFRSF25 agonist, reduced the suppressive activity of regulatory T cells and enhanced CD4+ T cell effector responses, in the presence of tumor antigens, in a murine melanoma model. 2021
2Tahiliani et al. A novel TNFRSF25 agonist, PTX35, synergizes with Gp96-Ig/OX40L-Ig to enhance effector and memory anti-tumor CD8+ T cell responses and delay tumor growth. 2020