HiFiBiO Therapeutics, a multinational clinical-stage biotherapeutics company, announced today that the first patient has been dosed with HiFiBiO’s HFB200301, a first-in-class agonistic anti-TNFR2 monoclonal antibody, in combination with tislelizumab, an investigational anti-PD-1 immune checkpoint inhibitor, for the treatment of advanced solid tumor indications preselected by HiFiBiO’s proprietary Drug Intelligence Science (DIS®) platform.
This open-label, multi-center, Phase 1a/b study of HFB200301 and tislelizumab (NCT05238883) investigates the safety and tolerability of this combination therapy. Data from the trial will inform combination dose and dosing regimen, further indication selection, and biomarker strategy.
“Having the first patient dosed with HFB200301 and tislelizumab combination therapy is a significant milestone for HiFiBiO,” commented Liang Schweizer, PhD, Founder, CEO, and Chairperson of HiFiBiO Therapeutics, “This marks a major step toward further understanding the therapeutic activity of HFB200301 and how we can best deliver safe and effective treatment strategies for cancer patients where other therapeutic options have failed.”
Under the terms of the previously announced clinical supply agreement, Novartis will supply tislelizumab for use in combination with HFB200301 and HiFiBiO Therapeutics will maintain control of the HFB200301 program, including global R&D and commercial rights.
HFB200301 is a first-in-class agonistic anti-TNFR2 antibody that binds potently and selectively to TNFR2, and induces the activation of CD4 T cells, CD8 T cells and NK cells. HFB200301 demonstrates potent antitumor activity as a single agent and in combination with anti-PD-1 in animal models. HiFiBiO is applying a biomarker strategy by leveraging its DIS® platform to select indications that may benefit the most from HFB200301 as a monotherapy as well as combination therapy.
Tislelizumab is an investigational humanized IgG4 anti-PD-1 monoclonal antibody specifically designed to minimize binding to Fc-gamma (Fcγ) receptors on macrophages. In pre-clinical studies, binding to Fcγ receptors on macrophages has been shown to compromise the anti-tumor activity of PD-1 antibodies through activation of antibody-dependent macrophage-mediated killing of T effector cells.