Announcement • Jun 11
BioInvent International AB (publ)'s TNFR2 Antibody BI-1808 Delivers Meaningful Responses and Immune Activation as Single Agent and in Combination with KEYTRUDA in Advanced CTCL (EHA 2026)
BioInvent International AB (publ) announced that clinical data from its ongoing Phase 2a trial evaluating BI-1808, its novel anti-TNFR2 monoclonal antibody, in patients with advanced CTCL is being presented at the European Hematology Association (EHA) 2026 Congress in Stockholm, Sweden in a poster titled “Targeting TNFR2 with BI-1808 with or without pembrolizumab: Immune activation and promising responses in advanced cutaneous T-cell lymphomas (CTCLs).” The poster is being presented by Stefan K. Barta, MD, MS, Associate Professor of Medicine (Hematology-Oncology) and Director of the T-Cell Lymphoma Program at the Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania in Philadelphia, US, and these data underscore BI-1808’s potential as both a single agent and combination therapy in this difficult-to-treat cancer with limited therapeutic options. The poster highlights emerging translational, efficacy and safety findings from the Phase 2a cohort in patients with advanced CTCL, including mycosis fungoides and Sézary syndrome. Patients in these cohorts received BI-1808 either as monotherapy or in combination with MSD’s (Merck & Co. Inc., Rahway, NJ., USA) anti-PD-1 therapy KEYTRUDA® (pembrolizumab). Advanced cutaneous T-cell lymphomas are associated with poor long-term outcomes, and patients who relapse after multiple lines of systemic therapy face limited and often short-lived treatment options. Durable responses remain uncommon, underscoring the need for novel therapeutic approaches. TNFR2 is highly upregulated in the tumor microenvironment. With its differentiated mechanism of action, depleting immunosuppressive Treg cells and reprogramming myeloid cells to unleash CD8+ T cell antitumor immunity, BI-1808 offers a promising new approach to cancer immunotherapy. Against this backdrop, the BI-1808 data are particularly significant, demonstrating meaningful and durable clinical activity alongside strong immune activation in a heavily pretreated CTCL population. By selectively targeting TNFR2 and reshaping the tumor immune microenvironment, BI-1808 has the potential to translate immune activation into sustained clinical benefit, both as monotherapy and in combination with pembrolizumab. BI-1808 has received FDA Orphan Drug Designation for T-cell lymphoma and FDA Fast Track Designation for relapsed or refractory MF and SS, as well as a positive opinion from the European Medicines Agency (EMA) for Orphan Drug Designation in CTCL, collectively underscoring the significant unmet medical need and supporting an accelerated path to approval. BI-1808 Single Agent Cohort Fully Enrolled with Responses Across Both MF and SS Subtypes: The signal-seeking portion of the Phase 2a study has been fully enrolled. Twenty patients with advanced-stage CTCL received BI-1808 1000 mg Q3W as monotherapy (12 mycosis fungoides (MF), 8 Sézary syndrome (SS)). Nine patients received BI-1808 in combination with pembrolizumab 200 mg Q3W (6 MF, 3 SS), representing a heavily pretreated population with a median of 6 prior systemic lines of therapy (range 1–18), no prior anti-PD-1 exposure, and 4 patients having received prior mogamulizumab. BI-1808 Monotherapy Achieves 40% ORR Including a Complete Response Ongoing at Two Years: Of 15 patients evaluable by the modified Severity Weighted Assessment Tool (mSWAT), the standard measure of skin disease burden in CTCL, BI-1808 achieved an ORR of 40%, with 5 confirmed partial responses across both MF and SS subtypes, and one Sézary syndrome patient achieving a complete response that remains ongoing at approximately two years. Eight additional patients achieved stable disease as best response, corresponding to a disease control rate (DCR) of 93%. Two patients with peripheral T-cell lymphoma (PTCL), an aggressive type of lymphoma, were also evaluable, with one achieving a partial response and one stable disease. Combination with Pembrolizumab Delivers 50% ORR in Patients with No Prior Anti-PD-1 Exposure: Of 8 evaluable patients in the combination arm, 4 achieved a partial response at first assessment and 2 achieved stable disease, resulting in an ORR of 50% and a DCR of 75%. The lower DCR of 75% in the combination arm compared to 93% in the monotherapy arm is consistent with the smaller, more heavily pretreated patient population evaluated to date. Translational Data Confirm Immune Activation and Provide a Mechanistic Basis for Durable Responses: Translational data from the study provides important mechanistic support for BI-1808's activity. Sustained depletion of CD4+ T cells in blood was observed in patients with disease control during the first treatment cycle, consistent with the drug's Fc?R-mediated depletion of regulatory T cells. Elevated serum levels of IL-12, CXCL11, and CCL19 were observed in responders compared to non-responders, indicating an important myeloid reprogramming, CD8+ T cell activation, and the formation of tertiary lymphoid structures which are biomarker signals associated with durable and sustained anti-tumor immune responses. Low Rate of Severe Side Effects Allows Patients to Remain on Treatment Long-Term: BI-1808 was very well tolerated as a single agent. The most commonly reported treatment-related adverse events (TRAEs) included fatigue, flares (a transient worsening of cutaneous symptoms such as erythema and pruritus shortly after the first dose that is recognized in this patient population), and hypertension. The combination with pembrolizumab was generally well tolerated in this heavily pretreated population, with the most frequently reported TRAEs including fatigue, chills, pyrexia, and infusion-related reactions, consistent with the known profiles of both agents.
Taken together, these data support TNFR2 as a compelling therapeutic target in CTCL and highlight BI-1808’s potential as a novel immunotherapeutic approach, both as monotherapy and in combination with immune checkpoint inhibition.
