공고 • Jul 28
BioInvent International Publishes Preclinical Proof-Of-Concept Data Supporting Mechanistic Rationale For BI-1206 And BI-1607 In Combination With Immune Checkpoint Blockade BBioInvent International AB had preclinical proof-of-concept data supporting the mechanistic rationale for BI-1206 and BI-1607 in combination with immune checkpoint blockade published in the peer-reviewed Journal of Experimental & Clinical Cancer Research (JECCR). The publication, titled "Tailored Fc?R Blockade Enhances Immune Checkpoint Therapy and Overcomes Resistance," identifies tailored Fc?R blockade as a strategy to overcome resistance to checkpoint therapy. BI-1206, an anti-Fc?RIIB antibody with a wild-type Fc domain, was shown to enhance the activity of the approved anti-PD-1 antibodies nivolumab and pembrolizumab by protecting effector CD8+ T cells from macrophage-mediated PD-1 depletion. These findings provide the mechanistic foundation for ongoing Phase 2a evaluation of BioInvent's BI-1206 in combination with pembrolizumab in first-line NSCLC and uveal melanoma, with initial data expected in the second half of 2026. In the same study, structurally distinct anti-Fc?RIIB antibody variants, BI-1607 and its murine surrogate, engineered with an Fc-silenced domain, were shown to enhance anti-CTLA-4 antibodies, including ipilimumab, through selective Fc?RIIB blockade. The BI-1607 program is currently paused as BioInvent focuses resources on advancing its lead programs BI-1206 and BI-1808. Mechanistic basis for enhancing PD-1 and CTLA-4 checkpoint therapy: Immune checkpoint inhibitors have transformed cancer treatment, yet most patients either do not respond or develop resistance during therapy. Understanding and overcoming that resistance is one of the most pressing challenges. Further limiting patient benefit, CTLA-4 checkpoint therapy is often dose-limited by toxicity. Fc gamma receptors (Fc?Rs) regulate therapeutic antibody activity by engaging immune effector cells. Prior work established that different checkpoint antibodies have opposing Fc?R requirements: anti-PD-1 antibodies can be undermined by Fc?R-dependent depletion of the very effector CD8+ T cells they are designed to reactivate, whereas anti-CTLA-4 antibodies rely on Fc?R engagement to deplete tumor-infiltrating regulatory T cells. The JECCR study reconciles these opposing requirements and identifies tailored Fc?R blockade with BI-1206 as a strategy to overcome anti-PD-1 resistance and with BI-1607 to enhance anti-CTLA-4 efficacy in a tumor-selective manner, potentially improving tolerability. The study was conducted by researchers at BioInvent International and the University of Southampton's Antibody and Vaccine Group, School of Cancer Sciences. The processed and raw single-cell RNA sequencing data have been deposited in the NCBI Gene Expression Omnibus under accession number GSE335831. BI-1206: Fc?RIIB is an inhibitory Fc gamma receptor often upregulated in the tumor microenvironment. Alongside activating Fc gamma receptors, Fc?RIIB expressed on immune effector cells can limit the efficacy of checkpoint therapy. BI-1206 is a human anti-Fc?RIIB monoclonal antibody with a wild-type Fc domain, designed to block Fc?Rs on tumor-associated macrophages, thereby preventing macrophage-mediated depletion of PD-1-coated CD8+ T cells and preserving anti-PD-1 antitumor activity. A Phase 2a study of BI-1206 in combination with MSD's KEYTRUDA (pembrolizumab) therapy is ongoing in treatment-naïve patients with advanced or metastatic non-small cell lung cancer (NSCLC) and uveal melanoma, with initial data expected in the second half of 2026 (NCT04219254). BI-1206 is also being evaluated in a separate Phase 2a triple combination with rituximab and Calquence (acalabrutinib) in relapsed/refractory non-Hodgkin's lymphoma, where the antibody addresses a distinct resistance mechanism relevant to CD20-directed therapy (NCT03571568). 공고 • Jul 17
BioInvent International AB Abstract On BI-1808 In Platinum-Resistant Ovarian Cancer Accepted For Poster Presentation At ESMO 2026 BioInvent International AB announced that its abstract describing immune-modulatory BI-1808 in recurrent platinum-resistant ovarian cancer (PROC) has been accepted for a poster presentation at the European Society for Medical Oncology (ESMO) Congress 2026, taking place October 23-27, 2026, in Madrid, Spain. Recurrent ovarian cancer that has progressed after platinum-based chemotherapy represents a significant unmet need. Pembrolizumab monotherapy has historically achieved an 8% response rate in this setting (KEYNOTE-100), while the addition of BI-1808 pushes the response rate to 24% and in a much more heavily pretreated patient population. BioInvent's first-in-class antibody targeting TNFR2 depletes immunosuppressive regulatory T cells, activates myeloid cells in the tumor microenvironment (TME), activates CD8+ T cells, and displays complementary activity with PD-1 blockade. At ASCO in May 2026, BioInvent presented preliminary Phase 2a data showcasing 56% disease control rate (DCR) in the BI-1808 plus pembrolizumab combination arm, including multiple durable responses extending beyond 10 months with patients still on treatment. The combination exhibits a very favorable safety profile, and, in contrast to chemotherapy-based regimens, results in very low rates of treatment discontinuations. The upcoming ESMO poster will include updated data compared to ASCO 2026 and the full data set (approx. 40 patients) is expected before year-end 2026. Poster presentation details: Title: From Modest to Meaningful: Targeting TNFR2 with BI-1808 to Unlock Checkpoint Inhibitor Efficacy in Recurrent Platinum Resistant Ovarian Cancer (PROC), Abstract number: 7852, Presentation type: Poster. This Phase 2a trial (NCT04752826) is designed to assess the safety and tolerability of BI-1808 as a single agent (Part A), in combination with pembrolizumab (Part B) and in a triple combination with pembrolizumab and paclitaxel (Part C). The study aims to characterize safety, pharmacokinetics and pharmacodynamics, and assess preliminary antitumor activity by ORR, DoR (duration of response), and progression-free survival (PFS), as measured by RECIST and iRECIST v1.1. The BI-1808 antibody is part of BioInvent’s tumor-associated regulatory T cells (Treg) anti-TNFR2 targeting program. TNFR2 is particularly upregulated on Tregs of the tumor microenvironment and has been shown to be important for tumor expansion and survival, representing a new and promising target for cancer immunotherapy. BI-1808 is a first-in-class drug candidate in clinical development for the treatment of lymphoma and solid tumors. BI-1808 has shown T-cell activity as well as excellent safety and tolerability, in monotherapy and in combination with pembrolizumab in an ongoing Phase 1/2a study for the treatment of solid tumors and lymphomas. A manuscript detailing the mechanism of action of BI-1808 (and BI-1910) is available on BioRxiv.com. BI-1808 is a ligand-blocking FcgR-engaging antibody that depletes immunosuppressive Treg cells and reprograms myeloid cells. BI-1808 shows potent anti-tumor efficacy across multiple syngeneic mouse tumor models, can effectively be combined with anti-PD-1, and triggers effective CD8+ T cell antitumor immunity. 공고 • Mar 25
BioInvent International AB (publ), Annual General Meeting, Apr 29, 2026 BioInvent International AB (publ), Annual General Meeting, Apr 29, 2026, at 16:00 W. Europe Standard Time. Location: elite hotel, ideon on scheelevagen 27 in lund, Sweden 공고 • Mar 17
BioInvent International AB (publ) to Report Fiscal Year 2025 Final Results on Mar 31, 2026 BioInvent International AB (publ) announced that they will report fiscal year 2025 final results on Mar 31, 2026 공고 • Jan 05
Bioinvent Reports Promising Data from Ongoing Phase 2A Study for Bi-1808 with Keytruda®(Pembrolizumab) in Recurrent Ovarian Cancer BioInvent International AB announced encouraging interim results from its ongoing Phase 2a signal-seeking study evaluating BI-1808, a novel immuno-oncology candidate, in combination with MSD's (Merck & Co. Inc., Rahway, NJ, USA) anti-PD-1 therapy KEYTRUDA® (pembrolizumab) in patients with recurrent ovarian cancer who have progressed following platinum-based therapy. The interim data from the signal-seeking cohort of patients with recurrent ovarian cancer demonstrates an overall response rate (ORR) of 24%, which represents a meaningful improvement over pembrolizumab monotherapy. Some responses have been observed after several months of treatment, suggesting that additional responses with potentially important impact on PFS (Progression Free Survival) may be observed. The combination was generally safe and well-tolerated, and all adverse events were manageable with standard medical treatments. Exploratory analyses indicate strong activity in both high-grade serous and clear cell ovarian cancer subtypes. The Phase 2a expansion will enroll an additional 20 patients focusing on these subtypes to validate and quantify the signal with an expected readout in H2 2026. Clinical trial collaboration and supply agreement. KEYTRUDA® is a registered trademark of Merck Sharp & Dohme LLC, a subsidiary of Merck & Co. Inc., Rahway, NJ., USA, to evaluate the combination of BI-1808 and MSD's anti-PD-1 therapy, KEYTRUDA (pembrolizum AB). This Phase 2a trial (NCT04752826) is designed to assess BI-1808 administered as a single agent (Part A) and in combination with pembrolizumab (Part B) at the respective recommended Phase 2 dose (RP2D) determined in Phase 1. Phase 2a expansion is being conducted in indication specific cohorts of subjects. The aim of the Phase 2a is to further assess the safety and tolerability of BI-1808 as a single agent (PartA) and in combination with p Embrolizumab (PartB), characterize its PK and pharmacodynamics, and assess preliminary antitumor activity by ORR, DoR (duration of response), and progression-free survival (PFS), as measured by RECIST v1.1 and iRECIST. BI-1808 is a ligand-blocking FcgR-engaging antibody that depletes immunosuppressive Treg cells and reprograms myeloid cells. BI-1910 is a pure agonist antibody that directly co-stimulates T and NK cells through partially FcgR-independent mechanisms. 
