Rituximab biosimilar(Merck Sharp & Dohme)

LUND, SE / ACCESS Newswire / June 1, 2026 / BioInvent International AB ("BioInvent") (Nasdaq Stockholm:BINV), a leader in the discovery of novel immune-modulatory antibodies, today announced that it will host an in-person and virtual key opinion leader (KOL) event at GT30, Grev Turegatan 30 in Stockholm on Thursday, June 11, 2026 at 11:45 AM CEST. The event will feature Guilherme Perini MD, PhD (Hospital Israelita Albert Einstein), and Stefan K. Barta, MD, MS (Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania) who will join company management to discuss the treatment landscape, unmet need, and future outlook in non-Hodgkin's lymphoma (NHL) and cutaneous T-cell lymphoma (CTCL). To register for the in-person event, click here . RSVP June 4, 2026. The event will highlight the clinical progress and commercial potential of BioInvent's lead programs in hematology, BI-1206 and BI-1808. Presentations will include new insights into BI-1206's ability to overcome resistance to rituximab through FcγRIIB blockade, including encouraging activity observed in the triple combination with rituximab and Calquence® (acalabrutinib) in patients with relapsed or refractory NHL. In addition, the session will feature BI-1808, a novel anti-TNFR2 immunotherapy, highlighting data from the Phase 2a study in patients with advanced CTCL. Patients in these cohorts received BI-1808 as monotherapy or in combination with MSD's (Merck & Co., Inc., Rahway, NJ, USA) anti-PD-1 therapy KEYTRUDA® (pembrolizumab). Early clinical findings demonstrating meaningful and sustained responses, alongside evidence of immune activation, support its potential as both a monotherapy and combination treatment. Agenda (CEST) 11:45am | BioInvent's BI-1206 & BI-1808 opportunities in hematology | Martin Welschof, CEO 11:50am | NHL treatment landscape, medical need and future outlook | Guilherme Perini, MD, PhD 12:05pm | BI-1206 in NHL: Targeting the Resistance to Rituximab through FcγRIIB Blockade: BI-1206 + Rituximab + Acalabrutinib Shows Powerful Activity in R/R NHL | Andres McAllister, CMO 12:20pm | BI-1206: Market opportunity in NHL | Sylvie Ryckebusch, CBO 12:30pm | Q&A BI-1206 in NHL | All 12:45pm | Coffee break | - 1:00pm | CTCL treatment landscape, medical need and future outlook | Stefan Barta, MD, MS 1:15pm | BI-1808: A Novel Immunotherapy Approach in CTCL: TNFR2 Blockade Shows Durable and Meaningful Responses | Andres McAllister, CMO 1:30pm | BI-1808: Market opportunity in CTCL | Sylvie Ryckebusch, CBO 1:40pm | Q&A BI-1808 in CTCL | All 1:55pm | Closing remarks | Martin Welschof, CEO The event will be conducted in English and a live webcast will be available here . A replay of the webcast will be made available on BioInvent's website following the event. This event is the second in a two-part KOL series. The first event, held on May 27, 2026, focused on BI-1808 for the treatment of ovarian cancer. About Guilherme Perini, MD, PhD Dr. Guilherme Perini is a board-certified hematologist in Brazil, with a focus on lymphoid malignancies. He is the current Director of the Department of Excellence in Lymphoid Malignancies at Hospital Israelita Albert Einstein in São Paulo, Brazil. He is also the Head of Oncology Research at ARO - Academic Research Organization, at Einstein. Dr. Perini is currently the principal investigator in more than 20 clinical trials in lymphoma and chronic lymphocytic leukemia (CLL). About Stefan K. Barta, MD, MS Stefan K. Barta, MD, MS is Associate Professor of Medicine (Hematology-Oncology) directing the T-cell lymphoma program at the University of Pennsylvania and serve as the Executive Officer of the NCI-sponsored Consortium for Advancing Management and Prevention of Cancer in People with HIV (AMC). Additionally, he is an active member of the AMC Lymphoma Working group and the ECOG Lymphoma Core Committee. Dr. Barta is a recognized expert in T-cell lymphomas, including cutaneous T-cell lymphoma (CTCL), and has served as lead author and principal investigator on multiple clinical studies evaluating novel immunotherapies for hematologic malignancies. About the BI-1206 Phase 2a part of the study The triple combination arm in the ongoing Phase 2a part of the study ( NCT03571568 ) combines the subcutaneous formulation of BI-1206 with rituximab and acalabrutinib in subjects with indolent B-cell non-Hodgkin's lymphoma (NHL) who have relapsed or are refractory to rituximab. Patient enrolment (approximately 30 patients) has been completed in Spain, Germany, USA, and Brazil. BioInvent has a clinical supply agreement with AstraZeneca (LSE/STO/Nasdaq: AZN) providing Calquence ® (acalabrutinib) for the combination arm. About BI-1206 FcγRIIB is overexpressed in several forms of NHL and overexpression has been associated with poor prognosis in difficult-to-treat forms of NHL, such as mantle cell lymphoma. By blocking the receptor FcγRIIB on tumor cells, BI-1206 is expected to recover and enhance the activity of rituximab and acalabrutinib in the treatment of several forms of NHL. The drug candidate is evaluated in two separate clinical Phase 1/2a programs, one for the treatment of solid tumors and one for the treatment of non-Hodgkin's lymphoma (NHL), a type of blood cancer. Both programs show encouraging clinical activity along with good tolerability. About the BI-1808 Phase 2a Study ThisPhase 2a trial ( NCT04752826 ) is designed to assess the safety and tolerability of BI-1808 as a single agent (Part A) and in combination with pembrolizumab (Part B), characterize its pharmacokinetics and pharmacodynamics, and assess preliminary antitumor activity by ORR, DoR (duration of response), and progression-free survival (PFS). The modified Severity-Weighted Assessment Tool (mSWAT) was used to assess disease activity. About BI-1808 The anti-TNFR2 antibody BI-1808 is part of BioInvent's tumor-associated regulatory T cells (Treg)-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 T-cell lymphoma and solid tumors. A manuscript detailing the mechanisms of action of the BI-1808 and differentiated BI-1910 anti-TNFR2 antibodies is available on BioRxiv.com , an open-access online repository for yet unpublished research manuscripts (preprints). Both anti-TNFR antibodies show potent anti-tumor efficacy across multiple syngeneic mouse tumor models, can effectively be combined with anti-PD-1, and trigger CD8+ T cell antitumor immunity, albeit by different mechanisms; BI-1808 is a ligand-blocking FcyR-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 FcyR-independent mechanisms. About BioInvent BioInvent International AB (Nasdaq Stockholm: BINV) is a clinical-stage biotech company that discovers and develops novel and first-in-class immuno-modulatory antibodies for cancer therapy, with drug candidates in ongoing clinical programs in Phase 1/2 trials for the treatment of hematological cancer and solid tumors. The Company's validated, proprietary F.I.R.S.T™ technology platform identifies both targets and the antibodies that bind to them, generating many promising new immune-modulatory candidates to fuel the Company's own clinical development pipeline and providing licensing and partnering opportunities. The Company generates revenues from research collaborations and license agreements with multiple top-tier pharmaceutical companies, as well as from producing antibodies for third parties in the Company's fully integrated manufacturing unit. More information is available at . For further information, please contact: Cecilia Hofvander, VP Investor Relations Phone: +46 (0)46 286 85 50 Email: cecilia.hofvander@bioinvent.com BioInvent International AB (publ) Co. Reg. No.: 556537-7263 Visiting address: Ideongatan 1 Mailing address: 223 70 LUND Phone: +46 (0)46 286 85 50 Attachments BioInvent to Host a KOL Event in Stockholm on June 11, 2026, to Discuss Updated BI-1206 & BI-1808 Data in Hematology SOURCE: BioInvent International View the original press release on ACCESS Newswire

Scientists at MIT and Stanford have unveiled a promising new way to help the immune system recognize and attack cancer cells more effectively. Their strategy targets a hidden “off switch” that tumors use to stay invisible to immune defenses—special sugar molecules on the cancer cell surface that suppress immune activity. Early tests show it can supercharge immune responses and outperform current antibody therapies.A research team from MIT and Stanford University has developed a new technique designed to push the immune system to go after tumor cells. The strategy is aimed at helping cancer immunotherapy succeed in far more patients than it does today. At the center of the work is a way to undo a built in "brake" that tumors can trigger to keep immune cells from attacking. That brake is tied to sugars called glycans, which sit on the surface of cancer cells. The scientists found that blocking these glycans with proteins known as lectins can greatly strengthen immune activity against cancer cells. To do this in a targeted way, they built multifunctional molecules called AbLecs that pair a lectin with an antibody that homes in on tumors. "We created a new kind of protein therapeutic that can block glycan-based immune checkpoints and boost anti-cancer immune responses," says Jessica Stark, the Underwood-Prescott Career Development Professor in the departments of Biological Engineering and Chemical Engineering. "Because glycans are known to restrain the immune response to cancer in multiple tumor types, we suspect our molecules could offer new and potentially more effective treatment options for many cancer patients." Stark, who is also a member of MIT's Koch Institute for Integrative Cancer Research, led the study as the paper's lead author. Carolyn Bertozzi, a Stanford professor of chemistry and director of the Sarafan ChEM Institute, served as the senior author. The findings were published in Nature Biotechnology. How Cancer Uses Immune Brakes One of the biggest goals in cancer treatment is teaching the immune system to spot tumor cells and eliminate them. A major group of immunotherapy drugs called checkpoint inhibitors works by interrupting the interaction between two proteins, PD-1 and PD-L1. By blocking that connection, these medicines remove a brake that tumors use to keep immune cells such as T cells from killing cancer cells. Checkpoint inhibitors that target the PD-1 PD-L1 pathway are already approved for several cancers. For some people, they can produce long lasting remission. For many others, however, they provide little benefit or none at all. Because of that gap, researchers are searching for other ways tumors suppress the immune system. One promising target involves interactions between tumor glycans and receptors on immune cells. Siglecs, Sialic Acid, and a Sugar Based Checkpoint Glycans appear on nearly all living cells, but cancer cells often carry versions not found on healthy cells. Many of these tumor specific glycans include a sugar building block called sialic acid. When sialic acids attach to lectin receptors on immune cells, they can switch on an immune dampening pathway. The lectins that recognize sialic acid are called Siglecs. "When Siglecs on immune cells bind to sialic acids on cancer cells, it puts the brakes on the immune response. It prevents that immune cell from becoming activated to attack and destroy the cancer cell, just like what happens when PD-1 binds to PD-L1," Stark says. So far, no approved medicines directly target the Siglec sialic acid interaction, even though many approaches have been explored. One idea has been to create lectins that bind to sialic acids and block their contact with immune cells. But this has struggled because lectins typically do not bind strongly enough to build up in large numbers on the surface of cancer cells. AbLecs Combine Antibodies and Lectins To solve that problem, Stark and her team used antibodies as delivery vehicles to bring more lectins to tumors. The antibody portion targets cancer cells, and once it arrives, the attached lectin can bind sialic acid. That blocks sialic acid from engaging Siglec receptors on immune cells, which lifts the immune brake and lets immune cells including macrophages and natural killer (NK) cells attack the tumor. "This lectin binding domain typically has relatively low affinity, so you can't use it by itself as a therapeutic. But, when the lectin domain is linked to a high-affinity antibody, you can get it to the cancer cell surface where it can bind and block sialic acids," Stark says. A Plug and Play Design Tested in Cells and Mice For this study, the researchers built an AbLec using trastuzumab, an antibody that binds to HER2 and is approved for treating breast, stomach, and colorectal cancers. To create the AbLec, they replaced one arm of the antibody with a lectin, choosing either Siglec-7 or Siglec-9. In lab experiments with cultured cells, this AbLec changed how immune cells behaved, pushing them to attack and kill cancer cells. The team also tested the AbLecs in mice engineered to express human Siglec receptors and human antibody receptors. After the mice were given cancer cells that formed lung metastases, treatment with the AbLec led to fewer lung metastases than treatment with trastuzumab alone. The researchers also demonstrated that the approach is flexible. They could swap in different tumor targeting antibodies such as rituximab, which targets CD20, or cetuximab, which targets EGFR. They could also exchange the lectin portion to target other immunosuppressive glycans, or use antibodies that target checkpoint proteins such as PD-1. "AbLecs are really plug-and-play. They're modular," Stark says. "You can imagine swapping out different decoy receptor domains to target different members of the lectin receptor family, and you can also swap out the antibody arm. This is important because different cancer types express different antigens, which you can address by changing the antibody target." Next Steps and Funding Stark, Bertozzi, and colleagues have launched a company called Valora Therapeutics to develop lead AbLec candidates. They aim to start clinical trials in the next two to three years. Funding for the work came in part from a Burroughs Wellcome Fund Career Award at the Scientific Interface, a Society for Immunotherapy of Cancer Steven A. Rosenberg Scholar Award, a V Foundation V Scholar Grant, the National Cancer Institute, the National Institute of General Medical Sciences, a Merck Discovery Biologics SEEDS grant, an American Cancer Society Postdoctoral Fellowship, and a Sarafan ChEM-H Postdocs at the Interface seed grant.