Ipilimumab

iStock, Deagreez If AstraZeneca and Bristol Myers Squibb were to successfully become one company, analysts say it could reset the current deal environment, which has picked up greatly in the first half of the year. News broke over the weekend that Bristol Myers Squibb and AstraZeneca—both massive pharma companies worth more than $130 billion each—have held talks to merge. Analysts largely brushed off the idea as “unlikely,” given the companies have major competing products that would likely snarl the deal in antitrust review. On Monday morning, AstraZeneca’s shares fell more than 4% in pre-market trading to $162.13. On the flip side, BMS rose nearly 6% to $69.20. Rumors of such a deal were reported by The Financial Times on Sunday. If the mega-merger did come to pass, it would be the largest in the pharma industry’s history. But analysts are skeptical. ezstandalone.cmd.push(function () { ezstandalone.showAds(129); }); “Based on significant business overlap, we believe a deal is less likely to materialize,” BMO Capital Markets wrote on Sunday evening. The analysts pointed to the heavy scrutiny the deal would likely receive from antitrust officials on both sides of the pond. “Looking across both Bristol and AstraZeneca’s commercial portfolio, we note several areas of overlap that could reduce the odds of a successful merger,” BMO said. Most notably, the companies compete in non-small cell lung cancer with BMS’s Opdivo and AstraZeneca’s Imfinzi. Opdivo brought in $10.05 billion worldwide in 2025, while Imfinzi took in $6.06 billion. “Multiple other therapeutic overlaps exist between the two companies to varying degrees of competition, likely raising FTC questions on potential anti-competitive issues with a deal,” BMO said. BMS is no stranger to mega deals. The company bought Celgene in 2019 for $74 billion. To complete that deal, BMS was ordered to divest psoriasis and psoriatic arthritic drug Otezla to Amgen. Deals Bristol-Myers Squibb Plans to Sell Celgene’s Otezla in Attempt to Expedite Acquisition “Bristol-Myers Squibb is committed to working with regulatory authorities around the world on the proposed combination with Celgene,” the company stated. “The company is focused on realizing the promise of the transaction, and is continuing to work to complete the transaction on a timely basis.” June 24, 2019 · 2 min read · Mark Terry Read more Neither BMS nor AstraZeneca has the firepower to buy the other outright, BMO added, making a direct acquisition unlikely. The analysts put BMS’s deal capacity at about $32 billion and AstraZeneca’s around $37 billion. BMS has a current market cap of $133.41 billion, while AstraZeneca is larger at $195.93 billion, according to data from S&P Capital IQ. If the deal does manage to overcome all the hurdles in front of it, analysts suspect the achievement could reset the current deal environment, which has already been busy in the first half of the year. “A successful AZN-BMS merger could trigger a new wave of M&A among large global pharma companies,” Jefferies wrote on Sunday. A new paradigm in cancer treatment The joining of AstraZeneca and BMS would also reset the cancer landscape, Jefferies noted. The combined company would rake in $100 billion in annual sales with the “deepest oncology portfolio in the industry,” the firm wrote. “The strategic rationale may be extending beyond cost synergies to a competition for larger portfolios of complementary assets that can support complex combination regimens,” Jefferies said. Up until now, AstraZeneca has successfully combined its Imfinzi with the Daiichi Sankyo–partnered drug Enhertu and Datroway. Should BMS join AstraZeneca, it would open the door for Opdivo combos. “A combination with BMS would remove the commercial barriers to exploring more combinations with Opdivo, which has a broader scientific and commercial footprint than Imfinzi,” Jefferies wrote. The companies could also look at triplet regimens by pairing targeted therapies with immuno-oncology drugs and antibody-drug conjugates (ADCs). AstraZeneca has many of these targeted options in its portfolio, including Tagrisso, Lynparza, Truqap and the investigational camizestrant, which is under FDA review . BMS, meanwhile, has immuno-oncology asset Yervoy and next-generation programs in the clinic, Jefferies said. Working together, BMS and AstraZeneca could create complex treatment regimens in lung, breast, ovarian and gastrointestinal cancers, Jefferies said. “Combination therapies increasingly define the standard of care in oncology, and the ability to develop and commercialize more complex multi-drug regimens without cross-company negotiations may ultimately prove one of the most compelling strategic rationales for a merger.” Earnings AstraZeneca has no plans to ramp up dealmaking in wake of Wainua failure AstraZeneca remains “very much on track” to hit its 2030 goal of reaching $80 billion in revenue despite the recent late-stage failure of Wainua in ATTR-cardiomyopathy, CEO Pascal Soriot said during the company’s Q2 earnings presentation on Monday. July 27, 2026 · 3 min read · Tristan Manalac Read more

Preclinical proof-of-concept data support two distinct FcγR-blockade strategies to enhance cancer antibody therapies and overcome resistance BI-1206 boosts αPD-1 antibody activity by protecting effector CD8+ T cells from macrophage-mediated depletion, a mechanism identified as limiting αPD-1 efficacy Findings reinforce the mechanistic rationale for BI-1206's ongoing Phase 2a evaluation with pembrolizumab in first-line NSCLC and uveal melanoma; initial data expected second half of 2026 Complementary Fc-engineered variant BI-1607 enhances αCTLA-4 antibody activity, including ipilimumab, by deepening intratumoral Treg depletion Lund, Sweden – July 28, 2026 – BioInvent International AB (“BioInvent”) (Nasdaq Stockholm: BINV), a leader in the discovery of novel immune‑modulatory antibodies, today announce that preclinical proof‑of‑concept data supporting the mechanistic rationale for BI-1206 and BI-1607 in combination with immune checkpoint blockade have been published in the peer-reviewed Journal of Experimental & Clinical Cancer Research (JECCR). The publication, titled "Tailored FcγR Blockade Enhances Immune Checkpoint Therapy and Overcomes Resistance," identifies tailored FcγR blockade as a strategy to overcome resistance to PD-1-directed checkpoint therapy. BI-1206, an anti-FcγRIIB antibody with a wild-type Fc domain, was shown to enhance the activity of the approved αPD-1 antibodies nivolumab and pembrolizumab by protecting effector CD8+ T cells from macrophage-mediated depletion. These findings provide the mechanistic foundation for BioInvent's ongoing Phase 2a evaluation of 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-FcγRIIB antibody variants, BI-1607 and its murine surrogate, engineered with an Fc-silenced Fc domain, were shown to enhance αCTLA-4 antibodies, including ipilimumab, through selective FcγRIIB blockade. The BI-1607 program is currently paused as BioInvent focuses resources on advancing its lead programs BI-1206 and BI-1808. "This work resolves a longstanding question in the field: whether and how FcγRs affect immune checkpoint blockade efficacy," said Björn Frendéus, Chief Scientific Officer of BioInvent and corresponding author of the study. "The answer depends on which immune cells express the checkpoint target. When a checkpoint target sits on suppressive regulatory T cells, as with CTLA-4, FcγR engagement helps antibodies deplete them, an effect BioInvent's Fc-silenced BI-1607 was designed to amplify. When the target sits on the effector CD8+ T cells that deliver anti-tumor activity, as with PD-1, FcγR engagement causes those cells to be cleared instead. Blocking all FcγRs with an Fc-competent antibody like BI-1206 protects those CD8+ T cells and preserves αPD-1 efficacy. These findings provide the mechanistic foundation for BI-1206, our lead FcγRIIB-blocking antibody, and directly support the ongoing Phase 2a evaluation of BI-1206 in combination with pembrolizumab in first-line NSCLC and uveal melanoma." "Despite the transformative impact of checkpoint inhibitors, most patients still fail to benefit long-term from these therapies," said Mark S. Cragg, Professor of Experimental Cancer Biology, Antibody and Vaccine Group, School of Cancer Sciences, University of Southampton and co-senior author of the study. "The mechanistic insights described in this paper give us a clear path to designing next-generation antibody combinations that address the underlying biology limiting current immunotherapy responses. This has been another highly productive collaboration between the Antibody and Vaccine Group at Southampton and BioInvent, and we look forward to seeing these principles translate into meaningful clinical benefit." Publication overview: Mechanistic basis for enhancing PD-1 and CTLA-4 checkpoint therapyImmune 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 field's most pressing challenges. Further limiting patient benefit, CTLA-4 checkpoint therapy is often dose-limited by toxicity. Fc gamma receptors (FcγRs) regulate therapeutic antibody activity by engaging immune effector cells. Prior work established that different checkpoint antibodies have opposing FcγR requirements: αPD-1 antibodies can be undermined by FcγR-dependent depletion of the very effector CD8+ T cells they are designed to reactivate, whereas αCTLA-4 antibodies rely on FcγR engagement to deplete tumor-infiltrating regulatory T cells. The JECCR study reconciles these opposing requirements and identifies tailored FcγR blockade with BI-1206 as a strategy to overcome αPD-1 resistance and with BI-1607 to enhance αCTLA-4 efficacy in a tumor-selective manner, potentially improving tolerability. About the StudyThe study was conducted by researchers at BioInvent International and the University of Southampton's Antibody and Vaccine Group, School of Cancer Sciences. Stephen A. Beers and Mark S. Cragg (University of Southampton) and Ingrid Teige and Björn Frendéus (BioInvent) share senior authorship; Frendéus is corresponding author. The processed and raw single-cell RNA sequencing data have been deposited in the NCBI Gene Expression Omnibus under accession number GSE335831. About BI-1206FcγRIIB is an inhibitory Fc gamma receptor often upregulated in the tumor microenvironment. Alongside activating Fc gamma receptors, FcγRIIB expressed on immune effector cells can limit the efficacy of PD-1-directed checkpoint therapy. BI-1206 is a human anti-FcγRIIB monoclonal antibody with a wild‑type Fc domain, designed to block FcγRs on tumor-associated macrophages, thereby preventing macrophage-mediated depletion of PD-1-coated CD8+ T cells and preserving αPD-1 antitumor activity. A Phase 2a study of BI-1206 in combination with MSD's (Merck & Co., Inc., Rahway, NJ, USA) anti-PD-1 therapy KEYTRUDA® (pembrolizumab) 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). About BioInventBioInvent 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 on the Company’s website. For further information, please contact:Cecilia Hofvander, VP Investor RelationsPhone: +46 (0)46 286 85 50Email: cecilia.hofvander@bioinvent.comBioInvent International AB (publ)Co. Reg. No.: 556537-7263Visiting address: Ideongatan 1Mailing address: 223 70 LUNDPhone: +46 (0)46 286 85 50www.bioinvent.com The press release contains statements about the future, consisting of subjective assumptions and forecasts for future scenarios. Predictions for the future only apply as the date they are made and are, by their very nature, in the same way as research and development work in the biotech segment, associated with risk and uncertainty. With this in mind, the actual outcome may deviate significantly from the scenarios described in this press release.