On April 17, 2026 Precision Biologics, Inc. reported a new target in Acute Myeloid Leukemia (AML) for CAR-NK therapy. Recent data for several human AML subtypes expressing truncated core 1 O-glycans will be presented in a poster at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting on April 19th, 2026, in San Diego, CA, USA.

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Poster title: NEO-201-recognized truncated Core 1 O-glycans represent a new target for CAR-NK therapy in AML

Presentation of the poster will be made in person on the following date and location:

Sunday, April 19th, 2:00pm – 5:00pm PT

San Diego Convention Center, San Diego, CA, USA

Exhibit Hall

Session Category: Immunology

Session Title: Alternative Cell Type and in Situ Cell Therapies

Location: Poster Section 7

Poster Board Number: 7

Poster Number: 133

Abstract Number: 7933 (published in Cancer Research: View Source)

BACKGROUND:

Acute myeloid leukemia (AML) continues to have poor long-term outcomes, particularly in high-risk and relapsed/refractory disease. Progress in AML immunotherapy has been hindered by the scarcity of antigens selectively expressed on leukemic cells while sparing hematopoietic stem/progenitor cells (HSPCs).

Recent data to be presented for the first time at AACR (Free AACR Whitepaper), clearly identifies truncated Core 1 O-glycans recognized by NEO-201 as a novel AML-associated antigen present across multiple subtypes and largely absent from early hematopoietic progenitors. The potent antileukemic activity of NEO-201CAR NK cells in preclinical systems highlights the promise of this approach and sets the stage for advancing truncated Core 1 O-glycan-directed Cellular therapies into translational and clinical development.

"What was surprising to us was this novel target originally was discovered in solid tumors not healthy tissue, but its expression is also found in hematologic cancers. This provides the basis of targeting this specific glycan when developing cellular therapies for the treatment of refractory leukemias" said Dr. Philip M. Arlen, of Precision Biologics, Inc.

With a 5-year relative survival of only 32.9% from 2015 – 2021, it’s estimated that in the US in 2025 AML claimed about 22,000 new cases, with over 11,000 deaths. (seer.cancer.gov)

(Press release, Precision Biologics, APR 17, 2026, View Source [SID1234664490])

On April 17, 2026 Boundless Bio (Nasdaq: BOLD), a clinical-stage oncology company interrogating extrachromosomal DNA (ecDNA) biology to deliver transformative therapies to patients with previously intractable oncogene amplified cancers, reported preclinical data supporting its lead ecDNA-directed therapy (ecDTx), BBI-940, at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026. Boundless has identified a novel kinesin target ("Kinesin") essential to ecDNA segregation and inheritance in cancer cells, but non-essential in healthy cells. BBI-940, a potentially first-in-class, oral, and selective Kinesin degrader, is currently being evaluated in the Phase 1 KOMODO-1 trial (NCT07408089) in patients with advanced or metastatic ER+/HER2- breast cancer and TNBC-LAR.

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"Extrachromosomal DNA is well established as a distinct enabler of chromosomal instability associated with oncogene amplification, therapeutic resistance, and poor outcomes for patients," said Chris Hassig, Ph.D., Chief Scientific Officer of Boundless Bio. "We have discovered and validated a novel kinesin target that plays a critical role in ecDNA segregation during cell division, thereby affording tumors with a high degree of genomic plasticity. Our data demonstrate that selective degradation of this target delivered potent antitumor activity in validated breast cancer models, particularly those with ecDNA. Our genetic, in vitro, in vivo, and toxicity profile of BBI-940 supports our recently initiated, first-in-human KOMODO-1 clinical trial evaluating BBI-940 in ER+/HER2- and TNBC-LAR breast cancer patients."

Details of the presentation are as follows:

Title: Selective degradation of a novel kinesin as a potential therapeutic strategy addressing high-risk extrachromosomal DNA (ecDNA) positive cancers, including breast cancer
Abstract Number: LB361
Session Title: Late-Breaking Research: Experimental and Molecular Therapeutics 3
Session Date and Time: Tuesday April 21, 2026, 2:00 PM – 5:00 PM PT
Location: Poster Section 53
Poster Board Number: 18

Genetic and pharmacologic degradation of Kinesin caused ecDNA mis-segregation, ecDNA depletion, and reduced viability of ecDNA+ cancer cells. Selective degradation of Kinesin in a panel of tumor cell lines demonstrated sensitivity across multiple tumor types and 32% sensitivity in breast cancer cell lines, including those positive for ecDNA and FGFR1 gain. This molecularly defined subgroup for Kinesin degradation was further validated in vivo with demonstrated monotherapy tumor regressions in an ecDNA+ TNBC-LAR model, and significant antitumor activity as monotherapy and combination in an ecDNA+/FGFR1+ ER+ breast cancer model.

About BBI-940
Our lead ecDTx, BBI-940, is a novel, oral, and selective kinesin degrader being evaluated in the ongoing, first-in-human Phase 1 KOMODO-1 (Kinesin Oral Molecular Degrader for Oncology) clinical trial (NCT07408089) in patients with advanced or metastatic estrogen receptor-positive, HER2-negative (ER+/HER2-) breast cancer or triple-negative breast cancer of the luminal androgen receptor subtype (TNBC-LAR). BBI-940 targets a specific kinesin protein, "Kinesin", essential for ecDNA segregation and inheritance in cancer cells, but non-essential in healthy cells. BBI-940 is designed to exploit the heightened dependence of ecDNA-positive tumors on mitotic machinery by degrading Kinesin to induce mitotic catastrophe and cell death.

(Press release, Boundless Bio, APR 17, 2026, View Source [SID1234664506])

On April 16, 2026 SOPHiA GENETICS (NASDAQ: SOPH), a global leader in AI-driven precision medicine, reported that the Mount Sinai Health System, one of the leading academic health systems in the United States, will adopt the AI-powered SOPHiA DDM Platform to advance cancer research and enhance genomic testing capabilities.

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Mount Sinai, a National Cancer Institute-designated Comprehensive Cancer Center in New York City, supports care for more than 4,000 oncology patients annually. Mount Sinai’s Molecular Pathology team will leverage SOPHiA DDM to strengthen next-generation sequencing (NGS) capabilities for blood cancers and solid tumors. The Platform is designed to enable detection and interpretation of a wide range of complex genomic variants while improving operational efficiency by consolidating critical steps in the analysis pipeline and reducing manual interpretation time.

By combining Mount Sinai’s clinical excellence with SOPHiA DDM’s advanced AI-powered analytics, the hospital will be equipped to interpret complex genomic datasets at scale and optimize laboratory resources, enabling teams to focus on direct patient care.

Jane Houldsworth, Ph.D., Director of Molecular Oncology Pathology of the Mount Sinai Health System, said: "The collaboration between Mount Sinai and SOPHiA GENETICS reinforces our commitment to scientific innovation by integrating powerful digital tools into our workflows to support high-quality, data-driven cancer care. Leveraging SOPHiA DDM has enabled us to reduce hands-on analysis time and improve our testing turnaround times, enabling our clinicians to provide better patient care."

John Carey, Managing Director, North America, SOPHiA GENETICS, said: "Mount Sinai is widely regarded as one of the world’s leading centers for cancer research and was recently ranked No. 1 globally among health care institutions in the Nature AI Index, underscoring its leadership in artificial intelligence and data-driven innovation. We are honored to support their teams with an AI-native platform and global network designed to deliver faster results, greater operational efficiency, and deeper genomic understanding to help shape the future of precision oncology."

By utilizing the SOPHiA DDM for Blood Cancers and SOPHiA DDM for Solid Tumors applications, Mount Sinai joins a growing network of more than 990 global institutions using SOPHiA GENETICS’ decentralized platform to accelerate precision medicine. This collaboration underscores SOPHiA GENETICS’ mission to democratize data-driven medicine, delivering scalable, cloud-native solutions that empower healthcare institutions to expand access to advanced genomic testing and improve patient outcomes worldwide.

The collaboration was announced from the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting in San Diego. Learn more by connecting with SOPHiA GENETICS at AACR (Free AACR Whitepaper) booth #4248 from April 17 – 22, 2026.

(Press release, Mount Sinai Hospital, APR 16, 2026, View Source [SID1234664442])

On April 16, 2026 INmune Bio Inc. (NASDAQ: INMB) (the "Company"), a clinical-stage biotechnology company focused on developing therapies that harness the patient’s innate immune system, reported new preclinical data for INB03 (XPro1595 for oncology). The data will be presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 in San Diego on April 17-22.

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The poster, titled, "Soluble TNF blockade overcomes tyrosine kinase inhibitors resistance in HER2-positive breast cancer," details how INB03 ("XPro"), a first-in-class dominant-negative soluble TNF (sTNF) inhibitor, significantly enhances the anti-tumor activity of the tyrosine kinase inhibitors (TKIs) lapatinib and tucatinib while reducing metastatic spread to the brain, lungs, and liver in HER2-positive breast cancer models. It was authored by collaborators from the Instituto de Biología y Medicina Experimental (IBYME-CONICET) in Buenos Aires, Argentina.

Key Scientific Findings:

Overcoming Resistance in Vitro: The combination of INB03 (10 µg/mL) with either lapatinib (1 µM) or tucatinib (10 µM) produced statistically superior inhibition of cell proliferation and migration in both HER2+ JIMT-1 and brain-metastatic JIMT-1 Br3-luc cell lines compared to TKIs alone (p < 0.05 to p < 0.0001).
Enhanced Tumor Control In Vivo: In female nude mice bearing JIMT-1 or JIMT-1 Br3-luc tumors, INB03 + TKI combinations markedly slowed tumor growth compared to TKIs alone.
Reduction of Metastatic Spread: The addition of INB03 significantly reduced the incidence of metastases to brain, lung, and liver (quantified by ex-vivo IVIS luminescence imaging). Notably, it further enhanced tucatinib’s effect on lung metastases (p < 0.05 to p < 0.0001).
Mechanism of Action: These results support prior research showing that selective sTNF neutralization with INB03 down-regulates MUC4, a protein that shields the HER2 molecule and prevents therapies from binding effectively.
"These results build on our prior work showing that selective sTNF neutralization with INB03 down-regulates MUC4, restoring sensitivity to HER2-targeted therapies," said Roxana Schillaci, Ph.D., lead investigator. "The ability of INB03 to overcome TKI resistance and limit metastatic dissemination, including to the brain, highlights its potential to address key unmet needs in advanced HER2-positive breast cancer."

David Moss, CEO of INmune Bio, added, "INB03 continues to demonstrate broad therapeutic potential across solid tumors by targeting the soluble TNF pathway. These AACR (Free AACR Whitepaper) data reinforce our confidence in advancing INB03 combinations in the clinic for patients who have developed resistance to standard TKIs or who are at high risk for brain metastases."

The poster will be available for viewing during the AACR (Free AACR Whitepaper) 2026 meeting on April 21st.

About XPro (INB03)

XPro is a next-generation inhibitor of tumor necrosis factor (TNF) that is currently in clinical trial and acts differently than currently available TNF inhibitors in that it neutralizes soluble TNF (sTNF), without affecting trans-membrane TNF (tmTNF) or TNF receptors. XPro could have potential substantial beneficial effects in patients with neurologic disease by decreasing neuroinflammation. For more information about the importance of targeting neuroinflammation in the brain to improve cognitive function and restore neuronal communication visit this section of INmune Bio’s website.

(Press release, INmune Bio, APR 16, 2026, View Source [SID1234664458])

On April 16, 2026 Mabwell (688062.SH), an innovation-driven biopharmaceutical company with a fully integrated industry chain, reported that it has established a licensing and commercialization agreement with a strategic business partner ("the partner") in Malaysia for its Denosumab biosimilar products MAILISHU (a biosimilar of Prolia) and MAIWEIJIAN (a biosimilar of Xgeva) ("the products"). Under the agreement, the partner is responsible for the registration and commercialization of the products in Malaysia, while Mabwell is responsible for the development, production and commercial supply for the products.

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Malaysia has a population of approximately 35.97 million, with a GDP at a leading level in Southeast Asia. As a full member of PIC/S, Malaysia boasts the most mature and well-regulated pharmaceutical regulatory framework in the ASEAN region. In terms of the pharmaceutical market, Malaysia’s market size stood at approximately USD 3.4 billion in 2025, maintaining a compound annual growth rate of about 6%, indicating big market potential.

Mr. Huiguo Hu, Board Member, Senior Vice President and Board Secretary of Mabwell, said, "We are delighted to see that we have reached a collaboration on denosumab in another ASEAN country. Malaysia has an internationally aligned regulatory environment, strong regional recognition and significant space for development. This collaboration will further deepen Mabwell’s presence in the ASEAN market. We look forward to rapidly advancing the product’s local registration and commercialization with our partner’s strong commercial capabilities, bring high-quality, affordable treatment options to more patients in the region."

(Press release, Mabwell Biotech, APR 16, 2026, View Source [SID1234664443])