Xenetic Biosciences Reports ASCO 2026 Data Showing DNase I Boosts CAR-T Expansion And Anti-Tumor Activity In B-Cell Cancer Models

New preclinical and translational findings position DNase I as a potentially transformative adjunct therapy for CAR-T treatment in aggressive B cell malignancies

Data highlight potential of DNase I to improve CAR-T cell expansion, reduce exhaustion and enhance tumor control across hematologic cancer models

Findings support continued clinical development of DNase I as a combinatorial strategy to augment CAR-T cell therapies in difficult-to-treat cancers

Data to be presented today as a poster presentation at the ASCO 2026 annual meeting

FRAMINGHAM, MA / ACCESS Newswire / June 1, 2026 / Xenetic Biosciences, Inc. (NASDAQ:XBIO) ("Xenetic" or the "Company"), a biopharmaceutical company focused on advancing innovative immuno-oncology technologies addressing difficult to treat cancers, today announced positive preclinical data will be presented at the 2026 American Society of Clinical Oncology (ASCO) Annual Meeting demonstrating that DNase I significantly enhances CAR-T cell expansion, persistence, and antitumor efficacy in aggressive hematologic cancer models.

Presentation Details:

Session Title: Hematologic Malignancies - Plasma Cell Dyscrasia (Poster Session)

Abstract Title: Targeting cfDNA and NETs with DNase I to augment CAR-T cell function and antitumor efficacy

Poster Board: 410

Presentation Date & Time: June 1, 2026, 9:00 AM - 12:00 PM CDT

Presenter: Alexey V. Stepanov, PhD

The poster presentation, titled "Targeting cfDNA and NETs with DNase I Augments CAR T-Cell Function and Antitumor Efficacy," highlights evidence that extracellular DNA and neutrophil extracellular traps (NETs) act as key drivers of CAR-T cell exhaustion and persistence, leading to therapeutic failure. The findings demonstrate that DNase I degrades these immunosuppressive barriers and restores CAR-T functionality.

In preclinical studies, DNase I efficiently degraded extracellular DNA, preserved CAR-T cell effector function, improved CD8-positive T cell ratios and reduced expression of exhaustion markers including PD-1, LAG-3 and TIM-3 across multiple rounds of tumor rechallenge in vitro.

In vivo, DNase I significantly enhanced CAR-T cell expansion and persistence following infusion in both NALM-6 B cell leukemia and Raji Burkitt lymphoma xenograft models. Combination therapy with DNase I resulted in improved tumor control, delayed relapse upon rechallenge and prolonged survival compared to CAR T-cell therapy alone.

The poster also includes translational observations from a pediatric patient with highly refractory Burkitt lymphoma, where DNase I co-administration was associated with marked CAR-T cell expansion and progressive reduction in tumor burden following prior CAR-T cell failure.