On March 18, 2026, Genprex, Inc. ("Genprex" or the "Company") issued a press release announcing that its research collaborators will present at the upcoming 2026 American Association for Cancer Research ("AACR") Annual Meeting being held April 17-22, 2026, in San Diego, California. The collaborators will present positive preclinical data from studies of its lead drug candidate, Reqorsa® Gene Therapy (quaratusugene ozeplasmid, also referred to as "Quar Oze"), for the treatment of lung cancer. The press release noted that these findings advance the Company’s understanding of TUSC2’s therapeutic mechanisms and its impact on lung cancer. Additionally, the Company believes that the identification of TROP2 and PTEN as potential biomarkers of response to TUSC2 gene therapy in non-small cell lung cancer ("NSCLC") is a pivotal development, providing insights that could refine patient selection strategies and optimize the therapeutic efficacy of REQORSA in a clinical setting.

The first of the featured Genprex-supported posters to be presented at the 2026 AACR is titled "TROP2 and PTEN are biomarkers of primary resistance to TUSC2 gene therapy in non-small cell lung cancer." In this study, researchers established models primarily resistant to TUSC2 gene therapy to find biomarkers indicative of TUSC2 gene therapy resistance in NSCLC cell lines, PDX-derived organoids, and patient-derived xenografts. A panel of 10 NSCLC cell lines screened for TUSC2 sensitivity showed resistance in 50% of the cell lines, as assessed by annexin V staining and colony formation assays. Researchers evaluated TUSC2 sensitivity in 12 NSCLC PDXOs using ATP-based viability assays in 3D culture following TUSC2 or empty vector transfection. While some PDXOs were highly responsive to TUSC2 within 72 hours post-transfection, 50% of PDXOs exhibited primary resistance.

The second poster to be presented at the 2026 AACR is titled "Quaratusugene ozeplasmid mediated TUSC2 upregulation in EML4-ALK bearing non-small cell lung carcinoma induces apoptosis and is highly effective in preclinical studies." In this study, researchers evaluated TUSC2 expression in a range of ALK+ cell lines and patient-derived organoids, both prior to and following exposure to Quar Oze. The findings show that Quar Oze-driven TUSC2 overexpression initiates a robust pro-apoptotic response in ALK-positive models, not only in cells that are sensitive but also with acquired resistance to the ALK inhibitor, alectinib.

The third poster to be presented at the 2026 AACR is titled "Restoring TUSC2 function boosts NK cell cytotoxicity and antitumor immunity in vivo and in vitro." This study suggests TUSC2 acts as a critical enhancer of innate antitumor immunity by boosting NK cell cytotoxic function. Therapeutic delivery of TUSC2 via Quar Oze suppresses tumor progression and, in many cases, drives complete tumor elimination. These results highlight TUSC2 as a potent immunomodulatory tumor suppressor and support its development as a dual-function therapeutic that directly targets tumor cells while also activating NK cell-mediated immunity.

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