Genprex Collaborators to Present Positive Preclinical Data on the Use of Reqorsa® Gene Therapy for the Treatment of Lung Cancer at the 2026 AACR Annual Meeting
Research Collaborators Identify Biomarkers that May Predict Patient Response to Reqorsa® Gene Therapy
REQORSA is a Potential Treatment for ALK-EML4 Positive Translocated Non-Small Cell Lung Cancer
REQORSA Boosts Natural Killer (NK) Cell Antitumor Activity
AUSTIN, Texas — (March 18, 2026) — Genprex, Inc. (“Genprex” or the “Company”) (NASDAQ: GNPX), a clinical-stage gene therapy company focused on developing life-changing therapies for patients with cancer and diabetes, today announced 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 selection of three distinct abstracts for presentation at the 2026 American Association for Cancer Research underscores the robust preclinical evidence supporting REQORSA’s multi-faceted potential in the treatment of cancer,” said Ryan Confer, President and Chief Executive Officer at Genprex. “These findings advance our understanding of TUSC2’s therapeutic mechanisms and its impact on lung cancer. Additionally, the identification of TROP2 and PTEN as potential biomarkers of response to TUSC2 gene therapy in non-small cell lung cancer is a pivotal development, providing insights that could refine patient selection strategies and optimize the therapeutic efficacy of REQORSA in a clinical setting.”
The featured Genprex-supported posters to be presented at AACR 2026:
Title: “TROP2 and PTEN are biomarkers of primary resistance to TUSC2 gene therapy in non-small cell lung cancer (NSCLC)”
Session Category: Experimental and Molecular Therapeutics
Session Title: Mechanisms of Drug Resistance 1
Session Date and Time: April 19, 2026 from 2-5 p.m. PT
Location: Poster Section 16
Poster Board Number: 24
Abstract Presentation Number: 391
In this study, researchers established models primarily resistant to TUSC2 gene therapy (REQORSA or Quar Oze) to find biomarkers indicative of TUSC2 gene therapy resistance in NSCLC cell lines, PDX-derived organoids (PDXOs), and patient-derived xenografts (PDXs). 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. TC314AR (Acquired Resistance) PDX tumors and xenograft models (A549AR, H1299AR, H23AR) were developed, grown in NSG mice, and then treated with TUSC2 gene therapy. 20-30% of tumors in every model showed resistance, with no significant reduction in size compared to the control tumors after treatment. Protein expression profiling using reverse-phase protein array (RPPA) analysis of 500 proteins showed distinct expression signatures, with several candidate biomarkers significantly altered in resistant cell lines and PDXOs. RPPA analysis of residual tumors from both the xenograft and PDX models revealed significant but model-specific alterations in protein expression between responders and non-responders. Comparative analyses across the three models showed low expression of TROP2 and high expression of PTEN as potential biomarkers of primary resistance. Overexpression of TROP2 in H1299 and H460 cells increased TUSC2-induced apoptosis. These findings suggest that TROP2 and PTEN may serve as biomarkers to predict TUSC2 response and guide therapeutic strategies in NSCLC.
Title: “Quaratusugene ozeplasmid mediated TUSC2 upregulation in EML4-ALK bearing non-small cell lung carcinoma induces apoptosis and is highly effective in preclinical studies”
Session Category: Experimental and Molecular Therapeutics
Session Title: RNA, Gene and Cell Therapies, and Enabling Assay Technologies
Session Date and Time: April 19, 2026 from 2-5 p.m. PT
Location: Poster Section 19
Poster Board Number: 12
Abstract Presentation Number: 469
In this study, researchers evaluated TUSC2 expression in a range of ALK+ cell lines and patient-derived organoids (PDOs), both prior to and following exposure to quaratusugene ozeplasmid (Quar Oze). The findings show that Quar Oze-driven TUSC2 overexpression initiates a robust pro-apoptotic response in ALK-positive (ALK+) models, not only in cells that are sensitive but also with acquired resistance (generated in the lab) to the ALK inhibitor, alectinib. This is evidenced by increased pro-apoptotic markers and lower cell viability when Quar Oze is used in combination with alectinib. To further assess the Quar Oze and alectinib combination, researchers tested it in two in vivo models: (1) an alectinib-sensitive model using subcutaneous injection of NCI-H2228 ALK+ cells into nude mice, and (2) an alectinib-resistant model using ALK167 PDX implants in NSG mice. Once tumors reached ~ 100 mm³, mice were randomized into four groups: vehicle control; Quar Oze alone (25 μg/mouse, IV, every three days); alectinib alone (0.5 mg/kg for sensitive or 15 mg/kg for resistant, oral, daily); and Quar Oze plus alectinib at the same doses. In the sensitive model, tumors in the alectinib-treated group shrank by 60%. Notably, treatment with Quar Oze alone, and particularly Quar Oze combined with alectinib, resulted in 79% tumor shrinkage (p value 0.0135 versus control), demonstrating a 23% improved outcome compared to alectinib alone. This suggests that Quar Oze might serve as a valuable adjunct therapy, especially for patients who have advanced disease and/or experience resistance to TKIs.
In the resistant model, the Quar Oze and alectinib combination produced a synergistic effect, achieving the greatest tumor reduction and improved overall survival (p value 0.0001 versus control), further supporting the clinical potential of this therapeutic strategy in ALK+ NSCLC. Altogether, the in vitro and in vivo studies indicate that Quar Oze-mediated TUSC2 overexpression in ALK+ NSCLC effectively curtails tumor growth and proliferation via activation of apoptotic pathways, providing a compelling rationale for progressing toward a clinical trial.
Title: “Restoring TUSC2 function boosts NK cell cytotoxicity and antitumor immunity in vivo and in vitro”
Session Category: Immunology
Session Title: Immune Cell Biology and Tumor-Immune Crosstalk
Session Date and Time: April 19, 2026 from 2-5 p.m. PT
Location: Poster Section 8
Poster Board Number: 7
Abstract Presentation Number: 164
Tusc2 knockout (Tusc2 KO) and wild-type (Tusc2 WT) mice were challenged with syngeneic tumor cells (344SQ) and treated with TUSC2-expressing lipoparticles (quaratusugene ozeplasmid, Quar Oze). The therapeutic group received Quar Oze after tumor establishment starting at day 8 from cell line injection, while the prophylaxis group received Quar Oze before tumor establishment, starting 2 days before injection of cell lines. Control groups received empty lipoparticles. After three weeks from cell line injection, tumor volumes were assessed, and mice were euthanized for collection of tumors, spleens, and tumor-draining lymph nodes (TDLN). Immune cell phenotypes and cytotoxic markers were analyzed using flow cytometry. In vitro studies evaluated NK cell cytotoxic function following Quar Oze treatment by measuring CD107a degranulation and CellTrace Violet–based proliferation. In the therapeutic treatment group, 67% of Tusc2 KO mice and 33% of Tusc2 WT mice achieved complete tumor regression, with all remaining mice showing significant tumor reduction compared with controls. Prophylactic administration did not induce complete tumor clearance but consistently reduced tumor growth across all mice. Immune profiling of the tumor microenvironment revealed that Quar Oze robustly enhanced NK cell cytotoxicity, particularly increasing granzyme B and perforin expression. In vitro assays confirmed that TUSC2 restoration significantly increased NK cell degranulation and proliferation, supporting the in vivo findings.
In conclusion, 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.
About TUSC2
TUSC2 is the tumor suppressor gene used in REQORSA (quaratusugene ozeplasmid or Quar Oze). REQORSA consists of a TUSC2 gene expressing plasmid encapsulated in non-viral lipid-based nanoparticles in a lipoplex form (the Company’s Oncoprex® Delivery System), which has a positive charge. REQORSA is injected intravenously and specifically targets cancer cells. REQORSA is designed to deliver the functioning TUSC2 gene to negatively charged cancer cells while minimizing uptake by normal tissue. Laboratory studies show that the uptake of TUSC2 in tumor cells in vitro after REQORSA treatment was 10 to 33 times the uptake in normal cells.
The aforementioned 2026 AACR posters will be available on Genprex’s website following the completion of their live presentations.
About Genprex, Inc.
Genprex, Inc. is a clinical-stage gene therapy company focused on developing life-changing therapies for patients with cancer and diabetes. Genprex’s technologies are designed to administer disease-fighting genes to provide new therapies for large patient populations with cancer and diabetes who currently have limited treatment options. Genprex works with world-class institutions and collaborators to develop drug candidates to further its pipeline of gene therapies in order to provide novel treatment approaches. Genprex’s oncology program utilizes its systemic, non-viral Oncoprex® Delivery System which encapsulates the gene-expressing plasmids using lipid-based nanoparticles in a lipoplex form. The resultant product is administered intravenously, where it is taken up by tumor cells that then express tumor suppressor proteins that were deficient in the tumor. The Company’s lead product candidate, Reqorsa® Gene Therapy (quaratusugene ozeplasmid), is being evaluated in two clinical trials as a treatment for NSCLC and SCLC. Each of Genprex’s lung cancer clinical programs has received a Fast Track Designation from the FDA for the treatment of that patient population, and Genprex’s SCLC program has received an FDA Orphan Drug Designation. Genprex’s diabetes gene therapy approach is comprised of a novel infusion process that uses an AAV vector to deliver Pdx1 and MafA genes directly to the pancreas. In models of Type 1 diabetes, GPX-002 transforms alpha cells in the pancreas into functional beta-like cells, which can produce insulin but may be distinct enough from beta cells to evade the body’s immune system. In a similar approach for Type 2 diabetes, where autoimmunity is not at play, GPX-002 is believed to rejuvenate and replenish exhausted beta cells.
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Statements contained in this press release regarding matters that are not historical facts are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. These forward-looking statements are made on the basis of the current beliefs, expectations and assumptions of management, are not guarantees of performance and are subject to significant risks and uncertainty. These forward-looking statements should, therefore, be considered in light of various important factors, including those set forth in Genprex’s reports that it files from time to time with the Securities and Exchange Commission and which you should review, including those statements under “Item 1A – Risk Factors” in Genprex’s Annual Report on Form 10-K for the year ended December 31, 2024.
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