Genprex Collaborators to Present Positive Preclinical Data on the Use of Reqorsa® Gene Therapy for the Treatment of Lung Cancer at the 2025 AACR-NCI-EROTC International Conference on Molecular Targets and Cancer Therapeutics

Rhea-AI Summary

Genprex (NASDAQ: GNPX) collaborators will present positive preclinical data for Reqorsa® (quaratusugene ozeplasmid) at the 2025 AACR‑NCI‑EROTC conference in Boston on October 25, 2025. Studies show QO upregulates TUSC2 and induces apoptosis in ALK‑EML4 positive NSCLC models.

Key findings: QO alone and combined with alectinib reduced tumor volume by 79% in an NCI‑H2228 mouse model versus 60% for alectinib alone; QO increased caspase 3/7 activity, pro‑apoptotic markers, DNA fragmentation, and reduced colony formation. Results support a potential clinical trial pathway for REQORSA in ALK+ NSCLC.

Insights

Translational Oncology Scientist

Preclinical data show Reqorsa (QO) induces apoptosis in ALK‑EML4 NSCLC and shrinks tumors more than alectinib in mice.

Reqorsa (quaratusugene ozeplasmid) delivers functional TUSC2 via lipid nanoparticles and raised TUSC2 expression in ALK+ cell lines and patient‑derived organoids, triggering apoptosis measured by caspase 3/7, pro‑apoptotic protein upregulation, DNA fragmentation, and reduced colony formation. In a murine NCI‑H2228 xenograft model, single‑agent QO produced 79% tumor shrinkage versus 60% for alectinib; QO plus alectinib matched the 79% result and slowed regrowth at the measured timepoint.

The biology supports a clear mechanism: restoring a tumor suppressor (TUSC2) induces apoptosis in ALK+ cells, including those with acquired alectinib resistance. Key dependencies include translation of nanoparticle delivery and expression levels from mouse to human tissues and confirmation that apoptosis and tumor control persist beyond the short treatment window; safety and biodistribution data in relevant models will also matter. Watch for a formal clinical trial announcement and any reported safety/toxicity results or pharmacodynamic biomarkers in 2025–near term pre‑IND communications.

Clinical Development Strategist

Positive preclinical efficacy creates a plausible path toward a clinical trial, contingent on safety and translational biomarkers.

Researchers demonstrated activity across in vitro ALK+ models and in vivo xenografts, including models with acquired alectinib resistance, suggesting QO could serve as a single agent or a companion to ALK inhibitors. The reported effect size—79% tumor reduction versus 60% with alectinib—and slower regrowth after combination therapy provide actionable efficacy signals for development planning.

Risks remain: preclinical efficacy does not guarantee human benefit and dosing, delivery, and toxicity must be defined. Concrete near‑term milestones to monitor are any IND/CTA filing, first‑in‑human trial design and inclusion criteria (ALK+ and alectinib‑resistant cohorts), and early safety/PD readouts expected within the typical first 12–18 months after filing.

Reqorsa® Gene Therapy is a Potential Treatment for ALK-EML4 Positive Translocated Non-Small Cell Lung Cancer

Research Suggests that REQORSA May Be an Effective Treatment in Patients Progressing on Alectinib

AUSTIN, Texas, Oct. 23, 2025 /PRNewswire/ -- 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 positive preclinical data at the upcoming 2025 AACR-NCI-EROTC International Conference on Molecular Targets and Cancer Therapeutics taking place October 22-26, 2025 at the Hynes Convention Center in Boston. The collaborators will present positive preclinical data from a study of Genprex's lead drug candidate, Reqorsa® Gene Therapy (quaratusugene ozeplasmid), for the treatment of ALK-EML4 positive non-small cell lung cancer (NSCLC).

"We are delighted to have our academic partners present this compelling preclinical evidence that supports the therapeutic use of REQORSA in ALK Positive NSCLC," said Ryan Confer, President and Chief Executive Officer at Genprex. "Our researchers found that REQORSA alone or in combination with alectinib was able to shrink tumors by 79 percent, suggesting that REQORSA may be active as a single agent and may also be an ideal companion drug for patients with advanced disease. These data support a pathway for a potential future clinical trial for REQORSA."

The featured Genprex-supported poster to be presented at the 2025 EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics:

Title: "Quaratusugene ozeplasmid mediated TUSC2 upregulation in EML4-ALK bearing non-small cell lung carcinoma induces apoptosis and is highly effective in preclinical studies"

Collaborator: The University of Michigan Rogel Cancer Center

Session: Poster Session C

Session Date and Time: Saturday, October 25, 2025 from 12:30 – 4:00 p.m. ET

The featured Genprex-supported abstract to be presented at the 2025 EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics:

NSCLC bearing the EML4-ALK fusion (Echinoderm microtubule-associated protein-like 4- Anaplastic Lymphoma Kinase) occurs in approximately 5% of NSCLC. Tumors bearing the fusion are sensitive to ALK Tyrosine Kinase Inhibitors (TKIs), that form the first and second line of treatment for these patients. However, ALK+ lung cancers invariably develop resistance to ALK inhibitors, creating the need for newer treatment strategies.

Tumor Suppressor Candidate 2 (TUSC2) is a tumor suppressor gene that is known to have low endogenous expression in NSCLC. REQORSA Gene Therapy, referred to as quaratusugene ozeplasmid (QO) in the abstract and developed by Genprex, is a gene therapy (TUSC2 plasmid encapsulated in non-viral lipid nanoparticles) that upregulates TUSC2 expression in cancer cells by delivering the functional TUSC2 gene.

Researchers evaluated TUSC2 expression in several ALK+ cell lines and patient derived organoids (PDOs), both before and after exposure to QO. The studies indicate that QO mediated overexpression of TUSC2 significantly induced apoptosis in ALK+ cell lines and PDOs, as demonstrated by increase in caspase 3/7 activity of the cells, increased protein expression of pro-apoptotic markers, reduced colony formation ability of the cells, and increased DNA fragmentation. Furthermore, researchers have observed a robust pro-apoptotic response in ALK+ NSCLC cell lines with acquired resistance to the ALK inhibitor, alectinib, resulting in reduced cell viability when treated with QO and alectinib in combination. To better understand how QO and alectinib work in combination, researcher subcutaneously injected NCI-H2228 ALK+ cells into nude mice and when the tumors developed to approximately 100mm3, mice were randomized into 4 groups. Mice from group 1 were treated with vehicle control, group 2 were treated with QO (25ug/mouse, i.v., every three days), group 3 were treated with alectinib (0.5mg/kg/mouse, oral gavage, every day) and group 4 were treated with QO and alectinib in combination at the same concentration and frequency of dosing for up to a month.

The results showed that alectinib shrunk tumors by 60% (group 3). However, QO alone (group 2) and in combination with alectinib (group 4) were able to shrink the tumors by 79%. This finding showed that QO has a 23% improved outcome than alectinib, leading to the hypothesis that QO may be an ideal companion drug for patients with advanced disease or a treatment for patients who cannot tolerate alectinib. Researchers are also currently monitoring the mice for survival, and tumor measurements recorded at 2 weeks after the end of treatment indicate that tumors in mice that received single drug treatment are regrowing faster than tumors in mice that received combined treatment of QO and alectinib, further emphasizing the clinical relevance of this novel combination in ALK+ NSCLC.

Taken together, the in vitro and in vivo data suggest that QO mediated overexpression of TUSC2 in ALK+ NSCLC is effective in decreasing growth and proliferation through the activation of apoptotic pathways, thereby paving the way for a potential clinical trial.

About Reqorsa® Gene Therapy
REQORSA (quaratusugene ozeplasmid) consists of a plasmid containing the TUSC2 gene 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 conducted at MD Anderson show that the uptake of TUSC2 in tumor cells in vitro after REQORSA treatment was 10 to 33 times the uptake in normal cells.

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.

Interested investors and shareholders are encouraged to sign up for press releases and industry updates by visiting the Company Website, registering for Email Alerts and by following Genprex on Twitter, Facebook and LinkedIn.

Cautionary Language Concerning Forward-Looking Statements
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.

Because forward-looking statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. Such statements include, but are not limited to, statements regarding: Genprex's ability to advance the clinical development, manufacturing and commercialization of its product candidates in accordance with projected timelines and specifications; the timing and success of Genprex's clinical trials, its intended regulatory submissions and any resulting regulatory approvals; the effect of Genprex's product candidates, alone and in combination with other therapies, on cancer and diabetes; including as a potential treatment for ALK-EML4 positive translocated non-small cell lung cancer; Genprex's future growth and financial status, including Genprex's ability to maintain compliance with the continued listing requirements of The Nasdaq Capital Market and to continue as a going concern and to obtain capital to meet its long-term liquidity needs on acceptable terms, or at all; Genprex's commercial and strategic partnerships, including those with its third party vendors, suppliers and manufacturers and their ability to successfully perform and scale up the manufacture of its product candidates; Genprex's intellectual property and licenses; and Genprex's current expectations, estimates, forecasts and projections about the industry and markets in which it operates.

These forward-looking statements should not be relied upon as predictions of future events and Genprex cannot assure you that the events or circumstances discussed or reflected in these statements will be achieved or will occur. If such forward-looking statements prove to be inaccurate, the inaccuracy may be material. You should not regard these statements as a representation or warranty by Genprex or any other person that Genprex will achieve its objectives and plans in any specified timeframe, or at all. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date of this press release. Genprex disclaims any obligation to publicly update or release any revisions to these forward-looking statements, whether as a result of new information, future events or otherwise, after the date of this press release or to reflect the occurrence of unanticipated events, except as required by law.

Genprex, Inc.
(877) 774-GNPX (4679)

GNPX Investor Relations
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GNPX Media Contact
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FAQ

What preclinical result did Genprex collaborators report for REQORSA (GNPX) at AACR‑NCI‑EROTC on October 25, 2025?

Collaborators reported that REQORSA (QO) alone or with alectinib shrank tumors by 79% in a mouse ALK+ NSCLC model, versus 60% for alectinib alone.

How does REQORSA (quaratusugene ozeplasmid) work in ALK‑EML4 positive NSCLC according to the October 23, 2025 report?

REQORSA delivers a functional TUSC2 gene via lipid nanoparticles, increasing TUSC2 expression and inducing apoptosis in ALK+ cell lines and patient‑derived organoids.

What dosing and model produced the 79% tumor shrinkage reported for REQORSA in the Genprex presentation?

In the study, mice received QO at 25 µg/mouse i.v. every three days and/or alectinib at 0.5 mg/kg daily; combined or QO alone produced 79% tumor shrinkage.

Does the Genprex preclinical data suggest REQORSA could help patients resistant to alectinib (GNPX)?

Researchers observed robust pro‑apoptotic responses in ALK+ cell lines with acquired alectinib resistance when treated with QO, supporting potential use in resistant cases.

When and where will the Genprex‑supported poster on REQORSA be presented at the 2025 conference?

The poster from the University of Michigan Rogel Cancer Center will be presented in Poster Session C on Saturday, October 25, 2025 from 12:30–4:00 p.m. ET at the Hynes Convention Center, Boston.