On May 14, 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, reported that its research collaborators presented positive preclinical data on the Company’s diabetes gene therapy drug candidate at the 2026 American Society of Gene and Cell Therapy (ASGCT) (Free ASGCT Whitepaper) Annual Meeting. The collaborators presented preclinical data demonstrating that the diabetes gene therapy (Pdx1/MafA gene therapy, PM or GPX-002) can reverse hyperglycemia in Type 2 diabetic (T2D) mouse models.

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"We are pleased to have our collaborators present this promising preclinical data in Type 2 diabetes at the ASGCT (Free ASGCT Whitepaper) Annual Meeting," said Ryan Confer, President and Chief Executive Officer at Genprex. "We believe this preclinical data is a pivotal step toward a transformative treatment for Type 2 diabetes by directly addressing beta-cell dysfunction. Our therapy holds the potential to offer long-term glycemic control, moving beyond symptomatic management to fundamentally address the disease for diabetic patients."

The featured Genprex-supported abstract and poster at the 2026 ASGCT (Free ASGCT Whitepaper) Annual Meeting:

Title: "Pancreatic Delivery of AAV-Pdx1/MafA Reverses Hyperglycemia in a Preclinical Model of Type 2 Diabetes"

Abstract ID: 2419

Topic: Gene-Based Therapies in Pre-Clinical Models of Genetic Disease

Poster Presentation Date: Wednesday, May 13, 2026

Poster Presentation Time: 5-6:30 p.m. ET

In this study, eight-week-old male C57BL/6 mice were maintained on a regular diet (RD) or high fat diet (HFD) for 24 weeks. HFD mice then either remained unoperated or underwent retrograde infusion into the pancreatic duct of adeno-associated virus (AAV-8) encoding Pdx1 and MafA (PM) cassettes under the CMV promoter (global–islet cell targeting) or the rat insulin promoter (RIP) (β-cell–specific targeting) or received a control virus. The diet remained unchanged after surgery. At two and/or four weeks after surgery, researchers performed intraperitoneal glucose tolerance testing (IPGTT), insulin tolerance testing (ITT), glucose-stimulated insulin secretion (GSIS), calculated HOMA-IR and assessed glucagon secretion. Mice were then euthanized for pancreatic histology, quantification of β- and α-cell mass, electron microscopy (EM), and islets were isolated for ex-vivo glucose-stimulated insulin secretion (GSIS) and single-cell RNA sequencing. The results at four weeks showed major improvements in the control of diabetes.

At four weeks after surgery, ex-vivo GSIS showed that islets isolated from HFD+CMV-PM-GFP treated mice had insulin secretion similar to islets from RD mice, and both groups had increased insulin secretion

compared to islets from the control HFD groups, indicating improved β-cell function with PM treatment.

Similarly, and importantly, treatment of HFD mice with RIP-PM-GFP, which selectively targets β-cells,

reversed hyperglycemia and improved ex-vivo GSIS. In addition, EM imaging showed that PM treatment in HFD mice increased the number of total and mature insulin granules and decreased the number of immature insulin granules compared with HFD controls. Furthermore, transcriptomic pseudotime analysis demonstrated a shift in β-cells from an immature state toward a more mature state after PM treatment.

PM gene therapy reverses hyperglycemia, likely in large part by specifically enhancing β-cell

function and maturation. This approach is technically translatable to humans using endoscopic retrograde

cholangiopancreatography to deliver PM gene therapy to the pancreas.

To view the poster presented at the 2026 ASGCT (Free ASGCT Whitepaper) Annual Meeting, please visit Genprex’s website here.

(Press release, Genprex, MAY 14, 2026, View Source [SID1234665704])