Genprex's Reqorsa Gene Therapy Shows 79% Tumor Reduction in ALK-Positive Lung Cancer Preclinical Study
核心洞察
Genprex's Reqorsa gene therapy demonstrated a 79% tumor reduction in ALK-positive non-small cell lung cancer (搜索) models during preclinical studies presented at the 2025 AACR-NCI-EROTC Conference.
The combination of Reqorsa with alectinib improved treatment outcomes by 23% compared to alectinib alone, suggesting potential as a companion therapy for advanced disease.
The positive preclinical data supports the advancement of Reqorsa toward clinical trials for ALK-EML4 positive NSCLC (搜索), a subset that primarily affects young, non-smoking individuals.
Genprex's lead gene therapy candidate Reqorsa (quaratusugene ozeplasmid) achieved a 79% tumor reduction in preclinical models of ALK-positive non-small cell lung cancer (搜索) (NSCLC), according to data presented at the 2025 AACR-NCI-EROTC International Conference on Molecular Targets and Cancer Therapeutics. The study, conducted by collaborators at the University of Michigan Rogel Cancer Center, demonstrated the therapy's ability to induce apoptosis in ALK (搜索)-positive lung cancer cells.
Combination Therapy Shows Enhanced Efficacy
The preclinical study revealed that combining Reqorsa with alectinib, an established ALK (搜索) inhibitor, improved treatment outcomes by 23% compared to alectinib monotherapy. This finding positions Reqorsa as a potential companion drug for treating advanced ALK-EML4 positive translocated NSCLC, a subset that predominantly affects young, non-smoking individuals.
"We are thrilled that our collaborators have once again been selected to present positive preclinical data on the use of REQORSA and its ability to induce apoptosis in ALK positive (搜索) lung cancer," said Ryan Confer, President and Chief Executive Officer at Genprex. "These preclinical data further validate REQORSA as a potential treatment for many types of cancer, including another subset of lung cancer, and we look forward to continuing our studies of REQORSA in combination with ALK (搜索) inhibitors."
Targeted Delivery Mechanism
Reqorsa consists of a TUSC2 (搜索) tumor suppressor gene expressing plasmid encapsulated in non-viral lipid-based nanoparticles through Genprex's Oncoprex Delivery System. The positively charged lipoplex formulation is administered intravenously and specifically targets negatively charged cancer cells while minimizing uptake by normal tissue.
Laboratory studies demonstrate the therapy's selective targeting capability, showing that TUSC2 (搜索) gene uptake in tumor cells after Reqorsa treatment was 10 to 33 times higher than uptake in normal cells. This selective delivery mechanism allows the therapy to restore tumor suppressor protein function specifically in cancer cells that have lost this critical cellular function.
Research Collaboration and Clinical Development
The preclinical study was conducted under a Sponsored Research Agreement between Genprex and the University of Michigan Rogel Cancer Center, established in October 2024. The collaboration also involves ALK Positive (搜索), a non-profit patient-driven research organization dedicated to improving outcomes for ALK (搜索)-positive lung cancer patients.
The poster presentation, titled "Quaratusugene ozeplasmid mediated TUSC2 (搜索) upregulation in EML4-ALK (搜索) bearing non-small cell lung carcinoma induces apoptosis and is highly effective in preclinical studies," was featured during Poster Session C on Saturday, October 25, 2025.
Regulatory Status and Clinical Pipeline
Reqorsa is currently being evaluated in two clinical trials as a treatment for NSCLC and small cell lung cancer (搜索) (SCLC). Both of Genprex's lung cancer clinical programs have received Fast Track Designation from the FDA, with the SCLC program also receiving FDA Orphan Drug Designation.
The positive preclinical data supports the potential advancement of Reqorsa toward clinical trials specifically for ALK-EML4 positive NSCLC (搜索), representing a significant step forward in addressing treatment options for this patient population with limited therapeutic alternatives.