Qualigen Therapeutics to Present Five Posters at the American Association for Cancer Research Annual Meeting 2023

Rhea-AI Summary

Qualigen Therapeutics (Nasdaq: QLGN) announces participation at the AACR Annual Meeting 2023 in Orlando, FL, held from April 14-19. The company will present five posters, highlighting their lead program QN-302 and a study on QN-247 in Triple Negative Breast Cancer. Key presentations include a comparison of QN-302 and CX-5461, findings on S100P gene down-regulation, and anti-tumor activity of QN-302. QN-302 targets G-Quadruplex structures in various tumors, while QN-247 focuses on nucleolin-expressing cancers. Orphan Drug Designation for QN-302 in pancreatic cancer was granted in January 2023.

CARLSBAD, Calif., March 15, 2023 (GLOBE NEWSWIRE) -- Qualigen Therapeutics, Inc. (“Qualigen” or “the Company,” Nasdaq: QLGN), a diversified life sciences company focused on developing treatments for adult and pediatric cancers with potential for Orphan Drug Designation, while also commercializing diagnostics, today announces the Company will be presenting five posters at the American Association for Cancer Research (AACR) Annual Meeting 2023 to be held April 14-19 in Orlando, FL. The AACR Conference is a focal point of the cancer research community, where scientists, clinicians, other healthcare professionals, survivors, patients, and advocates gather to share the latest advances in cancer science and medicine.

The Company will be presenting four posters regarding its lead program, QN-302, and one poster regarding an in-vivo study of program QN-247 in Triple Negative Breast Cancer (TNBC).

QN-302 Posters

• “A comparison of the activity of the quadruplex-targeting experimental drugs QN-302 and CX-5461 (Pidnarulex) in wild-type and gemcitabine-resistant pancreatic cancer cell lines” Ahmed Ahmed, Tariq Arshad, and Stephen Neidle
• “The potent quadruplex-binding compound QN-302 down-regulates the S100P gene in vitro and in vivo models of pancreatic cancer: a potential therapeutic target and biomarker for PDAC^” Nicole Williams, Jenny Worthington, Ahmed Ahmed, Tariq Arshad, and Stephen Neidle 
• “The potent quadruplex-binding compound QN-302 shows anti-tumor activity as a monotherapy in an orthotopic in vivo model of pancreatic cancer” Nicole Williams, Danielle Santos, Jenny Worthington, Ahmed Ahmed, Tariq Arshad and Stephen Neidle 
• “Structure-based design rules for potent quadruplex-binding compounds based on the naphthalene diimide core” Stephen Neidle 

QN-247 Poster:

• “Nano-immunotherapy: Efficacy of nanoconjugate QN-247 in a Triple Negative Breast Cancer (TNBC) mouse model” Tariq Arshad, Stephen Fait, Guy Gammon, Andrew Hertig, Mark J. Sarno
  

About QN-302

QN-302 is a small molecule G-Quadruplex (G4)-selective transcription inhibitor in development for the treatment of G4-expressing tumors, such as pancreatic cancer (PDAC), prostate cancer, sarcomas, Gastrointestinal Stromal Tumors (GIST), and others. Orphan Drug Designation (ODD) was granted by the FDA in January of this year for pancreatic cancer. QN-302 is currently in IND enabling studies toward submission of an Investigational New Drug (IND) application (in the coming months).

About QN-247

QN-247 is a nucleolin-targeted therapeutic with potential indications against nucleolin expressing malignancies such as Triple Negative Breast Cancer (TNBC), Acute Myeloid Leukemia (AML), Glioblastoma (GBM), and others. The company is currently seeking partners to advance QN-247 program in TNBC and other malignancies.

About Qualigen Therapeutics, Inc.

Qualigen Therapeutics, Inc. is a diversified life sciences company focused on developing treatments for adult and pediatric cancer, while also commercializing diagnostics. Our investigational QN-302 compound is a small molecule selective transcription inhibitor with strong binding affinity to G4s prevalent in cancer cells; such binding could, by stabilizing the G4s against “unwinding,” help inhibit cancer cell proliferation. The investigational compounds within Qualigen’s family of RAS oncogene protein-protein interaction inhibitor small molecules are believed to inhibit or block the binding of mutated RAS genes’ proteins to their effector proteins, thereby leaving the proteins from the mutated RAS unable to cause further harm. In theory, such mechanism of action may be effective in the treatment of about one quarter of all cancers, including certain forms of pancreatic, colorectal, and lung cancers. Our investigational QN-247 compound inhibits nucleolin, a key multi-functional regulatory protein that is overexpressed in cancer cells; QN-247 may thereby be able to inhibit the cells’ proliferation. QN-247 has shown promise in preclinical studies for the treatment of acute myeloid leukemia (AML). In addition to its oncology drug pipeline, Qualigen has an established diagnostics business which manufactures and distributes proprietary and highly accurate rapid blood testing systems to physician offices and small hospitals for the management of prostate cancer and other diseases and health conditions.

For more information about Qualigen Therapeutics, Inc., please visit www.qualigeninc.com.

Contact:

Jules Abraham
JQA Partners, Inc.
917-885-7378
jabraham@jqapartners.com

Source: Qualigen Therapeutics, Inc.

FAQ

What is Qualigen Therapeutics presenting at AACR Annual Meeting 2023?

Qualigen Therapeutics will present five posters, focusing on QN-302 and QN-247.

What are the main topics of the QN-302 posters?

The posters cover comparisons with CX-5461, S100P gene down-regulation, anti-tumor activity, and design rules for quadruplex-binding compounds.

What is the significance of QN-302 in cancer treatment?

QN-302 is being developed for G4-expressing tumors, including pancreatic cancer, and received Orphan Drug Designation from the FDA.

What does QN-247 target in cancer therapy?

QN-247 is aimed at nucleolin-expressing cancers, including Triple Negative Breast Cancer and Acute Myeloid Leukemia.

When is the AACR Annual Meeting taking place?

The AACR Annual Meeting 2023 is scheduled from April 14-19 in Orlando, FL.