Qualigen Therapeutics Presents Data on its RAS Inhibitor Program at the American Association for Cancer Research: Targeting RAS Conference


Data demonstrates potential anti-RAS activity with Qualigen’s novel RAS small molecule in both pancreatic and breast cancer in vivo models

CARLSBAD, Calif., March 09, 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 presentation of data in two posters at the American Association for Cancer Research (AACR) Special Conference: Targeting RAS. The two posters outlined preclinical studies of the Company’s RAS-targeted program that showed potential anti-RAS activity in both pancreatic and breast cancer models. The conference took place at the Philadelphia Marriott in Philadelphia, Pennsylvania from March 5-8, 2023.

Details of the posters include:

Title:A Novel RAS inhibitor for Pancreatic Cancer
Authors:Clark, et. al.
Highlights:The study examines anti-RAS activity in a series of RAS inhibitors with a predicted unique interaction region. The compounds, in development at Qualigen Therapeutics, bind wild type KRAS and HRAS, but exhibit preferential binding to specific mutations of KRAS. Investigators observed suppression of mutant RAS signaling and inhibition of 3D cell growth of mutant RAS cell lines with these agents. They also enhanced the effects of both MRTX-1133 against K-RAS G12D cells and had a similar effect on AMG-510 in K-RAS G12C cell lines. According to Qualigen’s Chief Medical Officer, Tariq Arshad, MD, these agents may serve as novel anti-RAS therapeutics with the potential to enhance activity or suppress resistance to these investigational compounds.
  
Title:A Novel RAS Inhibitor for Luminal B and Triple Negative Breast Cancers
Authors:Clark, et. al.
Highlights:RAS pathways are frequently hyper-activated in breast cancers, and genetic/ epigenetic inactivation of RAS-negative regulators is common. Qualigen’s novel small molecules bound all three main RAS proteins (KRAS, HRAS, and NRAS) and suppressed RAS function. This was validated by (1) Microscale Thermophoresis to quantify recombinant protein interaction (2) 3D growth inhibition and protein-based RAS signaling assays (3) demonstration of antitumor effect in vivo against a Luminal B cell line xenograft. 
  

1. https://seer.cancer.gov/statfacts/html/common.html

Qualigen’s Chief Medical Officer, Tariq Arshad, M.D., M.B.A. commented, “Given that Luminal B tumors are typically less sensitive to therapy and have a high frequency of relapse, we find these data to be encouraging and supportive of further development of our RAS-targeted compounds. These data demonstrate that Qualigen’s compounds may provide meaningful anti-RAS activity, as a novel approach to breast cancer. RAS is among the most common cancer oncogenes, and RAS-driven tumors represent an area of significant unmet medical need. The development of our RAS-targeted program is focused on the creation of novel small molecules that bind to RAS isoforms while blocking the ability for RAS to bind and signal through its effectors.”

About RAS

RAS is the most common cancer oncogene. Activating mutations in one of the three human RAS gene isoforms (KRAS, HRAS, or NRAS) are present in about one-fourth of all cancers. For example, mutant KRAS is found in 98% of pancreatic ductal adenocarcinomas, 52% of colon cancers, and 32% of lung adenocarcinomas. According to the National Cancer Institute, mutant KRAS subsets of these three cancers alone are diagnosed in more than 170,000 people each year in the United States and cause more than 120,000 deaths annually.1 Substantial scientific and pharmaceutical industry interest is evident by the compounds either approved or in development to treat devastating RAS-driven advanced solid tumors, such as non-small cell lung cancer (NSCLC) and pancreatic cancer.

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.

Attachments


F3 Compounds Cooperate with Checkpoint Inhibitors and Other RAS Inhibitors F3-8-60 inhibits RAS RAF interaction and blocks RAS Signaling F3-8-60 is active in vivo against pancreatic cancer models F3-8-60 suppresses RAS mitogenic signaling pathways in Panc1 cells (KRAS12D) F3860 inhibits Luminal B tumor growth in vivo Inhibition of RAS signaling pathways RAS binding of compounds