RAS-F3

Fourth RAS Initiative Symposium Highlights Preclinical Data in Solid Tumor Models CARLSBAD, Calif., Oct. 19, 2022 (GLOBE NEWSWIRE) -- Qualigen Therapeutics, Inc. (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 two posters detailing the Company’s RAS-Targeted platform at the National Cancer Institute-sponsored Fourth RAS Initiative Symposium to be held October 17-19, 2022 at The Advanced Technology Research Facility of the National Cancer Institute in Frederick, Maryland. “RAS is a key cancer oncogene present in about one quarter of all cancers. RAS development is an active field with substantial interest from the scientific community and biopharmaceutical industry. Only one FDA-approved targeted RAS inhibitor exists today and it is specific to the KRAS G12C mutation. Thus, an unmet need to discover and develop more broadly acting RAS-targeted compounds exists,” commented Michael Poirier, Qualigen’s Chairman and CEO. “Our RAS targeted platform aims to identify a small molecule that inhibits RAS-RAS protein interaction and acts more broadly across RAS forms to treat advanced solid tumors by blocking the ability of RAS to bind and signal through its effectors. These posters, which represent early findings in our partnership with Dr. Geoff Clark at the University of Louisville, demonstrate the potential of our approach to addressing RAS.” Poster highlights included: Abstract #: 39 Title: “A novel pan-RAS inhibitor for Malignant Peripheral Nerve Sheath Tumors” Author/s: Geoff Clark, Ph.D., et. al. Presentation Date: October 17, 2022 Following screening to identify an initial candidate inhibitor of RAS oncoproteins for malignant peripheral nerve sheath (MPNST) tumors, investigators measured in vitro and in vivo activity against these tumors. The lead candidate, designated by investigators as RAS-F suppressed RAS signaling pathways and suppressed MPNST tumor growth in animal models. VIEW POSTER Abstract #: 40 Title: “A Novel RAS Inhibitor for Pancreatic Cancer” Author/s: Geoff Clark Ph.D., et. al. Presentation Date: October 18, 2022 Following screening to identify an initial candidate inhibitor against pancreatic cancer tumor growth, investigators analyzed in vitro and in vivo activity against these tumors. The lead candidate, designated RAS-F, suppressed RAS signaling pathways and pancreatic tumor cell growth in vitro. It also suppressed xenograft development of human and mouse RAS-driven pancreatic tumor cell lines and reduced the growth of pancreatic cancer patient-derived xenograft models. The study also showed that RAS-F enhanced the effects of immune checkpoint therapy in syngeneic tumor xenografts. VIEW POSTER 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, resulting in 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 pancreatic cancer. AboutQualigenTherapeutics,Inc. Qualigen Therapeutics, Inc. is a diversified life sciences company focused on developing treatments for adult and pediatric cancer, as well as maintaining and expanding its core FDA-cleared FastPack® System, which has been used successfully in diagnostics for over 20 years. 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. 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 . Forward-Looking Statements This news release contains forward-looking statements by Qualigen that involve risks and uncertainties and reflect the Company's judgment as of the date of this release. These statements include those related to the Company's prospects and strategy, including statements related to the development of QN-302 and the Company’s other therapeutic drug candidates. Actual events or results may differ from the Company's expectations. For example, here can be no assurance that the Company will be able to successfully develop any drugs (including QN-302, QN-247 and RAS); that preclinical development of the Company's drugs (including QN-302, QN-247 and RAS, and the deprioritized infectious-disease drug candidate QN-165) will be completed on any projected timeline or will be successful; that any clinical trials will be approved to begin by or will proceed as contemplated by any projected timeline, or at all; that any future clinical trial data will be favorable or that such trials will confirm any improvements over other products or lack negative impacts; that any drugs will receive required regulatory approvals (or Fast Track designation or Orphan Drug status) or that they will be commercially successful; that patents will issue on the Company's owned and in-licensed patent applications; that such patents, if any, and the Company's currently owned and in-licensed patents would prevent competition; or that the Company will be able to procure or earn sufficient working capital to complete the development, testing and launch of the Company's prospective therapeutic products (including QN-302, QN-247 and RAS). The Company's stock price could be harmed if any of the events or trends contemplated by the forward-looking statements fails to occur or is delayed or if any actual future event otherwise differs from expectations. Additional information concerning these and other risk factors affecting the Company's business can be found in the Company's prior filings with the Securities and Exchange Commission, including its most recent Form 10-K, all of which are available at . The Company disclaims any intent or obligation to update these forward-looking statements beyond the date of this news release, except as required by law. This caution is made under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Contact: Jules Abraham JQA Partners, Inc. 917-885-7378 jabraham@jqapartners.com Source: Qualigen Therapeutics, Inc. Attachments Figure: 1 Figure: 2 Figure: 3 Figure: 4 Figure: 5 Figure: 6 Figure: 7 Figure: 1 Compound F3 and enhanced activity derivative F3-8-60 directly bind to K-RAS Figure: 2 F3 class compounds block RAS signaling. Figure: 3 F3-8-60 Suppresses MPNST cell line tumor growth Figure: 4 F3-8-60 suppresses MPNST pdx growth Figure: 5 NMR studies demonstrate F3-8-60 binds K-RaS12D and promotes changes in effector domain structure. Figure: 6 F3-8-60 is active in vivo against pancreatic cancer models. Figure: 7 F3-8-60 enhances the effect of Immune Checkpoint inhibitors.