Veralox Therapeutics Expands Its Pipeline with the Exclusive Option to Acquire Nudge Therapeutics

PR Newswire

FREDERICK, Md., Jan. 9, 2025

   -- Exclusive agreement to acquire Nudge Therapeutics includes their series 
      of cGAS inhibitors. 
 
   -- Nudge has developed novel potent small molecule cGAS inhibitors that 
      prevents the overproduction of Type 1 interferons which are implicated in 
      inflammatory and autoimmune diseases. 
 
   -- The addition of cGAS inhibitors complements the Company's focus on 
      VLX-1005, which is expected to achieve clinical PoC in 2025. 

FREDERICK, Md., Jan. 9, 2025 /PRNewswire/ -- Veralox Therapeutics, a clinical-stage biotechnology company developing a new class of therapies targeting the 12-lipoxygenase (12-LOX) pathway, announced today that it has entered into an exclusive agreement with Nudge Therapeutics to acquire the company and their preclinical cyclic AMP-GMP (cGAS) inhibitor compounds. The agreement allows Veralox to continue development of Nudge's compounds and trigger acquisition of the company upon achievement of downstream milestones. Financial terms were not disclosed.

"We are excited because this agreement allows Nudge to utilize the expertise of Veralox to drive our cGAS program towards a clinical candidate," said Robert Lowery, CEO of Nudge Therapeutics and CEO of Bellbrook Labs. "Veralox has unique experience with these assets which can be utilized to move the program forward quickly."

"This is an exciting time for Veralox as we look to build on our expertise in developing novel therapeutics that address serious autoimmune and inflammatory diseases," said Jonathan Mow, CEO of Veralox. "The potential for cGAS inhibitors to treat a variety of inflammatory conditions, including autoimmune, metabolic, cardiovascular, rare diseases, and neurodegenerative diseases complements our novel approach to the development of VLX-1005."

About cGAS

The cGAS-STING pathway is an innate immune sensor to detect both host-derived and foreign cytoplasmic DNA produced as a result of infection or cell damage and triggers an inflammatory response. In autoimmune diseases, the innate immune response is chronically activated, directly promoting inflammation and the development of autoimmunity, both in the periphery and the central nervous system $(CNS)$.

About VLX-1005

VLX-1005 is a novel, small molecule inhibitor of 12-lipoxygenase (12-LOX) intended for the treatment or prevention of thrombosis in adults with heparin-induced thrombocytopenia $(HIT)$. A potent and selective inhibitor of 12-LOX, VLX-1005 inhibits platelet 12-HETE production. Two Phase 1 studies completed in 96 healthy participants showed favorable safety and tolerability with no deaths, no serious adverse events and no trend in AE reporting with increased dosing of VLX-1005. A Phase 2 study (VLX-1005-003) to evaluate VLX-1005 in patients with suspected HIT is currently enrolling patients across 14 clinical sites. Additional information is available at clinicaltrials.gov, identifier NCT05785819.

About Veralox Therapeutics

Veralox Therapeutics Inc. is the leader in developing first-in-class therapeutics targeting 12- lipoxygenase, pioneering a new class of therapies that treat the underlying pathologies of serious immune-inflammatory diseases with unmet medical needs. The company's lead candidate, VLX-1005, is in development for the treatment of patients with heparin-induced thrombocytopenia $(HIT.AU)$. VLX-1005 has orphan drug designation in the United States and has been awarded Fast Track Designation by the U.S. Food and Drug Administration and has been awarded Orphan Drug Status in EMA for Receives New Designation for Treatment of Platelet-Activating Anti-Platelet Factor 4 (PF4) Disorders. Second generation therapeutic products are under development for type 1 diabetes and other immune-mediated and inflammatory diseases.

For more information, visit our website: https://veralox.com/.

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SOURCE Veralox Therapeutics

/CONTACT: Lisa Beck, Veralox Therapeutics, 919.413.6223, lbeck@veralox.com

(END) Dow Jones Newswires

January 09, 2025 17:35 ET (22:35 GMT)