- Halia Therapeutics will showcase its LRRK2 and NEK7 inhibitors targeting Alzheimer’s disease and obesity.
LEHI, Utah, Oct. 21, 2024 /PRNewswire/ — Halia Therapeutics, Inc. (Halia), a clinical-stage biopharmaceutical company pioneering innovative treatments for inflammatory and neurodegenerative diseases, today announced that it will showcase its scientific data and progressive pipeline at the upcoming Global Health Exhibition. The event will occur October 21–23, 2024, in Riyadh, Saudi Arabia.
Halia Therapeutics will host an exhibition booth to showcase its efforts in targeting two indications, Alzheimer’s disease and obesity. Halia’s candidate HT-4253 is a LRRK2 inhibitor administered orally with excellent brain penetration. LRRK2 is a key modulator of neuroinflammation, which plays a critical role in neurodegenerative diseases. HT-6184 is a first-in-class, selective and orally bioavailable inhibitor of the NEK7/NLRP3 inflammasome. HT-6184 is being tested in combination with semaglutide to target inflammation, which has been linked to obesity-related metabolic dysfunction. Halia’s drug candidates are designed to provide novel approaches to improve patients’ lives affected by neurodegenerative diseases and chronic inflammatory disorders.
Global Health Exhibition unites visionaries, policymakers, government agencies, healthcare luminaries, scientists and futurists to forge a healthier, more innovative future.
Visit Halia at booth H1C-W83 in the USA Pavillion.
To view the full agenda please visit https://www.globalhealthsaudi.com/en/congress/overview.html
About NLRP3
NLRP3, an innate immune sensor, is activated in response to various pathogenic and sterile stimuli. Activation of NLRP3 triggers the release of the pro-inflammatory cytokines IL-1β and IL-18 and induces a lytic cell death process called pyroptosis. These mechanisms lead to systemic chronic inflammation. Halia’s therapeutic inhibits NLRP3, preventing the formation of the NLRP3 inflammasome and promoting its disassembly once formed. This inhibition blocks the production and release of IL-1β and IL-18. Chronic NLRP3 inflammasome activation is believed to drive the onset and progression of many conditions, including fibrotic, dermatological, and auto-inflammatory diseases. Moreover, it plays a significant role in neurodegenerative and neuroinflammatory disorders such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis.
About HT-6184
HT-6184 is a groundbreaking drug candidate that targets the protein NEK7 through an allosteric mechanism. NEK7 plays a crucial role in the NLRP3 inflammasome, which is essential for its assembly and activity maintenance. In preclinical models, Halia demonstrated that inhibiting the NEK7’s ability to bind to NLRP3 disrupts inflammasome signaling and reduces the inflammatory response. HT-6184 not only prevents the formation of the NLRP3 inflammasome but also promotes its disassembly once activated. (Halia unpublished data).
About HT-4253
HT-4253 is an orally administered small molecule with excellent brain penetration that targets LRRK2, a key mediator of neuroinflammation. Chronic brain inflammation is a driver of several neurodegenerative diseases, including Parkinson’s and Alzheimer’s. Halia scientists have demonstrated that LRRK2’s essential role in regulating neuroinflammation. LRRK2 inhibition by HT-4253 offers a novel approach to treat neurodegenerative diseases with an inflammation component, potentially altering disease progression. HT-4253 is undergoing a Phase I trial to evaluate the safety and tolerability in healthy volunteers (NCT06537817).
About Halia Therapeutics, Inc.
Halia Therapeutics is pioneering novel therapeutics to enhance patients’ lives with chronic inflammatory disorders and neurodegenerative diseases. Halia’s initial programs target NEK7 and LRRK2.Headquartered in Lehi, Utah, Halia Therapeutics invites you to learn more about our work. Visit our website at www.haliatx.com, connect with us on LinkedIn, and follow our updates on Twitter (X).
Company Contact
Halia Therapeutics
info@haliatx.com
+1 (385) 355-4315