On January 31, 2024 Halia Therapeutics, a clinical-stage biopharmaceutical company pioneering a novel class of small molecule medications designed to combat inflammation, reported the completion of a $30 million Series C financing (Press release, Halia Therapeutics, JAN 31, 2024, View Source [SID1234639744]). The financing was led by Todd Pedersen, with continued participation from existing investors.
Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:
Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing
Schedule Your 30 min Free Demo!
Proceeds from the financing will be used to support the advancement of Halia’s lead asset, HT-6184, a selective and orally bioavailable first-in-class inhibitor of NLRP3/NEK7 inflammasome in Phase II clinical trials. Halia Therapeutics recently initiated a Phase IIa trial in India to treat patients with lower-risk myelodysplastic syndromes (LR-MDS). LR-MDS are a group of cancers in which the bone marrow produces underdeveloped cells that are abnormal in size, shape, or appearance and are therefore "dysplastic." The company also plans to evaluate HT-6184 in Phase II trials in the U.S. for the treatment of post-procedure inflammatory pain response, as well as begin a Phase I trial in Alzheimer’s patients. Funding will also support IND-enabling studies for Halia’s alternative programs that are developing Leucine-rich repeat kinase 2 (LRRK2) inhibitors to treat neurological diseases such as Parkinson’s and Alzheimer’s disease, in addition to building out clinical and regulatory teams further to support the global development of the company’s pipeline.
"We are grateful for the trust investors have in our therapeutic approach. Their confidence is the driving force behind our efforts in developing innovative therapies targeting chronic inflammation," said Dr. David Bearss, CEO of Halia Therapeutics. "This financing will help us to advance significantly our lead drug candidate, HT-6184, in ongoing global Phase II trials and will support the trajectory of our additional programs targeting neuroinflammation into the clinic, bringing us even closer to breakthrough treatments for inflammatory-related diseases."
"We believe that Halia’s unique approach of targeting the NLP3 inflammasome holds significant potential for addressing a wide range of inflammatory diseases, along with hematologic conditions and other malignancies," said Todd Pedersen. "The company’s expertise and patient-focused mindset will be invaluable for advancing these anti-inflammatory therapeutics and revolutionizing the approach for targeting chronic inflammation in patients."
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 processes lead to systemic chronic inflammation. Halia’s therapeutic inhibition of NLRP3 prevents the formation of the NLRP3 inflammasome and promotes its disassembly once formed, thereby inhibiting the production and release of IL-1β and IL-18. Persistent activation of the NLRP3 inflammasome is thought to drive the onset and progression of many conditions, including fibrotic, dermatological, and auto-inflammatory diseases. Significant neurological disorders such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis are also driven by NLRP3 activation.
About HT-6184
HT-6184 represents an innovative approach as it is the first drug candidate to target the protein NEK7 through an allosteric mechanism. NEK7 is an essential component of the NLRP3 inflammasome and is critical for its assembly and the maintenance of NLRP3 activity. In preclinical models, Halia has shown that inhibiting the ability of NEK7 to bind to NLRP3 leads to a disruption in the formation of the NLRP3 inflammasome complex, thereby inhibiting the signaling from the inflammasome and reducing the inflammatory response. Preclinical models also showed that in addition to disrupting the formation of the NLRP3 inflammasome, HT-6184 promotes the disassembly of the inflammasome once activated.