Halia Therapeutics Presents Two AAIC 2026 Posters on HT-4253 for Alzheimer's Prevention in APOE4 Carriers
Preclinical data show HT-4253 reduces neuroinflammation and tau pathology; a second details a Phase 2a biomarker trial in pre-symptomatic APOE4 carriers via UAE genomics
LONDON, July 13, 2026 /PRNewswire/ -- Halia Therapeutics today announced two posters at the Alzheimer's Association International Conference (AAIC) 2026, July 12–15, linking preclinical data on its LRRK2 inhibitor HT-4253 to a biomarker trial to prevent or delay Alzheimer's disease (AD).
Halia's approach is grounded in genetic resilience: some APOE4 carriers, protected by a RAB10 variant, never develop Alzheimer's. HT-4253 reproduces that protection by inhibiting LRRK2, an upstream regulator of the RAB10 pathway.
"Our preclinical data show HT-4253 engages LRRK2, lowering neuroinflammation and tau phosphorylation and restoring microglial function," said David Bearss, Ph.D., CEO of Halia Therapeutics.
AAIC Presentations:
HT-4253, A Brain-Penetrant LRRK2 Inhibitor, Targets Neuroinflammation and Tau Pathology for AD Prevention in APOE4 Carriers
Wednesday, July 15, 2026, 7:30 a.m.–4:15 p.m. • Session: [In-Person Posters Wed] Drug Development: Human • Location: Exhibit Hall • Poster: Wednesday-0025 (Abstract #3245)
In human cell-based models, HT-4253 inhibited LRRK2 autophosphorylation and Rab10 phosphorylation, confirming target engagement. In iPSC-derived microglia (2D and 3D organoids), it reduced pro-inflammatory cytokine secretion; in iPSC-derived neurons, it decreased tau phosphorylation; and it restored phagocytic function in interferon-γ–exhausted BV2 microglia.
Design of a Phase 2a Trial of LRRK2 Inhibitor HT-4253 in Pre-symptomatic APOE4 Carriers Identified via Population-scale Genomics in the UAE
Monday, July 13, 2026, 7:30 a.m.–4:15 p.m. • Session: [In-Person Posters Mon] Drug Development: Human • Location: Exhibit Hall • Poster: Monday-0081 (Abstract #5843)
After a Phase 1 trial with a favorable safety profile, Halia designed an early-intervention study using population-scale UAE genomics to identify cognitively normal APOE4 carriers. Candidates are screened with C2N Diagnostics' PrecivityAD2™ blood test for elevated AD biomarkers signaling emerging amyloid pathology. Eligible participants enroll in a 48-week study of once-daily HT-4253, tracking blood-based biomarkers to assess whether it can alter disease onset and progression.
ABOUT HT-4253 AND THE LRRK2–RAB10 PATHWAY
HT-4253 is a brain-penetrant, small molecule inhibitor of leucine-rich repeat kinase 2 (LRRK2), a stress-recruited endolysosomal kinase that regulates membrane trafficking by phosphorylating Rab GTPases, including Rab10. Halia's hypothesis: persistent LRRK2 signaling, particularly in microglia, links major Alzheimer's pathologies: impaired lysosomal clearance, tau pathology, and chronic neuroinflammation.
ABOUT HALIA THERAPEUTICS
Halia Therapeutics, headquartered in Lehi, Utah and founded in 2017, is the genetic resilience company. Its secondary program, HT-4253, is in clinical development to prevent or delay Alzheimer's disease in APOE4 carriers. Halia's pipeline targets the RAB10 pathway through LRRK2 (upstream) and NEK7 (downstream) to regulate NLRP3 inflammasome activation, a driver of inflammation implicated in Alzheimer's, cancer, cardiovascular disease, and other chronic conditions.
Investor Contact
Leigh Salvo
New Street Investor Relations
leigh@newstreetir.com
Media Contact
Taylor Avei, Head of Business Development
Halia Therapeutics
tavei@haliatx.com • haliatx.com
Preclinical data show HT-4253 reduces neuroinflammation and tau pathology; a second details a Phase 2a biomarker trial in pre-symptomatic APOE4 carriers via UAE genomics
LONDON, July 13, 2026 /PRNewswire/ -- Halia Therapeutics today announced two posters at the Alzheimer's Association International Conference (AAIC) 2026, July 12–15, linking preclinical data on its LRRK2 inhibitor HT-4253 to a biomarker trial to prevent or delay Alzheimer's disease (AD).
Halia's approach is grounded in genetic resilience: some APOE4 carriers, protected by a RAB10 variant, never develop Alzheimer's. HT-4253 reproduces that protection by inhibiting LRRK2, an upstream regulator of the RAB10 pathway.
"Our preclinical data show HT-4253 engages LRRK2, lowering neuroinflammation and tau phosphorylation and restoring microglial function," said David Bearss, Ph.D., CEO of Halia Therapeutics.
AAIC Presentations:
HT-4253, A Brain-Penetrant LRRK2 Inhibitor, Targets Neuroinflammation and Tau Pathology for AD Prevention in APOE4 Carriers
Wednesday, July 15, 2026, 7:30 a.m.–4:15 p.m. • Session: [In-Person Posters Wed] Drug Development: Human • Location: Exhibit Hall • Poster: Wednesday-0025 (Abstract #3245)
In human cell-based models, HT-4253 inhibited LRRK2 autophosphorylation and Rab10 phosphorylation, confirming target engagement. In iPSC-derived microglia (2D and 3D organoids), it reduced pro-inflammatory cytokine secretion; in iPSC-derived neurons, it decreased tau phosphorylation; and it restored phagocytic function in interferon-γ–exhausted BV2 microglia.
Design of a Phase 2a Trial of LRRK2 Inhibitor HT-4253 in Pre-symptomatic APOE4 Carriers Identified via Population-scale Genomics in the UAE
Monday, July 13, 2026, 7:30 a.m.–4:15 p.m. • Session: [In-Person Posters Mon] Drug Development: Human • Location: Exhibit Hall • Poster: Monday-0081 (Abstract #5843)
After a Phase 1 trial with a favorable safety profile, Halia designed an early-intervention study using population-scale UAE genomics to identify cognitively normal APOE4 carriers. Candidates are screened with C2N Diagnostics' PrecivityAD2™ blood test for elevated AD biomarkers signaling emerging amyloid pathology. Eligible participants enroll in a 48-week study of once-daily HT-4253, tracking blood-based biomarkers to assess whether it can alter disease onset and progression.
ABOUT HT-4253 AND THE LRRK2–RAB10 PATHWAY
HT-4253 is a brain-penetrant, small molecule inhibitor of leucine-rich repeat kinase 2 (LRRK2), a stress-recruited endolysosomal kinase that regulates membrane trafficking by phosphorylating Rab GTPases, including Rab10. Halia's hypothesis: persistent LRRK2 signaling, particularly in microglia, links major Alzheimer's pathologies: impaired lysosomal clearance, tau pathology, and chronic neuroinflammation.
ABOUT HALIA THERAPEUTICS
Halia Therapeutics, headquartered in Lehi, Utah and founded in 2017, is the genetic resilience company. Its secondary program, HT-4253, is in clinical development to prevent or delay Alzheimer's disease in APOE4 carriers. Halia's pipeline targets the RAB10 pathway through LRRK2 (upstream) and NEK7 (downstream) to regulate NLRP3 inflammasome activation, a driver of inflammation implicated in Alzheimer's, cancer, cardiovascular disease, and other chronic conditions.
Investor Contact
Leigh Salvo
New Street Investor Relations
leigh@newstreetir.com
Media Contact
Taylor Avei, Head of Business Development
Halia Therapeutics
tavei@haliatx.com • haliatx.com
About Halia Therapeutics
Halia Therapeutics is a clinical-stage biopharmaceutical company focused on treating the root causes of inflammation. Leveraging genetic insights and AI-enabled discovery, Halia is building a robust pipeline of novel therapeutics based on genetic resilience that targets inflammatory pathways in diseases ranging from metabolic disorders to neurodegeneration and hematologic malignancies.
Halia’s mission is to create data-driven therapies that not only extend life but also improve its quality. The company is headquartered in Lehi, Utah, and is actively advancing global partnerships in clinical research, drug discovery, and personalized medicine.
To learn more, visit www.haliatx.com or follow us on LinkedIn and Twitter @HaliaTx.