RESEARCH
Mitochondrial dysfunction is increasingly implicated in the onset of Alzheimer's disease.
We are developing small-molecule therapeutics that target bioenergetic failure — an early and potentially tractable driver of neurodegeneration.
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Three pillars of research
Our programs address the underlying biology of Alzheimer's disease, where mitochondrial health is critical to neuronal function.
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Neurodegenerative diseaseAlzheimer's and related diseases are our primary focus. We target the biological failures that drive them before significant damage has occurred. -
Cellular metabolismWhen cells can't produce enough energy, disease follows. We focus on restoring the metabolic machinery that keeps neurons healthy and resilient. -
NeuroinflammationChronic inflammation is both a symptom and a driver of neurodegeneration. We investigate the inflammatory pathways that accelerate disease and look for ways to interrupt them.
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From discovery to IND
Our programs address the underlying biology of Alzheimer's disease, where mitochondrial health is critical to neuronal function.
Basic to translational
Each program is grounded in the underlying disease biology and built on a mechanistic foundation before moving into animal models.
Data before decisions
Multi-modal datasets across tissues and timepoints guide candidate selection and progression criteria.
Machine learning integration
Computational models trained on multi-modal biological datasets accelerate pattern recognition across tissues, timepoints, and treatment groups.
IND-enabling by design
Programs are structured from the outset around the regulatory and scientific milestones required for clinical advancement.
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As mitochondrial function declines with age, the downstream consequences — neuroinflammation, synaptic loss, cellular death — follow predictably in Alzheimer's disease.
- Neurons depend on mitochondrial outputNeurons are among the most energy-demanding cells in the body, leaving them acutely vulnerable when mitochondrial output declines. Supporting mitochondrial function is a key focus of our therapeutic approach.
- Dysfunction appears before symptomsMitochondrial impairment manifests years before significant clinical decline — creating a therapeutic window for earlier therapeutic intervention.
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