Polku Therapeutics develops first-in-class, disease-modifying small molecule therapies targeting neurodegenerative conditions like Parkinson's disease and tauopathies. The platform modulates PREP/PP2A interaction to reduce toxic protein aggregation, enhance aggregate clearance via autophagy, and mitigate neuroinflammation. This approach aims to preserve neuronal vitality and slow the progression of debilitating central nervous system disorders.
Funding
$2M raised to dateRaised to date based on public sources. This may differ from the amount the company actually raised and is based only on what is publicly available on the internet.
Founders
Product
Problem
Neurodegenerative diseases, such as Parkinson's and Alzheimer's, are characterized by the accumulation of abnormal protein aggregates and neuroinflammation, leading to the progressive loss of neurons and cognitive decline. Current treatments often fail to address the underlying mechanisms of these diseases, offering only symptomatic relief.
Solution
Polku Therapeutics is developing disease-modifying therapies for neurodegenerative diseases by targeting protein aggregation and neuroinflammation. Their approach focuses on activating processes that reduce the buildup of toxic proteins like tau and alpha-synuclein, while simultaneously enhancing the clearance of existing aggregates through autophagy. By modulating PREP/PP2A interaction, Polku's therapies aim to dephosphorylate tau and α-syn, reduce oxidative stress, and dampen neuroinflammatory responses, creating a healthier environment for neurons to thrive and slowing disease progression. The company utilizes optimized small molecules that bind to a novel binding site to allosterically modulate PREP protein-protein interactions.
Target Audience
The primary target audience includes individuals suffering from neurodegenerative diseases like Parkinson's and Alzheimer's, as well as pharmaceutical companies and research institutions focused on developing and studying treatments for these conditions.
Features
- Modulation of PREP/PP2A interaction to restore protein dephosphorylation and autophagy.
- Promotion of autophagy to enhance the clearance of neurotoxic tau and α-syn aggregates.
- Reduction of oxidative stress through PP2A activation.
- Dampening of neuroinflammatory responses via PP2A activation to protect neurons.
- Optimized small molecules designed to bind to a novel binding site on PREP.
- Demonstrated disease-modifying effects on cognition and motor function in Parkinson's and tauopathy mouse models.