Parkinson’s Disease (PD)

Neuroinflammation and mitochondrial dysfunction with associated oxidative/endoplasmic reticulum (ER) stress all work synergistically to accelerate Parkinson’s disease (PD) progression.

Emergent data supports a crucial role of soluble epoxide hydrolase (sEH) in driving pathogenesis of human PD. sEH promotes neuronal inflammation, a-synuclein aggregation, neurotoxicity and death of dopaminergic neurons -
NeuroPn is pursuing novel inhibitors of soluble epoxide hydrolase (sEH) to develop disease modifying therapeutics for Parkinson’s disease with highly discriminatory (efficacy, safety, neuronal protection) vs. marketed drugs.

Oncology

NeuroPn approach balances inflammatory toxicities and regulates immunological response in tumor.

NeuroPn sEH inhibitors have potential to accomplish optimal efficacy while minimizing the adverse effects of currently available therapies.

Painful Peripheral Neurotheraphy

Inadequate efficacy and mechanism-based side effects continue to restrict the utility of marketed drugs for chronic neuropathic pain. Selective stimulation of the endogenous analgesic pathway that mimics a natural response to pain stimuli could yield novel agents with superior efficacy and reduced side effects over marketed drugs.

sEH inhibition stimulates endogenous pathways for pain relief and promotes nerve healing

Soluble epoxide hydrolase (sEH) is a regulatory enzyme that rapidly degrades protective mediators epoxyeicosatrienoic acids (EETs) to inactive dihydroxyeicosatrienoic acids (DHETs). Inhibition of sEH stimulates endogenous GABAergic and opioid pathways to provide effective pain relief without narcotic effects. Inhibitors of sEH reduce endoplasmic reticulum (ER) and oxidative stress, neuronal inflammation and neurodegeneration.
NeuroPn sEH-inhibitors provide a novel, non-narcotic, disease-modifying therapy for chronic neuropathic pain conditions.