A Novel Use of the Phytoestrogen Biochanin A in Neuroprotection
Reference #: 2009-022
Neural injury is often an irreversible event that results in lifelong consequences. Therapeutic options to reduce neuronal injury following central or peripheral nervous system disorder or injury, or any other kind of injury, surgery, or chronic neuropathy are necessary to reduce the lifelong effects associated with neuronal toxicity. As it stands, current treatment strategies to reduce neuronal injury have limited effectiveness and adverse side effects. Our invention describes a new use of a naturally occurring dietary supplement, Biochanin A to reduce and/or prevent nerve damage. Georgetown researchers demonstrate that Biochanin A effectively prevents or rescues neuronal injury by modulating p75 NTR expression. The present invention also describes a method of screening agents that modulate neuronal cell death, thereby allowing for cheap and efficient screening of neuroprotective agents.
- Treatment of pain and/or reducing the severity of any nerve damage caused by:
- Central nervous system injury or disorder such as spinal cord injuries or head injuries.
- Peripheral nervous system injury or disorder such as peripheral neuropathy
- Surgery, radiation or chemotherapy
- Diabetic neuropathy
- Other condition such as stroke, ischemia, a genetic disorder, infection, organ failure etc.
- A preventive regimen for patients that are at risk for a neural injury.
- A research tool for screening other novel neuroprotectant molecules as well as regulators of p75NTR and p38 MAPK expression
- Biochanin A protects from neural injury more effectively than dexamethasone, the current standard of care
- Biochanin A is effective at reducing the incidence of pain in a model of neuropathic pain
- Biochanin A is a readily available, naturally occurring phytoestrogen with no known side effects; this is in contrast to dexamethasone
- Biochanin A is cost-effective and easily obtained.
Stage of Development
Biochanin A has been demonstrated to protect from ibuprofen-induced neuronal injury caused by up-regulation of p75NTR. Proof of principle has been established in an animal model of neuropathic pain.
“Biochanin A reduces drug-induced p75NTR expression and enhances cell survival: a new in vitro assay for screening inhibitors of p75NTR expression”. El Touny LH et. al., Rejuvenation Research. 2010; 5: 227-237
“Quercetin promotes functional recovery following acute spinal cord injury”. Schültke E, et. al., J Neurotrauma. 2003 Jun; 20(6): 583-91.
Patent application has been filed.