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2-2021-1561

Controlled-release formulation in double microfluidic encapsulated emulsion for spinal cord injury, Ischemic Stroke and TBI

UNMET NEED
Neurotrauma causes accumulation of excess toxic glutamate and neurological damage. Anti-glutamatergic treatments have failed to reduce CNS (Central nerve system) glutamate levels after SCI, and there is no clinically available emergency treatment to prevent the damage and to promote functional recovery.
OUR SOLUTION
The new BGS formulation is intended to be the first emergency neuroprotective treatment given shortly after an accident by paramedics. BGS reduce the blood glutamate concentration, thus increasing the rate by which excess glutamate is cleared. The normal glutamate concentrations are very well regulated by several liver enzymes, the major one being glutamate Oxalo-Acetate Transaminase (GOT1).
Solution steps:
a. Encapsulation of the enzyme GOT1 and its substrates oxaloacetate and vitamin B6, using droplet-microfluidics device.   
b. Encapsulation protects the reagents from rapid oxidation and allows controlled- drug (enzyme) release.
c. Our treatment (encapsulated enzyme) can be given by intravenous (IV) injection shortly after the accident by paramedics. This is a crucial element. We anticipate that our solution will be given in ambulances.
 KEY FEATURES:
• Dramatically reduces secondary injury, compared to the current standard of care (at the ER) to minimize    spinal cord damage.
• Time is of essence to prevent major damage when it comes to spinal cord injuries. Our aim is to treat the earliest possible right after the injury to mitigate potential neuromotor damage.
• This is a novel emergency treatment, designed to provide an initial response before reaching the hospital.
STATUS
 BGS was demonstrated in vitro:  comparison of treatment with direct addition of GOT1 and its substrates, with treatment where the enzyme was added encapsulated in microfluidic droplets for suspense release.

 

 

INTELLECTUAL PROPERTY
Provisional patent application was submitted.