STROKE RESEARCH TRIALS

Several clinical research studies are underway at the Chattanooga Center for Neurolgic Research. The Center specializes in acute and secondary stroke prevention trials. The following are a summary of ongoing investigations.

BAYx 3702
BAYx 3702 is classified as a neuroprotectant therapeutic drug. During ischemic stroke, the immediate damage cannot be prevented or treated. Complex biochemical cascades and axonal and neuronal derangements follow ischemia, leading to delayed secondary deterioration and poor outcome.

The massive release of glutamate following acute cerebral ischemia results in a dramatic increase in the influx of calcium into neuronal cells, resulting in cell death. Excitatory neurotransmitter glutamate may also play a major role in secondary cell damage following ischemic stroke.

The BAYx investigation attempts to determine whether this medicine will act to prevent or reduce this highly deleterious glutamate-induced activity.

A 4.5 hour interventional window has been established for this study, starting from the time stroke symptoms first manifest to the initiation of therapy.

CHARISMA
Aspirin and the anti-platelet medication, Plavix, are combined in this clinical trial to determine whether together, they are more effective than either drug used individually.

DEDAS
The agent in this study is an advanced “clot-buster” that dissolves vascular obstructions in the brain. Because of its biochemical specificity, the drug used in DIAS is expected to be safer and more effective than t-PA, causing less systemic bleeding and hemorrhage.

FUJISAWA
Compound FK506 is currently approved as an immune suppressant and anti-inflammatory agent that prevents tissue rejection during organ transplants. During acute stroke these anti-inflammatory properties may potentially reduce neuronal brain injury. up to 12 hours after acute stroke onset. In this trial, FK506 may be administered either as monotherapy or else in combination with t-PA.

RREACT/ONO
This is an acute stroke trial using a compound which inhibits glial cell activation in the brain. Glial cells are thought to play an inflammatory role in ischemic brain injury that increases the size of the patient’s stroke. By inhibiting glial cell activation this compound may decrease the ultimate stroke area. Patients enrolled in this study must present within onset of stroke symptoms less than six hours old. This Phase II investigation will involve careful evaluation by a neurologist and neuro-imaging with MRI scans of the brain.