CGS 26303

11/01/2004 - "Total infarct areas were reduced when compared with vehicle-treated animals by 48%, 50%, and 57% in rats receiving CGS 26303 at 1, 3, and 10 mg/kg, respectively, while the neurological score was significantly improved in the highest-dose CGS 26303-treated group. "
11/01/2004 - "Total infarct areas were reduced by an average of 42-50% in the CGS 26303 treatment group. "
11/01/2004 - "The purpose of this study was to examine the effect of an endothelin-converting enzyme inhibitor, CGS 26303, on neurological deficit, infarct size, and extent of edema after transient occlusion of the middle cerebral artery and bilateral common carotid arteries (triple vessel occlusion) in rats. "

01/01/2014 - "Deficits in motor function were obvious in the SAH rats, and CGS 26303 significantly improved the rate of paraplegia. "
02/01/2007 - "The results showed that pretreatment with CGS 26303 significantly preserved the locomotor function and decreased the paraplegia rate at Days 1 and 3 as compared with a saline-treated group. "

04/01/2004 - "Thus, long-term treatment with CGS 26303 decreases both preload and afterload, increases cardiac output, and diminishes LV hypertrophy, dilatation, and cardiac fibrosis, suggesting that dual ECE-NEP inhibition might be beneficial in human CHF."
06/01/2005 - "Both temocapril and CGS 26303 ameliorated LV perivascular fibrosis, reduced mRNA levels of types I and III collagen, and decreased the heart weight/body weight ratio. "

04/01/2004 - "Thus, long-term treatment with CGS 26303 decreases both preload and afterload, increases cardiac output, and diminishes LV hypertrophy, dilatation, and cardiac fibrosis, suggesting that dual ECE-NEP inhibition might be beneficial in human CHF."

01/01/1998 - "Arterial narrowing was significantly attenuated in rabbits treated with CGS 26303 at 30 mg/kg. These results demonstrate that CGS 26303 may be an effective agent in prevention and reversal of cerebral vasospasm after aneurysmal SAH."
08/01/1997 - "The ECE inhibitor CGS 26303 thus represents a promising therapeutic agent for the treatment of cerebral vasospasm following aneurysmal SAH."
11/01/1996 - "Moreover, the findings indicate that blocking the conversion of Big ET-1 to its active ET-1 form using CGS 26303 may represent a feasible strategy for ameliorating cerebral vasospasm."
08/01/2001 - "Continuous intravenous infusion of CGS 26303 attenuated SAH-induced cerebral vasospasm in a dose-dependent manner in both the prevention and the reversal groups. "
11/01/2004 - "These data suggest that the reduction of cerebral vasospasm by CGS 26303 in rats subjected to experimental subarachnoid hemorrhage may result from both over-expression of heme-oxygenase-1 in brain tissue and suppression of endothelin biosynthesis in basilar arteries."