dibenzo(b,f)oxepin- 10- ylmethyl- methyl- prop- 2- ynyl- amine (TCH346)

12/01/2006 - "The discrepancy between the preclinical promise of TCH346 and the clinical outcome could have arisen because of the use of laboratory models that do not accurately reflect the pathogenesis of Parkinson's disease, the doses of study drug used, insensitive clinical endpoints, and the patient population selected for study."
01/01/2003 - "However, CGP 3466 pretreatment does not ameliorate survival and function of the dopaminergic neurons after grafting into a rat model of Parkinson's disease."
12/01/2000 - "In conclusion, our results indicate that CGP 3466 is able to prevent death of dopaminergic cells in in vitro and in vivo models of Parkinson's disease. "
12/01/2000 - "CGP 3466 protects dopaminergic neurons in lesion models of Parkinson's disease."
08/01/2000 - "CGP 3466B is suggested to be a valuable agent for inhibiting the dopaminergic degeneration in patients with Parkinson's disease."

01/01/2013 - "dy(2J) mice treated with 0.1 mg/kg/day omigapil showed decreased percent fibrosis in both gastrocnemius (p<0.03) and diaphragm (p<0.001) compared to vehicle, and in diaphragm (p<0.013) when compared to 1 mg/kg/day omigapil treated mice. "
01/01/2013 - "Omigapil therapy (0.1 mg/kg) improved respiratory rate and decreased skeletal and respiratory muscle fibrosis in dy(2J) mice. "
01/01/2013 - "Omigapil treatment decreases fibrosis and improves respiratory rate in dy(2J) mouse model of congenital muscular dystrophy."
08/01/2011 - "By combining mini-agrin with either transgenic Bcl2 expression or oral omigapil application, we show that the ameliorating effect of mini-agrin, which acts by restoring the mechanical stability of muscle fibres and, thereby, reduces muscle fibre breakdown and concomitant fibrosis, is complemented by apoptosis inhibitors, which prevent the loss of muscle fibres. "

01/01/2017 - "Administration of CGP3466B improved neurological function, downregulated the ROS level and alleviated brain edema at 24 h after TBI. "

08/21/2007 - "The trial revealed no evidence of a beneficial effect of TCH346 on disease progression in patients with ALS."
10/01/2000 - "CGP 3466B slowed disease progression as determined by a 57% increase in life-span, preservation of body weight and motor performance. "

06/01/2004 - "In November 2002, an advisory board meeting was convened by Novartis Pharma to provide recommendations and rationale for clinical trials designed to evaluate new treatments, such as TCH346, for amyotrophic lateral sclerosis (ALS). "