|1.||Ikonomidou, Chrysanthy: 1 article (10/2002)|
|2.||Turski, Lechoslaw: 1 article (10/2002)|
|3.||Akins, Paul T: 1 article (01/2002)|
|4.||Atkinson, Richard P: 1 article (01/2002)|
|5.||Hall, D: 1 article (12/2001)|
|6.||Aptiganel Acute Stroke Investigators: 1 article (12/2001)|
|7.||Goldstein, L B: 1 article (12/2001)|
|8.||Albers, G W: 1 article (12/2001)|
|9.||Lesko, L M: 1 article (12/2001)|
|10.||Brambilla, A: 1 article (03/2001)|
10/01/1999 - "This study assessed the safety and tolerability of non-weight-adjusted doses of aptiganel in patients with acute ischemic stroke. "
10/01/1999 - "Safety and tolerability study of aptiganel hydrochloride in patients with an acute ischemic stroke."
12/05/2001 - "Aptiganel was not efficacious in patients with acute ischemic stroke at either of the tested doses, and m ay be harmful. "
12/05/2001 - "At 7 days, placebo-treated patients exhibited slightly greater neurological improvement on the NIH Stroke Scale than high-dose aptiganel patients (mean improvement for placebo group, -0.8 points vs for high-dose aptiganel, 0.9 points; P =.04). "
12/05/2001 - "Patients were randomly assigned within 6 hours of stroke to receive 1 of 3 treatment regimens: high-dose aptiganel (5-mg bolus followed by 0.75 mg/h for 12 hours; n = 214); low-dose aptiganel (3-mg bolus followed by 0.5 mg/h for 12 hours; n = 200); or placebo (n = 214). "
10/01/1998 - "Aptiganel completely inhibited c-Jun expression (P < 0.001) but not Fos, improved functional outcome, and attenuated neuronal necrosis (P < 0.05). "
10/01/1998 - "Aptiganel inhibits c-Jun expression, attenuates neuronal necrosis, and improves outcome."
10/01/1997 - "Neuronal necrosis was observed in the brains of vehicle-treated lambs after 120 minutes of HCA but was significantly decreased (p < 0.05) in the lambs given aptiganel. "
10/01/1998 - "This study determined the induction profiles of immediate-early genes in the ovine brain after cardiopulmonary bypass (CPB) and hypothermic circulatory arrest (HCA), and the effects of the noncompetitive N-methyl-D-aspartate antagonist, aptiganel, on immediate-early gene expression, neuronal necrosis, and functional outcome. "
|3.||Spinal Cord Injuries (Spinal Cord Injury)
|4.||Brain Ischemia (Cerebral Ischemia)
03/01/2001 - "Effects of cerestat and NBQX on functional and morphological outcomes in rat focal cerebral ischemia."
12/05/2001 - "Aptiganel hydrochloride is a novel and selective ligand for the ion-channel site of the N-methyl-D-aspartate receptor-channel complex and a promising neuroprotective agent in animal models of focal brain ischemia. "
03/01/1998 - "Recent studies have demonstrated a neuroprotective effect of the noncompetitive N-methyl-D-aspartate receptor antagonist aptiganel HCl (Cerestat) in focal cerebral ischemia. "
01/01/1998 - "Recent studies revealed a neuroprotective effect of the non-competitive NMDA receptor antagonist Aptiganel HCL (Cerestat CNS 1102) in focal cerebral ischemia. "
10/01/1999 - "Aptiganel (CNS 1102) is a selective, noncompetitive antagonist that acts on the ion channel associated with the N-methyl-D-aspartate (NMDA) receptor and is neuroprotective in experimental focal cerebral ischemia models at a plasma concentration of 10 ng/mL. In human volunteers, dose-limiting effects of aptiganel are blood pressure increases and central nervous system (CNS) excitation or depression. "
|5.||Brain Injuries (Brain Injury)
03/01/1998 - "Taken together, aptiganel HCl exerts various beneficial effects following experimental traumatic brain injury. "
12/19/1997 - "CERESTAT (4, aptiganel CNS 1102) is currently undergoing clinical trial for the treatment of traumatic brain injury and stroke. "
03/01/1995 - "Both noncompetitive (aptiganel hydrochloride, dextrorphan) and competitive (selfotel, d-CPPene) antagonists have undergone tolerability studies in acute stroke and traumatic brain injury. "
09/15/1995 - "The high affinity noncompetitive N-methyl-D-aspartate receptor antagonist CNS 1102 (aptiganel hydrochloride, Cambridge NeuroScience, Cambridge, MA.) is neuroprotective in preclinical models of stroke when administered as pretreatment or up to 60 minutes postischemia, and has potential for treatment of acute stroke or traumatic brain injury in man. "
10/01/2002 - "Glutamate N-methyl-D-aspartate (NMDA) receptor antagonists (competitive receptor antagonists, ion channel blockers, and glycine antagonists)--such as selfotel, aptiganel, eliprodil, licostinel and gavestinel--failed to show efficacy in clinical trials of stroke or traumatic brain injury. "
|6.||Dizocilpine Maleate (Dizocilpine)
|7.||gacyclidine (GK 11)
|9.||Ion Channels (Ion Channel)
|10.||Glutamic Acid (Glutamate)
|1.||Cardiopulmonary Bypass (Heart-Lung Bypass)