|1.||Tortella, Frank C: 2 articles (09/2005 - 05/2002)|
|2.||Williams, Anthony J: 2 articles (09/2005 - 05/2002)|
|3.||Barton, Matthew E: 2 articles (03/2004 - 03/2004)|
|4.||White, H Steve: 2 articles (03/2004 - 03/2004)|
|5.||Dave, J R: 2 articles (11/2003 - 07/2000)|
|6.||Williams, A J: 2 articles (11/2003 - 07/2000)|
|7.||Tortella, F C: 2 articles (11/2003 - 07/2000)|
|8.||Castellino, Francis J: 1 article (01/2015)|
|9.||Dang, Alexander: 1 article (01/2015)|
|10.||Balsara, Rashna: 1 article (01/2015)|
|1.||Brain Ischemia (Cerebral Ischemia)
11/01/2003 - "In conclusion, CGX-1007 effectively attenuated gene expression associated with delayed cell death as related to a neuroprotective relief of cerebral ischemia."
05/07/2002 - "Intrathecal CGX-1007 is neuroprotective in a rat model of focal cerebral ischemia."
07/01/2000 - "Neuroprotective efficacy and therapeutic window of the high-affinity N-methyl-D-aspartate antagonist conantokin-G: in vitro (primary cerebellar neurons) and in vivo (rat model of transient focal brain ischemia) studies."
09/21/2005 - "The potent NMDA receptor antagonist, Conantokin-G (CGX-1007), a snail peptide, has an 8-h therapeutic window in rat focal cerebral ischemia. "
|2.||Middle Cerebral Artery Infarction (Middle Cerebral Artery Syndrome)
05/07/2002 - "Using the same model of middle cerebral artery occlusion (MCAo) in rats we now report the neuroprotective effects of CGX-1007 when delivered intrathecally (i.t.). "
11/01/2003 - "In this study we have evaluated the upregulation of several genes associated with delayed cell death (c-fos, bax, and bcl-2) during the initial 24 h of transient middle cerebral artery occlusion (MCAo) in the rat and the effects of postinjury treatment with the NR2B subunit specific NMDA receptor antagonist CGX-1007 (Conantokin-G, Con-G). "
03/01/2004 - "CGX-1007 has been reported to have highly potent, broad-spectrum anticonvulsant activity in animal seizure models. "
03/01/2004 - "In amygdala kindled rats, acute treatment with CGX-1007 blocked the secondarily generalized kindled seizure in a dose-dependent manner. "
03/01/2004 - "The present study was designed to assess the effects of CGX-1007 and CI-1041 on the acquisition and expression of kindled seizures. "
03/01/2004 - "Although both CI-1041 and CGX-1007 are reportedly NR2B specific antagonists, they differ in their ability to block amygdala-kindled seizures, suggesting that the mechanism of action of these compounds differs. "
03/01/2004 - "In the corneal kindled rat, CGX-1007 [Epilepsia 36 (1998) 39] and CI-1041, administered p.o., 2h prior to the kindling stimulation displayed time- and dose-dependent block of fully expressed corneal kindled seizures (ED50 = 300 pmol and 2.5mg/kg for CGX-1007 and CI-1041, respectively). "
|4.||Brain Injuries (Brain Injury)
11/01/2003 - "Treatment with the snail peptide CGX-1007 reduces DNA damage and alters gene expression of c-fos and bcl-2 following focal ischemic brain injury in rats."
01/01/2015 - "The neuroprotective activity of conantokin-G (con-G), a naturally occurring antagonist of N-methyl-D-aspartate receptors (NMDAR), was neurologically and histologically compared in the core and peri-infarct regions after ischemia/reperfusion brain injury in male Sprague-Dawley rats. "
05/07/2002 - "The NMDA antagonist CGX-1007 (Conantokin-G) has previously been shown to possess potent neuroprotective properties when administered intracranially following experimental ischemic brain injury. "
02/01/2009 - "In a model of neuropathic spinal cord injury pain, which is clinically difficult to treat, the combination of conantokin-G and omega-conotoxin MVIIA resulted in robust synergistic antinociception. "
02/01/2009 - "Antinociceptive effects of the marine snail peptides conantokin-G and conotoxin MVIIA alone and in combination in rat models of pain."
01/01/2012 - "Conantokin G (CTG), isolated from the venom of the marine cone snail Conus geographus, is an antagonist of N-methyl-d-aspartate receptors (NMDARs), the activation of which, especially those located on the central afferent terminals and dorsal horn neurons, leads to hypersensitivity and pain. "
|4.||N-Methyl-D-Aspartate Receptors (NMDA Receptors)