|1.||Callaway, J K: 6 articles (11/2006 - 10/2000)|
|2.||Jarrott, B: 5 articles (11/2006 - 10/2000)|
|3.||Beart, P M: 3 articles (07/2004 - 10/2000)|
|4.||Giardina, S F: 2 articles (07/2004 - 04/2001)|
|5.||Hermansson, Ann: 1 article (12/2012)|
|6.||Hultcrantz, Malou: 1 article (12/2012)|
|7.||Stenfeldt, Karin: 1 article (12/2012)|
|8.||Groth, Anita: 1 article (12/2012)|
|9.||Enoksson, Frida: 1 article (12/2012)|
|10.||Stalfors, Joacim: 1 article (12/2012)|
12/01/1999 - "The present findings suggest that AM-36 may have great promise in the acute treatment of human stroke."
07/01/2004 - "The present studies demonstrate Na+ channel blocking activity of AM-36 both in vitro and in vivo, together with significant neuroprotection when administration is delayed up to 5 h following experimental stroke."
11/01/2001 - "5. These studies indicate that AM-36 is a unique neuroprotective agent with multiple modes of action, making it an attractive candidate for the treatment of acute stroke in humans."
11/01/2001 - "AM-36 was neuroprotective even when administration was delayed until 3 h systemically, or 5 h intravenously, after induction of stroke. "
04/01/2001 - "This bifunctional profile of activity may underlie the potent neuroprotective effects of AM-36 recently found in a stroke model in conscious rats."
|2.||Middle Cerebral Artery Infarction (Middle Cerebral Artery Syndrome)
02/01/2008 - "The very high brain uptake of AM-36 supports previous in-vivo efficacy studies demonstrating the neuroprotective effects of this compound when administered to rats with middle cerebral artery occlusion."
10/15/2000 - "AM-36 (1.8 mg/kg i.p.) or vehicle, was administered 30 min, 24 and 48 h after endothelin-1-induced middle cerebral artery occlusion in conscious rats. "
12/01/1999 - "AM-36 (6 mg/kg IP) or vehicle was administered intraperitoneally 30, 60, or 180 minutes after middle cerebral artery occlusion. "
12/01/1999 - "Delayed treatment with AM-36, a novel neuroprotective agent, reduces neuronal damage after endothelin-1-induced middle cerebral artery occlusion in conscious rats."
11/01/2001 - "4. In a middle cerebral artery occlusion model of stroke in conscious rats, systemic administration of AM-36 markedly reduced both cortical and striatal infarct volume and significantly improved functional outcome in motor performance, neurological deficit and sensorimotor neglect tests. "
01/01/2010 - "The antinociception after morphine (3.2 mg/kg) was increased by co-administration with CNSB002 from 28.0 and 31.7% to 114.6 and 56.9% reversal of hyperalgesia in the inflammatory and neuropathic models, respectively (P < 0.01; one-way analysis of variance-significantly greater than either drug given alone). "
01/01/2010 - "The doses calculated to cause 50% reversal of hyperalgesia (ED50) were 7.54 (1.81) and 4.83 (1.54) in the carrageenan model and 44.18 (1.37) and 9.14 (1.24) in the STZ-induced neuropathy model for CNSB002 and morphine, respectively (mg/kg; mean, SEM). "
08/01/2008 - "To study the effect of Astrangalus mongholicus (AM) on the expression of Connective Tissue Growth Factor (CTGF) in SD rats with Unilateral Ureteral Obstruction (UUO) and elucidate the mechanism underlying the renorotective effects of AM. 36 Sprague-Dawley rats were randomly divided into 3 groups: sham-operation group (Sham), UUO group (UUO) and UUO + AM group (AM). "
|5.||Neuralgia (Stump Neuralgia)
01/01/2010 - "This study determined the antihyperalgesic effect of CNSB002, a sodium channel blocker with antioxidant properties given alone and in combinations with morphine in rat models of inflammatory and neuropathic pain. "
01/01/2010 - "Studies of synergy between morphine and a novel sodium channel blocker, CNSB002, in rat models of inflammatory and neuropathic pain."
|1.||Morphine (MS Contin)
|3.||Endothelin-1 (Endothelin 1)
|4.||Connective Tissue Growth Factor
|5.||Sodium Channels (Sodium Channel)
|6.||salicylhydroxamic acid (SHAM)
|7.||Potassium Channel Blockers (Blockers, Potassium Channel)
|8.||Brain-Derived Neurotrophic Factor (BDNF)
|9.||Reactive Oxygen Species (Oxygen Radicals)