Dextrorphan

Dextro form of levorphanol. It acts as a noncompetitive NMDA receptor antagonist, among other effects, and has been proposed as a neuroprotective agent. It is also a metabolite of DEXTROMETHORPHAN.

Also Known As:

Networked: 84 relevant articles (13 outcomes, 15 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Watterson, James H: 2 articles (10/2019 - 07/2017)
2.	Jhoo, Wang-Kee: 2 articles (05/2004 - 01/2003)
3.	Kim, Hyoung-Chun: 2 articles (05/2004 - 01/2003)
4.	Kim, Won-Ki: 2 articles (05/2004 - 01/2003)
5.	Shin, Eun-Joo: 2 articles (05/2004 - 01/2003)
6.	Altman, Ryan A: 1 article (04/2022)
7.	Sorrentino, Jacob P: 1 article (04/2022)
8.	Düfer, Martina: 1 article (10/2020)
9.	Gresch, Anne: 1 article (10/2020)
10.	Chou, Tz-Chong: 1 article (04/2020)

Related Diseases

1.	Brain Ischemia (Cerebral Ischemia) 11/01/1991 - "We studied the dose response characteristics of dextrorphan's neuroprotective efficacy and side effects, correlating these beneficial and adverse responses with plasma and brain levels in a rabbit model of transient focal cerebral ischemia. " 09/17/1993 - "The dose-response curve and time window of efficacy for dextrorphan in permanent focal brain ischemia leading to infarction was studied in the rat. " 09/18/1989 - "We studied the efficacy of systemic pre-treatment with dextrorphan (DX), a clinically tested N-methyl-D-aspartate (NMDA) antagonist, in a rabbit model of transient focal cerebral ischemia. " 02/01/1995 - "Dextrorphan hydrochloride is a noncompetitive N-methyl-D-aspartate antagonist that is neuroprotective in experimental models of focal brain ischemia. " 11/01/1991 - "Protection after transient focal cerebral ischemia by the N-methyl-D-aspartate antagonist dextrorphan is dependent upon plasma and brain levels."
2.	Wounds and Injuries (Trauma) 01/01/1993 - "Single-dose treatment with nalmefene, YM14673, or dextrorphan at 30 min after trauma each significantly improved behavioral recovery at two weeks as compared with vehicle-treated controls, confirming earlier studies with these agents. " 01/10/1990 - "Treatment with either dextrorphan or CPP, administered intrathecally 15 min after trauma, significantly improved chronic (4 weeks) behavioral recovery. " 03/02/1992 - "Pretreatment with dextrorphan attenuated the post-traumatic increase in extracellular levels of aspartate; although these differences did not reach significance when examined as absolute values, they were significant when analyzed as percent increase over pre-trauma baseline levels. " 05/19/1989 - "Treatment with the noncompetitive N-methyl-D-aspartate (NMDA) antagonist dextrophan or the competitive antagonist 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid limited the resultant neurological dysfunction; dextrorphan treatment also improved the bioenergetic state after trauma and increased the intracellular free magnesium. " 01/10/1990 - "The potential role of N-methyl-D-aspartate (NMDA) receptors in the pathophysiology of spinal cord injury was examined in rats by comparing the effects of the non-competitive NMDA antagonist dextrorphan and the competitive NMDA antagonist 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP) on the behavioral and anatomical consequences of impact trauma to the spinal cord. "
3.	Ischemia 09/17/1993 - "A dose-response study of dextrorphan in permanent focal ischemia." 11/01/1991 - "These results demonstrate that systemic treatment with dextrorphan after 1 h focal ischemia can significantly protect against cerebral damage if adequate plasma and brain levels of dextrorphan are achieved. " 04/01/1996 - "Dextrorphan (DX) 20-10 mg/kg given ip 15 min before ischemia reduced infarct volume in a dose-dependent manner with an apparent U-shaped dose-response curve; best protection was observed at 30 mg/kg. Posttreatment at 30 min, but not 60 min, was still effective. " 03/10/1988 - "DM and its active metabolite dextrorphan may prove to be clinically useful in protecting against hypoxia-ischemia." 08/01/1994 - "Dextrorphan, a noncompetitive N-methyl-D-aspartate receptor antagonist, has been shown to provide significant protection against cerebral damage after focal ischemia. "
4.	Stroke (Strokes) 02/01/1995 - "The purpose of this study was to determine the maximum loading dose and maintenance infusion of dextrorphan hydrochloride that are well tolerated in patients with an acute stroke. " 02/01/1995 - "An intravenous infusion of dextrorphan or placebo was begun within 48 hours of onset of a mild-to-moderate hemispheric stroke. " 02/01/1995 - "Safety, tolerability, and pharmacokinetics of the N-methyl-D-aspartate antagonist dextrorphan in patients with acute 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. " 01/01/2002 - "No improvement in clinical outcome of stroke has been seen with competitive NMDA antagonists (selfotel) and non-competitive NMDA antagonists (dextrorphan, GV150526, aptiganel and eliprodil). "
5.	Substance Withdrawal Syndrome (Withdrawal Symptoms) 05/01/2008 - "Dextromethorphan (DM) is a low-affinity, non-competitive NMDA receptor antagonist that has shown promise in preclinical and preliminary clinical studies for the reduction of opioid withdrawal symptoms, but when used at higher doses, it is associated with deleterious side effects attributed to its metabolite, dextrorphan. "

Related Drugs and Biologics

1.	N-Methylaspartate (NMDA)
2.	N-Methyl-D-Aspartate Receptors (NMDA Receptors)
3.	Dextromethorphan (Racemethorphan)
4.	Ketamine
5.	Opioid Analgesics (Opioids)
6.	6-chloro-2-(1-piperazinyl)pyrazine (CPP)
7.	Protein Kinases (Protein Kinase)
8.	aptiganel
9.	selfotel
10.	nalmefene (Revex)

Related Therapies and Procedures

1.	Intravenous Infusions
2.	Therapeutics
3.	Ligation
4.	Injections
5.	Oral Administration