Systematic (IUPAC) name
Clinical data
Legal status
  • Uncontrolled
Routes Oral
CAS number
ATC code None
Chemical data
Formula C19H25NO 
Mol. mass 283.41 g/mol

Dextrallorphan (DXA) is a drug of the morphinan class used in scientific research. It acts as a σ1 receptor agonist and NMDA receptor antagonist.[1][2][3][4] It has no significant affinity for the σ2, μ-opioid, or δ-opioid receptor, or for the serotonin or norepinephrine transporter.[5][2] As an NMDA receptor antagonist, in vivo, it is approximately twice as potent as dextromethorphan, and five-fold less potent than dextrorphan.[3]


Research using Dextrallorphan dates back to at least 1955, where researchers used it in a study that looked at the relationship between analgetics and acetylcholine metabolism. This study specifically looked to determine the concentration required for morphine and similar compounds, like dextrallorphan, to inhibit enzymatic activity in bovine erythrocytes, rat brain, dog serum, and the muscular wall of dog intestine. It was found that dextrallorphan inhibited 25% of bovine erythrocyte cholinesterase at a dose of 10-3 mole/liter, which corresponds to a concentration of up to 0.2 mg/kg in dog intestine. However, at this dose the drug showed no effect on the gut tone. In the same study, dextrallorphan was classified as a potent inhibitor of the intestinal and red blood cell cholinesterase based on the concentration of the drug needed to inhibit these enzymes in the cholinesterase preparations from the animals systems utilized. Simultaneously, dextrallorphan showed no analgesia and no change in intestinal tone. With these results dextrallorphan helped proved that there is no correlation between the inhibition of cholinesterase systems and analgetic or intestinal effects. [6]

In 1979, dextrallorphan was found to have a half maximal inhibitory concentration (IC50) for binding to the pituitary and brain receptor of 10,000 ± 1000 nM and 10,000 ± 1500 nM, respectively. While its stereoisomer, levellorphan, had a 10,000 times more potent dose, thus proving that binding to these receptors is stereospecific. [7]

See also


  1. ^ Su, T. P. (Nov 1982). Opioid Receptor: Binding of [3H]SKF-10047 to Etorphine-Inaccessible Sites in Guinea-Pig Brain"Sigma"Evidence for (pdf). The Journal of Pharmacology and Experimental Therapeutics 223 (2): 284–290.  
  2. ^ a b Codd, E. E.; Shank, R. P.; Schupsky, J. J.; Raffa, R. B. (Sep 1995). "Serotonin and Norepinephrine Uptake Inhibiting Activity of Centrally Acting Analgesics: Structural Determinants and Role in Antinociception" (pdf). The Journal of Pharmacology and Experimental Therapeutics 274 (3): 1263–1270.  
  3. ^ a b Shukla, V. K.; Lemaire, S. (Jan 1997). "N-Methyl-D-Aspartate Antagonist Activity of Alpha- and Beta-Sulfallorphans" (pdf). The Journal of Pharmacology and Experimental Therapeutics 280 (1): 357–365.  
  4. ^ Shannon, H. E. (Apr 1983). "Pharmacological Evaluation of N-Allynormetazocine (SKF 10,047) on the Basis of its Discriminative Stimulus Properties in the Rat". The Journal of Pharmacology and Experimental Therapeutics 225 (1): 144–152.  
  5. ^ He, X. S.; Bowen, W. D.; Lee, K. S.; Williams, W.; Weinberger, D. R.; de Costa, B. R. (Mar 1993). "Synthesis and Binding Characteristics of Potential SPECT Imaging Agents for Sigma-1 and Sigma-2 Binding Sites". Journal of Medicinal Chemistry 36 (5): 566–571.  
  6. ^ Young, D. C.; Vander Ploeg, A.; Featherstone, R. M.; Gross, E. G. (May 1955). "The Interrelationships Among the Central, Peripheral and Anticholinesterase Effects of Some Morphinan Derivatives" (pdf). The Journal of Pharmacology and Experimental Therapeutics 114 (2): 33–37.  
  7. ^ Simantov, R.; Snyder, S. H. (Dec 1976). "Opiate receptor binding in the pituitary gland" (pdf). Brain Research 124 (1): 178–184.