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Use of dextromethorphan and an oxidase inhibitor to treat dermatitis

Patent 5366980 Issued on November 22, 1994. Estimated Expiration Date: Icon_subject September 2, 2013. Estimated Expiration Date is calculated based on simple USPTO term provisions. It does not account for terminal disclaimers, term adjustments, failure to pay maintenance fees, or other factors which might affect the term of a patent.

Patent References

Method for enhancing the systemic delivery of dextromethorphan for the treatment of neurological disorders
Patent #: 5166207
Issued on: 11/24/1992
Inventor: Smith

Method for reducing emotional lability Patent #: 5206248
Issued on: 04/27/1993
Inventor: Smith

Inventor

Application

No. 114845 filed on 09/02/1993

US Classes:

514/289Two of the cyclos share at least three ring members (i.e., bridged) (e.g., morphinans, etc.)

Examiners

Primary: Raymond, Richard L.

Attorney, Agent or Firm

International Class

A61K 031/445

Abstract

This invention discloses a method for treating human patients suffering from dermatitis, particularly severe dermatitis which does not respond adequately to non-prescription drugs. Such patients are treated using dextromethorphan (DM), an antitussive agent normally used in cough syrup. If the patient is a so-called "extensive metabolizer," an antioxidant drug (such as quinidine) can be coadministered to inhibit the DM-degrading activity of debrisoquin hydroxylase, an enzyme that will rapidly convert DM into its metabolite, dextrorphan. This treatment has been shown to be highly effective in treating severe dermatitis, and in most patients this drug combination causes no significant adverse side effects.

Other References

  • Koppel, C., et al, "Urinary metabolism of dextromethorphan in man," Arzneim.-Forsch./Drug Research 37:1304-1306 (1987)
  • Guttendorf, R. J., et al, "Simplified phenotyping with dextromethorphan by thin-layer chromatography," Ther. Drug. Monit. 10:490-498 (1988)
  • Kupfer, A., et al, "Dextromethorphan as a safe probe for debrisoquine hydroxylation polymorphism," Lancet: 517-518 (Sep. 1, 1984)
  • Physician's Desk Reference, 44th Edition (1990), pp. 670-671 (Medical Economics Company, 1990)
  • Inaba, T., et al, "In vitro inhibition studies of two isozymes of human liver cytochrome P-450," Drug Metabolism and Diposition 13: 443-447 (1985)
  • Inbaba, T., et al, "Quinidine: Potent inhibition of sparteine and debrisoquin oxidation in vivo," Br. J. Clin. Pharmacol. 22: 199-200 (1986)
  • Broly, F., et al, "Effect of quinidine on the dextromethorphan O-methylase activity of microsomal fractions from human liver," Br. J. Clin. Pharmacol. 28: 29-36 (1989)
  • Broly, F., et al., "Inhibitory studies of mexiletine and dextromethorphan oxidation in human liver microsomes," Biochem. Pharmacol. 39: 1045-1053 (1990)
  • Brinn, R., et al, "Sparteine oxidation is practically abolished in quinidine-treated patients," Br. J. Clin. Pharmacol. 22: 194-197 (1986)
  • Brosen, K., et al, "Extensive metabolizers of debrisoquin become poor metabolizers during quinidine treatment," Pharmacol. Toxicol. 60: 312-314 (1987)
  • Nielsen, M. D., et al, "A dose-effect study of the in vivo inhibitory effect of quinidine on sparteine oxidation in man," Br. J. Clin. Pharmacol. 29: 299-304 (1990)
  • Walker, E. O., and Hunt, V. P., "An open label trial of dextromethorphan in Huntington's Disease," Clin. Neuropharmacol. 12: 322-330 (1989)
  • Albers, G. W., et al, "Safety and tolerance of oral dextromethorphan in patients at risk for brain ischemia," Stroke 22: 1075-1077 (1991)
  • Applebaum, J. S., et al, "Dextromethorphan in the treatment of ALS: A Pilot Study," Abstract number 960S (p. 393) in Neurology 41 (Suppl. 1), Mar. 199
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