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Patent · US5080899A · A · US

Method of treating pulmonary inflammation

(11) Publication number
US5080899A
(21) Application number
07/659,782
(22) Filing date
1991-02-22
(30) Priority date
1991-02-22
(43) Publication date
1992-01-14
(45) Date of grant
1992-01-14
(51) IPC
A61K 31/00; A61K 31/44; A61K 31/45; A61K 35/74; A61P 11/00; A61P 29/00; C07D 498/18; C12P 17/00
(52) CPC
  • A61K Preparations for medical, dental or toiletry purposes: 31/70, 31/44, 35/74
  • A61P Specific therapeutic activity of chemical compounds or medicinal preparations: 11/00, 29/00
(73) Assignee
American Home Products Corp
(72) Inventors
Robert J. Sturm; Laurel M. Adams; Barry M. Weichman
(54) Title
Method of treating pulmonary inflammation
(57) Abstract

This invention provides a method of preventing or reversing pulmonary inflammation in a mammal by administering an effective amount of rapamycin orally, parenterally, intranasally, or intrabronchially. As such, rapamycin is useful in providing the symptomatic relief of diseases in which pulmonary inflammation is a component such as, asthma, chronic obstructive pulmonary disease, emphysema, acute respiratory distress syndrome, bronchitis, and the like.

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Claims (8)

  1. A method of preventing or reversing pulmonary inflammation in a mammal in need thereof which comprises administering to said mammal an effective amount of rapamycin orally, parentally, intranasally, or intrabronchially.
  2. The method according to claim 1, which comprises administering rapamycin in a daily dose of 0.01 to 10 mg/kg.
  3. The method according to claim 1, which comprises administering rapamycin in a daily dose of 0.1 to 10 mg/kg.
  4. The method according to claim 1, which comprises administering rapamycin in a daily dose of 0.3 to 4 mg/kg.
  5. A method of providing symptomatic relief of asthma, chronic obstructive pulmonary disease, emphysema, acute respiratory distress syndrome, and acute bronchitis in a mammal in need thereof which comprises administering to said mammal an effective amount of rapamycin orally, parentally, intranasally, or intrabronchially.
  6. The method according to claim 5, which comprises administering rapamycin in a daily dose of 0.01 to 10 mg/kg.
  7. The method according to claim 5, which comprises administering rapamycin in a daily dose of 0.1 to 10 mg/kg.
  8. The method according to claim 5, which comprises administering rapamycin in a daily dose of 0.3 to 4 mg/kg.

Description

Asthma has recently been recognized as being mediated by an inflammatory response in the respiratory tract [DeMonchy, J., Am. Rev. Resp. Dis. 131: 373-376 (1985)]. Recent findings suggest that human T-lymphocytes play a major role in regulating the airway inflammation associated with allergic asthma [Frew, A. J., J. Allergy Clin. Immunol. 85: 533-539 (1990)] and chronic obstructive pulmonary disease [O'Connor, G. T., Am. Rev. Resp. Dis. 140: 225-252 (1989)].

In addition to the infiltration of other inflammatory cells into the pulmonary system, human asthmatics and atopics who are dual responders (i.e., show both early and late phase reactions) show a small but significant infiltration of T-lymphocytes following antigen challenge [Frew, A. J., and Kay, A. B., J. Immunol. 141: 4158-4164 (1988)]. More importantly, these recruited T-lymphocytes are almost entirely of the CD4 + (T-helper) type, and there appears to be a direct correlation between the influx of CD4 + cells, the influx of eosinophils, and the IgE-related allergic response in these individuals [Frew, A. M. and Kay, A. B., J. Immunol. 141: 4158-4164 (b 1988)]. In severe asthmatics, these CD4 + cells appear to be activated [Corrigan, C. J. and Kay, A. B. Am. Rev. Resp. Dis. 141: 970-977 (1990)] by virtue of the increase in IL-2 receptor positive cells. Thus, these cells are capable of producing cytokines (such as IL-3, IL-5, and granulocyte macrophage colony stimulating factor) which can directly affect the differentiation, maturation and activation state of the eosinophils and other inflammatory cells.

Citations (1)

  • US3929992A
Record as JSON
{
  "publication_number": "US5080899A",
  "country": "US",
  "kind": "A",
  "title": "Method of treating pulmonary inflammation",
  "abstract": "This invention provides a method of preventing or reversing pulmonary inflammation in a mammal by administering an effective amount of rapamycin orally, parenterally, intranasally, or intrabronchially. As such, rapamycin is useful in providing the symptomatic relief of diseases in which pulmonary inflammation is a component such as, asthma, chronic obstructive pulmonary disease, emphysema, acute respiratory distress syndrome, bronchitis, and the like.",
  "claims": [
    "1. A method of preventing or reversing pulmonary inflammation in a mammal in need thereof which comprises administering to said mammal an effective amount of rapamycin orally, parentally, intranasally, or intrabronchially.",
    "2. The method according to claim 1, which comprises administering rapamycin in a daily dose of 0.01 to 10 mg/kg.",
    "3. The method according to claim 1, which comprises administering rapamycin in a daily dose of 0.1 to 10 mg/kg.",
    "4. The method according to claim 1, which comprises administering rapamycin in a daily dose of 0.3 to 4 mg/kg.",
    "5. A method of providing symptomatic relief of asthma, chronic obstructive pulmonary disease, emphysema, acute respiratory distress syndrome, and acute bronchitis in a mammal in need thereof which comprises administering to said mammal an effective amount of rapamycin orally, parentally, intranasally, or intrabronchially.",
    "6. The method according to claim 5, which comprises administering rapamycin in a daily dose of 0.01 to 10 mg/kg.",
    "7. The method according to claim 5, which comprises administering rapamycin in a daily dose of 0.1 to 10 mg/kg.",
    "8. The method according to claim 5, which comprises administering rapamycin in a daily dose of 0.3 to 4 mg/kg."
  ],
  "description_excerpt": "Asthma has recently been recognized as being mediated by an inflammatory response in the respiratory tract [DeMonchy, J., Am. Rev. Resp. Dis. 131: 373-376 (1985)]. Recent findings suggest that human T-lymphocytes play a major role in regulating the airway inflammation associated with allergic asthma [Frew, A. J., J. Allergy Clin. Immunol. 85: 533-539 (1990)] and chronic obstructive pulmonary disease [O'Connor, G. T., Am. Rev. Resp. Dis. 140: 225-252 (1989)].\n\nIn addition to the infiltration of other inflammatory cells into the pulmonary system, human asthmatics and atopics who are dual responders (i.e., show both early and late phase reactions) show a small but significant infiltration of T-lymphocytes following antigen challenge [Frew, A. J., and Kay, A. B., J. Immunol. 141: 4158-4164 (1988)]. More importantly, these recruited T-lymphocytes are almost entirely of the CD4 + (T-helper) type, and there appears to be a direct correlation between the influx of CD4 + cells, the influx of eosinophils, and the IgE-related allergic response in these individuals [Frew, A. M. and Kay, A. B., J. Immunol. 141: 4158-4164 (b 1988)]. In severe asthmatics, these CD4 + cells appear to be activated [Corrigan, C. J. and Kay, A. B. Am. Rev. Resp. Dis. 141: 970-977 (1990)] by virtue of the increase in IL-2 receptor positive cells. Thus, these cells are capable of producing cytokines (such as IL-3, IL-5, and granulocyte macrophage colony stimulating factor) which can directly affect the differentiation, maturation and activation state of the eosinophils and other inflammatory cells.",
  "cpc": [
    "A61K 31/70",
    "A61K 31/44",
    "A61K 35/74",
    "A61P 11/00",
    "A61P 29/00"
  ],
  "ipc": [
    "A61K 31/00",
    "A61K 31/44",
    "A61K 31/45",
    "A61K 35/74",
    "A61P 11/00",
    "A61P 29/00",
    "C07D 498/18",
    "C12P 17/00"
  ],
  "assignees": [
    "American Home Products Corp"
  ],
  "inventors": [
    "Robert J. Sturm",
    "Laurel M. Adams",
    "Barry M. Weichman"
  ],
  "filing_date": "1991-02-22",
  "publication_date": "1992-01-14",
  "grant_date": "1992-01-14",
  "priority_date": "1991-02-22",
  "application_number": "US-65978291-A",
  "family_id": "24646823",
  "cited_by_count": 225,
  "citations": [
    "US3929992A"
  ]
}

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