Modulation of complement to treat pain

• US 20050222027A1
• Filed: 11/12/2004
• Published: 10/06/2005
• Est. Priority Date: 07/03/2003
• Status: Abandoned Application

• Current Assignee: Euroceltique SA
• Original Assignee: Euroceltique SA
• Inventors: Levin, Margaret E., Chiang, Lillian W.
• Application Number:
  US10/989,891
• Publication Number:
  US 20050222027A1
• Time in Patent Office: Days
• US Class Current: 424/94.630
• CPC Class Codes: A61K 38/1709 from mammals
• CPC Class Codes: C12Q 1/6883 for diseases caused by alterations of genetic material
• CPC Class Codes: C12Q 2600/158 Expression markers
• CPC Class Codes: G01N 2800/2842 Pain, e.g. neuropathic pain, psychogenic pain
• CPC Class Codes: G01N 2800/52 Predicting or monitoring the response to treatment, e.g. for selection of therapy based on assay results in personalised medicine; Prognosis
• CPC Class Codes: G01N 33/5023 on expression patterns
• CPC Class Codes: G01N 33/5058 Neurological cells

Abstract

The present invention provides compositions and methods for treating pain, including neuropathic pain, by modulating the expression or activity of one or more components of the complement pathway. The present invention further provides screening methods to identify therapeutic agents for treating pain by screening for compounds capable of modulating the expression or activity of one or more components of the complement pathway.

Claims

1-81. -81. (canceled)

82. A method for treating pain by modulating a biological activity of a complement component in a subject feeling pain, comprising administering to the subject a therapeutically effective amount of a compound that modulates a biological activity of a complement component, with the proviso that the compound is not cobra venom factor (CVF).

83. The method of claim 82, wherein the compound decreases a biological activity of a complement component.

84. The method of claim 83, wherein the complement component is a complement effector.

85. The method of claim 84, wherein the complement effector is C3, C3aR, C5aR, C5, C3 convertase, C5 convertase, Factor D, C1s, MASP-1, MASP-2, MASP-3, Factor B, C1r, or C5b-9.

86. The method of claim 82, wherein the compound inhibits an increase in a biological activity of a complement component.

87. The method of claim 82, wherein the compound increases a biological activity of a complement component.

88. The method of claim 87, wherein the complement component is an endogenous complement inhibitor.

89. The method of claim 88, wherein the complement inhibitor is decay accelerating factor (DAF), Factor H, Factor I, CRRY, CR1, clusterin, CD59, or C1 INH.

90. The method of claim 82, wherein the complement component is active in a pathway selected from the group consisting of the classical pathway, the MB-lectin pathway, the alternative pathway, and the downstream shared pathway.

91. The method of claim 82, wherein the type of pain is neuropathic pain, nociceptive pain, chronic pain, inflammatory pain, pain associated with cancer, or pain associated with rheumatic disease.

92-173. -173. (canceled)