US2005019322A1PendingUtilityA1

Treatment of central nervous system diseases by antibodies against glatiramer acetate

Priority: Jun 20, 2000Filed: Feb 10, 2004Published: Jan 27, 2005
Est. expiryJun 20, 2020(expired)· nominal 20-yr term from priority
A61P 37/02A61P 25/00C07K 16/18A61K 2039/505C07K 16/44A61P 3/00A61K 38/02C07K 2317/74
50
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0
Cited by
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References
0
Claims

Abstract

The present invention provides humanized polyclonal and humanized monoclonal antibodies directed against an epitope on glatiramer acetate, also known as Copolymer 1, Copolymer-1, Cop- 1 or Cop. Additionally, the subject invention concerns a pharmaceutical composition comprising an antibody directed against an epitope on glatiramer acetate for the treatment of a disease associated with demyelination of central nervous system axons. Also encompassed by the subject invention is a method of treating a subject suffering from a disease associated with demyelination of central nervous system axons. The subject invention further contains methods of stimulating remyelination of central nervous system axons. In addition, the subject invention provides a method of stimulating proliferation of lymphocytes.

Claims

exact text as granted — not AI-modified
1 - 18 . (canceled)  
     
     
         19 . A method of stimulating remyelination of central nervous system axons comprising contacting the axons with an antibody directed against an epitope on glatiramer acetate in an amount effective to stimulate remyelination of central nervous system axons.  
     
     
         20 . The method of  claim 19 , wherein the antibody is a humanized antibody.  
     
     
         21 . The method of  claim 19 , wherein the antibody is not cross-reactive with, myelin basic protein (MBP).  
     
     
         22 . The method of  claim 19 , wherein the antibody consists essentially of IgG1.  
     
     
         23 . The method of  claim 19 , wherein the antibody does not react with mature oligodendrocytes.  
     
     
         24 . The method of  claim 19 , wherein the antibody cross-reacts with spinal cord homogenate (SCH).  
     
     
         25 . The method of  claim 19 , wherein the antibody primarily reacts with cells exhibiting a macrophage or microglial phenotype.  
     
     
         26 . The method of  claim 19 , wherein the antibody is a monoclonal antibody.  
     
     
         27 . The method of  claim 19 , wherein the antibody is a polyclonal antibody.  
     
     
         28 . A method of treating a subject suffering from a disease associated with demyelination of central nervous system axons comprising administering to the subject an effective amount of an antibody directed against an epitope on glatiramer acetate in an amount effective to treat the disease associated with demyelination of central nervous system axons.  
     
     
         29 . The method of  claim 28 , wherein the antibody is a humanized antibody.  
     
     
         30 . The method of  claim 28 , wherein the antibody is not cross-reactive with myelin basic protein (MBP).  
     
     
         31 . The method of  claim 28 , wherein the antibody consists essentially of IgG1.  
     
     
         32 . The method of  claim 28 , wherein the antibody does not react with mature oligodendrocytes.  
     
     
         33 . The method of  claim 28 , wherein the antibody cross-reacts with spinal cord homogenate (SCH).  
     
     
         34 . The method of  claim 28 , wherein the antibody primarily reacts with cells exhibiting a macrophage or microglial phenotype.  
     
     
         35 . The method of  claim 28 , wherein the antibody primarily reacts with cells exhibiting a macrophage or microglial phenotype.  
     
     
         36 . The method of  claim 28 , wherein the antibody is a monoclonal antibody.  
     
     
         37 . The method of  claim 28 , wherein the antibody is a polyclonal antibody.  
     
     
         38 . The method of  claim 28 , wherein the disease associated with demyelination of central nervous system axons is selected from the group consisting of: multiple sclerosis, acute disseminated encephalomyelitis, transverse myelitis, demyelinating genetic diseases, spinal cord injury, virus-induced demyelination, Progressive Multifocal Leucoencephalopathy, Human Lymphotrophic T-cell Virus I (HTLVI)-associated myelopathy, and nutritional metabolic disorders.  
     
     
         39 . The method of  claim 38 , wherein the nutritional metabolic disorder is vitamin B 12  deficiency.  
     
     
         40 . The method of  claim 38 , wherein the nutritional metabolic disorder is central pontine myelinolysis.  
     
     
         41 . The method of  claim 28 , wherein the effective amount is an amount from 0.5 mg to 400 mg.  
     
     
         42 . The method of  claim 41 , wherein the effective amount is an amount from 0.5 mg to 250 mg.  
     
     
         43 . (canceled)  
     
     
         44 . A method of treating a subject suffering from a disease associated with demyelination of central nervous system axons comprising administering to the subject glatiramer acetate in an amount effective to treat the disease associated with demyelination of central nervous system axons, wherein the disease associated with demyelination of central nervous system axons is selected from the group consisting of: acute disseminated encephalomyelitis, transverse myelitis, demyelinating genetic diseases, spinal cord injury, virus-induced demyelination, Progressive Multifocal Leucoencephalopathy, Human Lymphotrophic T-cell Virus I (HTLVI)-associated myelopathy, and nutritional metabolic disorders.  
     
     
         45 . A method of stimulating proliferation of lymphocytes comprising contacting the lymphocytes with an antibody directed against an epitope on glatiramer acetate in an amount effective to stimulate lymphocyte proliferation.  
     
     
         46 - 53 . (canceled)

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