USRE43982EExpiredUtility

IGF-1 to improve neural outcome

53
Assignee: GENENTECH INCPriority: Aug 1, 1991Filed: Jun 27, 2003Granted: Feb 5, 2013
Est. expiryAug 1, 2011(expired)· nominal 20-yr term from priority
A61P 25/28A61K 38/30A61K 9/0085
53
PatentIndex Score
0
Cited by
45
References
20
Claims

Abstract

A method of treating injuries to or diseases of the central nervous system that predominantly effects glia and/or non-cholinergic neuronal cells characterized in that it comprises the step of increasing the active concentration(s) of insulin-like growth factor 1 and/or analogues thereof in the central nervous system of the patient. The present invention also provides therapeutic compositions comprising insulin-like growth factor 1 and/or analogues thereof for administration to a patient at or following a neural insult, which compositions are useful in minimizing damage to the central nervous system that would otherwise occur following the insult.

Claims

exact text as granted — not AI-modified
1. A method of treating neural damage suffered after a CNS insult affecting glia or other non-cholinergic cells in a mammal, comprising administering to the central nervous system of said mammal an effective amount of IGF-1 and/or a biologically active analogue of IGF-1. 
     
     
       2. A method of  claim 1  wherein the central nervous system injury is hypoxic injury. 
     
     
       3. A method of  claim 1  wherein the central nervous system injury is ischemic injury. 
     
     
       4. A method of  claim 1  wherein the central nervous system injury is traumatic injury. 
     
     
       5. A method of  claim 1  wherein the central nervous system injury affects non-cholinergic neuronal cells. 
     
     
       6. A method of  claim 1  wherein the central nervous system injury affects glial cells. 
     
     
       7. A method of  claim 1  wherein the central nervous system injury is a consequence of Parkinson's disease. 
     
     
       8. A method of  claim 1  wherein the central nervous system injury is a consequence of multiple sclerosis. 
     
     
       9. A method of  claim 1  wherein the central nervous system injury is a consequence of a demyelinating disorder. 
     
     
       10. A method of  claim 1  wherein the IGF-1 and/or biologically active analogue of IGF-1 is administered in the period from the time of the central nervous system injury to 100 hours after the injury. 
     
     
       11. A method of  claim 1  wherein the IGF-1 and/or biologically active analogue of IGF-1 is administered at least once in the period from the time of the central nervous system injury to about 8 hours subsequently. 
     
     
       12. A method of  claim 1  wherein the IGF-1 and/or biologically active analogue of IGF-1 is administered to the mammal in an amount from about 0.1 to 1000 μg of IGF-1 per 100 gm of body weight of the mammal. 
     
     
       13. A method of  claim 1  wherein the biologically active analogue of IGF-1 is selected from the group consisting of insulin-like growth factor 2 (IGF-2) and truncated IGF-1 (des 1-3 IGF-1). 
     
     
       14. A method of  claim 1  wherein the IGF-1 and/or biologically active analogue of IGF-1 is administered to the mammal through a surgically inserted shunt into the cerebro ventricle of the mammal. 
     
     
       15. A method of  claim 1  wherein the IGF-1 and/or biologically active analogue of IGF-1 is administered peripherally into the mammal for passage into the lateral ventricle of the brain. 
     
     
       16. A method of treating non-cholinergic cells damaged from CNS injury, comprising administering to the CNS of a mammal in need thereof, an effective amount of a biological analog of IGF-1, wherein the CNS injury is an injury to the hippocampus and further wherein said analog is selected from the group consisting of naturally-occurring analogs, IGF-2, and des 1-3 IGF-1. 
     
     
       17. A method according to claim 16, wherein the injury to the hippocampus comprises an injury to the dentate gyrus. 
     
     
       18. A method of treating non-cholinergic cells damaged from CNS injury, comprising administering to the CNS of a mammal in need thereof, an effective amount of a biological analog of IGF-1, wherein the CNS injury is an injury to the striatum and further wherein said analog is selected from the group consisting of naturally-occurring analogs, IGF-2, and des 1-3 IGF-1. 
     
     
       19. A method of treating non-cholinergic cells damaged from CNS injury, comprising administering to the CNS of a mammal in need thereof, an effective amount of a biological analog of IGF-1, wherein the CNS injury is an injury to the thalamus and further wherein said analog is selected from the group consisting of naturally-occurring analogs, IGF-2, and des 1-3 IGF-1. 
     
     
       20. A method of treating non-cholinergic cells damaged from CNS injury, comprising administering to the CNS of a mammal in need thereof, an effective amount of a biological analog of IGF-1, wherein the CNS injury is an injury to the cortex and further wherein said analog is selected from the group consisting of naturally-occurring analogs, IGF-2, and des 1-3 IGF-1.

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