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 Title: |
US5559095:
Delayed treatment method of reducing ischemia-related neuronal damage
[ Derwent Title ]
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| Country: |
US United States of America
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| Inventor: |
Miljanich, George P.; Redwood, CA
Bowersox, Stephen S.; Menlo Park, CA
Fox, James A.; Palo Alto, CA
Valentino, Karen L.; San Carlos, CA
Bitner, Robert S.; West Lafayette, IN
Yamashiro, Donald H.; Cleveland Heights, OH
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| Assignee: |
Neurex Corporation, Menlo Park, CA
other patents from NEUREX CORPORATION (397535) (approx. 15)
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| Published / Filed: |
1996-09-24
/ 1991-11-12
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| Application Number: |
US1991000789913
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| IPC Code: |
Advanced:
C07K 14/435;
A61K 38/00;
Core:
more...
IPC-7:
A61K 38/16;
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| ECLA Code: |
C07K14/435;
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| U.S. Class: |
Current:
514/012;
514/013;
530/324;
530/325;
530/326;
Original:
514/012;
514/013;
530/324;
530/325;
530/326;
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| Field of Search: |
514/012,13-15,21
530/350,324,325,326,327
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| Priority Number: |
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| Abstract: |
A method and compositions for reducing neuronal damage related to an ischemic condition in a mammalian subject are described. The method includes administration of a voltage-gated calcium channel-blocking compound to the subject, 4-24 hours after the onset of the ischemic condition. Such a calcium channel blocking compound is effective to block norepinephrine release in mammalian CNS neuronal cells and is characterized by specific, high affinity binding to omega-conotoxin MVIIA binding sites. Also disclosed are novel peptide structures useful in the treatment method of the invention.
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| Attorney, Agent or Firm: |
Stratford, Carol A. ;
Dehlinger, Peter J. ;
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| Primary / Asst. Examiners: |
Schain, Howard E.; Lukton, David
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| Maintenance Status: |
E3 Expired Check current status
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| INPADOC Legal Status: |
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Family Legal Status Report
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| Parent Case: |
This application is a continuation-in-part of application Ser. No. 561,766 filed Aug. 2, 1990, now U.S. Pat. No. 5,189,020 which is in turn a continuation-in-part of application Ser. No. 440,094 filed Nov. 22, 1989, now U.S. Pat. No. 5,051,403.
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| Designated Country: |
BE CH FR GB IT LI LU NL SE HU KR NO RU SU
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| Family: |
Show 23 known family members
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First Claim:
Show all 5 claims |
It is claimed:
1. A method of reducing neuronal damage resulting from an ischemic condition in the central nervous system of a mammalian subject, comprising
- parenterally administering to the subject, at a time 6-24 hours following the onset of the ischemic condition, a pharmaceutically acceptable amount of an OCT peptide effective to inhibit voltage-gated calcium channels selectively in neuronal tissue, as evidenced by the ability of the OCT peptide to
- (a) bind to an MVIIA omega-conotoxin binding site in neuronal tissue with an affinity which is at least as great as that exhibited by any of the omega-conotoxins MVIIA, GVIA, TVIA and SNX-207 for said binding site; and
- (b) inhibit norepinephrine release at a given site in neuronal tissue with at least the same potency as that exhibited by any of the omega-conotoxins MVIIA, GVIA, TVIA and SNX-207 at said neuronal site.
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| Background / Summary: |
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| Drawing Descriptions: |
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| Description: |
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| Forward References: |
Show 9 U.S. patent(s) that reference this one
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| Foreign References: |
None
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| Other Abstract Info: |
CHEMABS 115(25)270696K
CHEMABS 125(23)293039U
CHEMABS 119(13)131535B
CHEMABS 119(17)174217S
CHEMABS 125(23)293039U
DERABS C1991-192969
DERABS C1993-085564
DERABS C1993-182487
DERABS C1993-385665
DERABS C1995-223694
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| Other References: |
Olivera et al, Biochemistry 26, 2086, 1987.
(5 pages)
Cited by 19 patents
Feuerstein et al. J. Pharmacol Exp Ther 252, 778, 1990.
(8 pages)
Ahmad, S., and G. P. Miljanich, "The calcium channel antagonist, ω-conotoxin, and electric organ nerve terminals: binding and inhibition of transmitter release and calcium influx," Brain Research 453:247-256 (1988).
(10 pages)
Cited by 3 patents
Bielenberg, G. W., et al., "Effects of Nimodipine of Infarct Size and Cerebral Acidosis After Middle Cerebral Artery Occlusion in the Rat," Stroke 21:IV90-IV92 (1990).
(3 pages)
Buchan, A., and W. A. Pulsinelli, "Hypothermia But Not the N-Methyl-D-Aspartate Antagonist, MK-801, Attenuates Neuronal Damage in Gerbils Subjected to Transient Global Ischemia," J. Neurosci. 10:311-316 (1990).
(6 pages)
Cited by 5 patents
Dirnagl, U., et al., "Pre-and post-treatment with MK-801 but not pretreatment alone reduces neocortical damage after focal cerebral ischemia in the rat," Brain Res. 527:62-68 (1990).
(7 pages)
Gill, R., et al., "MK-801 is Neuroprotective in Gerbils When Administered During the Post-Ischaemic Period," Neurosci. 5(3):847-855 (1988).
(9 pages)
Cited by 8 patents
Goldberg, M., et al., "N-Methyl-D-Aspartate Receptors Mediate Hypoxic Neuronal Injury in Cortical Culture," J. Pharmacol. Exp. Therapeutics 243:784-791 (1987).
(8 pages)
Cited by 8 patents
Gray, W., et al., "Peptide Toxins From Venomous Conus Snails," Ann. Rev. Biochem. 57:665-700 (1988).
(36 pages)
Cited by 11 patents
Hartley, D., and D. Choi, "Delayed Rescue of N-Methyl-D-Aspartate Receptor-Mediated Neuronal Injury on Cortical Culture," J. Pharmacol. Exp. Therapeutics 250:752-758 (1989).
(7 pages)
Cited by 2 patents
Jacewicz, M., et al., "Continuous Nimodipine Treatment Attenuates Cortical Infarction in Rats Subjected to 24 Hours of Focal Cerebral Ischemia," J. Cereb. Blood Flow Metab. 10:89-96 (1990).
(8 pages)
Kaplan, B., et al., "Temporal Thresholds for Neocortical Infarction in Rats Subjected to Reversible Focal Cerebral Ischemia," Stroke 22:1032-1039 (1991).
(8 pages)
[ISI abstract]
Kirino, T., "Delayed Neuronal Death in the Gerbil Hippocampus Following Ischemia," Brain Res. 239:57-69 (1932).
McCleskey, E. W., et al., "ω-Conotoxin: Direct and persistent blockade of specific types of calcium channels in neurons but not muscle," Proc. Natl. Acad. Sci. USA 84:4327-4331 (1987).
(5 pages)
Cited by 8 patents
Nedergaard, M., "Neuronal injury in the infarct border: A neuropathological study in the rat," Acta Neuropathol. (Berl.) 73:267-274 (1987).
(8 pages)
Newberg, L., et al., "Failure of Flunarizine to Improve Cerebral Blood Flow of Neurologic Recovery in a Canine Model of Complete Cerebral Ischemia," Stroke 15:666-671 (1984).
(6 pages)
Nowycky, M. C., et al., "Three types of neuronal calcium channel with different calcium agonist sensitivity," Nature (London) 316:440-443 (1985).
(4 pages)
Cited by 6 patents
Olivera, B., et al., "Purification and Sequence of a Presynaptic Peptide Toxin from Conus geographus Venom," Biochemistry 23:5087-5090 (1984).
(4 pages)
Cited by 13 patents
Pulsinelli, W. A., et al., "A New Model of Bilateral Hemispheric Ischemia in the Unanesthetized Rat," Stroke 10:267-272 (1979).
(6 pages)
Cited by 6 patents
Pulsinelli, W. A., et al. "Temporal Profile of Neuronal Damage in a Model of Transient Forebrain Ischemia," Ann. Neurol. 11:491-498 (1982).
(8 pages)
Cited by 15 patents
Sano, K., et al., "Effects of synthetic ω-conotoxin, a new type Ca2+ antagonist, on frog and mouse neuromuscular transmission," Eur. J. Pharmacol. 141:235-241 (1987).
(7 pages)
Cited by 3 patents
Sher, E., et al., "Physiopathology of neuronal voltage-operated calcium channels," FASEB J. 5:2677-2683 (1991).
(7 pages)
[ISI abstract]
Tateishi, A., et al., "Nimodipine Does Not Improve Neurologic Outcome After 14 Minutes of Cardiac Arrest in Cats," Stroke 20:1044-1050 (1989).
(7 pages)
Cited by 2 patents
Wauquier A., et al., "Cerebral Resuscitation: Pathophysiology and Therapy," Neurosci. Biobehav. Rev. 11:287-306 (1987).
(20 pages)
Cited by 3 patents
Widmann,R., et al., "[14 C]Leucine Incorporation into Brain Proteins in Gerbils After Transient Ischemia: Relationship to Selective Vulnerability of Hippocampus," J. Neurochem. 56(3):789-796 (1991).
(8 pages)
[ISI abstract]
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