Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Peptide containing doai
Reexamination Certificate
2007-04-17
2007-04-17
Kemmerer, Elizabeth (Department: 1649)
Drug, bio-affecting and body treating compositions
Designated organic active ingredient containing
Peptide containing doai
C435S005000, C435S343000, C514S013800, C514S04400A
Reexamination Certificate
active
09957909
ABSTRACT:
Methods of suppressing the activation of microglial cells in the Central Nervous System (CNS), methods of ameliorating or treating the neurological effects of cerebral ischemia or cerebral inflammation, and methods of combating specific diseases that affect the CNS by administering a compound that binds to microglial receptors and prevents or reduces microglial activation are described. Also described are methods of screening compounds for the ability to suppress or reduce microglial activation.
REFERENCES:
patent: 4902505 (1990-02-01), Pardridge et al.
patent: 5017566 (1991-05-01), Bodor
patent: 5168045 (1992-12-01), Dyer et al.
patent: 5182364 (1993-01-01), Dyer et al.
patent: 5204327 (1993-04-01), Kiyota et al.
patent: 5473039 (1995-12-01), Dyer et al.
patent: 5604198 (1997-02-01), Poduslo et al.
patent: 5686416 (1997-11-01), Kozarich et al.
patent: 6245751 (2001-06-01), Crutcher et al.
patent: 6605588 (2003-08-01), Lees et al.
patent: WO 92/10512 (1992-06-01), None
patent: WO 95/06456 (1995-03-01), None
patent: WO 97/14437 (1997-04-01), None
patent: WO 98/01101 (1998-01-01), None
patent: WO 99/45950 (1999-09-01), None
patent: WO 2003/026479 (2003-04-01), None
patent: WO 2003/026479 (2003-04-01), None
Yan et al., Two-amino-acid molecular switch in an epithelial morphogen that regulates binding to two distinct receptors. Science 290: 523-527, 2000.
Voet et al. Biochemistry. 1990. John Wiley & Sons, Inc. 126-128 and 228-234.
Mickle JE et al. Genotype-phenotype relationships in cystic fibrosis. Med Clin North Am. May 2000;84(3):597-607.
Chen et al (1997). Motor and Cognitive Defecits in Apolipoprotein E-Deficient Mice After Closed Head Injury. Neuroscience 80: pp. 1255-1262.
Champe et al (2005). Lippincott's Illustrated Reviews: Biochemistry, 3rd ed. Lippincott Williams & Wilkins, Philadelphia, pp. 18-21.
Misra, et al., Apolipoprotein E and Mimetic Peptide Initiate A Calcium-dependent Signaling Response in Macrophages (2001)Jour. Leukocyte Bio., 70:677-683.
Aono, et al., Protective Effects of Peptides Corresponding to the Receptor Binding Region of Apolipoprotein E on NMDA Excitotoxicity in Primary Neuronol-Glial Cultures Trip Report: 31stAnnual Meeting of the Society for Neuroscience, San Diego, California, Nov. 10-15, 2001.
Laskowitz et al., “Downregulation of Microglial Activation by Apolipoprotein E and ApoE-Mimetic Peptides”, Experimental Neurology, 167:74-85 (2001).
Benazzouz, A., et al., “Riluzole Prevents MPTP-induced Parkinsonism in the Rhesus Monkey: A Pilot Study,”Eur. J. Pharmacol.284:299-307 (1995).
Gordon, I., et al., “Derangement in Stress Response of Apolipoprotein E-deficient Mice,”Neuroscience Letters206:212-214 (1996).
Jordan et al., “Isoform-Specific Effect of Apolipoprotein E on Cell Survival and β-Amyloid-induced Toxicity in Rat Hippocampal Pyramidal Neuronal Cultures,”J. Neurosci.18:195-204 (1998).
Marzolo, M., et al., “Expression of α2-Macroglobulin Receptor/Low Density Lipoprotein Receptor-Related Protein (LRP) in Rat Microglial Cells,”J. Neurosci. Res.60:401-411 (2000).
Tolar, M., et al., “Truncated Apoliprotein E (ApoE) Causes Increased Intracellular Calcium and May Mediate ApoE Neurotoxicity,”J. Neuroscience19(16): 7100-7110 (1999).
A. Cardin et al.; Inhibition of Lymphocyte Proliferation by Synthetic Peptides Homologous to Human Plasma Apolipoproteins B and E,Biochemical and Biophysical Research Communications, 154:741-745 (Jul. 1998).
A. Lalazar et al.; Site-specific Mutagenesis of Human Apolipoprotein E,The Journal of Biological Chemistry, 263:3542-3545 (1988).
Bowie, et al.; Deciphering the message in protein sequences: tolerance to amino acid substitutions,Science, vol. 247, pp. 1306-1310 (1990).
C. Dyer et al.; A Synthetic Peptide Mimic of Plasma Apolipoprotein E That Binds the LDL Receptor,The Journal of Biological Chemistry266:22803-22806 (Dec. 1991).
C. Dyer et al.; Only Multimers of a Synthetic Peptide of Human Apolipoprotein E Are Biologically Active,The Journal of Biological Chemistry266:15009-15015 (1991).
Christie et al., “Expression of the Very Low-Density Lipoprotein Receptor (VLDL-r), an Apolipoprotein-E Receptor, in the Central Nervous System and in Alzheimer's Disease”,Journal of Neuropathology and ExperimentalNeurolog, 55(4):491-498 (1996).
D. Laskowitz et al.; Apolipoprotein E Suppresses Glial Cell Secretion of TNFα,Journal of Neuroimmunology76:70-74 (1997).
D. Laskowitz et al.; Apolipoprotein E-Deficient Mice Have Increased Susceptibility to Focal Cerebral Ischemia,Journal of Cerebral Floww and Metabolism17:753-758 (1997).
Holtzman et al.: “Low density lipoprotein receptor-related protein mediates apolipoprotein E-dependent neurite outgrowth in a central nervous system-derived neuronal cell line”,Proc. Natl. Acad. Sci. USA, 92:9480-9484 (1995).
International Search Report for PCT US99/05221 (mailed Nov. 3, 1999).
K. Crutcher et al.; Neurite Degeneration Elicited by Apolipoprotein E Peptides,Experimental Neurology130:120-126 (1994).
K. Weisgraber et al.; The Receptor-binding Domain of Human Apolipoprotein E,Journal of Biological Chemistry258: 12348-12354 (1983).
L. Dong et al.; Enhanced Binding Activity of an Apolipoprotein E. Mutant, APO E5, to LDL Receptors on Human Fibroblasts,Biochemical and Biophysical Research Communications168:409-414 (Apr. 1990).
L. Dong et al.; Site-Directed Mutagenesis of an Apolipoprotein E Mutant, APO E5(GLU3→LYS) and its Binding to Low Density Lipoprotein Receptors,Biochemical and Biophysical Research Communications187:1180-1186 (Sep. 1992).
Laskowitz et al.: “Apolipoprotein E and the CNS Response to Injury”,J. Cereb. Blood Flow Metab., 18(5):465-471 (1998).
Laskowitz et al.: “Endogenous apolipoprotein E suppresses LPS-stimulated microglial nitric oxide production”,Clinical Neuroscience and Neuropathology, NeuroReport,9(4):615-618 (1998).
M. Clay et al.; Localization of a Domain in Apolipoprotein E with both Cytostatic and Cytotoxic Activity;Biochemistry34:11142-11151 (1995).
Pardrige, W.M., Chapter 12: Blood-brain barrier peptide transport and peptide delivery to the brain, Peptide-based drug design; Ed Taylor, et al.,American Chemical Society, pp. 265-296 (1995).
R. Mrak et al.; Glial Cytokines in Alzheimer's Disease: Review and Pathogenic Implications,Hum Pathol26:816-823 (Aug. 1995).
S. Barger et al.; Microglial Activation by Alzheimer Amyloid Precursor Protein and Modulation by Apolipoprotein E,Nature388:878-881 (Aug. 1997).
T. Innerarity et al.; Binding of Arginine-rich (E) Apoprotein after Recombination with Phospholipid Vesicles to the Low Density Lipoprotein Receptors of Fibroblast,The Journal of Biological Chemistry254:4186-4190 (1979).
Vitek et al.: “Modulation of Nitric Oxide Production in Human Macrophages by Apolipoprotein-E and Amyloid-Beta Peptide”,Biochemical and Biophysical Research Communications, 240:391-394 (1997).
Zielasek, J., et al.,Advances in Neuroimmunology; vol. 6, No. 2, pp. 191-222 (1996).
Laskowitz Daniel T.
Matthew William D.
McMillian Michael
Cognosci, Inc.
Cooley Godward Kronish LLP
Emch Gregory S.
Kemmerer Elizabeth
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