Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Peptide containing doai
Reexamination Certificate
1998-04-17
2002-10-15
Priebe, Scott D. (Department: 1636)
Drug, bio-affecting and body treating compositions
Designated organic active ingredient containing
Peptide containing doai
C424S184100, C424S185100, C424S192100, C435S069100, C435S320100, C435S325000, C530S350000, C530S351000, C530S380000, C536S023100, C536S023500, C536S023400
Reexamination Certificate
active
06465422
ABSTRACT:
BACKGROUND OF THE INVENTION
Throughout this application, various publications are referenced by author and date. Full citations for these publications may be found listed alphabetically at the end of the specification immediately preceding Sequence Listing and the claims. The disclosures of these publications in their entireties are hereby incorporated by reference into this application in order to more fully describe the state of the art as known to those skilled therein as of the date of the invention described and claimed herein.
An important means by which tumors grow and invade surrounding normal tissue is by a complex series of cell—cell and cell matrix interactions. We have focused on the interaction of tumor cells with matrix-associated components. The Receptor to AGE (RAGE) interacts with a range of physiologically and pathophysiologically-relevant ligands (1-5). In normal developing neurons of the central nervous system, the expression of RAGE is markedly enhanced and co-localizes with that of its ligand, amphoterin. Amphoterin, a matrix-associated polypeptide, is expressed in developing neurons and certain tumor cells, such as rat C6 glioma cells (6-12).
SUMMARY OF THE INVENTION
The present invention provides for a method for inhibiting tumor invasion or metastasis in a subject which comprises administering to the subject a therapeutically effective amount of a form of soluble Receptor for Advanced Glycation Endproducts (RAGE). The present invention also provides a method for evaluating the ability of an agent to inhibit tumor invasion in a local cellular environment which comprises: (a) admixing with cell culture media an effective amount of the agent; (b) contacting a tumor cell in cell culture with the media from step (a); (c) determining the amount of spreading of the tumor cell culture, and (d) comparing the amount of spreading of the tumor cell culture determined in step (c) with the amount determined in the absence of the agent, thus evaluating the ability of the agent to inhibit tumor invasion in the local cellular environment. The present invention also provides a pharmaceutical composition which comprises a therapeutically effective amount of the agent evaluated in the aforementioned method and a pharmaceutically acceptable carrier.
REFERENCES:
patent: WO9822138 (1998-05-01), None
Schmidt et al., Activation of Receptor for Advanced Glycation End Products A Mechanism for Chronic Vascular Dysfunction in diabetic Vasculopathy and Atherosclerosis, 1999, CIRC, RES., 84:489-497.*
Taguchi et al., Blockade of RAGE- amphoterin signalling suppresses tumor growth and metastases, May 2000, Nature 405:354-360.*
Mastrangelo et al., Gene therapy for human cancer: An essay for clinicians, Feb. 1996, Seminars in Oncology, vol. 23 No. 1 pp. 4-21.*
Blau et al., Molecular Medicine: Gene therapy-A novel form of drug delivery, 1995, The New England Journal of Medicine, vol. 333 No. 18 pp. 1204-1207.*
Kelloff et al., Cancer Chemoprevention: Progress and Promise, 1999, European Journal of Cancer, vol. 35 No. 14 pp. 2031-2038.*
Gomez-Navarro et al., Gene therapy for cancer, 1999, European Journal of Cancer, vol. 35 No. 6 pp. 867-885.*
Hori et al. ‘The Receptor for Advanced Gycation Endproducts: Implications for the Development of Diabetic Vascular Disease. Fundam. Clin. Cardiol.’ In: The Endothelium in Clinical Practice. Jan. 1997, Chapter 11, pp. 311-329 (Exhibit C).
Chen et al., Amyloid-beta Peptide- Receptor for Advanced Glycation Endproduct Interaction Elicits Neuronal Expression of Macrophage-Colony Stimulating Factor: A Proinflammatory Pathway in Alzheimer Disease. Proc. Natl. Acad. Sci. May 13, 1997, vol. 94, No. 10, pp. 5296-5301 (Exhibit D).
Schmidt et al. V-domain of Receptor for Advanced Glycation Endproducts (RAGE) Mediates Binding of AGEs: A Novel Target for Therapy of Diabetic Complications. Circulation. Oct. 21, 1997, vol. 96, No. 8 Suppl. p. 137, (Exhibit E).
Hori et al. The Receptor for Advanced Glycation Endproducts (RAGE) Is A Cell Surface Receptor for Amphoterin in the Development Central Nervous System (CNS) to Promote Neutrite Outgrowth, FASEB J. 1995, vol. 9, No. 3, p. A382,(Exhibit F).
International Search Report of International Application No. PCT/US99/08427, dated Jul. 29, 1999 (Exhibit G).
Hori, O. et al. (1995) “Receptor for Advanced Glycation End Products (RAGE) Is a Cellular Binding Site for Amphoterin.”J. Biol. Chem., 270(43): 25752-25761. (Exhibit 2).
Mohan, P. S. et al. (1992) “Sulfoglycolipids Bind to Adhesive Protein Amphoterin (P30) in the Nervous System.”Biochem.&Biophys. Research Comm., 182(2) 689-696 (Exhibit 3).
Neeper, M. et al. (1992) “Cloning and Expression of a Cell Surface Receptor for Advanced Glycosylation End Products of Proteins.”J. Biol. Chem., 267(21): 14998-15004 (Exhibit 4).
Price, J. T. et al. (1997) “The Biochemistry of Cancer Dissemination.”Critical Reviews in Biochemistry and Molecular Biology, 32(3): 175-253 (Exhibit 5).
Schmidt, A. M. et al. (1992) “Isolation and Characterization of Two Binding Proteins for Advances Glycolation End Products from Bovine Lung Which Are Present on the Endothelial Cell Surface.”J. Biol. Chem., 267(21): 14987-14997 (Exhibit 6).
Schmidt, A. M. et al. (1998) “RAGE: A Receptor with a Taste for Multiple Ligands and Varied Pathophysiologic States.”Hormones and Signaling, 1: 41-63 (Exhibit 7).
Sigh, S. P. et al (1997) “Role of Gq&agr; in Insulin-Stimulated Glucose Uptake by C6 Glioma Cells.”NeuroReport, 8: 2359-2363 (Exhibit 8).
Yan, S. D. et al. (1997) “Amyloid-&bgr; Peptide-Receptor for Advanced Glycation Endproduct Interaction Elicits Neuronal Expression of Macrophage-colony Stimulating Factor: A Proinflammatory Pathway in Alzheimer Disease.”Proc. Natl. Acad. Sci. USA, 94: 5296-5301 (Exhibit 9).
Yan, S. D. et al. (1996) “RAGE and Amyloid-&bgr; Pepetide Neurotoxicity in Alzheimer's Disease.”Nature, 382:685-691 (Exhibit 10).
Schmidt Ann Marie
Stern David
Cooper & Dunham LLP
Kausnal Sumesh
Priebe Scott D.
The Trustees of Columbia University in the City of New York
White John P.
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