Appeal 2007-1614
Application 09/779,447
(Specification 1). Abnormal or uncontrolled angiogenesis features
prominently in a number of diseases (id. at 2). Tumor growth, for example,
depends on angiogenesis (id.). Thus, “[i]n breast carcinoma, intratumoral
endothelial cells proliferate 45 times faster than endothelial cells in adjacent
benign stroma, and the rate of tumor progression correlates with increased
intratumoral microvascular density. Neovascularization supports tumor
growth by allowing ‘perfusion’ of nutrients, oxygen, and waste products
through a crowded cell population” (id.).
The Specification discloses that tunicamycin reduces endothelial cell
proliferation in cell culture, with 70% of the cells entering “into apoptosis
(i.e., ‘programmed cell death’) after an exposure to [1 μg/ml] tunicamycin
for 32 hours” (id. at 56). The Specification discloses methods of inhibiting
angiogenesis by administering nucleosides, including tunicamycin, “to a
patient in need of such treatment, e.g., a patient having disease state
characterized by an abnormally high amount of angiogenesis. For instance,
the present invention may inhibit neovascularization of a solid tumor tissue”
(id. at 37).
DISCUSSION
1. CLAIMS
Claims 9, 14, and 18 are pending and on appeal. Claim 9 is
representative and reads as follows:
Claim 9: A method for inhibiting angiogenesis, comprising:
administering a nucleoside in an amount effective to
inhibit angiogenesis, to a patient in need of such treatment, the
nucleoside comprising glucosamine, and wherein the
glucosamine comprises at least one tunicamycin and functional
derivatives thereof, and wherein the at least one of tunicamycin
2
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