Appeal No. 2006-3253 Page 3
Application No. 10/276,547
The specification also states that
[A]gents which modulate this gene . . . or its products are useful for
treating obesity/overweight-associated comorbidities including
hypertension, type 2 diabetes, coronary artery disease, hyperlipidemia,
stroke, gallbladder disease, gout, osteoarthritis, sleep apnea and
respiratory problems, some types of cancer . . . , thrombolic disease,
polycystic ovarian syndrome; reduced fertility, complications of pregnancy,
menstrual irregularities, hirsutism, stress incontinence, and depression.
Page 50, lines 13-20.
The specification also states that “[h]uman DA-like GPCRs provide a potential
target for treating cancer.” Page 50, line 22. Finally, the specification states that
[d]iabetes also can be potentially treated by regulating the activity of
human DA-like GPCR. . . .
Type 1 diabetes is initiated by an autoimmune reaction that attacks the
insulin secreting cells (beta cells) in the pancreatic islets. Agents that
prevent this reaction . . . are potential therapies for this disease. Other
agents that induce beta cell proliferation and regeneration are also
potential therapies.
Type II diabetes is the most common of the two diabetic conditions. . . .
Therapies that increase the response by the beta cell to glucose would
offer an important new treatment for this disease.
The defect in insulin action in Type II diabetic subjects is another target for
therapeutic intervention. Agents that increase the activity of the insulin
receptor in muscle, liver and fat will cause a decrease in blood glucose.
. . . Other therapies can directly activate the cellular end product . . . to
generate an insulin-like effect and therefore [ ] produce [a] beneficial
outcome. Because overweight subjects have a greater susceptibility to
Type II diabetes, any agent that reduces body weight is a possible
therapy.
Both Type I and Type [II] diabetes can be treated with agents that mimic
insulin action or that treat diabetic complications by reducing blood
glucose levels.
Page 51, line 28, to page 52, line 29.
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Last modified: November 3, 2007