Appeal No. 2006-2368 Page 5
Application No. 10/247,032
Choi2 to support their assertion that “[l]evels of CRP above 0.4 mg/dL have
simply not been demonstrated in all atherosclerosis patients.” Id. at 7-8.
Appellants arguments are not found to be convincing. As noted by the
examiner, Rosenblum teaches a method of treating atherosclerosis through the
administration of ezetimbre as the specific sterol adsorption inhibitor, and
simvastatin as the HMG-CoA reductase inhibitor. Thus, the issue becomes
whether treating a patient with atherosclerosis is treating a patient having a blood
level of c-reactive protein of greater than about 0.4 mg/dL, and thus treating
vascular inflammation (claim 1) or reducing vascular c-reactive protein levels
(claim 32).
As noted by appellant, Erren teaches that only 50% of patients with
coronary artery disease (CAD), but no peripheral artery disease (PAD), have c-
reactive protein (CRP) levels of 0.4 mg/dL. See Erren, Table 3. But stated
differently, 50% of atherosclerosis (CAD) patients had CRP levels greater than
0.4 mg/dL, and 25% had CRP levels greater than 14 mg/dL. Moreover, the use
of “about” in the claims to describe the 0.4 mg/dL would actually include a higher
percentage of patients that have CRP levels greater than about 0.4 mg/dL.
Thus, in treating atherosclerosis patients with ezetimibe as the specific sterol
adsorption inhibitor, and simvastatin as the HMG-CoA reductase inhibitor, as
taught by Rosenblum, Erren demonstrates that out of 100 patients, more than 50
patients will have CRP levels greater than about 0.4 mg/dL. Thus, the required
2 Choi et al. (Choi), “Association of High Sensitivity C-Reactive Protein with Coronary Heart
Disease Prediction, but Not with Carotoid Athersclerosis, in Patients with Hypertension,” Circ. J.,
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