Appeal 2007-4148
Application 09/148,012
and murine homologs of SR-BI, an AcLDL and LDL binding scavenger
receptor . . . ha[ve] been isolated and characterized” (id. at 5).
“Direct binding studies show that SR-BI expressed in mammalian
cells . . . binds HDL, without cellular degradation of the HDL-apoprotein,
and lipid is accumulated within cells expressing the receptor” (id. at 6).
SR-BI . . . mediates the uptake and transport of cholesteryl ester
from high density lipoproteins. It has been demonstrated that
transgenic animals which do not produce SR-BI are healthy,
with the exception that the females are infertile. This provides
evidence that inhibition of uptake, binding or transport of
cholesteryl ester to SR-BI can be used to inhibit pregnancy.
The same pathway can also be used to decrease production of
steroids, and therefore be used as a therapy for disorders
involving steroidal overproduction.
(Id. at 7.)
DISCUSSION
1. CLAIMS
Claims 1-9, 12, 15, 16, and 20-22 are on appeal. Claim 19 is also
pending but has been withdrawn from consideration by the Examiner.
The claims have not been argued separately and therefore stand or fall
together. 37 C.F.R. § 41.37(c)(1)(vii). We will focus on claim 1, the
broadest claim on appeal. Claim 1 reads as follows:
1. A method for inhibiting pregnancy or decreasing production of
steroids in a mammal comprising
administering a compound inhibiting uptake, binding or
transport of cholesteryl ester by SR-BI in the mammal in an amount
effective to inhibit pregnancy or to decrease production of steroids in
disorders involving steroidal overproduction.
2
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