Appeal No. 2004-2170 Page 3
Application No. 09/901,429
Specification, pages 3-4.
Finally, the specification indicates that “[p]ost-traumatic net proteolysis is
primarily a result of a large increase in protein degradation, which outweighs a lesser
increase in total protein synthesis” (id., page 30), but “[p]ropranolol induced an increase
in the intracellular recycling of free amino acids” (id.), and “[a]n acceleration in protein
synthesis in propranolol treated subjects was seen” (id.). When patients were tested
after four weeks of treatment with propranolol, “[t]he net balance of protein synthesis
and breakdown [had] achieved anabolic levels” (id., page 29).
DISCUSSION
Independent claim 1 is directed to a method of treating a burn patient by
administering a pharmacologically effective dose of a beta-adrenergic antagonist,
wherein treatment with the beta-adrenergic antagonist improves skeletal muscle protein
kinetics in the patient as compared with an untreated patient. Dependent claim 3
specifies that the dose is effective to decrease the patient’s heart rate by about 25%.
There is no dispute that Herndon administers propranolol, a $-adrenergic
antagonist, to burn patients, at a dose of 2 mg/kg per day – a dose effective to
decrease patients’ heart rates to the required level, and also within the range asserted
in the specification to be effective in improving skeletal muscle protein kinetics (see
pages 7-8). According to the examiner, Herndon anticipates the claimed invention
because “the critical elements (i.e., the effective therapeutic dosage regimen (2 mg/kg),
the burn patients and the successful outcome) required by the instant claims have been
taught and acknowledged” (Answer, page 4). As further explained by the examiner,
“the underlying mechanism recited in the claims (i.e., [skeletal] [muscle] protein kinetics)
[is] not considered as a critical element having [patentable] weight because the
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