Ex Parte Pardridge

Board of Patent Appeals and Interferences

Jul 22, 2010

11061956 (B.P.A.I. Jul. 22, 2010)

UNITED STATES PATENT AND TRADEMARK OFFICE
UNITED STATES DEPARTMENT OF COMMERCE
United States Patent and Trademark Office
Address: COMMISSIONER FOR PATENTS
P.O. Box 1450
Alexandria, Virginia 22313-1450
www.uspto.gov
APPLICATION NO. FILING DATE FIRST NAMED INVENTOR ATTORNEY DOCKET NO. CONFIRMATION NO.
11/061,956 02/17/2005 William M. Pardridge 407J-001910US 5758
7590 07/22/2010
Quine Intellectual Property Law Group, P.C.
P.O. Box 458
Alameda, CA 94501
EXAMINER
DAHLE, CHUN WU
ART UNIT PAPER NUMBER
1644
MAIL DATE DELIVERY MODE
07/22/2010 PAPER
Please find below and/or attached an Office communication concerning this application or proceeding.
The time period for reply, if any, is set in the attached communication.
PTOL-90A (Rev. 04/07)

UNITED STATES PATENT AND TRADEMARK OFFICE
__________

BEFORE THE BOARD OF PATENT APPEALS
AND INTERFERENCES
__________

Ex parte WILLIAM M. PARDRIDGE
__________

Appeal 2009-012932
Application 11/061,956
Technology Center 1600
__________

Before ERIC GRIMES, LORA M. GREEN, and
JEFFREY N. FREDMAN, Administrative Patent Judges.

FREDMAN, Administrative Patent Judge.

DECISION ON APPEAL1
This is an appeal under 35 U.S.C. § 134 involving claims to a
composition for delivering a large lysosomal enzyme across the blood brain

1 The two-month time period for filing an appeal or commencing a
civil action, as recited in 37 C.F.R. § 1.304, or for filing a request
for rehearing, as recited in 37 C.F.R. § 41.52, begins to run from
the “MAIL DATE” (paper delivery mode) or the
“NOTIFICATION DATE” (electronic delivery mode) shown on
the PTOL-90A cover letter attached to this decision.
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barrier. The Examiner has rejected the claims as obvious. We have
jurisdiction under 35 U.S.C. § 6(b). We affirm.
Statement of the Case
The Claims
Claims 1, 2, 5-8, 22, and 23 are on appeal. Claims 1, 2, 7, and 23 are
separately argued. The remaining claims are not argued separately and
therefore stand or fall together. 37 C.F.R. § 41.37(c)(1)(vii). Claims 1, 2, 7,
and 23 read as follows:
1. A composition that is capable of delivering a
large lysosomal enzyme across the blood brain
barrier in vivo, said composition comprising:
a large lysosomal enzyme; and
a monoclonal antibody that binds to an
insulin receptor wherein said monoclonal antibody
is linked to said large lysosomal enzyme.

2. A composition according to claim 1,
wherein the monoclonal antibody is a humanized
monoclonal antibody that binds to a human insulin
receptor.

7. A composition according to claim 1
wherein said monoclonal antibody is linked to said
large enzyme by genetic fusion to form a fusion
protein consisting essentially of said monoclonal
antibody and said large enzyme.

23. The composition of claim 1, wherein the
enzyme is an α-L-iduronidase and the monoclonal
antibody binds to the human insulin receptor,
wherein the α-L-iduronidase is genetically fused to
the monoclonal antibody.

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The prior art
The Examiner relies on the following prior art references to show
unpatentability:
Pardridge WO 99/00150 Jan. 7, 1999
Radin et al. US 5,929,304 Jul. 27, 1999

McGrath et al., Bifunctional Fusion Between Nerve Growth Factor
and a Transferrin Receptor Antibody, 47 J. NEUROSCIENCE RESEARCH 123-
133 (1997).

The issues
A. The Examiner rejected claims 1, 2, 5, 6, 8, and 22 under 35 U.S.C. §
103(a) as obvious over Pardridge and Radin (Ans. 3-5).
B. The Examiner rejected claims 7 and 23 under 35 U.S.C. § 103(a) as
obvious over Pardridge, Radin, and McGrath (Ans. 5-6).
C. The Examiner objected to claim 23 (Final Rej. 2).

A. 35 U.S.C. § 103(a) over Pardridge and Radin
The Examiner finds that “one skilled in the art could have combined
monoclonal antibody specific for human insulin receptor and human IDUA
[α-L-iduronidase] by known methods with no change in their respective
functions and the combination would have yielded predictable results of
transferring lysosomal enzymes such as IDUA across BBB [blood brain
barrier] to release brain symptoms suffered by patients with lysosomal
storage disorders” (Ans. 4).
Appellant contends that “the Examiner fails to address the problem of
predictability in any meaningful way. At most, the Examiner argues that
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there was ‘no change in [the] respective functions’ of the antibody and
enzyme components in the overall claimed composition, making the
combination predictable” (App. Br. 10). Appellant contends that
there was no way to know whether an antibody could be
linked with a large lysosomal enzyme while retaining
activity of the antibody and the enzyme; there was no way to
know if the human insulin receptor could internalize such a
large antibody-enzyme complex; there was no [way] to
know if the enzyme would be active after crossing the blood
brain barrier.

(App. Br. 10). Appellant also contends that “Dr. Pardridge establishes in his
declaration of June 7, 2007 (Appendix D), a variety of references show that
other systems that were expected to work for enzyme delivery across the
blood brain barrier simply failed” (App. Br. 17).
The issues with respect to this rejection are: Does the evidence of
record support the Examiner’s conclusion that Pardridge and Radin provide
a reasonable expectation of success in delivering a lysosomal enzyme linked
to an insulin receptor monoclonal antibody across the blood brain barrier?
Findings of Fact
1. Pardridge teaches “to prepare a radiolabeled peptide
pharmaceutical conjugated to a BBB delivery system” (Pardridge 2, ll. 4-5).
2. Pardridge teaches that “[r]adiolabeled truncated analogs of
Aβ1-43 conjugated to a BBB drug delivery system are enabled to enter the
brain from blood to a high degree, which allows for imaging amyloid
plaques in AD brain tissue following systemic (intravenous) injection”
(Pardridge 2, ll. 12-14).
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3. Pardridge teaches that a “typical BBB delivery system is the
83-14 monoclonal antibody (Mab) to the human insulin receptor (HIR). The
83-14 HIRMAb undergoes receptor-mediated transcytosis through the BBB
of Old World primates” (Pardridge 5, ll. 2-4).
4. Figure 11 of Pardridge is reproduced below:

“Scheme depicting the multifunctionality and three domains of the peptide
radiopharmaceutical conjugated to the blood-brain barrier (BBB) delivery
system. The imaging agent is comprised of amyloid binding domain, a
linker domain, and a BBB transport domain” (Pardridge 4, ll. 8-11).
5. Pardridge teaches that the “immunogenicity of the MAb portion
of the delivery vector may be minimized by ‘humanization’ of the murine
framework sequences of the MAb” (Pardridge 16, l. 32 to 17, l. 2).
6. Pardridge teaches that “when the peptide pharmaceutical was
administered conjugated to the BBB delivery system, there was robust
uptake of the peptide radiopharmaceutical” (Pardridge 12, ll. 4-5).
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7. Radin teaches “the production of human or animal lysosomal
enzymes in transformed or transfected cells” (Radin, col. 7, ll. 11-12).
8. Radin teaches a “construct comprises nucleotide sequence
encoding a human α-L-iduronidase (IDUA)” (Radin, col. 7, ll. 30-32).
9. Radin teaches that the “plant expression systems and the
recombinant lysosomal enzymes produced therewith have a variet[y] of
uses, including but not limited to: (1) the production of enzymatically active
lysosomal enzymes for treatment of lysosomal storage diseases” (Radin, col.
7, ll. 38-42).
10. Radin teaches that the hGC enzyme had “an apparent molecular
weight of about 66-69 kDa (Fig. 5B). The size of the immuno-reactive
protein w[]as reduced to about 58 kDa after N-glucanase treatment,
indicating that the enzyme was glycosylated” (Radin, col. 24, ll. 59-63).
11. Radin teaches that the “IDUA (92 kD) from IDUA-9 tobacco
extract migrated slightly faster than secreted IDUA from CHO cells. This
presumably is due to differences in glycan composition” (Radin, col. 31, ll.
23-26).
12. Radin teaches that the tobacco synthesized IDUA is
enzymatically active (see Radin, col. 31, ll. 53-67).
13. The Specification teaches that the “delivery of a large
molecular weight (MW) enzyme to the brain . . . mimics a process that has
been previously demonstrated for a range of peptide drugs, such as
vasoactive intestinal peptide (VIP), which has a MW of about 5000 Daltons,
to recombinant CD4, which has a MW of about 40,000 Daltons. However,
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many of the missing lysosomal enzymes have molecular weights of 50,000
to 100,000 Daltons” (Spec. 7 ¶ 00017; reference citations omitted).
14. The Specification teaches “a 150,000 Dalton receptor-specific
Mab acting as a BBB molecular Trojan horse” (Spec. 7 ¶ 00017).
15. The Specification teaches that:
Prior work has shown that drugs or gene medicines can be
ferried across the BBB using molecular Trojan horses that
bind to BBB receptor/transport systems. These Trojan
horses may be modified proteins, endogenous peptides, or
peptidomimetic monoclonal antibodies (Mab’s). For
example, HIR MAb 83-14 is a murine MAb that binds to the
human insulin receptor (HIR). This binding triggers
transport across the BBB of MAb 83-14 (Pardridge et al,
1995), and any drug or gene payload attached to the MAb
(Wu et al., 1997).

(Spec. 2 ¶ 0005).
16. The Specification states that β-glucuronidase “forms a homo-
tetramer, and the MW of tetramer is 390,000 Daltons. It is not known if
BBB molecular Trojan horses can carry across the BBB therapeutic agents
of this large size and with such high MW” (Spec. 7 ¶ 00017; reference
citations omitted).
Principles of Law
The question of obviousness is resolved on the basis of underlying
factual determinations including: (1) the scope and content of the prior art;
(2) the level of ordinary skill in the art; (3) the differences between the
claimed invention and the prior art; and (4) secondary considerations of
nonobviousness, if any. Graham v. John Deere Co., 383 U.S. 1, 17 (1966).
The Supreme Court has emphasized that “the [obviousness] analysis need
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not seek out precise teachings directed to the specific subject matter of the
challenged claim, for a court can take account of the inferences and creative
steps that a person of ordinary skill in the art would employ.” KSR Int’l v.
Teleflex Inc., 550 U.S. 398, 418 (2007). As noted by the Court in KSR, “[a]
person of ordinary skill is also a person of ordinary creativity, not an
automaton.” 550 U.S. at 421.
Analysis
Claim 1
Pardridge teaches that a “typical BBB delivery system is the 83-14
monoclonal antibody (Mab) to the human insulin receptor (HIR). The 83-14
HIRMAb undergoes receptor-mediated transcytosis through the BBB of Old
World primates” (Pardridge 5, ll. 2-4; FF 3). Pardridge teaches that
“[r]adiolabeled truncated analogs of Aβ1-43 conjugated to a BBB drug
delivery system are enabled to enter the brain from blood to a high degree”
(Pardridge 2, ll. 12-13; FF 2). Pardridge teaches that “when the peptide
pharmaceutical was administered conjugated to the BBB delivery system,
there was robust uptake of the peptide radiopharmaceutical” (Pardridge 12,
ll. 4-5; FF 6).
Radin teaches that human α-L-iduronidase (IDUA) is 92,000 daltons
(FF 8, 11). Radin teaches “the production of enzymatically active lysosomal
enzymes for treatment of lysosomal storage diseases” (Radin, col. 7, ll. 38-
42; FF 9). Radin teaches that the tobacco synthesized IDUA is
enzymatically active (see Radin, col. 31, ll. 53-67; FF 12).
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We agree with the Examiner that a preponderance of the evidence
supports a determination that the claimed invention would have been
obvious over Pardridge and Radin. In KSR, the Supreme Court stated that an
invention may be found obvious if it would have been obvious to a person
having ordinary skill to try a course of conduct:
When there is a design need or market pressure to solve a
problem and there are a finite number of identified,
predictable solutions, a person of ordinary skill has good
reason to pursue the known options within his or her
technical grasp. If this leads to the anticipated success, it is
likely the product not of innovation but of ordinary skill and
common sense. In that instance the fact that a combination
was obvious to try might show that it was obvious under §
103.

KSR, 550 U.S. at 421. We agree with the Examiner that the ordinary
practitioner would recognize that it would have been obvious to deliver
Radin’s enzymatically active IDUA using Pardridge’s blood brain barrier
delivery system (FF 1-12).
Appellant contends that “the Examiner fails to address the problem of
predictability in any meaningful way. At most, the Examiner argues that
there was ‘no change in [the] respective functions’ of the antibody and
enzyme components in the overall claimed composition, making the
combination predictable” (App. Br. 10). Appellant contends that
there was no way to know whether an antibody could be
linked with a large lysosomal enzyme while retaining
activity of the antibody and the enzyme; there was no way to
know if the human insulin receptor could internalize such a
large antibody-enzyme complex; there was no [way] to
know if the enzyme would be active after crossing the blood
brain barrier.
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(App. Br. 10). Appellant also contends that “Dr. Pardridge establishes in his
declaration of June 7, 2007 (Appendix D), a variety of references show that
other systems that were expected to work for enzyme delivery across the
blood brain barrier simply failed” (App. Br. 17).
We are not persuaded. In the instant situation, Appellant’s
Specification acknowledges that the prior art demonstrates delivery of
compounds from 5,000 to 40,000 daltons across the blood brain barrier (FF
13). The Specification teaches that “HIR MAb 83-14 is a murine MAb that
binds to the human insulin receptor (HIR). This binding triggers transport
across the BBB of MAb 83-14 (Pardridge et al, 1995), and any drug or gene
payload attached to the MAb (Wu et al., 1997)” (Spec. 2 ¶ 0005; FF 15).
The Specification also teaches that “a 150,000 Dalton receptor-specific Mab
acting as a BBB molecular Trojan horse” (Spec. 7 ¶ 00017; FF 14).
We have considered the Pardridge Declaration, which states that
“Prince showed enhanced uptake by cells in culture, but could not
demonstrate enhanced BBB transport in vivo” (Pardridge ¶ Dec. 7). We
have reviewed Prince, and find that Prince2 teaches that:
We have produced and characterized fusions between RAP
and two lysosomal enzymes IDU and GAA. The fusions
retained some key features of each fusion partner. The
fusions bound to members of the LDLR family and were
routed to the lysosome after being endocytosed. The fusions

2 Prince et al., Lipoprotein Receptor Binding, Cellular Uptake, and
Lysosomal Delivery of Fusions between the Receptor-associated
Protein (RAP) and α-L-Iduronidase or Acid α-glucosidase, 279 J.
BIOLOGICAL CHEMISTRY 35037-35046 (2004).
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had appropriate enzymatic activity that was resistant to the
conditions in the lysosome.

(Prince 35044, col. 2 to 35045, col. 1). Prince teaches that “RAP itself was
recently demonstrated to cross the blood-brain barrier” (Prince 35046, col.
1). While it is true that Prince does not demonstrate enhanced BBB
transport in vivo, this is not surprising since Prince does not attempt BBB
transport in vivo. As the Examiner notes, this “does not mean that fusion
protein of lysosomal enzyme and RAP does not work in vivo” (Ans. 12).
We balance Appellant’s contention of unpredictability of delivery of
large lysosomal enzymes (see App. Br. 10; Pardridge Dec. ¶¶ 7-8) against
the express teaching by Pardridge of the delivery of a complex comprising a
150,000 dalton monoclonal antibody (FF 14), the protein streptavidin, a
linker and Aβ1-43 (FF 4) and the teaching by the Specification that proteins
up to 40,000 daltons have been transferred (FF 13). Radin teaches that
IDUA is 92,000 daltons (FF 11). Given the absence of any definition of
“large” in the claim or Specification, the “large lysosomal enzyme” can
range from the 50,000 daltons disclosed in the Specification (FF 13) to the
92,000 daltons of IDUA (FF 11) to the 390,000 Dalton tetramer which was
the only size therapeutic agent identified by the Specification as being
uncertain for transport by BBB molecular Trojan horses (FF 16).
Based on these facts, we conclude there is a reasonable expectation of
success. Kubin stated that “[r]esponding to concerns about uncertainty in
the prior art influencing the purported success of the claimed combination,
this court [in O’Farrell] stated: ‘[o]bviousness does not require absolute
predictability of success … all that is required is a reasonable expectation of
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success.”’ In re Kubin, 561 F.3d 1351, 1360 (Fed. Cir. 2009) (citing In re
O’Farrell, 853 F.2d 894, 903-904 (Fed. Cir. 1988)).
Appellant also contends that “no one had any idea how to transport an
enzyme across the blood brain barrier – or even whether it was possible”
(App. Br. 10). Appellant argues that “the lack of blood brain barrier
targeting programs was directly attributed by the Author [Dr. Pardridge] to a
lack of knowledge and predictability, prior to the invention, regarding
delivery mechanisms to transport large molecules across the blood brain
barrier” (App. Br. 7).
This argument appears to implicate the doctrine of long felt need.
Evidence of long felt need must show that the problem solved by Applicant's
invention was known but not solved prior to the invention. See Al-Site Corp.
v. VSI, Inc., 174 F.3d 1308, 1325 (Fed. Circ. 1999). To show failure of
others, the evidence must establish that others skilled in the art tried and
failed to find a solution for the problem solved by the Applicant. Stratoflex
Inc. v. Aeroquip, 713 F.2d 1530, 1540 (Fed. Cir. 1983).
One must also show that the others who failed had knowledge of the
critical prior art. In re Caveney, 386 F.2d 917, 923 (CCPA 1967). While the
Pardridge Declaration does provide evidence that delivery across the blood
brain barrier was a known problem, Appellant has failed to establish that
those in the prior art had knowledge of the critical prior art of Pardridge, the
art applied by the Examiner.
As pointed out by the Examiner, “there is no evidence that if persons
skilled in the art . . . knew of the teachings of Pardridge (WO 99/00150) and
Radin et al., they would still have been unable to solve the problem” (Ans.
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10). That is, the comparison argued here by Appellant is not with the closest
prior art of Pardridge, but rather with earlier failures. Thus the evidence
presented is not probative of the knowledge of the ordinary artisan aware of
the teachings of the closest prior art of Pardridge.
Claim 2
Appellant argues that “[i]t is not clear from the rejection how one of
skill could have predictably humanized the Ab, based solely on the prior art,
particularly in light of the actual difficulty in humanizing this Ab that was
experienced by Appellant” (App. Br. 5).
We are not persuaded. As Pardridge evidences, humanization of
antibodies was known to the ordinary artisan (FF 5). The Specification
cites known methods for performing the humanization (see Spec. 23 ¶
00062). O’Farrell states that “[o]bviousness does not require absolute
predictability of success.” In re O’Farrell, 853 F.2d 894, 903 (Fed. Cir.
1988). O’Farrell identifies
two kinds of error. In some cases, what would have been
“obvious to try” would have been to vary all parameters or
try each of numerous possible choices until one possibly
arrived at a successful result, where the prior art gave either
no indication of which parameters were critical or no
direction as to which of many possible choices is likely to be
successful…. In others, what was “obvious to try” was to
explore a new technology or general approach that seemed
to be a promising field of experimentation, where the prior
art gave only general guidance as to the particular form of
the claimed invention or how to achieve it.

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O’Farrell, 853 F.2d at 903. The instant facts do not fit O’Farrell’s first kind
of error, since the prior art of Pardridge specifically points the practitioner to
humanizing antibodies for use in human therapeutics (FF 5).
The instant fact pattern also does not represent a situation where the
prior art only provides a “general approach”, since there is no dispute that
Appellant did not invent antibody humanization, rather the prior art teaches
specific known methods by which antibodies are humanized (see, e.g., Spec.
23 ¶ 00062). We therefore find that there was a reasonable expectation of
success in humanizing the antibody of Pardridge (FF 5). See In re Kubin,
561 F.3d 1351, 1359 (Fed. Cir. 2009).
Conclusion of Law
The evidence of record supports the Examiner’s conclusion that
Pardridge and Radin provide a reasonable expectation of success in
delivering a lysosomal enzyme linked to an insulin receptor monoclonal
antibody across the blood brain barrier.

B. 35 U.S.C. § 103(a) over Pardridge, Radin, and McGrath
The Examiner finds that “McGrath et al. teach that antibody fusion
protein provides an alternative to chemical conjugation for producing
precisely defined homogeneous bifunctional molecules with both NGF and
transferrin receptor targeting activities and can be used to deliver proteins to
CNS” (Ans. 6). The Examiner finds that the “combination of the teachings
of Pardridge, Radin et al. and McGrath et al. would yield the predictable
results of a composition capable of transferring lysosomal enzymes across
BBB wherein the composition comprises monoclonal antibody to insulin
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receptor wherein said antibody is genetically fused to lysosomal enzymes
such as α-L-iduronidase” (Ans. 6).
Appellant contends that “when attempting to fuse a functional enzyme
to a functional antibody, as in the claimed invention of claims 7 and 23, the
issue of unpredictability faced by the practitioner was actually severely
compounded by the teachings of McGrath” (App. Br. 18). Appellant
contends that:
The above considerations would leave the artisan unsure
what even to attempt, even had the idea of a HIRMAb-
lysosomal enzyme been presented to them. If they followed
McGrath, they would fuse the Enz, including the Enz signal
peptide, to the NT of the HIRMAb, but would risk lo[]sing
biologic activity of the HIRMAb. If they were concerned
about the effect of the large 80 kDa ENZ on the NT and
CDRs of the HIRMAb, they would fuse the ENZ to the CT
of the antibody, and risk losing enzyme activity owing to
improper folding of the ENZ.

(App. Br. 20).
The issue with respect to this rejection is: Does the evidence of record
support the Examiner’s conclusion that formation of a fusion protein of an
antibody and lysosomal enzyme would have been obvious?
Additional Findings of Fact
17. McGrath teaches that “[a]ntibody engineering has provided an
alternative to chemical conjugation for producing precisely defined,
homogenous bifunctional molecules with both NGF activity and TfR
targeting activity” (McGrath 124, col. 1).
18. McGrath teaches that “the constraints imposed by the presence
of the relatively large antibody molecule at the C-terminus of human NGF
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does not affect the association between NGF monomers or significantly
affect the ability of the molecule to adopt an active conformation” (McGrath
131, col. 1).
19. McGrath teaches that “[i]t is noteworthy that the affinity of the
antibody carrying NGF at the C-terminus of the heavy chain, when analyzed
in its purified form (Fig. 6), is uncompromised relative to the unmodified
human chimera” (McGrath 131, col. 1).
20. McGrath teaches that “fusions with NGF at the amino terminus
of the light chain or both chains also resulted in antibodies that still bound
the TfR” (McGrath 131, col. 1).
21. McGrath teaches that “gene fusions between the neurotrophins
and antibodies may represent a useful method to non-invasively deliver
these and other proteins to the CNS” (McGrath 131, col. 2).
Analysis
McGrath teaches that a fusion of NGF and an antibody resulted in
obtaining a fusion where both NGF and the antibody retained the desired
functional properties (FF 17-20). McGrath teaches that this approach may
be a useful method to deliver proteins to the central nervous system (FF 21).
Appellant contends that “when attempting to fuse a functional enzyme
to a functional antibody, as in the claimed invention of claims 7 and 23, the
issue of unpredictability faced by the practitioner was actually severely
compounded by the teachings of McGrath” (App. Br. 18).
We are not persuaded. As we balance the argument of Appellant,
which lacks evidentiary support, against the express success of McGrath in
synthesizing a fusion protein which retains activity of both the desired
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protein and antibody partners, we conclude that there is a reasonable
expectation of success. Appellant has provided no evidence to rebut the
successful showing in McGrath. See In re Pearson, 494 F.2d 1399, 1405
(CCPA 1974) (“Attorney's argument in a brief cannot take the place of
evidence.”).
Conclusion of Law
The evidence of record supports the Examiner’s conclusion that
formation of a fusion protein of an antibody and lysosomal enzyme would
have been obvious.

C. Objection to Claim 23
Appellant submits “that the objection is improper and respectfully
request that the rejection [be] withdrawn by the Examiner or reversed by the
Board” (App. Br. 21).
We do not have jurisdiction to review the objection to claim 23, as
this is a matter that is reviewable by petition to the Director under 37 C.F.R.
§ 1.181. See MPEP § 1201 (the Board will not ordinarily hear a question that
is reviewable by petition); In re Berger, 279 F.3d 975, 984 (Fed. Cir. 2002)
(citing In re Hengehold, 440 F.2d 1395, 1403-04 (CCPA 1971) (stating that
there are many kinds of decisions made by examiners that are not appealable
to the Board when they are not directly connected with the merits of issues
involving rejections of claims, and holding that “the kind of adverse
decisions of examiners which are reviewable by the board must be those
which relate, at least indirectly, to matters involving the rejection of
claims”)); and In re Mindick, 371 F.2d 892, 894 (CCPA 1967) (holding that
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the refusal of an examiner to enter an amendment of claims is reviewable by
petition under 37 C.F.R. § 1.181, and not by appeal to the Board). Therefore,
we are not reviewing the Examiner’s objection to claim 23.
SUMMARY
In summary, we affirm the rejection of claims 1 and 2 under 35
U.S.C. § 103(a) as obvious over Pardridge and Radin. Pursuant to 37 C.F.R.
§ 41.37(c)(1)(vii)(2006), we also affirm the rejection of claims 5, 6, 8, and
22 as these claims were not argued separately.
We affirm the rejection of claims 7 and 23 under 35 U.S.C. § 103(a)
as obvious over Pardridge, Radin, and McGrath.
We do not review the Examiner’s objection to claim 23.

No time period for taking any subsequent action in connection with
this appeal may be extended under 37 C.F.R. § 1.136(a)(1)(iv)(2006).

AFFIRMED

dm

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