Ex Parte ZENG et al

Patent Trial and Appeal Board

Sep 20, 2016

12762091 (P.T.A.B. Sep. 20, 2016)

UNITED STA TES p A TENT AND TRADEMARK OFFICE
APPLICATION NO. FILING DATE FIRST NAMED INVENTOR
121762,091 04/16/2010
77974 7590 09/22/2016
Stanford University Office of Technology Licensing
Bozicevic, Field & Francis LLP
1900 University Avenue
Suite 200
East Palo Alto, CA 94303
DefuZENG
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
ATTORNEY DOCKET NO. CONFIRMATION NO.
CAP576B US 2635
EXAMINER
DIBRINO, MARIANNE
ART UNIT PAPER NUMBER
1644
NOTIFICATION DATE DELIVERY MODE
09/22/2016 ELECTRONIC
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.
Notice of the Office communication was sent electronically on above-indicated "Notification Date" to the
following e-mail address( es):
docket@bozpat.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte DEFU ZENG and SAMUEL STROBER1
Appeal2014-006351
Application 12/762,091
Technology Center 1600
Before DONALD E. ADAMS, MELANIE L. McCOLLUM, and
TIMOTHY G. MAJORS, Administrative Patent Judges.
McCOLLUM, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal under 35 U.S.C. § 134 involving claims to an
autoantibodies reduction method. The Examiner has rejected the claims as
obvious. We have jurisdiction under 35 U.S.C. § 6(b). We affirm.
STATEMENT OF THE CASE
"Systemic lupus erythematosus (SLE) is an autoimmune disease
characterized by polyclonal B cell activation, which results in a variety of
anti-protein and non-protein autoantibodies" (Spec. ,-i 2). The present
Specification discloses that "[t]reatment with anti-CDl monoclonal
1 Appellants identify the real party in interest as The Leland Stanford Junior
University (App. Br. 2).
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Application 12/762,091
antibodies significantly delays the onset of proteinuria, reduces the levels of
serum IgG and anti-dsDNA IgG and prolongs survival in a model system for
SLE" (id. iJ 13).
Claims 1, 6, 7, 15, and 16 are pending and on appeal (App. Br. 2).
The claims subject to each rejection have not been argued separately and
therefore stand or fall together. 37 C.F.R. § 41.37(c)(l)(iv). Claims 1 and
16 are representative and read as follows:
1. A method of reducing the level of anti-dsDNA IgG autoantibodies
in the serum of a human Systemic Lupus Erythematosus patient in need
thereof, comprising: administering to said human Systemic Lupus
Erythematosus patient an effective dose of an antibody that specifically
binds to CDld, wherein the antibody interferes with T cell recognition of the
CD 1 d receptor on a B cell, and wherein the interfering causes a reduction in
the level of IgG isotype anti-dsDNA antibodies in the serum of the patient.
16. The method according to claim 1, further comprising
administering to said patient a second therapeutic agent selected from the
group consisting of a non-steroidal anti-inflammatory drug, corticosteroid,
immunomodulating drug, and anticoagulant.
Claims 1, 6, 7, and 15 stand rejected under 35 U.S.C. § 103(a) as
obvious over Amano2 in view of Zeng, 3 Somnay-W adgaonkar, 4 and Hughes5
2 Masahiko Amano et al., CDJ Expression Defines Subsets of Follicular and
Marginal Zone B Cells in the Spleen: /32-Microglobulin-Dependent and
Independent Forms, 161 J. Immunol. 1710-17 (1998).
3 Defu Zeng et al., Subsets of Transgenic T Cells That Recognize CD 1
Induce or Prevent Murine Lupus: Role of Cytokines, 187 J. Exp. Med. 525-
536 (1998).
4 Kaumudi Somnay-Wadgaonkar et al., lmmunolocalization of CD Id in
Human Intestinal Epithelial Cells and Identification of a /32-Microglobulin-
Associated Form, 11 Int. Immunol. 383-92 (1999).
5 David Hughes, Therapeutic Antibodies Make a Comeback, 3 Drug Disc.
Today 439--42 (1998).
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Application 12/762,091
as evidenced by admissions in the specification at [0013] and [0033]
(Ans. 2).
Claim 16 stands rejected under 35 U.S.C. § 103(a) as obvious over
Amano in view of Zeng, Somnay-W adgaonkar, and Hughes as evidenced by
admissions in the specification at [0013], [0033], [0076], [0085], and [0079]
and further in view of the Merck Manual6 (Ans. 14-15).
Claims 1, 6, and 15 stand rejected under 35 U.S.C. § 103(a) as
obvious over Porcelli7 in view of Amano (Ans. 16).
Claims 7 and 16 stand rejected under 35 U.S.C. § 103(a) as obvious
over Porcelli in view of Amano, the Merck Manual, and Hughes (Ans. 21 ).
PRINCIPLES OF LAW
"It is a general rule that merely discovering and claiming a new
benefit of an old process cannot render the process again patentable." In re
Woodruff, 919 F.2d 1575, 1578 (Fed. Cir. 1990). "Where ... the claimed
and prior art products are identical or substantially identical ... the PTO can
require an applicant to prove that the prior art products do not necessarily or
inherently possess the characteristics of his claimed product." In re Best,
562 F.2d 1252, 1255 (CCPA 1977).
I
The Examiner rejects representative claim 1 as obvious over Amano
in view of Zeng, Somnay-W adgaonkar, and Hughes as evidenced by
admissions in the specification (Ans. 2). The Examiner concludes:
6 The Merck Manual of Diagnosis & Therapy 1317-21 (16th ed. 1992).
7 Porcelli et al., WO 95/00163 Al, Jan. 5, 1995.
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Application 12/762,091
It would have been prima facie obvious to one of ordinary skill
in the art at the time the invention was made to have used the
anti-CDld mAb taught by Zeng et al or Amano et al or the anti-
CDld antibodies taught by Somnay-Wadgaonkar et al (such as
3C 11 or 51.1) to block CD 1 recognition by T cells as taught by
Amano et al, by administering them to human patients with SLE
to reduce the level of anti-dsDNA IgG autoantibodies in said
patients, including with humanized or human versions of the said
antibodies as taught by Hughes.
(Id. at 10.)
The Examiner rejects claim 16, which depends from claim 1, as
obvious over Amano in view of Zeng, Somnay-W adgaonkar, and Hughes as
evidenced by admissions in the specification and in view of the Merck
Manual (id. at 14-15). In particular, the Examiner finds that the "Merck
Manual teaches treatment of SLE with corticosteroid treatment ... in
combination with immunosuppressive agents" (id. at 15).
Appellants do not separately argue the rejection of claim 16 (App.
Br. 4--42). We will therefore discuss these rejections together.
Findings of Fact
1. The present Specification discloses methods "for inhibiting
pathogenic polyclonal B cell activation ... in B cells associated with the
development of [SLE]" (Spec. ,-i 13). In particular, the Specification
discloses:
Binding molecules that specifically interact with CD 1 antigen
recognition, but do not activate signaling (blocking agents), are
administered to a patient, and act to inhibit the function of T cells
that recognize CD 1. When CD 1 mediated signaling is thus
blocked, the T cell response is diminished, resulting in reduced
polyclonal B cell activation and lg class switching. Treatment
with anti-CDl monoclonal antibodies significantly delays the
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Application 12/762,091
(Id.)
onset of proteinuria, reduces the levels of serum IgG and anti-
dsDNA IgG and prolongs survival in a model system for SLE.
2. Amano discloses:
CDl is a nonpolymorphic, class I MHC-like molecule that
associates noncovalently with B2-microglobulin (B2m)3 .... Two
subgroups of CD 1 proteins have been identified in humans;
group 1 includes the closely related CD 1 a, CD 1 b, and CD 1 c
proteins, and group 2 contains the more distantly related CD 1 d
protein . . . . Only the homologue of the CD 1 d protein has been
identified in mice . . . . [M]ouse and human gastrointestinal
epithelial cells express CD 1 d . . . . The predominant form of
CDld in the latter cells is a nonglycosylated /hm-independent
molecule, as judged by analyses of immunoprecipitates with the
anti-CDl mAb 3Cl 1.
(Amano 1710.)
3. Amano also discloses: "The CDl molecule itself or in
combination with endogenous Ags appears to be recognized by an
autoreactive subset of T cells expressing the NKl .1 surface marker ....
The NKl .1 + T cell subset in the thymus is positively selected by CD4+CD8+
thymocytes that express CD 1." (Id.)
4. In addition, Amano discloses:
LPS-activated spleen cells from . mice stimulated the
proliferation of a CDl-restricted VB9/Va4.4 T cell clone. This
T cell proliferation was CD I-dependent, because it was inhibited
by the anti-CD 1 mAb 3C 11 and was also induced by CD 1-
transfected but not nontransfected A20 cells. Thus, either a B2m-
independent form of CD 1 itself or a molecule that cross-reacts
with the 3Cl 1 mAb is expressed on the surface ofLPS-activated
B cells. This possibility is consistent with recent studies on anti-
CD l T cell hybridomas that have shown that some VBI4-
expressing T cells recognize a B2m-independent form of CDl,
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whereas VB14+ hybridomas only recognize a B2m-dependent
form .... As T cell proliferation was not blocked by lBl, which
was the second anti-CD 1 mAb used here, the current study
confirms previous data showing that 1B1 recognizes only a B2m-
dependent form of CDl ... and indicates that the 3Cl 1 mAb
recognized both the B2m-dependent and the B2m-independent
forms of CDl.
(Id. at 1716.)
5. Citing to Zeng (id. at 1717 (citation 33)), Amano also discloses:
The T cell recognition of CD 1 on the surface of B cells may play
an important role in the pathogenesis of systemic lupus. CD4 +
and CD8+ T cells expressing anti-CD 1 TCR trans genes ... will
induce lupus when transferred into syngeneic BALB/c nude
hosts (33). These mice develop anti-dsDNA Abs, proteinuria,
and ascites (33). Furthermore, the transgenic T cells can activate
[wild-type] BALB/c B cells via the cross-linking of surface CDl
to secrete both IgM and IgG in vitro (33). Thus, the interaction
between anti-CDl T cells and B cells expressing surface CDl
leads to a mutual activation of both cell types that results in
i.. 1 h 1" . r1 • • • • • _i_iypergammag_Louu_i1nem1a anu systemic auto1mmun1ty 1n vivo
(33). More recent studies have shown that the spontaneous
secretion in vitro of both IgM and IgG by spleen cells from lupus-
prone New Zealand Black/New Zealand White mice is mediated
by the CD 1 high subset of B cells.
(Id. at 1716.)
6. Zeng discloses that "some subsets of T cells (i.e., NKl .1 + T
cells) have been- reported to recognize the nonpolymorphic, class I MHC-
like molecule CD 1 ... , and other T cells can recognize sugar and/or lipid
antigens in the context of CD l" (Zeng 525).
7. Zeng also discloses:
In the current study, transgenic CD4+ and CD8+ cells that
recognize CD 1 on syngeneic B cells and activate them to secrete
immunoglobulins were tested for their capacity to induce lupus
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(Id.)
in irradiated syngeneic (BALB/c) nude hosts. These T cells were
obtained from the spleen of a line of transgenic BALB/c mice
that expressed the TCR-a and -B chain genes from an anti-CDl
BALB/c T cell clone .... The transgenic CD4+ and CD8+ T cells
induced lupus in the irradiated hosts, and the majority developed
severe immune complex glomerulonephritis and anti-ds DNA
antibodies. On the other hand, CD4-CD8- T cells from the bone
marrow (BM) of transgenic mice expressing the same TCR-a and
-B chain genes prevented lupus when coinjected with inducing T
cells. The ... T cells [that induced lupus] secreted large amounts
of IFN-y and little IL-4, whereas the preventive T cells secreted
large amounts of IL-4 and little IFN-y.
8. In addition, Zeng discloses that an "alternative pathway of T
cell-induced polyclonal activation of B cells and/or help for the secretion of
autoantibodies to nonprotein antigens (i.e., nucleotides, phospholipids, and
phosphodiesters) in lupus is via T cell recognition of the nonpolymorphic
MHC class I-like, CDl molecule" (id. at 532).
9. Somnay-Wadgaonkar discloses that "anti-CDld mAb, D5 and
51.1, have been described previously" and that the "3C 11 mAb (IgM) is a rat
anti-mouse CDld mAb that cross-reacts with human CDld" (Somnay-
Wadgaonkar 385).
Analysis
Claim 1 is directed to a method comprising administering to a human
SLE patient an effective dose of an antibody that specifically binds to CD 1 d
to reduce the level of anti-dsDNA IgG autoantibodies in the patient's serum.
As evidenced by the Specification, the Examiner finds that "[t]reatment with
anti-CD 1 monoclonal antibodies ... [inherently] reduces the level of serum
IgG and anti-ds-DNA IgG" (Ans. 9, citing Spec. ,-i 13 (Finding of Fact (FF)
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Application 12/762,091
1) ). Thus, we conclude that the issue is whether the applied references
suggest administering to a human SLE patient a dose of an antibody that
specifically binds to CD 1 d, wherein the dose would be effective to reduce
the level of anti-dsDNA IgG autoantibodies in the patient's serum, not
whether the references suggest that the administering would reduce the level
of anti-dsDNA IgG autoantibodies in the patient's serum. For at least this
reason, we are not persuaded by Appellants' various arguments that the
applied references do not suggest "a link ... between CD 1 stimulation and
the secretion of IgG isotype anti-dsDNA antibodies" (App. Br. 19). 8
Appellants also argue:
Amano and Zeng did not provide any indication as to whether T
cells that express an anti-CDl receptor were naturally in
circulation in SLE patients, and assuming they were, whether
such T cells interacted with B cells, and assuming they did,
whether such interaction produced immune tolerance or B cell
activation.
(Id.) The Examiner responded to this argument at pages 36-37 of the
Examiner's Answer. We conclude that Appellants have not adequately
explained why the Examiner's reasoning is incorrect.
8 We have reviewed the Declaration of Dr. Samuel Strober signed
October 24, 2012 (submitted November 6, 2012), which Appellants have
relied upon to support their position (see, for example, App. Br. 26).
However, for the same reason, we do not agree that the Examiner needs to
demonstrate that "the skilled artisan would ... have been motivated to
modify the cited references to achieve ... a reduction in the level of serum
IgG anti-DNA antibodies" or that "the skilled artisan would ... have had a
reasonable expectation of success in achieving a reduction in the level of
serum IgG anti-DNA antibodies" (Deel. ,-i 8).
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In addition, Appellants argue that "none of these references teach an
'effective dose' of an anti-CDl antibody- that is, none of these references
teaches what dose of such an antibody would be effective to reduce the
serum concentration of anti-dsDNA IgG antibodies" (App. Br. 22). We are
not persuaded.
In view of the above findings of facts (see, in particular, FF 5 & 8),
we conclude that the Examiner has set forth a prima facie case that it would
have been obvious to administer to a human SLE patient a dose of an
antibody that specifically binds to CDld. In addition, it would have been
obvious to use a dose that is effective to treat SLE. We conclude that the
evidence supports the conclusion that such a dose would have been effective
to reduce the serum concentration of anti-dsDNA IgG antibodies (FF 1 ). In
re Best, supra.
Appellants also argue that "Amano teaches away from the ... use of
antibodies to CD 1 that have no inhibitory effect on proliferation" (App.
Br. 39). In addition, Appellants argue that, "[ d]espite the fact that lB 1 had
been previously shown to have no effect on inhibiting T cell proliferation,
this antibody reduced the serum level of both IgM and IgG antibodies to
dsDNA in the mice" (id.). Appellants also argue that this is "surprising and
unexpected" (id.). We are not persuaded.
Even if we assume that the cited art teaches away from lBl,
Appellants have not adequately explained why it would not have been
obvious to use other anti-CD 1 d antibodies, such as 3C 11 (FF 2, 4, & 9),
which are also encompassed by claim 1. As a result, even if it is unexpected
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Application 12/762,091
that lBl reduces the serum level of both IgM and IgG antibodies to dsDNA
in mice, this is not commensurate with the scope of claim 1.
In addition, Appellants argue that "Zeng teaches away from the
invention as claimed" (App. Br. 40). In particular, Appellants argue: "Zeng
itself demonstrated that in some contexts, T cell interaction with CD 1 may
actually prevent SLE. In this respect, persons having ordinary skill in the art
would not have considered targeting/blocking CD 1 out of concern for
inhibiting the T cell interaction that produces a SLE-preventing effect." (Id.)
We are not persuaded.
The Examiner responded to this argument at page 54 of the
Examiner's Answer. We conclude that Appellants have not adequately
explained why the Examiner's reasoning is incorrect. Moreover, we note
that an "assertion of what seems to follow from common experience is just
attorney argument and not the kind of factual evidence that is required to
rebut a prima facie case of obviousness." In re Geisler, 116 F.3d 1465, 1470
(Fed. Cir. 1997).
For the same reasons, we are not persuaded by these arguments in the
context of claim 16.
Conclusion
The evidence supports the Examiner's conclusion that Amano, Zeng,
Somnay-W adgaonkar, and Hughes, as evidenced by admissions in the
specification, suggest the method of claim 1. We therefore affirm the
obviousness rejection of claim 1 over these references. Claims 6, 7, and 15
fall with claim 1.
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The evidence also supports the Examiner's conclusion that Amano,
Zeng, Somnay-W adgaonkar, Hughes, and the Merck Manual, as evidenced
by admissions in the specification, suggest the method claim 16. We
therefore affirm the obviousness rejection of claim 16 over these references.
II
In a second rejection of representative claim 1, the Examiner relies on
Porcelli for teaching "inhibiting CD I -mediated antigen presentation by a
CD 1 + APC in order to treat autoimmune disease, including in human
patients, by administering a CD 1 blocking agent, including a monoclonal
antibody (mAb) that binds to CDl," and "that CDld is a CDl gene product
that presents antigen to T cells" (Ans. 16-17). The Examiner relies on
Amano for teaching the deficiencies in Porcelli (id. at 17-19). The
Examiner concludes:
It would have been prima facie obvious to one of ordinary skill
in the art at the time the invention \'1/as made to have treated an
autoimmune disease with a CD 1 blocking agent, that is an anti-
CD l monoclonal antibody that blocks CDld/antigen complex-
TCR interaction and activation as taught by [Porcelli], wherein
the autoimmune disease being treated is SLE as taught by Amano
et al and wherein the anti-CDld antibody is 3Cl 1 or another
antibody with similar functionality.
(Id. at 19.)
The Examiner rejects representative claim 16 as obvious over Porcelli
in view of Amano, the Merck Manual, and Hughes (id. at 21). Appellants
do not separately argue the rejection of claim 16 (App. Br. 42-55). We will
therefore discuss these rejections together.
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Findings of Fact
10. Porcelli discloses that "[ fJive CD 1 genes have thus far been
identified in humans: CDla, CDlb, CDlc, CDld and CDle" (Porcelli 10:
19-20).
11. Porcelli also discloses: "The present invention is ... based on
the observation that CD I -mediated antigen presentation can serve as a basis
for the development of autoimmune disease. Based on this observation, the
present invention provides methods of and means for inhibiting CD I -
mediated antigen presentation by a CDl + APC." (Id. at 17: 15-19.)
12. In addition, Porcelli defines a "CDJ blocking agent" as a
"composition or compound which is capable of blocking the interaction of a
CDl-presented antigen with CDl, or of blocking the interaction between
CD 1 :antigen complexes and their cognate T cell receptors" and indicates
that "[b]locking agents include (1) agents which bind to CDl" (id. at 27: 22-
25).
13. Porcelli also discloses that "examples of blocking agents
include, but are not limited to, (1) polyclonal or monoclonal antibodies
which bind to and block the portion of a CD 1 molecule that binds a CD I -
presented antigen" (id. at 31: 27-29).
14. In addition, Porcelli discloses that "CD 1 blocking agents, [such
as an antibody which binds a CD 1 molecule and thus prevents the
interaction of the CD 1 molecule and a CD I-presented antigen,] are useful
for controlling undesired T cell-mediated immunity which occurs, e.g., in
autoimmune diseases" (id. at 51: 19 to 52: 6).
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Analysis
In view of the foregoing findings of fact, including the findings of fact
provided in section I above concerning Amano, we conclude that the
Examiner has set forth a prima facie case that Porcelli and Amano suggest
the method of claim 1.
Appellants argue, however, that Porcelli "does not teach or suggest
administering an antibody that specifically binds to CD 1 d in a human SLE
patient, and does not even suggest that the prophetic, non-specific antibodies
to CDl to which it refers could be useful for this purpose" (App. Br. 47).
We are not persuaded.
Porcelli discloses that "CD 1 blocking agents, [such as an antibody
which binds a CD 1 molecule and thus prevents the interaction of the CD 1
molecule and a CD I-presented antigen,] are useful for controlling undesired
T cell-mediated immunity which occurs, e.g., in autoimmune diseases"
(FF 14). Porcelli also discloses that "[fJive CDl genes have thus far been
identified in humans: CD la, CDl b, CDlc, CDld and CD le" (FF 10).
Porcelli does not specifically teach that the CD 1 blocking agent is a CD 1 d
antibody or that the autoimmune disease is SLE. However, Appellants do
not adequately explain why this would not have been obvious in view of
Amano (see, in particular, FF 2-5).
Appellants also argue that the "examiner has not identified where in
[Porcelli] as combined with Amano, the key limitation of a reduction in the
level of IgG isotype anti-dsDNA antibodies in the serum of the patient can
be found" (App. Br. 48). We are not persuaded.
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The Examiner does not find that Porcelli and Amano "teach that
administration of the anti-Cdld antibody will reduce the level of anti-
dsDNA IgG autoantibodies in the serum of a lupus patient" (Ans. 20).
Instead, the Examiner finds that the suggested method would necessarily
meet this recitation and places the burden on Appellants "to show an
unobvious distinction between the method of the instant invention and that
of the prior art" (id.). We conclude that the Examiner properly shifted the
evidentiary burden to Appellants and that Appellants have not met this
burden.
In addition, Appellants argue that "none of these references teaches
what dose of such an antibody would be effective to reduce the serum
concentration of anti-dsDNA IgG antibodies" (App. Br. 48). We are not
persuaded by this argument for the reasons discussed in section I above.
Appellants also argue that the Examiner's position "is devoid of a
motivation to combine and/or modify the cited art" (id. at 50). We are not
persuaded.
The Examiner concludes:
One of ordinary skill in the art at the time the invention was made
would have been motivated to do this in order to treat SLE,
particularly in light of the teaching of Amano et al that the
interaction between anti-CDld NK-T cells and B cells
expressing surface CD 1 d leads to a mutual activation of both cell
types that results in hypergammaglobulinemia and systemic
autoimmunity in vivo (in SLE).
(Ans. 19.) Appellants have not adequately explained why this position is in
error.
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In this regard, we acknowledge Appellants' argument:
"[T]reatment of SLE" represents a gross oversimplification of
the invention. The invention relates to a specific kind of SLE
treatment- a reduction ofigG isotype anti-dsDNA antibodies in
the serum. The question is not whether a person having ordinary
skill in the art would have been motivated to treat SLE, but
whether a person having ordinary skill in the art would have been
motivated to administer an anti-CD 1 antibody for purposes of
reducing IgG isotype anti-dsDNA antibodies in the serum ofSLE
patients in view of the teachings of [Porcelli] and Amano.
(App. Br. 51.) However, in view of how we are interpreting claim 1, as
discussed in section I above, we do not agree.
In addition, Appellants argue that "persons having ordinary skill in the
art would not have reasonably expected that blocking CD 1 would have had
any effect on the serum level of IgG anti-DNA antibodies" (id. at 54). We
are not persuaded.
As noted above, the Examiner does not find that Porcelli and Amano
"teach that administration of the anti-Cdld antibody will reduce the level of
anti-dsDNA IgG autoantibodies in the serum of a lupus patient" (Ans. 20).
Instead, the Examiner finds that this is an inherent effect of administering
the antibody to treat SLE (id.). Thus, we do not agree with Appellants that it
is necessary to demonstrate that there would have been a reasonable
expectation of success that the treatment would have inherently reduced the
serum level of IgG anti-DNA antibodies.
For the same reasons, we are not persuaded by these arguments in the
context of claim 16.
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Conclusion
The evidence supports the Examiner's conclusion that Porcelli and
Amano suggest the method of claim 1. We therefore affirm the obviousness
rejection of claim 1 over these references. Claims 6 and 15 fall with claim 1.
The evidence also supports the Examiner's conclusion that Porcelli,
Amano, the Merck Manual, and Hughes suggest the method claim 16. We
therefore affirm the obviousness rejection of claim 16 over these references.
Claim 7 falls with claim 16.
TIME PERIOD FOR RESPONSE
No time period for taking any subsequent action in connection with
this appeal may be extended under 37 C.F.R. § l.136(a).
AFFIRMED
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