Atul J. Butte et al.

Patent Trials and Appeals Board

Jan 2, 2020

13575904 - (D) (P.T.A.B. Jan. 2, 2020)

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.
13/575,904 11/30/2012 Atul J. Butte STAN-669 1001
77974 7590 01/02/2020
STANFORD UNIVERSITY OFFICE OF TECHNOLOGY LICENSING
BOZICEVIC, FIELD & FRANCIS LLP
201 REDWOOD SHORES PARKWAY
SUITE 200
REDWOOD CITY, CA 94065
EXAMINER
GAMBEL, PHILLIP
ART UNIT PAPER NUMBER
1644
NOTIFICATION DATE DELIVERY MODE
01/02/2020 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 ATUL J. BUTTE and KEIICHI KODAMA1
Appeal 2018-004007
Application 13/575,904
Technology Center 1600

Before ERIC B. GRIMES, RYAN H. FLAX, and
CYNTHIA M. HARDMAN, Administrative Patent Judges.

GRIMES, Administrative Patent Judge.

DECISION ON APPEAL
This is an appeal under 35 U.S.C. § 134(a) involving claims to
methods of reducing insulin resistance, which have been rejected as obvious
and lacking adequate written description. We have jurisdiction under
35 U.S.C. § 6(b).
We AFFIRM the rejection for inadequate written description.
STATEMENT OF THE CASE
The Specification discloses that “polymorphisms in the CD44 locus
and the CD44 ligand (SPP1, osteopontin) . . . are predictive of a

1 Appellant identifies the real party in interest as the Board of Trustees of the
Leland Stanford Junior University. Appeal Br. 2. We use the word Appellant
to refer to “applicant” as defined in 37 C.F.R. § 1.42(a).
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susceptibility in an individual to development of type 2 diabetes. Serum
levels of CD44 are also diagnostic of insulin resistance.” Spec. ¶ 8.
“Methods of treatment target the product of these genes, particularly
targeting CD44 and/or osteopontin.” Id.
Claims 1, 2, 4, 5, and 30–32 are on appeal. Claims 1 and 30,
reproduced below, are illustrative:
1. A method of reducing insulin resistance in an
individual having Type 2 diabetes, the method comprising:
administering to said individual an effective dose of an
antibody that inhibits CD44.

30. A method of reducing insulin resistance in an insulin
resistant human subject, the method comprising:
administering to said subject an antibody that binds to an
extracellular domain of a CD44 splice variant expressed on
adipose tissue macrophages, and which antibody blocks
interaction between CD44 and a CD44 ligand, in a dose
effective to improve glucose homeostasis in said subject.

The claims stand rejected as follows:
Claims 1, 2, 4, 5, and 30–32 under 35 U.S.C. § 112, first paragraph,
for lack of adequate written description in the Specification (Final Action2
3), and

2 Office Action mailed March 7, 2017.
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Claims 1, 2, 4, 5, and 30–32 under 35 U.S.C. § 103(a) as obvious
based on Naor,3 Hentsch,4 Chabas,5 Bingham,6 Kiefer,7 Schultz,8 and
Tracey9 (Final Action 8).
OPINION
Written Description
The Examiner finds that “the instant specification does not describe
any particular anti-CD44 antibody, including any particular anti-CD44
antibody having the claimed properties.” Final Action 4. According to the
Examiner, the “specification does not provide a single particular anti-CD44
antibody having the specificity and the functional properties argued by
applicant and disclosed in the specification and recited / encompassed by the
claimed methods, including sufficient species representing” the antibodies
recited in the claims. Id. at 5.
The Examiner also finds that the “specification discloses that the anti-
CD44 antibody has certain specificities (a splice variant, exon 3 of CD44,
extracellular domain of CD44) and certain functional properties (inhibits
ligand binding activity, etc.) (see paragraphs [0054]-[0055]) in order to carry

3 US 2006/0019340 A1 (publ. Jan. 26, 2006).
4 EP 1 647 556 A1 (publ. Apr. 19, 2006).
5 US 2005/0119204 A1 (publ. June 2, 2005).
6 US 2011/0008328 A1 (publ. Jan. 13, 2011).
7 Kiefer et al., Osteopontin deficiency prevents obesity-associated hepatic
steatosis and insulin resistance, Diabetologia 52:S33, abstr. no. 65 (2009).
8 Schultz et al., Expression levels and functional aspects of the hyaluronan
receptor CD44: Effects of insulin, glucose, IGF-I, or growth hormone on
human arterial smooth muscle cells, Metabolism Clinical and Experimental
54:287–295 (2005).
9 US 2003/0212104 A1 (publ. Nov. 13, 2003).
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out the claimed methods,” but “the specification as filed does not provide the
correlation between structure and function of anti-CD44 antibodies.” Id. at 4.
The Examiner concludes that
the instant application has not provided a sufficient
description showing possession of the necessary functional
characteristics coupled with a known or disclosed correlation
between function and structure, or by a combination of such
identifying characteristics, sufficient to show the applicant was
in possession of the genus of anti-CD44 antibodies . . .
encompassed by the claimed invention.
Id. at 6.
We agree with the Examiner that the claims are not supported by a
description that satisfies 35 U.S.C. § 112, first paragraph. “[T]he test for
sufficiency [of the written description] is whether the disclosure of the
application relied upon reasonably conveys to those skilled in the art that the
inventor had possession of the claimed subject matter as of the filing date.”
Ariad Pharms., Inc. v. Eli Lilly & Co., 598 F.3d 1336, 1351 (Fed. Cir. 2010)
(en banc).
A “sufficient description of a genus . . . requires the disclosure of
either a representative number of species falling within the scope of the
genus or structural features common to the members of the genus so that one
of skill in the art can ‘visualize or recognize’ the members of the genus.” Id.
at 1350. “[A]n adequate written description requires a precise definition,
such as by structure, formula, chemical name, physical properties, or other
properties, of species falling within the genus sufficient to distinguish the
genus from other materials.” Id.
“[F]unctional claim language can meet the written description
requirement when the art has established a correlation between structure and
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function.” Id. “But merely drawing a fence around the outer limits of a
purported genus is not an adequate substitute for describing a variety of
materials constituting the genus and showing that one has invented a genus
and not just a species.” Id.
The written description standard set out in Ariad applies to antibodies.
See Amgen, Inc. v. Sanofi, 872 F.3d 1367, 1376–79 (Fed. Cir. 2017)
(applying the Ariad standard to antibodies claimed based on their binding
and blocking activities); AbbVie Deutschland GmbH & Co. v. Janssen
Biotech, Inc., 759 F.3d 1285, 1298–1300 (Fed. Cir. 2014) (same).
The claims here are directed to methods of using antibodies, rather
than the antibodies themselves, but the same standard applies with regard to
the written description requirement. See University of Rochester v. G.D.
Searle & Co., 358 F.3d 916, 926 (Fed. Cir. 2004):
Regardless whether a compound is claimed per se or a method
is claimed that entails the use of the compound, the inventor
cannot lay claim to that subject matter unless he can provide a
description of the compound sufficient to distinguish infringing
compounds from non-infringing compounds, or infringing
methods from non-infringing methods.
In University of Rochester, the “claimed method depend[ed] upon
finding a compound that selectively inhibits PGHS-2 activity. Without such
a compound, it is impossible to practice the claimed method of treatment.”
Id. (citation omitted). Similarly here, the claimed methods cannot be
practiced without antibodies having the inhibiting or blocking activities
recited in the claims. Appellant’s argument that the claims are adequately
described because they are directed to a method, not a composition of matter
(Appeal Br. 7), is therefore unpersuasive.
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The instant Specification does not describe any specific antibodies
that are suitable for use in the claimed methods. The Specification states that
one aspect of the invention is “prevention or treatment of type 2 diabetes, by
administering to an individual an inhibitor of CD44 activity. . . . Such
inhibitors include, without limitation, antibodies, nucleic acid inhibitors . . . ;
inhibitory osteopontin peptides, small molecules inhibitors, and the like.”
Spec. ¶ 9; see also id. ¶ 56 (“Representative CD44 inhibitory agents include,
but are not limited to: antisense oligonucleotides; antibodies;” etc.).
Because the Specification fails to describe any single antibody having
any of the functions recited in the claims, it necessarily fails to describe a
representative number of species within the claimed genera. In addition, the
Specification fails to describe structural features common to members of the
genus that would allow a skilled artisan to distinguish antibodies
encompassed by the claim language from other antibodies. Finally, the
Specification fails to disclose any correlation between the structure and
function of the antibodies encompassed by the claim language. Therefore,
the Specification fails to describe the antibodies required to practice the
claimed method in a manner that reasonably conveys to those skilled in the
art that Appellant was in possession of the claimed method as of the filing
date of the instant application.
Appellant argues that “[t]he present invention is based on
Appellant[’]s surprising finding that CD44 and osteopontin were associated
with insulin resistance in a screen of human genome sequences.” Appeal Br.
6. Appellant argues that the Specification shows that “a knock-out of the
CD44 gene in an animal model for diabetes prone mice was able to improve
insulin resistance and glucose homeostasis in these animals.” Id.
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This argument is unpersuasive, because the claimed methods require
using antibodies that have specific functional properties. Even if the
Specification shows that reducing CD44 activity improves insulin resistance,
the claims require using antibodies having specific properties, and the
Specification does not describe those antibodies in the manner required by
35 U.S.C. § 112, first paragraph.
Appellant also points to a post-filing publication10 as evidence that
“administering daily injections of anti-CD44 monoclonal antibody (mAb) in
a high-fat-diet mouse model . . . reduced fasting blood glucose levels, weight
gain, liver steatosis, and insulin resistance to levels comparable to or better
than therapy with the drugs metformin and pioglitazone.” Appeal Br. 6.
This argument is also unpersuasive. It is unclear which, if any, of the
functional limitations in the claims are purportedly met by the antibody
described in the post-filing reference but, in any event, written descriptive
support depends on “whether the disclosure of the application relied upon
reasonably conveys to those skilled in the art that the inventor had
possession of the claimed subject matter as of the filing date.” Ariad, 598
F.3d at 1351 (emphasis added). Appellant’s post-filing evidence does not
make up for the Specification’s deficiency.
Appellant argues that “many antibodies that bind to human CD44 are
known in the art and commercially available, as evidenced by Exhibit C.”
Appeal Br. 6. Exhibit C is said to “provide[] an example of commercially
available monoclonal antibodies reactive with human CD44, from one

10 Kodama et al., Anti-CD44 Antibody Treatment Lowers Hyperglycemia
and Improves Insulin Resistance, Adipose Inflammation, and Hepatic
Steatosis in Diet-Induced Obese Mice, Diabetes 64:867–875 (2015).
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supplier, Novus Biologicals. 36 antibodies are available from this single
supplier.” Id. at 4.
However, Exhibit C lacks any indicia that would indicate that the
listed antibodies were commercially available at the time the instant
application was filed. In addition, Appellant has not provided evidence that
the listed antibodies have the specific inhibiting or blocking properties
required by the claims. This argument is therefore unpersuasive.
Finally, Appellant argues that
[p]roperties of antibodies and methods of generating antibodies
are described in the specification at paragraphs 66–73.
Paragraph 74 further provides guidance for one of skill in the
art to test candidate antibodies for the desired activity. Further,
at paragraphs 130–133, assays are provided that allow one of
skill in the art to screen available antibodies and determine
which are suitable for use in the methods of the invention.
Appeal Br. 6–7.
This argument is unpersuasive. “[T]o satisfy the statutory requirement
of a description of the invention, it is not enough for the specification to
show how to make and use the invention, i.e., to enable it.” Amgen v. Sanofi,
872 F.3d at 1377; see also University of Rochester, 358 F.3d at 927 (the
patent at issue described assays for screening compounds for those having
the desired activity, but without disclosure of which compounds had that
activity, the claimed method had not been described); AbbVie, 759 F.3d at
1300 (“One needs to show that one has truly invented the genus, i.e., that
one has conceived and described sufficient representative species
encompassing the breadth of the genus. Otherwise, one has only a research
plan.”).
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In summary, we affirm the rejection of claims 1 and 30 under 35
U.S.C. § 112, first paragraph, for lack of adequate written description.
Claims 2, 4, 5, 31, and 32 fall with claims 1 and 30. 37 C.F.R.
§ 41.37(c)(1)(iv) (2016).
Obviousness
Claims 1, 2, 4, 5, and 30–32 stand rejected as obvious based on Naor,
Hentsch, Chabas, Bingham, Kiefer, Schultz, and Tracey. Final Action 8. The
Examiner finds that Naor teaches “the applicability of anti-CD44 antibodies
and antigen binding fragments . . . to treat a variety of inflammatory
conditions . . . including diabetes.” Id. at 11. The Examiner notes that Naor
“differs from the claimed methods by not describing treating type 2 diabetes
per se with anti-CD44 antibodies and that osteopontin as [sic] another ligand
of CD44.” Id.
The Examiner finds that Hentsch teaches “inhibiting signals via CD44
for the treatment of hyperproliferative disorders, including insulin dependent
diabetes and non-insulin dependent diabetes (i.e., type 2 diabetes).” Id. The
Examiner finds that Chabas teaches “methods of treating various disorders
including diabetes / insulin-dependent diabetes . . . with various inhibitors of
osteopontin-mediated binding and activity . . . and notes that CD44 was a
known ligand for osteopontin as well as the blocking via CD44 binding.” Id.
at 13. The Examiner finds that Bingham teaches “the treatment of insulin-
resistance associated with obesity, aging and type 2 diabetes . . . with various
osteopontin inhibitors . . . and notes that osteopontin binds to CD44.” Id.
The Examiner finds that Kiefer teaches “the known role of
osteopontin . . . in the pathogenesis of obesity-induced insulin resistance,
which, in turn, could be a therapeutic approach to prevent obesity-associated
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metabolic disorders, including type 2 diabetes.” Id. at 14. The Examiner
finds that Schultz teaches “the functional consequences of accumulated
hyaluronan through binding to CD44 as a feature of diabetic
macroangiopathy, where CD44 and its isoform CD44v3 play a role in cell
response to metabolic and hormonal disorders of diabetes.” Id. The
Examiner finds that Tracey “teach[es] that treating Type 2 diabetes is
associated with various conditions and manifestations, including diabetic
macroangiopathy and insulin resistance syndrome.” Id.
The Examiner concludes that it would have been obvious “to provide
CD44 antagonists . . . for the treatment of various diseases / disorders
including type 2 diabetes / non-insulin-dependent diabetes with anti-CD44
antibodies, given the teachings of the prior art to target CD44 as well as
osteopontin binding . . . to treat various diseases / orders [sic] including type
2 diabetes.” Id. at 15. The Examiner reasoned that a skilled artisan would
have “administer[ed] CD44 antagonists such as anti-CD44 antibodies . . .
with an expectation of success, since such properties and advantages are
consistent with human therapeutic regimens associated with treating said
conditions.” Id.
Appellant argues that Naor does not teach using anti-CD44 antibodies
for “the treatment of Type 2 diabetes, which is a condition distinct from the
inflammation and autoimmune responses associated with Type 1 diabetes.”
Appeal Br. 8. Appellant argues that Hentsch discloses providing “short
peptide motifs referred to as CD44v6 peptides, which have the activity of
inhibiting complex formation between Met, hepatocyte growth factor and
CD44” and provides no reason to “believe that such peptides or CD44
variant are involved in Type 2 diabetes.” Id. at 10. Appellant notes that
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Hentsch discloses non-insulin dependent diabetes as one of a “laundry list”
of diseases to be treated, but argues that Hentsch “does not provide any
evidence of a common mechanism in the extensive list of disorders” that
would lead a skilled artisan to expect that inhibiting CD44 would reduce
insulin resistance. Id. at 12.
Appellant argues that Chabas discloses a method of inducing an
immune response in order to inhibit osteopontin, and that Bingham “fails to
teach the use of antibodies to CD44 in the reduction of insulin resistance in a
patient with Type 2 diabetes.” Id. at 13–14. Appellant argues:
While osteopontin is a ligand for CD44, both of osteopontin
and CD44 interact with numerous other molecules including a
number of integrins. One of skill in the art would have not have
a reasonable expectation that inhibition of osteopontin, and
inhibition of CD44, would lead to any similarity of biological
results.
Id. at 14.
Finally, Appellant argues that Schultz “relates to effects of insulin and
glucose on the behavior of human arterial smooth muscle cells, which cells
may be effected by diabetes, but which cells do not have a causative role in
insulin resistance”; that Tracey “relates to an entirely unrelated pathway, a
sodium-hydrogen exchanger type 1 (NHE-1) inhibitor, for treatment of
[certain] disorders”; and that, while Kiefer “is cited for teaching a role for
osteopontin in obesity-associated metabolic disorders,” and “osteopontin is
known to be one ligand of CD44, each of these proteins interacts with
numerous other ligands.” Id. at 15–16.
Appellant concludes that “the combined references fail to provide any
motivation or specific teaching that would lead one of skill in the art to treat
reduce insulin resistance in an individual having Type 2 diabetes by
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administering to the individual an effective dose of an antibody that inhibits
CD44.” Id. at 16.
We agree with Appellant that the Examiner has not shown that the
claimed method would have been prima facie obvious to a person of
ordinary skill in the art based on the cited references. “In rejecting claims
under 35 U.S.C. § 103, the examiner bears the initial burden of presenting a
prima facie case of obviousness.” In re Rijckaert, 9 F.3d 1531, 1532 (Fed.
Cir. 1993). “[O]bviousness requires . . . showing that a person of ordinary
skill at the time of the invention would have selected and combined th[e]
prior art elements in the normal course of research and development to yield
the claimed invention.” Unigene Labs., Inc. v. Apotex, Inc., 655 F.3d 1352,
1360 (Fed. Cir. 2011).
Naor states that its invention relates to, among other things,
“antibodies specific for [a] novel CD44 polypeptide variant, . . . and the use
of these antibodies . . . in the diagnosis and treatment of inflammatory
diseases such as rheumatoid arthritis.” Naor ¶ 3. Naor states that CD44 and
variants thereof are known to be involved in autoimmune diseases, and that
monoclonal antibodies against various variant CD44 regions have been
suggested as treatments of autoimmune diseases. Id. ¶¶ 17–18. Naor
suggests using antibodies against its CD44 variant (CD44vRA) to treat
Type 1 diabetes (id. ¶¶ 207–213). However, as the Examiner concedes (Final
Action 11), Naor does not describe treating Type 2 diabetes per se with anti-
CD44 antibodies, and the Examiner has not pointed to any description of
treating insulin resistance.
Hentsch discloses “short peptide motifs, derived from the CD44 v6
region, which are capable of interfering with HGF [hepatocyte growth
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factor] signaling via inhibition of the formation of the trimeric complex
made up by c-Met, HGF and CD44.” Hentsch ¶ 3. Hentsch states that each
of these proteins has been associated with tumor metastasis (id. ¶ 2), and
inhibiting their interaction “might be therapeutically useful for . . .
hyperproliferative diseases like cancer or diseases associated with invasive
processes of cells.” Id. ¶ 3.
Hentsch also suggests
the formation of complexes of CD44 involving other growth
factor recetors [sic], such as, but not limited to, FGFR, PDGFR,
ErbB2, EGFR, Osteopontin, and integrins, followed by a CD44
mediated signaling of these growth factor receptors, so that an
inhibition of the formation of such complexes might be
therapeutically benefical [sic] in diseases in which the
formation of such complexes contributes to the disease onset,
manifestation or progression.
Id. ¶ 55. Hentsch states that such diseases include “insulin dependent
diabetes mellitus, non-insulin dependent diabetes [aka Type 2 diabetes].” Id.
Chabas discloses a method of treating “a disorder in which expression
of osteopontin contributes to the pathogenesis,” including autoimmune
diseases like Type 1 diabetes, by inducing an immune response that reduces
the level of osteopontin in the patient. Chabas ¶ 13. Similarly, Bingham
discloses “a method of controlling glucose uptake and/or insulin sensitivity
by administration of an inhibitor to OPN [osteopontin].” Bingham ¶ 7.
Kiefer likewise relates to targeting osteopontin, not CD44, as a potential
treatment for type 2 diabetes. Kiefer, abstract.
However, the Examiner has not pointed to any disclosure in Chabas,
Bingham, or Kiefer of inhibiting CD44, as required by the claims. The
evidence supports Appellant’s position that osteopontin and CD44 both bind
to proteins other than each other. See Bingham ¶ 5 (“OPN binds to integrins
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and CD44”); Hentsch ¶ 55 (“complexes of CD44 involving . . . FGFR,
PDGFR, ErbB2, EGFR, Osteopontin, and integrins”). The Examiner has not
persuasively explained why a skilled artisan would have been led to
administer a CD44-inhibiting antibody based on the disclosure of inhibiting
osteopontin in Chabas, Bingham, or Kiefer.
Schultz “investigate[d] the relationship between some of the
components in the metabolic disorders of diabetes and the CD44 quantity
and function on human[] arterial SMCs [smooth muscle cells].” Schultz 288,
left col. Schultz states that its data “support a role of CD44 and its isoform,
CD44v3, in the SMC response to the metabolic and hormonal disorders of
diabetes.” Id. at 287, abstract. The Examiner has not explained how
Schultz’s finding, that CD44 has an effect on arterial smooth muscle cells in
diabetic patients, would have suggested inhibiting CD44 to treat Type 2
diabetes or insulin resistance.
Finally, Tracey discloses “methods of treating or preventing type 2
diabetes, . . . and/or insulin resistance syndrome (IRS) in mammals,
particularly in humans.” Tracey ¶ 2. However, Tracey’s method
“administer[s] a sodium-hydrogen exchanger type 1 (NHE-1) inhibitor.” Id.
The Examiner has not explained why Tracey’s treatment would have
provided a reason to administer an anti-CD44 antibody to treat insulin
resistance or Type 2 diabetes.
In summary, the disclosure in the cited references that is most relevant
to the claimed invention is Hentsch’s suggestion that formation of
complexes of CD44 and receptors such as FGFR, PDGFR, ErbB2, EGFR,
osteopontin, or integrins “might be therapeutically benefical [sic] in diseases
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in which the formation of such complexes contributes to the disease onset,
manifestation or progression.” Hentsch ¶ 55.
In our view, however, Hentsch’s disclosure would not have suggested
the claimed method without the benefit of hindsight. Hentsch does not
suggest inhibiting CD44 complex formation using any compounds other
than short peptide motifs derived from CD44 itself, rather than by using an
anti-CD44 antibody, as required by the claims. Nor has the Examiner
articulated any basis for extrapolating the effect of Hentsch’s complex-
inhibiting peptides to an effective treatment of Type 2 diabetes via an
antibody that inhibits CD44. Thus, although Hentsch includes “non-insulin
dependent diabetes” as one of the many diseases in which “inhibition of the
formation of such [CD44-containing] complexes might be therapeutically
benefical [sic],” we conclude that a skilled artisan would not have been led
to modify Hentsch’s method by using an anti-CD44 antibody instead of
Hentsch’s peptides, without the benefit of hindsight gleaned from
Appellant’s Specification.
We therefore conclude that the cited references do not support a prima
facie case of obviousness, and reverse the rejection of claims 1, 2, 4, 5, and
30–32 under 35 U.S.C. § 103(a) based on Naor, Hentsch, Chabas, Bingham,
Kiefer, Schultz, and Tracey.
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DECISION SUMMARY
In summary:
Claims
Rejected
35 U.S.C. § Reference(s)/Basis  Affirmed Reversed
1, 2, 4, 5,
30–32
112, first
paragraph
Written Description 1, 2, 4, 5,
30–32

1, 2, 4, 5,
30–32
103(a) Naor, Hentsch,
Chabas, Bingham,
Kiefer, Schultz, Tracey
1, 2, 4, 5,
30–32
Overall
Outcome
1, 2, 4, 5,
30–32

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. § 1.136(a). See 37 C.F.R.
§ 1.136(a)(1)(iv).
AFFIRMED