Ex Parte Prochiantz et al

Patent Trial and Appeal Board

Aug 21, 2018

12812139 (P.T.A.B. Aug. 21, 2018)

UNITED STA TES p A TENT AND TRADEMARK OFFICE
APPLICATION NO. FILING DATE
12/812,139 11/17/2010
9629 7590 08/23/2018
MORGAN LEWIS & BOCKIUS LLP (WA)
1111 PENNSYLVANIA A VENUE NW
WASHINGTON, DC 20004
FIRST NAMED INVENTOR
Alain Prochiantz
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.
045636-5143 4490
EXAMINER
WANG, CHANG YU
ART UNIT PAPER NUMBER
1649
NOTIFICATION DATE DELIVERY MODE
08/23/2018 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):
patents@morganlewis.com
karen.catalano@morganlewis.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte ALAIN PROCHIANTZ and
LEE MOYA KENNETH 1
Appeal2017-009072
Application 12/812,139
Technology Center 1600
Before RICHARD M. LEBOVITZ, JOHN G. NEW, and
RICHARD J. SMITH, Administrative Patent Judges.
NEW, Administrative Patent Judge.
DECISION ON APPEAL
1 Appellants state that the real parties-in-interest are the Centre National de
la Recherche Scientifique and the Ecole Normale Superieure. App. Br. 1.
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Application 12/812, 139
SUMMARY
Appellants file this appeal under 35 U.S.C. § I34(a) from the
Examiner's Final Rejection of claims 1-3, 8, and 10-13. Specifically,
claims 1, 2, 8, 11, and 12 stand rejected as unpatentable under 35 U.S.C.
§ I02(b) as being anticipated by or, in the alternative, under 35 U.S.C.
§ I03(a) as being obvious over, Furukawa (EP 1 591 127 Al, November 2,
2005) ("Furukawa '127"), or Furukawa (US 2006/0122111 Al, June 8,
2006) ("Furukawa '111 "), or Furukawa (US 7,858,346 B2, December 28,
2010) ("Furukawa '346"), as evidenced by Reh et al. (US 7,541,186 B2,
June 2, 2009) ("Reh"), E.M. Ullian et al., Invulnerability of Retinal
Ganglion Cells to NMDA Excitotoxicity, 26 MOL. CELL. NEUROSCI. 544--57
(2004) ("Ullian"), K.R. Kendell et al., Primary Open-Angle Glaucoma is not
Associated with Photoreceptor Loss, 36(1) INVEST. OPHTHALMOL. & VISUAL
SCI. 200-05 (1995) ("Kendell"), and D.M. Berson, Phototransduction in
Ganglion-Cell Photoreceptors, 454 EUR. J. PHYSIOL. 849-55 (2007)
("Berson").
Claims 1-3, 8, and 10-13 stand rejected as unpatentable under
35 U.S.C. § I03(a) as being obvious over Furukawa '127, Furukawa '111
Furukawa '346, Reh, Ullian, Kendell, and Berson.
Claims 1-3, 8, and 10-13 also stand provisionally rejected as
unpatentable under the nonstatutory doctrine of obviousness-type double
patenting.
We have jurisdiction under 35 U.S.C. § 6(b).
We AFFIRM.
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NATURE OF THE CLAIMED INVENTION
Appellants' invention is directed to a method for improving the
survival of ganglionic neurons, comprising bringing a homeoprotein of the
Otx subfamily, and in particular an Otx2 homeoprotein, or a composition
comprising said homeoprotein, into contact with said ganglionic neurons.
Spec. 4.
REPRESENTATIVE CLAIM
Claim 1 is representative of the claims on appeal and recites:
1. A method of reducing excitotoxicity-induced retinal
ganglion neuron degeneration in a subject in need thereof,
comprising administering to said subject a functional
orthodenticle homolog 2 (Otx2) homeoprotein having a
polypeptide sequence at least 90% identical to SEQ ID NO: 1 or
SEQ ID NO: 2 in an amount sufficient to reduce the
excitotoxicity-induced retinal ganglion neuron degeneration,
wherein the subject does not exhibit photoreceptor neuron
degeneration, and
the functional Otx2 homeoprotein has a homeodomain
having at least 98% sequence identity with residues 3 8-97 of
SEQIDNO: 1.
App. Br. 15.
ISSUES AND ANALYSES
We are persuaded by, and expressly adopt, the Examiner's findings
and conclusions establishing that Appellants' claims are prima facie
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anticipated by, or obvious over, the combined cited prior art. We address
the arguments raised by Appellants below.
A. Claims 1, 2, 8, 11, and 12 under 35 U.S.C. §§ 102(b) and 103(a)
Issue 1
Appellants argue that the Examiner erred because the cited references
fail to disclose the limitation of claim 1 reciting: "wherein the subject does
not exhibit photoreceptor neuron degeneration." App. Br. 5.
Analysis
Appellants argue that, in making the rejections, the Examiner found
that each of the Furukawa references suggests a method of treating
glaucoma, and that glaucoma is a condition due to cell death of retinal
ganglion cells. App. Br. 5 ( citing Interview Summary 5-6, June 1, 2016).
According to Appellants, the Examiner concluded that, regardless of what
molecular mechanisms are involved in glaucoma, Furukawa teaches a
patient population (i.e., glaucoma) identical to the claimed population. Id.
Appellants dispute the Examiner's findings and conclusions, asserting
that the glaucoma patients disclosed in the Furukawa references are not
identical to the recited population that does not exhibit photoreceptor neuron
degeneration as required claim 1. App. Br. 5---6. Appellants assert that the
genus of glaucoma patients disclosed in Furukawa does not disclose the
species of glaucoma patient that does not exhibit photoreceptor neuron
degeneration. Id. at 6.
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Appellants assert that different types of glaucoma patients include
glaucoma patients exhibiting photoreceptor neuron degeneration. App. Br.
6. In support of this assertion, Appellants cite I.M. Velten et al., The A-
Wave of the Dark Adapted Electroretinogram in Glaucomas: Are
Photoreceptors Affected?, 85 BR. J. 0PHTHALMOL. 397--402 (2001)
("Velten"), and P. Janssen et al., Evidence for glaucoma-induced horizontal
cell alterations in the human retina, 5 GER. J. OPHTHALMOL. 378-85 (1996)
("Janssen"). Id. Appellants argue that Velten teaches that photoreceptors
are involved in glaucomatous damage and that Janssen discloses that
photoreceptors are affected by advanced glaucoma. Id. ( citing Janssen
Abstr.).
Appellants dispute the Examiner's finding that Velten and Janssen are
not dispositive because the involvement of photoreceptor cells only occurs
in advanced glaucoma and that neither the Furukawa references nor the
claims on appeal recite advanced glaucoma. App. Br. 6 ( citing Final Act. 6).
Appellants assert that the Examiner's finding is, in this respect, irrelevant in
determining the genus or species of the recited subject. Id. Appellants argue
that, in evaluating whether Furukawa references disclose the recited subject
that does not exhibit photoreceptor neuron degeneration, it is irrelevant
whether the present claims recite advanced glaucoma. Id. Furthermore,
Appellants argue, even assuming, arguendo, that the photoreceptor neuron
degeneration of Velten and Janssen are related only to advanced glaucoma
as alleged by the Examiner, these references still support that there is a
subset of glaucoma ( e.g., advanced glaucoma) that exhibits photoreceptor
neuron degeneration. Id. Therefore, Appellants argue, there are at least two
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species of glaucoma, one that exhibits photoreceptor neuron degeneration,
and the other that does not exhibit photoreceptor neuron degeneration. Id.
Appellants argue, without citing support, that a genus does not always
anticipate a claim to a species within the genus. App. Br. 6. Appellants
acknowledge that when a species is expressly named in a reference, the
species claim is anticipated no matter how many other species are
additionally named. Id. ( citing Ex parte A, 17 USPQ2d 1716 (BP AI 1990);
see also MPEP § 213I.02(II)). However, argue Appellants, in this case,
none of the cited references disclose the species of glaucoma patient that
does not exhibit photoreceptor neuron degeneration. Id. Therefore,
Appellants contend, the genus of glaucoma patients disclosed in the
Furukawa references does not anticipate the claims reciting the subject that
does not exhibit photoreceptor neuron degeneration. Id.
We are not persuaded by Appellants' arguments. Appellants do not
dispute the Examiner's finding that the Furukawa references disclose the
genus of subjects with glaucoma. See, e.g., Furukawa '127 ,r,r 6, 54--55;
Furukawa' 111 ,r,r 31, 82-83, 124; Furukawa '346 col. 3, 11. 40-50, col. 16,
11. 4--12. However, Appellants contend the Furukawa references do not
disclose the species within that genus consisting of subjects who do not
exhibit photoreceptor neuron degeneration.
We disagree. "[W]hether a generic disclosure necessarily anticipates
everything within the genus ... depends on the factual aspects of the specific
disclosure and the particular products at issue." Sanofi-Synthelabo v.
Apotex, Inc., 550 F.3d 1075, 1083 (Fed. Cir. 2008); see also Osram Sylvania
Inc. v. American Induction Tech. Inc., 701 F.3d 698, 706 (Fed. Cir. 2012)
("[H]ow one of ordinary skill in the art would understand the relative size of
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a genus or species in a particular technology is of critical importance"); see
also MPEP § 2131.02(III). The Examiner cites Kendell as demonstrating
that it was well known in the art that primary open-angle glaucoma is the
most common type of glaucoma in humans and is not associated with
photoreceptor loss. See Ans. 18 (citing Kendell 200,203, table 2; see also
The Glaucoma Foundation, Primary Open-Angle Glaucoma (POAG),
available at: http://www.glaucomafoundation.org/primary_open-
angle_glaucoma.htm (last visited August 3, 2018) ("Approximately one
percent of all Americans have this form of glaucoma, making it the most
common form of glaucoma in our country"). Because this species of
glaucoma is the most common form of glaucoma and because it is not
associated with photoreceptor damage, we agree with the Examiner that a
person of ordinary skill in the art of diseases of the retina would understand
that the majority of the genus of subjects with primary glaucoma would
necessarily consist of a majority of subjects who do not exhibit
photoreceptor degeneration.
Furthermore, Appellants point to Janssen, which Appellants contend
teaches that photoreceptors are affected by advanced glaucoma. App. Br. 6
(citing Janssen Abstr.). Furukawa teaches that by administering the Otx2
homeoprotein in "retinal diseases such as retinitis pigmentosa, senile
macular degeneration, diabetic retinopathy, retinal detachment, glaucoma
and retinal vessel occlusion can be prevented or treated, or progression of
such disease can be suppressed." Furukawa' 127 ,r 6. In other words, a
person of ordinary skill in the art would have understood that treatment of
individuals with the most common type of glaucoma by the methods of
Furukawa can prevent individuals with no photoreceptor degeneration from
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progressing to advanced glaucoma, in which photoreceptors are adversely
affected.
We therefore agree with the Examiner that a person of ordinary skill
in the art would necessarily envisage that the genus of individuals with
glaucoma, as disclosed in the Furukawa references, includes the subjects
recited in the disputed limitation of claim 1.
Issue 2
Appellants argue the Examiner erred because the combination of the
cited references fails to teach or suggest all the claim elements of the
invention, either explicitly or inherently. App. Br. 7.
Analysis
Appellants argue that the Examiner relies upon Reh as demonstrating
what was known in the art at the time of invention, and that Reh teaches that
glaucoma is a condition arising from the death of retinal ganglion cells.
App. Br. 7.
Appellants argue that, with respect to Reh, even if glaucoma is due to
retinal ganglion cell death, the ganglion cells are in a different retinal layer
from the photoreceptor neurons. App. Br. 7. According to Appellants, the
Examiner's rejection is deficient because the "Examiner failed to establish
that a glaucoma patient population having the retinal ganglion cell death
would render obvious the recited subject that does not exhibit photoreceptor
neuron degeneration Id .. With respect to Kendell, Appellants argue that the
fact that the primary open-angle glaucoma, which has no photoreceptor
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neuron degeneration, is encompassed by glaucoma suggested in the cited
reference is not sufficient to support the outstanding rejections. Id. at 8.
We are not persuaded. The combination of Reh and Kendell, as
indicative of what was known in the art at the time of invention, teaches that
retinal ganglion cell degeneration is caused by glaucoma, and that the most
common form of glaucoma, primary open-angle glaucoma, does not involve
photoreceptor degeneration. However, Appellants admit that advance
glaucoma patients later show photoreceptor generation. Appeal Br. 6. Thus,
the skilled worker would had reason to administer Otx2 to patients prior to
experiencing photodegeneration to prevent and treat it. We are therefore not
persuaded by Appellants' argument.
Issue 3
Appellants argue further that the Examiner erred because a person of
ordinary skill in the art would have had no reasonable expectation of success
in practicing the methods disclosed by the Furukawa references ( and recited
in the claims) upon the species of subjects with glaucoma who do not exhibit
photoreceptor degeneration. App. Br. 9.
Analysis
Appellants argue that a person of ordinary skill in the art would have
no reasonable expectation of success in treating glaucoma patients disclosed
in Kendell which do not exhibit photoreceptor neuron degeneration by the
method disclosed by Furukawa, because the latter method acts to regenerate
photoreceptor cells. App. Br. 9. According to Appellants, Furukawa treats a
degenerative retinal disease by regenerating or newly producing a retinal
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photoreceptor cell, whereas the differentiation of retinal stem cells into other
retinal cells is suppressed. Id. (citing Furukawa '127 i-fi-f 91-92). Appellants
point to the Furukawa references' disclosure that: "[t]he present invention
relates to an agent for inducing differentiation into retinal photoreceptor
cells" and that: "the number of retinal photoreceptor cells was increased by
about 10% ... differentiation from a [ retinal] stem cell into a bipolar cell, an
amacrine cell and a Muller glia[l] cell was strongly suppressed, and almost
[all] of [the] retinal stem cells are differentiated into retinal photoreceptor
cells." Id. (quoting Furukawa '127 i-fi-f 91-92).
Appellants assert that the Examiner has acknowledged that
Furukawa's development of more photoreceptor cells from retinal
stem/progenitor cells has "nothing to do with a condition of [Kendell's]
glaucoma that is a condition due to the cell death of retinal ganglion cells."
App. Br. 10 (quoting Final Act. 10). Therefore, Appellants argue, a person
of ordinary skill in the art, understanding the disclosures of Furukawa,
would have concludes that Furukawa's method of regenerating or newly
producing retinal photoreceptor cells could not reasonable have been
expected to be successful in treating Kendell's patients without
photoreception neuron degeneration. Id.
The Examiner responds that, regardless of the mechanism of
pathogenesis of glaucoma, the active step and the material used in the
method (i.e., administering to said subject a Otx2 having a polypeptide
sequence at least 90% identical to SEQ ID NO: 1 or 2) and the patient
population (i.e., subjects with glaucoma) disclosed by the method of
Furukawa are identical to those in the claimed method. Ans. 26. Therefore,
the Examiner concludes, the Furukawa references anticipate the claimed
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invention or, alternatively, substantially overlap the limitations of the
claimed method and thus render the claimed invention obvious. Id.
As an initial matter, a "reasonable expectation of success" is irrelevant
to an anticipation analysis under 35 U.S.C. § 102. "For a claim to be
anticipated, each claim element must be disclosed, either expressly or
inherently, in a single prior art reference, and the claimed arrangement or
combination of those elements must also be disclosed, either expressly or
inherently, in that same prior art reference." Therasense, Inc. v. Becton,
Dickinson and Co., 593 F.3d 1325, 1332-33 (Fed. Cir. 2010). Appellants do
not dispute that the Furukawa references teach the steps of the method
recited in the claims, but rather dispute whether Furukawa's disclosure of
the genus of subjects with glaucoma includes the species of individuals
without photoreceptor degeneration. We have explained why we agree with
the Examiner that a person of ordinary skill in the art would recognize that
the genus disclosed by Furukawa also includes Appellants' recited species,
and why we are not persuaded by Appellants' arguments to the contrary.
We agree that Furukawa teaches that administration of Otx2 promotes
photoreceptor development from retinal stem cells. However, while,
Kendell teaches that individuals with primary glaucoma may not experience
photoreceptor degeneration, as admitted by Appellants, Janssen teaches that
individuals with advanced glaucoma experience photoreceptor degeneration.
App. Br. 6 (citing Janssen Abstr.). The Furukawa references teach that
treatment with Otx2 can prevent or treat, or stop the progression of such
glaucoma. Furukawa' 127 ,r 6. We therefore agree with the Examiner that a
person of ordinary skill would have understood that Otx2, administered to
individuals with primary glaucoma, who do not experience photoreceptor
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degeneration, can prevent or stop the progression of glaucoma to its
advanced form.
Issue 4
Appellants argue the Examiner erred because Furukawa teaches away
from administering a functional Otx2 homeoprotein to a subject that does
not exhibit photoreceptor neuron degeneration. App. Br. 10.
Analysis
Appellants argue that the Furukawa references teach that Otx2
regenerates retinal photoreceptor cells but prevents regeneration of other
retinal cells, such as the recited retinal ganglion neuron. App.Br. 10.
Appellants argue that the Examples disclosed by Furukawa teach that, by
expressing an Otx2 gene, almost all of retinal stem cells are differentiated
into retinal photoreceptor cells, whereas the differentiation of retinal stem
cell to other retinal cells is suppressed. Id. (citing Furukawa' 127 ,r,r 91-92).
Therefore, argue Appellants, a person of ordinary skill in the art,
apprehending the teachings of Furukawa, would have no reason to
administer the recited Otx2 homeoprotein to a subject that does not exhibit
photoreceptor neuron degeneration. Id.
We are not persuaded by Appellants' arguments. As an initial matter,
an argument that a reference "teaches away" is irrelevant to an anticipation
analysis under 35 U.S.C. §102. See Celeritas Techs., Ltd. v. Rockwell Int'!
Corp., 150 F.3d 1354, 1361 (Fed. Cir. 1998) ("A reference is no less
anticipatory if, after disclosing the invention, the reference then disparages
it. ... [T]he question whether a reference 'teaches away' from the invention
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isinapplicable to an anticipation analysis."). Even assuming, arguendo, that
the Furukawa references teach away from Appellants' claimed invention,
Appellants' argument is inapplicable if, as we conclude, the references
anticipate Appellants' claimed invention.
Nor are we persuaded, in the context of the obviousness rejection, that
Furukawa teaches away from Appellants' claimed invention. A teaching
away requires a reference to actually criticize, discredit, or otherwise
discourage the claimed solution, such that "a person of ordinary skill, upon
reading the reference, would be discouraged from following the path set out
in the reference, or would be led in a direction divergent from the path that
was taken by the applicant." In re Fulton, 391 F.3d 1195, 1201 (Fed. Cir.
2004) (quoting In re Gurley, 27 F.3d 551, 553 (Fed. Cir. 1994)). Appellants
point to no teaching in the Furukawa references that would directly
discourage or divert a person of ordinary skill.
To the contrary, Furukawa' 127 is directed to: "an agent for
preventing, treating or suppressing progression of retinal diseases of the
present invention can be particularly effectively used in congenital retinal
degenerative disease, retinitis pigmentosa, macular degeneration, diabetic
retinapathy, retinal detachment, glaucoma or retinal vessel occlusion."
Furukawa '127 i-f 55 (emphasis added). We acknowledge, as we have
explained supra, that the Furukawa references teach that Otx2 promotes the
development of retinal photoreceptors from retinal stem cells. But we
discern no teaching of Furukawa that would directly discourage or divert a
person of ordinary skill from using Otx2 to treat glaucoma, including those
in individuals with no photoreceptor degeneration. This is especially so
because Furukawa expressly teaches that Otx2 can be used in preventing the
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progression of congenital retinal disease. In other words, the skilled worker
knowing that advanced glaucoma can involve photoreceptor degeneration,
would have had reason to administer Otx2 prior to experiencing
photodegeneration to prevent and treat the disease progression that leads to
photoreceptor degeneration.
We consequently affirm the Examiner's rejection of the claims as
being anticipated and/or obvious.
B. Claims 1-3, 8, and 10-13 under 35 U.S.C. § 103(a)
Analysis
Appellants repeat their arguments presented in the preceding section
of this Decision. App. Br. 11.
Additionally, with respect to claims 3 and 8, which recite: "contacting
isolated retinal ganglion neurons with a functional orthodenticle homolog 2
(Otx2) homeoprotein," Appellants argue that Furukawa's teaching of
"photoreceptor cells or cells derived from eye ball tissue" do not include
retinal ganglion cells as recited in the claims. App. Br. 11. Appellants point
to Figure 3 of Furukawa '127, which, Appellants argue, depicts a frozen
section of retina showing that the retinal photoreceptor cells ("R"). Id.
Appellants state that such photoreceptor cells (i.e., rods and cones) are
positioned in the outer cell layer of the retina and that the term
"photoreceptor" as used by Furukawa does not include the recited retinal
ganglion neurons. Id.
Appellants also contend that Furukawa teaches that the eye-ball
tissue-derived cells can be, e.g., a fetal neural retina, a pigmented epithelial
cell or a retinal pigment epithelial cell, a corpus ciliare epithelial cell, and an
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iris cell, excluding any retinal ganglion neurons. App. Br. 12 ( citing
Furukawa '127 ,r 48).
We do not agree. Furukawa teaches: "expressing an Otx2 protein, or
increasing an amount of expression of an Otx2 protein in an eye ball tissue-
derived cell, an embryonic stem cell, a neural stem cell or a neural precursor
cell." Furukawa ,r 5. Furukawa subsequently teaches:
Preferable examples of the "eye ball tissue" include an inner
layer tissue of the optic cup. Such tissue may be derived from an
adult, or may be derived from an individual at an embryonic
stage. Examples of the "eye ball tissue-derived cell" include a
fetal neural retina, a corpus ciliare cell such as a corpus ciliare
pigment epithelial cell or a retinal pigment epithelial cell, a
corpus ciliare epithelial cell, and an iris cell.
Id. at ,r 48. Retinal ganglion cells are, as Appellants acknowledge,
undeniably eye ball tissue-derived cells. Although Furukawa' 127 does not
name retinal ganglion cells in its list of examples, this does not alter the fact
that retinal ganglion cells are nevertheless eye ball tissue-derived cells. See
Merck & Co. v. Biocraft Labs., Inc., 874 F.2d 804, 807 (Fed. Cir. 1989)
("[ A ]11 disclosures of the prior art, including unpreferred embodiments, must
be considered." ( citation omitted)).
We consequently affirm the Examiner's rejection of the claims on this
ground.
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C. Claims 1-3, 8, and 10-13 under the nonstatutory doctrine of
obviousness-type double patenting
Appellants rely upon the same arguments presented supra. For the
reasons explained, we find them no more persuasive with respect to this
ground of rejection, and we similarly affirm the Examiner's rejection.
DECISION
The Examiner's rejection of claims 1, 2, 8, 11, and 12 under 35 U.S.C.
§ 102(b) and/or§ 103(a) is affirmed.
The Examiner's rejection of claims 1-3, 8, and 10-13 under 35 U.S.C.
§ 103(a) is affirmed.
The Examiner's rejection of claims 1-3, 8, and 10-13 under the
nonstatutory doctrine of obviousness-type double patenting is affirmed.
No time period for taking any subsequent action in connection with
this appeal may be extended under 37 C.F.R. § 1.136(a)(l )(iv).
AFFIRMED
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