Ex Parte Schmidt

Patent Trial and Appeal Board

Nov 23, 2016

11316570 (P.T.A.B. Nov. 23, 2016)

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.
11/316,570 12/21/2005 Karl-Georg Schmidt 930008-2206 2127
20999 7590 11/28/2016
FROMMER LAWRENCE & HAUG
745 FIFTH AVENUE- 10TH EL.
NEW YORK, NY 10151
EXAMINER
ANTHOPOLOS, PETER
ART UNIT PAPER NUMBER
1611
NOTIFICATION DATE DELIVERY MODE
11/28/2016 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):
prosecutiondocketing@flhlaw.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte KARL-GEORG SCHMIDT
Appeal 2014-002984
Application 11/316,570
Technology Center 1600
Before MELANIE L. McCOLLUM, ULRIKE W. JENKS, and
TAWEN CHANG, Administrative Patent Judges.
JENKS, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal under 35 U.S.C. § 134(a) involving claims to a
method of treating open-angle glaucoma with flupirtine. The Examiner
rejects the claims as obvious. We have jurisdiction under 35 U.S.C. § 6(b).
We AFFIRM.
Appeal 2014-002984
Application 11/316,570
STATEMENT OF THE CASE
Claims 13, 24, and 29 are on appeal, and can be found in the Claims
Appendix of the Appeal Brief. Claim 13 is representative of the claims on
appeal, and reads as follows:
13. A method of treating human open-angle glaucoma, which
comprises administering a therapeutically effective amount of a
composition comprising flupirtine in capsule form to a patient
in need thereof.
Appellant seeks review of the Examiner’s rejection of the claims 13,
24, and 29 under 35 U.S.C. § 103(a) as unpatentable over Osborne1 in view
of Kerrigan2 and Rote Liste3.
The issue is: Does the preponderance of evidence of record support
the Examiner’s conclusion that the claims are obvious based on the
combined teachings of the references?
Findings of Fact
We adopt the Examiner’s findings of fact and reasoning regarding the
scope and content of the prior art (Final Act. 3—8; Ans. 3—8). For emphasis
only we highlight the following:
FF1. “Ischemia is defined as an arrest of blood flow and consequent
reduction of oxygen supply” (Osborne SI06). “Ischemic neuronal
death has traditionally been attributed to necrosis. Recently,
1 Osborne et al., Neuroprotection in Relation to Retinal Ischemia and
Relevance to Glaucoma, 43 Survey of Opthalmology SI02—SI28 (1999)
(“Osborne”).
2 Kerrigan et al., TUNEL-Positive Ganglion Cells in Human Primary Open-
angle Glaucoma, 115 Arch Ophthalmol. 1031-1035 (1997).
3 Rote Liste® 05 042 (2002).
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Application 11/316,570
morphologic studies have characterized two distinct types of cell
death: necrosis and apoptosis” {id. at SI08).
FF2. Osborne teaches that “[rjecent reports indicate that apoptosis is a
cause of ganglion cell death in both primary open-angle glaucoma and
AION [anterior ischemic optic neuropathy]” {id. at SI07).
FF3. Osborne teaches that “ischemia-induced insults to the retina in vivo
are ameliorated by MK-801, dextromethorphan, flupirtine, and
memantine” {id. at SI 15).
FF4. As noted by the Examiner, Osborne “identifies flupirtine as a
pharmaceutical that (1) maintains energy supply to the retina,
(2) inhibits NMDA receptor activation, and (3) prevents apoptotic cell
death” (Ans. 4 (citing Osborne SI 17, Table 7)).
FF5. Osborne teaches:
[D]rugs that can reduce NMDA-receptor activity by acting
more indirectly on the modulatory redox site of the NMDA
receptor may be more useful for human use. Present evidence
suggests that flupirtine acts in this way, functioning as an
oxidizing agent and thereby suppressing or facilitating channel
opening on activation of the NMDA receptor. This provides an
explanation as to why flupirtine has already been used clinically
for other purposes without apparent side effects. The nontoxic
effect of flupirtine, its effectiveness as a NMDA antagonist, and
its ability to blunt insults that lead to necrotic or apoptotic
injury make flupirtine a possible drug for use in the treatment
of glaucoma.
(Osborne SI 18 (emphasis added).)
FF6. Kerrigan teaches that “[a]poptosis seems to be a mechanism of cell
death in human eyes with primary open-angle glaucoma” (Kerrigan,
Abstract; Final Act. 5). “There are potential therapeutic approaches to
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Application 11/316,570
block cell death by interfering with the apoptotic pathway” (Kerrigan,
1035; Final Act. 5).
FF7. The Examiner finds that “Rote Liste® 2002 teaches that flupirtine is
commercially available in capsule form (see Entry No. 05 042). It is
worth noting that kaspeln is the German word for capsule” (Final
Act. 5).
Principle of Law
“The combination of familiar elements according to known methods
is likely to be obvious when it does no more than yield predictable results.”
KSR Inti Co. v. Teleflex Inc., 550 U.S. 398, 416 (2007). As expressly
recognized in KSR, any art recognized need or problem can provide a reason
for combining claim elements. Id. at 416.
Analysis
Appellant contends that “different types of glaucoma share neither
common therapeutic characteristics nor common clinical appearances with
the instantly-claimed open-angle glaucoma” (Br. 3).
We are not persuaded by Appellant’s contention. We agree with the
Examiner’s fact finding, statement of the rejection and responses to
Appellant’s arguments as set forth in the Answer and Final Action. We find
that the Examiner has provided evidence to support a prima facie case of
obviousness for applying flupirtine to prevent apoptotic cell death associated
with diseases of the eye including open angle glaucoma.
To summarize, Osborne discloses that the “nontoxic effect of
flupirtine, its effectiveness as a NMDA antagonist, and its ability to blunt
insults that lead to necrotic or apoptotic injury make flupirtine a possible
drug for use in the treatment of glaucoma” (FF5). In addition, Osborne
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Application 11/316,570
“identifies flupirline as a pharmaceutical that. . . prevents apoptotic cell
death” (FF4). Kerrigan teaches that “[a]poptosis seems to be a mechanism
of cell death in human eyes with primary open-angle glaucoma” and that
“[t]here are potential therapeutic approaches to block cell death by
interfering with the apoptotic pathway” (FF6; see also FF2). Based on these
findings, the Examiner concludes that the combination of references would
have motivated the ordinary artisan to “administer[] capsules comprising
flupirtine (an inhibitor of apoptosis) to a patient suffering from primary
open-angle glaucoma, in an effort to treat primary open-angle glaucoma by
inhibiting apoptosis of retinal ganglion cells” (Final Act. 5—6; see FF1—FF7).
We find no error with the Examiner’s rationale.
Appellant contends that in “examining Osborne in its entirety, it
clearly pertains to prevention of ganglion cell or retinal neuron death, which
is induced by retinal ischemia” (Br. 4). However, “open-angle glaucoma,
unlike other types of glaucoma, does not show any signs of ischemia” {id.).
“The minimal increase in intra-ocular pressure associated with open-angle
glaucoma is insufficient to cause any impediment to the drainage of fluid in
the eye, and therefore causes no reduction in blood supply, and therefore
no ischemia” {id. at 3).
We are not persuaded. As the Examiner explains, Kerrigan suggests
that a therapeutic approach is to inhibit apoptosis regardless of the reason for
initiating programmed cell death (Ans. 8; FF6). Osborne teaches that
flupirtine is a drug that prevents apoptotic death and is suggested for
treatment in glaucoma based on the prevention of apoptosis (FF1—FF6). The
test for obviousness is what the combined teachings of the references as a
whole would have suggested to those of ordinary skill in the art. In re
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Application 11/316,570
Keller, 642 F.2d 413, 425 (CCPA 1981). Here, both references suggest the
application of apoptosis inhibitors to prevent programmed cell death in cells
of the eye; this is regardless of the mechanism that leads to the initiation of
apoptosis.
According to the Schmidt Declaration,4 “open-angle glaucoma unlike
other glaucomas slowly develops over years” (Schmidt Decl. 7).
Specifically, “open angle glaucoma is very unusual when compared to other
glaucoma types,” and that teachings from one type of glaucoma cannot be
generalized to other types {id. at 8). “Most notably, open-angle glaucoma
does not show any signs of ischemia, like other glaucomas” {id.)
As explained by the Examiner, the Schmidt Declaration is insufficient
to overcome the prima facie case of obviousness because it “fails to address
the teachings of Kerrigan et al., which are considered extremely relevant”
(Ans. 7). Specifically, Kerrigan teaches that apoptosis is the mechanism of
cell death in open-angle glaucoma and that there “are potential therapeutic
approaches to block cell death by interfering with the apoptotic pathway”
(FF6). We agree with the Examiner’s position, and further note that
although open angle glaucoma may be unlike other glaucomas in its
etiology, the therapy applied is common therapy as suggested by Ritch5 {see
Schmidt Decl. 8). Specifically, Ritch suggests that for open angle glaucoma
the treatment is “only common therapy, no specific therapy, medicinal
and/or surgical decrease of pressure; although the pressure is not necessarily
excessively increased” (Ritch 2). In other words, even if the underlying
4 Declaration under 35U.S.S. § 1.132 by Karl-Georg Schmidt dated June 15,
2012 (“Schmidt Deck”).
5 Ritch et al., Glaucoma-different types of therapies, The Glaucomas (1989).
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pathological issues leading to the development of open-angle glaucoma are
not known, the art suggests applying therapies used for other glaucoma
types. This disclosure buttresses the Examiner’s combination of Osborne,
which teaches conventional therapies including the use of apoptosis
inhibitors (FF5), and Kerrigan, which proposes apoptosis as the mechanism
of cell death in open angle glaucoma and suggests a similar therapeutic
approach (FF6).
We conclude that the evidence cited by the Examiner supports a prima
facie case of obviousness with respect to claim 13, and Appellants have not
provided sufficient evidence of secondary considerations that outweighs the
evidence supporting the prima facie case. As Appellant does not argue the
claims separately, claims 24 and 29 fall with claim 13. 37 C.F.R. § 41.37
(c)(l)(iv).
SUMMARY
We affirm the rejection of all claims.
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).
AFFIRMED
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