Ex Parte Prentice et al

Patent Trial and Appeal Board

Dec 5, 2016

13463440 (P.T.A.B. Dec. 5, 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.
13/463,440 05/03/2012 Howard M. PRENTICE 7018-0019 6080
112994 7590 12/07/2016 EXAMINERCHS Pharma Inc
5425 Park Central Court FAY, ZOHREH A
Suite 111
Naples, EL 34109 ART UNIT PAPER NUMBER
1621
NOTIFICATION DATE DELIVERY MODE
12/07/2016 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):
sakptomail@iplawpro.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte HOWARD M. PRENTICE,
HERBERT WEISSBACH, and JANET BLANKS
Appeal 2015-004241
Application 13/463,440
Technology Center 1600
Before MELANIE L. McCOLLUM, JEFFREY N. FREDMAN, and
RYAN H. FLAX, Administrative Patent Judges.
FREDMAN, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal1 under 35 U.S.C. § 134 involving a method of
protecting a retinal cell by treatment with a sulindac agent. The Examiner
rejected the claims as anticipated. We have jurisdiction under 35 U.S.C.
§ 6(b). We affirm.
Statement of the Case
Background
The Specification explains, “[djamage to RPE [retinal pigment
epithelial] cells by oxidative stress is a central factor in the initiation and
1 Appellant identifies the Real Party in Interest as CHS Pharma, Inc. (see Br.
3).
1
Appeal 2015-004241
Application 13/463,440
progression of macular degeneration and protection of the RPE cells against
oxidative stress is an important therapeutic strategy for preventing the
disease” (Spec. 127). “Sulindac has been shown to protect normal cells
from oxidative stress” (Spec. 127).
The Claims
Claims 7 and 8 are on appeal. Claims 7 and 8 read as follows:
7. A method of protecting a retinal cell from dying in
response to oxidative stress, the method comprising the step of
contacting the cell with an amount of a sulindac agent effective
to protect the cell from dying in response to the oxidative stress,
wherein the sulindac agent is selected from the group consisting
of sulindac, sulindac metabolites, and sulindac derivatives.
8. The method of claim 7, wherein the retinal cell is a
retinal pigment epithelial (RPE) cell.
The Issue
The Examiner rejected claims 7 and 8 under 35 U.S.C. § 102(b) as
anticipated by D’Amato* 2 (Final Act. 2—3).
The Examiner finds D’Amato teaches:
the use of non-steroidal anti-inflammatory compounds ... for
inhibiting angiogenesis related disorders. See the abstract. The
treatment of angiogenic conditions, such as macular
degeneration and retinpathy is taught in Para [0007], [0029],
[0033] and claim 20. The use of sulindac for the treatment of
angiogenesis dependent disorders is taught in Para [0097]. The
ophthalmic use is taught in Para [0101]. . . . The oxidative
stress is considered to be a major component of macular
degeneration and retinopathy. Therefore, the use of the use of
2 D’Amato, R, US 2003/0191098 Al, published Oct. 9, 2003 (“D’Amato”).
2
Appeal 2015-004241
Application 13/463,440
sulindac for the treatment of macular degeneration reads on the
protecting retinal death due to oxidative stress.
(Final Act. 2).
The issue with respect to this rejection is: Does the evidence of
record support the Examiner’s conclusion that D’Amato anticipates claims 7
and 8?
Findings of Fact
1. D’Amato teaches “[diseases associated with retinal/choroidal
neovascularization include, but are not limited to, diabetic retinopathy,
macular degeneration” (D’Amato 1 8).
2. D’Amato teaches “treating certain ocular neovascular diseases
such as macular degeneration. The compounds which are contemplated as
part of the present invention preferably can be given orally to the patient and
thereby halt the progression of the disease. Other disease that can be treated
using the present invention are diabetic retinopathy” (D’Amato 129).
3. D’Amato teaches “the invention also includes the inhibition of
angiogenesis and the treatment of angiogenesis dependent diseases by
administering antiinflammatory compounds .... Examples of NSAIDs
which may be used in the invention include . . . sulindac, sulindac sulfone,
sulindac sulfide” (D’Amato Tflf 95—96).
4. D’Amato teaches “formulations include those suitable for . . .
ophthalmic . . . administration” (D’Amato | 101).
5. Example 9 of D’Amato teaches a “Corneal Micropocket Assay”
where neovascularization was induced in mouse corneas as “pellets
containing bFGF were implanted 1.0-1.2 mm from the limbal vessels, while
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Appeal 2015-004241
Application 13/463,440
the pellets containing VEGF were implanted 0.5-0.7 mm from the limbal
vessels” (D’Amato 1148). “The mice were then treated with varying doses
of antiinflammatory drugs as shown in the table” reproduced in part, below:
AGTINT DOSE bFGF' VEGF2 n p-value
Suii:n.d.fs c 25 mg/kg 50 55 15/15 <.01/