Ex Parte Kleemann et al

Patent Trial and Appeal Board

Mar 20, 2017

13885199 (P.T.A.B. Mar. 20, 2017)

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.
13/885,199 06/25/2013 Robert Kleemann 078168.7 3555
27805 7590 03/22/2017
THOMPSON HTNF T T P
EXAMINER
10050 Innovation Drive LONG, SCOTT
Suite 400
DAYTON, OH 45342-4934 ART UNIT PAPER NUMBER
1633
NOTIFICATION DATE DELIVERY MODE
03/22/2017 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):
ipdocket @ thompsonhine. com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte ROBERT KLEEMANN, REINOUT STOOP,
JOHAN HENDRIKUS VERHEIJEN, PETER YDO WIELINGA, and
TEAKE KOOISTRA1
Appeal 2016-004008
Application 13/885,199
Technology Center 1600
Before ERIC B. GRIMES, JOHN G. NEW, and RACHEL H. TOWNSEND,
Administrative Patent Judges.
GRIMES, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal under 35U.S.C. § 134 involving claims relating to
an animal model for treating or preventing diabetic complications, which
have been rejected on several grounds. We have jurisdiction under 35
U.S.C. § 6(b).
We reverse.
1 Appellants identify the Real Party in Interest as Nederlandse Organisatie
voor Toegepast-Natuurwetenschappelijk Onderzoek (Netherlands
Organization for Applied Scientific Research). (Br. 1.)
Appeal 2016-004008
Application 13/885,199
STATEMENT OF THE CASE
The invention relates to a method of using an animal model for micro-
and macrovascular complications of diabetes such as diabetic nephropathy.
(Spec. 1:2—9.) The Specification discloses that “low density lipoprotein
receptor-deficient mice (LDLr" ") mice when fed with high energy diets
produce controllable, progressively developing and consistent diabetic
complications, especially renal damage, similar to the human
pathophysiology and biological response.” {Id. at 2:23—27.)
Claims 1, 4, 5, and 9-11 are on appeal. Claim 1 is the only
independent claim and reads as follows (emphasis added):
1. A method for discovering a preventive or therapeutic
regimen for the prevention or treatment of diabetic micro- or
macrovascular complications, comprising the steps of:
a) feeding LDLr-/- mice, which have not been treated
with streptozotocin, with a high energy diet without
supplemented cholesterol;
b) before, during and/or after this diet treating the mice
with the preventive or therapeutic regimen;
c) checking whether any change in the micro- or
macrovascular system of the animal occurs.
The claims stand rejected as follows:
Claims 1, 4, 5, and 9-11 under 35 U.S.C. § 112, second paragraph, as
indefinite (Non-final Action2 5);
2 Office Action mailed Feb. 24, 2015.
2
Appeal 2016-004008
Application 13/885,199
Claims 1, 5, and 9-11 under 35 U.S.C. § 102(b) as anticipated by
Wouters3 as evidenced by Wu4 (Non-final Action 10);
Claim 4 under 35 U.S.C. § 103(a) as obvious based on Wouters and
Wu (Non-final Action 13); and
Claims 1, 4, 5, and 9-11 under 35 U.S.C. § 112, first paragraph, as
including new matter (Non-final Action 15—16).
DISCUSSION
The Examiner has rejected all of the claims on appeal as indefinite
and including new matter, on the basis that Appellants’ Specification
describes “high energy” diets as including fat sources that include
cholesterol, such as lard, and thus include cholesterol “added” to the base
rodent chow. (Non-final Action 3—7, 15—19; Ans. 4—5, 8.) Similarly, the
Examiner has rejected all of the claims as either anticipated or obvious,
based on “interpret[ing] the new claim limitations, ‘a high energy diet
without exogenous [sic, supplemented] cholesterol, ’ to encompass high
energy diets with supplemental cholesterol.” (Non-final Action 8, see also
13-14.)
Thus, all of the rejections depend on a single issue: What is the
broadest reasonable interpretation of a “high energy diet without
supplemented cholesterol”?
3 Wouters et al., Dietary Cholesterol, Rather than Liver Steatosis, Leads to
Hepatic Inflammation in Hyperlipidemic Mouse Models of Nonalcoholic
Steatohepatitis, 48 Hepatology 474-486 (2008).
4 Wu et al., Diabetic atherosclerosis mouse models, 191 Atherosclerosis
241-249 (2007).
3
Appeal 2016-004008
Application 13/885,199
Appellants argue that “the specification defines ‘high energy diet’ to
mean ‘diets in which the lipid or fat content is increased [relative to a normal
diet],’ and which include fats or oils, preferably animal fats, with a high
content of saturated fatty acids and monounsaturated fatty acids (p. 5 lines
10-16).” (Br. 6.) Appellants argue that they “differentiate types of diets.
Appellants state that ‘[althero genic diets differ from diabetogenic diets in
several ways: they typically contain less fat (in w/w% as well as in En%)
and they typically are supplemented with cholesterol at a concentration of
0.1% w/w and 1% w/w’ (specification p. 5 lines 21—24; emphasis added).”
(Id.) Appellants argue that the “claims do not recite ‘a diet without
supplemented cholesterol’, but instead recite ‘a high energy diet [as defined]
without supplemented cholesterol’ (emphasis added).” (Id. at 7.)
We agree with Appellants that the Examiner’s interpretation of “a
high energy diet without supplemented cholesterol” to include “a high
energy diet with supplemented cholesterol” is broader than is reasonable
when the claim language is read in light of the Specification. Specifically,
we conclude that the Examiner’s interpretation either redefines “high energy
diet” in conflict with the Specification or essentially reads out of the claims
the requirements that go along with a high energy diet.
The Specification states that “[h]igh energy diets are diets in which
the lipid content is increased, especially in the form of fats or oils.
Preferably animal fats, such as lard, beef tallow, butter, and ghee are used.
These diets are typical diabetogenic diets.” (Spec. 5:10-13.) Thus, a high
energy diet is described as one in which lipid content is increased, preferably
with animal fats, which (as the Examiner noted) contain cholesterol. We
4
Appeal 2016-004008
Application 13/885,199
agree with Appellants that the “increased” lipid content would be understood
by one of ordinary skill in the art to be relative to normal chow. (See, e.g.,
Figure 1 (comparing the increase in body weight of rodents fed “chow” and
those fed a certain percentage energy Lard diet).) Moreover, the
Specification equates such “high energy diets” with “diabetogenic diets.”
(Spec. 5:10-13.)
The Specification distinguishes, however, between a high energy/
diabetogenic diet and an atherogenic diet:
Atherogenic diets differ from diabetogenic diets in several ways:
they typically contain less fat ... and they typically are
supplemented with cholesterol at a concentration of 0.1% w/w
and 1% w/w). Some investigators also add choclate [sic] to the
atherogenic diets to stimulate cholesterol uptake and to increase
plasma cholesterol. A typical atherogenic diet contains for
instance 15% w/w cocoa and 1% w/w palm oil and 1%
cholesterol as fat source.
(Id. at 5:21-27.)
The Specification provides an example in which “LDLr-/- male mice
. . . were fed a high fat diet” containing different concentrations of lard
defined by the provision of a certain energy percentage “En %”. (Id. at 9:4—
12.) Thus, these high fat diets providing energy percentages of 30 En%
Lard, 45 En% Lard, and 60 En% Lard are high energy as compared to
“chow control.” The Specification reports that “vascular inflammation
markers (VCAM and E-selectin) were significantly elevated indicating
macro-and micro vascular dysfunction.” (Id. at 10:18—19.) The
Specification also provides an example in which LDLr-/- mice were fed one
of the diets described in the first example and various interventions were
started after nine weeks. (Id. at 11:2—11.) Finally, The Specification also
5
Appeal 2016-004008
Application 13/885,199
provides an example (Example 3) in which “LDLr-/- mice . . . were fed a
high fat diet (45% En% Lard diet)... for 10 weeks, and for an additional 6
weeks high fat diet enriched with 1% (w/w) cholesterol.” (Id. at 13:11—13.)
Thus, the Specification distinguishes both in Examples and when
differentiating between atherogenic and diabetogenic diets between a “high
energy” (or “high fat”) diet and a high energy diet that was supplemented,
i.e., “enriched,” with cholesterol. We conclude that, when read in light of
the Specification, “a high energy diet” means one in which the normal diet
(“chow,” Spec. 9:9) has been modified with extra fat, which may or may not
contain cholesterol. Thus, the broadest reasonable interpretation of “a high
energy diet without supplemented cholesterol,” in light of the Specification,
is one in which the diet can contain added fat as compared to normal chow,
and from any source, but does not contain cholesterol beyond that found in
the fat source in the “high energy” diet.
That claim interpretation resolves all of the rejections on appeal. We
conclude that the claims are not indefinite, because the meaning of the claim
language is reasonably clear in light of the Specification. We also finds that
the Specification’s description demonstrates possession of “a high energy
diet without supplemented cholesterol,” as that phrase would be understood
by those of skill in the art. And, because we conclude that “a high energy
diet without supplemented cholesterol” excludes deliberately added
cholesterol, we conclude that the Examiner has not shown that the claims are
anticipated by Wouters or obvious in view of Wouters and Wu.
6
Appeal 2016-004008
Application 13/885,199
SUMMARY
We reverse all of the rejections on appeal.
REVERSED
7