Moustafa, Tarek et al.

Patent Trials and Appeals Board

Sep 30, 2019

12670639 - (D) (P.T.A.B. Sep. 30, 2019)

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.
12/670,639 08/26/2010 Tarek Moustafa 116138-5001-US 3955
13356 7590 09/30/2019
Morgan, Lewis & Bockius LLP (CH)
1111 Pennsylvania Avenue, NW
Washington, DC 20004
EXAMINER
CORNET, JEAN P
ART UNIT PAPER NUMBER
1628
NOTIFICATION DATE DELIVERY MODE
09/30/2019 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):
kcatalano@morganlewis.com
patents@morganlewis.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
________________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
________________

Ex parte TAREK MOUSTAFA, MICHAEL TRAUNER
and PETER FICKERT1
________________

Appeal 2019-004162
Application 12/670,639
Technology Center 1600
________________

Before DONALD E. ADAMS, JOHN G. NEW, and
RACHEL H. TOWNSEND, Administrative Patent Judges.

NEW, Administrative Patent Judge.

DECISION ON APPEAL

1We use the word “Appellant” to refer to the “applicant” as defined in 37
C.F.R. § 1.142”. Appellant identifies Medizinische Univeristät Graz as the
real party-in-interest. App. Br. 1.
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SUMMARY
Appellant files this appeal under 35 U.S.C. § 134(a) from the
Examiner’s Final Rejection of claims 8 and 9 as unpatentable under 35
U.S.C. § 103(a) as being obvious over the combination of Zadini et al. (WO
2007/061820 A2, May 31, 2007) (“Zadini”) B.I. Cohen et al., Differing
Effects of Nor-ursodeoxycholic or Ursodeoxycholic Acid on Hepatic
Histology and Bile Acid Metabolism in the Rabbit, 91 GASTROENTEROL.
189–97 (1986) (“Cohen”), and Castagnola et al. (US 4,892,868, January 9,
1990) (“Castagnola”).
Claims 8 and 9 stand further rejected as unpatentable under the
combination of Trauner et al. (WO 2006/119803 A1, November 16, 2006)
(“Trauner”), P. Fickert et al., Primary Sclerosing Cholangitis – The
Arteriosclerosis of the Bile Duct?, 6:3 LIPIDS IN HEALTH AND DISEASE, 1–8
(January 25, 2007) (“Fickert”), and Sasahara et al. (US 2007/0203115 A1,
August 30, 2007) (“Sasahara”).
We have jurisdiction under 35 U.S.C. § 6(b).
We AFFIRM.

NATURE OF THE CLAIMED INVENTION
Appellant’s invention is directed to the use of nor-bile acids and their
pharmaceutically acceptable salts, esters, and/or derivatives in the treatment
of arteriosclerosis. Abstr.
REPRESENTATIVE CLAIM
Claim 8 is representative of the claims on appeal and recites:
8. A method of treating arteriosclerosis in a human or animal
subject comprising the step of administering at least nor-
ursodeoxycholic acid and/or at least one pharmaceutically
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acceptable salt and/or ester thereof, wherein the oral dosage form
is a controlled release dosage form that releases the at least nor-
ursodeoxycholic acid and/or the at least one pharmaceutically
acceptable salt and/or ester thereof only after the oral dosage
form has reached the stomach or the gastro-intestinal tract.

App. Br. 21.

ISSUES AND ANALYSES
We adopt the Examiner’s findings, reasoning, and conclusion that the
claims on appeal are prima facie obvious over the cited prior art. We
address the arguments raised by Appellant below.

A. Rejection of the claims over Zadini, Cohen, and Castagnola
Issue
Appellant argues the Examiner erred because Zadini, Cohen, and/or
Castagnola fail to provide, either individually or in combination, any
teaching, suggestion, or motivation that would have led a skilled artisan to
combine the references to arrive at the claimed method. App. Br. 11.

Analysis
The Examiner finds that Zadini teaches a method of treating
atherosclerosis comprising administering a list of biliary compound to a
human, in which the compound is orally ingested, and is a slow-release
pharmaceutical preparation. Final Act. 4 (citing Zadini claims 1, 3, 11, 6,
12). The Examiner finds that Zadini teaches that the orally-ingested
composition is in an oral dosage form, and that the slow release corresponds
to claim 8’s recitation of “controlled release.” Id. The Examiner further
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finds that Zadini teaches that its orally-ingested dosage form comprises an
intestinal absorption enhancer. Id. (citing Zadini claim 18). The Examiner
therefore finds that Zadini teaches that its slow-release dosage form
formulated with an intestinal absorption enhancer would be understood by a
skilled artisan to correspond to the controlled-release dosage form that
releases the nor-ursodeoxycholic acid (“nor-UDCA”) only after the
compound has reached the gastro-intestinal tract, as recited in claim 8. Id.
The Examiner notes that Appellant’s Specification defines controlled-
release dosage form as a composition that releases the active agent only after
the dosage form has reached a certain site of the body, e.g., the stomach or
the gastro-intestinal tract, or, additionally or alternatively, it may designate a
dosage form, which releases the active agent over a prolonged period of
time. Final Act. 4 (citing Spec. 21).
The Examiner also finds that Zadini teaches biliary compounds,
including nor-bile acid derivatives such as 23-methylursodeoxycholic acid
and 24-nor-UDCA. Final Act. 4 (citing Zadini 21, ll. 15–16). The Examiner
finds that Zadini teaches biliary compounds include 3-hydroxy-5-cholen-24-
oic acid 3-sulfate ester (see page 19, line 18) and hyodeoxycholate-6-O-
glucuronidel (see page 20, line 11).
The Examiner finds that Cohen teaches that, from a therapeutic
standpoint, not only is nor-UDCA not hepatotoxic in humans, but also that if
administered in its unconjugated form, it will not accumulate in the
enterohepatic circulation, unlike ursodeoxycholic acid (“UDCA”). Final
Act. 5.
The Examiner finds that Castagnola teaches that nor-UDCA, and its
salts, derivatives, and esters, have been shown to have significantly
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improved properties as regards to cholesterol-dissolving ability, higher
critical micellar concentration and stimulation of the bile flow compared to
ursodeoxycholic acid (UDCA). Final Act. 5. The Examiner finds that these
properties are combined with an exceptional stability against natural
degradation and remarkable hepatic tolerance, enabling these compounds for
long term treatment. Id. (citing Castagnola col. 2, ll. 1–59). The Examiner
further finds that Castagnola teaches that these compounds can be
administered via oral and parenteral routes. Id. (citing Castagnola col. 7, ll.
38–40).
The Examiner concludes that it would have been prima facie obvious
to a person of ordinary skill in the art to select nor-UDCA, or a salt or ester
thereof, because Cohen teaches that nor-UDCA is not hepatotoxic in humans
because it does not accumulate in the enterohepatic circulation compared to
its amidates (i.e., UDCA), and also because Castagnola teaches that nor-
UDCA, salts, derivatives, and esters thereof, have been shown to have
significantly improved properties with respect to cholesterol-dissolving
ability, higher critical micellar concentration and stimulation of the bile flow
compared to UDCA, exceptional stability and low hepatotoxicity. Final Act.
5–6. The Examiner finds that a person of ordinary skill in the art would
have been motivated to select nor-UDCA due to its advantages over UDCA.
Id. at 6.
Appellant argues that Zadini and Cohen each teach away from the
claimed invention and that Castagnola does not cure these deficiencies.
App. Br. 11. With respect to Zadini, Appellant argues that Zadini teaches
that bile acids, including nor-UDCA, should not be administered using the
oral-digestive route of administration. According to Appellant, Zadini
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further teaches that, if oral-digestive administration is used, nor-UDCA must
be chemically modified. Id.
By way of example, Appellant contends that Zadini teaches that:
“biliary compounds can be administered via many routes, except that they
cannot be administered via the oral digestive route, because when ingested
they are […] sequestered in the enterohepatic circulation.” App. Br. 12
(quoting Zadini 29). Appellant points out that Zadini further teaches that:
In animals, as in human bodies, bile salts however are confined
to the digestive system, in the so called enterohepatic circulation,
and do not come in contact with arteries either of the systemic or
pulmonary circulation, therefore the biliary salts in nature are
prevented from displaying their benefits on atherosclerotic
plaques.

Id. (quoting Zadini 5). Appellant notes that Zadini therefore teaches a
number of methods for administering bile acids or their salts via means
which bypass the enterohepatic circulation, including via: “[o]ral mucous
membrane, such as sublingual,” but not via oral ingestion. Id. (quoting
Zadini 31).
Appellant therefore argues that Zadini neither teaches nor suggests the
oral administration of nor-UDCA. App. Br. 13. Rather, Appellant contends,
oral-sublingual administration of nor-UDCA, or its pharmaceutically
acceptable salts or esters, is expressly excluded by claim 8, which requires
that the oral dosage form be released “only after the oral dosage form has
reached the stomach or the gastro-intestinal tract.” Id.
Appellant acknowledges that Zadini teaches that:
Biliary compounds can also be chemically manipulated and
designed in such a way that they are not captured by the liver in
any significant amount to be sequestered into the entero-hepatic
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circulation once introduced into the body by any route including
the oral-digestive route. The use of these types of compounds
makes oral administration possible even with biliary compounds,
expanding even further the possibilities of the disclosed
treatment of atherosclerosis.

App. Br. 13 (quoting Zadini 34). Appellant contends that Zadini thus
teaches that, to the extent oral-digestive administration of nor-UDCA is
contemplated, despite Zadini’s teachings to the contrary, nor-UDCA must be
chemically modified to turn it into another chemical compound that would
be suitable for such use. Id. Appellant asserts that Zadini teaches the oral-
digestive administration of a nor-UDCA derivative, and not the oral-
digestive administration of unmodified nor-UDCA, or pharmaceutically
acceptable salt or ester thereof, as required by claim 8. Id.
With respect to Cohen, Appellant argues that the reference teaches
that nor-UDCA taken up via the stomach will not enter systemic blood
circulation. App. Br. 13 (citing Cohen Fig. 1). According to Appellant,
chronic administration of nor-UDCA causes hepatotoxicity because chronic
ingestion of natural bile acids leads to the accumulation of the toxic
metabolite, lithocholate, in the liver. Id. at 14. Appellant contends that
Cohen teaches, however that nor-UDCA does not cause lithocholate
accumulation or hepatotoxicity in the liver of rabbits. Id. Appellant asserts
that Cohen therefore concludes that nor-UDCA is not hepatotoxic, and that
the absence of lithocholate accumulation is caused by enzymatic
modification of nor-UDCA that occurs during hepatic passage; in short, the
nor-UDCA is converted to nor-UDCA-glucuronide and excreted. Id. (citing
Cohen 194–95).
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Therefore, Appellant contends, Cohen teaches that nor-UDCA does
not reach systemic blood circulation, and therefore cannot reach the
coronary arteries, where atherosclerosis is predominant. App. Br. 15. In
view of this, argues Appellant, a person of ordinary skill in the art would
have understood that nor-UDCA administered via the oral-digestive route
would not be able to be used to treat arteriosclerosis, and would have also
understood that Cohen teaches away from the administration of nor-UDCA
via an oral-digestive route for the treatment of arteriosclerosis. Id.
With respect to Castagnola, Appellant argues that the reference
teaches that nor-UDCA has the ability to dissolve cholesterol at a higher
critical micellar concentration and stimulation of the bile flow as compared
to UDCA. App. Br. 16 (citing Castagnola col. 2, ll. 24–27). Appellant
contends that Castagnola does not provide any teaching or suggestion
regarding the intestinal absorption and hepatic metabolism of nor-UDCA.
Id.
Appellant therefore argues that it would not have been obvious to a
person of ordinary skill in the art to choose nor-UDCA, or a salt or ester
thereof, for use in oral-digestive administration to treat arteriosclerosis.
App. Br. 16. Appellant asserts that a person of ordinary skill in the art
would not be motivated to administer nor-UDCA via the oral-digestive route
in view of the teachings of Zadini and Cohen that doing so would be
unsuccessful, since the nor-UDCA would not reach the circulatory system
and could not do so without potentially deleterious modifications. Id.
Furthermore, argues Appellant, there would be no reasonable expectation of
successfully administering nor-UDCA, or a salt or ester thereof, via an oral-
digestive route to treat arteriosclerosis, because, as taught by Zadini and
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Cohen, the nor-UDCA would not enter the blood circulatory system and
therefore would not be able to affect any arteriosclerotic vessels. Id. at
16–17.
We do not find Appellant’s arguments persuasive. We acknowledge
that Zadini teaches the passages quoted by Appellant. However, Zadini
expressly teaches the oral administration of biliary salts, including nor-DCA.
See Zadini claim 11 (“The treatment of claim 2 wherein said compound is
orally ingested”); see also Abstr. (“A pharmacological substance namely a
biliary salt or acid or precursor or derivative with emulsifying properties …
administered into the systemic circulation of a patient via a variety of routes
of administration including topical-mucous membrane such as sublingual,
topical-dermatological such as via a skin patch, oral, [etc.]”) (emphasis
added).
Furthermore, Zadini teaches that:
Biliary compounds can also be chemically manipulated and
designed in such a way that they are not captured by the liver in
any significant amount to be sequestered into the entero-hepatic
circulation once introduced into the body by any route including
the oral-digestive route. The use of these types of compounds
makes oral administration possible even with biliary compounds,
expanding even further the possibilities of the disclosed
treatment of atherosclerosis.

Zadini 34. Zadini further teaches, by way of example, that: “Biliary
compounds being designed to enter the systemic circulation through oral-
digestive route of administration can be associated with intestinal absorption
enhancers so that their bioavailability in the systemic circulation is
maximized.” Id. Appellant’s claims do not recite any “chemical
manipulation or design” in the administration of nor-UDCA, nor do they
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claim association with “intestinal absorption enhancers,” however, the
claims do recite: “A method of treating arteriosclerosis in a human or animal
subject comprising the step of administering at least nor-ursodeoxycholic
acid and/or at least one pharmaceutically acceptable salt and/or ester thereof
….” The use of the transition term “comprising” does not exclude any
additional steps or limitations from the scope of the claim. See Crystal
Semiconductor Corp. v. TriTech Microelectronics Int’l, Inc., 246 F.3d 1336,
1348 (Fed. Cir. 2001) (“Use of the transition “comprising” in the language
of a claim creates a presumption ... that the claim does not exclude
additional, unrecited elements”).
Finally, Cohen teaches that nor-UDCA is “glucuronidated during
hepatic passage” and suggests that: “it is a reasonable conclusion that the
glucuronide was not reabsorbed from the gastrointestinal tract, as other
glucuronides are not reabsorbed from the intestine.” Cohen 195. Zadini,
however, teaches that:
An interesting compound among the biliary acids is the
hyodeoxycholic acid. As reported by Sacquet E. et al.[2] … once
it reaches the liver through the portal venous system after
absorption by the intestinal mucosa, the hyodeoxycholic acid
largely escapes, in healthy humans, the enterohepatic circulation
entering the systemic circulation to be excreted through the
kidneys in the urine in a very significant amount. It appears that
the hyodeoxycholic acid escapes the enterohepatic circulation
after having undergone a process of glucuronidation by the
hepatic cell. The Applicants believe that this peculiarity of the
hyodeoxycholic acid to enter the systemic circulation in theory
could be exploited to directly emulsify/dissolve the lipid core of
atherosclerotic plaques. Another advantage of the

2 Sacquet E. et al., Intestinal Absorption, Excretion, and Biotransfonnation
of Hyodeoxycholic Acid in Man, 24 J. LIPID RES. 604–13 (1983).
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hyodeoxycholic acid is that it can be administered via oral-
intestinal route.

Zadini 12 (emphasis added). Cohen thus teaches that nor-UDCA is
converted in the liver to a glucuronide, just as hyodeoxycholic acid is
similarly converted (and unlike UDCA; see Cohen 194–95; Fig. 1). Cohen
hypothesizes that the converted glucuronide is removed from the body via
the intestinal system, but does not test this hypothesis, nor does Cohen
determine whether nor-UDCA enters systemic circulation. We find that,
because both nor-UDCA and hyodeoxycholic acid are capable of
glucuronidation, and because, when glucuronidated, hyodeoxycholic acid
can pass into systemic circulation, it would not be an unreasonable inference
by a person of ordinary skill in the art to conclude that, like hyodeoxycholic
acid, nor-UDCA is also able to pass into the systemic circulation.3
In summary, we are not persuaded by Appellant that the balance of
evidence presented by the cited prior art teaches away from the claims on
appeal. A teaching away requires a reference to actually criticize, discredit,
or otherwise discourage the claimed solution. See In re Fulton, 391 F.3d
1195, 1201 (Fed. Cir. 2004). As we have explained the combination of

3 We also note here that hyodeoxycholic acid and nor-UDCA are highly
similar structures, as illustrated below:

Structures of nor-UDCA (left) and hyodeoxycholic acid (right)
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Zadini and Cohen suggests that oral administration is at least feasible as a
means of introducing nor-UDCA into systemic circulation. We
consequently are not persuaded by Appellant’s arguments, and we affirm the
Examiner’s rejection.

B. Rejection of the claims over Trauner, Fickert, and Sasahara
Issue 1
Appellant argues that the Examiner erred by failing to articulate any
teaching, suggestion, or motivation in the prior art that would have led a
person of ordinary skill to combine the references to arrive at Appellant’s
claimed invention. App. Br. 17.

Analysis
The Examiner finds that Trauner teaches a method of treating liver
diseases, and preferably primary sclerosing cholangitis (“PSC”) or primary
biliary cirrhosis (“PBC”) comprising nor-UDCA, and/or its
pharmaceutically acceptable salt and esters, in an amount of 10 to
8000 mg. Final Act. 8 (citing Trauner 5, 6, claims 1, 4, 5). The Examiner
finds that Trauner teaches various delivery systems, including sustained
release form. Id. (citing Trauner 8). The Examiner points to Appellant’s
Specification as disclosing that sustained release is a form of controlled
release and, therefore, Trauner’s teaching of sustained release falls within
the scope of “controlled release,” as recited in the claims. Id. at 8–9 (citing
Spec. ¶ 116). The Examiner also finds that Trauner teaches that the
sustained release dosage form can be administered as a solid oral dosage
form. Id. at 9 (citing Trauner 6).
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The Examiner finds that Trauner does not teach arteriosclerosis or
atherosclerosis; however, the Examiner finds that Fickert teaches that
arteriosclerosis and PSC may share common disease mechanisms, based on
similar pathogenic features and mediators found in both. Final Act. 9 (citing
Fickert 1). The Examiner further finds that Fickert teaches that research on
PSC may greatly benefit from translating pathogenic concepts from
advanced work in arteriosclerosis to the study of cholestasis. Id. (citing
Fickert 7).
The Examiner finds that Sasahara teaches therapeutic agents, viz.
novel benzodiazepine compounds which are useful for treating
arteriosclerosis, PSC, and PBC. Final Act. 9 (citing Sasahara ¶¶ 4, 9).
The Examiner concludes that it would have been prima facie obvious
to a person of ordinary skill in the art to employ the method of treatment
taught by Trauner to treat arteriosclerosis (which, the Examiner finds,
includes atherosclerosis). Final Act. 9. The Examiner finds that a skilled
artisan would have been motivated to do so because Fickert teaches that PSC
and arteriosclerosis have common disease mechanisms. Id. Therefore, the
Examiner finds, a person of ordinary skill would have had a reasonable
expectation of success in employing the treatments taught by Trauner to treat
arteriosclerosis, because Sasahara teaches that treatments for PSC can also
be used to treat arteriosclerosis. Id.
Appellant argues that, although PSC and arteriosclerosis share some
similarities regarding their pathogenesis, they affect different areas of the
body: PSC affects the liver, whereas arteriosclerosis occurs predominantly in
the coronary arteries. App. Br. 17–18. Therefore, argues Appellant, a drug
that is effective in treating PSC must reach the liver, whereas a drug that is
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used in the treatment of arteriosclerosis must reach the coronary arteries. Id.
at 18.
Appellant contends that a person of skill in the art would have known,
at the time Appellant’s application was filed, that bile acids like nor-UDCA
are kept away from systemic blood circulation upon oral-digestive uptake,
because it is confined in the enterohepatic circulation. App. Br. 18. As a
result, Appellant contends, such acids reach the liver, but not the systemic
circulation, and therefore do reach the coronary arteries where
arteriosclerotic plaques occur. Id. Therefore, Appellant asserts, it would
have been reasonable to treat PSC with an oral-digestive dosage form
containing nor-UDCA, as disclosed by Trauner, since nor-UDCA can reach
the liver and achieve a high concentration in the liver via cholohepatic
shunting. Id. However, Appellant argues, it would not have been
reasonable to use nor-UDCA to treat a condition, such as arteriosclerosis,
that requires nor-UDCA to enter the systemic circulation and, in particular,
sclerotic arteries. Id. Appellant asserts that it was well-known that when
administered via an oral-digestive dose, nor-UDCA would not reach the
blood circulatory system and that bile acids, such as nor-UDCA, accumulate
in the liver, resulting in hepatotoxicity. Id.
Therefore, Appellant argues, the mechanism by which nor-UDCA is
beneficial in the treatment of PSC, would not have suggested that nor-
UDCA would be beneficial in, or even capable of, the treatment of
arteriosclerosis, which requires that the nor-UDCA accumulate in the system
arteries affected by sclerosis. App. Br. 18 (citing Zadini 5).
We do not find Appellant’s argument persuasive. Although Zadini
and Cohen are not cited, in this rejection, as bases for the rejection,
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Appellant’s argument nevertheless explicitly relies upon the arguments
presented supra with respect to the teachings of Zadini and Cohen, as
indicating that the prior art at the time of Appellant’s invention taught away
from the idea that oral administration of nor-UDCA can reach the systemic
circulation.
As an initial matter, Cohen directly contradicts Appellant’s contention
that “bile acids, such as nor-UDCA, accumulate in the liver, resulting in
hepatotoxicity.” See App. Br. 18. To the contrary, Cohen expressly teaches
that nor-UCDA is converted to a glucuronide and consequently does not
accumulate as the hepatotoxic metabolite, lithocholate, in the liver. See
Cohen Abstr. (“Ingestion of nor-[UDCA] … did not cause hepatotoxicity,
and neither it nor its presumed metabolite, nor-lithocholate, accumulated in
biliary bile acids”).
Furthermore, we have explained supra, why we are not persuaded that
the prior art at the time of invention would have taught a person of ordinary
skill in the art that oral administration of nor-UDCA could not reach the
systemic circulation. To the contrary, we have found that a person of
ordinary skill, given the combined teachings of the prior art, and particularly
those of Zadini and Cohen, would have believed that there was a reasonable
expectation of success that nor-UDCA could be introduced into the systemic
circulation, either via chemical manipulation and design in such a way that it
would not be captured by the liver, as taught by Zadini (see Zadini 34), or
via hepatic conversion to glucuronide, as suggested by the combined
teachings of Zadini and Cohen. See Zadini 12, Cohen 194–95. We
consequently do not find Appellant’s arguments persuasive.
Issue 2
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Appellant argues that the Specification discloses the unexpected result
that oral-digestive administration of nor-UDCA is effective in the treatment
of arteriosclerosis in mice. App. Br. 19 (citing Spec. Ex. 1). Appellant
contends that this is a surprising result because Appellant contends that the
knowledge in the art at the time of Appellant’s invention taught that there is
no oral-digestive uptake of nor-UDCA. Id.
Additionally, Appellant points to the allegedly unexpected discovery
that nor-UDCA has positive effects on the liver, including acting as an anti-
inflammatory, when compared to UDCA. App. Br. 20 (citing, e.g., Spec.
27–30, Figs. 7, 8, 9, 12). According to Appellant, treatment in mice with
nor-UDCA reduced white adipose tissue as compared to treatment with
UDCA. Id. (citing, e.g., Spec. 30–33, Fig. 18). Appellant contends that
these effects upon treatment with nor-UDCA were unexpected and support
the nonobviousness of the instantly claimed invention.
We do not agree. As we have explained, we do not find Appellant’s
arguments supra persuasive of the contention that the prior art at the time of
Appellant’s invention taught away from the oral administration of nor-
UDCA as a means of introducing it into the systemic circulation. Appellant
points to no direct evidence in the prior art demonstrating that oral
administration of nor-UDCA would not be effective in introducing the
composition into systemic circulation, and we have explained how we have
found that the prior art suggests that it could be so used.
Furthermore, as found by the Examiner, the combined teachings of the
combined cited prior art also directly suggests that nor-UDCA could be
effective in the treatment of atherosclerosis.
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Finally, the fact that nor-UDCA is beneficial to the liver, as compared
to UDCA, which promotes hepatotoxicity via the accumulation of the
metabolite lithocholate, is expressly taught by Cohen. See Cohen Abstr.
194–95. Moreover, the effect of nor-UDCA in reducing white adipose tissue
in mice, as argued by Appellant, is not relevant to the claims and is
insufficient to overcome the Examiner’s conclusion that the claims are
prima facie obvious. See In re Baxter Travenol Labs., 952 F.2d 388, 392
(Fed. Cir. 1991) (holding that “[m]ere recognition of latent properties in the
prior art does not render nonobvious an otherwise known invention”). We
consequently affirm the Examiner’s rejection upon this ground.

DECISION
The Examiner’s rejection of claims 8 and 9 under 35 U.S.C.
§ 103(a) 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)(1)(iv).

AFFIRMED

Claims Rejected Basis Affirmed Reversed
8, 9 § 103(a) over Zadini,
Cohen, Castagnola
8, 9
8, 9 § 103(a) over
Trauner, Fickert,
Sasahara
8, 9
Overall Outcome 8, 9