ECONUGENIS INC

Patent Trials and Appeals Board

Nov 24, 2021

2021003788 (P.T.A.B. Nov. 24, 2021)

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.
16/687,447 11/18/2019 ISAAC ELIAZ ECON-0015-CIPCONT3 2818
80308 7590 11/24/2021
The Kelber Law Group
6701 Democracy Blvd
Suite 300
Bethesda, MD 20817
EXAMINER
BERRY, LAYLA D
ART UNIT PAPER NUMBER
1623
NOTIFICATION DATE DELIVERY MODE
11/24/2021 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):
steve@kelberlawgroup.com
susan@kelberlawgroup.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte ISAAC ELIAZ
Appeal 2021-003788
Application 16/687,447
Technology Center 1600
Before TAWEN CHANG, RACHEL H. TOWNSEND, and
DAVID COTTA, Administrative Patent Judges.
TOWNSEND, Administrative Patent Judge.
DECISION ON APPEAL
Pursuant to 35 U.S.C. § 134(a), Appellant1 appeals from the
Examiner’s decision to reject claims directed to a method of treating a
mammal with kidney damage by reducing active galectin-3 levels as being
obvious. Oral argument was heard November 15, 2021. We have
jurisdiction under 35 U.S.C. § 6(b).

1 We use the word “Appellant” to refer to “applicant” as defined in 37
C.F.R. § 1.42. Appellant identifies the real party in interest as ecoNugenics,
Inc. (Appeal Br. 2.)
Appeal 2021-003788
Application 16/687,447

2
We AFFIRM but because our reasoning differs somewhat from the
Examiner’s, we designate the affirmance as a NEW GROUND OF
REJECTION pursuant to 37 C.F.R. § 41.50(b).
STATEMENT OF THE CASE
Galectin-3 is a protein that contains a carbohydrate-recognition-
binding domain, and “has been shown to be involved in a large number of
biological processes, including cell adhesion, cell migration, cell invasion,
cell activation and chemoattraction, cell growth and differentiation, cell
cycle and apoptosis.” (Spec. ¶ 2.) It has also “been demonstrated to be
involved in a large number of disease states of medical implications.” (Id.)
Research has demonstrated that low molecular weight pectins (MCPs) bind
galectin-3 molecules. (Id. ¶ 4.) And “it is now clear that administering
PectaSol-C MCP or other low molecular weight pectins at the dosage levels
of 5–1,500 mg/kg of body weight per day, with a preferred range of 10
mg/kg/day to 1,000 mg/kg/day inherently binds galectin-3 molecules in
mammals . . . providing therapeutic benefit against many of the disease
conditions mentioned.” (Id.) Appellant’s Specification explains:
The inhibition of the growth and transformation of various
cancers, the inhibition of fibrosis in a variety of organs and
organ systems, the reduction in inflammation associated with
galectin-3, all combine to provide a powerful method of
treatment in a wide variety of situations.
(Spec. ¶ 13.) Moreover, Appellant’s Specification states:
The binding of galectin-3 achieved by administration of low
molecular weight pectins (at least as reflected in U.S. Patent
Application Serial No. 11/485,955 10,000 -20,000 Daltons
molecular weight such as PectaSol MCP) is effective in
reducing trauma due to kidney injury. Kolatsi-Jannou et al,
PlusOne, 6, 4, el8683 (2011).
Appeal 2021-003788
Application 16/687,447

3
(Id. ¶ 3.)
Appellant has discovered that administration of MCPs between
10,000 Daltons (10 kDa) and 20 kDa “inherently binds cellular, serum and
circulating galectin-3.” (Spec. ¶ 11.) Appellant’s claims are directed to a
method that takes advantage of that inherent binding.

Claims 7 and 8 are on appeal, both of which are reproduced below.
7. A method of treating a mammal which benefits from a
reduction in available circulating galectin-3, comprising the
steps of:
a) Identifying a mammal in need of treatment for kidney
damage, and
b) Administering to said mammal an amount of modified
pectin of molecular weight of 3,000-13,000 Daltons, in an
amount of 10-750 mg/kg/day, for a period of time sufficient such
that said mammal exhibits a reduction in active galectin-3 levels
in said mammal and thereby treat kidney damage in said
mammal.

8. A method of treating a mammal which benefits from a
reduction in available galectin-3, comprising the steps of:
a) Identifying a mammal in need of treatment for kidney
damage, and
b) Administering to said mammal modified pectin of low
molecular weight of 10,000-20,000 Daltons, in an amount of 5-
1,500 mg/kg/day, for a period of time sufficient for said mammal
to exhibit a reduction in active galectin-3 levels in said mammal
and thereby treat kidney damage in said mammal.
(Appeal Br., Revised Claims Appendix.2)

2 The Revised Claims Appendix is dated February 19, 2021.
Appeal 2021-003788
Application 16/687,447

4
The prior art relied upon by the Examiner is:
Name Reference Date
Maria Kolatsi-Joannou
et al. (“KJ”)
Modified Citrus Pectin
Reduces Galectin-3
Expression and
Disease Severity in
Experimental Acute
Kidney Injury, 6(4)
e18683 PloS ONE, 1–9
2011
Juan Yan and Aaron
Katz
PectaSol-C Modified
Citrus Pectin Induces
Apoptosis and
Inhibition of
Proliferation in Human
and Mouse Androgen-
Dependent and
Independent Prostate
Cancer Cells, 9(2)
Integrative Cancer
Therapies, 197–203
2010

The following ground of rejection by the Examiner is before us on
review:
Claims 7 and 8 under 35 U.S.C. § 103(a) as unpatentable over
Kolatsi-Joannou and Yan.
DISCUSSION
The Examiner found that Kolatsi-Joannou (KJ) teaches that modified
citrus pectin (MCP), PectaSol, may be used to reduce renal injury in acute
kidney injury via modulation of galectin-3. (Final Action 4, 5; Ans. 5.) The
Examiner noted that KJ indicates
“Modulating” galectin-3 was beneficial in the FA-induced acute
kidney injury model, and that MCP administration reduces
Appeal 2021-003788
Application 16/687,447

5
galectin-3 upregulation (page 4, left column), and that MCP
decreased levels of galectin-3 in concert with significantly
improved renal fibrosis (end of left column, page 7).
(Final Action 6; see also Ans. 5 (“Administration of MCP reduced gal-3
expression at day 14 (Figure 3), when mice are in the recovery phase (last
paragraph on page 4).”).) The Examiner acknowledged that KJ “does teach
that MCP might not act only through galectin 3 (page 6, last paragraph), but
[it] focuses on modulation of galectin-3 as a strategy to reduce acute kidney
injury (see the title, abstract, page 6, first paragraph, and page 8, last
paragraph).” (Ans. 4 (emphasis added).) Moreover, the Examiner found
that KJ indicated that “the effect of MCP was long-term.” (Final Action 5;
Ans. 4.)
Regarding treatment, the Examiner points to “the last paragraph of KJ,
which states that MCP is a potential therapy o[f] acute kidney injury, and
suggests to examine the timing of treatment.” (Final Action 5.) The
Examiner further found that KJ teaches that the MCP that was administered
was a 1% solution. (Id. at 4.) The Examiner found that “[t]here was a
reasonable expectation of success [for acute kidney therapy] because KJ
identified at least one mechanism for the suggested treatment (galectin-3
pathway) and because the effect of MCP was long-term.” (Ans. 4; see also
id. at 5 (“K-J teaches that MCP treats kidney injury, regardless of whether
multiple pathways are involved”).) The Examiner states “[t]he skilled
artisan would administer MCP to reduce gal-3 expression as taught by K-J.”
(Id.)
The Examiner found that Yan teaches that MCP antagonizes galactin-
3, which results in suppression of cancer metastasis. (Final Action 4; Ans. 5
(citing Yan 197, last paragraph).) In particular, the Examiner noted that
Appeal 2021-003788
Application 16/687,447

6
“Yan teaches that MCP binds to and suppresses the activity of gal-3 (page
201, last paragraph).” (Ans. 4, 5.) In addition, the Examiner found that Yan
teaches that PectaSol-C, which is an MCP with a molecular weight between
5 kDa and 10 kDa, was used in human clinical trials in a dose of 15 g per
day for treating cancer, as was PectaSol, which is an MCP with a molecular
weight between 12 kDa and 16 kDa. (Final Action 4, Ans. 6.) The
Examiner further found that Yan teaches that PectaSol-C “might have better
bioavailability in vivo” but otherwise teaches PectaSol-C is effective for the
same purpose as PectaSol. (Id.) The Examiner acknowledged that Yan
teaches treating a different disorder than KJ, but explained that, like KJ,
“Yan is using MCP for modulating galectin-3, . . . so the skilled artisan
would look to Yan for guidance based on mechanism of action.” (Id. at 6.)
The Examiner found that based on the teachings of KJ and Yan, one
of ordinary skill in the art would have found it obvious to administer either
PectaSol or PectaSol-C for treatment of kidney injury, and to use 15 g per
day which “would equal 300 mg/kg/day for a 50 kg human or 166
mg/kg/day for a 100 kg human, well within the claimed ranges.” (Final
Action 4.) The Examiner further noted that “the skilled artisan would look
to Yan for guidance in dosage, and would optimize the dose using routine
experimentation with the purpose of reducing galectin-3 as taught by both
KJ and Yan.” (Id. at 7; see also Ans. 6 (“Yan teaches that MCP suppresses
cancer metastasis by suppressing the activity of gal-3. MCP was used at a
dose of 15 g/day for treating cancer, and one mechanism for that treatment is
suppression of gal-3 (page 201, last paragraph).”).) Furthermore, the
Examiner found that “[t]here is no evidence in the specification that the
claimed range is critical.” (Ans. 5.) In addition, the Examiner found that
Appeal 2021-003788
Application 16/687,447

7
“the effects of administering MCP are inherent because a compound and its
properties are inseparable.” (Id. at 7.)
We agree with the Examiner’s conclusion of obviousness. In
particular, we agree with the Examiner that KJ would have provided a
person of ordinary skill in the art with a reasonable expectation of treating
acute renal injury with the administration of MCP, such as PectaSol, which
Appellant does not dispute has a molecular weight of between 12 kDa and
16 kDa, and which overlaps with the ranges recited in claims 7 and 8. We
agree with the Examiner that Yan, although directed to treating cancer,
would have provided one of ordinary skill in the art with a reason to select
15 g of MCP per day to administer to a human patient with a reasonable
expectation of lowering galectin-3, which KJ teaches is a mechanism of
action that reduces fibrosis in acute kidney injury.
We begin our analysis with claim construction.

a. Claim requirements
During prosecution, we interpret terms in a claim using the broadest
reasonable interpretation in light of the Specification. In re Morris, 127 F.3d
1048, 1056 (Fed. Cir. 1997).
Claims 7 and 8 are directed to “[a] method of treating a mammal.”
The positive method steps of both claim 7 and 8 require 1) identifying a
mammalian patient that is in need of “treatment for kidney damage” and
then 2) administering MCP (a) within a recited molecular weight range, (b)
within a recited dosage range, and (c) for a time sufficient to achieve “a
reduction in active galectin-3 levels in said mammal” and “thereby treat
kidney damage in the mammal.” In other words, the treatment of kidney
Appeal 2021-003788
Application 16/687,447

8
damage is expressly noted by the claim to be a function of simply reducing
active galectin-3 levels. This reduction in active galectin-3 levels
corresponds to the term “treating” as recited in the preamble: a “method of
treating a mammal which benefits from a reduction in available circulating
galectin-3.”
Other than the specific dosage range claimed, KJ teaches the method
of treating required by the claims.
b. Administering MCP for a period of time sufficient to reduce active
galectin-3 levels and thereby treat kidney damage
Many of Appellant’s arguments are premised on the position that KJ
“does not attribute improvements [in the kidneys of treated mice] to
reduction of galectin-3 expression” (see, e.g., Appeal Br. 13–14; Reply Br.
17 (“Nowhere in K-J is there the slightest indication that AKI treatment is
effected by reducing active galectin-3 levels.”). We do not agree with
Appellant’s position.
1. reducing active galectin-3 levels
KJ studied a mouse model of acute renal injury induced by high dose
folic acid (FA) treatment, which treatment damages the kidney tubules and
results in interstitial fibrosis and inflammation. (See KJ 1, 4.) KJ explains
that “kidneys of FA-exposed animals (Group II) contained significantly
higher galectin-3 mRNA levels than sham controls (Group I) at both
experimental day 2 and 14 (Figure 3A).” (Id. at 4.) It was also explained
that in this model, galectin-3 expression was more widespread than in
normal kidneys, as well as being “observed in fibrotic areas consistent with
macrophage localization.” (Id. at 4.)
Appeal 2021-003788
Application 16/687,447

9
KJ teaches that the “principal findings [of its study] were that MCP[3]
reduced acute renal enlargement and proliferative responses in the initial
phases of FA nephropathy, then decreased renal apoptosis, inflammation and
fibrosis in the later phase.” (Id. at 6.) KJ also reports that MCP
administration “significantly decreased galectin-3 levels” which was
associated with “decreased renal apoptosis, inflammation and fibrosis.” (Id.
at 6; Id. at 4 (“Administration of MCP (Group III) did not significantly alter
galectin-3 mRNA levels at 2 days but there was a statistically significant
reduction at day 14 (Figure 3A)” (emphasis added)); id. at 7 (“MCP
decreased renal mRNA and protein levels of galectin-3 at 14 days after FA
injection, in concert with significantly improved renal fibrosis as assessed by
reduced expression of multiple fibrotic genes.”).)
Thus, KJ teaches that galectin-3 levels were statistically significantly
reduced by the 14th day of administration of MCP after the induction of
acute kidney injury, which “reduction was confirmed at the protein level.”
(Id. at 4.)
2. the relationship between reduced galectin-3 levels and
treatment
As just noted, KJ reports findings at two phases of the FA model of
acute kidney injury; namely, (a) at “initial phases” or “acute phase” of the

3 The MCP administered was PectaSol and was administered as 1% MCP
provided in the animals drinking water. (Id. at 2.) KJ teaches that “[t]his
dose of MCP previously led to effective galectin-3 blockade and was non-
toxic in murine cancer studies examining parameters such as tumour growth,
angiogenesis and spontaneous metastasis.” (Id.) KJ also teaches that lower
doses of MCP “prevent galectin-3 mediated functions in-vitro including
chemotaxis and cell adhesion, but there is no data showing this would be
replicated in-vivo.” (Id.)
Appeal 2021-003788
Application 16/687,447

10
injury (called FA nephropathy) and (b) in the later “recovery” phase. (KJ 4,
6.) KJ notes that although MCP administered prior to induction of acute
renal injury did not prevent “severely impaired kidney function” as
measured at day 2 after induction, i.e., the initial or acute phase of injury,
from a clinical standpoint (“clinically”), it did “reduce[] the severity of the
disease” that was induced as measured at that same time. (Id. at 4.) KJ
states:
FA also caused severely impaired kidney function in MCP
maintained mice, with increases in serum creatinine and BUN
comparable to those given normal drinking water. Clinically,
however, the MCP mice had reduced severity of disease: they
had preserved body weight (mean 23.6 g), which is similar to
sham controls (Figure 4, Table 1 ), whilst kidney weights (0.16
g) were higher than shams but significantly reduced compared
to those exposed to FA but maintained on water alone (Figure
4, Table 1). Histologically, MCP administration significantly
reduced the number of proliferating cells in FA-treated animals
(water/FA 17.9±3.3; MCP/FA 7.2±2.8) but did not significantly
alter levels of apoptosis (water/FA 2.7±0.6, MCP/FA 1.8 ±0.6).
(Id.) It is in this initial phase of injury only that KJ found that no differences
in galectin-3 expression were observed as related to treatment of acute
kidney injury (Appeal Br. 13 (citing KJ 6 (“MCP treatment reduced tubular
proliferation two days following FA administration with no differences in
galectin-3 expression”).)
However, as already noted, KJ explains that after 14 days of treatment
of the acute renal injury with MCP, galectin-3 protein levels were
statistically significantly reduced. (Id.) And, KJ explains that although
“[t]he whole of the kidney does not return to normal,” there was an
attenuation of kidney injury. (Id. at 4–5.) In particular, KJ reports that after
14 days of treatment of the acute renal injury with MCP, MCP caused
Appeal 2021-003788
Application 16/687,447

11
“significant attenuation of” the increases of most fibrotic markers caused by
the administration of FA which created the acute renal injury and fibrosis.
(KJ 5.) KJ explains regarding fibrotic markers that:
The growth factor TGF-β plays a key role in the progression of
renal fibrosis by promoting myofibroblastic differentiation [36]
and galectin-3 has been implicated in this type of differentiation
and extracellular matrix production in hepatic stellate cells [37].
MCP reduced TGF-β mRNA here, which may have contributed
to reduced myofibroblast formation as evidenced by decreased
αSMA levels.
(Id. at 7.) KJ states: “MCP decreased renal mRNA and protein levels of
galectin-3 at 14 days after FA injection, in concert with significantly
improved renal fibrosis as assessed by reduced expression of multiple
fibrotic genes.” (Id. (emphasis added).)
In addition, KJ reports that MCP administration “led to significantly
decreased levels of [the cytokines] IL-1β and TNF-α.” (Id. at 5.)
Thus, while KJ found that in the initial injury phase of the MCP
treated mice (2 days after MCP administration post FA induced injury) MCP
“did not alter galectin-3 initially,” the continued use of MCP post initial
injury did ultimately “significantly decrease[] galectin-3 levels” which
decreased levels were associated with “decreased renal apoptosis,
inflammation and fibrosis.” (Id. at 6; id. at 7.)4 Thus, KJ teaches the steps
required by the claim, other than the dosage range claimed.

4 Appellant does seem to recognize MCP treatment did decrease galectin-3
expression 14 days and acute kidney injury was induced, but then
confusingly notes that KJ describes other experimental kidney diseases that
are not acute kidney injury where it is believed that galectin-3 is beneficial.
(Appeal Br. 13.) KJ’s reporting on galectin-3 levels in other kidney disease
models is simply irrelevant to the fact that KJ teaches that galectin-3 is
lowered 14 days after MCP administration in acute kidney injury compared
Appeal 2021-003788
Application 16/687,447

12
For the foregoing reasons, we find Appellant’s argument that “even
though the treated mice were given MCP for a week in advance of the
administration of folic acid, the article expressly found that there was no
impact on expression of gal-3 due to administration of MCP” (Appeal Br.
13; see also Appeal Br. 17–18 (noting KJ “makes it clear that at best,
administration, even pretreatment, to mammals (mice) with MCP did not
reduce gal-3 levels for 14 days after the date of injury”)) to be misleading
because the reduction of galectin-3 levels due to administration of MCP of
mice having acute kidney injury is expressly established in KJ. Thus
Appellant’s argument is unpersuasive of error in the Examiner’s rejection.5
Furthermore, KJ explains that galectin-3, which is “abundantly
expressed by subsets of macrophages, can induce monocyte migration or
alternative macrophage and regulate cytokine expression,” and proposes that
“MCP effects on inflammation in FA-nephropathy may in part be mediated
by galectin-3.” (KJ 8.) In other words, not only does KJ link a reduction of
galectin-3 to improvement of kidney fibrosis that occurs in acute kidney
injury, KJ suggests that the reduction in inflammation of the kidney
observed with administration of MCP in acute renal injury is also related to a
reduction in available galectin-3. We determine that a reduction of
inflammation would also be considered a “treatment,” as that term is used in

to mice who were not treated with MCP and were induced to have acute
kidney injury.
5 Moreover, Appellant’s arguments related to the statements in KJ that
galectin-3 is beneficial in some experimental kidney disease which are not
acute kidney injury (Appeal Br. 13, 16) are irrelevant to the Examiner’s
rejection, which is focused on the teachings of KJ with respect to galectin-3
levels in the acute kidney injury model—in which injury was induced by
administering FA—after the treatment with MCP when injury was induced.
Appeal 2021-003788
Application 16/687,447

13
the pending claims. Indeed, Appellant’s specification links a reduction in
inflammation to “treatment.” (Spec. ¶ 13 (“The inhibition of the growth and
transformation of various cancers, the inhibition of fibrosis in a variety of
organs and organ systems, the reduction in inflammation associated with
galectin-3, all combine to provide a powerful method of treatment in a wide
variety of situations.”).)
Appellant urges error in the rejection because KJ suggests that MCP
acts in modulating proliferation, apoptosis, fibrosis and inflammation
through a number of pathways that are not related to galectin-3 expression.
(Appeal Br. 14 (citing KJ 7); see also Appeal Br. 18 (“K-J also teaches those
of skill in the art that kidney injury improvements observed may have
nothing at all to do with gal-3 levels.”).) This argument is not persuasive.
As noted, KJ states: “MCP decreased renal mRNA and protein levels of
galectin-3 at 14 days after FA injection, in concert with significantly
improved renal fibrosis as assessed by reduced expression of multiple
fibrotic genes.” (KJ 7 (emphasis added).) KJ then teaches that MCP acts in
modulating proliferation, apoptosis, fibrosis and inflammation by more than
just binding to the carbohydrate recognition domain of galectin-3 and
impairing the lectin’s carbohydrate binding-related functions. (KJ 7.) In
particular, KJ states that
it could be postulated that if MCP acted only through galectin-3
in FA nephropathy it would not have any effect on intracellular
actions including proliferation and apoptosis, while modulating
extracellular functions such as inflammation. This proved not
the case.
(Id.) KJ indicates that it may be that “it is not just galectin-3 levels” that
modulate proliferation, apoptosis, and inflammation, but also galectin-3’s
bioavailability. (Id. (emphasis added).) KJ posits that “[i]t is possible that
Appeal 2021-003788
Application 16/687,447

14
similar levels of galectin-3 have less biological effects when MCP is present
because its carbohydrate binding roles will be abrogated.” (Id.)6 While KJ
undoubtedly observed that the improvements to the mice kidneys having
acute kidney injury that were administered MCP could be due to a number
of pathways, it nevertheless specifically linked the improvement in fibrosis
and inflammation to the lowering of levels of active galectin-3 as a
definitive pathway that is involved in the treatment of the damaged kidney.
In light of the foregoing teachings of KJ, we disagree with Appellant
that KJ provides “pure speculation as to the pathway and effect” (Appeal Br.
16). KJ acknowledges that the data from its study suggests there may be
additional helpful activity in treating acute renal injury by the administration
of MCP through other molecular pathways that are not due to reducing
active galectin-3 (Appeal Br. 14; KJ 7). However, this does not contradict
the fact that KJ teaches that the treatment of a mammalian patient with acute
renal injury with administration of MCP, such as PectaSol, not only results
in reduction in available circulating galectin-3 but that reduction is linked to

6 For this reason, we disagree with Appellant that KJ “does not suggest that
MCP binds galectin-3” (Reply Br. 15). We note, however, that whether or
not KJ suggests MCP binds galectin-3 is not important to our affirmance of
the Examiner’s rejection. The claim does not require such binding, and as
explained in the opinion, KJ teaches the elements the claims require, i.e.,
administering MCP of the requisite molecular weight for a time sufficient
such that the mammal treating exhibits a reduction in active galectin-3 levels
and thereby treating kidney damage. Additionally, that MCP has no effect
on normal mice (Reply Br. 15), is immaterial regarding what is
demonstrated with regard to mice having acute kidney injury.
Appeal 2021-003788
Application 16/687,447

15
the treatment of the damaged kidney, i.e., fibrosis7, as well as reducing
inflammation, renal apoptosis, and proliferation.
Based on its study’s results, KJ explains that because the data
indicates “that MCP is protective in experimental nephropathy through
modulation of proliferation, apoptosis, fibrosis and inflammation,” MCP is a
potential therapy for acute renal injury. (KJ 8.) KJ indicates for further
studies, that an “examin[ation of] different doses of MCP, [and] timing of
treatment are warranted.” (Id.)
In light of all of the foregoing, relevant to the claim requirements, KJ
teaches that treatment of a mammalian patient with acute renal injury—
which injury causes an increase of galectin-3—by administration of MCP,
such as PectaSol, not only results in reduction in active galectin-3 levels
(levels of available circulating galectin-3), but that reduction is a treatment
of the damaged kidney because, at a minimum, it reduces fibrosis of the
kidney compared to an untreated patient with acute renal injury and reduces
inflammation.
Appellant’s generic assertions about the complicated science of
experimental biology (Appeal Br. 15) notwithstanding, in light of the
foregoing, we conclude that one of ordinary skill in the art would have had a
reasonable expectation of success of carrying out the claimed invention from
the clear teachings of KJ, including identifying a patient having acute kidney

7 For all the reasons discussed, we reject Appellant’s assertion that the study
described in KJ only “offers a tantalizing possibility that perhaps there is
some interrelation between gal-3 levels and MCP administration” (Appeal
Br. 16). KJ expressly states that the administration of MCP reduced the
levels of galectin-3 and resulted in treating fibrosis of the damaged kidney
and inflammation.
Appeal 2021-003788
Application 16/687,447

16
injury and in need of treatment, administering MCP for a time sufficient to
reduce active galectin-3 levels, and thus treating kidney fibrosis and
inflammation, i.e., kidney damage.
This is true, even though KJ states that the study identifies “a new
potential therapy for acute kidney injury” (KJ 8), because KJ specifically
indicates that MCP administration achieves all of the endpoints required by
Appellant’s claim, i.e., reduction in active galectin-3 levels and thereby
treating fibrosis and inflammation, i.e., kidney damage in acute kidney
injury. As the Examiner explained in the Answer, only a reasonable
expectation of success is required, and KJ establishes that with the response
observed in a mouse model for acute kidney injury that showed reduced
galectin-3 and reduced fibrosis with administration of PectaSol and the
determination that the observed improvement in the damaged kidney was
due at least in part to the reduction in available galectin-3.
Appellant urges that “the USPTO has found that reducing
inflammation by administration of MCP is patentably distinct from reducing
fibrosis by administration of MCP and both to be patentably distinct from
treating kidney injury by reducing gal-3 by reason of administration of
MCP.” (Appeal Br. 11.) Appellant does not direct our attention toward any
evidence of record in support of that position and our review of the file
history of the application on appeal does not support Appellant’s assertion.
We are aware that the application on appeal is a continuation of US
Application of 15/453,972, which itself was a continuation of US
Application 15/215,514, which was a continuation of US Application
13/153,648. Notably, the application on Appeal is not designated as a
Divisional application of any of the foregoing applications, which itself is an
Appeal 2021-003788
Application 16/687,447

17
indication that there has been no identification by the Patent Office of a
patentable distinctness of the present claims directed to treating kidney
injury and the claims in the patents that issued from the noted related
applications. We are aware that the following restriction was made in the
’648 application:
I. Claims 1 and 9, drawn to a method of treating a mammal
comprising steps of selecting a mammal in need of at least one
of inhibition of cancer progression, inhibition of cancer
transformation, or the inhibition of the spread of cancer
metastases, classified in 514/54 plus.
II. Claims 7 and 10, drawn to a method of treating a mammal
comprising steps of selecting a mammal in need of at least one
of inhibition or reduction of inflammation, classified in 536/124
plus.
III. Claims 8 and 11, drawn to a method of treating a mammal
comprising steps of selecting a mammal in need of at least one
of inhibition or reduction of formation of fibroses, classified in
536/124 plus.
(’648 Application File History, Final Action dated Oct. 22, 2013.) Thus,
there was not a restriction made between reducing inflammation by
administration of MCP from treating kidney injury by reducing galectin-3 by
reason of administration of MCP, nor was there a restriction made between
reducing fibrosis by administration of MCP and from treating kidney injury
by reducing galectin-3 by reason of administration of MCP. Applicant
elected to pursue claims to group I in the ’648 application. (Id. at Response
to Restriction Requirement dated June 4, 2014.) Applicant pursued claims
to group III (fibroses) in the ’514 Application. And, in the ’972 application,
Applicant pursued claims not involved in the restriction, namely a method of
treating a mammal in need of treatment for chronic heart failure in. Thus,
we do not find Appellant’s argument that the PTO has found there to be a
Appeal 2021-003788
Application 16/687,447

18
patentable distinction between reducing fibrosis by administration of MCP
and treating kidney injury by reducing galectin-3 by reason of administration
of MCP persuasive.

c. Dosage limitation
The only remaining issue to consider for the obviousness rejection is
whether the teachings of KJ and Yan suggest administering an MCP such as
Pectasol or Pectasol-C with a dosage amount within that which is claimed.
We conclude that it does. Although, here, our reasoning differs somewhat
from the Examiner’s.
First, we note that KJ teaches administration in a mouse model. One
of ordinary skill in the art would have found it obvious to scale the dosage
upwards to reduce galectin-3 in a larger mammalian patient, such as a
human, and thus achieve reduction in fibrosis. Indeed, Azémar8, a reference
Appellant provided in the Appendix for this Appeal, teaches that scaling
dosage upwards for treatment in humans is within the level of ordinary skill
in the art based on “pre-clinical animal studies as well as on clinical
experience.” Azémar 75. In fact, Azémar teaches that 15 g total, divided
into 5g of MCP three times a day, was provided to human patients, and that
“[a]ll patients tolerated the therapy well without any severe therapy-related
adverse events.” (Id.) Furthermore, KJ based its dosage choice for MCP in
the mouse model based on prior murine cancer studies. (KJ 2.)

8 Marc Azémar et al., Clinical Benefit in Patients with Advanced Solid
Tumors Treated with Modified Citrus Pectin: A Prospective Pilot
Study, Clinical Medicine: Oncology, 73–80, 2007.
Appeal 2021-003788
Application 16/687,447

19
Turning now to Yan, irrespective of the fact that Yan’s “[a]im [was]
[t]o demonstrate the efficacy of PectaSol-C modified citrus pectin (MCP) on
prostate cancer in vitro” (Yan, Abstr), Yan makes clear that 15 g per day of
the MCPs PectaSol and PectaSol-C is an amount that may be given to a
human with a reasonable expectation that the MCP would bind to galectin-3
making galectin-3 incapable of binding to its receptors. Yan teaches that it
was known that “MCP acts as a ligand for galectin-3” and that “MCP is
thought to render galectin-3 incapable of binding its receptors.” (Yan 198.)
Yan also describes that it demonstrated that MCP bound to galectin-3 on
cells and suppressed the activity of galectin-3. These teachings in Yan are in
accord with KJ’s teaching that MCPs not only lower the available galectin-3
levels but may inhibit the bioavailability of galectin-3 “because its
carbohydrate binding roles will be abrogated” with MCP binding to galectin-
3 (KJ 7).
Yan teaches that there have been clinical trials administering the
MCPs PectaSol and PectaSol-C to humans for therapeutic purposes and that
these are “the only MCPs that have been used in human clinical trials.”
(Yan 198.) And Yan teaches the amount administered that achieved a
therapeutic end point (“improved quality of life”) was 15 g of MCP per day.
(Id.) Although the study in Yan was not directed to administering 15 g of
MCP per day to a human, Yan is prior art for all that it teaches. In re Fritch,
972 F.2d 1260, 1265 (Fed. Cir. 1992) (“It is well settled that a prior art
reference is relevant for all that it teaches to those of ordinary skill in the
art.”).
We conclude that one of ordinary skill in the art knowledgable of KJ’s
teaching to “examine effects of different doses of MCP” for treating acute
Appeal 2021-003788
Application 16/687,447

20
kidney injury (KJ 8), would have found it obvious from Yan’s teachings
regarding what was known from clinical trials administering PectaSol or
PectaSol-C to humans, to start with 15 g per day of PectaSol or PectaSol-C,
a known safe amount to administer to humans, with a reasonable expectation
from KJ’s teaching that (a) available galectin-3 levels would be reduced, and
(b) fibrosis of the kidney and inflammation at a minimum would be reduced
and (c) thus the kidney damage would be treated.
For the foregoing reasons, we do not find Appellant’s arguments
concerning the specifics of Yan’s study (Appeal Br. 19, 21; Reply Br. 18)
persuasive of non-obviousness.
Thus, we affirm the Examiner’s rejection of claims 7 and 8 as being
obvious from the teachings of Kolatsi-Joannou and Yan. However, because
our reasoning differs in some respects to the Examiner’s for finding the
dosage range recited to be non-obvious, we designate our affirmance a new
ground of rejection.
DECISION SUMMARY
In summary:
Claims
Rejected
35 U.S.C.
§
Reference(s)/Basis Affirmed Reversed
7, 8 103 Kolatsi-Joannou,
Yan
7, 8

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). See 37 C.F.R.
§ 1.136(a)(1)(iv).
Appeal 2021-003788
Application 16/687,447

21
37 C.F.R. § 41.50(b) also provides that the Appellant, WITHIN TWO
MONTHS FROM THE DATE OF THE DECISION, must exercise one of
the following two options with respect to the new ground of rejection to
avoid termination of the appeal as to the rejected claims:
(1) Reopen prosecution. Submit an appropriate
amendment of the claims so rejected or new Evidence relating
to the claims so rejected, or both, and have the matter
reconsidered by the examiner, in which event the prosecution
will be remanded to the examiner. . . .
(2) Request rehearing. Request that the proceeding be
reheard under § 41.52 by the Board upon the same Record. . . .

Further guidance on responding to a new ground of rejection can be
found in the Manual of Patent Examining Procedure § 1214.01.
AFFIRMED; 37 C.F.R. 41.50(b)