BOARD OF SUPERVISORS OF LOUISIANA STATE UNIVERSITY AND AGRICULTURAL AND MECHANICAL COLLEGE

Patent Trials and Appeals Board

Oct 1, 2020

2020001651 (P.T.A.B. Oct. 1, 2020)

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.
15/478,437 04/04/2017 Charles D. NICHOLS 50971-007003 9246
21559 7590 10/01/2020
CLARK & ELBING LLP
101 FEDERAL STREET
BOSTON, MA 02110
EXAMINER
WU, JULIE ZHEN QIN
ART UNIT PAPER NUMBER
1643
NOTIFICATION DATE DELIVERY MODE
10/01/2020 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):
patentadministrator@clarkelbing.com
smmichaud@clarkelbing.com
PTOL-90A (Rev. 04/07)

UNITED STATES PATENT AND TRADEMARK OFFICE
____________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
____________

Ex parte CHARLES D. NICHOLS and BANGNING YU 1
____________

Appeal 2020-001651
Application 15/478,437
Technology Center 1600
____________

Before JEFFREY N. FREDMAN, DEBORAH KATZ, and
JOHN G. NEW, Administrative Patent Judges.

NEW, Administrative Patent Judge.

DECISION ON APPEAL

1 We use the word “Appellant” to refer to “applicant” as defined in 37
C.F.R. § 1.42. Appellant identifies Board of Supervisors of Louisiana
State University and Agricultural and Mechanical College as the real
party-in-interest. App. Br. 3.

Appeal 2020-001651
Application 15/478,437

2

SUMMARY
Appellant files this appeal under 35 U.S.C. § 134(a) from the
Examiner’s Final Rejection of claims 17 and 18 as unpatentable under 35
U.S.C. § 102(b)(pre-AIA) as being anticipated by May et al. (US 6,664,286
B1, December 16, 2003) (“May”).2
We have jurisdiction under 35 U.S.C. § 6(b).
We AFFIRM.

NATURE OF THE CLAIMED INVENTION
Appellant’s claimed invention is directed to a method of treating an
inflammatory disorder by administering (R)-1-(2,5-dimethoxy-4-
iodophenyl)-2-aminopropane (“(R)-DOI”). Abstr.

REPRESENTATIVE CLAIM
Claim 17 is representative of the claims on appeal and recites:
17. A method for the treatment of an inflammatory
disorder in a mammal, said method comprising

administering to a mammal in need of such treatment a
therapeutically effective amount of (R)-1-(2,5-dimethoxy-4-
iodophenyl)-2-aminopropane ((R)-DOI), or a salt thereof,

in a pharmaceutically acceptable carrier.

2 The Examiner further rejected claims 17 and 18 as unpatentable under the
nonstatutory doctrine of obviousness-type double patenting over claims 1–
7 of Nichols et al. (US 9,642,819 B2, May 19, 2007) (the “’819 patent”).
Appellant filed a terminal disclaimer that was approved on December 28,
2019. See Reply Br. 2. Accordingly, the nonstatutory double patenting
rejection is moot and no longer before us on appeal.
Appeal 2020-001651
Application 15/478,437

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App. Br. 7.

ISSUES AND ANALYSIS
We agree with, and expressly adopt, the Examiner’s findings,
reasoning, and conclusion that the claims are anticipated. We address below
the arguments raised by Appellant.

Issue
Appellant argues that May’s treatment of glaucoma using (R)-DOI
does not necessarily treat an inflammatory disorder and thus May does not
inherently anticipate the claims. Reply Br. 4.

Analysis
The Examiner finds that May discloses administering (R)-DOI to treat
glaucoma in a person. Ans. 3. The Examiner finds that Acute Glaucoma
Discovered to be an Inflammatory Disease, UC San Diego Health
Newsroom, July 11, 2014, available at: https://health.ucsd.edu/news/
releases/Pages/2014-07-14-acute-close-angle-glaucoma.aspx (last visited
September 18, 2020)(“Newsroom”) provides extrinsic evidence that
glaucoma is an inflammatory disease. Id. The Examiner also finds that R.
Vohra, et al., The Role of Inflammation in the Pathogenesis of Glaucoma, 58
SURVEY OF OPHTHALMOLOGY 311–320 (2013) (“Vohra”) provides extrinsic
evidence that inflammatory molecules, e.g., tumor necrosis factor-α (“TNF-
α”), are up-regulated in glaucoma. Id. at 7. Because the extrinsic evidence
teaches that glaucoma is an inflammatory response, the Examiner finds that,
Appeal 2020-001651
Application 15/478,437

4

when used in the treatment of glaucoma, May’s process inherently treats an
inflammatory disorder as claimed. Id. at 8–9.
Appellant argues that the Examiner misapplies the doctrine of
inherency and May does not inherently anticipate the claims. App. Br. 4.
Appellant argues that May discloses treating glaucoma generally, and not
inflammatory glaucoma specifically. Id. Appellant argues that not all types
of glaucoma are inflammatory disorders and, therefore, May does not
necessarily treat an inflammatory disorder by treating glaucoma. Id.
Appellant submits the Declaration of Dr. Angelo Tanna (the “Tanna
Declaration”) as evidence that treating glaucoma does not necessarily treat
an inflammatory disorder. App. Br. 5. Dr. Tanna attests that “[g]laucomas
are a group of optic neuropathies” that include both primary and secondary
variants of open-angle glaucoma and narrow-angle glaucoma. Tanna Decl.
¶ 4. Dr. Tanna attests that “inflammation is not generally thought to play a
role in the etiology of primary open-angle glaucoma” and that primary open-
angle glaucoma patients “have elevated intraocular pressure without
showing signs of inflammation.” Id. ¶ 5 (emphasis omitted). In contrast,
Dr. Tanna attests that the disclosures of Newsroom3 are limited to a mouse
model of acute-intraocular pressure that is “not representative of the vast
majority of cases of human glaucoma.” Id. ¶ 6 (emphasis omitted). Dr.
Tanna attests that “severe IOP elevation, as is observed in the setting of the

3 Dr. Tanna’s Declaration refers to the full article cited by Newsroom: W.
Chi et al., Caspase-8 promotes NLRP1/NLRP3 inflammasome activation
and IL-1β production in acute glaucoma, 111 PNAS 11181–11186 (2014)
(submitted September 26, 2018).
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Application 15/478,437

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rare condition known as acute primary angle closure, is associated with
clinical signs of inflammation and breakdown of the blood-aqueous barrier.”
Id. Dr. Tanna concludes by stating that “the inflammatory mechanism
described by Chi does not necessarily apply to any human glaucoma, much
less to every type of primary and secondary glaucoma discussed above.” Id.
¶ 7.
Appellant further argues that Vohra refers to a “possible role of low-
grade inflammation as a causal factor in the pathogenesis of glaucoma.”
App. Br. 6 (emphasis omitted). Appellant argues that Vohra’s proposed
inflammatory signaling is limited to specific types of glaucoma, and does
not establish that all types of glaucoma relate to inflammatory disease. Id.
We are not persuaded by Appellant’s argument and evidence.
“[W]hen considering a prior art method, the anticipation doctrine examines
the natural and inherent results in that method without regard to the full
recognition of those benefits or characteristics within the art field at the time
of the prior art disclosure.” Perricone v. Medicis Pharm. Corp., 432 F.3d
1368, 1378 (Fed. Cir. 2005). Accordingly, we consider whether the claimed
method is the natural and inherent result of the prior art.
The claims recite treating an inflammatory disorder by administering
a therapeutically effective amount of (R)-DOI. The Specification defines a
“therapeutically effective amount” as an amount that “inhibits or reduces the
release of proinflammatory compounds to a clinically significant degree.”
Spec. ¶ 88. The Specification explains that 5-HT2A receptor agonists, e.g.,
(R)-DOI, “potently inhibits TNF-α-induced inflammation.” Id. ¶ 16.
Accordingly, the claimed method encompasses treating an inflammatory
disorder by inhibiting or reducing TNF-α.
Appeal 2020-001651
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May discloses that “serotonergic compounds which possess agonist
activity at 5HT2 receptors,” e.g., (R)-DOI, unexpectedly “lower and control
[intraocular pressure (“IOP”)] and are useful for treating glaucoma.” May
col. 2, l. 66–col. 3, l. 2. May does not explain the underlying mechanism of
5HT2 agonists, e.g., (R)-DOI, in lowering IOP and treating glaucoma. See
id. at col. 2, ll. 53–55. However, May expressly discloses a method of
treating glaucoma, specifically reducing acute IOP, by administering a
pharmaceutically effective amount of (R)-DOI to a mammal in an actual
working example. See id. at col. 6, ll. 15–45; col. 8, ll. 61–64 (claim 1); col.
9, ll. 3–5 (claim 4). See In re Montgomery, 677 F.3d 1375, 1381 (Fed. Cir.
2012) (“[W]e agree with the Board that even if the claim includes an
efficacy requirement, efficacy is inherent in carrying out the claim steps.”)
Vohra discloses “several studies have shown that TNF-α induces
[retinal ganglion cells (“RGC”)] death, suggesting that inflammation in
response to ischemia may play a crucial role in the development and
progression of glaucoma.” Vohra 315–316. Vohra discloses that RGC
death “has been shown to be ameliorated by inhibition of TNF-α.” Id. at
316. Vohra summarizes the literature as indicating “that inflammation in
response to either ischemia or increased IOP induces enhanced TNF-α
levels, thus promoting RGC death through [tumor necrosis factor receptor 1
(“TNFR1”)]. Id.
Vohra does not describe inflammation as limited to specific types of
glaucomas, contrary to Appellant’s argument.4 Rather, Vohra discloses that

4 Dr. Tanna does not address Vohra’s disclosure. See generally Tanna Decl.
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the characteristic feature of glaucoma, i.e., progressive loss of RGC (Vohra
311), is associated with elevated TNF-α. Vohra 316. Appellant’s
Specification acknowledges that (R)-DOI is a potent inhibitor of TNF-α.
See supra. Accordingly, May’s method of treating glaucoma with a
pharmaceutically effective amount of (R)-DOI naturally and inherently
inhibits or reduces TNF-α, thereby ameliorating RGC death. Because May
“discloses the very same methods as claimed,” we find that “the particular
benefits must naturally flow from those methods even if not recognized as
benefits at the time of [May’s] disclosure.” Perricone, 432 F.3d at 1378.
Consequently, we sustain the Examiner’s rejection based on inherent
anticipation.

CONCLUSION

The rejection of claims 17 and 18 as unpatentable under 35 U.S.C.
§ 102(b), 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).

AFFIRMED
Claims
Rejected
35 U.S.C. § Reference(s)/Basis Affirmed Reversed
17, 18 102(b) May 17, 18