Ex Parte Laughlin et al

Patent Trial and Appeal Board

Feb 10, 2017

13278465 (P.T.A.B. Feb. 10, 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.
13/278,465 10/21/2011 Leo Timothy Laughlin II 11736 5551
27752 7590 02/14/2017
THE PROCTER & GAMBLE COMPANY
Global IP Services
Central Building, C9
One Procter and Gamble Plaza
CINCINNATI, OH 45202
EXAMINER
LEE, ANDREW P
ART UNIT PAPER NUMBER
1621
NOTIFICATION DATE DELIVERY MODE
02/14/2017 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):
centraldocket. im @ pg. com
pair_pg @ firsttofile. com
mayer.jk @ pg. com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte LEO TIMOTHY LAUGHLINII, TOMOHIRO HAKOZAKI,
WENZHU ZHAO, JIAZHEN WANG, and
JOHN CRIST BIERMAN1
Appeal 2015-000947
Application 13/278,465
Technology Center 1600
Before ERIC B. GRIMES, JOHN G. NEW, and TAWEN CHANG,
Administrative Patent Judges.
GRIMES, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal under 35U.S.C. § 134 involving claims to a
screening method, which have been rejected as obvious. We have
jurisdiction under 35 U.S.C. § 6(b).
We reverse.
1 Appellants identify the Real Party in Interest as The Procter & Gamble
Company. (Appeal Br. 1.)
Appeal 2015-000947
Application 13/278,465
STATEMENT OF THE CASE
Melanogenesis, or melanin synthesis (Spec. 1 5), can result in age
spots when cumulative UV damage causes melanocytes to overproduce
melanin (id. 1 6). Adrenergic receptors (ADRs) (id. 8) include ADRpi and
ADRP2, which can contribute to melanogenesis by increasing the level of
cyclic AMP (cAMP) in melanocytes. (Id. H 31—34.) ADRP3 receptors, by
contrast, stimulate nitric oxide production, which reduces cAMP levels. (Id.
| 51.) And “the antagonism of ADRalB and ADRa2C receptors is believed
to impede melanogenesis.” (Id. 1 58.)
Claims 1—10, 13, 16, and 19 are on appeal. Claims 1 and 16 are
illustrative and read as follows:
1. A screening method for determining whether a test agent,
which is suitable for use in a topical cosmetic composition, is
effective for modifying the appearance of pigmented skin, the
method comprising:
contacting a cell, a cell culture, or bulk cells with the test agent,
wherein the cell, the cell culture, or the bulk cells comprise
ADRpi receptors and wherein the test agent is a cosmetic
agent; and
determining based on the binding interaction of the test agent
with the ADRpi receptors whether the test agent is an effective
ADRpi receptor antagonist suitable for modifying the
appearance of pigmented skin, wherein the test agent is
considered to be an effective ADRpi receptor antagonist when
it defines a half maximal inhibitory concentration of less than
about 1000 ppm.
16. A screening method for determining at least one test agent
as effective for modifying the appearance of pigmented skin,
the method comprising:
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Application 13/278,465
contacting a cell, a cell culture, or bulk cells with the test agent,
wherein the cell, the cell culture, or the bulk cells comprise
ADRalB receptors; and
determining based on the binding interaction of the test agent
with the ADRalB receptors whether the test agent is an
ADRalB receptor antagonist suitable for modifying the
appearance of pigmented skin.
Claims 13 and 19 are also independent. Claim 13 is similar to claim 1
but recites ADRP3 receptors and “an ADRP3 receptor agonist,” rather than
claim l’s ADRpi receptors and an “ADRpi receptor antagonist.” Claim 19
is similar to claim 16 but recites ADRa2C receptors and “an ADRa2C
receptor antagonist,” rather than claim 16’s ADRalB receptors and “an
ADRalB receptor antagonist.”
The claims stand rejected as follows:
Claims 1, 3—5, 9, 10, and 13 under 35 U.S.C. § 103(a) as obvious
based on Potenza2 and Yang3 (Ans. 34);
2 Potenza et al., A Method for Evaluating the Effects of Ligands upon Gs
Protein-Coupled Receptors Using a Recombinant Melanophore-Based
Bioassay, 206 Analytical Biochem. 315—322 (1992).
3 Yang et al., Norepinephrine upregulates VEGF, IL-8, andIL-6 expression
in human melanoma tumor cell lines: Implications for stress-related
enhancement of tumor progression, 23 Brain, Behavior, and Immunity 267—
275 (2009).
4 The Examiner states that “[t]he prior rejection line of claims 1, 3-5, 9, 10,
and 13 incorrectly cited Yang, but the rejection of claim 1 does not rely on
Yang.” (Ans. 3.) However, the Examiner continues to cite Yang in
responding to Appellants’ arguments. (Ans. 13—16.) Therefore, we have
considered the rejections as relying on Yang in addition to the other cited
reference(s).
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Application 13/278,465
Claim 2 under 35 U.S.C. § 103(a) as obvious based on Potenza, Yang,
and Heintz5 (Ans. 5);
Claim 6 under 35 U.S.C. § 103(a) as obvious based on Potenza, Yang,
and Mahalingam6 (Ans. 7);
Claims 7 and 8 under 35 U.S.C. § 103(a) as obvious based on
Potenza, Yang, and Tan7 (Ans. 9); and
Claims 16 and 19 under 35 U.S.C. § 103(a) as obvious based on
Potenza, Yang, and Mullins8 (Ans. 11);
I
The Examiner has rejected claims 1, 3—5, 9, 10, and 13 as obvious
based on Potenza and Yang. The Examiner finds that “Potenza discloses the
claimed invention except for testing for an IC50 value of less than about
1000 ppm.” (Ans. 5.) The Examiner finds that “Yang teaches that the
expression of ADRj31 receptors (which would be stimulated by a test agent
as taught by Potenza) would lead to the upregulation of ADRj31 genes in
melanocytes.” {Id. at 13.)
The Examiner concludes that an IC50 value is a result-effective
variable, and it would have been obvious “to create the invention of Potenza
with an IC50 value of less than about 1000 ppm since it has been held that
5 Heintz et al., US 2011/0071049 Al, published Mar. 24, 2011.
6 Mahalingam et al., US 2006/0013782 Al, published Jan. 19, 2006.
7 Tan et al., US 2004/0072287 Al, published Apr. 15, 2004.
8 Mullins et al., Melatonin Agonists Induce Phosphoinositide Hydrolysis in
Xenopus Laevis Melanophores, 9 Cell. Signal. 169—173 (1997).
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Application 13/278,465
discovering an optimum value of a result effective variable involves only
routine skill in the art.” (Id. at 5.) The Examiner also reasons that
[t]he claimed invention is broadly drawn to the active steps of
contacting a cell, a cell culture, or bulk cells with a test agent. . . .
[T]he recitation of “wherein the test agent is considered to be an
effective ADRpi receptor antagonist when it defines a half
maximal inhibitory concentration of less than about 1000 ppm[”]
does not actually require an active step of measuring such an
IC50. . . . Potenza thus teaches the active steps of the claimed
invention.
(Id. at 13.)
Appellants argue that “[tjhere is no disclosure in the combination of
Potenza and Yang of a [] test agent being considered an effective ADRpi
receptor antagonist when it defines a half maximal inhibitory concentration
of less than about 1000 ppm.” (Appeal Br. 5.)
We agree with Appellants that the cited references would not have
made obvious the last step of claim 1:
determining based on the binding interaction of the test agent
with the ADRpi receptors whether the test agent is an effective
ADRpi receptor antagonist suitable for modifying the
appearance of pigmented skin, wherein the test agent is
considered to be an effective ADRpi receptor antagonist when it
defines a half maximal inhibitory concentration of less than
about 1000 ppm.
(Claim 1.)
In our view, this claim language requires determining the IC50 for a
test agent, based on the binding of the test agent with ADRpi receptors.
While the claimed method can be performed even if the IC50 for a given
agent is greater than 1000 ppm, the method nonetheless requires a step of
determining the IC50 for the agent.
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Application 13/278,465
Neither Potenza nor Yang suggest determining the IC50 for an agent
based on its binding with ADRpi receptors. Potenza describes a method of
screening agents for their effect in agonizing or antagonizing stimulatory
guanine nucleotide (Gs) proteins. (Potenza 315, abstract.) Potenza’s method
involves transfecting Xenopus laevis cells with a plasmid encoding human
ADRP2 (which Potenza refers to as P2 AR). (Id.) Potenza states that the
X. laevis cells express an endogenous Pi-like adrenergic receptor (id.) but
that, using its method, “it is possible to rapidly evaluate the effects of
antagonists on the P2 AR without apparent interference from the endogenous
P AR.” (Id. at 321, right col.) Thus, Potenza does not provide a reason for a
skilled artisan to determine the IC50 of a test agent “based on the binding
interaction of the test agent with the ADRpi receptors,” as recited in claim 1.
Yang discloses that norepinephrine (NE) upregulated production of
VEGF, IL-8, and IL-6 in human melanoma cells, and this effect was
mediated by both Pi and P2 ARs. (Yang 267, abstract.) Yang states that
“[treatment with the P-AR antagonist propranolol completely abrogated the
NE-induced upregulation of VEGF, IL-8, and IL-6 mRNA levels in all three
cell lines. These data indicate that the NE-dependent upregulation of VEGF,
IL-8, and IL-6 mRNA levels ... is mediated by the P-ARs.” (Id. at 271, left
col.) Yang does not, however, disclose treatment with a test agent that binds
specifically with ADRpi receptors.
Thus, Yang also does not provide a reason for a skilled artisan to
determine the IC50 of a test agent “based on the binding interaction of the
test agent with the ADRpi receptors,” as recited in claim 1. Likewise,
neither Potenza nor Yang provide a reason for a skilled artisan to determine
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Application 13/278,465
the IC50 of a test agent “based on the binding interaction of the test agent
with the ADR03 receptors,” as recited in claim 13.
We therefore conclude that Potenza and Yang do not support a prima
facie case that the method of claim 1 or claim 13 would have been obvious
to a person of ordinary skill in the art. The rejections of dependent claims 2
and 6—8 rely on the same reasoning as the rejection of claim 1, and are
reversed for the same reason.
II
The Examiner has rejected claims 16 and 19 as obvious based on
Potenza, Yang, and Mullins. Claims 16 and 19 are similar to claim 1 but
require determining the interaction of a test agent with ADRalB or
ADRa2C receptors, respectively.
The Examiner finds that “Mullins teaches prazosin, an alpha-
adrenergic antagonist, having a demonstrated affinity for low affinity
melatonin binding sites the [sic, on the?] dermal melanophores.” (Ans. 12.)
The Examiner concludes that it would have been obvious “to perform a
screening method wherein the test agent interacts with ADRal or ADRa2
receptors for the modification of pigmented skin since there would be a
reasonable expectation of success that test agents that interact with alpha-
adrenergic receptors would bind with melatonin sites.” (Id.)
Appellants argue that none of the cited references disclose using an
ADRalB receptor or ADRa2C receptor. (Appeal Br. 9.)
We agree with Appellants that the cited references do not support a
prima facie case of obviousness. Mullins discloses that melatonin has been
implicated in a variety of neurobiological effects. (Mullins 170, left col.)
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Application 13/278,465
Mullins discloses that “melatonin binding sites in Xenopus Laevis
melanophores are functionally coupled to phosphoinositide hydrolysis as a
second messenger system.” {Id. at 171, right col.) Mullins states that
“[pjhosphoinositide hydrolysis induced by 2-iodomelatonin (0.1 pM) was
blocked by . . . prazosin (10 pM), an alpha-adrenergic antagonist which has
been shown to have affinity for low affinity melatonin binding sites.” {Id. at
171, left col.) Mullins also states that “[responses mediated by 2-
iodomelatonin were not sensitive to . . . phentolamine (10 pM), an alpha-
adrenergic antagonist, which shows no affinity for melatonin binding sites.
This suggests that the phosphoinositide responses observed were not due to
stimulation of. . . alpha-adrenergic receptors.” {Id.)
Thus, while Mullins discloses that prazosin is an antagonist of alpha-
adrenergic receptors, it also states that its results were due to prazosin’s
binding to low affinity melatonin binding sites, not stimulation of alpha-
adrenergic receptors. Mullins therefore does not provide a reason for a
skilled artisan to determine the binding interaction of a test agent for either
ADRalB receptors or ADRa2C receptors, as required by claims 16 and 19,
respectively.
SUMMARY
We reverse all of the rejections on appeal.
REVERSED
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