Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claim Status
Applicant’s election without traverse to Group I, drawn to claims 1, 3, 6-13, 15-17, 19-21, 27-28, 30, 34, and 36-37, and species election to an effective amount of a nicotinic acetylcholine receptor (nAchR) agonist or pharmaceutically acceptable salt thereof as recited in claims 2-3 in the reply filed on 24 Apr 2026 is acknowledged.
Amendments to the claims filed 24 Apr 2026 are acknowledged. Claim 2 is canceled. Claims 1 and 3 are amended. Claims 11, 65, and 71 are withdrawn.
Claims 1, 3, 6-13, 15-17, 19-21, 27-28, 30, 34, 36-37, 65, and 71 are pending. Claims 1, 3, 6-10, 12-13, 15-17, 19-21, 27-28, 30, 34, and 36-37 are considered on the merits.
Information Disclosure Statement
The listing of references in the specification is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered.
Specification
The use of the term "mesoscale discovery assay" in par. 625, which is a trade name or a mark used in commerce, has been noted in this application. The term should be accompanied by the generic terminology; furthermore, the term should be capitalized wherever it appears or, where appropriate, include a proper symbol indicating use in commerce such as ™, SM , or ® following the term. Although the use of trade names and marks used in commerce (i.e., trademarks, service marks, certification marks, and collective marks) are permissible in patent applications, the proprietary nature of the marks should be respected and every effort made to prevent their use in any manner which might adversely affect their validity as commercial marks.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. § 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1, 3, 6-10, 12-13, 15-17, and 36 are rejected under 35 U.S.C. § 102(a)(2) as being anticipated by Nau (US 2021/0379066 A1, filed 08 Jan 2021).
The applied reference has a common assignee (Oyster Point Pharma, Inc.) and joint inventor (Jeffrey Alan Nau) with the instant application. Based upon the earlier effectively filed date of the reference, it constitutes prior art under 35 U.S.C. § 102(a)(2). This rejection under 35 U.S.C. § 102(a)(2) might be overcome by: (1) a showing under 37 CFR 1.130(a) that the subject matter disclosed in the reference was obtained directly or indirectly from the inventor or a joint inventor of this application and is thus not prior art in accordance with 35 U.S.C. § 102(b)(2)(A); (2) a showing under 37 CFR 1.130(b) of a prior public disclosure under 35 U.S.C. § 102(b)(2)(B) if the same invention is not being claimed; or (3) a statement pursuant to 35 U.S.C. § 102(b)(2)(C) establishing that, not later than the effective filing date of the claimed invention, the subject matter disclosed in the reference and the claimed invention were either owned by the same person or subject to an obligation of assignment to the same person or subject to a joint research agreement.
Regarding claims 1 and 36, Nau discloses a method of treating dry eye disease (an ocular surface disorder and a cornea disorder) in a subject by administering a positive allosteric modulator (a primary therapeutic agent) to the nasal cavity (tissue in fluidic communication with the eye via the nasolacrimal duct) and a nicotinic acetylcholine receptor (nAchR) agonist (par. 2 and 6).
Regarding claim 3, Nau discloses that the nAchR agonist may be varenicline, a pharmaceutically acceptable salt of varenicline, compound 1, which is (R)-5-((E)-2-pyrrolidin-3-ylvinyl)pyrimidine (CAS Registry No. 753015-44-0), a pharmaceutically acceptable salt of compound 1, or a full agonist of nAchR subtypes α4β2, α3β4, α3α5β4, or α4α6β2 (par. 6 and 50).
Regarding claims 6-7, Nau discloses that the nAchR agonist may be administered to the nose by nasal spray (par. 134).
Regarding claims 8 and 12-13, Nau discloses that the positive allosteric modulator (primary therapeutic agent) may be delivered topically (to the cornea) (par. 540).
Regarding claims 9-10, Nau discloses that the nAchR agonist (treatment that increases tear production) may be administered beginning 7-14 days subsequent to administration of the positive allosteric modulator (primary therapeutic agent) (par. 145).
Regarding claims 15-17, Nau is silent as to the results of the amount of primary therapeutic agent in the tear film or cornea. However, under the principles of inherency, when the claim recites an old composition or structure and the "use" is directed to a result or property of that composition or structure, the claim is anticipated. In re May, 574 F.2d 1082, 1090, 197 USPQ 601, 607 (CCPA 1978). See MPEP § 2112.02(II). Because Nau teaches the same composition used in the same method claimed, the result of "an increased amount of the primary therapeutic delivered to" the tear film (claims 15 and 17) or cornea (claim 16) "of an eye of the subject in a predetermined time compared to administration of the primary therapeutic agent alone", "wherein the determined time is between about 5 minutes to about 1 hour" (claim 17) is inherent to the method disclosed by Nau.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. § 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claims 1, 3, 6-7, and 36 are rejected under 35 U.S.C. § 103 as being unpatentable over Gong (N. Gong, et al., Invest Ophthalmol Vis Sci, 2007) in view of Yerxa (US 6,277,855 B1, 2001) and as evidenced by de Moura (F.B. de Moura and J. Bergman, J Pharmacol Exp Ther, Jan 2021).
Regarding claims 1 and 36, Gong teaches administration of a recombinant adenoviral vector comprising a polynucleotide encoding nerve growth factor (NGF) (a primary therapeutic agent and a gene product) for the prevention of corneal transplant rejection (treatment of a corneal wound, a corneal disorder) (Abstract and Materials and Methods p. 1044).
Gong additionally teaches that local administration of a gene therapy is more effective in preventing corneal allograft rejection than systemic expression of the gene (Discussion p. 1049). Gong further teaches that immunosuppression is required for prevention of corneal transplant rejection and that application of NGF as a single agent is insufficient to achieve long term graft survival (Discussion p. 1050).
Gong does not teach administering a treatment comprising a nicotinic acetylcholine receptor (nAchR) agonist that increases tear production as required by claims 1, 3, 6-8, and 36.
However, Yerxa teaches administration of nAchR agonists to increase "hydration and lubrication of lacrimal tissues" (increase tear production, claim 1) (Abstract). Yerxa further teaches that administration of an nAchR agonist is useful for treating dry eye disease and corneal injury in part by reducing inflammation on ocular surfaces (Abstract and col. 4).
Regarding claim 3, Yerxa teaches administration of epibatidine, which is a full agonist of the α4β2 nAchR subtype, for increasing tear production (Yerxa col. 4 and de Moura Discussion p. 105).
Regarding claims 6-7, Yerxa teaches that the nAchR agonist may be administered locally to the nasal cavity by nasal spray (col. 8).
Therefore, it would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to combine the method of preventing corneal transplant rejection by administration of a recombinant adenoviral vector comprising a polynucleotide encoding NGF as taught by Gong with nasal spray administration of the nAchR α4β2 agonist epibatidine to increase tear production as taught by Yerxa to arrive at the claimed invention. One would be motivated to make such a combination as Gong teaches that immunosuppression is required for prevention of corneal transplant rejection and that application of NGF as a single agent is insufficient to achieve long term graft survival and as Yerxa teaches that nAchR agonism reduces inflammation on the ocular surface, which would aid in immunosuppression. One would have a reasonable expectation of success in making the combination as Yerxa demonstrates increased tear production when administering an nAchR agonist.
Claims 8-10, 12-13, 15-17, 19-21, 27, 30, 34, and 37 are rejected under 35 U.S.C. § 103 as being unpatentable over Gong (N. Gong, et al., Invest Ophthalmol Vis Sci, 2007) and Yerxa (US 6,277,855 B1, 2001) as applied to claims 1, 3, 6-7, and 36 and in further view of Thomas (P.B. Thomas, et al. Invest Ophthalmol Vis Sci, 2010) and as evidenced by Dieckmann (G. Dieckmann, et al. Ocular Surface, 2019) and Alimohammadi (H. Alimohammadi and W.L. Silver, Chem Senses, 2000).
Gong and Yerxa teach a method of treating a cornea disorder by administration of a recombinant adenoviral vector comprising a polynucleotide encoding nerve growth factor (NGF) for the prevention of corneal transplant rejection (treatment of a corneal wound, a corneal disorder) and an nAchR agonist as discussed in the rejection of claims 1, 3, 6-7, and 36 under 35 U.S.C. § 103 above.
Regarding claim 21, the viral vector taught by Gong is an adenovirus vector (Materials and Methods p. 1044).
Regarding claim 27, Gong teaches that adeno-associated viruses (AAV) or lentiviruses should be considered as vectors for NGF gene therapy because AAV and lentiviruses are less immunogenic than adenoviruses (Discussion p. 1051).
Gong further teaches administration of an adenovirus comprising a polynucleotide encoding NGF by intraperitoneal injection (Materials and Methods p. 1044). Gong further teaches that local administration of a gene therapy is more effective in preventing corneal allograft rejection than systemic expression of the gene (Discussion p. 1049). Gong further teaches that immunosuppression is required for prevention of corneal transplant rejection and that application of NGF as a single agent is insufficient to achieve long term graft survival (Discussion p. 1050).
Gong and Yerxa do not teach administration of the gene product to at least one lacrimal gland as required by claims 8-10, 12-13, 15-17, 19-21, 27, 30, 34, and 37.
However, Thomas teaches delivery of an adeno-associated virus (AAV) serotype 2 (AAV2, claim 27) comprising a polynucleotide encoding interleukin 10 (IL-10, a similar gene product as NGF taught by Gong) to the inferior lacrimal gland (claims 8, 12-13, 19, and 37) (Abstract and Materials and Methods p. 5138).
Regarding claims 19, 27, and 30, Thomas teaches that "adenovirus-mediated gene transfer results only in transient transgene expression" and that their previous attempts to transfect interleukin 10 (IL-10) using an adenovirus resulted in expression of IL-10 protein in tears for less than two weeks, whereas AAV vectors "have been found to mediate long-term transgene expression with minimal pathogenicity in many organs" (Introduction p. 5138). Thomas demonstrates that expression of IL-10 protein persists in the tear film for at least 12 weeks in animals transduced with an AAV2 vector comprising a nucleotide encoding for IL-10 (Results p. 5140 and Table 2).
Regarding claims 15-17 and 34, Dieckmann teaches that intranasal stimulation of trigeminal nerve endings can stimulate the nasolacrimal reflex to rapidly induce tear production and that within 5 min of stimulation, tear production increases and that the protein and lipid content of the tears remains equivalent to tear composition prior to stimulation, indicating that stimulation further stimulates release of proteins and lipids from secretory vesicles (pp. 20 and 25). Furthermore, Alimohammadi teaches that nicotinic acetylcholine receptors are expressed on the ends of the trigeminal nerve within the nasal cavity and that nAchR agonism can stimulate the trigeminal nerve (Abstract). Therefore, the result of an increased amount of NGF (primary therapeutic agent and gene product) in the tear film on the surface of the cornea about 5 min to about 1 h subsequent to administration of an nAchR agonist to induce tear production compared to administration of administration of an AAV2 vector comprising a polynucleotide encoding NGF alone is considered inherent to the combined teachings of Gong, Yerxa, Thomas.
Regarding claims 9-10, Gong further teaches that expression of high levels of NGF can be measured in corneal allografts virally transfected ex vivo after 3 days (Results p. 1045). Therefore, a skilled artisan would recognize that administration of an AAV2 vector comprising a polynucleotide encoding NGF requires time, on the order of days, for transfection of lacrimal gland cells to result in significant expression of NGF in the lacrimal gland and thus, administration of an nAchR agonist would increase delivery of NGF to the tear film if applied subsequent to administration of the gene product. Gong, Yerxa, and Thomas do not teach administration of nAchR agonist 4 to 10 days subsequent to administration of the primary therapeutic as required by claim 10. However, a prima facie case of obviousness exists where the claimed ranges or amounts do not overlap with the prior art but are merely close. Titanium Metals Corp. of America v. Banner, 778 F.2d 775, 783, 227 USPQ 773, 779 (Fed. Cir. 1985) (Court held as proper a rejection of a claim directed to an alloy "having 0.8% nickel, 0.3% molybdenum, up to 0.1% iron, balance titanium" as obvious over a reference disclosing alloys of 0.75% nickel, 0.25% molybdenum, balance titanium and 0.94% nickel, 0.31% molybdenum, balance titanium. "The proportions are so close that prima facie one skilled in the art would have expected them to have the same properties."). It is routine procedure to optimize component amounts to arrive at an optimal product that is superior for its intended use, since it has been held where the general conditions of a claim are disclosed in the prior art, discovering the optimum or workable ranges involves only routine skill in the art. See MPEP § 2144.05. Skilled artisan would be able to optimize the timing of administration of an nAchR based on sufficient expression of the gene product in the lacrimal gland.
Therefore, it would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to substitute intraperitoneal delivery of the adenovirus vector taught by Gong for injection of an AAV2 vector into the lacrimal gland as taught by Thomas to arrive at the claimed invention. One would be motivated to substitute an adenovirus for an AAV2 vector as both Gong and Thomas teach that adenoviruses can only achieve transient expression of a transgene and are immunogenic and Thomas teaches that AAV vectors can achieve long term transgene expression in many tissues. One would be motivated to substitute intraperitoneal injection for injection into the lacrimal gland as Gong teaches that local viral transfection of NGF is more effective than systemic and as Thomas teaches that lacrimal gland transfection results in secretion of a gene product to the ocular surface for an extended period. One would be motivated to administer an nAchR agonist subsequent to administration of a gene therapy as Gong teaches that significant expression of NGF can be measured 3 days after administration of the viral vector and that Dieckmann and Alimohammadi show that nAchR agonism can induce release of lacrimal gland proteins, which would include a virally transfected gene product, to the tear film. One would have a reasonable expectation of success in substituting an adenovirus vector for an AAV2 vector as Thomas teaches that adenovirus transfection results in expression of the gene product for less than two weeks whereas AAV2 transfection results in expression of the gene product for at least 12 weeks. One would have a reasonable expectation of success in substituting systemic administration of a viral vector comprising NGF with lacrimal gland injection as Thomas demonstrates expression of a similar gene product in the tear film for at least 12 weeks. One would have a reasonable expectation of success in administering an nAchR agonist subsequent to administration an AAV2 vector comprising a polynucleotide encoding NGF as Gong teaches that significant expression of NGF takes days and Dieckmann teaches that intranasal stimulation of the nasolacrimal reflex results in rapid induction of tear production.
Claim 28 is rejected under 35 U.S.C. § 103 as being unpatentable over Gong (N. Gong, et al., Invest Ophthalmol Vis Sci, 2007), Yerxa (US 6,277,855 B1, 2001), and Thomas (P.B. Thomas, et al. Invest Ophthalmol Vis Sci, 2010) as applied to claims as applied to claims 1, 3, 6-10, 12-13, 15-17, 19-21, 27, 30, 34, and 36-37 above and in further view of François (A. François, et al., Methods & Clin Develop, 2018).
Gong, Yerxa, and Thomas teach a method of treating a cornea disorder by administration of an adeno-associated virus serotype 2 (AAV2) vector comprising a polynucleotide encoding nerve growth factor (NGF) to the lacrimal gland for the prevention of corneal transplant rejection (treatment of a corneal wound, a corneal disorder) and an nAchR agonist as discussed in the rejection of claims as applied to claims 1, 3, 6-10, 12-13, 15-17, 19-21, 27, 30, 34, and 36-37 under 35 U.S.C. § 103 above.
Thomas further teaches administration of 108 plaque forming units (PFU) in 200 μL (5 x 108 PFU/mL) of the AAV2 vector (Materials and Methods p. 5139). Thomas further teaches that a certain dose threshold is required "before useful proteins are produced at therapeutic levels" (Discussion p. 5143).
Gong, Yerxa, and Thomas do not teach administration of about 1012 or about 6.2 x 1012 genome copies/mL of the AAV vector as required by claim 28.
However, François teaches that plaque assays are an inaccurate method for determining infectious titer because AAV infection does not result in a cytopathic effect (Introduction pp. 223-224). François further teaches that accurate measurement of viral titer is critical to ensure efficacy of an AAV gene therapy product and that one of the most widely used methods is measurement of viral genome replication by quantitative PCR to determine number of genome copies (Introduction p. 224).
Furthermore, a prima facie case of obviousness exists where the claimed ranges or amounts do not overlap with the prior art but are merely close. Titanium Metals Corp. of America v. Banner, 778 F.2d 775, 783, 227 USPQ 773, 779 (Fed. Cir. 1985) (Court held as proper a rejection of a claim directed to an alloy "having 0.8% nickel, 0.3% molybdenum, up to 0.1% iron, balance titanium" as obvious over a reference disclosing alloys of 0.75% nickel, 0.25% molybdenum, balance titanium and 0.94% nickel, 0.31% molybdenum, balance titanium. "The proportions are so close that prima facie one skilled in the art would have expected them to have the same properties."). It is routine procedure to optimize component amounts to arrive at an optimal product that is superior for its intended use, since it has been held where the general conditions of a claim are disclosed in the prior art, discovering the optimum or workable ranges involves only routine skill in the art. See MPEP § 2144.05.
A skilled artisan would be able to optimize the viral titer taught by changing the method of measuring the titer and adjusting the amount of virus delivered to achieve a therapeutic effect.
Therefore, it would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to substitute the method of measuring AAV dose by plaque assay as taught by Gong, Yerxa, and Thomas with measurement of genome copy number as taught by François and to optimize the dose of AAV particles delivered arrive at the claimed invention. One would be motivated to make such a substitution as François teaches that plaque assays are an inaccurate approach to AAV dosing and as measurement of genome copies is more reliable. One would be motivated to optimize the dose of AAV particles delivered as routine optimization is obvious to a skilled artisan. One would have a reasonable expectation of success in making the combination as François teaches that quantitative PCR to measure viral genome replication is widely used in the art. One would have a reasonable expectation of success in optimizing the dose of AAV particles delivered as routine optimization is obvious to a skilled artisan.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1, 3, and 6 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 5 of U.S. Patent No. US 9,504,644 B2 (hereafter '644) in view of Yerxa (US 6,277,855 B1, 2001). Claim 5 of '644 recites a method of increasing tear production comprising local administration of one or more substances that prevent the entry or reduce the entry of the nicotinic acetylcholine receptor (nAchR) into the desensitized state (administering an effective amount of a primary therapeutic agent to the eye, claim 1 step (a)) and administration into the nasal cavity (local nasal administration, claim 6) varenicline (claim 3), which is an nAchR agonist that increases tear production (claim 1 step (b)). The nasal cavity is in fluidic communication with the eye via the nasolacrimal duct.
Claim 5 of '644 does not recite treatment of an ocular surface disorder, corneal disorder, or anterior chamber disorder as required by claims 1, 3, and 6 of the immediate application.
However, Yerxa teaches that administering an nAchR agonist via nasal spray (local nasal administration) increases hydration and lubrication of lacrimal tissues in a subject (increases tear production) and that the method is useful for the treatment of dry eye disease (an ocular surface disorder) and corneal injury (a corneal disorder) (Abstract). Yerxa further teaches that administration of the nAchR agonist metanicotine could alleviate symptoms in a rabbit model of dry eye disease (Example 1, col. 10).
Therefore, it would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to apply the known method of increasing tear production by administration of an nAchR agonist and a primary therapeutic agent as recited in claim 5 of '644 to the treatment of dry eye disease as taught by Yerxa to arrive at the claimed invention. One would be motivated to apply the method as Yerxa teaches that increasing tear production is useful in the treatment of dry disease. One would have a reasonable expectation of success in making the combination as Yerxa demonstrates that increased tear production using a similar nAchR agonist could alleviate symptoms of dry eye disease.
Claims 1, 3, and 6 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 5 of U.S. Patent No. US 9,532,944 B2 (hereafter '944) in view of Yerxa (US 6,277,855 B1, 2001) and as evidenced by Tsubota (K. Tsubota, et al., Int J Mol Sci, 2020). Claim 5 of '944 recites a method of improving ocular comfort comprising local administration of one or more substances that prevent the entry or reduce the entry of the nicotinic acetylcholine receptor (nAchR) into the desensitized state (administering an effective amount of a primary therapeutic agent to the eye, claim 1 step (a)) and administration into the nasal cavity (local nasal administration, claim 6) varenicline (claim 3), which is an nAchR agonist that increases tear production (claim 1 step (b)). The nasal cavity is in fluidic communication with the eye via the nasolacrimal duct.
Claim 5 of '944 does not recite treatment of an ocular surface disorder, corneal disorder, or anterior chamber disorder as required by claims 1, 3, and 6 of the immediate application.
However, Yerxa teaches that administering an nAchR agonist via nasal spray (local nasal administration) increases hydration and lubrication of lacrimal tissues in a subject (increases tear production) and that the method is useful for the treatment of dry eye disease (an ocular surface disorder) and corneal injury (a corneal disorder) (Abstract). Yerxa further teaches that administration of the nAchR agonist metanicotine could alleviate symptoms in a rabbit model of dry eye disease (Example 1, col. 10). Ocular discomfort is defining characteristic of dry eye disease (Tsubota, Abstract).
Therefore, it would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to apply the known method of increasing tear production by administration of an nAchR agonist and a primary therapeutic agent as recited in claim 5 of '944 to the treatment of dry eye disease as taught by Yerxa to arrive at the claimed invention. One would be motivated to apply the method as Yerxa teaches that increasing tear production is useful in the treatment of dry disease. One would have a reasonable expectation of success in making the combination as Yerxa demonstrates that increased tear production using a similar nAchR agonist could alleviate symptoms of dry eye disease.
Claims 1, 3, and 6 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 5 of U.S. Patent No. 9,597,284 B2 (hereafter '284). Although the claims at issue are not identical, they are not patentably distinct from each other because claim 5 of '284 recites a method of treating dry eye (an ocular surface disorder) comprising local administration of one or more substances that prevent the entry or reduce the entry of the nicotinic acetylcholine receptor (nAchR) into the desensitized state (administering an effective amount of a primary therapeutic agent to the eye, claim 1 step (a)) and administration into the nasal cavity (local nasal administration, claim 6) varenicline (claim 3), which is an nAchR agonist that increases tear production (claim 1 step (b)). The nasal cavity is in fluidic communication with the eye via the nasolacrimal duct.
Claims 1, 3, and 6 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 25 of U.S. Patent No. 10,456,396 B2 (hereafter '396). Although the claims at issue are not identical, they are not patentably distinct from each other because claim 25 of '396 recites a method of treating dry eye (an ocular surface disorder) comprising local administration of one or more substances that prevent the entry or reduce the entry of the nicotinic acetylcholine receptor (nAchR) into the desensitized state (administering an effective amount of a primary therapeutic agent to the eye, claim 1 step (a)) and administration into alternating nostrils (local nasal administration, claim 6) varenicline (claim 3), which is an nAchR agonist that increases tear production (claim 1 step (b)). The nasal cavity is in fluidic communication with the eye via the nasolacrimal duct.
Conclusion
No claim is allowed.
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Eric B Wright, PhD
Examiner
Art Unit 1632
/Eric B Wright/Examiner, Art Unit 1632 /VALARIE E BERTOGLIO/Primary Examiner, Art Unit 1632
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