DETAILED ACTION
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Status of the Application
Receipt is acknowledged of Applicants’ amendment and remarks, filed on 02/20/2026, in which claims 16-21 are newly added.
Claims 1-21 are pending and are examined on the merits herein.
Priority
The instant application is a 371 of PCT/JP2020/024916, filed on 06/24/2020, which claims foreign priority of JP 2019-117642 filed on 06/25/2019.
Information Disclosure Statement
The information disclosure statement (IDS) dated 02/20/2026 complies with the provisions of 37 CFR 1.97, 1.98 and MPEP § 609. Accordingly, the information disclosure statement has been considered by the examiner.
The following are maintained or new grounds of rejection necessitated by Applicant’s amendment, in which claims 16-21 are newly added.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 1-6, 12, 14, 16, and 19 are rejected under 35 U.S.C. 103 as being unpatentable over Jester et al. (BMC Ophthalmology, 2015; PTO-892 09/30/2024) in view of Imai et al. (US 10,925,888 B2; PTO-892) and Zeev et al. (Clinical Ophthalmology 2014; PTO-892 08/20/2025).
Jester discusses the causes and symptoms of meibomian gland dysfunction (MGD) (abstract). Jester teaches that MGD is a common eyelid disorder with the incidence increasing with age (page 3, paragraph 1). The meibomian glands excrete lipid onto the surface of the eye to form the lipid layer of the tear film to reduce aqueous tear evaporation and MGD causes loss of glands resulting in decreased tear film lipid (page 3, paragraph 1). Defects in meibomian gland acinar differentiation and function leading to gland atrophy play a critical role in the development of clinical MGD (paragraph bridging pages 4-5). Specifically, Jester teaches that repeated stress-induced hyperproliferation of the meibomian gland may lead to early exhaustion of the progenitor or stem cell population within the gland that is necessary for maintenance of acinar function. Because of this, repeated exposure to environmental stress such as ocular surface drying is one cause of the loss of acinar cells (paragraph bridging pages 8-10). Jester teaches that recent analysis of MGD uses non-invasive and non-contact imaging systems and focuses on gland dropout, the severity of which has been shown to be highly correlated with meibomian gland lipid changes (page 5, paragraph 1). Jester further teaches that ocular surface inflammation is associated with dry eye (page 8, paragraph 2).
The teachings of Jester differ from that of the instantly claimed invention in that Jester does not teach administration of nicotinamide mononucleotide or inspection of a meibomian gland.
Imai teaches that dry eye is one of the most prevalent eye disorders, particularly among the elderly (col 2, lines 41-43). Imai discloses methods and compositions for treating conditions including age-related changes in eye function, comprising administering nicotinamide mononucleotide (NMN) to a subject (abstract). Specifically, Imai discloses a method of treating dry eye in a subject, comprising administering to a subject in need of treatment a pharmaceutically effective amount of NMN (claim 1). Imai teaches that the dry eye may be age-associated dry eye (claim 2). Imai teaches that the composition may be administered topically by direct ocular application including eye drops (claim 9 and col. 5, lines 28-29). Example 7 discloses a dose dependent increase in tear production in mice administered NMN, which Imai teaches as providing an effective intervention to protect eye function from dry eye diseases (col. 49, lines 40-57).
Zeev discusses the state of the art in the diagnosis of dry eye disease (abstract). Zeev teaches that lid margin assessment is performed by examining meibomian glands using a slit-lamp by pulling down on the lower lid and up on the upper lid. The glands are expressed and the consistency and contents of the glands evaluated. The lid margin assessment should also include evaluation of gland dropout, telangiectasias, meibomian gland plugging, and collarettes (page 587, paragraph 3). Zeev teaches that, due to its complex and varied presentation, dry eye disease often tends to be misdiagnosed and so it is critical to rely heavily on careful clinical history-taking, a detailed slit-lamp examination, and utilization of tests such as tear break-up time and eyelid margin assessment for the diagnosis of dry eye disease (page 588, paragraph 2).
It would have been prima facie obvious before the effective filing date of the invention to treat patients experiencing MGD as taught by Jester using the method of administration of NMN as taught by Imai because Imai teaches that the method is suitable for treatment of patients with age-associated dry eye, and Jester teaches that MGD is a common eyelid disorder with the incidence increasing with age and further teaches that patients suffering from age-related MGD are expected to be susceptible to dry eye disease. Furthermore, although the teachings of Jester do not expressly teach inspecting a meibomian gland function, it would have been prima facie obvious before the effective filing date of the invention for one of ordinary skill in the art to do so because Imai teaches that the composition comprising NMN is administered to a patient suffering from dry eye disease and Zeev teaches that eyelid margin assessment includes the expression of the meibomian gland and is routinely used in the process of diagnosing dry eye disease such that a practitioner would have examined the function of the meibomian gland in the diagnosis of dry eye prior to administering the composition comprising NMN.
Regarding instant claims 2 and 3, it would have been prima facie obvious before the effective filing date of the invention that treating dry eye through the administration of NMN as taught by Imai would increase a number of meibomian gland acinar cells and thereby increase the amount of lipid secretion in the patient, as described by Jester, because Jester suggests that the number of acinar cells is decreased by meibomian gland dysfunction and in particular by ocular surface drying that leads to early exhaustion of the progenitor or stem cell population and Imai teaches administering NMN as providing an effective intervention to protect eye function. It would be prima facie obvious that treating dry eye using the method of administering NMN taught by Imai would reduce the ocular surface drying that is taught by Jester as decreasing the number of acinar cells. As a result, if dry eye is treated such that there is no longer ocular surface drying, one of ordinary skill in the art would have a reasonable expectation of success in improving the number of acinar cells and lipid secretion in a meibomian gland using the method taught by Imai because Jester teaches that ocular surface drying leads to a decrease in the number of acinar cells.
Claims 17-18 and 20-21 are rejected under 35 U.S.C. 103 as being unpatentable over Jester et al. (BMC Ophthalmology, 2015; PTO-892 09/30/2024) in view of Imai et al. (US 10,925,888 B2; PTO-892) and Zeev et al. (Clinical Ophthalmology 2014; PTO-892 08/20/2025) as applied to claims 1 and 5, further in view of Braidy et al. (Antioxidants and Redox Signaling, 2019; PTO-892).
The combined teachings of Jester, Imai, and Zeev are as above. Imai further teaches that NMN can be delivered in prodrug form (col. 9, line 3). Imai states that prodrugs can refer to compounds that can be transformed in vivo to yield NMN (col. 9, lines 27-28). Imai further teaches that the composition may include nicotinamide mononucleotide (NMN), a salt thereof and/or a prodrug thereof (col. 16, lines 1-4). Imai teaches methods of augmentation of NAD+ levels during aging through NMN administration to maintain an NSPC pool (col. 15, lines 58-61).
The combined teachings of Jester, Imai, and Zeev differ from that of the instantly claimed invention in that they do not teach administration of nicotinamide riboside (NR).
Braidy teaches that boosting the NAD+ pool by utilizing precursor molecules may have multiple health benefits and a diverse range of therapeutic implications. Braidy further teaches that NA, NAM, NMN, and NR are known as potent NAD+ boosters. NMN and NR may also be used as a general supplement in patients who have adverse responses to NA and NAM (page 273, paragraph 3). Braidy further teaches that NR is safe in mice and humans with no adverse effects reported (paragraph bridging page 273-274). Figure 2 on page 255 shows the NAD+ metabolome and states that NR is phosphorylated to form NMN by NRK1/NRK2, which is then subsequently converted to NAD+ by NMNAT1-3.
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It would have been prima facie obvious before the effective filing date of the claimed invention to exchange the NMN in the method suggested by the combined teachings of Jester, Imai, and Zeev with NR or a combination of NMN and NR to arrive at the instantly claimed invention because Imai teaches methods of augmentation of NAD+ levels during aging through NMN administration and Braidy teaches that NMN and NR are both known as potent NAD+ boosters and that NR is a precursor to NMN in vivo. One of ordinary skill in the art would have a reasonable expectation of success because Imai teaches that NMN can be delivered in prodrug form such as a compound that can be transformed in vivo to yield NMN, and that the composition may include a combination of NMN and a NMN prodrug.
Claims 1, 4, 7-11, and 16 are rejected under 35 U.S.C. 103 as being unpatentable over Findlay et al. (Aust Prescr, 2018; cited in PTO-892 09/30/2024) in view of Imai et al. (US 10,925,888 B2; PTO-892) and Zeev et al. (Clinical Ophthalmology 2014; PTO-892 08/20/2025).
Findlay teaches the state of the art in treating dry eye disease, which is also known as keratoconjunctivitis sicca, is characterized by a loss of homeostasis of the tear film as well as ocular surface inflammation and damage (page 160, paragraph 1). Findlay teaches that advancing age is a major risk factor from dry eye disease (page 160, paragraph 6). Findlay teaches that MGD is extremely common in dry eye disease and contributes to the inflammatory process (abstract). Blepharitis, or lid margin inflammation, is both a cause and an effect of MGD (page 160, paragraph 5). Findlay teaches that treating MGD includes expression of blocked glands (page 162, paragraph 3). Findlay teaches that the material excreted from meibomian glands is meibum (page 161, paragraph 8). Findlay teaches that patients with dry eye disease often report foreign body sensation and ocular discomfort (page 160, paragraph 7).
The teachings of Findlay differ from that of the instantly claimed invention in that Findlay does not teach administration of nicotinamide mononucleotide or inspection of a meibomian gland.
Imai discloses methods and compositions for treating conditions including age-related changes in eye function, comprising administering nicotinamide mononucleotide (NMN) to a subject (abstract). Specifically, Imai discloses a method of treating dry eye in a subject, comprising administering to a subject in need of treatment a pharmaceutically effective amount of NMN (claim 1). Imai teaches that the composition may be administered topically by direct ocular application including eye drops (claim 9 and col. 5, lines 28-29). Example 7 discloses a dose dependent increase in tear production in mice administered NMN, which Imai teaches as providing an effective intervention to protect eye function from dry eye diseases (col. 49, lines 40-57).
Zeev discusses the state of the art in the diagnosis of dry eye disease (abstract). Zeev teaches that lid margin assessment is performed by examining meibomian glands using a slit-lamp by pulling down on the lower lid and up on the upper lid. The glands are expressed and the consistency and contents of the glands evaluated. The lid margin assessment should also include evaluation of gland dropout, telangiectasias, meibomian gland plugging, and collarettes (page 587, paragraph 3). Zeev teaches that, due to its complex and varied presentation, dry eye disease often tends to be misdiagnosed and so it is critical to rely heavily on careful clinical history-taking, a detailed slit-lamp examination, and utilization of tests such as tear break-up time and eyelid margin assessment for the diagnosis of dry eye disease (page 588, paragraph 2).
It would have been prima facie obvious before the effective filing date of the invention to treat patients experiencing MGD and blepharitis, that is, excessive lipid accumulation in the duct of the meibomian gland, as well as foreign body sensation and ocular discomfort as taught by Findlay using the method of administration of NMN as taught by Imai because Findlay teaches that dry eye disease is caused by blepharitis which is both a cause and an effect of MGD and Imai teaches that the method is suitable for treatment of patients with dry eye. Furthermore, although the teachings of Findlay do not expressly teach inspecting a meibomian gland function, it would have been prima facie obvious before the effective filing date of the invention for one of ordinary skill in the art to do so because Imai teaches that the composition comprising NMN is administered to a patient suffering from dry eye disease and Zeev teaches that eyelid margin assessment includes the expression of the meibomian gland and is routinely used in the process of diagnosing dry eye disease such that a practitioner would have examined the function of the meibomian gland in the diagnosis of dry eye prior to administering the composition comprising NMN.
Claims 2-3 and 12-15 are rejected under 35 U.S.C. 103 as being unpatentable over Findlay et al. (Aust Prescr, 2018; cited in PTO-892 09/30/2024) in view of Imai et al. (US 10,925,888 B2; PTO-892) and Zeev et al. (Clinical Ophthalmology 2014; PTO-892 08/20/2025), as applied to claim 1 above, further in view of Jester et al. (BMC Ophthalmology, 2015; PTO-892 09/30/2024).
The combined teachings of Findlay, Imai, and Zeev are as above.
The combined teachings of Findlay, Imai, and Zeev differ from that of the instantly claimed invention in that they do not teach increasing a number of meibomian gland acinar cells (instant claim 2) or lipid secretion from the meibomian gland (instant claim 3).
Jester discusses the causes and symptoms of meibomian gland dysfunction (MGD) (abstract). Jester teaches that MGD is a common eyelid disorder with the incidence increasing with age (page 3, paragraph 1). The meibomian glands excrete lipid onto the surface of the eye to form the lipid layer of the tear film to reduce aqueous tear evaporation and MGD causes loss of glands resulting in decreased tear film lipid (page 3, paragraph 1). Defects in meibomian gland acinar differentiation and function leading to gland atrophy play a critical role in the development of clinical MGD (paragraph bridging pages 4-5). Specifically, Jester teaches that repeated stress-induced hyperproliferation of the meibomian gland may lead to early exhaustion of the progenitor or stem cell population within the gland that is necessary for maintenance of acinar function. Because of this, repeated exposure to environmental stress such as ocular surface drying is one cause of the loss of acinar cells (paragraph bridging pages 8-10). Jester teaches that recent analysis of MGD uses non-invasive and non-contact imaging systems and focuses on gland dropout, the severity of which has been shown to be highly correlated with meibomian gland lipid changes (page 5, paragraph 1). Jester further teaches that ocular surface inflammation is associated with dry eye (page 8, paragraph 2).
It would have been prima facie obvious before the effective filing date of the invention that treating dry eye through the administration of NMN as taught by Imai would increase a number of meibomian gland acinar cells in the patients of Findlay and thereby increase the amount of lipid secretion in the patient, as described by Jester, because Jester suggests that the number of acinar cells is decreased by meibomian gland dysfunction and in particular by ocular surface drying that leads to early exhaustion of the progenitor or stem cell population and Imai teaches administering NMN as providing an effective intervention to protect eye function. It would be prima facie obvious that treating dry eye using the method of administering NMN taught by Imai would reduce the ocular surface drying that is taught by Jester as decreasing the number of acinar cells. As a result, if dry eye is treated such that there is no longer ocular surface drying, one of ordinary skill in the art would have a reasonable expectation of success in improving the number of acinar cells and lipid secretion in a meibomian gland in the patients of Findlay using the method taught by Imai because Jester teaches that ocular surface drying leads to a decrease in the number of acinar cells.
Claims 17-18 are rejected under 35 U.S.C. 103 as being unpatentable over Findlay et al. (Aust Prescr, 2018; cited in PTO-892 09/30/2024) in view of Imai et al. (US 10,925,888 B2; PTO-892) and Zeev et al. (Clinical Ophthalmology 2014; PTO-892 08/20/2025) as applied to claims 1, further in view of Braidy et al. (Antioxidants and Redox Signaling, 2019; PTO-892).
The combined teachings of Findlay, Imai, and Zeev are as above. Imai further teaches that NMN can be delivered in prodrug form (col. 9, line 3). Imai states that prodrugs can refer to compounds that can be transformed in vivo to yield NMN (col. 9, lines 27-28). Imai further teaches that the composition may include nicotinamide mononucleotide (NMN), a salt thereof and/or a prodrug thereof (col. 16, lines 1-4). Imai teaches methods of augmentation of NAD+ levels during aging through NMN administration to maintain an NSPC pool (col. 15, lines 58-61).
The combined teachings of Findlay, Imai, and Zeev differ from that of the instantly claimed invention in that they do not teach administration of nicotinamide riboside (NR).
Braidy teaches that boosting the NAD+ pool by utilizing precursor molecules may have multiple health benefits and a diverse range of therapeutic implications. Braidy further teaches that NA, NAM, NMN, and NR are known as potent NAD+ boosters. NMN and NR may also be used as a general supplement in patients who have adverse responses to NA and NAM (page 273, paragraph 3). Braidy further teaches that NR is safe in mice and humans with no adverse effects reported (paragraph bridging page 273-274). Figure 2 on page 255 shows the NAD+ metabolome and states that NR is phosphorylated to form NMN by NRK1/NRK2, which is then subsequently converted to NAD+ by NMNAT1-3.
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It would have been prima facie obvious before the effective filing date of the claimed invention to exchange the NMN in the method suggested by the combined teachings of Findlay, Imai, and Zeev with NR or a combination of NMN and NR to arrive at the instantly claimed invention because Imai teaches methods of augmentation of NAD+ levels during aging through NMN administration and Braidy teaches that NMN and NR are both known as potent NAD+ boosters and that NR is a precursor to NMN in vivo. One of ordinary skill in the art would have a reasonable expectation of success because Imai teaches that NMN can be delivered in prodrug form such as a compound that can be transformed in vivo to yield NMN, and that the composition may include a combination of NMN and a NMN prodrug.
Response to Arguments
Applicant's arguments filed 02/20/2026 have been fully considered but they are not persuasive.
Applicant argues that the instant rejection impermissibly connects different medical and pathological models disclosed in the cited references because Imai demonstrates that oral administration of nicotinamide mononucleotide (NMN) increases the amount of the aqueous component of tears secreted from the lacrimal gland (Remarks, page 6, paragraph 7) whereas Jester and Findlay discuss meibomian gland dysfunction (MGD) (Remarks, page 7, paragraph 1). This is not persuasive.
As discussed in the above grounds of rejection, Jester teaches that repeated exposure to environmental stress such as ocular surface drying is one cause of the loss of acinar cells (Jester, paragraph bridging pages 8-10). Jester also teaches that defects in meibomian gland acinar differentiation and function leading to gland atrophy play a critical role in the development of clinical MGD (Jester, paragraph bridging pages 4-5). Thus Jester suggests that ocular surface drying and environmental stress broadly are a cause of MGD and suggests that any reduction in ocular surface drying would be expected to reduce the loss of acinar cells and minimize MGD. Imai teaches methods of treating dry eye in a subject resulting in an increase in tear production.
Thus both references discuss ocular surface drying and the method of Imai providing protection from eye function from dry eye diseases would also be expected to reduce the loss of acinar cells and minimize MGD described by Jester.
Applicant similarly argues that because although both Imai and Jester use the same term "dry eye," the disease subtype addressed, the target tissue, and the therapeutic mechanism are fundamentally different between the two references that thus a person of ordinary skill in the art would not have looked to the treatment of Imai for the condition of Jester (Remarks, page 10, paragraph 6). Applicant argues that the teachings of Imai are limited to showing that NMN can increase secretion of the aqueous component of tears via improvement of lacrimal gland function and Imai is silent regarding meibomian gland function (page 9, paragraph 3). This is not persuasive.
As discussed in the above grounds of rejection, Jester suggests that ocular surface drying and environmental stress broadly are a cause of MGD. Jester suggests reduction in ocular surface drying in order to reduce the loss of acinar cells and minimize MGD. The teachings of Imai as a whole teach improvement of age-related changes in eye function (Imai, abstract). Although Imai states that "decrease in lacrimal gland secretory function might be a possible cause of age-associated dry eye diseases" (Imai, col. 2, lines 45-46) and provides specific examples of increasing tear production, Imai does not state that the methods of improving dry eye disease are limited to improvement of lacrimal gland function. Imai broadly teaches increase in tear production and reduction of ocular surface drying and thus teaches a treatment that would be expected to reduce the loss of acinar cells and minimize the MGD described by Jester.
MPEP 2123(I) states that "The use of patents as references is not limited to what the patentees describe as their own inventions or to the problems with which they are concerned. They are part of the literature of the art, relevant for all they contain...A reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill in the art. MPEP2123(II) states that "Disclosed examples and preferred embodiments do not constitute a teaching away from a broader disclosure or nonpreferred embodiments." Thus the teachings of Imai as a whole teach the improvement of age-related dry eye broadly such that one of ordinary skill in the art would have looked to the teachings of Imai to treat the patients of Jester.
Applicant further argues that Jester teaches MGD as an irreversible condition (Remarks, page 10, paragraph 4) such that one or ordinary skill in the art would not expect to improve the function of a meibomian gland (Remarks, page 10, paragraph 6). This is not persuasive.
As discussed in the above grounds of rejection, Jester teaches that repeated stress-induced hyperproliferation of the meibomian gland may lead to early exhaustion of the progenitor or stem cell population within the gland that is necessary for maintenance of acinar function (Jester, paragraph bridging pages 8-10). Thus Jester teaches that the body has a progenitor cell population of acinar cells which are in use to maintain acinar cell population after acinar cell drop out. Thus one would understand that the body is capable of producing newly differentiated acinar cells. Jester also teaches that defects in meibomian gland acinar differentiation and function leading to gland atrophy play a critical role in the development of clinical MGD (Jester, paragraph bridging pages 4-5).
Applicant further argues that one of ordinary skill in the art would not have been directed to administer NMN to the eye because the experimental example of Imai relating to dry eye demonstrates an effect of oral administration of NMN on promoting tear secretion and does not experimentally support ocular administration for the treatment of dry eye (page 7, paragraph 7). This is not persuasive.
The teachings of the prior art are not limited to experimental examples. Rather, Imai specifically claims a method of treating dry eye comprising administration of a composition comprising NMN topically by direct ocular application including eye drops. Thus Imai directs administration to the eye. MPEP 2143.02(I) states that conclusive proof of efficacy is not required to show a reasonable expectation of success, and that efficacy data is not always required for a reasonable expectation of success.
Applicant further argues that the lid margin assessment described in Zeev is intended to improve the diagnostic accuracy of dry eye disease, and is not positioned as an essential step for evaluating therapeutic efficacy or for determining a treatment regimen such that a person of ordinary skill in the art to understand that such an evaluation step should be incorporated as a mandatory step in a treatment method using NMN (Remarks, page 13, paragraphs 1-2). This is not persuasive.
As discussed in the above grounds of rejection, Zeev teaches that, due to its complex and varied presentation, dry eye disease often tends to be misdiagnosed and so it is critical to rely heavily on methods including eyelid margin assessment for the diagnosis of dry eye disease. Because Zeev teaches that eyelid margin assessment includes the expression of the meibomian gland and is routinely used in the process of diagnosing dry eye disease, one of ordinary skill in the art would have understood that a practitioner would have been motivated to examine the patients eyes, including examining the function of the meibomian gland in order to achieve a correct diagnosis of dry eye prior to treating the condition. MPEP 2143.02(II) states that obviousness does not require absolute predictability, but at least some degree of predictability is required.
Applicant further argues that a person of ordinary skill in the art who seeks to treat MGD based on Findlay would have no rational motivation to apply the lacrimal-gland-oriented therapeutic technology disclosed in Imai to the treatment of meibomian gland dysfunction (Remarks, page 14, paragraph 2). This is not persuasive.
As discussed in the above grounds of rejection, the teachings of Imai as a whole teach improvement of age-related changes in eye function (Imai, abstract). Although Imai states that "decrease in lacrimal gland secretory function might be a possible cause of age-associated dry eye diseases" (Imai, col. 2, lines 45-46) and provides specific examples of increasing tear production, Imai does not state that the methods of improving dry eye disease are limited to improvement of lacrimal gland function. MPEP 2123(I) states that "The use of patents as references is not limited to what the patentees describe as their own inventions or to the problems with which they are concerned. They are part of the literature of the art, relevant for all they contain...A reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill in the art. MPEP2123(II) states that "Disclosed examples and preferred embodiments do not constitute a teaching away from a broader disclosure or nonpreferred embodiments." Thus the teachings of Imai as a whole teach the improvement of age-related dry eye broadly such that one of ordinary skill in the art would have looked to the teachings of Imai to treat the patients of Findlay.
Because Applicant’s arguments are not persuasive, the instant claims are rejected for the reasons of record with modifications made to account for the claim amendments filed 02/20/2026.
Conclusion
No claims are allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any extension fee pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the date of this final action.
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/S.G.H./Examiner, Art Unit 1693
/SCARLETT Y GOON/Supervisory Patent Examiner, Art Unit 1693
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