DETAILED ACTION
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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 4/2/2026 has been entered.
Claims 1-3, 5, 10-11, 14, 28-29 and 33-35 are currently pending and under consideration.
Claim Interpretation
Claim 1 recites “A method of treating cognitive impairment in a patient in need thereof suffering from a mitochondrial disease, the method comprising administering a total oral daily dose of 15 mg of compound I, wherein treatment results in improvements in attention, attention span,… improved executive function or a combination thereof.”. Accordingly, the claims encompass what appears to be a patient that is suffering from a mitochondrial disease and a potential subpopulation which also is in need of improving cognitive improvement.
Applicants disagreed with the Examiners previous interpretation of a patient in need of treating cognitive impairment as a patient suffering from mitochondrial disease since the specification teaches that patients can be those that have not been formally diagnosed with mild cognitive impairment or dementia (see specification, paragraph 00100). Specifically, Applicants have shown that patients suffering from cognitive impairment and a mitochondrial disease are a subpopulation of patients suffering from a mitochondrial disease. As such, the examiner has adopted this interpretation.
Note: This addresses sections “Diversity of Mitochondrial Diseases and Symptoms” and “Subpopulation Targeted by the Instant Claims” of the response.
Compact Prosecution:
In the Final Rejection of 12/03/2025, the examiner questioned Applicants assertion that it is well known that mitochondrial function decreases with age (and similarly mitochondrial dysfunction increases with age), and as such elderly patients are good models for patients with mitochondrial disease. Moreover, the Examiner questioned Applicants assertion that one of skill in the art would recognize that cognitive impairment is a general term describing deficits in one or more higher function, wherein it would be caused by different medical conditions/diseases and can be manifested with different symptoms. Further that cognitive impairment associated with or as a result of mitochondrial disease would not be expected to respond the same way as cognitive impairment not associated with or as a result of mitochondrial disease.
In response to these questions, Applicants submit two articles by Tranah G.J. et al. Sci. Rep. 2018; 8(1):11887 and Wallace, D.C. Annu Rev Genet. 2005;39:359-407 to show that elderly patients are good models for patients with mitochondrial disease. Regarding Tranah G.J. et al., Applicants contend that Tranah G.J. discloses that mtDNA mutation m.3243A>G is a common mutation in “several mitochondrial diseases” and showed that elderly patients without a mitochondrial disease (i.e. generally otherwise healthy) had increased m3243A>G levels, wherein elevated “levels were associated with significantly impaired strength, cognition, cardiovascular, metabolic function, and mortality consistent with the diverse mitochondrial diseases”. Regarding Wallace, DC, Applicants contend that Wallace states that “mitochondrial decline and mtDNA damage are central to the etiology of the age-related metabolic and degenerative diseases” and that “[a]s the number of mtDNA-associated diseases identified increased, it became clear that mitochondrial diseases commonly have a delayed onset and progressive course and that they result in the same clinical problems as observed in age-related disease and in the elderly”. (pages 3 and 7).
In response to this submission, the Examiner has reviewed each of the articles and cannot find any specific teaching or suggestion that elderly patients are good models for patients with mitochondrial disease or that cognitive impairment associated with or as a result of mitochondrial disease would not be expected to respond the same way as cognitive impairment not associated with or as a result of mitochondrial disease. Moreover, it would appear that some of the citations are taken out of context. For example, while Tranah G.J. et al. does discloses elevated “levels were associated with significantly impaired strength, cognition, cardiovascular, metabolic function, and mortality consistent with the diverse mitochondrial diseases”, it is unclear whether this statement only pertained to the “non-disease” presenting participants as asserted by Applicants. For example, Tranah G.J., in the sentence following this statement, specifically calls out the non-disease presenting participants as having circulating m.3243A>G heteroplasmy ranged from 0-19% with clear impairment at the highest tertiles (page 3, Last sentence). In view of this, it seems like only a certain percentage of the “non-disease” presenting participants had measurable circulating m.3243A>G. Moreover, Tranah G.J. teaches that previous research has shown that m3243A>G heteroplasmy levels of 10-30% are associated with type 1 and type II diabetes and autism, heteroplasmy levels of 50-90% are associated with encephalomyopathies including MELAS, and heteroplasmy levels of 90%-100% lead to Leigh Syndrome or perinatal fatality (5, lines 2-5). Accordingly, it would appear that these levels would fall into the type 1 and type II diabetes and autism. Lastly, it is important to note that Applicants have presented the instant claimed patients to be a subpopulation of the generic mitochondrial diseases, e.g. patients suffering from both cognitive impairment and a mitochondrial disease. In other words, not all patients with a mitochondrial disease have cognitive impairment. If this is true, it is unclear how “healthy elderly” participants would encompass this subpopulation. For example, as mentioned by Applicants “Thus, it is clear from Moore, and even Finsterer, that while cognitive impairment may be present in some, or even many, patients with mitochondrial diseases, there is significant variation within patient populations. Further, Moore (specifically Table 3) clearly demonstrates that not everyone with a mitochondrial disease will display signs of cognitive impairment” (see remarks Page 7, 1st full paragraph). Accordingly, it would appear that “healthy” elderly patients may or may not have cognitive impairment.
Rejections Maintained:
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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claim(s) 1-3, 5, 10-11, 14, 28-29 and 33-34 remain rejected and new claim 35 is under 35 U.S.C. 103 as being unpatentable over Ironwood Pharmaceuticals (WO2018/045276A1, 2018-03-08, IDS) referred to herein as Ironwood in view of Moore et al. (European Journal of Neurology 2020; 27:3-17, first published 2019-08-25).
Ironwood teaches stimulators of soluble guanylate cyclase (sGC), pharmaceutical formulations comprising them and their uses thereof, alone or in combination with one or more additional agents, for treating various disease, wherein an increase in the concentration of nitric oxide (NO) or an increase in the concentration of cyclic Guanosine Monophosphate (cGMP), or both, or an upregulation of the NO pathway is desirable (Abstract). With regards to the stimulator, the WO document teaches a stimulator referred to as compound I-1 that appears to be the preferred compound and which is identical to the compound of formula I claimed in the instant application (page 26, Table I). With regards to the diseases, the WO document teaches that the disease is a CNS disease or health condition such as Alzheimer’s disease, dementia, vascular dementia, mixed dementia, Lewy body dementia and mild cognitive impairment (MCI)(page 65 (9)). With regards to the combination with one or more additional agents, the WO document teaches that additional agents include drugs used for the treatment of dementia such as galantamine, rivastigmine, donepezil and tacrine (page 89 (50)). Moreover, Ironwood teaches numerous in vivo studies using compound I-1. For example, Ironwood teaches assessing the ability of compound I-1 to enhance memory in cognitive deficit induced rats, wherein compound I-1 (0.01, 0.1 and 1 mg/KG) was orally administered to rats 60 minutes prior to training and showed clear efficacy in saving the NOR memory after treatment of MK-801 (Page 154, Example 10). Lastly, Ironwood teaches the pharmaceutical compositions will be formulated, dosed and administered in a fashion, i.e., amounts, concentrations, schedules, course, vehicles, and route of administration, consistent with good medical practice, wherein factors for consideration in this context include the particular disorder being treated, the particular mammal being treated, the clinical condition of the individual patient, the cause of the disorder, the site of delivery, the method of administration, the scheduling of administration, and other factors known to medical practitioners, such as the age, weight, and response of the individual patient (paragraph 0097).
Ironwood does not specifically teach that patient is in need of treatment of cognitive function and has a mitochondrial disorder. Moreover, Ironwood does not specifically teach a dose of 15 mg of compound I-1 or a dosing protocol/schedule encompassing a first and second dose of compound I-1.
Moore et al. provide a systematic review of cognitive deficits in adult mitochondrial disease (Title). Moreover, Moore et al. teach that examination of the case literature commonly revealed dementia, cognitive impairment and cognitive decline, as well as other memory problems in patients with mitochondrial diseases (page 15, 1st column, 1st full paragraph). For example, Moore et al. teach that the cognitive assessments of Lang showed that patients with KSS performed best and those with MELAS performed worse, wherein over half of all patients demonstrated memory impairment and five patients (MELAS, 3; PEO, 2) were diagnosed with dementia (page 14, 1st column, 3rd full paragraph).
It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to modify the method taught by Ironwood to include patients in need of treatment of cognitive function and suffer from a mitochondrial disease such as MELAS in view of the teachings of Moore et al.. One of ordinary skill in the art would have been motivated to make such a modification, with a reasonable expectation of success, because:
- Moore et al. teach that the examination of the case literature commonly revealed dementia, cognitive impairment and cognitive decline, as well as other memory problems in patients with mitochondrial diseases; and
-Ironwood teaches that the compound I-1 can be used for CNS disease or health conditions such as Alzheimer’s disease, dementia, vascular dementia, mixed dementia, Lewy body dementia and mild cognitive impairment (MCI)(page 65 (9)), and further, assessed the ability of compound I-1 to enhance memory in cognitive deficit induced rats, wherein compound I-1 (0.01, 0.1 and 1 mg/KG) was orally administered to rats 60 minutes prior to training and showed clear efficacy in saving the NOR memory after treatment of MK-801 (Page 154, Example 10).
Moreover, it would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to modify the amount and dosing schedule of compound I-1 taught by Ironwood for treating cognitive function in a patient suffering from a mitochondrial disease. One of ordinary skill in the art would have been motivated to make such a modification, with a reasonable expectation of success, because:
-Ironwood teaches the pharmaceutical compositions will be formulated, dosed and administered in a fashion, i.e., amounts, concentrations, schedules, course, vehicles, and route of administration, consistent with good medical practice.
Generally, differences in concentration or temperature will not support the patentability of subject matter encompassed by the prior art unless there is evidence indicating such concentration or temperature is critical. "[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation." In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955).
In response to the rejection, Applicants contend that Ironwood is silent regarding mitochondrial disease, and thus does not disclose or make obvious the treatment of cognitive impairment in patients with a mitochondrial disease, let alone the specific improvement in cognitive function as recited in amended claims 1. Thus, Applicants contend that based on the complexities of cognitive disorders and impairments, there would be no reasonable expectation that cognitive impairment associated with or as a result of a mitochondrial disease would respond the same way as cognitive impairment not associated with or as a result of a mitochondrial disease. Regarding the combination of Ironwood and Moore, Applicants contend that Moore does not overcome the deficiencies of Ironwood. In particular, Applicants contend that Moore gives no indication that Compound I would be able to treat this cognitive impairment in patients with mitochondrial diseases and certainly not the specific improvements in claim 1. Regarding the specific improvement in claim 1, Applicants assert that the claimed cognitive improvements related to attention, focus and brain speed of processing function are not taught or suggested by Ironwood nor Moore and cannot be reasonably expected or predicted based on their teachings. Therefore, Applicants assert that these do not “flow naturally” from the teachings of Ironwood and Moore.
These arguments have been carefully considered, but are not found persuasive.
Regarding Applicants contention that there would be no reasonable expectation of success that cognitive impairment associated with or as a result of a mitochondrial disease would respond the same way as cognitive impairment not associated with or as a result of a mitochondrial disease. The Examiner recognizes that applicants have not provided a factual basis to show these are different. In the instant case, Ironwood teaches using the instantly claimed compound to treat Alzheimer’s disease, dementia, vascular dementia, mixed dementia, Lewy body dementia and mild cognitive impairment (MCI)(page 65 (9)) and further provides in vivo studies using compound I-1. For example, Ironwood teaches assessing the ability of compound I-1 to enhance memory in cognitive deficit induced rats, wherein compound I-1 (0.01, 0.1 and 1 mg/KG) was orally administered to rats 60 minutes prior to training and showed clear efficacy in saving the NOR memory after treatment of MK-801 (Page 154, Example 10). As such, there is motivation to use compound I-1 to treat cognitive function in a patient with a mitochondrial disease because Moore et al. teach that dementia, cognitive impairment and cognitive decline, as well as other memory problems in patients with mitochondrial diseases. Regarding Applicants arguments pertaining to the specific improvement in claim 1, the examiner recognizes that the combination of Ironwood and Moore teach using the same compound for the same patient population. As such, it would appear that such improvements would necessarily be present. "Products of identical chemical composition cannot have mutually exclusive properties." In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990). A chemical composition and its properties are inseparable. Therefore, if the prior art teaches the identical chemical structure, the properties applicant discloses and/or claims are necessarily present. Id. Assuming, arguendo, that the dose imparts the claimed improvements, it is noted that Applicants have not shown any criticality in the amount in that they have only provided one dose 15mg which has this property and have not shown that doses outside of this amount do not also possess this property.
Rejections Maintained but amended in view of the claim interpretation
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, 5, 10-11, 14, 28-29 and 33-34 remain and new claim 35 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-4 of U.S. Patent No. 12,220,414B2 to Hadcock (2025-02-11) in view of Ironwood Pharmaceuticals (WO2018/045276A1, 2018-03-08, IDS) referred to herein as Ironwood in view of Moore et al. (European Journal of Neurology 2020; 27:3-17, first published 2019-08-25).
US Patent No. 12,220,414B2 claims a method of treating MELAS (Mitochondrial myopathy, encephalomyopathy, lactic acidosis, stroke-like symptoms) in a patient in need thereof, comprising administering a compound having the formula
PNG
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145
167
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Greyscale
which appears to be identical to compound I of the instant application (claim 1). Moreover, the patent claims that the compound of formula I is administered in combination with arginine. (claim 2).
US Patent No. 12,220,414B2 does not claim that the patient is in need of treatment of cognitive function and has a mitochondrial disorder. Moreover, the US Patent does not specifically claim a dose of 15 mg of compound I-1 or a dosing protocol/schedule encompassing a first and second dose of compound I-1.
Ironwood teaches stimulators of soluble guanylate cyclase (sGC), pharmaceutical formulations comprising them and their uses thereof, alone or in combination with one or more additional agents, for treating various disease, wherein an increase in the concentration of nitric oxide (NO) or an increase in the concentration of cyclic Guanosine Monophosphate (cGMP), or both, or an upregulation of the NO pathway is desirable (Abstract). With regards to the stimulator, the WO document teaches a stimulator referred to as compound I-1 that appears to be the preferred compound and which is identical to the compound of formula I claimed in the instant application (page 26, Table I). With regards to the diseases, the WO document teaches that the disease is a CNS disease or health condition such as Alzheimer’s disease, dementia, vascular dementia, mixed dementia, Lewy body dementia and mild cognitive impairment (MCI)(page 65 (9)). With regards to the combination with one or more additional agents, the WO document teaches that additional agents include drugs used for the treatment of dementia such as galantamine, rivastigmine, donepezil and tacrine (page 89 (50)). Moreover, Ironwood teaches numerous in vivo studies using compound I-1. For example, Ironwood teaches assessing the ability of compound I-1 to enhance memory in cognitive deficit induced rats, wherein compound I-1 (0.01, 0.1 and 1 mg/KG) was orally administered to rats 60 minutes prior to training and showed clear efficacy in saving the NOR memory after treatment of MK-801 (Page 154, Example 10). Lastly, Ironwood teaches the pharmaceutical compositions will be formulated, dosed and administered in a fashion, i.e., amounts, concentrations, schedules, course, vehicles, and route of administration, consistent with good medical practice, wherein factors for consideration in this context include the particular disorder being treated, the particular mammal being treated, the clinical condition of the individual patient, the cause of the disorder, the site of delivery, the method of administration, the scheduling of administration, and other factors known to medical practitioners, such as the age, weight, and response of the individual patient (paragraph 0097).
Moore et al. provide a systematic review of cognitive deficits in adult mitochondrial disease (Title). Moreover, Moore et al. teach that examination of the case literature commonly revealed dementia, cognitive impairment and cognitive decline, as well as other memory problems in patients with mitochondrial diseases (page 15, 1st column, 1st full paragraph). For example, Moore et al. teach that the cognitive assessments of Lang showed that patients with KSS performed best and those with MELAS performed worse, wherein over half of all patients demonstrated memory impairment and five patients (MELAS, 3; PEO, 2) were diagnosed with dementia (page 14, 1st column, 3rd full paragraph).
It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to modify the method claimed by the US Patent to include patients in need of treatment of cognitive function and suffer from a mitochondrial disease such as MELAS in view of the teachings of Ironwood Moore et al.. One of ordinary skill in the art would have been motivated to make such a modification, with a reasonable expectation of success, because:
- Moore et al. teach that the examination of the case literature commonly revealed dementia, cognitive impairment and cognitive decline, as well as other memory problems in patients with mitochondrial diseases; and
-Ironwood teaches that the compound I-1 can be used for CNS disease or health conditions such as Alzheimer’s disease, dementia, vascular dementia, mixed dementia, Lewy body dementia and mild cognitive impairment (MCI)(page 65 (9)), and further, assessed the ability of compound I-1 to enhance memory in cognitive deficit induced rats, wherein compound I-1 (0.01, 0.1 and 1 mg/KG) was orally administered to rats 60 minutes prior to training and showed clear efficacy in saving the NOR memory after treatment of MK-801 (Page 154, Example 10).
Moreover, it would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to modify the amount and dosing schedule of compound I-1 claimed in the US Patent for treating cognitive function in a patient suffering from a mitochondrial disease. One of ordinary skill in the art would have been motivated to make such a modification, with a reasonable expectation of success, because:
-Ironwood teaches the pharmaceutical compositions will be formulated, dosed and administered in a fashion, i.e., amounts, concentrations, schedules, course, vehicles, and route of administration, consistent with good medical practice.
Generally, differences in concentration or temperature will not support the patentability of subject matter encompassed by the prior art unless there is evidence indicating such concentration or temperature is critical. "[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation." In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955).
Conclusion
Therefore, No claim is allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to BRANDON J FETTEROLF whose telephone number is (571)272-2919. The examiner can normally be reached M-F 6AM-4PM.
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/BRANDON J FETTEROLF/ Primary Examiner, Art Unit 1626
Prosecution Insights