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 .
Election/Restrictions
Applicant’s election without traverse of Group III corresponding to claims 4 and 3, and further amended claims 5-15 and 22-26, in the reply filed on 10/15/2025 is acknowledged.
Priority
Acknowledgement is made to Applicant’s claim to priority to U.S. Provisional App. No. 63/145,250 filed 02/03/2021.
Status of Claims
This Office Action is responsive to the claims filed on 10/15/2025. Claims 5, 6, 10-15, and 23-25 have been amended in response to the requirement for restriction/election. Claims 1-26 are presently pending in this application. Claims 1, 2, and 16-21 are presently withdrawn from consideration following the response to the requirement for restriction/election.
Claim Objections
Claim 3 is objected to because of the following informalities:
Claim 3, line 7: The extra semicolon in “level;.” should be removed.
Appropriate correction is required.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 6-9, 13, and 23 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
A broad range or limitation together with a narrow range or limitation that falls within the broad range or limitation (in the same claim) may be considered indefinite if the resulting claim does not clearly set forth the metes and bounds of the patent protection desired. See MPEP § 2173.05(c). In the present instance, claim 6 recites the broad recitation “using magnetic resonance imaging (MRI), positron emission tomography (PET), or magnetic resonance spectroscopy (MRS)”, and the claim also recites “preferably proton Magnetic Resonance Spectroscopy (iH MRS)” which is the narrower statement of the range/limitation. The claim(s) are considered indefinite because there is a question or doubt as to whether the feature introduced by such narrower language is (a) merely exemplary of the remainder of the claim, and therefore not required, or (b) a required feature of the claims. For the purpose of examination, this is understood to mean “using magnetic resonance imaging (MRI), positron emission tomography (PET), or magnetic resonance spectroscopy (MRS)” and that proton Magnetic Resonance Spectroscopy (iH MRS) is not required.
A broad range or limitation together with a narrow range or limitation that falls within the broad range or limitation (in the same claim) may be considered indefinite if the resulting claim does not clearly set forth the metes and bounds of the patent protection desired. See MPEP § 2173.05(c). In the present instance, claim 13 recites the broad recitation “at least once a day for at least a week”, and the claim also recites “a month, three months, six months, or a year” which is the narrower statement of the range/limitation. The claim(s) are considered indefinite because there is a question or doubt as to whether the feature introduced by such narrower language is (a) merely exemplary of the remainder of the claim, and therefore not required, or (b) a required feature of the claims. For the purpose of examination, this is understood to mean “at least once a day at least a week”.
A broad range or limitation together with a narrow range or limitation that falls within the broad range or limitation (in the same claim) may be considered indefinite if the resulting claim does not clearly set forth the metes and bounds of the patent protection desired. See MPEP § 2173.05(c). In the present instance, claim 23 recites the broad recitation “younger than 21 years old”, and the claim also recites “18 years old, or 15 years old” which is the narrower statement of the range/limitation. The claim(s) are considered indefinite because there is a question or doubt as to whether the feature introduced by such narrower language is (a) merely exemplary of the remainder of the claim, and therefore not required, or (b) a required feature of the claims. For the purpose of examination, this is understood to mean “the subject is younger than 21 years old”.
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 3-8, 10, 11, 13-15, and 22-24 are rejected under 35 U.S.C. 103 as being unpatentable over Chez (Non-Patent Literature: Chez, M. et al. 2007. Memantine as Adjunctive Therapy in Children Diagnosed With Autistic Spectrum Disorders: An Observation of Initial Clinical Response and Maintenance Tolerability. Journal of Child Neurology. Vol. 22, 5. May 2007. Pg. 574-579) in view of Joshi (Non-Patent Literature: Joshi, G. et al. 2012. Magnetic resonance spectroscopy study of the glutamatergic system in adolescent males with high-functioning autistic disorder: a pilot study at 4T. Eur Arch Psychiatry Clin Neurosci. 18 Sept. 2012. 263:379-394).
Regarding claim 4, Chez teaches a method of treating a subject with autism spectrum disorder (ASD) (Pg. 574, Abstract; Open-label add-on therapy was offered to 151 patients with prior diagnoses of autism or Pervasive Developmental Disorder Not Otherwise Specified over a 21-month period), the method comprising:
(i) providing a subject identified as having ASD (Pg. 575, Methods; The present study included 151 patients with prior diagnostic criteria for autism); and
(ii) administering to the subject a therapeutically effective amount (Pg. 575, right col., para. 1; The starting dose of memantine was 5 mg, but the range of dosing for the first 3 weeks was 2.5 to 20 mg (mean = 5.83, SD = 2.69). These patients were gradually titrated up to a maximum dose ranging from 2.5 to 30 mg/day (mean = 12.67, SD = 6.52).) of a glutamate modulating agent (Pg. 575, Methods; Patients were offered a prescription for treatment with memantine; Pg. 574, right col. Para. 1; memantine is a moderate antagonist that binds to NMDA receptors and blocks glutamate access to cells).
Chez does not explicitly teach the ASD is characterized by increased glutamate activity in one or more selected brain regions of interest (ROIs) in the brain of the subject.
Joshi, however, teaches a method of characterizing ASD (Pg. 379, Abstract; pilot study aimed at examining the neural glutamatergic activity in autism) comprising providing a subject identified as having ASD (Pg. 380, Methods; Fourteen subjects (7 ASD…) took part in the study) characterized by increased glutamate activity (Pg. 381, Results; Results indicated significant increased Glu in the ACC of ASD versus control subjects) in one or more selected brain regions of interest (ROIs) in the brain of the subject (Pg. 381, Left col.; Proton spectra were acquired at 4T using a two-dimensional J-resolved (2D-JPRESS) MRS protocol. An 8-cc single voxel was placed in the ACC; Pg. 379, Abstract; Results indicated significantly high glutamate (Glu) levels in the anterior cingulate cortex of autistic disorder versus control subjects).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the invention to have modified the method of Chez to have included subjects identified as having ASD characterized by increased glutamate activity in one or more selected brain regions of interest (ROIs) in the brain of the subject as taught by Joshi because it would have allowed treating patients which have increased glutamate and thus more receptive to treatments involving glutamate modulating therapy (Joshi, Pg. 383, left col.).
Regarding claim 3, together Chez and Joshi teach all of the limitations of claim 4 as noted above.
Chez does not explicitly teach identifying a subject as having ASD characterized by increased glutamate activity in one or more selected brain regions of interest (ROIs) in the brain of the subject comprises:
(i) identifying a subject who has ASD;
(ii) determining a level of glutamate in one or more selected brain regions of interest (ROIs) in the brain of the subject; and
(iii) comparing the level of glutamate in the ROI to a reference level;.
Joshi, however, further teaches identifying a subject as having ASD characterized by increased glutamate activity in one or more selected brain regions of interest (ROIs) in the brain of the subject comprises:
(i) identifying a subject who has ASD (Pg. 380-381, Methods; Fourteen subjects 7 ASD… The DSM-IV-based diagnosis of ASD was established by a comprehensive psychiatric evaluation conducted by a board-certified psychiatrist experienced in evaluating ASD);
(ii) determining a level of glutamate in one or more selected brain regions of interest (ROIs) in the brain of the subject (Pg. 381-382, Table 1; Glu Levels (IU) in ACC of ASD patients: 1.43 ± 0.20); and
(iii) comparing the level of glutamate in the ROI to a reference level (Pg. 381-382; Results indicated significant increased Glu in the ACC of ASD versus control subjects; Table 1, Glu Levels (IU) in ACC of HCS patients: 0.96 ± 0.18);.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the invention to have modified the method of Chez in view of Joshi to have further included the steps of (i) identifying a subject who has ASD; (ii) determining a level of glutamate in one or more selected brain regions of interest (ROIs) in the brain of the subject; and (iii) comparing the level of glutamate in the ROI to a reference level as taught by Joshi because it would have allowed determining cases of ASD associated with dysregulated glutamate activity (Pg. 379, introduction).
Regarding claim 5, together Chez and Joshi teach all of the limitations of claim 4 as noted above.
Chez does not explicitly teach at least one ROI comprises all or part of the pregenual anterior cingulate cortex (PgACC).
Joshi, however, further teaches at least one ROI comprises all or part of the pregenual anterior cingulate cortex (PgACC) (Pg. 381, Left col.; An 8-cc single voxel was placed in the ACC; Fig. 1(a) shows the voxel contains at least part of the pregenual ACC which is understood to read on the claimed limitation as understood in its broadest reasonable interpretation).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the invention to have modified the method of Chez in view of Joshi such that at least one ROI comprises all or part of the pregenual anterior cingulate cortex (PgACC) as taught by Joshi because The ACC is functionally associated with cognitive, affective, and social processing and response and therefore is a region of interest in autism. The ACC also has close anatomic connections to the amygdala and participates in emotional regulation (Pg. 380, Left col., para. 2). Furthermore, increased Glu is detected in the ACC of ASD subjects (Pg. 381, Results).
Regarding claim 6, together Chez and Joshi teach all of the limitations of claim 3 as noted above.
Chez does not explicitly teach determining a level of glutamate in one or more selected ROIs comprises using magnetic resonance imaging (MRI), positron emission tomography (PET), or magnetic resonance spectroscopy (MRS), preferably proton Magnetic Resonance Spectroscopy (iH MRS).
Joshi, however, further teaches determining a level of glutamate in one or more selected ROIs comprises using magnetic resonance spectroscopy (MRS), preferably proton Magnetic Resonance Spectroscopy (iH MRS) (Pg. 381, left col.; Proton spectra were acquired at 4T using a two-dimensional J-resolved (2D-JPRESS) MRS protocol).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the invention to have modified the method of Chez in view of Joshi to have further included using magnetic resonance spectroscopy (MRS), preferably proton Magnetic Resonance Spectroscopy (1H MRS) as taught by Joshi because it would have allowed good separation of the overlapping J-coupled metabolite resonances of Glu and Gln in the ACC and MTLs, thereby allowing more accurate measurements of glutamate in the subject (Pg. 383, left col.).
Regarding claim 7, together Chez and Joshi teach all of the limitations of claim 6 as noted above.
Chez does not explicitly teach determining a level of glutamate in the ROI comprises acquiring and/or analyzing a proton spectra using 1H MRS.
Joshi, however, teaches determining a level of glutamate in the ROI comprises acquiring and/or analyzing a proton spectra using 1H MRS (Pg. 380; Proton magnetic resonance spectroscopy (1HMRS) ; Pg. 381, left col.; Proton spectra were acquired at 4T using a two-dimensional J-resolved (2D-JPRESS) MRS protocol; Spectral analysis was conducted in a fully automated fashion using the commercially available LCModel package).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the invention to have modified the method of Chez in view of Joshi to have further included d acquiring and/or analyzing a proton spectra using 1H MRS as taught by Joshi because Proton magnetic resonance spectroscopy (1HMRS) is a brain imaging technique that permits non-invasive quantification of brain chemistry and has been employed to study Glu concentrations (Pg. 380, Left col. Para 1).
Regarding claim 8, together Chez and Joshi teach all of the limitations of claim 7 as noted above.
Chez does not explicitly teach the proton spectra is acquired at 3 or 4 Tesla (3T or 4T) using a two-dimensional J-resolved (2D-JPRESS) 1H MRS.
Joshi, however, teaches the proton spectra is acquired at 3 or 4 Tesla (3T or 4T) using a two-dimensional J-resolved (2D-JPRESS) 1H MRS (Pg. 381, left col.; Proton spectra were acquired at 4T using a two-dimensional J-resolved (2D-JPRESS) MRS protocol).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the invention to have modified the method of Chez in view of Joshi to have further included acquiring at 3 or 4 Tesla (3T or 4T) using a two-dimensional J-resolved (2D-JPRESS) 1H MRS as taught by Joshi because relying on a field strength of 4T was an important consideration for acquiring MRS data from young children who have smaller brain volumes than adults. In addition, SNR was increased, enabling more accurate metabolite quantification, including differentiation of Glu and Gln (Pg. 382, right col.).
Regarding claim 10, together Chez and Joshi teach all of the limitations of claim 4 as noted above.
Chez further teaches the glutamate modulating agent is memantine (Pg. 575, Methods; Patients were offered a prescription for treatment with memantine).
Regarding claim 11, together Chez and Joshi teach all of the limitations of claim 4 as noted above.
Chez does not explicitly teach the reference level represents a level in a cohort of subjects who have a level of glutamate in the ROI that is above the level of glutamate in the ROI of a cohort of healthy control subjects.
Joshi, however, further teaches the reference level represents a level in a cohort of subjects who have a level of glutamate in the ROI that is above the level of glutamate in the ROI of a cohort of healthy control subjects (Pg. 380; Methods; Fourteen subjects (7 age-, sex-, and IQ-matched healthy comparison subjects); Pg. 381, Right col.; Statistical analysis was performed using the IBM SPSS software, and t tests were used to compare T2, cerebrospinal fluid, and GM fraction corrected Glu levels across groups. Results; Results indicated significant increased Glu in the ACC of ASD versus control subjects).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the invention to have modified the reference level Chez in view of Joshi to have represented a level in a cohort of subjects who have a level of glutamate in the ROI that is above the level of glutamate in the ROI of a cohort of healthy control subjects as taught by Joshi because findings suggest increased Glu levels in the ACC region and normal in the MTL in high-functioning adolescent males compared to the healthy control group (Pg. 382, Discussion).
Regarding claim 13, together Chez and Joshi teach all of the limitations of claim 4 as noted above.
Chez further teaches the treatment comprises administration of the glutamate modulating agent at least once a day for at least a week, a month, three months, six months, or a year (Pg. 575, right col., para. 1; participants were started on 5 mg/day of memantine once or twice daily… The length of treatment observation at the time that data collection closed for this article in February 2005 ranged from 1 to 20 months).
Regarding claim 14, together Chez and Joshi teach all of the limitations of claim 4 as noted above.
Chez further teaches the therapeutically effective amount is sufficient to result in an improvement in one or more impairments measured in the Clinical Global Impression (CGI) severity scale (Pg. 575, right col., para. 3; After all assessments were conducted, they were formulated into a Clinical Global Impression Improvement scale; Pg. 576, Results and Table 1; The Clinical Global Impression Improvement scale for language showed scores of very much improved or much improved (scores of 1 or 2, respectively) in 34/150 and 71/150 of patients, respectively, for a combined percentage of significant clinical improvement in 70.0% of patients).
Regarding claim 15, together Chez and Joshi teach all of the limitations of claim 4 as noted above.
Chez does not explicitly teach the subject has high-functioning ASD (HF-ASD) and/or is intellectually capable.
Joshi, however, further teaches the subject has high-functioning ASD (HF-ASD) (Title; in adolescent males with high-functioning autistic disorder; Pg. 382, Discussion; Our findings of increased Glu levels in the ACC region and normal in the MTL in high-functioning adolescent males).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the invention to have modified the method of Chez in view of Joshi to have performed the method with a subject that has high-functioning ASD (HF-ASD) as taught by Joshi because it has been shown that high-functioning adolescent males with autistic disorder have increased Glu levels in the ACC region (Pg. 382, Discussion) and that should Glu contribute to the pathophysiology of ASD, it is reasonable to suggest that agents modulating Glu may have some utility in its treatment (Pg. 383, left col.).
Regarding claim 22, together Chez and Joshi teach all of the limitations of claim 15 as noted above.
Chez further teaches the glutamate modulating agent is memantine (Pg. 575, Methods; Patients were offered a prescription for treatment with memantine).
Regarding claim 23, together Chez and Joshi teach all of the limitations of claim 4 as noted above.
Chez further teaches the subject is younger than 21 years old, 18 years old, or 15 years old (Pg. 575, Methods; There were 129 male and 22 female patients, ranging in age from 2.58 to 26.33 years (mean = 9.31, SD = 4.16)).
Regarding claim 24, together Chez and Joshi teach all of the limitations of claim 4 as noted above.
Chez further teaches the glutamate modulating agent is memantine (Pg. 575, Methods; Patients were offered a prescription for treatment with memantine).
Claim 9 is rejected under 35 U.S.C. 103 as being unpatentable over Chez in view of Joshi as applied to claim 6 above, and further in view of Jia (Jia, Y. et al. 2020. Glutamate Chemical Exchange Saturation Transfer (GluCEST) Magnetic Resonance Imaging in Pre-clinical and Clinical Applications for Encephalitis. Frontiers in Neuroscience. July 2020. Vol 14, 750.).
Regarding claim 9, together Chez and Joshi teach all of the limitations of claim 6 as noted above.
Together Chez and Joshi do not explicitly teach determining a level of glutamate in the ROI comprises using a glutamate chemical exchange saturation transfer (GluCEST) imaging.
Jia, however, teaches a method comprising determining a level of glutamate (Pg. 1, Methods; imaging with different concentrations of glutamate and other major metabolites in the brain; Pg. 4, Right col.; GluCEST imaging was used to directly observe Glu in vivo.) in the ROI (Pg. 4, Right col.; Hence, using GluCEST MRI to map the distribution of Glu in human brain structures) comprises using a glutamate chemical exchange saturation transfer (GluCEST) imaging (Pg. 4, GluCest Imaging in vivo in Patients With Encephalitis; Hence, using GluCEST MRI to map the distribution of Glu in human brain structures is feasible using a 3.0 T MR system. Compared with the HC group, the signal intensity of GluCEST was elevated in patients with encephalitis, Fig. 4).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the invention to have modified the method of Chez in view of Joshi to have further included using a glutamate chemical exchange saturation transfer (GluCEST) imaging as taught by Jia because GluCEST imaging could be used for real-time, quantitative, and non-invasive monitoring of its dynamic change without requiring the injection of any exogenous imaging contrast agents. In addition, GluCEST imaging could be used to observe the spatial alteration of Glu before and after treatment and then evaluate the therapeutic effect (Pg. 10, left col.).
Claim 12 is rejected under 35 U.S.C. 103 as being unpatentable over Chez in view of Joshi as applied to claim 11 above, and further in view of Shinohe (Shinohe, A. et al. 2006. Increased serum levels of glutamate in adult patients with autism. Progress in Neuro-Psychopharmacology & Biological Psychiatry. July 2006. Vol. 30, Pg. 1472-1477).
Regarding claim 12, together Chez and Joshi teach all of the limitations of claim 11 as noted above.
Together Chez and Joshi do not explicitly teach the reference level represents a level of glutamate that is at least one standard deviation above the level of glutamate in the cohort of healthy subjects.
Shinohe, however, teaches a level of glutamate that is at least one standard deviation above the level of glutamate in the cohort of healthy subjects (Pg. 1475, Results; The serum levels (mean=89.2 μM, S.D.=21.5) of glutamate in the patients with autism were significantly (t=−4.48, df=35, p<0.001) higher than those (mean=61.1 μM, S.D.=16.5) of normal controls).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the invention to have modified the reference level of Chez in view of Joshi to have been at a level of glutamate that is at least one standard deviation above the level of glutamate in the cohort of healthy subjects as taught by Shinohe because levels of glutamate in adult patients with autism are significantly higher than those of normal healthy controls, and that there is a positive correlation (r=0.523, p=0.026) between serum glutamate levels and ADI-R social scores in patients (pg. 1475, Discussion). Choosing a level which reflects this significance would allow for a more targeted treatment.
Claims 25 and 26 are rejected under 35 U.S.C. 103 as being unpatentable over Chez in view of Joshi as applied to claim 4 above, and further in view of Lipton (US 20200368177).
Regarding claim 25, together Chez and Joshi teach all of the limitations of claim 4 as noted above.
Together Chez and Joshi do not explicitly teach the glutamate modulating agent is a nitro-aminoadamantane compound, or a pharmaceutically acceptable salt thereof.
Lipton, however, teaches that a glutamate modulating agent (Claims 1-3; treating a juvenile-onset neurological condition in a subject in need thereof with an inhibitor of N-methyl-D-aspartate type of glutamate receptor… wherein the inhibitor of NMDAR comprises NitroSynapsin) is a nitro-aminoadamantane compound (Paragraph [0037] and Scheme 1; NitroMemantine (aka NitroSynapsin); NitroSynapsin is the molecule described in Applicant pg. 44, ln. 10), or a pharmaceutically acceptable salt thereof (Paragraph [0003]; or a pharmaceutically acceptable salt thereof).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the invention to have substituted the glutamate modulating agent of Chez in view of Joshi with a nitro-aminoadamantane compound, or a pharmaceutically acceptable salt thereof as taught by Lipton because NitroSynapsin is able to restore synaptic number and function (Paragraph [0037]) and shows improved treatment of NMDAR over memantine (Paragraph [0108]) while maintaining the ability to regulate glutamate (paragraphs [0026], [0040], [0043], [0051], and claims 1-3).
Regarding claim 26, together Chez, Joshi, and Lipton teach all of the limitations of claim 4 as noted above.
Chez does not explicitly teach the nitro-aminoadamantane compound is a compound of any one of formulas (I)-(V).
Lipton, however, further teaches the nitro-aminoadamantane compound is a compound of any one of formulas (I)-(V) (Paragraph [0037] and Scheme 1; NitroMemantine (aka NitroSynapsin); NitroSynapsin is the molecule described in Applicant pg. 44, ln. 10).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the invention to have further modified the nitro-aminoadamantane compound of Chez in view of Joshi, and Lipton to have been a compound of any one of formulas (I)-(V) as taught by Lipton because NitroSynapsin is able to restore synaptic number and function (Paragraph [0037]) and shows improved treatment of NMDAR over memantine (Paragraph [0108]) while maintaining the ability to regulate glutamate (paragraphs [0026], [0040], [0043], [0051], and claims 1-3).
Conclusion
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/DEAN N EDUN/Examiner, Art Unit 3797
/ANH TUAN T NGUYEN/Supervisory Patent Examiner, Art Unit 3795
12/15/25