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 .
Detailed Action
Summary
This is the Final Office Action based on application 17/633917 RCE response filed 12/10/2025.
Claims 1, 6, 11-12, 15, 20, 25, 30-31, 35, 37-38 & 59, 61-62 are pending and have been fully considered.
Claims 2-3, 5, 7-10, 13-14,16-19, 21-24, 26-39, 32-36, 39-58, 60 have been cancelled.
Claim Objections/Claim Interpretation
Claims 1, 20 & 38 are objected to because of the following informalities:
With respect to Claims 1 & 20, it is the examiner’s understanding, that applicant means to limit Claims 1 & 20 to always require the claimed treatment. However, in Claim 1, step (b)- there is a “when,” clause, which leaves the claims open to no treatment occurring and therefore just a diagnosis. Claim 20, contains a similar limitation in that the level is only altered, “upon progression,” and “when sampled at a later timepoint.” Applicant can remedy this by positively reciting detection altered levels of the claimed biomarkers and therefore necessitating the treatments in Claim 1, step c) and Claim 20, step b).
Claim 38 is only drawn towards “treating,” but also contains this “when,” clause which makes the claim read as that the claimed “metho of treatment,” is not always required to result in a treatment, but only “when”. Therefore- this claim broadly reads on any treatment with the claimed c-Ab1 inhibitor or PARP inhibitor, as there is no claimed measurement required.
Appropriate correction is required.
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.
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 non-obviousness.
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.
Claims 1, 6, 12, 20, 25, 31, 37 are rejected under 35 U.S.C. 103 as being obvious by DAWSON in, “Parkin Plays Role in Sporadic Parkinson’s Disease,” in view of SPUR in US 20110229883 and further in view of MITSUHASHI in US 20190219578.
With respect to Claim 1, DAWSON teaches of a method of monitoring chronic progressive neurologic disorder (abstract). DAWSON more specifically teach of detecting Parkin, C-Ab1, AIMP2, and PARIS (ZNF746) in Parkinson’s disease patients (Page 1, results). DAWSON also teaches of monitoring alpha-synuclein in Parkinson’s disease patients (Page 2, last paragraph, Page 3, first paragraph).
DAWSON teaches of detection and association of these biomarkers with neurodegenerative disease and further teaches that overexpression of them is what causes or is associated to conditions associated with the diseases (Page 2, paragraphs 2 & 3).
DAWSON even further teaches of using c-AB1 inhibitors for treatment in Parkinson’s disease (Page 3, paragraph 2).
DAWSON does not teach of detecting or monitoring PARP1, PAR, or alpha-synuclein. Further, DAWSON does not specifically call out measurement or detection of “expression level.”
SPUR is used to remedy this and further teaches of utilizing biochemical markers and genetic markers to diagnose, predict, and/or monitor intervention of a number of diseases and conditions that have unresolved oxidative stress as an important component. The system, methods and assays are applicable to various diseases, including autism, asthma, and Alzheimer's disease (abstract). SPUR further teaches that the condition can be one of a number of neurodegenerative diseases including Parkinson’s and Alzheimer’s (paragraph 0021), and that the PARP 1 and poly ADP ribose (PAR) genes are associated with Alzheimer’s disease (Table 0006). SPUR further teaches that a-synuclein can also be a biomarker used and associated with the neurodegenerative disease (paragraph 0164).
SPUR further teaches of determination of gene expression and specifically of determining the gene expression of the biomarkers in Table 6 (paragraph 0013, 0017, 0024, 0168), of determining altered levels of the gene or protein expression (paragraph 0157-0158) and that continued monitoring including the biomarkers and expression of the genetic markers enables regular assessment and therapeutic management for the patients (paragraph 0165).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant invention to detect the biomarkers as done in SPUR in the method of monitoring/detecting the neurodegenerative condition of DAWSON due t the need in the art for methods and assays to diagnose, monitor and determine susceptibility to diseases and conditions associated with unresolved or altered oxidative stress like neurodegenerative diseases and further due to the need for improved methods and additional relevant biochemical and genetic markers are therefore needed (DAWSON, paragraph 0010).
Neither DAWSON or SPUR teach of detection in exosomes.
MITSUHASHI teaches of methods of detecting exosomal biomarkers to diseases (abstract). MITSUHASHI further teaches that the disease which is diagnosed can be Alzheimer’s, Parkinson’s, multiple system atrophy, Lewy body dementia, or another neurodegenerative disease and that the biomarker which is detected can be alpha-synuclein present in the exosomes and of detecting phosphorylation (paragraph 0008-0010). The instant application specification PGPub, paragraph 0008 indicates that a-synuclein is part of c-AB1 pathway, so an inhibitor of the c-Ab1 pathway can be read as an a-synuclein inhibitor.
MITSUHASHI teaches that the vesicles or exosomes detected can be isolated (paragraphs 0007-0008). MITSUHASHI also teach of detecting expression levels (paragraph 0060). MITSUHASHI further teaches of using the method to diagnose, prognose, and treat the disease (paragraph 0006, 0008-0010) and of comparison of the measured levels to a control and of any deviation indicating disease (paragraph 0024). MITSUHASHI further teaches that the control can be from a control sample (paragraph 0024) or from a healthy/non patient subject (paragraph 0141) and that the values are measured over time (paragraph 0095-0096).
MITSUHASHI teaches that the detected biomarker can be a-synulein, and that if this is detected the subject is treated (paragraph 0017, 0021). The instant application specification PGPub, paragraph 0008 indicates that a-synuclein is part of c-AB1 pathway, so an inhibitor of the c-Ab1 pathway can be read as an a-synuclein inhibitor.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant invention to detect the gene expression or protein expression levels of the neurodegenerative disease biomarkers in exosomes as is done in MITSUHASHI, in the methods of DAWSON and SPUT due to the advantage exosomes have shown in being useful diagnostically for various diseases since they carry the physiological materials of the mother cells from which they originate and the microenvironment near their mother cells (MITSUHASI, paragraph 0003, 0006).
With respect to Claim 6, SPUR further teaches that a-synuclein can also be a biomarker used and associated with the neurodegenerative disease (paragraph 0164) of determining altered levels of the gene or protein expression (paragraph 0157-0158). SPUR further teaches PARP 1 and poly ADP ribose (PAR) genes are associated with Alzheimer’s disease (Table 0006) and of detecting altered (increased or decreased) levels (paragraph 0157-0158).
MITSUHASHI teaches of detecting a biomarker monomer, oligomer, or phosphorylated form of tau, amyloid beta, or alpha-synuclein (paragraph 0008). MITSHUHASHI further teaches of detecting if the biomarker and seeing if it is elevated in comparison to a control (paragraph 0024).
With respect to Claim 12, SPUR teaches of the sample being blood (paragraph 0025, 0122). MITSUHASHI teaches of the sample being blood, serum, or plasma (paragraph 0007).
With respect to Claim 20, DAWSON teaches of a method of monitoring chronic progressive neurologic disorder (abstract). DAWSON more specifically teach of detecting Parkin, C-Ab1, AIMP2, and PARIS (ZNF746) in Parkinson’s disease patients (Page 1, results). DAWSON also teaches of monitoring alpha-synuclein in Parkinson’s disease patients (Page 2, last paragraph, Page 3, first paragraph).
DAWSON teaches of detection and association of these biomarkers with neurodegenerative disease and further teaches that overexpression of them is what causes or is associated to conditions associated with the diseases (Page 2, paragraphs 2 & 3).
DAWSON even further teaches of using c-AB1 inhibitors for treatment in Parkinson’s disease (Page 3, paragraph 2).
DAWSON does not teach of detecting or monitoring PARP1, PAR, or alpha-synuclein. Further, DAWSON does not specifically call out measurement or detection of “expression level.”
SPUR is used to remedy this and further teaches of utilizing biochemical markers and genetic markers to diagnose, predict, and/or monitor intervention of a number of diseases and conditions that have unresolved oxidative stress as an important component. The system, methods and assays are applicable to various diseases, including autism, asthma, and Alzheimer's disease (abstract). SPUR further teaches that the condition can be one of a number of neurodegenerative diseases including Parkinson’s and Alzheimer’s (paragraph 0021), and that the PARP 1 and poly ADP ribose (PAR) genes are associated with Alzheimer’s disease (Table 0006). SPUR further teaches that a-synuclein can also be a biomarker used and associated with the neurodegenerative disease (paragraph 0164).
SPUR further teaches of determination of gene expression and specifically of determining the gene expression of the biomarkers in Table 6 (paragraph 0013, 0017, 0024, 0168), of determining altered levels of the gene or protein expression (paragraph 0157-0158) and that continued monitoring including the biomarkers and expression of the genetic markers enables regular assessment and therapeutic management for the patients (paragraph 0165).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant invention to detect the biomarkers as done in SPUR in the method of monitoring/detecting the neurodegenerative condition of DAWSON due t the need in the art for methods and assays to diagnose, monitor and determine susceptibility to diseases and conditions associated with unresolved or altered oxidative stress like neurodegenerative diseases and further due to the need for improved methods and additional relevant biochemical and genetic markers are therefore needed (DAWSON, paragraph 0010).
Neither DAWSON or SPUR teach of detection in exosomes.
MITSUHASHI teaches of methods of detecting exosomal biomarkers to diseases (abstract). MITSUHASHI further teaches that the disease which is diagnosed can be Alzheimer’s, Parkinson’s, multiple system atrophy, Lewy body dementia, or another neurodegenerative disease and that the biomarker which is detected can be alpha-synuclein present in the exosomes and of detecting phosphorylation (paragraph 0008-0010). The instant application specification PGPub, paragraph 0008 indicates that a-synuclein is part of c-AB1 pathway, so an inhibitor of the c-Ab1 pathway can be read as an a-synuclein inhibitor.
MITSUHASHI teaches that the vesicles or exosomes detected can be isolated (paragraphs 0007-0008). MITSUHASHI also teach of detecting expression levels (paragraph 0060). MITSUHASHI further teaches of using the method to diagnose, prognose, and treat the disease (paragraph 0006, 0008-0010) and of comparison of the measured levels to a control and of any deviation indicating disease (paragraph 0024). MITSUHASHI further teaches that the control can be from a control sample (paragraph 0024) or from a healthy/non patient subject (paragraph 0141) and that the values are measured over time (paragraph 0095-0096).
MITSUHASHI teaches that the detected biomarker can be a-synulein, and that if this is detected the subject is treated (paragraph 0017, 0021). The instant application specification PGPub, paragraph 0008 indicates that a-synuclein is part of c-AB1 pathway, so an inhibitor of the c-Ab1 pathway can be read as an a-synuclein inhibitor.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant invention to detect the gene expression or protein expression levels of the neurodegenerative disease biomarkers in exosomes as is done in MITSUHASHI, in the methods of DAWSON and SPUT due to the advantage exosomes have shown in being useful diagnostically for various diseases since they carry the physiological materials of the mother cells from which they originate and the microenvironment near their mother cells (MITSUHASI, paragraph 0003, 0006).
With respect to Claim 25, SPUR further teaches that a-synuclein can also be a biomarker used and associated with the neurodegenerative disease (paragraph 0164) of determining altered levels of the gene or protein expression (paragraph 0157-0158). SPUR further teaches PARP 1 and poly ADP ribose (PAR) genes are associated with Alzheimer’s disease (Table 0006) and of detecting altered (increased or decreased) levels (paragraph 0157-0158).
MITSUHASHI teaches of detecting a biomarker monomer, oligomer, or phosphorylated form of tau, amyloid beta, or alpha-synuclein (paragraph 0008). MITSHUHASHI further teaches of detecting if the biomarker and seeing if it is elevated in comparison to a control (paragraph 0024).
With respect to Claim 31, SPUR teaches of the sample being blood (paragraph 0025, 0122). MITSUHASHI teaches of the sample being blood, serum, or plasma (paragraph 0007).
With respect to Claim 37, MITSUHASHI teaches of testing multiple sample at successive (multiple= two or more) timepoints for the same patient (paragraph 0095). MITSUHASHI teaches of detecting a biomarker monomer, oligomer, or phosphorylated form of tau, amyloid beta, or alpha-synuclein (paragraph 0008). MITSHUHASHI further teaches of detecting if the biomarker and seeing if it is elevated in comparison to a control (paragraph 0024).
Claim 38 is rejected under 35 U.S.C. 103 as being obvious by DAWSON in, “Parkin Plays Role in Sporadic Parkinson’s Disease,” in view of SPUR in US 20110229883 and further in view of MITSUHASHI in US 20190219578 and further in view of in view of NAKAMORI in US 20190008886.
With respect to Claim 38, DAWSON teaches of using c-AB1 inhibitors for treatment in Parkinson’s disease (Page 3, paragraph 2).
MITSUHASHI teaches of methods of detecting exosomal biomarkers to diseases (abstract). MITSUHASHI further teaches that the disease which is diagnosed can be Alzheimer’s or another neurodegenerative disease and that the biomarker which is detected can be alpha-synuclein present in the exosomes and of detecting phosphorylation (paragraph 0008-0010). The instant application specification PGPub, paragraph 0008 indicates that a-synuclein is part of c-AB1 pathway, so an inhibitor of the c-Ab1 pathway can be read as an a-synuclein inhibitor. MITSUHASHI also teach of detecting expression levels (paragraph 0060). MITSUHASHI further teaches of using the method to diagnose, prognose, and treat the disease (paragraph 0006, 0008-0010) and of comparison of the measured levels to a control and of any deviation indicating disease (paragraph 0024). See reason for combination as shown above.
If it is unclear that DAWSON, SPUR and MITSUHASHI teach specifically of administration to the patient NAKAMORI is used to remedy this.
It is noted that the instant application specification PGPub, paragraph 0008 indicates that a-synuclein is part of c-AB1 pathway, so an inhibitor of the c-Ab1 pathway can be read as an a-synuclein inhibitor.
NAKAMORI remedies this and teaches of a pharmacological composition which inhibits the expression of a-synuclein (abstract and paragraph 0001), and which is used to treat Parkinson’s disease or other neurodegenerative disease (paragraph 0056-0060, 0003, 0007, 0173). NAKAMORI further teaches of administering the pharmacological compound to the patient (paragraph 0057-0060).
It would have been obvious to one of ordinary skill in the art to treat a patient with neurodegenerative disease with an a-synuclein inhibitor as is done in NAKAMORI to treat the diseases in the methods of DAWSON, SPUR, and MITSUHASHI due to the adverse affect a-synuclein has in diseases such as Parkinson’s and dementia since they are a main component of lewy bodies (paragraph 0006-0010, 00019).
Claims 11 & 30 are rejected under 35 U.S.C. 103 as being obvious by DAWSON in, “Parkin Plays Role in Sporadic Parkinson’s Disease,” in view of SPUR in US 20110229883 and further in view of MITSUHASHI in US 2019021957 and further view of MAHUL- MELLIER in c-ABl phosphorylates alpha synuclein and regulates its degradation: implication for alpha synuclein clearance and contribution to the pathogenesis of Parkinson’s disease (as cited on IDS dated 12/19/2023).
With respect to Claims 11 & 30, DAWSON and SPUR teach of the claimed invention as shown in the above rejection. MITSUHASHI teaches of methods of detecting exosomal biomarkers to diseases (abstract). MITSUHASHI further teaches that the disease which is diagnosed can be Alzheimer’s or another neurodegenerative disease and that the biomarker which is detected can be alpha-synuclein present in the exosomes and of detecting phosphorylation (paragraph 0008-0010). The instant application specification PGPub, paragraph 0008 indicates that a-synuclein is part of c-AB1 pathway, so an inhibitor of the c-Ab1 pathway can be read as an a-synuclein inhibitor. MITSUHASHI also teach of detecting expression levels (paragraph 0060). MITSUHASHI further teaches of using the method to diagnose, prognose, and treat the disease (paragraph 0006, 0008-0010) and of comparison of the measured levels to a control and of any deviation indicating disease (paragraph 0024).
DAWSON, SPUR, and MATSUHASHI do not teach of detecting the specifically claimed phosphorylations.
MAHUL-MELLIER is used to remedy this and teaches of method of monitoring C-Abl protein in Parkinson’s disease and particularly the proteins alpha synuclein and parkin (abstract). MAHUL-MELLIER further teach of an increase in alpha synuclein causes increase in phosphorylation of c-Ab1 in PD patients, and that this could be monitoring and suggesting that inhibition of c-ABl could protect against alpha synuclein toxicity in Parkinson’s disease patients (Page 2859, column 2, paragraph 1
MAHUL-MELLIER further teaches of monitoring tyrosine Y39 and Y125 and that the increase phosphorylation occurs at tyrosine 39, but it has also been shown at tyrosine 125 (Page 2859, second column, results, Figure 1, & Page 2860, column 2, last paragraph). MAHUL-MELLIER further teach that increased phosphorylation at Y412 is indicative of alzheimer’s disease (Page 2859, column 1, paragraph 2). It would have been obvious to one of ordinary skill in the art to monitor for phosphorylation increase as is done in MAHUL-MELLIER and one would have reasonable expectation of success in the method of DAWSON, SPUR, and MATSUHASHI due to the advantage this monitoring could have for preventing alpha synuclein toxicity in PD patients (Page 2859, column 2, paragraph 1).
Claim 15 is rejected under 35 U.S.C. 103 as being obvious by DAWSON in, “Parkin Plays Role in Sporadic Parkinson’s Disease,” in view of SPUR in US 20110229883 and further in view of MITSUHASHI in US 2019021957 and in further view of SPETZLER in US 20140148350.
With respect to Claim 15, DAWSON and SPUR teach of the claimed invention as shown above. MITSUHASHI teaches of methods of detecting exosomal biomarkers to diseases (abstract). MITSUHASHI further teaches that the disease which is diagnosed can be Alzheimer’s or another neurodegenerative disease and that the biomarker which is detected can be alpha-synuclein present in the exosomes and of detecting phosphorylation (paragraph 0008-0010). The instant application specification PGPub, paragraph 0008 indicates that a-synuclein is part of c-AB1 pathway, so an inhibitor of the c-Ab1 pathway can be read as an a-synuclein inhibitor. MITSUHASHI also teach of detecting expression levels (paragraph 0060). MITSUHASHI further teaches of using the method to diagnose, prognose, and treat the disease (paragraph 0006, 0008-0010) and of comparison of the measured levels to a control and of any deviation indicating disease (paragraph 0024).
DAWSON, SPUR, and MITSUHASHI do not teach of detecting L1CAM.
SPETZLER is used to remedy this and teaches of detecting biomarkers for different diseases (abstract). SPETZZLER further teach of detecting Parkinson’s and Alzheimer’s disease (paragraphs 0073-0075) and further that the sample can include assessing various vesicles such as exosomes (paragraph 0190).
SPETZLER more specifically teaches od L1CAM detection (paragraph 1173, table 43). It would have been obvious to one of ordinary skill in the art to detect L1CAM as is done in SPETLZER in the methods of MUHLER MELLIER, DAWSON, SPUR, and MATSUHASHI and one would have had reasonable expectation of success due to that fact that L1CAM is a circulating biomarker the advantage that monitoring circulating biomarkers offer for detection of disease or disease severity (SPETZLER, paragraph 0005).
Claims 59, 61-62 are rejected under 35 U.S.C. 103 as being obvious by DAWSON in, “Parkin Plays Role in Sporadic Parkinson’s Disease,” in view of SPUR in US 20110229883 and further in view of MITSUHASHI in US 2019021957 and further in view of GOURHARI in US 20150152118.
With respect to Claims 59-60, DAWSON, SPUR, and MITSUHASHI teach of the claimed invention as shown above.
They do not teach of using one of the claimed inhibitors of c-AB1 pathway (or a PARP inhibitor) as a treatment for the dementia related disorder.
GOURHARI is used to remedy this and teach of a method of treatment with PARP inhibitors (abstract). These treatments are using for things such as treatment of Parkinson’s disease (paragraph 0260). GOURHARI teaches that the treatments can include imatinib (paragraph 0268, Claim 11).
It would have been obvious to one of ordinary skill in the art to use a PARP inhibitor such as imatinib as is done in GOURHARI in the method of DAWSON, SPUR, and MITSUHASHI and NAKAMORI to treat Parkinson’s or related dementia disorder due to the fact that PARP inhibitors have been show to be effective and PARP has been indicated in Parkinson’s disease (GOURHARI, paragraph 0007).
With respect to Claim 61, DAWSON, SPUR, ad MITSUHASHI teach of the claimed invention as shown above for Claim 60. They do not teach of a PARP1 inhibitor. GOURHARI teaches of the invention as shown above and further teaches of a PARP 1 inhibitor (Example 21, paragraphs 0889-0892, table 1). See reason for combination from Claim 59.
With respect to Claim 62, DAWSON, SPUR, and MITSUHASHI teach of the claimed invention as shown above for Claim 60. They do not teach of a PARP1 inhibitor being one of the claimed compounds. GOURHARI teaches of the invention as shown above and further teaches of a PARP 1 inhibitor (Example 21, paragraphs 0889-0892, table 1), and even further teaches of using benzamide (paragraph 0034). See reason for combination from Claim 59. It would have been further obvious to use these benzamide compounds due to the advantage they have shown as PARP inhibitors (GOURHARI, paragraph 0001).
Response to Arguments
Applicant's arguments filed 12/10/2025 have been fully considered but they are not persuasive.
With respect to the prior 112, a, scope of enablement rejection--- applicant has overcome it, due to amendments made 12/10/2025.
However, it is noted that a claim objections/claim interpretation section has been added to the rejection as shown in the above rejection. The examiner is happy to speak with applicant’s representative about this in a telephonic interview if desired.
Applicant’s arguments with respect to claim(s) have been considered but are moot because the new ground of rejection does not rely on the combination of references applied in the prior rejection of record for any teaching or matter specifically challenged in the argument. Notably, a new primary reference, DAWSON, and a new secondary reference, SPUR is used, and they are used to teach of the claimed newly amended combination of biomarkers as now claimed in the independent claims.
In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
MITSUHASHI, which was the primary reference used in prior actions, is now used only as the third reference, due to applicant’s amendments dated 12/10/2025, which necessitated a new grounds of rejection and which makes DAWSON in view of SPUR, in view of MITSUHASHI the best found prior art.
Applicant argues that MITSUHASHI does not teach of detecting the claimed biomarkers to diagnose/treat from specifically emphasized parkinsons or lewy body dementia patients. The examiner disagrees. MITSUHASHI teaches that the disease which is diagnosed and treated can be Alzheimer’s, Parkinson’s, multiple system atrophy, Lewy body dementia, or another neurodegenerative disease and that the biomarker which is detected can be alpha-synuclein present in the exosomes and of detecting phosphorylation (paragraph 0008-0010). Further- both DAWSON and SPUR teach of detection of the claimed biomarkers as shown in the above rejection.
The examiner admits that MITSUHASHI does not call out the specifically claimed treatment, however, the newly used reference, DAWSON does in fact teach of this.
Applicant only argues about the MAHUL-MELLIER references and SPETZLER references do not teach of the purported deficiencies with the primary references. NAKAMORI is no longer used for what applicant argues it is used for.
All claims remain rejected.
Conclusion
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 nonprovisional extension fee (37 CFR 1.17(a)) 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 mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to REBECCA M FRITCHMAN whose telephone number is (303)297-4344. The examiner can normally be reached 9:30-4:30 MT Monday-Friday.
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/REBECCA M FRITCHMAN/Primary Examiner, Art Unit 1758