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 Non-Final Office Action based on application 17/633917 RCE filed 04/30/2026.
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.
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 05/22/2026 has been entered.
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, 15, 20, 25, 31, 37, 38, are rejected under 35 U.S.C. 103 as being obvious by SPETZLER in US 20140148350 in view of DAWSON in, “Parkin Plays Role in Sporadic Parkinson’s Disease.
With respect to Claim 1, SPETZLER teaches of a method for detecting biomarkers for different diseases (abstract) and specifically for neurodegenerative diseases (Table 1). 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, 0196).
Even further, SPETZLER teaches that phosphorylation of the biomarkers is detected and whether the biomarker is elevated or decreased, “altered,” with respect to a reference or control level (paragraph 0329) which can include alpha synuclein (paragraph 0642), and that the reference or control of the vesicles or exosomes is from a healthy patient (paragraph 0340). SPETZLER also teaches that the biomarker can include PARKIN (Table 5), and that a PARP inhibitor (Table 11) can be used to treat the patient.
If it is unclear that the inhibitor treatment is used specifically for neurodegenerative treatment, DAWSON is used to remedy this
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).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant invention to use the inhibitor of DAWSON in the method of SPETZLER to treat neurodegenerative disease due to the advantage these inhibitor compounds are thought to have not only in cancers, but for being a disease modifying therapy for Parkinson’s Disease (Page 3, paragraph 2).
With respect to Claim 6, SPETZLER teaches of the above, but does not teach of the claimed increase or decreases specifically.
DAWSON is used to remedy this and teaches AIMP2 increase (which means the expression level of AIMP2 is increased) (Page 2, paragraph 2).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant invention to detect elevated AIMP2 as is done in DAWSON in the method of SPETZLER due to the advantage this has in showing elevated levels in Parkinson’s patients (Page 2, paragraph 2).
With respect to Claim 12, SPETZLER teaches of the sample being blood (paragraph 0006, 0011).
With respect to Claim 15, SPETZLER more specifically teaches of detecting L1CAM detection (paragraph 1173, table 43).
With respect to Claim 20, SPETZLER teaches of a method for detecting biomarkers for different diseases (abstract) and specifically for neurodegenerative diseases (Table 1). SPETZLER 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, 0196).
Even further, SPETZLER teaches that phosphorylation of the biomarkers is detected and whether the biomarker is elevated or decreased, “altered,” with respect to a reference or control level (paragraph 0329) which can include alpha synuclein (paragraph 0642), and that the reference or control of the vesicles or exosomes is from a healthy patient (paragraph 0340). SPETZLER also teaches that the biomarker can include PARKIN (Table 5), and that a PARP inhibitor (Table 11) can be used to treat the patient.
SPETZLER teaches of monitoring the biomarkers and multiple time points (paragraph 0032, 0201, 0330) to monitor progression of disease (abstract).
If it is unclear that the inhibitor treatment is used specifically for neurodegenerative treatment, DAWSON is used to remedy this
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).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant invention to use the inhibitor of DAWSON in the method of SPETZLER to treat neurodegenerative disease due to the advantage these inhibitor compounds are thought to have not only in cancers, but for being a disease modifying therapy for Parkinson’s Disease (Page 3, paragraph 2).
With respect to Claim 25, SPETZLER teaches of the above, but does not teach of the claimed increase or decreases specifically.
DAWSON is used to remedy this and teaches AIMP2 increase (which means the expression level of AIMP2 is increased) (Page 2, paragraph 2).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant invention to detect elevated AIMP2 as is done in DAWSON in the method of SPETZLER due to the advantage this has in showing elevated levels in Parkinson’s patients (Page 2, paragraph 2).
With respect to Claim 31, SPETZLER teaches of the sample being blood (paragraph 0006, 0011).
With respect to Claim 37, SPETZLER teaches of monitoring the biomarkers and multiple (two or more) time points (paragraph 0032, 0201, 0330) to monitor progression of disease (abstract).
With respect to Claim 38, SPETZLER teaches of a method for detecting biomarkers for different diseases (abstract) and specifically for neurodegenerative diseases (Table 1). 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, 0196).
Even further, SPETZLER teaches that phosphorylation of the biomarkers is detected and whether the biomarker is elevated or decreased, “altered,” with respect to a reference or control level (paragraph 0329) which can include alpha synuclein (paragraph 0642), and that the reference or control of the vesicles or exosomes is from a healthy patient (paragraph 0340). SPETZLER also teaches that the biomarker can include PARKIN (Table 5), and that a PARP inhibitor (Table 11) can be used to treat the patient.
If it is unclear that the inhibitor treatment is used specifically for neurodegenerative treatment, DAWSON is used to remedy this
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).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant invention to use the inhibitor of DAWSON in the method of SPETZLER to treat neurodegenerative disease due to the advantage these inhibitor compounds are thought to have not only in cancers, but for being a disease modifying therapy for Parkinson’s Disease (Page 3, paragraph 2).
Claims 11 & 30 are rejected under 35 U.S.C. 103 as being obvious by SPETZLER in US 20140148350 in view of DAWSON in, “Parkin Plays Role in Sporadic Parkinson’s Disease 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, SPETZLER in view of DAWSON teach of the claims as shown above. They 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 SPETZLER and DAWSON due to the advantage this monitoring could have for preventing alpha synuclein toxicity in PD patients (Page 2859, column 2, paragraph 1).
Claims 59, 61-62 are rejected under 35 U.S.C. 103 as being obvious SPETZLER in US 20140148350 in view of DAWSON in, “Parkin Plays Role in Sporadic Parkinson’s Disease and further in view of GOURHARI in US 20150152118.
With respect to Claims 59-60, SPTEZLER and DAWSON 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 SPETZLER and DAWSON to treat Parkinson’s or related dementia disorder due to the fact that PARP inhibitors have been shown to be effective and PARP has been indicated in Parkinson’s disease (GOURHARI, paragraph 0007).
With respect to Claim 61, SPETZLER and DAWSON 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, SPETZLER and DAWSON 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 04/30/2026 have been fully considered but they are not persuasive.
Applicant’s arguments with respect to claim(s) have been considered but are moot because the new ground of rejection does not rely on any reference applied in the prior rejection of record for any teaching or matter specifically challenged in the argument. Notably, a new primary reference has been used due to amendments dated 04/30/2026. This piece of prior art was used before, but not in the same way and instead had only been used as a supporting reference. Therefore, as the scope of the claims has changed, so has the rejection. Therefore, applicant’s arguments which focus on DAWSON as the primary reference, do not carry the same weight as DAWSON is now used only as a secondary reference.
All claims remain rejected.
Conclusion
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
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