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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 03/13/2026 has been entered.
Status of the Claims
Claims 1 and 21-25 are currently pending. Claims 1 and 21-25 are rejected.
Response to Amendment/Arguments
The amendment filed 10/01/2025 is compliant with the requirements of 37 CFR 1.121(c), accordingly the amendment has been entered. Applicant’s arguments have been fully considered and are addressed below:
35 USC § 103 Rejection
Applicant’s arguments with respect to the rejection of claims 1 and 16-25 under 35 USC 103 for being obvious over Harrison et al., in view of Henderson et al. have been fully considered, but are not persuasive.
In the amendment filed 03/13/2026, Applicant has narrowed the subject matter of the claims to a method of treating, delaying the onset of, or ameliorating at least one symptom of, dementia associated with b-amyloid (Ab) accumulation by administering the previous elected species
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. Applicant did not offer arguments or evidence to rebut the prima facie case of obviousness set forth in the Office Action mailed 12/15/2025 (beginning on page 5).
The rejection is therefore maintained.
Maintained 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 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.
Claims 1 and 21-25 are rejected under 35 U.S.C. 103 as being unpatentable over Harrison et al., “Novel Class of LIM-Kinase 2 Inhibitors for the Treatment of Ocular Hypertension and Associated Glaucoma” J. Med. Chem., 2009, pages 6515-6518, as cited in the IDS dated 3/24/2022 in view of Henderson et al., “Pharmacologic inhibition of LIMK1 provides dendritic spine resilience against beta-amyloid” Science Signaling, June 2019, pages 1-12, Vol. 12, eaaw93118, as cited in the IDS dated 3/24/2022.
Determining the scope and contents of the prior art. (See MPEP § 2141.01)
Harrison et al. teach a method of using compound 14 to inhibit LIMK1, see Table 6 on page 6517. Prior art compound 14, as shown in Table 5 on page 6517:
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, is identical to the instantly claimed compound.
Henderson et al. teach that “Treatment of hAPP mice with a LIMK1 inhibitor rescued Aβ-induced hippocampal spine loss and morphologic aberrations. Our data suggest that therapeutically targeting LIMK1 may provide dendritic spine resilience to Aβ, and therefore may benefit cognitively normal patients that are at high risk for developing dementia” (see abstract). Further, Henderson teaches that the LIMK1 inhibition with the compound SR7826 protects against Aβ-induced neuronal hyperexcitability. See page 4, left column, second paragraph.
Ascertaining the differences between the prior art and the claims at issue. (See MPEP § 2141.02)
Harrison et al. do not teach using compound 14 for the treatment of dementia, nor do they teach a relationship between LIMK1 and dementia.
Henderson et al. do not teach the use of the instantly claimed compound.
Considering objective evidence present in the application indicating obviousness or nonobviousness. (See MPEP § 2142-2144)
Given that Harrison et al. teach the presently claimed compound (compound 14) as an inhibitor of LIMK1 and that Henderson et al. teach a relationship between LIMK1 inhibition and dementia, it would have been obvious to a person having ordinary skill in the art to use the known compound 14 found in Harrison et al. as a treatment for dementia associated with Aβ accumulation in light of the known effect that inhibition of LIMK1 has on treating Aβ-induced diseases, such as Alzheimer’s disease, as taught by Henderson et al. This combination would have been expected to yield the predictable result wherein compound 14 of Harrison et al. would treat dementia associated with Aβ accumulation. Thus claim 1 is obvious in view of the prior art.
As it relates to dependent claim 21, which recites the limitation “wherein the dementia is Alzheimer’s disease”, Henderson et al. teaches the use of LIMK1 inhibitor SR7826 as a treatment for Alzheimer’s disease in a rat hippocampal model. See abstract and the first paragraph of the Results section on page 1. Therefore, it would have been obvious to substitute the LIMK1 inhibitor from Harrison et al. for Henderson’s SR7826 inhibitor and expect success in treating Alzheimer’s disease.
As it relates to dependent claim 22, which recites the limitation “wherein the at least one symptom of the dementia comprises memory deficits and/or aberrations or disintegration of neuronal networks” and claim 23 which further limits with “wherein aberrations or disintegration of neuronal networks are associated with excitotoxicity or Aβ toxicity”, Henderson et al. teaches that “Aβ oligomers have detrimental effects on actin cytoskeleton rearrangement in neurons” (page 3, left column, second paragraph). Later in the same paragraph, Henderson et al. report that when rat hippocampal neurons were treated simultaneously with SR7826 and Aβ42 oligomers, there was no damage to the neurons indicating that SR7826, by inhibiting LIMK1, “prevented Aβ42-induced spine degradation. See also Fig. 2C. Therefore, it would have been obvious to a skilled artisan to substitute the LIMK1 inhibitor from Harrison et al. for Henderson’s SR7826 inhibitor and expect success when using the inhibitor to treat a form of dementia associated with Aβ toxicity.
As it relates to independent claims 24 and 25, which recite a method for improving memory (claim 24) and reducing Aβ toxicity in neurons (claim 25) by administering an inhibitor of LIMK1, it would have been obvious to a skilled artisan to substitute the LIMK1 inhibitor taught by Harrison et al. for SR7826 as taught by Henderson et al. because Henderson teaches that “maintenance and retention of dendritic spines are hypothesized to facilitate memory and information processing in patients who harbor substantial Aβ pathology but are cognitively normal. Therefore, therapeutics that protect spines from Aβ could be useful to prevent dementia onset.” See paragraph bridging pages 3 and 4. In the same paragraph, SR7826 can be used to increase spine density in hippocampal neurons over time and Henderson et al report that “pharmacological inhibition of LIMK1 can generate spines under normal conditions but protects spines in the presence of Aβ42 oligomers.” Therefore, it would have been obvious to a skilled artisan to use the LIMK1 inhibitor taught by Harrison et al. in a method to protect neurons from Aβ-induced toxicity and improve memory and expect success given the findings from Henderson et al. with similar LIMK1 inhibitor SR7826.
Conclusion
Claims 1 and 21-25 are rejected.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Jalisa H. Ferguson whose telephone number is (703)756-1489. The examiner can normally be reached Monday - Friday 9:00am - 5:00pm.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Amy L. Clark can be reached at (571) 272-1310. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/J.H.F./Examiner, Art Unit 1626
/KAMAL A SAEED/Primary Examiner, Art Unit 1626
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