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 .
Priority
Acknowledgement is made of Applicants’ claim for benefit to prior filed US Provisional Application 63/024466, filed on 05/13/2020.
This application claims the benefit of priority to Patent Application PCT/US21/31983. Acknowledgement is made of Applicants’ claim for benefit to prior filed to Patent Application
Number PCT/US21/31983, filed on 05/12/2021.
Information Disclosure Statement
The Information Disclosure Statements filed 02/27/2023, 09/18/2023, 11/29/2023, 04/17/2024, 06/11/2024, 01/10/2025, and 11/14/2025 have been considered by the Examiner.
Status of Claims
Claims 1, 3-4, 10-13, 15-16, 24, 26, 48, and 52-56 are under examination.
Claim 2, 5-9, 14, 17-22, 23, 25, 27-47, 49-51, and 57-63 are cancelled.
Claim Rejections - 35 USC § 102
Rejection of claims 1, 3, 4, 10-13, 15-16, 24, 26, and 52-56 under 35 U.S.C. 102(a)(1) as being anticipated by Burns et al. (WO 2020/077295 Al) are withdrawn in view of the applicant’s amendments.
Claim Rejections - 35 USC § 103
Rejection of claims 21 and 22 under 35 U.S.C. 103 as being unpatentable over Burns et al. (WO 2020/077295 Al) and further in view of Suzuki et al. (Scientific Reports, 2017) have been withdrawn in view of the applicant’s cancellation of the claims.
Rejection to claim 48 under 35 U.S.C. 103 as being unpatentable over Wen et al (Biochemical and Biophysical Research Communications, 2019) is withdrawn in view of applicant’s cancellation of the claim.
New rejections to claims 1, 3, 4, 10-13, 15-16, 24, 26, and 52-56 are necessitated by the amendment filed 11/14/2025.
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.
Claims 1, 3, 4, 10-13, 15-16, 24, 26, and 52-56 are rejected under 35 U.S.C. 103 as being unpatentable over Burns et al. (WO 2020/077295 Al) and further in view of Suzuki et al. (Scientific Reports, 2017).
Regarding claim 1, Burns et al. teach an AAV1 vector comprising a coding sequence of an SLC26A4 gene operably linked to a promoter (page 9, E106).
Burns et al. does not teach the particle comprises AAV capsid that is or is derived from an Anc80 capsid.
Suzuki et al. teach AAV2/Anc80L65 is an AAV of which the main capsid proteins were synthesized to approximate the ancestral sequence state of AAV2, AAV8, AAV9 and several other serotypes (page 2, paragraph 2).
It would have been obvious to one of ordinary skill in the art at the time the invention was made to have modified the teachings of Burns et al. for an AAV vector with an AAV1 capsid with the teachings of Suzuki et al. for a vector where the main capsid proteins were synthesized to an AAV Anc80 capsid (page 8, Methods). Suzuki et al. provide motivation by teaching the “designer” vector, AAV2/Anc80L65 in their work should be useful for future development of gene therapies for sensorineural hearing loss (page 2, paragraph 2). One of skill in the art would have had a reasonable expectation of success at combining Burns et al. and Suzuki et al. because they both teach AAV vector based gene therapy methods relating to auditory dysfunction.
Regarding claim 3, Burns et al. teach the SLC26A4 gene is a human SLC26A4 gene, which reads on primate gene (page 43, Table 3 line 11).
Regarding claim 4, Burns et al. teach the SLC26A4 gene is a human SLC26A4 gene, which reads on human gene (page 43, Table 3 line 11).
Regarding claim 10, Burns et al. teach the promoter could be a ubiquitous promoter or a cell type-specific promoter (page 53, lines 36-39).
Regarding claim 11, Burns et al. teach cell type-specific promoter to induce or increase expression of the polynucleotide in one or more inner ear cell types (page 53, lines 36-39).
Regarding claim 12, Burns et al. teach the inner ear cell-specific promoter is a GJB2 promoter, a SLC26A4 promoter, a SYN1 promoter, a GFAP promoter, SOX2 promoter, a FGFR3 promoter, a LGR5 promoter, a HES1 promoter, a HES5 promoter, a NOTCH1 promoter, or a JAG1 promoter (pages 54-55, table 5).
Regarding claim 13, Burns et al. teach the promoter of the AAV particle is a CAG promoter, CMV promoter, or a CBA promoter (page 15, E235).
Regarding claim 15, Burns et al. teach retention of functional flanking ITR sequences, which are two AAC inverted terminal repeats flanking the coding sequences (page 59, line 5).
Regarding claim 16, Burns et al. teach the AAV1 vector comprises AAV2 inverted terminal repeat sequences (ITRs) (page 81, claim 89).
Regarding claim 24, Burns et al. teach a composition comprising an AAV1 vector comprising a coding sequence of an SLC26A4 gene operably linked to a promoter (page 59, lines 5-10).
Regarding claim 26, Burns et al. teach physiologically and pharmaceutically acceptable carriers for compositions which contain AAV vectors(page 60, lines 1-12).
Regarding claim 52, Burns et al. teach a method of treating hearing loss comprising introducing a composition containing AAV viral vectors (page 67, limes 10-11), which can be administered to a human subject (page 1, lines 31-33).
Regarding claim 53, Burns et al. teach various methods of delivery for the composition which could be via a round window injection (page 67, lines 13).
Regarding claim 54, Burns et al. teach mutations that cause hearing loss and/or vestibular dysfunction have been identified in a variety of different cell types in the inner ear. Burns et al. teach mutations in genes expressed in cochlear hair cells, cochlear supporting cells, and/or spiral ganglion neurons have been associated with hearing loss, auditory neuropathy, deafness, and tinnitus, as has damage, injury, degeneration, or loss (e.g., death) of these cells (page 34, lines 15-18). The polynucleotide of the AAV vector encodes SLC26a4 as a treatment for hearing loss (page 13, E206).
Regarding claim 55, Burns et al. teach a physician can indirectly assess gene expression and/or protein production and monitor the patient's hearing by performing ABR and distortion product of otoacoustic emissions (DPOAE) following administration of the composition. Burns et al. teach hearing measurements collected post-treatment can be compared to measurements obtained prior to treatment (page 70, lines 15-20).
Regarding claim 56, Burns et al. teach the composition described can be provided in a kit for use in treating sensorineural hearing loss or vestibular dysfunction (page 65, pages 30-31).
Response to Arguments
Applicant’s arguments have been fully considered and are not persuasive.
Applicant’s Arguments: Applicants argue that a person of ordinary skill in the art would not have modified the teachings of Burns by exchanging the AAV1 capsid for an Anc80 capsid of Suzuki. Applicants argue that Suzuki do not provide motivation because they do not teach that Anc80, has low antigenic similarity to naturally circulating AAV vectors, including the AAV1 capsid of Burns.
Applicant argues that because Burns was first filed two years after Suzuki was published and four years after the first publication of Anc80 capsids there would not be a motivation to combine. Applicant further argues that since Burns never mentions using an Anc80 capsid that it would not be reasonable to combine Burns and Suzuki.
Applicant argues that neither Burns nor Suzuki demonstrate that an SLC26A4 construct can be delivered using any AAV particle. Applicant further argues that Burns and Suzuki do not provide data showing that an AAV particle comprising an Anc80 capsid can be used to deliver an SLC26A4 gene.
Examiner’s response: Suzuki et al. teach various improvements of using a “designer” AAV vector, AAV2/Anc80L65, for gene therapy. Suzuki et al. teach AAV2/Anc80L65 maximizes transduction efficiencies(page 2, paragraph 2). Suzuki et al. teach AAV2/Anc80L65 via posterior semicircular canal injections targets virtually 100% of IHCs throughout the cochlear spiral, as well as a significant fraction of OHCs. Suzuki et al. teach the injections transduce all of the supporting cells in all the sensory epithelia of the saccule, utricle and semicircular canals(page 2, paragraph 2). Suzuki et al. further teach the combination of technical approaches used in their work should be useful for future development of gene therapies for sensorineural hearing loss (page 2, paragraph 2). Suzuki et al. teach evaluation of the Anc80L65 capsid is designed to mimic an ancestral form of several AAV serotypes in order to minimize antigenic similarity to naturally circulating AAV that poses a problem in clinical translation of AAV gene therapies (page 2, paragraph 2). Anc80L65 was pursued as it demonstrated compelling transduction characteristics in organotypic explant cultures(page 7, paragraph 2).
Suzuki and Burns read on the limitations of the claims at present and therefore their publication dates in relation to one another have no bearing on their weight as prior art.
Burns et al. teach an AAV1 vector comprising a coding sequence of an SLC26A4 gene operably linked to a promoter (page 9, E106), for gene therapy of a patient suffering from sensorineural hearing loss, deafness, auditory neuropathy, tinnitus and/or vestibular dysfunction. Burns et al. do not teach the Anc80 capsid, however Suzuki et al. teach the use of the Anc80 capsid for gene therapies for sensorineural hearing loss (page 2, paragraph 2). Further the combination of teachings from Burns et al. and Suzuki et al. would have a reasonable expectation of success because both teach AAV gene therapy and provide motivation for treatment of sensorineural hearing loss. Burns did not use an Anc80 capsid, however the motivation to use an Anc80 capsid over AAV1 of Suzuki et al. is relevant and persuasive in order to further improve the invention of Burns. While data is not available for the combination there is a reasonable expectation that this combination would be successful based upon the improvements taught by Suzuki et al., motivation, and clinical benefits.
Conclusion
THIS ACTION IS MADE FINAL. 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 Catherine L McCormick whose telephone number is (703)756-5659. The examiner can normally be reached Monday-Friday, 8:30 am-5:30 pm.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Tracy Vivlemore can be reached at (571) 272-2914. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/C.L.M./Examiner, Art Unit 1638
/Anna Skibinsky/
Primary Examiner, AU 1635
Prosecution Insights