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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 10/30/2025 has been entered.
Status of claims
Claims 1-22 as filed on 10/30/2025 are pending and under examination in the instant office action.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 1, 3, 4, 6-8, 10-20 and 22 are rejected under 35 U.S.C. 102 (a) (1) as being anticipated by Zhou et al (IDS reference; “Abstract 305: AAV9 Mediated cardiac Bin1 gene therapy attenuates pressure overload-induced heart failure in mice”. Circulation Research, AHA Journal. Published 18 February 2019, page 1) as evidenced by US 8,999,659 (Shaw).
Zhou teaches that administering a transgene encoding “a cardiac isoform of Bridging Integrator 1, cBIN1” by injection of adeno-associated viral vector comprising cBIN1 to heart tissues of a group of cardiac specific heterozygous BIN1 deleted mice (thus, mice with pre-existing heart failure condition) provided for robust protective effects of cBIN1 relatively to control group of BIN1 deleted mice that were administered adeno-associated viral vector comprising GFP (see abstract). The cardiac specific heterozygous BIN1 deleted mice are subjects with pre-existing heart failure condition because low level of BIN1 is recognized to be a marker of pre-existing heart failure as evidenced/taught by US 8,999,659 (Shaw); and Zhou explicitly states that BIN1 deleted mice have “less cBIN1” then normal adult mice.
Thus, the cited reference by Zhou teaches administration by injection to the heart tissue or myocardium of the same therapeutic agent to the same subject with pre-existing heart failure as encompassed by the amended claims 1, 3, 4, 6-8, 18, 19. Instant claims 10-17 and 22 are drawn to intended final effects. Thus, the cited method anticipates these claims as result of practicing identical method.
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 1, 3, 4, 6-8, 10-20 and 22 are rejected under 35 U.S.C. 103 as being unpatentable over Zhou et al (IDS reference; “Abstract 305: AAV9 Mediated cardiac Bin1 gene therapy attenuates pressure overload-induced heart failure in mice”. Circulation Research, AHA Journal. Published 18 February 2019, page 1) as evidenced by US 8,999,659 (Shaw et al) and in view of Liu et al (IDS reference: “Abstract 92: Cardiac Bridging Integrator 1 Gere Transfer Improves Left Ventricular Lusitropy in Mice With Continuous Infusion of isoproterenol", CIRCULATION RESEARCH, vol. 121, no. suppl 1, 30 January 2018, page 1).
The cited reference by Zhou discloses of a method for rehabilitation of heart tissue by administering a transgene encoding “a cardiac isoform of Bridging Integrator 1, cBIN1” to two animal mammalian models including:
1) a group of cardiac specific heterozygous BIN1 deleted mice; thus, mice with pre-existing heart failure condition because low level of BIN1 is recognized to be a marker of pre-existing heart failure as evidenced/taught by US 8,999,659 (Shaw); and Zhou explicitly states that BIN1 deleted mice have “less cBIN1” then normal adult mice; and
2) normal adult mice that received injection of cBIN1 after traverse aortic constriction (TAC) treatment which induces heart failure.
The cited reference by Zhou-2019 clearly concludes that BIN1 gene transfer (administration of BIN1) and normalization of CBIN1 level (as result of administration of BIN1) can postpone, if not prevent, pathological manifestations during heart failure (HF) progression. Thus, the cited reference clearly suggests rehabilitation of heart tissue by administration of BIN1 to a subject experiencing HF progression, thus, having pre-exiting HF.
The additional reference by Liu 2018 also concludes that exogenous cBIN1 can reverse symptoms of HF, thus, treating subjects with pre-exiting HF.
Therefore, it would have been obvious to one having ordinary skill in the art at the time the claimed invention was filed to practice administration of BIN1 to subjects with pre-existing HF with a reasonable expectation of success in rehabilitating heart tissues of subjects having HF as taught and suggested by the cited references because exogenous cBIN1 can reverse symptoms of HF.
Thus, the claimed invention as a whole was clearly prima facie obvious, especially in the absence of evidence to the contrary.
The claimed subject matter fails to patentably distinguish over the state art as represented be the cited references. Therefore, the claims are properly rejected under 35 USC § 103.
Claims 1-22 are rejected under 35 U.S.C. 103 as being unpatentable over Zhou et al (IDS reference; “Abstract 305: AAV9 Mediated cardiac Bin1 gene therapy attenuates pressure overload-induced heart failure in mice”. Circulation Research, AHA Journal. Published 18 February 2019, page 1) as evidenced by US 8,999,659 (Shaw et al) and in view of Liu et al (IDS reference; “Abstract 92: Cardiac Bridging Integrator 1 Gere Transfer Improves Left Ventricular Lusitropy in Mice With Continuous Infusion of isoproterenol", CIRCULATION RESEARCH, vol. 121, no. suppl 1, 30 January 2018, page 1) as applied to claims 1, 3, 4, 6-8, 10-20 and 22 above, and further in view of US 8,999,659 (Shaw et al ) and WO 2019/060454 (Kirn et al).
The references by Zhou-2019, US 8,999,659 (Shaw et al) and Liu-2018 as above.
Further as applied to pending claims 2 and 5: The cited reference by Zhou does not explicitly describe whether or not the blood levels of cBIN1 were measured. But US 8,999,659 (Shaw et al ) clearly teaches the use body fluid BIN1 as a marker of cardiac health (abstract) and diagnosing heart failure by measuring BIN1 level in a sample including blood (entire document including abstract, col. 1, lines 62-67 and col. 2, line 11) for mammalians including humans (col. 5, lines 60-63).
Therefore, it would have been obvious to one having ordinary skill in the art at the time the claimed invention was filed to practice diagnosing heart failure by measuring BIN1 blood level with a reasonable expectation of success in diagnosing heart failure because it has been taught and suggested by the prior art as evidenced by the cited US 8,999,659 (Shaw et al).
Thus, the claimed invention as a whole was clearly prima facie obvious, especially in the absence of evidence to the contrary.
The claimed subject matter fails to patentably distinguish over the state art as represented be the cited references. Therefore, the claims are properly rejected under 35 USC § 103.
As applied to pending claims 9 and 21: The cited reference by Zhou does not explicitly describe doses of transgene. But the cited document WO 2019/060454 (Kirn et al) teaches a method for treating muscle disorders and diseases including heart failure (see abstract; see par. 0154, page 70, line 3 from the bottom) by administration by injection into cardiac muscle or myocardium (par. 00172) an effective dose of 108 -1016 of recombinant virions or “vector genomes” (par 00171, page 81, lines 1-4) comprising BIN1 (page 74, par. 0158, line 5). The cited document WO 2019/060454 (Kirn et al) clearly recognizes that doses of therapeutic transgene delivered via viral vector as required to achieve the desired treatment effects can be readily appreciated and/or optimize by the ordinary skilled artisan (par. 00171 bridging pages 80-81). The subjects under treatment are mammalians including mice, dogs and humans (par. 0083, 0084).
Therefore, it would have been obvious to one having ordinary skill in the art at the time the claimed invention was filed to provide cBIN1 via viral vector in the claim-recited amounts with a reasonable expectation of success because it has been taught and suggested by the prior art as evidenced by the cited US 8,999,659 (Shaw et al).
Thus, the claimed invention as a whole was clearly prima facie obvious, especially in the absence of evidence to the contrary.
The claimed subject matter fails to patentably distinguish over the state art as represented be the cited references. Therefore, the claims are properly rejected under 35 USC § 103.
Response to Arguments
Applicant's arguments filed on 10/30/2025 have been fully considered but they are not found persuasive.
With regard to claim rejection under 35 U.S.C. 102 (a) (1) as being anticipated by Zhou et al (IDS reference; “Abstract 305: AAV9 Mediated cardiac Bin1 gene therapy attenuates pressure overload-induced heart failure in mice”. Circulation Research, AHA Journal. Published 18 February 2019, page 1) Applicants argue that the cited reference describes two sets of experiments and applicants address only the second experiment with normal adult mice that received injection of cBIN1 after traverse aortic constriction (TAC) treatment which induces heart failure; and, therefore, the subject under treatment in the second experiment is not “having pre-existing heart failure” as required by the claims.
However, the office action relied on description of the first experiment, wherein a model is cardiac specific heterozygous BIN1 deleted mice, thus, a subject “having pre-existing heart failure”. It appears from the cited disclosure that this model “having pre-existing heart failure “ also received the same injection of cBIN1 as the normal model in the experiment 2. Applicants did not clarify or argue this treatment on the record. Instead applicants argue that Zhou does not explicitly teaches that BIN1 deleted mice inherently have a pre-existing heart failure. This argument is not found persuasive because low level of BIN1 is considered to be a marker of pre-existing heart failure as evidenced/taught by US 8,999,659 (Shaw) and Zhou explicitly states that BIN1 deleted mice from first experiment have “less cBIN1” then normal adult mice from the second experiment.
With regard to claim rejection under 35 USC § 103 applicants argue that there is no suggestion to combine references. However, the cited references are in the same field of endeavor (such as treating heart failure by administration of exogenous therapeutic transgene including BIN1) and they seek to solve the same problems as the instant application and claims (such as rehabilitating heart tissue and ameliorating symptoms of heart failure) provide for a semen extender composition), and one of skill in the art is free to select components available in the prior art, In re Winslow, 151 USPQ 48 (CCPA, 1966).
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to VERA AFREMOVA whose telephone number is (571)272-0914. The examiner can normally be reached Monday-Friday: 8.30am-5pm EST.
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, Sharmila Landau can be reached at (571) 272-0614. 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.
Vera Afremova
March 1, 2026
/VERA AFREMOVA/ Primary Examiner, Art Unit 1653