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 .
Status of claims
Claims 1-22 as filed on 5/27/2026 are pending and under examination in the instant office action.
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 remain 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 remain 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
Applicants’ arguments and contents of Declaration by Ting-Ting Hong and by Robin Mark Shaw filed on 5/27/2026 have been fully considered but they are not all found persuasive.
The rejection of claims under 35 U.S.C. 102 (a) (1) as being anticipated by Zhou et al (“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) has been withdrawn in view of Applicants’ Declaration (it. 9) that interpretation of the disclosure by the office action is not correct, that Applicant is a co-author of the cited reference and that the mice with deleted BIN1 in set 1 of the disclosed experiments were not treated with any AAV9-cBIN1 gene therapy.
With regard to claim rejection under 35 USC § 103 Applicants’ arguments (response page 7) and contents of Declaration (it. 10) are based on the idea that the cited references by Zhou and Liu solely disclose prophylactic studies using cBIN1 gene therapies but not a treatment of subjects having pre-existing hear failure; and ,thus, there would not an obvious teaching and/or suggestion for treating subjects having pre-existing hear failure by administering cBIN1 gene therapy.
These arguments are not found particular persuasive because preventing a disease with a drug serves as strong evidence or reasonably provides a strong suggestion that the drug modifies the underlying biological pathway or risk factors of the disease. In the instant case, the cited references clearly teach that low or reduced levels of cBIN1 in blood samples are markers of heart failure (Liu et al; Shaw et al) and that progression of heart failure goes along with a decline of expression of BIN1 (Zhou), thereby, linking underlying biological pathway or risk factors of the heart failure with a levels of cBIN1 and drugs based on cBIN1-delivery or administration. Moreover, the references by Zhou and Liu teach that cBIN1 gene administration before actual heart failure (model with TAC performed after injection of cBIN1 delivered by viral vector) postpones and reverses the actual heart functions associated with heart failure (see section conclusions”).
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 a subject with a pre-existing HF with a reasonable expectation of success in rehabilitating heart tissue of the subject 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.
No claims are allowed.
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 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
August 10, 2026
/VERA AFREMOVA/ Primary Examiner, Art Unit 1653
Prosecution Insights