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 .
Applicant's arguments filed 8/3/2026 have been fully considered but they are not persuasive.
Claims 3-4, 10-12, 17-18, and 20 have been cancelled.
The rejection of claims 1-2, 4, 6, 17, and 19 under 35 U.S.C. 102(a)(1) as being anticipated by Tokudome et al. (of record, available 18 March 2020) is withdrawn in view of the Otani Declaration under 37 CFR 1.130(a) submitted 8/3/2026. This attribution declaration invokes an exception under 102(b)(1)(A) with respect to the Tokudome et al. reference. See MPEP 717.01(a), 717.01(a)(1), and 717.01(c).
The rejection of claims 1-2, 4, 6, 9, and 16-19 under 35 U.S.C. 103 as being unpatentable over Tokudome et al. (of record, available 18 March 2020) in view of Kakehi et al. (U.S. Patent Application Publication 2018/0148509) and Kaplon et al. is withdrawn in view of the Otani Declaration under 37 CFR 1.130(a) submitted 8/3/2026.
Election/Restrictions
Applicant’s election without traverse of the IL-6 antibody inhibitor satralizumab against the IL-6 receptor (IL-6R) in the reply filed on 1/20/2026 is again acknowledged.
Claims 1-2, 5-9, 13-16, and 19 are under consideration in view of the current claim amendments.
Claim Objections
Applicant is advised that should claim 15 be found allowable, claim 19 will be objected to under 37 CFR 1.75 as being a substantial duplicate thereof. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
. Claims 15 and 19 both depend from claim 1 and recite the same limitations. They are of the same scope.
Claim Rejections - 35 USC § 102
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 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 1-2, 5-8, 14-15, and 19 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Wakabayashi et al. (of record).
Wakabayashi et al. discloses administering anti-IL-6R antibodies such as MR16-1 and tocilizumab to inhibit preterm delivery induced by inflammation. The dosage was 12 mg/kg. The anti-IL-6R antibody MR16-1 is the same antibody administered in the examples of the instant specification. It was administered to pregnant mice who subsequently delivered. See at least abstract and pages 719-720 and 725.
Tocilizumab is a recombinant, monoclonal, humanized anti-IL-6 receptor IgG1 antibody that binds human IL-6R as evidenced by Bao et al. (U.S. Patent Application Publication 2012/0301460). It is a neutralizing antibody. See at least paragraphs [0006 and 0055-0056]. The tocilizumab antibody meets the antibody limitations of instant claims 1 and 5-8. Bao et al. is cited to establish the inherent structure of tocilizumab.
MR16-1 is a monoclonal anti-mouse IL-6R antibody as evidenced by Tamura et al. See at least abstract. It does not bind human IL-6R as evidenced by Okazaki et al. See at least abstract. The MR16-1 antibody meets the antibody limitations of instant claims 1, 5, and 7. Tamura et al. and Okazaki et al. are cited to establish the inherent structure of MR16-1.
The 12 mg/kg dosage is disclosed in the instant application as being an effective dose for the claimed methods. See at least paragraph [0108] of the instant specification. As such, the treatment disclosed by Wakabayashi et al. would inherently treat or prevent peripartum cardiomyopathy in the pregnant mice and by extension inherently prevent or treat peripartum cardiomyopathy in lactating subjects or subjects in puerperium. The reference does not report any occurrence of peripartum cardiomyopathy.
Applicant’s arguments are unpersuasive. Absent evidence to the contrary (which has not been provided by applicant), administration of MR16-1 or tocilizumab in the amount of 12 mg/kg would inherently treat or prevent cardiomyopathy in the pregnant mice and by extension inherently prevent or treat peripartum cardiomyopathy in lactating subjects or subjects in puerperium. The amount administered by Wakabayashi et al. is disclosed in the instant application as being an effective amount to treat and prevent peripartum cardiomyopathy. The prior art discloses administering the claimed therapeutic (i.e. an IL-6 receptor antibody that is an IL-6 inhibitor) to the subject population in need of treatment or prevention (i.e. pregnant subjects that subsequently delivered and would lactate following delivery) in an amount expected to be therapeutic. The position of inherency is supported by the results of the instant application when administering the IL-6R antibody inhibitor MR16-1. See at least paragraphs [0027] and [0145] of the instant specification. In addition, the instant specification specifically suggests using the antibody tocilizumab. See at least paragraph [0096] of the instant specification. Note that any argument or evidence to the contrary will be considered an admission that the instant claims are not enabled for their scope.
Note that the instant claims require no particular therapeutic outcome for treatment. The instant specification discloses a wide range of therapeutic effects for “treatment.” See at least paragraph [0098] of the instant specification.
Applicant’s arguments with respect to LPS are not persuasive. The instant claims do not preclude pregnant subjects that have been treated with LPS or that have an infection.
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.
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 1-2, 5-9, 13-16, and 19 are rejected under 35 U.S.C. 103 as being unpatentable over Wakabayashi et al. view of Kakehi et al. (U.S. Patent Application Publication 2018/0148509), Kaplon et al., and Takeshita et al. (U.S. Patent Application Publication 2022/0220210).
Wakabayashi et al. is applied as above.
Kakehi et al. discloses antibodies for treating IL-6 related diseases. The anti-IL-6 receptor antibody SA237 is disclosed. See at least paragraphs [0009 and 0027] and claims 16, 18, 20, and 21. The SA237 antibody corresponds to the satralizumab of instant claims 9 and 16 as evidenced by Kaplon et al. at page 230, right column.
Takeshita et al. is cited to establish that SA237 is a humanized anti-human IL-6 receptor neutralizing antibody. It could be monoclonal and recombinantly produced. See at least paragraphs [0004, 0072, and 0075]. The SA237 (i.e. satralizumab) antibody meets the antibody limitations of instant claims 1, 5-9, and 16.
It would have been obvious to administer the SA237 antibody (i.e. satralizumab) of Kakehi et al. in place of the anti-IL-6R antibody MR16-1 or tocilizumab in the method of Wakabayashi. One would have been motivated to do so as satralizumab would have been a known and suitable anti-IL-6R antibody. Administration of the satralizumab would have produced the therapeutic effect required by the instant claims. A product and its properties cannot be separated.
Claims 1-2, 5-9, 13-16, and 19 are rejected under 35 U.S.C. 103 as being unpatentable over Li et al. (of record) in view of Sarojini et al., Kakehi et al. (U.S. Patent Application Publication 2018/0148509), Kaplon et al., Takeshita et al. (U.S. Patent Application Publication 2022/0220210), and Sheriff et al. (U.S. Patent Application Publication 2012/0225069)
Kakehi et al. (U.S. Patent Application Publication 2018/0148509), Kaplon et al., and Takeshita et al. are applied as above.
Li et al. (of record) discloses that IL-6 knock-out (KO) improved cardiac function and inhibited myocardial remodeling. IL-6 KO suppressed the myocardial apoptosis level in mice with dilated cardiomyopathy (DCM). IL-6 knockout inhibited the phosphorylation of STAT3 in heart tissues of DCM mice. See at least abstract and page 3049. Treating pregnant, lactating, or peripartum subjects is not specifically disclosed.
Sarojini et al. discloses that increased IL-6 levels are a predictor for mortality in peripartum cardiomyopathy. Peripartum cardiomyopathy is a disorder in which symptoms of heart failure occur between the last month of pregnancy and 5 months post-partum. See at least abstract and first paragraph of the introduction. Patients who died had larger left ventricular (LV) dimensions (e.g. left ventricular end-diastolic diameter (LV EDD) and left ventricular end-systolic diameter (LV ESD)) (i.e. dilated cardiomyopathy) compared with those who survived. See at least page 238, right column, first paragraph, and Table 3.
Sheriff et al. discloses that anti-IL-6 receptor antibodies can be used to treat dilated cardiomyopathy. See at least abstract; claims; and paragraphs [0011-0013 and 0032]. Treating pregnant, lactating, or peripartum subjects is not specifically disclosed.
It would have been obvious to reduce IL-6 signaling in pregnant females to treat or prevent peripartum cardiomyopathy. Li et al. makes clear that reducing IL-6 signaling improves cardiac function and inhibits myocardial remodeling and Sarojini et al. makes clear that increased IL-6 levels (and by inference the signaling through the IL-6 receptor) is a predictor for mortality in peripartum cardiomyopathy. Those who died had myocardial remodeling as compared to those who did not. Sheriff et al. makes clear that anti-IL-6R antibodies can be used to treat cardiomyopathy. One would have been motivated to administer in anti-IL-6R antibody such as satralizumab as taught by Kakehi et al. and Kaplon et al. to block IL-6 signaling in pregnant females thereby preventing or treating peripartum cardiomyopathy. As peripartum cardiomyopathy would have been known to occur during and following pregnancy as taught by Sarojini et al., it would have been obvious to administer satralizumab to a pregnant subject, lactating subject, and/or subject in puerperium.
Applicant’s arguments are not persuasive. While Li et al. uses a Coxsackievirus B3-induced dilated cardiomyopathy (DCM) model, the conclusions of Li et al. are not limited to dilated cardiomyopathy that occurs only as a result of Coxsackievirus B3. The prior art when considered as a whole suggests reducing IL-6 signaling to treat peripartum cardiomyopathy and that this reduction could be achieved by blocking the IL-6R with an inhibitor such as satralizumab.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). 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 MARIANNE P ALLEN whose telephone number is (571)272-0712. The examiner can normally be reached 7:00-3:30 EST Monday-Friday.
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/Marianne P Allen/Primary Examiner, Art Unit 1647
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