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
This application, filed 29 November, 2021, is a national stage application of PCT/US2020/0634609, filed 27 May, 2020, which claims the benefit of U.S. Provisional Application N° 62/855,372, filed 31 May, 2019.
Information Disclosure Statement
Two information disclosure statements (IDS) submitted on 20 February, 2026 and 29 June, 2026 are acknowledged and have been considered.
Status of the Application
Receipt is acknowledged of Applicant's claimed invention, filed 15 June, 2026, in the matter of Application No. 17/614,826. Said documents have been entered on the record.
Claim 1 is amended. Claim 22 is canceled. No new matter was introduced.
Thus, Claims 1 and 21 represent all claims currently under consideration.
Response to Arguments
Claim 22 has been canceled. Therefore, the rejections of this claim under 35 U.S.C. 112(b) and 103 are moot.
Applicant's arguments and amendments, filed 15 June, 2026, have been fully considered but they are not persuasive. Applicant has amended Claim 1 to amend a subject “post myocardial injury having myocardial scarring.” Although Applicant has added the limitation “having myocardial scarring,” the amendment does not resolve the uncertainty regarding the scope of “post myocardial injury.” The claim still does not define the nature, type, severity, or temporal stage of the myocardial injury encompassed by this limitation. Further, this amendment does not distinguish the claimed method from the cited prior art. As discussed in the previous rejections under U.S.C. 103, Tassoni and Levin each teach administration of the same compound to patient populations suffering from myocardial injury, ischemic injury, or heart-failure-associated remodeling through the same mechanism of shifting myocardial metabolism from fatty acid oxidation toward glucose oxidation. Such patient populations are recognized in the art as undergoing myocardial remodeling associated with fibrosis and myocardial scarring. Accordingly, the added limitation merely identifies a characteristic of the treated patient population and does not alter the operative step of administering the same compound by the same mechanism for the same therapeutic purpose.
Applicant’s arguments continue to focus on the asserted therapeutic result of the claimed method, namely inhibition of cardiac fibrosis or myocardial scarring, rather than on a patentably distinct treatment step. The cited references teach administration of the same compound under conditions in which the claimed biological effect would reasonably be expected to occur. The recitation of the intended result, or the recognition of a previously unappreciated property or benefit of a known method, does not render the claimed method patentable. See MPEP § 2141.02(III).
Furthermore, the additional recitation “having myocardial scarring” does not provide objective boundaries for claim scope. The claim does not specify whether the recited scarring must result from the myocardial injury, the degree or extent of scarring required, or the criteria by which a subject is determined to possess the claimed scarring. Thus, even as amended, one of ordinary skill in the art cannot determine with reasonable certainty which subjects fall within the scope of the claim.
Accordingly, for the reasons discussed above and in the previous Office Action, the rejections under U.S.C. 112(b) and 103 are maintained, even where updated due to amendment.
Claim Rejections - 35 USC § 112 MAINTAINED
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 1 and 21 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 1 recites “a subject post myocardial injury having myocardial scarring”, which introduces uncertainty because the claim does not define the nature, type, severity, or temporal stage of myocardial injury encompassed by this term. As drafted, it is unclear whether “post myocardial injury having myocardial scarring” refers to the immediate acute phase following infarction, the subacute healing period, chronic remodeling, ischemic injury short of infarction, microinfarcts, cardiomyopathic injury, or other forms of myocardial stress. In the absence of objective boundaries or criteria establishing which clinical states fall within the scope of the claim, a person of ordinary skill in the art cannot determine with reasonable certainty whether a given subject satisfies the “post myocardial injury having myocardial scarring” limitation. Further, it is unclear whether the recited myocardial scarring is intended to define the timing of the injury, the severity of the injury, the extent of fibrosis, or merely an additional clinical characteristic of the subject. Thus the amendment does not provide objective boundaries for determining claim scope.
Claim 21 further requires that the myocardial injury be “associated with a disease, disorder, or condition,” but the claim does not set forth the degree, type, or temporal relationship of the required association, nor whether the listed disease must cause the injury or may merely coexist. Without such objective boundaries, a person of ordinary skill in the art cannot determine the scope of the claim with reasonable certainty.
Claim Rejections - 35 USC § 103 (MAINTAINED)
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
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 are rejected under 35 U.S.C. 103 as being unpatentable over Tassoni et al. (WO 2007/096251, previously cited, and in IDS), hereinafter Tassoni.
Regarding Claim 1, Tassoni teaches 1-(2-hydroxyethyl)-4-(2,3,4-trimethoxybenzyl)piperazine (‘251, Pg. 12, Line 10), and other CPT-1 inhibitors in the treatment of heart disorders such as congestive heart failure (CHF) (‘251, Abstract and Pg. 10, Lines 16-17.) Tassoni further discloses the action of these compounds seems to take place, at least in part, by promoting a shift in the cellular metabolism in the myocardium which leads to the preferential use of glucose reducing the oxidation of the fatty acids by inhibiting the activity of CPT1 (‘251, Pg. 2, Lines 6-9.)
While Tassoni fails to specify inhibition of cardiac fibrosis, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention, to administer the claimed compound to a subject post myocardial injury having myocardial scarring, as Tassoni teaches administering the instant compound to heart failure patients, a population well recognized in the art as undergoing post-myocardial remodeling characterized by myocardial fibrosis and scarring. A person of ordinary skill in the art would have been motivated to treat such patients to improve cardiac outcomes, including reducing or preventing fibrotic remodeling associated with heart failure. There would have been a reasonable expectation of success that administering the compound as taught in the art would inherently inhibit or reduce cardiac fibrosis; the “thereby inhibiting cardiac fibrosis” clause is an intended result that does not alter the method steps.
Regarding Claim 21, the additional limitation that “the myocardial injury is associated with a disease, disorder, or condition” does not patentably distinguish over Tassoni, which teaches administration to heart failure, a condition well known to be associated with post-myocardial remodeling characterized by myocardial fibrosis and scarring. Thus, Claim 21 is obvious for the reasons set forth above.
Claims 1 and 21 are rejected under 35 U.S.C. 103 as being unpatentable over Tassoni (WO 2007/096251), as applied to Claims 1 and 21 above, and further in view of Karwi et al. (Frontiers in Cardiovascular Medicine, Vol. 5, Article 68, June 6, 2018, previously cited, and in IDS), hereinafter Karwi.
The teachings of Tassoni (2007) are set forth in the above 35 U.S.C. 103 Rejections and are incorporated herein. Tassoni teaches the instant compound (Formula IX) and other CPT-1 inhibitors in the treatment of heart disorders such as congestive heart failure (CHF) and discloses the action of these compounds takes place, at least in part, by promoting a shift in the cellular metabolism in the myocardium which leads to the preferential use of glucose reducing the oxidation of the fatty acids by inhibiting the activity of CPT1.
Regarding Claims 1 and 21, Karwi teaches two molecules, namely etomoxir and perhexiline, are shown to inhibit CPT1 (Figure 3) and limit fatty acid oxidation with parallel increase in glucose oxidation in mouse and rat models of heart failure (Karwi, Pg. 10, § Inhibiting Fatty Acid Oxidation.)
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention, to substitute the CPT-1 inhibitor of Karwi for the alternative CPT-1 inhibitor of Tassoni, as both references disclose CPT-1 inhibition as a therapeutic strategy for treating patients with heart failure by shifting cardiac energy metabolism away from fatty oxidation and toward glucose oxidation.
One of ordinary skill would have been motivated to make such a substitution because the art establishes CPT-1 inhibition as a recognized mechanism of action for improving cardiac function in heart failure, and the skill artisan would have reasonably expected structurally different CPT-1 inhibitors to be interchangeable for this purpose.
There would have been a reasonable expectation of success that the compound taught by Tassoni, when used in the method of Karwi, would provide the same therapeutic benefit in heart failure patients, and therefore those post myocardial injury having myocardial scarring, since both references target the same enzyme and metabolic pathway to achieve the same clinical effect.
Claims 1 and 21 are rejected under 35 U.S.C. 103 as being unpatentable over Levin (US 2018/0360975, cited in IDS.)
Reference shares an inventor with the instant application.
Regarding Claims 1 and 21, Levin teaches the same Formula IX compound (‘975, Pg. 2, Para 0020), which shifts cardiac metabolism from fatty acid oxidation to glucose oxidation (‘975, Pg. 3, Para 0028 and 0029), in methods of treating conditions by providing compositions of the invention, wherein the condition may be heart disease, such as heart failure (‘975, Pg. 11, Para 0177, and Pg. 33, Claims 54-58.)
While Levin fails to specify inhibition of cardiac fibrosis, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention, to administer the claimed compound to a subject post myocardial injury having myocardial scarring, as Levin teaches administering the instant compound to heart failure patients, a population well recognized in the art as having post-myocardial remodeling characterized by myocardial fibrosis and scarring. A person of ordinary skill in the art would have been motivated to treat such patients to improve cardiac outcomes, including reducing or preventing fibrotic remodeling associated with heart failure. There would have been a reasonable expectation of success that administering the compound as taught in the art would inherently inhibit or reduce cardiac fibrosis; the “thereby inhibiting cardiac fibrosis” clause is an intended result that does not alter the method steps.
Regarding Claim 21, the additional limitation that “the post myocardial injury having myocardial scarring” is associated with a disease, disorder, or condition” does not patentably distinguish over Levin, which teaches administration to heart failure, a condition well known to be associated with myocardial injury. Thus, Claim 21 is obvious for the reasons set forth above.
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.
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/D.M.N./Examiner, Art Unit 1627
/SARAH PIHONAK/Primary Examiner, Art Unit 1627
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