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 .
DETAILED ACTION
Applicant’s amendment of 18 May 2026, in which claim 33 has been amended, is acknowledged.
Claims 33, 41, 43-44 are pending in the instant application.
Claims 33, 41, 43-44 are examined herein.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 19 February 2026 and 29 June 2026 are acknowledged and considered.
Response to arguments of 18 May 2026
In view of Applicant’s amendment of 18 May 2026, the objection to the Specification is herein withdrawn. Applicant has corrected a mistake in the Specification.
Applicant’s arguments (Remarks of 18 May 2026, page 5) against the rejection of claims 33, 41, 43-44 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, written description/new matter, have been considered. Applicant states that the rejection has been overcome because the claims no longer recite a comparison between oral administration of CV-8814 and an equivalent amount of trimetazidine.
On 18 May 2026, Applicant has amended independent claim 33 to recite
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Applicant’s arguments (Remarks of 18 May 2026, pages 6-8) against the rejections of claims 33, 41, 43-44 under 35 U.S.C. 103 over Morita and Murai, in view of Fillmore, in further view of Masso; and over Morita and Aoyanagi, in view of Steggall, in further view of Masso, have been considered.
On 18 May 2026, Applicant has amended claim 33 to recite a method of improving cardiac function in a human subject. New/modified rejections are made below, based on Applicant’s amendment of 18 May 2026.
Applicant’s arguments (pages 6-8) are focused on this newly added limitation. Applicant argues that none of the cited references teach that administration of CV-8814 results in greater improvement in cardiac symptoms than trimetazidine while also providing a lower brain-to-plasma ratio of trimetazidine in humans than from administration of an equivalent amount of trimetazidine, resulting in fewer Parkinsonian symptoms.
These arguments are not persuasive. It is noted that therapeutic agents are usually developed to treat human patients. While data may be collected in relevant models of disease, the goal of treatment is ultimately to treat human patients. That is the case with the instant application, as well. The examiner notes that, for obvious reasons, there is no data in the instant application showing what is now claimed, namely that the administration of CV-8814 to a human patient, results in a lower brain-to-plasma ratio of trimetazidine than administration of an equivalent amount of trimetazidine. Such data is generated using animal experiments (page 94, Specoification), in this case rats.
Further, the cited prior art teaches administering CV-8814 (compound IX) to human patients.
It is noted that the claims are drawn to a method of improving cardiac function in a human subject suffering from heart failure, comprising administering to the subject a therapeutically effective amount of a compound of formula (IX). Since it is known that attaching an ethylene glycol (CH2CH2O)nH linker to the piperazine N in TMZ results in a compound more effective than TMZ as coronary vasodilator (Morita Figure 2), and having better PK compared to TMZ (Fig. 1, Morita, n2-TMZ is excreted more slowly than TMZ over a long period of time), a person of ordinary skill in the art would have reasonably expected that such a compound having better vasodilator properties and better PK properties than TMZ will be more effective than TMZ in treating heart failure.
Since prior art teaches administration of compound IX to a human subject, the claimed limitation brain-to-plasma ratio appears to be a result or property of the administration of
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. As such, the claimed limitations appear to be met by the prior art. Applicants are reminded that the office does not have the facilities and resources to provide the factual evidence needed in order to establish that the product of the prior art does not possess the same material, structural and functional characteristics of the claimed method. In the absence of evidence to the contrary, the burden is on the applicant to prove that the function of the product is different from those taught by the prior art and to establish patentable differences. See In re Best 562F.2d 1252, 195 USPQ 430 (CCPA 1977) and Ex parte Gray 10 USPQ 2d 1922 (PTO Bd. Pat. App. & Int. 1989).
Further, the ability to cross the blood brain barrier in a human patient is an inherent characteristic of a compound. It is noted that compound IX is more hydrophilic than trimetazidine and thus less likely to cross the blood-brain barrier, thus a lower brain-to-blood ratio for compound IX than that seen with TMZ, is expected.
New/modified rejections are made below, based on Applicant’s amendment of 18 May 2026.
Claim Rejections- 35 USC 103
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 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.
Claim interpretation: the recitation “an equivalent amount of trimetazidine” in claim 33 is interpreted to mean a comparable amount (as in Specification, page 25).
Claims 33, 41, 43-44 are rejected under 35 U.S.C. 103 as being unpatentable over Morita et al. (US 4,574,156 of 4 March 1986, cited in PTO-892 of 6 April 2022) and Murai et al. (US 4,100,285, cited in IDS), in view of Fillmore et al. (British Journal of Pharmacology 2014, 171, 2080-2090, cited in PTO-892 of 23 January 2020), in further view of Masso et al. (Therapies 2005, 60 (4), 419-422, cited in PTO-892 of 25 October 2024).
Morita (US 4,574,156) teaches that compound n2-TMZ (column 11, lines 13-15) below
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where R is methoxy and n = 2,
is superior to trimetazidine TMZ
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as being excreted over a long period of time (Figure 1, also column 11, lines 5-22),
and is superior to TMZ as a long-acting vasodilator having both peripheral blood vessel vasodilator action (Figure 2, column 11, lines 23-42) and coronary artery vasodilator action (column 11, lines 43-65).
Morita specifically teaches (Figure 2, also column 11, lines 35-38) that n2-TMZ, even at a dose of 13.3 mg/kg, is more effective than a similar dose (10 mg/kg) of TMZ in mice.
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Thus, Morita clearly teaches that compound n2-TMZ is superior to trimetazidine (TMZ) as coronary and peripheral vasodilator (Morita, column 11); further, compound n2-TMZ is superior to TMZ in terms of PK (Fig. 1, Morita), being excreted more slowly over a long period of time.
Morita administers n2-TMZ as a pharmaceutical composition, as in instant claim 41, intravenously, at a dose of 13.3 mg/kg in rats (column 11, lines 23-37) or 20 mg/kg in dogs (column 11, lines 43-55).
Morita teaches that trimetazidine TMZ is a coronary vasodilator (column 1, lines 19-23) in human patients and the compounds of the invention specifically n2-TMZ have excellent drug efficacy (column 1, lines 39-43) and improve the duration in blood of TMZ administered (column 1, lines 23-26) without losing its action as coronary vasodilator.
Morita does not specifically teach that the compound n2-TMZ above, or a pharmaceutical composition thereof, is effective to treat heart failure, as in the instant claims.
Morita does not specifically teach tablets comprising the compound above, as pharmaceutical compositions for oral administration, as in instant claims, administered at a dosage of 1 mg/kg/day to 10 mg/kg/day, as in instant claim 44.
Morita does not teach that compound n2-TMZ induces Parkinsonian symptoms in the subject upon administration.
Murai (US 4,100,285) teaches the following compound (Examples 10a-f, column 4-5)
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, which is the very compound (IX) of instant claim 33,
as having excellent pharmacodynamics effects on the coronary circulation system such as coronary artery vasodilative action or cardiac movement controlling action, useful in medicinal preparations (column 1, lines 19-24). Such medicinal preparations are pharmaceutical compositions, as in instant claim 41. Murai teaches (column 1, lines 30-32) administration of the compounds of the invention into the human body by internal administration (column 1, lines 28-31), as in instant claims, at a recommended dose 10 to 500 mg/day for internal administration, which overlaps with the dose in instant claim 44 (1 mg/kg/day to 10 mg/kg/day, which, for a human weighing 70 kg, corresponds to 70 mg/day to 700 mg/day).
Thus, Murai teaches that the compound above is a coronary artery vasodilator.
Murai teaches (Table 1, Example 10) the cardiovascular activity of the compound above measured according to Langedorff’s method by using the removed guinea pig heart: at a concentration of 10-4 g/ml, the compound above is effective to reduce coronary perfusion pressure by 4.4%, and is effective to reduce heart movements amplitude and to reduce heart rate by 10.7%.
Murai does not specifically teach that the compound above, or a pharmaceutical composition thereof, is effective to treat heart failure, as in the instant claims.
Murai does not specifically teach tablets comprising the compound above, as pharmaceutical compositions for oral administration, as in instant claims, administered at a dosage of 1 mg/kg/day to 10 mg/kg/day, as in instant claim 44.
Murai does not teach that
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induces Parkinsonian symptoms in the subject upon administration.
Fillmore teaches (Figure 3) that trimetazidine improves cardiac function in heart failure in human patients.
Masso et al. (Therapies 2005, 60 (4), 419-422) teaches (Abstract) that trimetazidine induces Parkinsonism in some of the patients (human subjects, as in the instant claims).
It would have been obvious to administer
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in a method of treating heart failure in a human patient suffering from heart failure, because Murai teaches that the compound above has excellent coronary artery vasodilative action in human patients, Morita teaches that compound n2-TMZ and trimetazidine (TMZ) are coronary vasodilators, and Morita teaches that n2-TMZ is superior to TMZ as a long-acting vasodilator, and Fillmore teaches that TMZ (taught by Morita to be a coronary vasodilator) is effective to treat heart failure and improves cardiac function in heart failure.
Since coronary vasodilator (Morita) trimetazidine (TMZ) is taught by Fillmore to be effective to treat heart failure/improve cardiac function in heart failure in human patients, the person of ordinary skill in the art would have administered
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, a compound structurally similar to TMZ, to a human patient suffering from heart failure, with the expectation that the compound above, which is taught by Murai to be a coronary vasodilator, is effective to treat heart failure and improve cardiac function in heart failure. Since it is known that compound n2-TMZ is more effective than TMZ as coronary vasodilator, and has better PK compared to TMZ, a person of ordinary skill in the art would have reasonably expected that
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will have better vasodilator properties and better PK properties than TMZ and will be more effective than TMZ in treating heart failure.
Further, the person of ordinary skill in the art would have administered
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orally as a tablet, as in instant claim 43, because formulating a therapeutic agent as a tablet for oral administration in the method of treatment is well within the skill of the artisan. The person of ordinary skill in the art would have further determined the therapeutic dose of compound in the method of treatment, as in instant claim 44, because such exploration of different therapeutic amounts/day, with the aim of optimizing the therapeutic effect achieved in a method of treatment is routine, well within the skill of the artisan.
Regarding the limitation “wherein the method results in fewer Parkinsonian symptoms in the subject than from the administration of an equivalent amount of trimetazidine”,
it would be obvious to modify the method of treating heart failure with
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(based on the combined teachings of Morita, Murai, and Fillmore) to include monitoring of side effects, such as Parkinsonian symptoms, and a comparison with TMZ, which is known to produce Parkinsonian symptoms in some patients (Maso et al.). Since prior art Murai teaches administration of
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to a patient, the side effect, in this case, Parkinsonian symptoms, inherently occurs upon administration of said compound to the patient.
Since prior art Murai teaches administration of
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to a patient, the brain-to-plasma ratio of trimetazidine achieved is the result of/inherently occurs upon/ administration of said compound to the patient. The ability of a compound to cross the brain blood barrier is an inherent property of the compound.
While Murai does not explicitly teach that the administration of
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“results in a lower brain-to-plasma ratio of trimetazidine than from administration of an equivalent amount of trimetazidine, whereby the method results in fewer Parkinsonian symptoms in the subject than from the administration of an equivalent amount of trimetazidine”, the claimed limitation appears to be a result or property of the administration of the effective amount of the
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. As such, the claimed limitations appear to be met by the prior art. Applicants are reminded that the office does not have the facilities and resources to provide the factual evidence needed in order to establish that the product of the prior art does not possess the same material, structural and functional characteristics of the claimed method. In the absence of evidence to the contrary, the burden is on the applicant to prove that the function of the product is different from those taught by the prior art and to establish patentable differences. See In re Best 562F.2d 1252, 195 USPQ 430 (CCPA 1977) and Ex parte Gray 10 USPQ 2d 1922 (PTO Bd. Pat. App. & Int. 1989).
As such, claims 33, 41, 43-44 are rejected as prima facie obvious.
Claims 33, 41, 43-44 are rejected under 35 U.S.C. 103 as being unpatentable over Morita et al. (US 4,574,156 of 4 March 1986, cited in PTO-892 of 6 April 2022) and Aoyanagi et al. (JP 57131777, published 14 August 1982, cited in PTO-892 of 23 January 2020; human translation in PTO-892 of 10 March 2021), in view of Steggall et al. (Diseases 2017, 5 (14), pages 1-18, published 10 May 2017, cited in IDS), in further view of Masso et al. (Therapies 2005, 60 (4), 419-422, cited in PTO-892 of 25 October 2024).
Morita (US 4,574,156) teaches that compound n2-TMZ (column 11, lines 13-15) below
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where R is methoxy and n = 2,
is superior to trimetazidine TMZ
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as being excreted over a long period of time (Figure 1, also column 11, lines 5-22),
and is superior to TMZ as a long-acting vasodilator having both peripheral blood vessel vasodilator action (Figure 2, column 11, lines 23-42) and coronary artery vasodilator action (column 11, lines 43-65).
Morita administers n2-TMZ as a pharmaceutical composition, as in instant claim 41, intravenously, at a dose of 13.3 mg/kg in rats (column 11, lines 23-37) or 20 mg/kg in dogs (column 11, lines 43-55).
Morita teaches that trimetazidine TMZ is a coronary vasodilator (column 1, lines 19-23) in human patients and the compounds of the invention specifically n2-TMZ have excellent drug efficacy (column 1, lines 39-43) and improve the duration in blood of TMZ administered (column 1, lines 23-26) without losing its action as coronary vasodilator.
Morita specifically teaches (Figure 2, also column 11, lines 35-38) that n2-TMZ, which is compound (IX) in the instant claims, even at a dose of 13.3 mg/kg, is more effective than a similar dose (10 mg/kg) of TMZ in mice.
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Thus, Morita clearly teaches that compound n2-TMZ (which is the very compound (IX) in the instant claims, is superior to trimetazidine (TMZ) as coronary and peripheral vasodilator (Morita, column 11); further, compound n2-TMZ is superior to TMZ in terms of PK (Fig. 1, Morita), being excreted more slowly over a long period of time.
Morita does not specifically teach that the compound n2-TMZ above, or a pharmaceutical composition thereof, is effective to treat heart failure in a human patient, as in the instant claims.
Morita does not specifically teach tablets comprising the compound above, as pharmaceutical compositions for oral administration, as in instant claims, administered at a dosage of 1 mg/kg/day to 10 mg/kg/day, as in instant claim 44.
Morita does not teach that compound n2-TMZ induces Parkinsonian symptoms in the human subject upon administration.
Aoyanagi teaches the following compound (Examples 1, Z is –CH2CH2OH)
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which is compound (IX) of instant claim 33.
Aoyanagi teaches (Table 1, Z is –CH2CH2OH) that, at a concentration of 10-4 g/ml (thus in a pharmaceutical composition, as in instant claim 41), the compound above is effective to reduce coronary perfusion pressure by 4.4%, and is effective to reduce heart movements amplitude and to reduce heart rate by 10.7%.
Aoyanagi teaches (page 2, second paragraph, human translation) that the compounds of the invention have pharmaceutical action on the coronary circulatory system such as coronary vasodilatory action. Thus, Aoyanagi teaches that the compound above is a coronary vasodilator.
Aoyanagi teaches (page 2, third paragraph, human translation attached) that, when the compounds of the invention are administered to humans, it is preferably to be administered orally, as in instant claims, at a recommended dose 10 to 500 mg/day for oral administration, which overlaps with the dose in instant claim 44 (1 mg/kg/day to 10 mg/kg/day, which, for a human weighing 70 kg, corresponds to 70 mg/day to 700 mg/day).
Aoyanagi does not specifically teach that the compound above, or a pharmaceutical composition thereof, is effective to treat heart failure, as in the instant claims.
Aoyanagi does not specifically teach tablets comprising the compound above, as pharmaceutical compositions for oral administration, as in instant claim 43, administered at a dosage of 1 mg/kg/day to 10 mg/kg/day, as in instant claim 44.
Aoyanagi does not teach that
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induces Parkinsonian symptoms upon administration to a human patient.
Steggall (Diseases 2017, 5 (14), pages 1-18, published 10 May 2017) teaches (pages 4-6, Table 1) that trimetazidine is effective to treat heart failure, when administered to a human patient at twice daily dosing of 35 mg tablets (page 4, under 3.1, first 4 lines), as tablet, as in instant claim 43, at daily dose of 1 mg/kg/day (for a human subject weighing 70 kg), which is within the daily dose in instant claim 44.
Steggall (Table 1) that trimetazidine is effective to treat heart failure: treatment with trimetazidine in human patients with heart failure resulted in improvement in LVEF left ventricular ejection fraction (page 5, Table 1, Results for studies by Zhou, Zhang and Gao). Thus, Steggall teaches that trimetazidine is effective to improve cardiac function, and specifically the ejection fraction, in a subject suffering from heart failure.
Steggall does not teach a method of improving cardiac function in a human patient suffering from heart failure with a compound of formula (IX).
Masso et al. (Therapies 2005, 60 (4), 419-422) teaches (Abstract) that trimetazidine induces Parkinsonism in some of the patients (human subjects).
It would have been obvious to administer
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in a method of treating heart failure in a human patient, because Aoyanagi teaches that the compound above has excellent coronary artery vasodilative action, Morita teaches that compound n2-TMZ and trimetazidine (TMZ) are coronary vasodilators, and Morita teaches that n2-TMZ is superior to TMZ as a long-acting vasodilator; and Steggall teaches that TMZ (taught by Morita to be a coronary vasodilator) is effective to treat heart failure and to improve cardiac function, and specifically the ejection fraction, in a human subject suffering from heart failure.
Since coronary vasodilator (Morita) trimetazidine (TMZ) is taught by Steggall to be effective to treat heart failure and improve cardiac function in human patients with heart failure, the person of ordinary skill in the art would have administered
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, a compound structurally similar to TMZ, to a patient suffering from heart failure, with the expectation that the compound above, which is taught by Aoyanagi to be a coronary vasodilator, is effective to treat heart failure and improve cardiac function in heart failure. Since it is known that compound n2-TMZ is more effective than TMZ as coronary vasodilator, and has better PK compared to TMZ, a person of ordinary skill in the art would have reasonably expected that
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has better vasodilator properties and better PK properties than TMZ and will be more effective than TMZ in treating heart failure.
Further, the person of ordinary skill in the art would have administered the compound above orally as a tablet, as in instant claims 41, 43, because formulating a therapeutic agent as a tablet for oral administration in the method of treatment is well within the skill of the artisan. The person of ordinary skill in the art would have further determined the therapeutic dose of compound in the method of treatment, as in instant claim 44, because such exploration of different therapeutic amounts/day, with the aim of optimizing the therapeutic effect achieved in a method of treatment is routine, well within the skill of the artisan.
Regarding the limitation “wherein the method results in fewer Parkinsonian symptoms in the subject than from the administration of an equivalent amount of trimetazidine”,
it would be obvious to modify the method of treating heart failure with
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(based on the combined teachings of Morita, Aoyanagi and Steggall) to include monitoring of side effects, such as Parkinsonian symptoms, and a comparison with TMZ, which is known to produce Parkinsonian symptoms in some patients (Maso et al.). Since prior art Aoyanagi teaches administration of
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to a patient, the side effect, in this case, Parkinsonian symptoms, inherently occurs upon administration of said compound to the human patient.
Further, since prior art Aoyanagi teaches administration of
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to a human patient, the brain-to-plasma ratio of trimetazidine achieved is the result of/inherently occurs upon/ administration of said compound to the patient. The ability of a compound to cross the brain blood barrier is an inherent property of the compound.
While Aoyanagi does not explicitly teach that the administration of
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“results in a lower brain-to-plasma ratio of trimetazidine than from administration of an equivalent amount of trimetazidine, whereby the method results in fewer Parkinsonian symptoms in the subject than from the administration of an equivalent amount of trimetazidine”, the claimed limitation appears to be a result or property of the administration of the effective amount of the
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. As such, the claimed limitations appear to be met by the prior art. Applicants are reminded that the office does not have the facilities and resources to provide the factual evidence needed in order to establish that the product of the prior art does not possess the same material, structural and functional characteristics of the claimed method. In the absence of evidence to the contrary, the burden is on the applicant to prove that the function of the product is different from those taught by the prior art and to establish patentable differences. See In re Best 562F.2d 1252, 195 USPQ 430 (CCPA 1977) and Ex parte Gray 10 USPQ 2d 1922 (PTO Bd. Pat. App. & Int. 1989).
As such, claims 33, 41, 43-44 is rejected as prima facie obvious.
Conclusion
Claims 33, 41, 43-44 are rejected.
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 IRINA NEAGU whose telephone number is (571)270-5908. The examiner can normally be reached Mon-Fri 8-5.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, JEFFREY S. LUNDGREN can be reached on (571) 272-5541. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/IRINA NEAGU/Primary Examiner, Art Unit 1629
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