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
This Office Action is in response to Applicant’s Arguments and Amendment filed, 05/01/2026, wherein the Amendment amended claims 4, 7, 9, 11, 13, 15, 17, 21, and 44-48, and cancelled claims 41-43.
Claims 4, 7, 9, 11, 13, 15, 17, 21, and 44-48 are pending.
Note: Independent claim 21 is preceded by dependent claims 1, 4, 7, 9, 11, 13, 15, and 17. If the application is allowed, the claims will be renumbered, such that the independent claim precedes any dependent claims.
Priority
This application claims the following priority:
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Election/Restrictions
Applicant elected Group II, a method of use, and a) a combination of HDAC inhibitor and MR antagonist as the “combination of two or more histone acetylation code agents,” b) valproic acid as the HDAC inhibitor and canrenone as the MR antagonist, and c) ischemic damage as the single disclosed disease or condition that causes tissue and/or organ injury, in the reply filed on 09/18/2025.
In the course of the search, the MR antagonist was broadened to include spironolactone and eplerenone, and the disease was broadened to include myocardial infarction.
Claims 7, 11, 13, and 15 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected subject matter, there being no allowable generic or linking claim.
Claims 4, 9, 17, 21, and 44-48 are examined on the merits herein.
REJECTIONS WITHDRAWN
The status for each rejection and/or objection in the previous Office Action is set out below.
Claim Objections
Applicant’s amendment to claim 9 is sufficient to overcome this objection.
35 U.S.C. § 112(b)
Applicant’s amendments to claims 4 and 21 are sufficient to overcome these rejections.
35 U.S.C. § 112(a)
Applicant’s amendments to claim 21 that limits the method to a method of treating cardiac ischemic reperfusion injury, and limits the two or more histone acetylation code agents to VPA or a VPA derivative, and MR antagonist, are sufficient to overcome these rejections.
35 U.S.C. § 102 over Wang and 35 U.S.C. § 102 over de Groot
Applicant’s amendments to claim 21 that limits the two or more histone acetylation code agents to VPA or a VPA derivative, and MR antagonist, are sufficient to overcome these rejections.
REJECTIONS—MAINTAINED, MODIFIED, & NEW
Applicant’s amendment to claim 21 limits the treatment to a method of treating cardiac ischemic reperfusion injury and limits the two or more histone acetylation code agents to valproic acid or a valproic acid derivative, and a mineralocorticoid receptor antagonist. As such, the prior art rejections have been modified; Wang continues to be relied upon as a primary reference, and Le and Bossard continue to be relied upon as secondary references.
Applicant’s amendment to claim 48 is now commensurate in scope with the election of species of the combination of histone acetylation code agents. As such, claim 48 is no longer withdrawn and a new rejection is applied over claim 48.
Claim Objections
(new) Claim 48 is objected to because of the following informalities:
-In claim 48, line 4, the term “antagonist” should be inserted following “(MR).”
-In claim 48, line 4, the “and” following “suffered” should be replaced with - - an - -.
-In claim 48, line 6, prior to “formulation,” the article - - a - - should be inserted.
Appropriate correction is required.
Claim Rejections - 35 USC § 112(b)
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.
Claim 4 is 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 4 depends from claim 21, wherein claim 21 recites administering a combination of valproic acid or a valproic acid derivative and a mineralocorticoid receptor antagonist. Claim 4 recites further administering valproic acid or a valproic acid derivative. As such, it is not clear if the valproic acid or valproic acid derivative of claim 21 meets this limitation, or if the recitation of valproic acid and valproic acid derivative in claim 4 is a typo, or if claim 4 is intended to be limited to a greater amount of valproic acid or valproic acid derivative.
In view of compact prosecution, for the purpose of applying prior art, a teaching of valproic acid or valproic acid derivative that applies to claim 21 is interpreted as meeting the limitations of claim 4 since the instant specification teaches valproic acid or valproic acid derivatives as HDAC inhibitors (pg. 2).
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.
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.
(modified) Claims 4, 9, 17, 21, and 44-47 are rejected under 35 U.S.C. 103 as being unpatentable over US 2018/0325850 to Wang (published 2018, PTO-892 of 10/02/2026), in view of Le (Low-Dose Spironolactone Prevents Apoptosis Repressor With Caspase Recruitment Domain Degradation During Myocardial Infarction, Hypertension, published 2012, PTO-892 of 01/02/2026).
Wang teaches a method of treating and reducing the risk of myocardial infarction (MI) and/or reducing tissue damage caused by MI in a subject comprising administering an effective a dose of valproic acid or a related form thereof (title; abstract; pg. 8, claims 1-3, 4).
Wang specifically teaches the subject as suffering from myocardial ischemia, and teaches the method as reducing tissue damage caused by the MI or by reperfusion (pgs. 8-9, claims 3, 11-12).
Wang teaches co-administering, in a single formulation, the valproic acid with an additional agent (pgs. 8-9, claims 6-7, 11-12, 22-25; [0049]-[0050]).
Regarding claim 21, while Wang teaches a method of treating MI and/or reducing tissue damage caused by MI, by administering valproic acid, it differs from that of instant claim 21, in that it does not teach an MR antagonist.
Le teaches that when hearts from rats are subjected to regional ischemia followed by reperfusion, and then treated with low dose spironolactone or eplerenone, the infarct size is significantly reduced. Spironolactone also prevents cleavage of the apoptotic chromatin condensation inducer in the nucleus of the inhibitor of caspase activated DNAse induced by ischemic-reperfusion, thereby abolishing chromatin condensing and inter-nucleosome cleavage. Ischemia-reperfusion induced activation of caspases 2, 3, and 9, is prevented by spironolactone. Low-dose spironolactone and eplerenone prevents loss of the apoptosis repressor with the caspase recruitment domain and reduced myocyte death. Thus, low dose MR antagonists, such as spironolactone and eplerenone, reduce infarct size and apoptosis in the re-perfused myocardium by preventing apoptosis repressor with caspase recruitment domain degradation (abstract; pg. 1168).
It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to add the spironolactone or eplerenone of Le, to the valproic acid compositions of Wang, to arrive at instant claim 21. One of ordinary skill in the art would have been motivated to make such an addition, with a reasonable expectation of success, because:
-both Wang and Le teaches methods of treating myocardial infarction,
-Wang teaches co-administering the valproic acid with an additional prophylactic agent in a coformulation,
-Wang specifically teaches the additional agent as reducing tissue damage resulting from MI and/or reperfusion ([0050]-[0052]),
-Le teaches that MR antagonists, such as spironolactone and eplerenone, reduce infarct size and apoptosis in the re-perfused myocardium, and
-"It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art." In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980). MPEP 2144.06
As such, an ordinary skilled artisan would have been motivated to make such an addition to predictably arrive at a more therapeutically effective method of treating MI by decreasing infarct size and apoptosis.
Regarding claim 4, Wang teaches valproic acid. See the 112(b) rejection above for the interpretation of claim 4.
Regarding claim 9, Le teaches spironolactone and eplerenone.
Regarding claim 17, Wang teaches coformulations comprising valproic acid and an additional agent.
Regarding claims 44 and 46, the combination of Wang and Le teaches a method of treating myocardial infarction, and Le teaches myocardial infarction as triggering apoptosis, (programmed cell death) and progressive loss of cardiomyocytes (pg. 1164; pg. 1165, 1st paragraph).
Regarding claim 45, Wang teaches administering the valproic acid during an MI event or after (pg. 9, claims 16-17).
Regarding claim 47, Wang teaches oral or injection administration (pgs. 8-9, claims 5, 21).
(new) Claim 48 is rejected under 35 U.S.C. 103 as being unpatentable over US 2018/0325850 to Wang (published 2018, PTO-892 of 10/02/2026) in view of Le (Low-Dose Spironolactone Prevents Apoptosis Repressor With Caspase Recruitment Domain Degradation During Myocardial Infarction, Hypertension, published 2012, PTO-892 of 10/02/2026), and Collett (Dosage regimens, published 06/02/2016, PTO-892).
Wang and Le are applied as discussed above and incorporated herein.
Regarding claim 48, the combination of Wang and Le differs from that of instant claim 48 in that it does not teach intravenous administration in a clinical setting followed by oral administration.
Wang further teaches that dosing is dependent on severity and responsiveness of the disease state or condition to be treated, with the course of treatment lasting from several days to several months, or until a cure is effected or a diminution of the disease state of risk imposed thereby is achieved. In some embodiments, treatment is administered in one or more courses, where each course comprises one or more doses per day for several days or weeks. In some embodiments courses of treatment are administered sequentially, while in other embodiments, a break of 1 or more days, weeks, or months is provided between courses. Optimal dosing schedules can be calculated from measurements of drug accumulation in the body of the patients. The administering clinician can readily determine optimum dosages, dosing methodologies, and repetition rates. The treating clinician can estimate repetition rates for dosing based on measured residence times and concentrations of the drug in bodily fluids or tissues ([0047]-[0048]).
Wang teaches oral and intravenous administration ([0030]; [0039]-[0044]).
Collett teaches that the design of a dosage regimen determines the therapeutic benefit for patients. The principles of clinical pharmacokinetics are applied to design a dosage regimen for a patient that ensures the appropriate formulation of drug is chosen for an appropriate route of administration. One the basis of the patient’s drug handling parameters, which require an understanding of absorption, distribution, metabolism and excretion, the dosage regimen for the medicine in a particular patient, can be optimized. The pharmacist needs to ensure the appropriate regimen is prescribed to achieve optimal efficacy and minimal toxicity (pg. 2, 1st paragraph).
Collett teaches that clinical pharmacokinetics provides a basic understanding of the principles required to design a dosage regimen, wherein pharmacokinetics provides a mathematical basis to assess the time course of drug and their concentration in the body and enables absorption, distribution, metabolism, and excretion (ADME) to be quantified (pg. 2, 2nd paragraph).
Collett teaches that the design of the regimen, i.e. formulation, route of administration, dose size, and dose frequency, are important factors which influence what plasma concentration is achieved and maintained in the body over the prescribed course of drug treatment. Collett further teaches that other factors that require consideration are patients’ individuals needs and lifestyles (pg. 3, 3rd paragraph).
Collett teaches that to understand how the design of dosage regimen influences the time course of a drug in the body, consideration of the complex pharmacokinetic process of drug input, output, and distribution within the body must be considered (pg. 3, last paragraph). Collett teaches that pharmacokinetic models are hypothetical constructs which describe the fate of a drug in a biological system following its administration. The purpose of modeling is to characterize the ADME profile for a drug to indicate how the drug is handled by the patient and to characterize basic parameters (pg. 4, 1st paragraph).
Collett teaches that the greater the rate of drug input relative to the rate of drug output from the body compartment over the net absorption phase, the higher will be the peak concentration achieved in the body or plasma following oral administration of a single dose of drug.
It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to modify the dosing regimen of the combination of Wang and Le, to arrive at instant claim 48. One of ordinary skill in the art would have been motivated to make such a modification, with a reasonable expectation of success, because:
-Wang teaches that a clinician knows how to modify the dosing amounts, frequencies, and regimens to arrive at an optimal method of treatment,
-Collett teaches that in designing a dosage regimen, formulation, route of administration, dose size, and dose frequency, are important factors which influence what plasma concentration is achieved and maintained in the body over the prescribed course of drug treatment,
-Collett teaches that other factors that require consideration are patients’ individual needs and lifestyles, and
-"[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation," MPEP 2144.05(II).
Thus, an ordinary skilled artisan would have been motivated to make such a modification to predictably arrive at a dosing regimen that treats the MI during the MI and after the MI to minimize cardiac damage, i.e., cardiac ischemic reperfusion damage.
(modified) Claims 4, 9, 17, 21, and 44-47 are rejected under 35 U.S.C. 103 as being unpatentable over US 2018/0325850 to Wang (published 2018, PTO-892 of 10/02/2026), in view of Bossard (Mineral-corticoid receptor antagonists in patients with acute myocardial infarction—A systematic review and meta-analysis of randomized trials, published 2018, PTO-892 of 10/02/2026).
Wang is applied to as discussed above and incorporated herein.
Regarding claim 21, while Wang teaches a method of treating MI and/or reducing tissue damage caused by MI, by administering valproic acid, it differs from that of instant claim 21, in that it does not teach an MR antagonist, such as canrenone.
Bossard teaches that administration of MR antagonists reduces mortality after acute myocardial infarction, especially in patients with heart failure (abstract; pg. 67).
Bossard teaches canrenone as a MR antagonist (pg. 61, Col. 2; pg. 62, Fig. 1).
It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to add the canrenone taught by Bossard to the valproic acid compositions of Wang to arrive at instant claim 21. One of ordinary skill in the art would have been motivated to make such an addition, with a reasonable expectation of success, because:
-both Wang and Bossard teach methods of treating myocardial infarction,
-Wang teaches co-administering the valproic acid with an additional agent in a coformulation,
-Wang specifically teaches the additional agent as reducing tissue damage resulting from MI and/or reperfusion ([0050]-[0052]),
-Bossard teaches that administration of MR antagonists, such as canrenone, reduces mortality after acute myocardial infarction, especially in patients with heart failure, and
-"It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art." In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980). MPEP 2144.06
As such, an ordinary skilled artisan would have been motivated to make such an addition to predictably arrive at a therapeutically effective method of treating MI in patients by reducing mortality, especially in patients with heart failure.
Regarding claim 4, Wang teaches valproic acid. See the 112(b) rejection above for the interpretation of claim 4.
Regarding claim 9, Bossard teaches canrenone.
Regarding claim 17, Wang teaches coformulations comprising valproic acid and an additional agent.
Regarding claim 44, Bossard teaches MI as causing cardiomyocyte apoptosis and myocardial fibrosis (pg. 65, paragraph spanning Cols. 1-2).
Regarding claim 45, Wang teaches administering the valproic acid during an MI event or after (pg. 9, claims 16-17).
Regarding claim 46, the combination of Wang and Bossard teaches a method of treating myocardial infarction.
Regarding claim 47, Wang teaches oral or injection administration (pgs. 8-9, claims 5, 21).
(new) Claim 48 is rejected under 35 U.S.C. 103 as being unpatentable over US 2018/0325850 to Wang (published 2018, PTO-892 of 10/02/2026) in view of Bossard (Mineral-corticoid receptor antagonists in patients with acute myocardial infarction—A systematic review and meta-analysis of randomized trials, published 2018, PTO-892 of 10/02/2026) and Collett (Dosage regimens, published 06/02/2016, PTO-892).
Wang and Bossard are applied as discussed above and incorporated herein.
Regarding claim 48, the combination of Wang and Bossard differ from that of instant claim 48 in that it does not teach intravenous administration in a clinical setting followed by oral administration.
Wang further teaches that dosing is dependent on severity and responsiveness of the disease state or condition to be treated, with the course of treatment lasting from several days to several months, or until a cure is effected or a diminution of the disease state of risk imposed thereby is achieved. In some embodiments, treatment is administered in one or more courses, where each course comprises one or more doses per day for several days or weeks. In some embodiments courses of treatment are administered sequentially, while in other embodiments, a break of 1 or more days, weeks, or months is provided between courses. Optimal dosing schedules can be calculated from measurements of drug accumulation in the body of the patients. The administering clinician can readily determine optimum dosages, dosing methodologies, and repetition rates. The treating clinician can estimate repetition rates for dosing based on measured residence times and concentrations of the drug in bodily fluids or tissues ([0047]-[0048]).
Wang teaches or and intravenous administration ([0030]; [0039]-[0044]).
Collett is applied as discussed above and incorporated herein.
It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to modify the dosing regimen of the combination of Wang and Bossard, to arrive at instant claim 48. One of ordinary skill in the art would have been motivated to make such a modification, with a reasonable expectation of success, because:
-Wang teaches that a clinician knows how to modify the dosing amounts, frequencies, and regimens to arrive at an optimal method of treatment,
-Collett teaches that in designing a dosage regimen, formulation, route of administration, dose size, and dose frequency, are important factors which influence what plasma concentration is achieved and maintained in the body over the prescribed course of drug treatment,
-Collett teaches that other factors that require consideration are patients’ individuals needs and lifestyles, and
-"[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation," MPEP 2144.05(II).
Thus, an ordinary skilled artisan would have been motivated to make such a modification to predictably arrive at a dosing regimen that treats the MI during the MI and after the MI to minimize cardiac damage, i.e., cardiac ischemic reperfusion damage.
Response to Arguments
On pg. 7, Remarks, Applicant argues that Wang, Le, and Bossard do not teach or suggest the claimed combination.
This argument has been fully considered, but is not found persuasive. The above rejections are obviousness type, 35 USC 103 rejections, and not anticipatory 35 USC 102 rejections. It is the combination of the teachings of Wang and Le, and the teachings of Wang and Bossard, that are applied to arrive at the instant claims.
On pg. 7, Remarks, Applicant argues that In re Kerkhoven does not apply to the 35 USC 103 rejections.
On pg. 8, Remarks, Applicant further argues that Wang and Le/Bossard address overlapping but pharmacologically distinct aspects of cardiac injury through fundamentally different mechanisms. Applicant further argues that the fact that both classes of agents have been investigated in the general context of cardiac injury does not provide a motivation to combine them into a single therapy.
On pg. 9, Remarks, Applicant argues that the combination of VPA and MR antagonist is not a straightforward mixing of two interchangeable composition for the same purpose, but is a deliberate pairing of two agents that converge on a common molecular target through distinct and complementary mechanisms.
These arguments have been fully considered, but are not found persuasive. Though Applicant argues that both class of agents have been investigated in the general context of cardiac injury, it is respectfully pointed out that Wang specifically teaches valproic acid for the treatment of myocardial infarction, Le specifically teaches spironolactone and eplerenone for the treatment of myocardial infarction, and Bossard specifically teaches canrenone for the treatment of myocardial infarction. As such, all three compounds are “taught by the prior art to be useful for the same purpose.” As such, In re Kerkhoven is properly applied.
Moreover, Applicant is respectfully reminded that the reason or motivation to modify the reference may often suggest what the inventor has done, but for a different purpose or to solve a different problem. It is not necessary that the prior art suggest the combination to achieve the same advantage or result discovered by applicant, MPEP 2144 (IV).
On pg. 8, Remarks, Applicant argues that the cited references do not recognize any mechanistic relationship between HDAC inhibition and MR pathway modulation that would motivate a person of ordinary skill in the art to combine VPA with an MR antagonist.
On pgs. 8-9, Remarks, Applicant further argues that HCAC inhibitors can cause acetylation of MR, and acetylation of MR inhibits is transcriptional activity thereby promoting cell protection, and that MR antagonists independently block MR activation, and that the combination of these types of drugs, targets the mineralocorticoid receptor pathway through two distinct and complimentary mechanisms, and that the cited references do not teach or suggest this dual-mechanism approach.
These arguments have been fully considered, but are not found persuasive. As discussed above, the prior art teaches valproic acid for the treatment of myocardial infarction and teaches MR antagonists for the treatment of myocardial infarction. As such, an ordinary skilled artisan would have been motivated to combine valproic acid and MR antagonists to arrive at a more therapeutically effective method of treating MI. See the above rejections for a more detailed obviousness rationale. Moreover, Applicant is respectfully reminded that:
-“Mere recognition of latent properties in the prior art does not render nonobvious an otherwise known invention. . .’The fact that appellant has recognized another advantage which would flow naturally from following the suggestion of the prior art cannot be the basis for patentability when the differences would otherwise be obvious,’” MPEP 2145(II); and
-the reason or motivation to modify the reference may often suggest what the inventor has done, but for a different purpose or to solve a different problem. It is not necessary that the prior art suggest the combination to achieve the same advantage or result discovered by applicant, MPEP 2144 (IV).
On pg. 8, Remarks, Applicant argues that Maron teaches that outcomes from combined interventions in cardiac ischemia are uncertain and that Bell teaches that treatment depends on multiple injury specific factors, and that combining a VPA with a MR antagonist for an acute condition involves distinct pharmacological pathways.
This argument has been fully considered, but is not found persuasive. It is respectfully pointed out that Maron is directed toward patients with coronary disease and not patients with myocardial infarction. And Bell is directed toward soft tissue injuries in general and not toward myocardial infarction. As such, the patients populations of Maron and Bell are distinct from that of Wang, Le, Bossard, and the instant claims. Moreover, Maron is specifically directed toward the uncertainty of an invasive intervention plus a medical therapy, and does not teach the uncertainty of combining medical therapies, as argued by Applicant. Further, though Bell teaches that treatment of soft tissue injuries depends of several factors, such as severity, type of injury, and the particular join, muscle, or limb affect, Bell does not teach that it is uncertain to combine medicinal therapies for the treatment of myocardial infarction, as argued by Applicant.
On pg. 10, Remarks, Applicant argues that the instant specification provides unexpected results in Figures 2-5 and 7.
This argument has been fully considered, but is not found persuasive. It is respectfully pointed out that Figures 2-5 are specifically directed toward the effect of canrenone on heart function following ischemic reperfusion, and Figure 7 is specifically directed toward VPA improving donor heart ischemic tolerance. None of these figures provide data on the effects of a combination of VPA and canrenone. As such, it is not possible to evaluate whether or not a combination of VPA and canrenone produce an unexpected result in treating cardiac ischemic reperfusion injury. Moreover, data specifically directed toward canrenone is not commensurate in scope with instant independent claims 21 and 48, which are directed toward a combination of valproic acid or a VPA derivative, and any MR antagonist.
Applicant is reminded that unexpected results a) are greater than expected results, b) show superiority of a property shared with the prior art, c) exhibit the presence of an unexpected property, and/or d) exhibit the absence of an expected property. MPEP 716.02 additionally states that unexpected results must be commensurate in scope with the claimed invention and provide a comparison with the closest prior art.
For these reasons, Applicant’s arguments are not persuasive to overcome the instant rejections.
Conclusion
No claims are allowed.
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.
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