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, 07/22/2026, wherein the Amendment amended claims 1 and 24, and added claims 27-28.
Claims 1-3, 5-8, 12-15, 21-24, and 27-28 are pending, and examined on the merits herein.
Priority
This application claims the following priority:
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REJECTIONS WITHDRAWN
The status for each rejection and/or objection in the previous Office Action is set out below.
35 U.S.C. § 112(a)
Applicant’s amendment to independent claim 1 that deletes “cerebellar ataxia” and adds - -episodic ataxia type 2- -, is sufficient to overcome this rejection
REJECTIONS--MAINTAINED/MODIFIED
Applicant’s amendment to independent claim 1 has resulted in the below modified prior-art rejections.
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 (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 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.
(Modified) Claims 1-3, 5-7, 12-15, 21-22, 24, and 27-28 are rejected under 35 U.S.C. 103 as being unpatentable over Strupp (Episodic ataxia type 2, Springer Nature Link, published 2007, PTO-892) in view of Strupp 2 (Effects of acetyl-DL-leucine in patients with cerebellar ataxia: a case series, J. Neurol., published 2013, IDS of 09/04/2025, NPL210), Tomimitsu (Episodic ataxia type 2, published 2001, PTO-892), and WO 2021/048431 to McKnight (effectively filed 09/12/2019, PTO-892 of 06/04/2025), as evidenced by PubChem (“Acetylleucine,” PTO-892 of 06/04/2025).
Strupp teaches episodic ataxia type 2 (EA2) as a rare neurological disorder of autosomal dominant inheritance resulting from dysfunction of a voltage gated calcium channel. Strupp teaches that EA2 is caused most often by loss of function mutations of the calcium channel gene CACNA1A. Strupp teaches acetazolamide (ACTZ) as an effective treatment option for EA2 (Abstract, pgs. 268-269, “Clinical Features of Episodic Ataxia Type 2”).
Strupp teaches ACTZ as the drug of first choice for preventative treatment of EA with dosages of 250-1000 mg/day. ACTZ effectively prevents or attenuates the attacks in approximately 50-75% of all patients. ACTZ inhibits the carbonic anhydrase interconversion of CO2 + H20 ↔ H2CO3. It causes diuresis, initial kaliuresis, and metabolic acidosis. It lowers serum bicarbonate levels and reduces the amount of brain lactate and pyruvate, resulting in subsequent brain acidosis (pg. 270, “Treatment Options and Principles”). ACTZ additionally normalizes the abnormal intracellular pH levels in the cerebellum of patients, reducing potassium conductance of the cell membrane, and thus restoring the excitability and resting activity of neurons. Without ACTZ, Strupp teaches that attacks may be precipitated by exercise and stress (pg. 271).
Strupp teaches that side effects of ACTZ are dose related. Strupp teaches that even with adverse side effects, ACTZ is the drug of first choice (pg. 271).
Regarding claim 1, while Strupp teaches a method of treating EA2 by administering ACTZ, it differs from that of instant claim 1 in that it does not teach the administration of acetyl-DL-leucine.
Strupp 2 teaches the effects of acetyl-DL-leucine in patients with cerebellar ataxia (title).
Strupp 2 teaches administering 5 g/day of acetyl-DL-leucine to patients with degenerative cerebellar ataxia. Strupp 2 teaches this treatment as causing a remarkable decrease in the Scale for the Rating and Assessment of Ataxia, a significant improvement in motor function, and an overall increase in quality of life, and Strupp 2 teaches that this treatment has no reported side-effects. “In conclusion, acetyl-DL-leucine significantly improved ataxic symptoms without side effects and therefore showed a good risk-benefit profile” (abstract).
As evidenced by [0003], Specification, episodic ataxias are characterized by recurrent episodes of a cerebellar ataxia.
Tomimitsu teaches EA2 as an autosomal dominant cerebellar ataxia, caused by mutations in the CACNA1A gene (abstract).
McKnight teaches combining active ingredients for the treatment of ataxia, wherein the combined preparation is for simultaneous, separated or sequential use (pg. 1, lines 31-32; pg. 5, lines 6-9, 25-31; pg. 20, lines 1-9; pgs. 32-34, claims 9-10, 14).
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 acetyl-DL-leucine to the method of treating EA2 taught by Strupp, to arrive at instant claim 1. One of ordinary skill in the art would have been motivated to make such an addition, with a reasonable expectation of success, because:
-Strupp specifically teaches a method of treating EA2, wherein EA2 is a slow progression of cerebellar signs accompanied by atrophy of midline cerebellar structures,
-Tomimitsu teaches EA2 as a type of cerebellar ataxia,
-as evidenced by the instant Specification, episodic ataxias are characterized by recurrent episodes of a cerebellar ataxia,
-Strupp 2 teaches acetyl-DL-leucine as improving ataxic symptoms in patients with cerebellar ataxia,
-Strupp 2 teaches acetyl-DL-leucine as significantly improving ataxic symptoms and as improving the quality of life in patients with cerebral ataxia,
-McKnight teaches combining active ingredients for the treatment of ataxia, 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), see MPEP 2144.06.
As such, an artisan having ordinary skill in the art would have been motivated to make such an addition to predictably arrive at a more therapeutically effectively method of treating EA2 that treats a broader range of symptoms, and specifically a patient’s cerebellar symptoms, thereby improving the patient’s quality of life.
Moreover, Strupp teaches the side effects of ACTZ as being dose related. Thus, alternatively, an ordinary skilled artisan would have been motivated to add acetyl-DL-leucine to the methods of Strupp, to predictably arrive at a method of treating EA2 that decreases the side-effects of ACTZ, since an ordinary skilled artisan would predicably expect that adding another active ingredient would result in a decrease in the dosage of ACTZ.
Further regarding claim 1, and regarding claims 27-28, while the combination of Strupp, Strupp 2, Tomimitsu, and McKnight teaches a method of treating EA2 by administering therapeutically effective amounts of acetyl-leucine and acetazolamide, it differs from that of instant claim 1 in that it does not specifically teach the treatment duration.
Strupp additionally teaches that EA2 usually begins in early childhood and is characterized by recurrent attacks of ataxia lasting for several hours to days, wherein attacks may occur daily or over longer intervals, even years in some patients (pg. 268, Col. 2).
As such, 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 treat the patients in the combined method of Strupp, Strupp 2, Tomimitsu, and McKnight for about six months or more, one year or more, or two years or more, to arrive at instant claims 1, and 27-28. One of ordinary skill in the art would have been motivated to make such a selection, with a reasonable expectation of success, because:
-Strupp teaches EA2 as a life-long disease that often begins in early childhood,
-Strupp teaches attacks as lasting, in a range from several hours to years, 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)).
As such, an ordinary skilled artisan would have been motivated to modify the treatment duration based on the severity of the disease and the length of the attacks, to predictably arrive at a treatment that is optimized for therapeutic effectiveness and quality of life.
Regarding claims 2-3 and 24, since McKnight teaches the combined preparation for simultaneous, separated or sequential use (pg. 1, lines 31-32; pg. 5, lines 6-9, 25-31; pg. 20, lines 1-9; pgs. 32-34, claims 9-10, 14), an ordinary skilled artisan would have been motivated to combine the acetyl-DL-leucine and ACTZ in a single composition in the combined method of Strupp, Strupp 2, Tomimitsu, and McKnight, to predictably arrive at a method of simultaneous administration of the active ingredients. Since a single formulation must be contained, the limitations of claim 24 are met.
Regarding claims 5 and 24, since McKnight teaches sequential administration, an ordinary skilled artisan would have been motivated to sequentially administer the acetyl-DL-leucine and ACTZ, in the combined method of Strupp, Strupp 2, Tomimitsu, and McKnight, to predictably arrive at a method of sequential administration of the active ingredients. Since each formulation is contained, the limitations of claim 24 are met.
Regarding claims 6-7, while the combination of Strupp, Strupp 2, Tomimitsu, and McKnight does not teach which compound to administer first in the sequential administration, an artisan having ordinary skill in the art would have been motivated to modify the sequence of administration, to achieve an optimized therapeutic dosage regimen; "[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)).
Regarding claims 12-13, Strupp teaches administration of ACTZ daily (pg. 272, Col. 1) and Strupp 2 teaches daily administration of acetyl-DL-leucine (pg. 2557, Col. 2). An artisan having ordinary skill in the art would have been motivated to modify the times per day the active ingredients are administered to predictably arrive at a dosage regimen that is optimized for therapeutic effect and minimized for negative side-effects; "[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)).
Regarding claim 14, Strupp 2 teaches administration of 5g/day acetyl-DL-leucine (pg. 2557, Col. 2); in the case where the claimed ranges “overlap or lie inside ranges disclosed in the prior art” a prima facie case of obviousness exists. See MPEP 2144.05.
Regarding claim 15, Strupp teaches administration of 250-1000mg/day of ACTZ (pg. 270, Col. 2); in the case where the claimed ranges “overlap or lie inside ranges disclosed in the prior art” a prima facie case of obviousness exists. See MPEP 2144.05.
Regarding claim 21, Strupp 2 teaches acetyl-DL-leucine. As evidenced by PubChem (“Acetylleucine,” PTO-892), acetyl-DL-leucine is N-acetyl-DL-leucine (pg. 1).
Regarding claim 22, “A prima facie case of obviousness may be made when chemical compounds have very close structural similarities and similar utilities. . .Compounds which are position isomers (compounds having the same radicals in physically different positions on the same nucleus). . .are generally of sufficiently close structural similarity that there is a presumed expectation that such compounds possess similar properties,” see MPEP 2144.09. As such, an artisan have ordinary skill in the art would have been motivated to substitute the N-acetyl-DL-leucine with N-acetyl-L-leucine, to predictably arrive at a compound with similar activity to N-acetyl-DL-leucine, that is effective in treating EA2.
(Modified) Claim 8 is rejected under 35 U.S.C. 103 as being unpatentable over Strupp (Episodic ataxia type 2, Springer Nature Link, published 2007, PTO-892), Strupp 2 (Effects of acetyl-DL-leucine in patients with cerebellar ataxia: a case series, J. Neurol., published 2013, IDS of 09/04/2025, NPL210), Tomimitsu (Episodic ataxia type 2, published 2001, PTO-892), and WO 2021/048431 to McKnight (effectively filed 09/12/2019, PTO-892 of 06/04/2025), as evidenced by PubChem (“Acetylleucine,” PTO-892 of 06/04/2025), as applied to claims 1-3, 5-7, 12-15, 21-22, 24, and 27-28 above, and further in view of Fang (“Dose staggering as a strategy to reduce drug-drug interactions due to reversible enzyme inhibition between orally administered drugs with high first pass effect: a computer simulation study,” Biopharm. Drug. Dispos., published 2000, PTO-892 of 06/04/2025).
Strupp, Strupp 2, Tomimitsu, McKnight, and PubChem are applied as discussed above and incorporated herein.
Regarding claim 8, while the combination of Strupp, Strupp 2, Tomimitsu and McKnight teaches a method of treating EA2 by administering a combination of acetyl-DL-leucine and acetazolamide for a duration of about six months or more, it differs from that of the instantly claimed invention in that it does no teach administration of acetyl-DL-leucine and acetazolamide about 1 minute to about 6 hours apart.
Fang teaches that a physiological computer model was designed to simulate the metabolic drug-drug interactions between two orally co-administered drugs due to reversible enzyme inhibition using drug concentrations in the portal vein. It was demonstrated that the extent of the interactions can be strongly affected by a time interval between the two drug administrations. By delaying the administration of the inhibitor until after the absorption phase of the substrate, one can significantly reduce the extent of the drug-drug interactions. This is because drug concentrations in the portal vein and the liver are much higher than that in the systemic circulation during the absorption phase. The model showed that interactions involving substrates with a high extraction ratio, i.e. drugs with higher first-pass effect, can be more strongly affect by dose staggering. This observation suggests dose staggering as a simple and cost-effective way to reduce the extent of unwanted drug-drug interactions in clinical practice (abstract).
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 select administration of the acetyl-DL-leucine and acetazolamide in the combined method of Strupp, Strupp 2, Tomimitsu, and McKnight as about 1 minute to about 6 hours apart, to arrive at instant claim 8. One of ordinary skill in the art would have been motivated to make such a selection, with a reasonable expectation of success, because:
-McKnight teaches sequential administration, and
-Fang teaches that dose staggering is a simple and cost-effective way to reduce the extent of unwanted drug-drug interactions in clinical practice, 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).
As such, an ordinary skilled artisan would have been motivated to make such a selection to arrive at an optimized dosage regimen that reduces unwanted drug-drug interactions and optimizes therapeutic effectiveness.
(New) Claim 23 is rejected under 35 U.S.C. 103 as being unpatentable over Strupp (Episodic ataxia type 2, Springer Nature Link, published 2007, PTO-892), Strupp 2 (Effects of acetyl-DL-leucine in patients with cerebellar ataxia: a case series, J. Neurol., published 2013, IDS of 09/04/2025, NPL210), Tomimitsu (Episodic ataxia type 2, published 2001, PTO-892), and WO 2021/048431 to McKnight (effectively filed 09/12/2019, PTO-892 of 06/04/2025), as evidenced by PubChem (“Acetylleucine,” PTO-892 of 06/04/2025), as applied to claims 1-3, 5-7, 12-15, 21-22, 24, and 27-28 above, and further in view of Kim (Episodic Ataxia Type 2 due to a Deletion Mutation in the CACNA1A Gene in a Korean Family, published 2006, PTO-892 of 06/04/2025).
Strupp, Strupp 2, McKnight, Tomimitsu, and PubChem are applied as discussed above and incorporated herein.
Regarding claim 23, while the combination of Strupp, Strupp 2, Tomimitsu and McKnight teaches a method of treating EA2 by administering a combination of acetyl-DL-leucine and acetazolamide for a treatment duration of about six months or more, it differs from that of the instantly claimed invention in that it does not teach deletion of cytosine and thymidine at position 2070-2071 in exon 16 of the CACNA1A gene.
Strupp teaches that EA2 is caused most often by the loss of function mutations of the calcium channel gene CACNA1A, and that, to date, at least 30 mutations have been described (abstract; pg. 268, Col. 2; pg. 269, “Genetics and Pathophysiology”; pg. 270 “Animal Models of Episodic Ataxia Type 2”; pg. 271, Col. 1, last full paragraph). Strupp teaches that about 60% of patients with EP2 have CACNA1A mutations (pg. 268, Table 1).
Kim teaches that the underlying cause of EA2 is a genetic alteration of the voltage dependent calcium channel (CACNA1A), and specifically teaches this mutation in exon 16 (pg. 268; pg. 269, Fig. 2; pg. 270, Col. 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 select an EA2 patient with a deletion mutation in exon 16 of the CACNA1A gene, to arrive at instant claim 23. One of ordinary skill in the art would have been motivated to make such a selection, with a reasonable expectation of success, because:
-Strupp teaches that 60% of patients with EA2 have a CACNA1A gene mutation, and
-Kim teaches that the underlying cause of EA2 is a generic alteration of CACNA1A and further teaches this mutation in exon 16 of the CACNA1A gene.
As such, an artisan having ordinary skill would have been motivated to make such a selection to predictably identify and treat a patient with EA2. While the combination of Strupp, Strupp2, McKnight, Tomimitsu, and Kim do not expressly teach the deletion of cytosine and thymidine at position 2070-2071, a skilled artisan would have been motivated to select such a specific mutation since it is known in the art that mutations in exon 16 of CACNA1A gene are the underlying cause of EA2. Moreover, as discussed in the above rejection, Strupp teaches the side effects of ACTZ as being dose related. Thus, an ordinary skilled artisan would have been motivated to add acetyl-DL-leucine to the methods of Strupp, to predictably arrive at a method of treating EA2 that decreasing the side-effects of ACTZ by decreasing the dose of ACTZ, since an ordinary skilled artisan would predicably expect that adding another active ingredient for the treatment of EA2, would result in a decrease in the dosage of ACTZ.
Response to Arguments
On pg. 6, Remarks, Applicant argues that one of skill would not have expected the effect of the combination of acetyl-leucine and acetazolamide on reducing ataxia episodes and points to Example 2. Applicant argues that acetazolamide monotherapy reduced the frequency of episode to 2-3 times per week, but that the episodes returned to once per day. However, Applicant argues that the combined treatment stabilized the condition and reduced the episodes to only one in three months and two attacks of vertigo in three months.
These arguments have been fully considered, but are not found persuasive.
Applicant’s data in Example 2 is not sufficient to show unexpected results. Example 2 does not teach the dosage of acetazolamide administered to the patient or the frequency of the administration. Moreover, Example 2 does not provide any data on the administration of acetyl-DL-leucine, alone, on the frequency of episodes. As such, it is not clear if the combined treatment effect is expected based on the effects of acetyl-DL-leucine, alone, or if the combined treatment effects is expected based on the additive effects of the combination of acetazolamide and acetyl-DL-leucine.
Additionally, the results in Example 2 are not based on a treatment duration of about six months or more, as instantly claimed in independent claim 1.
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.
On pgs. 6-7, Remarks, Applicant argues that one of skill would not have expected that the combination of acetyl-leucine and acetazolamide would reduce ataxia episodes because of acetazolamide’s lack of long-term efficacy and intolerable side effects. Applicant specifically points to the teachings of Feil, Strupp, and Example 1 of the specification.
Regarding the 2013, Strupp publication, it is respectfully pointed out that the 2013 Strupp publication relied upon in the above rejection is not the same as the one relied upon on pgs. 6-7, Remarks. As such, it is not possible to evaluate these statements by Strupp.
Regarding Strupp, relied upon in the above rejections, Strupp teaches ACTZ as the drug of first choice for the preventative treatment and treatment of EA2. Thus, Strupp teaches ACTZ as not only known in the art to effectively treat EA2, but known in the art as the first choice treatment for EA2. Strupp additionally teaches that without ACTZ, attacks may be precipitated by exercise and stress. And Strupp teaches that even with adverse side effects ACTZ is the drug of first choice (pg. 271).
Regarding Feil, while Feil does teach that the side effects may limit the therapeutic use of acetazolamide, Feil does not teach that the side effects limit the therapeutic effects of acetazolamide in treating EA2 or teach that the side effects bar the use of acetazolamide for the treatment of EA2. Feil additionally teaches that 2/3 of patients responded to treatment with acetazolamide and teaches acetazolamide as a first-line treatment for EA2 for many years. Since side effects of pharmaceuticals are well known in the art, an ordinary skilled artisan would still reasonably be motivated to select acetazolamide for the treatment of EA2. Moreover, in view of these side effects, an ordinary skilled artisan would have been more motivated to pair the acetazolamide with another pharmaceutical known to be effective in treating EA2, to thereby mitigate the side-effects of the acetazolamide by modifying the dosage amount and frequency of administration of the acetazolamide.
Regarding Example 1 of the Specification, it is respectfully pointed out that Example 1 is directed toward patients with cerebellar ocular motor dysfunction, and not patients with EA2, as instantly claimed. Moreover, in [0128], it states “The patient did not respond to treatment with. . .acetazolamide.” As such, Example 1 is not persuasive to show that an ordinary skilled artisan would not have expected the combination of acetyl-leucine and acetazolamide to reduce ataxia episodes.
On pg. 7, Remarks, Applicant argues that one of skill in the art would not have selected acetazolamide for treating EA2 and would not have had a reasonable expectation of success because there are no placebo-controlled trials about the efficacy.
This argument has been fully considered, but is not found persuasive.
As taught by Strupp, ACTZ is the drug of first choice for the preventative treatment and treatment of EA2. Thus, Strupp teaches ACTZ as not only known in the art to effectively treat EA2, but known in the art as the first choice treatment for EA2. Strupp additionally teaches that without ACTZ, attacks may be precipitated by exercise and stress. And Strupp teaches that even with adverse side effects ACTZ is the drug of first choice (pg. 271). Thus, Applicant’s arguments are not persuasive to overcome the instant rejections.
Applicant is respectfully reminded that obviousness does not require absolute predictability, but a reasonable expectation of success. See MPEP 2143.02.
Regarding the arguments toward Tomimitsu on pg. 7, Remarks, it is respectfully pointed out that Tomimitsu is merely relied upon to teach that EA2 is a type of cerebellar ataxia, in reference to Strupp 2’s teaching of acetyl-leucine for the treatment of cerebellar ataxias.
Regarding the arguments toward McKnight on pg. 8, Remarks, it is respectfully pointed out that McKnight is merely relied upon to teach that it is known to combine active ingredient to treat ataxia.
Regarding the arguments toward PubChem on pg. 8, Remarks, it is respectfully pointed out that PubChem is merely relied upon as an evidentiary reference to teach that acetal-DL leucine and N-acetyl-DL-leucine are synonyms.
As such, these arguments are not persuasive to overcome the rejections.
These arguments have been fully considered, but are not found persuasive.
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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/LAUREN WELLS/Examiner, Art Unit 1622
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