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
The office acknowledges Applicants filing of the claim amendments, arguments and terminal disclaimer (for US 10899734) and arguments on 12/30/2025 in response to the office action mailed on 10/20/2025. Claims 5-7, 9, 16, 19-20, 27-35, and 37- 38 were previously canceled. Claims 2, 10-15, 17-18, 21-26, and 36 have been canceled and claims 39-47 have been newly added. The filing of the terminal disclaimer necessitated the withdrawal of ODP rejection over US 10899734. The rejections over the cancelled claims are withdrawn. Applicants arguments regarding the rejections that are maintained have been fully considered and are addressed below. In light of the amendments the 112(1) and ODP rejections have been modified and are presented below. Claims 1, 3-4, 8, and 39-47 are currently pending. Claim 4 do not read on the elected species. Claims 1, 3, 8, 39-47 are examined based on the merits herein.
Response to Applicants Arguments
112(1) rejection:
Applicants argue that the pending claims have been amended to further define both the compound structure and the CASTOR disease. Accordingly, it is believed that the pending claims address the Examiner's concerns with respect to the breadth of "the number of compounds and the diseases to be treated in the method."
In response, the scope of the compounds used in the method is still large. The method as claimed is for the treatment of CASTOR diseases selected from PKAN, glutaric acidemia type 1, methylmalonic academia, propionyl-CoA carboxylase deficiency, propionic academia, 3-methylcrotonyl carboxylase deficiency, or isovalerly-CoA dehydrogenase deficiency. As stated in the rejection below Applicants have provided support and guidance towards select compounds of claim 1, data with PZ-2891 compound that it prevents inhibition of purified human PANK3 in propionyl-CoA and PZ-3022 compound in Pcca mouse model which is specific for propionic acidemia.
As evidenced from the rejection below, CASTOR conditions are different genetic conditions and involve different genes/mutations. The mouse models used for testing methylmalonic acidemia or propionic acidemia or PKAN is different. Propionic acidemia (PA) is associated with mutations in the PCCA and PCCB genes and Mutki/ki and Mutko/ki mutations is associated with methylmalonic acidemia. It is noted that the pharmaceutical art is unpredictable, requiring each embodiment to be individually assessed for physiological activity.
The data provided by the Applicants with just two compounds is for treating propionic acidemia. There is no data provided demonstrating the pantothenate kinase activity of the compounds and no guidance or examples for treating the diseases as claimed. The scope of the genus of compounds to be used is large and there is no representative number of species shown in treating all the diseases as claimed. Applicants have failed to provide guidance or data or evidence as to how the skilled artisan would be able to extrapolate from the disclosed examples to make and possibly use of the claimed invention. In an unpredictable art, adequate written description of a genus which embraces widely variant species cannot be achieved by disclosing only one species within the genus. See Enzo Biochem, 323 F.3d at 966, 63 USPQ2d at 1615; Noelle v. Lederman, 355 F.3d 1343, 1350, 69 USPQ2d 1508, 1514 (Fed. Cir. 2004) (Fed. Cir. 2004); Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406.
ODP Rejections: 17/120,800, 18/257,680
Applicant states the rejection(s) is provisional, Applicant does not concede or agree with the merits of this rejection. However, Applicant respectfully requests that this provisional rejection be held in abeyance until such time as the Examiner otherwise finds allowable subject matter in this case so that a more complete determination regarding the merits of the rejection can be made.
In response, the rejections have been modified (necessitated by the amendments), maintained and are provided below.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1, 3, 8, 39-47 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
As the Federal Circuit has stated: The MPEP states that the purpose of the written description requirement is to ensure that the inventor had possession, as of the filing date of the application, of the specific subject matter later claimed.
As the Federal Circuit has stated: The MPEP states that the purpose of the written description requirement is to ensure that the inventor had possession, as of the filing date of the application, of the specific subject matter later claimed. The MPEP does state that for a generic claim the genus can be adequately described if the disclosure presents a sufficient number of representative species that encompass the genus. MPEP 2163. If the genus has a substantial variance, the disclosure must describe a sufficient variety of species to reflect the variation within that genus. See MPEP 2163. Although the MPEP does not define what constitute a sufficient number of representative species, the courts have indicated what do not constitute a representative number of species to adequately describe a broad generic. In Gostelli, the courts determined that the disclosure of two chemical compounds within a subgenus did not describe that subgenus. In re Gosteli, 872, F.2d 1008, 1012, 10 USPQ2d 1614, 1618 (Fed. Cir. 1989).
The factors considered in the Written Description requirement are:
(1) level of skill and knowledge in the art,
(2) partial structure,
(3) physical and/or chemical properties,
(4) functional characteristics alone or coupled with a known or disclosed correlation between structure and function, and
(5) the method of making the claimed invention
The examined claims are directed to:
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In the above formula,
A is selected from from O, CO, CH2,CF2, NH, N(CH3), and CH(OH);
Q1 is selected from CH or N;
Q2 is selected from:
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The dependent claims are limited to specific subgenus or species of the compound(s) and diseases.
It is noted that the core structure of the formula varies depending on the A, Q1 Q2 substituent(s). Accordingly there are hundreds and thousands of compounds based on the various substituents, A, Q1, Q2, R2, R3a, R3b and R23 that can be used in the method of treating the claimed CASTOR diseases.
(1) Level of skill and knowledge in the art:
The level of skill to practice the art of the instantly claimed invention is high and requires a variety of skills usually found in institutions and companies that employ highly trained and skilled scientists to carry out these tasks.
(2) Partial structure: (3) Physical and/or chemical properties: and (4) Functional characteristics:
The claims are very broad with respect to the number of compounds to be used in the treatment of CASTOR diseases claimed.
(5) Method of making the claimed invention:
(a) Actual reduction to practice and (b) disclosure of drawings or structural
chemical formulas:
The specification provides guidance to (i) select compounds of formula of claim 1 (ii) data with PZ-2891 compound that it prevents inhibition of purified human PANK3 in propionyl-CoA (iii) data demonstrating reduction of blood ammonia levels in response to PZ-2891 in a mouse model of propionic acidemia (iv) reduction of CoA levels in the livers of the Pcca Mouse model elevated by PZ-3022 treatment (v) elevation of CoA and acetyl-CoA in the livers of Pcca Mouse Model by PZ-3022 (vi) PZ-3022 Treatment Normalizes the Levels of Acyl-Carnitines in the Pcca Mouse Model (See Fig. 2, 4-7). The two compounds PZ-2891 and PZ-3022 as demonstrated in the examples have a specific backbone as far as A, Q1 and Q2 are concerned.
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, in both the compounds, Q1 is CH, Q2 is piperazinyl and A is CH.
It is noted that the data provided is PZ-3022 compound in Pcca mouse model which is specific for propionic acidemia.
Applicants claim treating Coenzyme A (CoA) sequestration, toxicity or redistribution, CASTOR diseases, selected from PKAN, glutaric acidemia type 1, methylmalonic academia, propionyl-CoA carboxylase deficiency, propionic academia, 3-methylcrotonyl carboxylase deficiency, and isovalerly-CoA dehydrogenase deficiency with a genus of compounds as in claim 1.
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The claims are very broad in scope in regards to the compounds for use in the CASTOR diseases to be treated.
As to the elected condition, PKAN, according to National Library of Medicine, pantothenate kinase-associated neurodegeneration (PKAN), the most prevalent form of neurodegeneration with brain iron accumulation (NBIA), is an autosomal recessive disorder caused by mutations in the PANK2 gene. This inborn error of CoA metabolism results in excessive iron deposition in the basal ganglia, leading to progressive extrapyramidal symptoms, including dystonia, rigidity, and choreoathetosis. Clinicians may recognize PKAN by its hallmark “eye-of-the-tiger” sign on T2-weighted brain magnetic resonance imaging (see Introduction). Although the precise etiology of PKAN remains unclear, case reports have suggested an inborn error of metabolism involving neuromelanin and the dopaminergic system (See Etiology). The mechanism by which basal ganglia iron uptake is increased in PKAN is unknown since systemic and cerebrospinal fluid iron levels and plasma ferritin, transferrin, and ceruloplasmin are all normal (See Pathophysiology). Various therapies for PKAN is taught (See p 7) (Asuncion, NLM, NIH, 2025).
NBIA teach that pantothenate kinase-associated neurodegeneration is one of the most common forms of NBIA. Approximately 30-35% of the NBIA population has PKAN. It is caused by mutations in the PANK2 gene on chromosome 20. This gene provides the instruction for making an enzyme called pantothenate kinase. Researchers are investigating how this missing enzyme damages nerve cells in the brain and causes iron to build up. There are two forms of PKAN: classic and atypical, although some people have symptoms that place them in between the two categories (See p 1). The reference teaches that the PANK2 mutation is thought to result in the reductions of cellular coenzyme A (CoA). CoA is cell autonomous and thus any effective PKAN therapy must penetrate both cellular membranes and the blood-brain barrier (BBB). This presents a challenge in finding a suitable drug that can perform these functions. Another challenge faced by PKAN researchers has been finding a suitable model on which to perform preliminary research. Using other species as models for the disease causes limitations on the implications of the research. In particular, PKAN researchers have lacked a compelling mammalian model in which an abnormality can be specifically attributed to a defect in PANK2. The state of the models is central to the development of therapeutic treatments (see p 4, last two paragraphs) (NBIA, https://www.nbiadisorders.org/about-nbia/pkan, 2025).
Mutations in the human PANK2 gene result in a rare and life-threatening neurological disorder known as PanK-associated neurodegeneration (PKAN) (Zhou et al. (2001) Nat. Genet. 28: 345-349; Johnson et al. (2004) Ann. N. Y. Acad. Sci. 1012: 282-298; Kotzbauer et al. (2005) J. Neurosci. 25: 689-698). PKAN is an inherited autosomal recessive disorder that leads to progressive dystonia, dysarthria, parkinsonism, and pigmentary retinopathy. Classic PKAN develops in the first 10 years of life, starting around age 3; and patients are at risk for early death. The PANK2 gene is highly expressed in human neuronal tissues and many of the mutations associated with PKAN result in truncated or inactivated PanK2 protein expression, or severely reduced activity (Zhang et al. (2006) J. Biol. Chem. 281:107-114). The PANK2 mutations are predicted to result in significantly lower CoA levels, thereby reducing neuronal metabolism and function in PKAN patients. Tools are lacking for investigation of the relationship(s) between CoA levels and neurodegeneration. Activation of the PanK1 or PanK3 proteins that are also expressed in neuronal tissues (Leonardi et al. (2007) FEBS Lett. 581:4639-4644) could compensate for the reduction in PanK2 activity because functional redundancy among the isoforms is demonstrated in the Pank1.sup.−/− and Pank2.sup.−/− mouse models (Leonardi et al. (2010) (See [0003] of Sharma et al. to US 20190300499).
In regards to PKAN, Sharma teaches select compounds that can be used in a method of treating PKAN (See WO 2017223474, also US 20190300499).
Subramanian teach the effects of BBP-71 that crosses the blood-brain barrier to correct the neuron-specific coenzyme A (CoA) deficiency and improve motor function in a mouse model of pantothenate kinase-associated neurodegeneration (See Abstract, The J of Pharm and Exp Therapeutics, p 171-180, 2024).
For example, methylmalonic acidemia refers to a group of inherited disorders in which the body is unable to process certain proteins and fats properly. Chen teach methylmalonic acidemia (MMA), also known as methylmalonic aciduria, is a congenital organic acidemia with multifactorial autosomal recessive inheritance (see Introduction, 26 Jan 2023). Methylmalonic acidemia (MMA) is mainly caused by the deficiency of methylmalonyl-coenzyme A mutase (MCM) or abnormal metabolism of adenosylcobalamin. Under normal circumstances, methylmalonyl-CoA generates succinyl-CoA under the action of MCM and adenosylcobalamin and participates in the tricarboxylic acid cycle (2. Etiology and Pathogenesis of MMA, para 1) (Chen, Front. Neurosci., 26 January 2023, vol. 17, p 01-09).
Yu teach 144 different types of mutations in the MMUT gene of mut-type MMA in methylmalonic acidemia patients (see 3.4, Mutation Analysis, table 2) (Yu, Mol Genet Genomic Med, 2021, 1-19).
Forny teach novel mouse models of methylmalonic aciduria, Mutki/ki and Mutko/ki
(See Abstract) (The J of Biol Chem, 291, 39, 2016, pp 20563-20573).
In regards to propionic acidemia (PA) Rivera-Barahona et al. teach that the disease is caused by mutations in the PCCA and PCCB genes (Abstract), Propionic acidemia is one of the most frequent life-threatening organic acidemias, caused by a deficiency of the mitochondrial propionyl-CoA carboxylase (PCC) enzyme (Introduction, col. 1, lines 1-3, p 266, Table 1) (Mol Gen and Metabolism, 2018, 266-275).
Mitchell teach methylmalonic acidemia and propionic acidemia as CASTOR diseases (Table 1). Mitchell teach each CASTOR disease is predicted to produce a distinct CoA profile, since its diagnostic patterns of urine organic acids and plasma acylcarnitines presumably reflect elevated intracellular concentrations of the corresponding CoA esters. Presumably this unique pattern, the intensity of which will be determined by the local flux of precursor degradation, gives rise to the clinical differences among different CASTOR conditions (see p 10, col.2, last two lines to first 6 lines, col. 1, Mitchell, Molecular Genetics and Metabolism, 94, 2008, 4-15).
As evidenced from above, CASTOR conditions are different genetic conditions that involve different genes/mutations. Propionic acidemia (PA) is associated with mutations in the PCCA and PCCB genes and Mutki/ki and Mutko/ki mutations is associated with methylmalonic acidemia. The mouse models used for testing methylmalonic acidemia or propionic acidemia or PKAN is different.
It is noted that the pharmaceutical art is unpredictable, requiring each embodiment to be individually assessed for physiological activity. The pharmaceutical industry is the prototypical example of a highly unpredictable field. Pfizer v. Teva Pharm., 482 F.Supp.2d 390, 413 (D.N.J. 2007); 2 Chisum on Patents § 5.04. It is not predictable from the data provided in the specification how all the claimed CASTOR diseases can be treated with the compounds of claim 1.
(c) Representative number of samples:
Applicants have provided data for treating propionic acidemia with select compound(s). The instant specification do not provide any data in regards to PKAN. In fact PKAN is mentioned just once in the specification in [0004]. The specification provides data and/or guidance to the treatment of propionic acidemia. The prior art provides guidance to disorder PKAN and its treatment with select compound(s) of instant claim 1 but do not provide evidence or data or guidance towards the treatment of all the CASTOR diseases as claimed with the genus of Markush compounds. In other words, applicants do not have possession of the treatment of all the diseases with the genus of compounds as claimed.
Applicants have failed to provide guidance or data or evidence as to how the skilled artisan would be able to extrapolate from the disclosed examples to make and possibly use of the claimed invention. “A description of what a material does, rather than of what it is, usually does not suffice." Rochester, 358 F 3d at 923; Eli Lilly, 119 at 1568. Instead, the “disclosure must allow one skilled in the art to visualize or recognize the identity of the subject matter purportedly described.”
The specification provides insufficient written description to support the genus encompassed by the claim, Vas- Gath Inc. v. Mahurkar, 19 USPQ2d 1111, makes clear that "applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the "written description" inquiry, whatever is now claimed." (See page 1117.) The specification does not "clearly allow persons of ordinary skill in tile art to recognize that [he or she] invented what is claimed" (See Vas-Gath at page 1116.)
The description requirement of the patent statue requires a description of an invention, not an indication of a result that one might achieve if one made that invention. See In re Wilder, 736, F.2d 1516, 1521,222 USPQ 369, 372-73 (Fed. Cir. 1984) (affirming rejection because the specification does "little more than outlin[e] goals appellants hope the claimed invention achieves and the problems the invention will hopefully ameliorate.").
Based on the specification as originally filed, one of ordinary skill in the art will not recognize that the applicants were in possession of treating all the CASTOR diseases with all the compounds as claimed.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1, 3, 8, 39-45 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 31-34, 36-40 of U.S. application No. 17120800 (now US 12552765 issued, yet to be published,) and Gregory (NCBI Bookshelf, NLM, NIH, Aug 3 2017).
The instant method claims are directed to:
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The dependent claims are limited to specific subgenus or species of the compound(s) and diseases.
‘800 reference claims are directed to:
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and claim 40 teach the use of the elected compound,
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. The dependent claims are limited to subgenus or specific compounds of the formula of claim 31 and to select diseases, neurodegeneration, hyperglycemia, diabetes.
Gregory has been cited to teach that pantothenate kinase-associated neurodegeneration (PKAN) is a type of neurodegeneration with brain iron accumulation (NBIA).
From Gregory it is obvious that PKAN is neurodegeneration disease associated with pantothenate kinase. A person skilled in the art from the reference claims would have found it obvious to administer an effective compound of the elected compound in treating PKAN in a subject with a reasonable amount of success. Thus claims 1, 3, 8, 39-42, 45 are addressed. As to claims 43-44, the same CASTOR disease PKAN being treated as claimed and hence cam be hereditary or acquired.
Claims 1, 3, 8, 39-45 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 3, 14, 15, 20, 22, 27, 43, 44, 55, 56, 75 of co-pending application, 18257680 (‘680).
The instant method claims as above.
‘680 reference claims are directed to:
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From the reference claims, a person of ordinary skill in the art would have found it obvious to administer the elected compound, a compound of the reference claim 55, in treating PKAN disease. Thus claims 1, 3, 8, 39-42, 45 are addressed. As to claims 43-44, the same CASTOR disease PKAN being treated as claimed and hence cam be hereditary or acquired.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Note: ODP rejection has not been made over the claims of US 11,891,378 because the reference claims teach non-elected compound(s) of claim and its pharmaceutical composition or over the claims of co-pending application(s) 18/390494 because it teach non-elected compounds in treating PKAN.
Conclusion
Applicant's amendment necessitated the modified 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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/Umamaheswari Ramachandran/Primary Examiner, Art Unit 1627