DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
This action is in response to the papers filed on 10/02/2025. Claims 1-25 are currently pending as per claims filed on 10/02/2025. Claims 3, 4, 6, 9, 13-15, 18, 19, 21, 23, and 25 are amended and claims 26-29 are canceled per applicant’s claim amendment filed 10/02/2025.
Therefore, claims 1-25 are subject to examination to which the
following grounds of rejection are applicable. Claim 1 is an independent claim.
Priority
The instant application is a 371 of PCT/ EP2023/057484 filed 03/23/2023.
The instant application claims benefit of foreign filed applications PORTUGAL 117925. Acknowledgment is made of applicant’s claim for foreign priority under 35 U.S.C. 119 (a)-(d) to PORTUGAL 117925 filed on 04/21/2022.
Filing of a certified translated copy of the application PORTUGAL 117925 is acknowledged.
The disclosure of the prior-filed foreign application, PORTUGAL 117925, fails to provide adequate support or enablement in the manner provided by 35 U.S.C. 112(a) or pre-AIA 35 U.S.C. 112, first paragraph for one or more claims of this application. The foreign application does not provide support for Claims 1-25. Accordingly, claims 1-25 of the instant application cannot claim the effective filing date of the foreign application, but are accorded the benefit of 03/23/2023 as the filing date of a prior-filed PCT application (PCT/ EP2023/057484) does provide support for claims 1-25.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 10/17/2024 were filed before the mailing date of the current office action. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Claim Objection
Claim 2 is objected to under 37 CFR 1.75 as being a substantial duplicate of claim 1. Claim 2 is no different in scope than claim 1; both claims recite increasing the concentration of MANF for increasing the regeneration of skeletal muscle. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 706.03(k).
Claim Rejections - 35 USC § 112
Written Description
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 1-25 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.
M.P.E.P. § 2163 recites, “The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number
of species by actual reduction to practice (see i)(A), above), reduction to drawings (see
i)(B), above), or by disclosure of relevant, identifying characteristics, i.e., structure or
other physical and/or chemical properties, by functional characteristics coupled with a
known or disclosed correlation between function and structure, or by a combination of
such identifying characteristics, sufficient to show the applicant was in possession of the
claimed genus (see i)(C), above). See Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406.”
Further, the written description inquiry is limited to that which is contained within the four corners of the specification, not the extent to which the skilled artisan, given his or her
knowledge of the art, would have considered it to expand with only routine
experimentation. See Ariad Pharms. Inc. v. Eli Lilly & Co., 598 F.3d 1336, 1351 (Fed.
Cir. 2010) (en banc); see also id. at 1352 (“[I]t is the specification itself that must
demonstrate possession A description that merely renders the invention obvious does
not satisfy the requirement.").
Claim 1 is directed to a method of increasing the regeneration of a skeletal muscle in an individual in need thereof comprising increasing the concentration of MANF in the skeletal muscle.
The specification does not disclose that any version of MANF (i.e. a nucleotide sequence of MANF, for instance), any agent to induce MANF expression at the RNA, DNA, or protein level, or any other method or intervention which would lead to increased MANF concentration is suffice to increase the regeneration of a skeletal muscle in any individual in need other than administering rhMANF intramuscularly in a mouse model. Similarly, the specification does not disclose any details pertaining to the variants of MANF, both for nucleic acid and amino acid sequences as recited in claims 5 and 7, such that the variants can increase the regeneration of skeletal muscle. In other words, one does not know the structure of the variants such that one could identify them, besides residues 25-182 of SEQ ID NO: 1 and SEQ ID NO: 2 in claims 5 and 7, respectively. Structural features that could distinguish the compounds of the claimed genus from others not encompassed by the genus are missing from the disclosure. No common structural attributes identify the members of the genus and there is no indication of the relationship of the structure required for its claimed function. As recited, the method lacks critical elements that provide necessary function. The broad and generic scope of the agents that is necessary to increase MANF renders the ability to perform the instant method unpredictable. Although the instant claims are directed to methods, adequate description of the methods first requires an adequate description of the materials, which provide the means for practicing the invention.
Applicant were referred to the guidelines for Written Description Requirement
published January 5, 2001 in the Federal Register, Vol.66, No.4, pp.1099-1110 (see
http://www.uspto.gov). The disclosure of a single species is rarely, if ever, sufficient to
describe a broad genus, particularly when the specification fails to describe the features
of that genus, even in passing. (see In re Shokal 113USPQ283(CCPA1957); Purdue
Pharma L. P. vs Faulding Inc. 56 USPQ2nd 1481 (CAFC 2000). The possession may
be shown by actual reduction to practice, clear depiction of the invention in a detailed
drawing, or by describing the invention with sufficient relevant identifying characteristics
(as it relates to the claimed invention as a whole) such that a person skilled in the art
would recognize that the inventor had possession of the claimed invention. See, e.g.,
Pfaff v. WellsElectronics, Inc., 525 U.S. 55, 68, 119 S.Ct. 304, 312, 48 USPQ2d 1641,
1647 (1998); Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406; Amgen, Inc. v. Chugai
Pharmaceutical, 927 F.2d 1200, 1206, 18 USPQ2d 1016, 1021 (Fed. Cir. 1991).
The “written description” requirement may be satisfied by using such descriptive
means as words, structures, figures, diagrams, formulas, etc., that fully set forth the
claimed invention. See Noelle v. Lederman, 355 F.3d 1343, 1349, 69 USPQ2d 1508,
1514 (Fed. Cir. 2004) and Lockwood v. American Airlines, Inc., 107 F.3d at 1572, 41
U.S.P.Q.2d at 1966. A definition by function alone “does not suffice” to sufficiently describe a coding sequence “because it is only an indication of what the gene does,
rather than what it is.” Regents of the University of California v. Eli Lilly & Co., 119 F.3 at
1568, 43 USPQ2d at 1406 (Fed. Cir. 1997) (discussing Amgen Inc. v. Chugai
Pharmaceutical Co., 927 F.2d 1200, 18 U.S.P.Q.2d 1016 (Fed. Cir. 1991)). In Fiers v.
Ravel, 984 F.2d at 1169-71, 25 U.S.P.Q.2d at 1605-06 (1993), the CAFC found that “a
mere wish or plan for obtaining the claimed chemical invention” is not sufficient to
describe a chemical invention (discussed in Eli Lilly at 1404).
In view of the large breadth of agents claimed by their function of increasing MANF and increasing muscle regeneration and variants of MANF protein and nucleic acid encompassed by the claims and the lack of adequate description of the structure-function relationship of the claimed genus in view of the teachings of the prior art, one of ordinary skill in the art would not have recognized Applicant as being in possession of the claimed genus. The limited disclosure in the specification is not deemed sufficient to reasonably convey to one skilled in the art that the applicants were in possessions of the genera of agents and methods of increasing the concentration of MANF in the skeletal muscle as recited in the claims at the time the application was filed. Thus, it is concluded that the written description requirement is not satisfied for the claimed genera.
Scope of Enablement
Claim 1-25 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for a method for increasing regeneration of a skeletal muscle in aged mice comprising administering a rhMANF intramuscularly to injured muscles of aged mice, does not reasonably provide enablement for any other embodiment. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
breadth of the claim; nature of the invention
The claims are broad, encompassing increasing regeneration of a skeletal muscle in any individual in need thereof comprising the steps of increasing, by any means, the concentration of Mesencephalic Astrocyte-derived Neurotrophic Factor (MANF) in the skeletal muscle. Thus, the claims are drawn to a genus of methods that can increase regeneration of a skeletal muscle in an individual in need, wherein one of ordinary skill in the art would need to determine which individual is in need as the specification does not teach how to identify those individuals, and the method causes an increase in MANF via any mechanism and using any agent. Claim 5 recites that MANF comprises an amino acid sequence or a variant thereof while Claim 6 recites that the agent is a nucleic acid sequence that encodes MANF or a variant thereof. Furthermore, claim 9 limits claim 6 reciting that the nucleic acid is contained in a vector and claim 10 further limits claim 9 reciting wherein the vector is a viral vector. Claim 11 recites that the agent can be a cell that expresses MANF. Hence, the invention encompasses a broad and structurally-distinct species of agents which can be a protein, a nucleic acid sequence (RNA or DNA), a cell, and a vector which can be contained in a vector such that the agent can increase the concentration of MANF and, therefore, increase the regeneration of the muscle.
the amount of direction provided by the inventor; the existence of working examples:
However, the specification does not disclose a reduction to practice for the broad method of increasing regeneration of a skeletal muscle in any individual in need thereof comprising the steps of increasing, by any means, the concentration of Mesencephalic Astrocyte-derived Neurotrophic Factor (MANF) in the skeletal muscle. While the specification recites methods for studying MANF’s role in skeletal muscle regeneration in aged mice (page 15-16 in Specification) by injecting into the injured muscle an agent wherein the agent is a recombinant human MANF protein, the specification does not teach, through working examples, any other method to increase the concentration of MANF through any other route of administration, and hence, increase the regeneration of skeletal muscle. Moreover, the specification is silent on what individual is a candidate for the claimed method as there is no indication by working examples of criteria to determine if an individual is in need of skeletal muscle regeneration. Indeed, there is no amount of direction with corresponding working examples for increasing the concentration of MANF (and therefore, the regeneration of skeletal muscle) using an agent that is a nucleic acid that encodes MANF, a vector that contains the nucleic acid encoding MANF, or a cell that expresses MANF. Consequently, there is no indication of success of using any agent, administered through any route, other than the intramuscular injection of recombinant human MANF (rhMANF) in injured muscles of aged mice as recited in the specification. Thus, the lack of working examples exacerbates the large breadth of the claims.
the state of the prior art; the level of predictability in the art:
The association of MANF and its role in the neuromuscular physiology has only been nascently shown in prior art, demonstrating that the technology for using MANF as a treatment of neuromuscular disease remains in its infancy stage of development and application. As aforementioned, the claims are recited to increase muscle regeneration by increasing MANF through an agent which increases MANF concentration in skeletal muscle, this could be, for example, any protein, a protein encoding MANF, any nucleic acid (DNA or RNA), a nucleic acid encoding MANF, a cell, a cell expressing MANF, or a vector containing the nucleic acid encoding MANF. Based on the recitation of the broad species of agents in the claims, the prior art indicates there exists a great level of unpredictably in use of any of the species recited in the claims for in vivo application, as described below.
In regards to the administration of an agent which is a protein, such as claim 5 which recites the MANF agent is an amino acid sequence, Liu et al (Acta Pharmaceutica Sinica B, 2025, pages 6342-6381), teaches that while peptide- and protein-based therapeutics offer potential benefits to health, there remains significant challenges in their widespread use due to substantial biological and physicochemical barriers such as enzymatic degradation causing instability, limited epithelial transport, and inherently low systemic bioavailability (abstract, page 1; 2.1. Intrinsic challenges of peptide and protein, page 2). Liu teaches the need to tailor the delivery route and anatomical target site, in conjunction with formulation design as a fundamental strategy to overcome the pharmacological and biopharmaceutical limitations of peptide and protein therapeutics (page 6369, right col, para 1). Hence, Liu emphasizes that administration of protein does not guarantee intended function due to obstacles related to administration and targeting sites of interest.
In regards to administration of nucleic acid sequences as the agent for increasing MANF expression without a carrier, as implied by claim 4-7 (i.e. a nucleic acid molecule without a carrier), it is well understood that nucleic acids hold promise as a gene therapy, however there remains challenges when attempting to administer for targeting across different tissues, organs, cell types, and regions of the body in different disorders. Uludag et al (Frontiers in Bioengineering and Biotechnology, 2019, pages 1-21) teaches that the route of administration has a significant influence on nucleic acid therapeutic biodistribution, bioavailability, and eventually its intended result (page 6, right col, para 1) and that more deep-seated maladies, naked nucleic acids (i.e. no carrier) may not be satisfactory as in this case they need to be administered systemically and are required to seek out the diseased tissue in the complex in vivo environment to be effective. For this, they need to be equipped with the right elements to identify target tissues and evade degradation, while still be biologically active (page 6, right col, para 1), thus demonstrating that use of nucleic acids as therapeutics for increasing MANF concentration can be unpredictable.
Despite claim 9 and 10 reciting that the nucleic acid is contained in a vector and the vector is a viral vector, the lack of specificity of the vector and viral type further reiterates the high level of unpredictability in the claimed method. While the claims are directed to increasing MANF in skeletal muscle through any means of administration of the any vector or a viral vector, the current state of the art indicates variability in achieving desirable end results when using any vector system, even viral vectors. Furthermore, claim 9 and 10 do not indicate the requirement of a promoter, which is a necessary element for proper transcription of nucleic acid in the cell. Ramamoorth et al (Journal of Clinical and Diagnostic Research, 2015, pages 1-6) teaches that delivery efficiency is the major hurdle for almost all of the non-viral vectors, indicating that use of the nucleic acid in a non-viral vector can lead to unpredictable results (page 4, right col, Discussion) and efficiency of vector transport and unloading into target cells, perseverance, activity, and immune response remain as large challenges in using vector-based gene therapy as various delivery systems exist wherein each system can lead to different results (page 1, right col, Technical challenges and limitations to successful Non-Viral Gene transfer). In regards to viral vectors, CD Genomics (CD Genomics Biomedical Application, first published December 2025, pages 1-15) teaches that while viral vectors are promising in effectively delivering therapeutic genes into cells for stable expression, inappropriate selection of the viral vector can bring a series of serious consequences. The mismatch between vector and target cell, abnormal gene expression regulation and other problems may lead to the failure of target gene expression, making it difficult to achieve the expected results. Therefore, careful and scientific selection of virus vectors is the key prerequisite for the successful development of gene therapy (page 1, para 2).
In regards to claim 11 reciting that the agent increasing the concentration of MANF in skeletal muscle is a cell expressing MANF, Azzag et al (Advanced Drug Delivery Reviews, 2026, pages 1-13) teaches that while cell therapy remains an attractive therapeutic option for maladies affecting skeletal muscle, there remains challenges in their effectiveness due to delivery and immune response (page 8, right col, para 3-4, Current challenge, limitations, and future directions). Azzag teaches that, for example, intraarterial injection of cells in DMD patients show limited engraftment, possibly due to number of cells delivered and status of the muscle physiology and other studies have shown inconsistencies between intraarterial and intramuscular injection of cells (page 8, right col, para 3-4, Current challenge, limitations, and future directions), further signifying the inconsistencies of administering cells for skeletal muscle therapeutic purposes.
The specification discloses a single working example for the intramuscular administration of rhMANF to an injured and aged mouse model. It is not clear how these results can be extrapolated to a multitude of other diverse conditions as claimed. In regards to using mouse models for translation to non-mouse subjects for administration of MANF, current literature indicates that the use of MANF remains in preclinical trial stage where several studies used murine model systems to determine effectiveness of MANF in treating maladies such as stroke and muscle injury (see the art of Anttila et al (Acta Neuropathologica Communications, 2024, pages 1-24; Sousa et al (bioRxiv, 2022, pages 1-24). In fact, applicant’s own art (Sousa et al (bioRxiv, 2022, pages 1-24) discloses that MANF emerges as a potential candidate to be used in a clinical setting where adult muscle stem cells are applied to the aged skeletal muscle (page 7 of Sousa et al). In regards to route of administration and purpose, the current art only indicates the enablement of administering MANF2 protein to the Striatum of rats (Saarma US 20190153052 A1; as cited in IDS) or intracerebral injection in rats (Saarma US 8853166 B2), administration of MANF protein intravitreally in mice (Neves US 20170274048 A1), or intramuscular injection of recombinant human MANF to aged mice (Sousa et al (bioRxiv, 2022, pages 1-24). A search of the scientific literature shows no current methods, let alone results, related to administering MANF (as a nucleic acid or protein) to any individual other than a mouse or rat, and administered in any route other than in the brain, muscle, or eye, again reiterating the lack of predictability in use of MANF for increasing skeletal muscle regeneration to any individual identified to be in need thereof, other than a mouse or rat and through any means of administration.
the quantity of experimentation needed to make or use the invention based on the content of the disclosure:
The skilled artisan would be required to perform undue levels of experimentation in order to practice the claimed invention. While the instant application discloses methods for increasing skeletal muscle regeneration by increasing MANF concentration in the skeletal muscle via intramuscular injection of rhMANF in an aged mouse, the art and disclosure would not allow one to determine the boundaries of the useable invention and hence would not enable one of ordinary skill in the art to use the invention as claimed. The skilled artisan would be forced to determine 1) which individuals are in need of the increased regeneration of skeletal muscle, 2) the appropriate agent that would increase the concentration of MANF in the skeletal muscle, 3) the route of administration of the MANF that would increase the concentration of MANF in the skeletal muscle, 4) the dosage of the agent required, and 5) determine if MANF is increased sufficiently and that regeneration of the skeletal muscle is sufficient.
conclusion
When all of the Wands factors are considered together, they establish a prima facie case that the specification is not enabling for the claims. While a lack of a working embodiment showing relevant data to support the methods cannot be a sole factor in determining enablement, the dearth number of results presented, in light of the unpredictable nature of the art, obstacles required to be overcome in administering therapeutics, and the minimal direction applicants present, provides additional weight to the scope of enablement in consideration of the Wands factors as a whole. Thus, one of ordinary skill in the art would not have had a reasonable expectation of success in making or using the claimed invention.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 1-3 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Sousa (Universidade Nova de Lisboa Thesis, first available March 14, 2022, pages 1-105).
The applied Sousa reference has a common inventor with the instant application. Based upon the earlier effectively filed date of the reference, it constitutes prior art under 35 U.S.C. 102(a)(1). The publication dated for Sousa is March 14, 2022. The earliest effective filing date of the instant application is March 23, 2023 (based on support by the disclosure in application PCT/ EP2023/057484).
Therefore rejection under 35 U.S.C. 103 CANNOT be overcome by: (1) a showing under 37 CFR 1.130(a) that the subject matter disclosed in the reference was obtained directly or indirectly from the inventor or a joint inventor of this application and is thus not prior art in accordance with 35 U.S.C.102(b)(2)(A); (2) a showing under 37 CFR 1.130(b) of a prior public disclosure under 35 U.S.C. 102(b)(2)(B); or (3) a statement pursuant to 35 U.S.C. 102(b)(2)(c) establishing that, not later than the effective filing date of the claimed invention, the subject matter disclosed and the claimed invention were either owned by the same person or subject to an obligation of assignment to the same person or subject to a joint research agreement. See generally MPEP § 717.02. Because the reference qualifies as prior art under 102(a)(1), the provisions of MPEP 717.02 do not apply.
Regarding claims 1-3 and 14-16, Sousa teaches that inducing injury to young (4 months of age) and old (25 months of age) mice by intramuscular injection of the chemical Barium Chloride (BaCl2) in the Tibialis Anterior or Quadriceps causes increased levels of MANF at the protein and mRNA level during the muscle regeneration process, thus increasing muscle regeneration (page 43-45, Figures 3.2 and 3.3; pages 48 Figure 3.6). Sousa teaches that the old mice have regenerative defects characterized by their aging condition (page 48, para 4).
Claims 1-4 and 14-16 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Sousa-Victor (Nature Metabolism, 2019, pages 1-36; as cited in IDS) as evidenced by Shoyaib et al (Pharm. Res. 2020, Page 1-30).
The applied Sousa-Victor reference has a common inventor with the instant application. Based upon the earlier effectively filed date of the reference, it constitutes prior art under 35 U.S.C. 102(a)(1). The publication dated for Sousa-Victor is Sept 5, 2019. The earliest effective filing date of the instant application is March 23, 2023 (based on support by the disclosure in application PCT/ EP2023/057484).
Therefore rejection under 35 U.S.C. 103 CANNOT be overcome by: (1) a showing under 37 CFR 1.130(a) that the subject matter disclosed in the reference was obtained directly or indirectly from the inventor or a joint inventor of this application and is thus not prior art in accordance with 35 U.S.C.102(b)(2)(A); (2) a showing under 37 CFR 1.130(b) of a prior public disclosure under 35 U.S.C. 102(b)(2)(B); or (3) a statement pursuant to 35 U.S.C. 102(b)(2)(c) establishing that, not later than the effective filing date of the claimed invention, the subject matter disclosed and the claimed invention were either owned by the same person or subject to an obligation of assignment to the same person or subject to a joint research agreement. See generally MPEP § 717.02. Because the reference qualifies as prior art under 102(a)(1), the provisions of MPEP 717.02 do not apply.
Regarding claims 1-4, Sousa-Victor teaches intra-peritoneal (i.p.) injections of human recombinant MANF (hrMANF) protein in old (21 months of age) mice which increases the concentration of MANF in circulation and demonstrated increased regeneration of the skeletal muscle (page 10, Supplemental Figure 10). It is noted that i.p. injection leads to the injected substance being absorbed and distributed throughout the body via systemic circulation, hence would cause increase in MANF in the skeletal muscle, as evidenced by Shoyaib (page 6, para 2).
Regarding claim 14-16, Sousa-Victor teaches that old animals (i.e mice used in their study) have reduced muscle mass (i.e. reduced regeneration), which is a defect due to reduced MANF which is caused by their old age (page 12, para 1).
Conclusion
No claims are allowed.
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/JULIANA IRENE CANDELARIA/ Examiner, Art Unit 1634
/MARIA MARVICH/ Primary Examiner, Art Unit 1634
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