DETAILED ACTION
Election/Restrictions
Applicant’s election without traverse of Group I, both a PC1 polypeptide and a pC2 polypeptide, EF1α and a CBh promoter in the reply filed on March 5 2026 is acknowledged. In light of the discovered prior art the promoter sequence has been expanded to include cytomegalovirus (CMV) promoter. Claims 1-11, 20-27, 30 and 49 are pending in the application. Claims 30 and 49 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on March 5 2026. Accordingly, claims 1-11 and 20-27 are being examined on the merits herein.
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 .
Priority
This application is a 371 of PCT/US2022/012461 (01/14/2022) which claims benefit of 63/221,196 (07/13/2021) and claims benefit of 63/137,629 (01/14/2021) as reflected in the filing receipt issued on June 13 2024.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on October 1 2024 and March 20 2025 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Drawings
The drawings are objected to for the following reasons: 37 CFR 1.84 (u)(1) states “Partial views intended to form one complete view, on one or several sheets, must be identified by the same number followed by a capital letter.” In the current case, the view numbers for the partial views for Figures 12A and 12B that appear on several sheets are followed by "Cont." instead of a capital letter such as FIG. 1A, FIG. 1B, etc.
Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
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 1-11 and 20-27 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 pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention.
The specification discloses chemicals, such as nucleic acid encoding a PC-1 polypeptide (SEQ ID NO: 1), a PC-1 polypeptide as set forth in SEQ ID NO: 2, a nucleic acid encoding a PC-2 polypeptide (SEQ ID NO: 3) or a PC-2 polypeptide as set forth in SEQ ID NO: 4 which meet the written description and enablement provisions of 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph. However, claim(s) 1, 6 and 11 is(are) directed to encompass variants which only correspond in some undefined way to specifically instantly disclosed chemicals. None of these variants meet the written description provision of 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, due to lacking chemical structural information for what they are and chemical structures are highly variant and encompass a myriad of possibilities. The specification provides insufficient written description to support the genus encompassed by the claim. Note: MPEP 2163.
The instant specification indicates a variant can have the amino acid sequence of a naturally occurring PC-1 polypeptide or PC-2 polypeptide with one or more (e.g. 1-10 or more) amino acid deletions, additions, substitutions or combinations thereof, provided that the variant retains the function of a naturally occurring PC-1 or PC-2 polypeptide (see page 21, lines 12-17; page 21-22, lines 29-32 and 1-2).
Table 1 of the instant specification shows examples of conservative amino acid substitutions which could be made. But non conservative substitutions are also suggested (see for example page 23-24).
Therefore, the instant specification appears to describe what could encompass a variant. The instant claims, however, require more than just a variant but that this variant is also capable of treating a mammal having polycystic kidney disease.
As recognized in the art, see for example Bergmann et al. (Nature Reviews, 2018, cited on PTO Form 1449), mutations in PKD1 or PKD2 which encode polycystin 1 (PC1) and polycystin 2 (PC2) are the most common cause of ADPKD (autosomal dominant polycystic kidney disease). Since the definition of variant include mutations (i.e. deletions, additions and/or substitution) and mutations are the cause of PKD, the specification must provide written description for the specific variants which can be made which allow for the variant to retain the function of the naturally occurring PC-1 or PC-2. However, the instant specification fails to describe what sequence is required to retain functionality, what mutations are allowed which results in retention of functionality or any particular sequence of a variant which maintains the functionality of the naturally occurring PC-1 or PC-2.
Vas-Cath Inc. v. Mahurkar, 19 USPQ2d 1111, (Fed. Cir. 1991), 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 the art to recognize that [he or she] invented what is claimed." (See Vas-Cath at page 1116.)
Univ. of Rochester v. G.D. Searle, 69 USPQ2d 1886, 1892 (CAFC 2004), further supports this by stating that:
The appearance of mere indistinct words in a specification or a claim, even an original claim, does not necessarily satisfy that requirement. A description of an anti-inflammatory steroid, i.e., a steroid (a generic structural term) described even in terms of its functioning of lessening inflammation of tissues fails to distinguish any steroid from others having the same activity or function. A description of what a material does, rather than of what it is, usually does not suffice…. The disclosure must allow one skilled in the art to visualize or recognize the identity of the subject matter purportedly described. (Emphasis added).
With the exception of the above specifically disclosed chemical structures, the skilled artisan cannot envision the detailed chemical structure of the encompassed variants, regardless of the complexity or simplicity of the method of isolation. Adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method for isolating it. The chemical structure itself is required. See Fiers v. Revel, 25 USPQ2d 1601, 1606 (Fed. Circ. 1993) and Amgen Inc. V. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016, (Fed. Cir. 1991). In Fiddes v. Baird, 30 USPQ2d 1481, 1483, (Bd. Pat. App. & Int. 1993), claims directed to mammalian FGF's were found unpatentable due to lack of written description for the broad class. The specification provided only the bovine sequence. Finally, University of California v. Eli Lilly and Co., 43 USPQ2d 1398, 1404, 1405 (Fed. Cir. 1997) held that:
...To fulfill the written description requirement, a patent specification must describe an invention and do so in sufficient detail that one skilled in the art can clearly conclude that "the inventor invented the claimed invention." Lockwood v. American Airlines, Inc., 107 F.3d 1565, 1572, 41 USPQ2d 1961, 1966 (Fed. Cir. 1997); In re Gosteli, 872 F.2d 1008, 1012, 10 USPQ2d 1614, 1618 (Fed. Cir. 1989) (" [T]he description must clearly allow persons of ordinary skill in the art to recognize that [the inventor] invented what is claimed."). Thus, an applicant complies with the written description requirement "by describing the invention, with all its claimed limitations, not that which makes it obvious," and by using "such descriptive means as words, structures, figures, diagrams, formulas, etc., that set forth the claimed invention." Lockwood, 107 F.3d at 1572, 41 USPQ2d at 1966.
Furthermore, to the extent that a functional description can meet the requirement for an adequate written description, it can do so only in accordance with PTO guidelines stating that the requirement can be met by disclosing “sufficiently detailed, relevant identifying characteristics,” including “functional characteristics when coupled with a known or disclosed correlation between function and structure.” Univ. of Rochester v. G.D. Searle, 68 USPQ2d 1424, 1432 (DC WNY 2003).
Therefore, only the above chemically structurally defined chemicals, but not the full breadth of the claim(s) meet the written description provision of 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph. The species specifically disclosed are not representative of the genus because the genus is highly variant. Applicant is reminded that Vas-Cath makes clear that the written description provision of 35 USC § 112 is severable from its enablement provision. (See page 1115.)
Claim Rejections - 35 USC § 103
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 of this title, 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 set forth in Graham v. John Deere Co., 383 U.S. 1, 148 USPQ 459 (1966), that are applied 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.
Claims 1-2, 4-11, 20 and 22-26 are rejected under 35 U.S.C. 103 as being unpatentable over Germino et al. (USPGPUB NO. 20140037652) in view of Hanaoka et al. (Nature, 2000), Kim et al. (Protein Science, 2004), Paul et al. (USPGPUB No. 20190153471) and Duan et al. (USPGPUB No. 20100003218).
Applicant Claims
The instant application claims a method for treating a mammal having a polycystic kidney disease (PKD), wherein said method comprises administering to said mammal:(a) nucleic acid encoding a PC-1 polypeptide or a variant of said PC-1 polypeptide, wherein said PC-1 polypeptide or said variant is expressed by kidney cells within said mammal; and (b) nucleic acid encoding a PC-2 polypeptide or a variant of said PC-2 polypeptide, wherein said PC-2 polypeptide or said variant is expressed by kidney cells within said mammal.
Determination of the Scope and Content of the Prior Art
(MPEP §2141.01)
Germino et al. is directed to the detection and treatment of polycystic kidney disease. Mutations in the PKD1 polynucleotide that cause ADPKD (autosomal dominant polycystic kidney disease) can lower the level of expression of the PKD1 polynucleotide or, alternatively, can cause inactive of substantially inactive PKD1 protein to be produced. In either instance, the result is an overall lower level of normal PKD1 activity in the tissue or cells in which PKD1 is normally expression. This lower level of PKD1 activity, then, leads to ADPKD symptoms. Thus, such PKD1 mutations represent dominant loss-of-function mutations (paragraph 0214). Normal PKD1 protein, at a level sufficient to ameliorate ADPKD symptoms can be administered to a patient exhibiting such symptoms or having a mutant PKD1 polynucleotide. Additionally, DNA sequences encoding normal PKD1 protein can be directly administered to a patient exhibiting ADPKD symptoms or administered to prevent or reduce ADPKD symptoms where they have been diagnosed as having a PKD1 mutation identified herein but have not yet demonstrated symptoms. Such administration can be at a concentration sufficient to produce a level of PKD1 protein such that ADPKD symptoms are ameliorated (paragraph 0215). Subjects with these types of mutations can be treated by gene replacement therapy. A copy of the normal PKD1 polynucleotide can be inserted into cells, renal cells, for example, using viral or non-viral vectors that include, but are not limited to vectors derived from, for example, retroviruses, vaccinia virus, adeno-associated virus, herpes viruses, bovine papilloma virus or non-viral vectors, such as plasmids (paragraph 0216). Constitutive expression with promoters including those from cytomegalovirus (CMV) (paragraph 0195). Mammalian subjects are expressly taught (paragraph 0026).
Ascertainment of the Difference Between Scope the Prior Art and the Claims
(MPEP §2141.02)
While Germino et al. teaches administration of a sequence encoding a normal PKD1 protein and other PKD-associated genes exist, such as PKD2, Germino et al. does not expressly teach administration of a sequence encoding a normal PKD2. However, this deficiency is cured by Hanaoka et al.
Hanaoka et al. is directed to the co-assembly of polycystin-1 and -2 produces unique cation-permeable currents. It is taught that in autosomal dominant polycystic kidney disease (ADPKD) cysts develop from renal tubules and enlarge independently. Mutations in either PKD1 or PKD2 are associated with ADPKD. It is taught that polycystin-1 and polycystin-2 interact to produce new calcium-permeable non-selective cationic currents. Disease-associated mutant forms of either polycystin protein that are incapable of heterodimerization do not result in new channel activity. Polycystin-1 and -2 co-assemble at the plasma membrane to produce a new channel and to regulate renal tubular morphology and function (page 990). Disease causing mutant forms of these proteins do not generate currently clearly shows that assembly of polycystin-1 and -2 is required for ion-channel function (page 993).
While Germino et al. suggest viral vectors with promoters, Germino et al. does not expressly teach the instantly claimed/elected promoters or the use of different promoters for PC1 and PC2. However, this deficiency is cured by Kim et al., Duan et al. and Paul et al.
Kim et al. is directed to two-promoter vector being highly efficient for overproduction of protein complexes. It is taught that the use of bicistronic vectors which contain two target genes under one promoter has been the most common practice for the heterologous production of binary protein complex. The major problem of this method is the much lower expression of the second gene compared with that of the first gene next to the promoter. Tested was whether inclusion of an additional promoter in front of the second gene may remove the problem. Taught is a significant increase in the second gene in a manner independent of the order of the target genes (page 1698; Fig. 1).
Duan et al. is directed to hybrid-AAV vectors to delivery large gene expression cassette. It is taught that a vector is often used to deliver the therapeutic, normal gene to the subject’s target cells. The adeno-associated virus (AAV) is attractive because it is not currently known to cause disease, infects dividing and non-dividing cells and may incorporate its genome into that of the host cell. However, it is limited by it 5 kb viral packaging limit (paragraph 0003). Taught is a hybrid-AAV (hdAAV) vector system which may be used with any target gene between 5kb and 10 kb (paragraph 0013). Taught is a cytomegalovirus promoter (paragraph 0038). The hdAAV is able to efficiently express therapeutic target genes larger than may be carried in a single AAV vector (paragraph 0039). Therapeutic target genes include polycystic kidney disease 1 (PKD1) and polycystic kidney disease 2 (PKD2) (paragraph 0043).
Paul et al. is directed to compositions for the treatment of disease. Taught are adeno-associated viral vectors which are widely used in gene therapy approaches (paragraph 0006). These vectors include a regulatory sequence operably linked to at least a first nucleic acid segment that encodes one or more polypeptides (paragraph 0011). Regulatory sequence comprise a promoter such as human elongation factor 1α-subunit (EF1α), cytomegalovirus (CMV) chicken β-actin (CBA) and its derivative(s) (paragraph 0014). Ubiquitous promoters include CMV, CBA (including derivatives CAG, CBh, etc.), EF-1alpha (paragraph 010). The use of two promoters such as an EF1alpha and CMV (paragraph 0120).
Finding of Prima Facie Obviousness Rationale and Motivation
(MPEP §2142-2143)
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teachings of Germino et al., Hanaoka et al., Kim et al., Duan et al. and Paul et al. and administer a nucleic acid encoding both polycystin-1 and polycystin-2 to a mammalian subject. Germino et al. clearly teaches administration of a nucleic acid encoding poycystin-1 to treat ADPKD. Hanaoka et al. teaches that mutations in either PKD1 or PKD2 are associated with ADPKD and that polycystin-1 and -2 co-assemble at the plasma membrane to produce a new channel and to regulate renal tubular morphology and function. Therefore, when treating ADPKD one skilled in the art would have been motivated to administer normal copies of polycystin-1 and -2 in order to restore function to subject with ADPKD. Since as taught by Hanaoka et al. these two peptides interact to regulate renal tubular morphology and function and mutations in both lead to ADPKD, one skilled in the art would have been motivated to administer both to subjects suffering from ADPKD.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teachings of Germino et al., Hanaoka et al., Kim et al., Duan et al. and Paul et al. and administer an hdAAV comprising two promoters with nucleic acids encoding both polycystin-1 and -2. One skilled in the art would have been motivated to utilize an hdAAV as these are designed to deliver larger genes as taught by Duan et al. Since Duan et al. specifically teaches that these vectors can be utilized with either polycystin-1 or -2 there is a reasonable expectation of success. One skilled in the art would have been motivated to operably link a promoter with polycystin-1 and a separate promoter with polycystin-2 in order to ensure expression of both. As taught by Kim et al. the use of one promoter can result in lower expression levels of the second target gene. Therefore, the use of two separate promoters would be expected to allow for increased expression of both of the target genes. One skilled in the art would have been to utilize CMV, EF1alpha or CBh promoters. One skilled in the art would have been motivated to utilize any of the known promoters used with AAV vectors. All of the claimed elements were known in the prior art and one skilled in the art could have combined the elements as claimed by known methods with no change in their respective functions and the combination would have yielded predictable results to one of ordinary skill in the art at the time of the invention. Note: MPEP 2143 KSR International Co. v. Teleflex Inc., 550 US 398, 82 USPQ 2d 1385 (2007).
Regarding claim 24, Germino et al. specifically teaches identifying a subject having or is at risk of having a PKD1-associated disorder (paragraph 0025).
Regarding claim 25, Germino et al. teaches mammalian subjects include humans (paragraph 0026).
Claims 3 and 21 are rejected under 35 U.S.C. 103 as being unpatentable over Germino et al. in view of Hanaoka et al., Kim et al., Paul et al. and Duan et al. as applied to claims 1-2, 4-11, 20 and 22-26 above and in further view of Vetrini et al. (Viruses, 2010).
Applicant Claims
The instant application claims said viral vector is a HDAd vector.
Determination of the Scope and Content of the Prior Art
(MPEP §2141.01)
The teachings of Germino et al., Hanaoka et al., Kim et al., Paul et al. and Duan et al.
Ascertainment of the Difference Between Scope the Prior Art and the Claims
(MPEP §2141.02)
While Germino et al. teaches viral vectors and Hanaoka et al. recognizes that normal AAV cannot support large genes, the use of a helper-dependent adenoviral vector is not expressly taught. However, this deficiency is cured by Vetrini et al.
Vetrini et al. is directed to gene therapy with helper-dependent adenoviral vectors current advances and future perspectives. Adenovirus (Ad)-derived gene therapy have 1) the ability to infect with high efficiency a variety of both quiescent and proliferating cell types, 2) Ad vectors can be easily grown to very high titer, allowing the experimenter to transduce a large number of cells and/or tissue target of large animals, and 3) the absence of vector genome integration thereby reduces the likelihood for germ-line transmission and insertional mutagenesis, which represents an important safety feature (page 1887). Helper-dependent adenoviral (HDAd) vectors are devoid of all viral coding sequences, and have shown tremendous potential for the treatment of genetic disease, allowing for persistent transgene expression for years in the apparent absence of any type of adaptive immune response and chronic toxicity. HDAds can mediate high efficiency transduction, do not integrate in the host genome, and have a large cloning capacity of up to 37 kb, which allows for the delivery of multiple transgenes or entire genomic loci, or large cis-acting elements to enhance or regulate tissue-specific transgene expression (page 1887).
Finding of Prima Facie Obviousness Rationale and Motivation
(MPEP §2142-2143)
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teachings of Germino et al., Hanaoka et al., Kim et al., Paul et al., Duan et al. and Vetrini et al. and utilize HDAd vectors to administer the nucleic acid encoding polycystin-1 and -2. One skilled in the art would have been motivated to utilize this vector as Germino et al. suggests viral vectors. Hanaoka et al. suggests the use of vectors which have larger capacity to delivery polycystin-1 and -2. Therefore, one skilled in the art would have been motivated to utilize an HDAd vector as it has a large cloning capacity. Furthermore, in light of the other advantages of HDAd taught by Ventrini et al. this provides more motivation to one skilled in the art to utilize this type of vector.
Claim 27 is rejected under 35 U.S.C. 103 as being unpatentable over Germino et al. in view of Hanaoka et al., Kim et al., Paul et al. and Duan et al. as applied to claims 1-2, 4-11, 20 and 22-26 above and in further view of Zahir et al. (Case Rep Urol., 2013) and Hato et al. (J Am Soc Nephrol, 2017) .
Applicant Claims
The instant application claims wherein said method further comprises, prior to said administering said nucleic acid, administering a lipopolysaccharides (LPS) to said mammal.
Determination of the Scope and Content of the Prior Art
(MPEP §2141.01)
The teachings of Germino et al., Hanaoka et al., Kim et al., Paul et al. and Duan et al.
Ascertainment of the Difference Between Scope the Prior Art and the Claims
(MPEP §2141.02)
While Germino et al. teaches treating subjects with ADPKD, Germino et al. does not expressly teach administration of a lipopolysaccharide prior to administering the nucleic acid encoding polycystin-1. However, this deficiency is cured by Zahir et al. and Hato et al.
Zahir et al. is directed to rupture in polycystic kidney disease presented as generalized peritonitis with sever sepsis. Infection of a cyst within a polycystic kidney is a serious complication of ADPKD, potentially leading to abscess, sepsis, and death.
Hato et al. is directed to endotoxin (aka lipopolysaccharide) preconditioning reprograms S1 tubules and macrophages to protect the kidney. It is taught that preconditioning with a low dose of endotoxin confers unparalleled protection against otherwise lethal models of sepsis. Exemplified is endotoxin preconditioning by administering lipopolysaccharide (LPS) intraperitoneal injection (page 113). In models of sepsis, endotoxin preconditioning conveys global protection. In the kidney, the tissue response to preconditioning is centered around S1 proximal tubular segments (page 113).
Finding of Prima Facie Obviousness Rationale and Motivation
(MPEP §2142-2143)
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teachings of Germino et al., Hanaoka et al., Kim et al., Paul et al., Duan et al., Zahir et al. and Hato et al. and precondition the kidney with lipopolysaccharides in order to protect the kidney from sepsis. Since as taught by Zahir et al. sepsis is a serious complication of ADPKD and Hao et al. teaches that the lipopolysaccharides can protect the kidney against sepsis, one skilled in the art would have been motivated to precondition with low doses of endotoxin in order to protect the kidney.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ABIGAIL VANHORN whose telephone number is (571)270-3502. The examiner can normally be reached M-Th 6 am-4 pm EST.
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/ABIGAIL VANHORN/Primary Examiner, Art Unit 1636
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