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 .
Applicant’s election without traverse of 1) the frameshift variant that occurs at position 240873025 of hg38 (an insertion of a A or C; P_000021.1:p.Leul93ProfsTer32); 2) a double stranded ribonucleic acid (dsRNA) agent, or a salt thereof; and 3) HAO1 in the reply filed on 10/10/25 is acknowledged. It is noted that given further consideration, the gene variants to be screened are considered to be obvious variations of each other and have therefore been rejoined.
Specification
The specification is objected to because there are structures that are not fully legible on pages 9 and 10, for example.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 1-5, 27, 72, 73, and 78-85 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claims 1 and 2 recite determination of the presence or absence of a heterozygous AGXT gene variant annotated in the Clinvar database as being pathogenic or pathogenic/likely pathogenic. The Clinvar database is not a static listing and it is regularly updated/amended. Therefore, the metes and bounds of the instant claims are not definite. Additionally, MPEP 2173.05(s) states in part “ [w]here possible, claims are to be complete in themselves. Incorporation by reference to a specific figure or table is permitted only in exceptional circumstances where there is no practical way to define the invention in words and where it is more concise to incorporate by reference than duplicating a drawing or table into the claim”. Applicant is required to refer to the variants, in the claims, by listing the variants. Claims 1 and 6 recite a database and claim 3 refers to Tables.
The remainder of the claims are rejected because they depend from the rejected claims and do not overcome the rejection.
Claim 1 recites the limitation "the kidney stone formation disease" in claim 1. There is insufficient antecedent basis for this limitation in the claim. The preamble recites “a kidney stone disease”, which is not consistent with “the kidney stone formation disease” later in the claim.
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 1-5, 27, 72, 73, and 78-85 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.
The claims are directed to a method of determining the presence or absence of a heterozygous alanine-glyoxylate amino transferase (AGXT) loss-of-function gene variant or a heterozygous AGXT gene variant annotated in the Clinvar database as being pathogenic or pathogenic/likely pathogenic gene variant in a sample obtained from the subject.
The specification discloses species of heterozygous alanine-glyoxylate amino transferase (AGXT) loss-of-function gene variants, but the specification does not adequately describe the structure required for an AGXT gene variant to be loss-of-function. Without further description of the structure required for the function, one would not be able to readily envision which heterozygous AGXT gene variants are necessarily included or excluded from the genus of loss-of-function gene variants. Determination of which variants are loss-of-function within all possible heterozygous AGXT gene variants involves computational analysis, experimental validation, and determination of which variants result in what level of loss-of-function. The specification does not ad2quately describe this genus and the species of the specification are not representative of the entire claimed genus.
Additionally, the claims are directed to delivery of a dsRNA (not necessarily a siRNA) that comprise the instantly recited sense and antisense strand that are 21 and 23 nucleotides in length, respectively.
The specification does not adequately describe the structure required for the function. The species of the specification are not representative of the entire claimed genus. The structure recited encompasses a large genus of dsRNAs that would not likely have the function of inhibiting the expression of any HAO1 gene. The dsRNA agent can be very long (i.e. 1,000 nucleotides) and comprise the instantly recited sequences. The species disclosed in the specification of siRNAs that comprise the instantly recited sequences are not representative of the entire claimed genus.
Additionally, the claims are directed to treatment of a “kidney stone disease”, a “recurrent kidney stone disease”, or a “calcium oxalate kidney stone disease or non-calcium oxalate kidney stone disease.
The specification does not adequately describe the requirements for a disease to be included or excluded from the genus of diseases that are a “kidney stone disease”, a “recurrent kidney stone disease”, or a “calcium oxalate kidney stone disease or non-calcium oxalate kidney stone disease.
Without further description of the criteria for the genus, one would not be able to readily envision the members of the genus. For example, Mihalopoulos et al. (Am J Clin Exp Urol 2022;10(5):277-298) teach that emerging evidence has implicated an association between kidney stones and upper urinary tract cancers (including renal cancer) (abstract). Mihalopoulos et al. teach that kidney stones are associated with increased risk of renal cell carcinoma (pages 280-281). Therefore, renal cancer would meet the instant limitation of a kidney stone disease. The specification does not adequately describe the instantly recited genus.
Luo et al. (Biology Direct, 2025, 20:42, 1-20) teach that the association of osteoporosis and kidney stones is well-established. Luo et al. teach that bone loss is associated with an increased risk of kidney stones (page 1). Luo et al. teach that despite their distinct clinical manifestations, recent studies have suggested the possibility of shared genetic or environmental risk factors between these two diseases (page 2). Therefore, osteoporosis could be considered to be a “kidney stone disease” as instantly recited because it is strongly associated to kidney stones.
Although the instant method requires determination of the presence of any heterozygous AGXT loss-of-function gene variant before treatment, the specification does not adequately describe which variants are loss-of-function variants and does not adequately describe which kidney stone diseases necessarily have these specific loss-of-function variants. Without further description, one would not be able to readily envision which kidney stone diseases necessarily have which variants.
The MPEP states 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. See 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 genus. In Gostelli, the courts determined that the disclosure of two chemical compounds within a subgenus did not describe that subgenus. In re Gostelli, 872, F.2d at 1012, 10 USPQ2d at 1618. Additionally, in Carnegie Mellon University v. Hoffman-La Roche Inc., Nos. 07-1266, -1267 (Fed. Cir. Sept. 8, 2008), the Federal Circuit affirmed that a claim to a genus described in functional terms was not supported by the specification’s disclosure of species that were not representative of the entire genus. Furthermore, for a broad generic claim, the specification must provide adequate written description to identify the genus of the claim. In Regents of the University of California v. Eli Lilly & Co. the court stated:
"A written description of an invention involving a chemical genus, like a description of a chemical species, 'requires a precise definition, such as by structure, formula, [or] chemical name,' of the claimed subject matter sufficient to distinguish it from other materials." Fiers, 984 F.2d at 1171, 25 USPQ2d 1601; In re Smythe, 480 F.2d 1376, 1383, 178 USPQ 279, 284985 (CCPA 1973) ("In other cases, particularly but not necessarily, chemical cases, where there is unpredictability in performance of certain species or subcombinations other than those specifically enumerated, one skilled in the art may be found not to have been placed in possession of a genus ...") Regents of the University of California v. Eli Lilly & Co., 43 USPQ2d 1398.
The claims are rejected under the written description requirement for failing to disclose adequate species to represent the claimed genus, the genus heterozygous AGXT loss-of-function gene variants, kidney stone diseases, and dsRNA agents of any length comprising the instantly recited sequences with the recited functions.
The Guidelines for Examination of Patent Applications under the 35 USC § 112, first paragraph, “Written Description” Requirement”, published at Federal Register, Vol. 66, No. 4, pp. 1099-1111 outline the method of analysis of claims to determine whether adequate written description is present. The first step is to determine what the claim as a whole covers, i.e., discussion of the full scope of the claim. Second, the application should be fully reviewed to understand how applicant provides support for the claimed invention including each element and/or step, i.e., compare the scope of the claim with the scope of the description. Third, determine whether the applicant was in possession of the claimed invention as a whole at the time of filing.
To achieve the desired function, it appears that the structure is required to be of a shorter length than the claimed genus which has no length limitation. With respect to siRNAs, as single species of RNAi agents, Elbashir et al. (The EMBO Journal, Vol. 20, No. 23, pages 6877-6888, 2001) teaches that duplexes of 21-23 nt RNAs are the sequence specific mediators of RNAi and that even single mismatches between the siRNA duplex and the target mRNA abolish interference (abstract and page 6888).
The claims encompass very long dsRNA, for example, that can trigger RNAi. Such dsRNA comprising the instantly recited sequences would not likely function as claimed. For example, Parrish et al. (Molecular Cell, Vol. 6, 1077–1087, November, 2000) teach that sequences of 1000 bp trigger RNAi (page 1078). The long dsRNA is cleaved into shorter fragments, which would not likely comprise the instantly recited sequences as a duplex after cleavage.
Thus, having analyzed the claims with regard to the Written Description guidelines, it is clear that the specification does not disclose a representative number of species for each genus that function as claimed. Thus, one skilled in the art would be led to conclude that Applicant was not in possession of the claimed invention at the time the application was filed.
Claims 1-5, 27, 72, 73, and 78-85 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 of inhibiting HAO1 via delivery of the instantly recited siRNA, does not reasonably provide enablement for a method of treating any possible kidney stone disease via broad delivery of the instantly recited dsRNA agent. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention commensurate in scope with these claims.
Factors to be considered in a determination of lack of enablement include, but are not limited to:
(A) The breadth of the claims;
(B) The nature of the invention;
(C) The state of the prior art;
(D) The level of one of ordinary skill;
(E) The level of predictability in the art;
(F) The amount of direction provided by the inventor;
(G) The existence of working examples; and
(H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure.
In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988)
The instant claims are directed to a method for treating any “kidney stone disease”, any “recurrent kidney stone disease”, or any “calcium oxalate kidney stone disease or non-calcium oxalate kidney stone disease” after determination of the presence of any heterozygous AGXT loss-of-function gene variant.
The specification discloses specific AGXT variants (Table 20) and correlation to individuals with the presence of ICD-10 (the specification refers to this as an increased risk of kidney stone disease). However, the claims are not limited to any specific kidney stone disease or a kidney stone disease with the presence of ICD-10. The claims are directed to the treatment of any kidney stone disease, which is a broader genus of possible diseases. Additionally, the claims are not limited to the AGXT variants of Example 1. The data in Example 1 demonstrates that not all patients having the AGXT variant necessarily had an increased risk of any specific kidney stone disease. The instant claims are directed to determining the presence of any heterozygous AGXT loss-of-function gene variant, not any specific variant that has been shown to identify a specific patient population that would be treated by inhibition of a HAO1 siRNA.
With regards to delivery, there is no guidance in the specification as filed that teaches how to deliver a siRNA and mediate RNA interference in vivo. Applicant is not enabled for mediating RNA interference in vivo by the broadly recited methods, as delivery is known in the art to be unpredictable with regards to dsRNA duplexes.
The references cited herein illustrate the state of the art for therapeutic in vivo applications using dsRNA.
For example, Elbashir et al. (The EMBO Journal, Vol. 20, No. 23, pages 6877-6888, 2001) teaches that duplexes of 21-23 nt RNAs are the sequence specific mediators of RNAi and that even single mismatches between the siRNA duplex and the target mRNA abolish interference (abstract and page 6888). The instant compounds can be much longer and comprise many mismatches.
Tang et al. (Journal of Controlled Release 341 (2022) 300–313) teach a polymeric siRNA carrier for selective delivery to injured kidneys. Specific nanoparticles carrying siRNAs were retained in injured kidneys (abstract). Tang et al. teaches: Although free siRNA displays natural renal tropism, there are several pharmaceutical challenges to the use of free siRNA in the treatment of AKI. The strong negative charge and macromolecular character of siRNA results in a poor ability to cross cell membranes and locate to its site of action in the cytoplasm (page 302). Tang et al. teach: An ideal siRNA delivery system not only requires stable interactions between siRNA and the carrier during systemic circulation, but also the ability to pass through biological barriers before reaching its cytoplasmic target (page 302). Tang et al. teach: Most of siRNA polyplexes usually have a short blood circulation times due to rapid renal clearance and phagocytic uptake (page 303). Therefore, Tang et al. is evidence that even post-filing, broad naked systemic delivery of dsRNA, as instantly claimed, would not likely have the effective action in the kidney.
As outlined above, it is well known that there is a high level of unpredictability in the RNAi art for therapeutic in vivo applications. The scope of the claims in view of the specification as filed together do not reconcile the unpredictability in the art to enable one of skill in the art to make and/or use the claimed invention, namely a broad method of treating any kidney stone disease encompassing in vivo effects.
MPEP 2164.01
Any analysis of whether a particular claim is supported by the disclosure in an application requires a determination of whether that disclosure, when filed, contained sufficient information regarding the subject matter of the claims as to enable one skilled in the pertinent art to make and use the claimed invention.
Also, MPEP 2164.01(a)
A conclusion of lack of enablement means that, based on the evidence regarding each of
the above factors, the specification, at the time the application was filed, would not have taught one skilled in the art how to make and/or use the full scope of the claimed
invention without undue experimentation. In re Wright, 999 F.2d 1557,1562, 27
USPQ2d 1510, 1513 (Fed. Cir. 1993).
Given the teachings of the specification as discussed above, one skilled in the art could not predict a priori whether introduction of any dsRNA comprising the instantly recited sequences in vivo by the broadly disclosed methodologies of the instantly claimed invention, would result in successful treatment of any kidney stone condition upon determination of the presence of any variant within the instantly recited genus. To practice the claimed invention, one of skill in the art would have to de novo determine; the stability of the dsRNA molecule in vivo, delivery of the dsRNA molecule to the whole organism, specificity to the target tissue in vivo, dosage and toxicity in vivo, and entry of the molecule into the cell in vivo and the effective action therein. Without further guidance, one of skill in the art would have to practice a substantial amount of trial and error experimentation, an amount considered undue and not routine, to practice the instantly claimed invention.
A conclusion of lack of enablement means that, based on the evidence regarding each of the above factors, the specification, at the time the application was filed, would not have taught one skilled in the art how to make and/or use the full scope of the claimed invention without undue experimentation (see MPEP 2164.01(a)).
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.
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 1-5, 27, 72, 73, and 78-85 is/are rejected under 35 U.S.C. 103 as being obvious over Erbe (WO 2019/014491 A1), in view of Matsuda et al. (ACS Chem. Biol. 2015, 10, 1181−1187), and Dulz et al. (Ophthalmic Genetics, 39, 2, 2018, 275-277).
The applied reference (Erbe) has a common inventor and assignee 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) and (a)(2).
Erbe teaches a siRNA targeting the human HAO1 gene (AD-65585) wherein the antisense strand is 100% identical to instant SEQ ID NO: 36 including the modification pattern and the sense strand is 100% identical to instant SEQ ID NO: 35 including the modification pattern. Erbe teaches that ALN-GO1 refers to the GalNac version of AD-65585 (see Example 1, page 101) (instant claim 1).
Erbe teaches that: Primary Hyperoxaluria Type 1 (PH1) is an autosomal recessive disorder of glyoxylate metabolism. Hepatic glyoxylate detoxification is impaired due to mutation of the AGXT gene, which encodes the liver peroxisomal alanine-glyoxylate aminotransferase (AGT) enzyme. AGT1 is the final enzyme in the metabolic breakdown of hydroxy proline. Loss of AGT function to convert the intermediate metabolite glyoxylate to glycine causes accumulation and reduction of glyoxylate to glycolate which is oxidized to oxalate by the enzyme glycolate oxidase (GO), also known as hydroxy acid oxidase (HAO1). Regulation of glyoxylate, the key precursor of oxalate, occurs at multiple cellular sites including the mitochondria, peroxisome and the cytosol. Excess oxalate in PHI patients is unable to be fully excreted by the kidneys leading to the formation and deposition of calcium oxalate crystals in the kidneys and urinary tract. Renal damage is caused by a combination of tubular toxicity from oxalate, nephrocalcinosis and renal obstruction by stones. Greater than 30% of patients advance to end stage renal disease (ESRD (page 1) (instant claim 79).
Erbe teaches that PH1 is a kidney stone forming disease (page 96). Application of the method to a recurrent kidney stone disease as recited in instant claim 5 is considered to be a matter of design choice given that Erbe teaches treating a kidney stone disease via the method. Certainly one would want to treat the disease if it is recurrent. Additionally, application of the method to a patient that has had surgery to remove a kidney stone as recited in instant claim 78 is considered to be a matter of design choice because certainly one would want to treat a patient having PH1 if they have already had a kidney stone removed and still require treatment for PH1. Erbe teaches a method of treating PH1 via delivery of the RNAi agent inhibiting the expression of HAO1 (abstract) (instant claim 1).
Erbe teaches: The present invention provides methods using RNAi agents, e.g., double-stranded iRNA agents, targeting HAO1 for inhibiting HAO1 expression, for treating HAO1 associated disorders, e.g. , PH1, and for increasing plasma glycolate and reducing urinary oxalate in a human subject (instant claim 4).
Therefore, Erbe teaches a method for treating a subject suffering from a kidney stone disease, PH1, the method comprising administering the instantly recited siRNA (instant claim 1).
Regarding determination of the presence or absence of a heterozygous AGXT loss-of-function gene variant, Erbe teaches that hepatic glyoxylate detoxification is impaired in PH1 due to mutation of the AGXT gene (page 1). Therefore, it would have been obvious to screen for mutation of the AGXT gene for diagnosis of PH1 before treatment with the siRNA.
Additionally, since Erbe teaches loss of AGT function to convert the intermediate metabolite glyoxylate to glycine causes accumulation and reduction of glyoxylate to glycolate which is oxidized to oxalate by the enzyme glycolate oxidase (GO), also known as hydroxy acid oxidase (HAO1), it would have been obvious to screen for an AGXT loss-of-function gene variant for diagnosis of PH1 before treatment with the siRNA. Erbe teaches diagnosis methods of PH1 (page 96).
Erbe teaches conjugation to a GalNAc ligand identical to the instantly recited structures (see Example 1, page 101, and the structures on pages 45-46) (instant claims 27 and 81). Erbe teaches attachment via a bivalent or trivalent linker (pages 43-44) (instant claim 80).
Although Erbe et al. does not recite the specific structure in instant claim 82, this was a known siRNA-GalNac conjugate schematic, as taught by Matsuda et al. (Figure 1) (instant claims 82 and 83). It would have been obvious to utilize this conjugate schematic in the method of Erbe because Matsuda et al. teaches that efficient receptor binding and hepatocellular uptake require multiple GalNAc units in close proximity as present in this schematic, as well as the schematic of Erbe.
Erbe teaches incorporation of various pharmaceutically acceptable salts including sodium counterions, for example sodium chloride (pages 60-61) (instant claim 84).
Erbe teaches that the pharmaceutical composition (instant claim 72) can be delivered subcutaneously (page 59) (instant claim 85).
Erbe teaches incorporation of an addition therapeutic (page 85) (instant claim 73).
Erbe recites: A method of treating a human subject having Primary Hyperoxaluria Type 1 (PHI), the method comprising subcutaneously administering to the subject quarterly doses of at least 2.0, at least 3.0, at least 4.0, or at least 5.0 mg ALN-GO1 per kg body weight of the subject (therapeutically effective amount as required in instant claim 1), thereby treating the subject, wherein a urinary oxalate excretion of the subject is reduced by at least 50% after treatment and/or a plasma glycolate level of the subject is increased and sustained until at least day 75 after treatment and/or a GO enzyme of the subject is inhibited by at least 90% after treatment compared to before treatment (claim 1).
Although Erbe offers motivation to screen for a loss-of-function gene variant of AGXT, Erbe does not teach determination of the presence of any specific heterozygous AGXT loss-of-function gene variant.
However, Dulz et al. teach that primary hyperoxaluria type 1 (PH1) is a rare congenital metabolic disorder of the glyoxylate pathway, which manifests with nephrocalcinosis, urolithiasis, and end-stage renal failure (ESRD) as well as deposition of oxalate crystals within ocular tissues. Dulz et al. teach siblings with PH1 with identical compound heterozygous alanine-glyoxylate aminotransferase (AGXT) mutations (background).
Dulz et al. teach patients with genetically confirmed heterozygous loss-of-function AGXT mutation (c.364C>T (p.R122X) and c.33dupC) (materials and methods). Therefore, Dulz et al. is evidence that such mutations were known to be present in PH1 patients. It would have been obvious to detect any known AGXT mutation before treatment of PH1 as a matter of design choice given that the relationship between AGXT mutation and PH1 was known, as evidenced by both Erbe and Dulz et al.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Amy R Hudson whose telephone number is (571)272-0755. The examiner can normally be reached M-F 8:00am-6:00pm.
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/AMY ROSE HUDSON/Primary Examiner, Art Unit 1636