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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 10/10/2025 has been entered.
Claim Status
Amended claims 1, 2, 17-19, 21-22, 38-40, 42-43 are pending and examined here, along with the following species: 1) hypertension, 2) Arg171Trp-Long, 3) genomic nucleic acid molecule of SEQ ID NO: 2 with thymine (T) at position 9519.
Priority
The application’s benefit to U.S. provisional applications 63/217,909 and 63/221031, filed on 07/02/2021 and 07/13/2021, respectively, is recognized. All claims enjoy the benefit of ‘909 filing date.
Nucleotide and/or Amino Acid Sequence Disclosures
The objection is withdrawn. The specification of 10/10/2025 displays SEQ ID NOs for sequences longer than 9 nt. of Table beginning on pg. 32.
Claim Rejections - 35 USC § 112
Rejection of claims 1, 2, 17-19, 21-22, 38-40, and 42-43 for lacking enablement requirement is maintained.
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, 2, 17-19, 21-22, 38-40, and 42-43 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 enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
When considering the scope of enablement, the Wands factors need to be reviewed, which poses whether the experimentation needed to practice the invention is undue or unreasonable. Determining undue experimentation requires analysis of, but 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 the instant case:
The breadth of the claims: The claims are drawn to a method of treating a subject having any type of elected hypertension or at risk of developing any type of hypertension by decreasing expression of SLC9A3R2 polypeptide in the subject, the method comprising administering to a subject a Solute Carrier Family 9 Isoform A3 Regulatory Factor 2 (SLC9A3R2) inhibitor, wherein the inhibitor comprises any inhibitory, modified nucleic acid molecule (NAM), which comprises antisense nucleic acid molecule (ASN), siRNA, or shRNA that hybridizes to an SLC9A3R2, wherein the subject is SLC9A3R2 reference or is heterozygous for an SLC9A3R2 missense variant nucleic acid molecule encoding the elected Arg171Trp-Long. Cl. 2 limits hypertension to secondary, resistant or malignant hypertension; cl. 17 recites method of cl. 1 further comprising detecting the presence or absence of SLC9A3R2 missense variant nucleic acid molecule encoding an SLC9A3R2 predicted loss-of-function polypeptide in a biological sample from the subject; cl. 18 further comprising administering any therapeutic agent for treating hypertension wherein the SLC9A3R2 missense variant nucleic acid molecule is absent; cl. 19 is to administer a recited dose of therapeutic agent that treats hypertension to a subject heterozygous for the SLC9A3R2 missense variant; cl. 21 limits SLC9A3R2 missense variant to recited encoded variants, cl. 22 recites an elected genomic variant according to SEQ ID NO: 2; Cl. 38-40, 42-43 recite a method of treating a subject with any therapeutic agent treating the elected hypertension, wherein the subject with hypertension or is at risk of developing hypertension by decreasing expression of a SLC9A3R2 polypeptide in a cell in the subject, the method comprising determining whether the subject has a SLC9A3R2 missense variant nucleic acid molecule encoding the recited variants, by obtaining sample from the subject, conducting sequencing of the sample, genotyping for one of the recited SLC9A3R2 missense variants; and administering or continuing to administer the therapeutic agent that treats elected hypertension to the subject who is SLC9A3R2 reference or is heterozygous for the recited SLC9A3R2 missense variants and/or administer SLC9A3R2 inhibitory, modified nucleic acid molecule, which is any ASN, siRNA or shRNA that hybridizes to an SLC9A3R2 nucleic acid molecule; cl. 43 recites SLC9A3R2 missense variant nucleic acid molecule is genomic nucleic acid according to SEQ ID NO: 2.
The nature of the invention: The invention is treating a subject with hypertension or at risk of hypertension by administering any therapeutic agent that treats elected hypertension and/or any recited SLC9A3R2 inhibitory, modified nucleic acid molecule, wherein the subject is SLC9A3R2 reference or is heterozygous for the SLC9A3R2 missense variant nucleic acid molecules encoding one of the recited variant, the method further comprising obtaining a sample from a subject, sequencing the sample, and genotyping for SLC9A3R2 missense variant encoding for the recited SLC9A3R2 missense variants for the subject that has or is at risk of developing hypertension.
The state of the prior art: Solute Carrier Family 9 Isoform A3 Regulatory Factor 2 (SLC9A3R2, also called Na+/H+ exchanger regulatory factor-2 (NHERF2) and the abbreviation will be used interchangeably) is a scaffolding protein that binds to Na+/H+ exchanger 3 (NHE3) (par. 4). NHEs, involved in sodium absorption, have been suggested to be involved in pathogenesis of hypertension (Kobayashi, 2004, pg. 1723). NHERF2 is localized in the kidney, amongst other tissues, and is co-localized with a complex of other proteins (par. 4). NHERF2 also plays a role in intestinal sodium absorption by regulating the activity of the NHE3 and may also regulate cystic fibrosis transmembrane regulator (CFTR) ion channel (par. 4).
Various studies have been conducted to understand the role of SLC9A3R2.
Genome Wide Studies: Genome/exome studies have identified the protective association with a loss-of-function variant of NHERF2 (Giri, in IDS). Further, Shiffman (US20170292159, pub. 10/12/2017, of record) indicate association of many genetic polymorphisms and cardiovascular diseases, including myocardial infarction and hypertension, and disclose a method of determining an altered risk for cardiovascular disease in humans following genotype testing to determine presence of single nucleotide polymorphism (SNP), including of SLC9A3R2 (abstract, cl. 1, see table 21 and table 22 for SLC9A3R2). But neither appears to disclose the claimed, elected variant (Arg171Trp-Long).
Non-GWAS studies: A mouse model of spontaneous/genetic hypertensive rats (SHR) was studied for understanding the pathophysiology of hypertension (Kobayashi, 2004, p. 1723). Since it is known that NHE3 has an essential role in sodium reabsorption, Kobayashi studied whether the family of NHERF scaffolding proteins (specifically NHERF1 and NHERF2) play a role in regulating NH3 in SHR (Kobayashi, pg. 1723-1724). In SHR, Kobayashi evaluated the activity of NHE (Na/H exchanger) and NHERF1 and NHERF2 expression levels in the kidney (Abstract). The authors concluded that decreased expression of NHERF1 may be related to the enhanced NHE activity in SHR and that these changes are likely to be genetically determined, whereas the increased NHERF2 expression may be induced as a compensatory mechanism for the genetic abnormality and “increased NHERF2 expression was not induced by hypertension” (Kobayashi, 2004, pg. 1729, 1727). This raises the question of whether reduction in NHERF2 would treat hypertension in SHR animals.
The level of predictability in the art:
Regarding the lack of studies associated with inhibitory nucleic acid molecules: One skilled in the art understands that considering only the canonical siRNA of 21 nt. for a target of SLC9A3R2 nucleic acid molecule (SEQ ID NO: 3 is identified as a reference sequence and is 2160 nt.) there is a possibility of some 2,139 siRNAs. Gavrilov (2012, Yale J. Biol. Med., 85, pg. 187-200) discloses that siRNA therapeutic is “extremely promising” but needs to overcome a number of intracellular and extracellular barriers, including siRNA stability and targeting, off-target silencing and its activation of immune response, delivery of the siRNA therapeutic to the target cell (pg. 190-192). Although these barriers can be addressed e.g. by improving stability by modifying the naked siRNA (it is noted that the specification provides a generic modification pattern for modifying a siRNA, see par. 52), identifying a carrier to deliver the siRNA therapeutic, there is still need of further testing. One of skill in the art is aware of many platforms that identify exemplary siRNAs, however, Gavrilov points out that “[o]ff-target silencing cannot be ignored in developing siRNA-based therapeutics, and all potential therapeutic siRNA candidate sequences must be heavily tested for perturbation of normal protein expression profiles” (pg. 191). Thus, the enablement requirement for methods of treatment with siRNAs is not met merely by identifying a functional siRNA. The state of the art calls for further testing to establish therapeutic efficacy. Thus, testing would be required to identify an efficient therapeutic siRNA or even one able to decrease expression of SLC9A3R2 effectively in a subject, and further a therapeutic siRNA would require heavy testing to potentially overcome the barriers noted above.
Exome sequencing studies – Although genome/exome sequence studies are gaining in prominence due to reduced costs, there are still issues concerning the causal link that is suggested between the genetic variation and a disease phenotype. Burgess et al. (2018, Ann. Rev. of Genomics and Human Genetics, 19, 303-327) disclose that an observational correlation between a suspected risk factor and an outcome does not necessarily imply that interventions on levels of risk factor will have a causal impact on the outcome (correlation is not causation) (Abstract). It could be an issue of confounders, common determinants of the risk factor and the outcome, that give rise to the association (pg. 305).
Further, even the specification discloses that an initial “low frequency missense variant in SLC9A3R2 (r5139491786, Arg171Trp, MAF=0.7%) was previously identified in a GWAS of blood pressure, but the signal was attributed to the nearby PKD1 gene variant (r5140869992, Arg2200Cys)” (par. 304). Thus, there is also an issue of mis-identifying the signal to a different gene variant.
Disease- As the specification points out, the cause of high blood pressure is unknown, but involves an interplay between many factors, include hormone systems, central-nervous system, stress, physical work and genetic influences/predisposition, and “derailment of one or more [these] systems results in high blood pressure” (par. 3). Thus, although it is potentially possible that targeting a single gene may be sufficient to control blood pressure, but without
All these issues in this section point to unpredictability in the art: NHERF2 is not clearly associated with hypertension and as Kobayashi demonstrated that the increased NHERF2 expression may be induced as a compensatory mechanism; and although siRNAs targeting NHERF2 are known, that does not equate to a predictable efficient therapeutic siRNA without carrying out further tests as pointed out by Gavrilov; association from genome wide studies are not causal but a correlative one as pointed out by Burgess; and on rare occasion, the positive signal is from a different gene, thus introducing another unpredictable factor based on the platform used to identify the association.
The amount of direction provided by the inventor/existence of working examples: The specification discloses an exome sequencing study of some ~450, 000 participants, where “a novel association was identified between a lower risk of hypertension and a burden of rare pLoFs and deleterious missense variants in SLC9A3r2)” (par. 303). Table 2 provides analysis of the association of deleterious missense variants of SLC9A3R2, which are the recited claimed subject matter.
MPEP 2164.03 indicates that more that is known in the prior art about the nature of the invention, how to make, and how to use the invention, and the more predictable the art is, the less information needs to be explicitly stated in the specification. In contrast, if little is known in the prior art about the nature of the invention and the art is unpredictable, the specification would need more detail as to how to make and use the invention in order to be enabling.
Here, the specification fails to, first, disclose a single, functional therapeutic claimed inhibitory nucleic acid molecule that binds to SLC9A3R2 and inhibits its expression in a subject, second, fails to disclose an example of a method of treating a subject with claimed conditions or at risk of claimed conditions by administering claimed inhibitory nucleic acid molecule, wherein the subject is SLC9A3R2 reference (lacks claimed SCL9A3R2 missense variant) or is heterozygous for a claimed SCL9A3R2 missense variant; and third, fails to disclose an example demonstrating that one of the claimed variants is protective in a subject with the claimed conditions. Further, even the specification indicates identification of “[a] burden of rare putative loss-of-function (LOF) and deleterious missense variants in the SLC9A3R2 gene associated with decreased risk of developing hypertension” (pg. 7, line 29-30). Thus, due to its rarity and being a putative LoF variant indicates a certain level of unpredictability and further information is required, such as whether the claimed variant(s) when expressed is indeed a LoF variant or whether its expression results in the indicated protective features. Data from suggested studies would provide information that would aid in removing unpredictability of the claimed subject matter. The lack of information noted above results in the art of the claimed subject matter being unpredictable, and consequently, the specification does not disclose sufficient enabling guidance of making claimed inhibitory nucleic acid molecule targeting SLC9A3R2 and using an inhibitory nucleic acid molecule of SCL9A3R2 in treating hypertension in a subject carrying SLC9A3R2 reference or its recited heterozygous variant(s).
The quantity of experimentation: Here the specification does not provide if a) predicted loss of function (pLoF) is an actual a loss-of-function mutation, i.e. a shortened mutant polypeptide; b) any functional studies demonstrating a causal link between the genetic variants and their protective nature, either in vivo or in vitro; c) or how the mutations are able to lower the risk of hypertension or hypertension, including studies to demonstrate suppression of SLC9A3R2 reduces hypertension or risk of hypertension; d) the specification also fails to identify an optimal or any inhibitory nucleic acid molecule that inhibits SLC9A3R2 in vivo or in vitro. Thus, there would be a need to conduct numerous undue experiments to practice the recited claims.
Thus, here the method of treating a subject by reducing the expression of SLC9A3R2 in a subject having hypertension or at risk of developing hypertension, the method comprising administering SLC9A3R2 inhibitor comprising a modified, inhibitory nucleic acid molecule, where in the subject is SLC9A3R2 reference or is heterozygous for claimed SLC9A3R2 variant recited in claimed subject matter would require unreasonable experimentation.
Response to Arguments
Applicant's arguments filed 10/10/2025 (“the Remarks”) have been fully considered but they are not persuasive.
The Remarks pg. 7-11 appears to be a copy of arguments made in previous Remarks of 07/11/2025, pg. 8-12, and have been addressed in the Advisory Action of 07/31/2025 (“the Advisory Action”).
The Remarks makes several arguments against the comments of the Advisory Action:
The Remarks note that a few examples noted from Khvorova to illustrate unpredictability “overstates the unpredictability and understates the sufficiency of the present disclosure” (pg. 12): Fig. 10b shows variation and not unpredictability of Khvorova’s rationale design, which “yields reproducible functional outcomes and increase the likelihood of effective silencing” (pg. 12-13). Further instant specification provides “general approach for siRNA design” along with additional methodology that is sufficient for a skilled artisan to practice instant claimed subject matter (pg. 13). Further, “[a]pplicant’s working examples establish a general correlation between disclosed structural features and the resulting inhibitory function” and thus the disclosure of predictive framework, multiple sequences, and empirical validation satisfies the Wands factor (pg. 13).
Proof of clinical efficacy is not required to demonstrate enablement. It is misguided to conflate enablement with “proof of clinical efficacy” and imposes a higher than required threshold, since the specification provides “ample molecular and functional guidance, including genetic data linking SLC9A3R2 to blood pressure regulation, hypertension and detailed antisense and detailed siRNA methodologies” (pg. 13).
The Office’s characterization of correlation versus causation is scientifically misplaced failing to consider the “mechanistic data disclosed,” i.e. a causal link between SLC9A3R2 modulation and blood pressure homeostasis by identifying functional variants (e.g. Arg171Trp) that affect sodium-hydrogen exchange activity (pg. 14). Further Curtis “reports a strong, statistically significant association (SLP=12.28) confirming that SLC9A3R2 variants are risk-lowering for hypertension” (pg. 14).
Curtis’s reported ‘difficulty in replication’ pertains to population-level statistical associations between genetic variants and phenotypic outcomes, not unpredictability in RNA interference or molecular inhibition” (pg. 14)..
Regarding the use of Chen, the Remarks note that pulmonary arterial hypertension is a distinct and more complex cardiopulmonary disease with different underlying molecular pathways than systemic hypertension as claimed (pg. 15). Since Chen does not disclose gene-silencing approach it is not relevant to RNA-based enablement and merely validates non-relevant genes as potential biomarkers thus has no bearing on unpredictability in antisense or siRNA design (pg. 15).
The argument is not persuasive.
Addressing argument 1) it is simply noted that Khvorova does not provide any examples of siRNAs targeting SLC9A3R2 nor does the instant specification detail any sequence of claimed inhibitory nucleic acid molecule, which is only one step in a multi-method claimed subject matter. Regardless of how the Applicant wants to designate the differences noted, Khvorova does not cure the unpredictability. Khvorova’s disclosure of designing siRNA is not a simple “plug and play,” e.g., the seventh embodiment (par. 60) requires “measuring the gene silencing ability of each siRNA from said set” (par. 60, (b); see also cl. 14) and then determining the amount of improved functionality by the presence or absence of at least one variable noted (par. 60, (c)). Thus, the design/algorithm embodiment requires “measuring” of silencing ability; the specification does not even provide a starting point in terms of a siRNA molecule since it does not provide a single claimed inhibitor. A skilled artisan would need to start from scratch and as noted in the Action above, based on the size of the target transcript, there are some potentially 2,139 siRNAs. Thus the disclosure requires an undue experimentation to identify a claimed inhibitory nucleic acid molecule targeting SLC9A3R2 to treat a subject with SLC9A32 reference genotype and having or at risk of claimed diseases.
Addressing argument 2) the Office is not requiring proof of clinical efficacy nor is raising the required enabling threshold. Clinical study of SLC9A3R2’s association with claimed hypertension or heart-related diseases/conditions would reduce the uncertainty. Clinical efficacy is just one of the factors that is analyzed under the Wands factor. The “genetic data linking SLC9A3R2 to blood pressure regulation, hypertension” appears to be an association and not a causation and uncertainty remains whether inhibiting SLC9A3R2 would treat a subject with misregulated blood-pressure/hypertension. The specification does not disclose the protein levels of SLC9A3R2 in subjects to illustrate decreased levels of SLC9A3R2 expression in subject heterozygous/homozygous for claimed variant compared to SLC9A3R2 reference patients, which would be another correlative factor that would also remove uncertainty. Here, little is known in the art thus more detail is required, and thus undue experimentation is required.
Addressing argument 3) Examiner did not mis-characterize the “mechanistic data” disclosed, the art does not consider GWAS-studies to provide causal link but rather an association between a genotype and a phenotype. A strong, statistical association between claimed SLC9A3R2 variant and claimed disease is not a causal link and, even if it is, it is still a single data point, which may not be sufficient to remove the uncertainty surrounding such a broad claimed subject matter: that administration of any SLC9A3R2 nucleic acid inhibitor molecule will treat any type of hypertension in a subject with SLC9A3R2 reference genotype, when the specification does not disclose a single, claimed SLC9A3R2 nucleic acid inhibitor molecule that is able to decrease expression of SLC9A3R2 in a subject, nor show that a decrease in SLC9A3R2 expression treats hypertension.
Addressing argument 4), the Remarks do not adequately address the unpredictability raised by the Curtis study, which was unable to pick up an association between SLC9A3R2 and hypertension in a similar GWAS study. The purpose of Curtis is for the unpredictability in GWAS studies, not RNAi or molecular inhibition. The Remarks, first attempt to dismiss Curtis by noting that “difficulty in replication’ pertains to population-level statistical association between genetic variants and phenotypic outcomes,” (pg. 14), thus noting that there is unpredictability in statistics when dealing with population-genome, i.e. GWAS, study. Similar observation was noted in specification as noted in prior action of 5/12/25, pg. 10: that initial signal with statistical significance was attributed to another gene, PKD1. Further Burgess provides other reasons (confounders, common determinants of the risk factor and outcome) for the association (pg. 10 of 05/12/2025 Action). Thus GWAS-studies, in addition to being difficult to replicate, have other issues and thus adds uncertainty to the art, and thus undue experimentation is required to clear up the uncertainty.
Giri (of record) indicates that even if a signal can be replicated, the signal may be irrelevant following further statistical analysis. Giri discloses a SLC9A3R2 variant (rs139491786, an Arg60Trp variant) that was identified as a rare exonic variants with suggestive evidence of association from the discovery sample and the variant was picked up following query for a replication in populations from BioVU and BP-ICE (pg. 52). However, following conditioning against sentinel common variant: “SNP rs139491786 in SLC9A3R2 showed a >50% reduction in effect size after condition on common variant rs140869992” (pg. 52, also see Table 2). Thus, highlighting the unpredictability concerning GWAS studies.
Addressing argument 5), the Remarks attempt to distinguish one species of hypertension (pulmonary arterial hypertension [PAH]) from another (systemic hypertension), but broadly claims the genus of hypertension and, regardless, encompasses the claimed subject matter since a subject with PAH is at risk of developing hypertension and/or CHD (see cl. 1, 38). Chen demonstrates that SLC9A3R2 expression levels are significantly downregulated in PAH patients, thus introducing uncertainty in the art, i.e. reduced SLC9A3R2 levels do not appear to lower the risk of hypertension, thus administering SLC9A3R2 inhibitory nucleic acid molecule to decrease expression of SLC9A3R2 will not treat a patient with PAH since their SLC9A3R2 levels are already reduced compared to normal patients). Although Chen identified putative genes using neural network models (“computational diagnostic”), they followed it up with examining the expression levels in patients (see Fig. 9K). Here, the specification does not follow up their GWAS study with additional studies, such as comparing the expression levels of SLC9A3R2 in patients with SLC9A3R2 reference genotype and ones with claimed variants or even that the variants claimed are indeed dysfunctional proteins/peptides in a subject, which would also be a correlative data point. Thus, due to the uncertainty in the art, undue experimentation is required.
Thus, the rejection of examined claims is maintained.
Conclusion
All claims are identical to or patentably indistinct from, or have unity of invention with claims in the application prior to the entry of the submission under 37 CFR 1.114 (that is, restriction (including a lack of unity of invention) would not be proper) and all claims could have been finally rejected on the grounds and art of record in the next Office action if they had been entered in the application prior to entry under 37 CFR 1.114. Accordingly, THIS ACTION IS MADE FINAL even though it is a first action after the filing of a request for continued examination and the submission under 37 CFR 1.114. See MPEP § 706.07(b). 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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/KEYUR A VYAS/Examiner, Art Unit 1637
/Soren Harward/Primary Examiner, TC 1600
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