Prosecution Insights
Last updated: April 19, 2026
Application No. 17/854,283

Methods Of Treating Asthma With Solute Carrier Family 27 Member 3 (SLC27A3) Inhibitors

Final Rejection §101§112
Filed
Jun 30, 2022
Examiner
KAPUSHOC, STEPHEN THOMAS
Art Unit
1683
Tech Center
1600 — Biotechnology & Organic Chemistry
Assignee
Regeneron Pharmaceuticals, Inc.
OA Round
2 (Final)
47%
Grant Probability
Moderate
3-4
OA Rounds
3y 11m
To Grant
99%
With Interview

Examiner Intelligence

Grants 47% of resolved cases
47%
Career Allow Rate
340 granted / 728 resolved
-13.3% vs TC avg
Strong +53% interview lift
Without
With
+52.9%
Interview Lift
resolved cases with interview
Typical timeline
3y 11m
Avg Prosecution
58 currently pending
Career history
786
Total Applications
across all art units

Statute-Specific Performance

§101
23.1%
-16.9% vs TC avg
§103
21.0%
-19.0% vs TC avg
§102
14.9%
-25.1% vs TC avg
§112
32.1%
-7.9% vs TC avg
Black line = Tech Center average estimate • Based on career data from 728 resolved cases

Office Action

§101 §112
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 Office Action is in reply to Applicants’ correspondence of 12/05/2025. Applicants’ remarks and amendments have been fully and carefully considered but are not found to be sufficient to put the application in condition for allowance. Any new grounds of rejection presented in this Office Action are necessitated by Applicants’ amendments. Any rejections or objections not reiterated herein have been withdrawn in light of the amendments to the claims or as discussed in this Office Action. This Action is made FINAL. Please Note: The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action. Withdrawn Claim Rejections - 35 USC § 112 - Indefiniteness The rejection of claims under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as set forth on pages 2-3 of the Office Action of 09/10/2025, is withdrawn in light of the amendments to the claims. Withdrawn Claim Rejections - 35 USC § 101 The rejection of claims under 35 U.S.C. 101, as set forth on pages 3-6 of the Office Action of 09/10/2025, is withdrawn in light of the amendments to the claims. Claim Rejections - 35 USC § 112 – Written Description Maintained in Part, Modified as Necessitated by Claim Amendments Claims 17-26, 28, 35 and 42-48 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. “[T]he purpose of the written description requirement is to ‘ensure that the scope of the right to exclude, as set forth in the claims, does not overreach the scope of the inventor’s contribution to the field of art as described in the patent specification.” Ariad Pharm., Inc. v. Eli Lilly & Co., 598 F.3d 1336, 1353-54 (Fed. Cir. 2010) (en banc) (quoting Univ. of Rochester v. G.D. Searle & Co., 358 F.3d 916, 920 (Fed. Cir. 2004)). To satisfy the written description requirement, the specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. Vas-Cath, Inc. v. Mahurkar, 935 F.2d 1555, 1562-63, 19 USPQ2d 1111 (Fed. Cir. 1991). See also MPEP 2163.04. For a claim to a genus, a generic statement that defines a genus of substances by only their functional activity does not provide an adequate written description of the genus. Reagents of the University of California v. Eli Lilly, 43 USPQ2d 1398 (CAFC 1997). The Federal Circuit has cautioned that, for claims reciting a genus of antibodies with particular functional properties, ‘‘[c]laiming antibodies with specific properties, e.g., an antibody that binds to human TNF-α with A2 specificity, can result in a claim that does not meet written description even if the human TNF-α protein is disclosed because antibodies with those properties have not been adequately described." Centocor Ortho Biotech Inc. v. Abbott Labs., 97 USPQ2d 1870, 1875, 1877-78 (Fed. Cir. 2011). ‘‘[A] sufficient description of a genus . . . requires the disclosure of either a representative number of species falling within the scope of the genus or structural features common to the members of the genus so that one of skill in the art can ‘visualize or recognize’ the members of the genus.” Ariad, 598 F.3d at 1350 (quoting Eli Lilly, 119 F.3d at 1568-69). A ‘‘representative number of species” means that those species that are adequately described are representative of the entire genus. AbbVie Deutschland GMBH v. Janssen Biotech, 111 USPQ2d 1780, 1790 (Fed. Cir. 2014). Thus, when there is substantial variation within the genus, one must describe a sufficient variety of species to reflect the variation within the genus to provide a "representative number” of species. The "structural features common to the members of the genus” needed for one of skill in the art to ‘visualize or recognize’ the members of the genus takes into account the state of the art at the time of the invention. For antibodies, the Federal Circuit has found that possession of a mouse antibody heavy and light chain variable regions provides a structural "stepping stone" to the corresponding chimeric antibody, but not to human antibodies. Centocor, 97 USPQ2d at 1875. The rejected claims are drawn to methods that require detecting a SLC27A3 variant that is “associated with a decreased risk of developing asthma” (as recited in each of claims 17 and 22). Relevant to the breadth of genetic structures encompassed by the claims, the specification (p. 7-8) teaches: “In some embodiments, the SLC27A3 variant nucleic acid molecule encoding an SLC27A3 predicted loss-of-function polypeptide is associated with a reduced in vitro response to SLC27A3 ligands compared with reference SLC27A3. In some embodiments, the SLC27A3 variant nucleic acid molecule encoding an SLC27A3 predicted loss-of-function polypeptide is an SLC27A3 variant that results or is predicted to result in a premature truncation of an SLC27A3 polypeptide compared to the human reference genome sequence. In some embodiments, the SLC27A3 variant nucleic acid molecule encoding an SLC27A3 predicted loss-of-function polypeptide is a variant that is predicted to be damaging by in vitro prediction algorithms such as Polyphen, SIFT, or similar algorithms. In some embodiments, the SLC27A3 variant nucleic acid molecule encoding an SLC27A3 predicted loss-of-function polypeptide is a variant that causes or is predicted to cause a nonsynonymous amino-acid substitution in SLC27A3 and whose allele frequency is less than 1/100 alleles in the population from which the subject is selected. In some embodiments, the SLC27A3 variant nucleic acid molecule encoding an SLC27A3 predicted loss-of-function polypeptide is any rare variant (allele frequency< 0.1%; or 1 in 1,000 alleles), or any splicesite, stop-gain, start-loss, stop-loss, frameshift, or in-frame indel, or other frameshift SLC27A3 variant.” The specification further provides a table of “SLC27A3 variants that can be used in the aggregate burden analysis”, as set forth on pages 29-89. While the structures of the mutation encompassed by the claims are generically broad, here it is noted that even with regard to the specifically disclosed mutations it is not clear that which of the particular disclosed variations are individually “associated with a decreased risk of developing asthma”. For example, rs1444740227 (identified as 1:153775126:C:T on page 29) is a variant that is upstream of the SCL27A3 gene, and it is not clear that there is any loss-of-function associated with alleles of the SNP. Even when a disclosed variant may encode a nonsynonymous mutation, it is not clear that such a mutation is itself specifically associated with pathology risk because the conclusion that SLC27A3 is associated with asthma is based on an aggregate burden of all variants in the SLC27A3 gene in cases versus controls. So it is not clear than any particular allele is found to be overrepresented in cases versus control. Even when considering mutations/allele with protein coding implications, the claims encompass variants causing the substitution of amino acid residues with conversative substitutions, which may have little or no effect on protein function, is known in the art (e.g.: French et al, 1983). It is further not clear which of the particular mutations disclosed in the specification may actually be overrepresented in cases versus control, and thus considered associated with decreased risk of developing asthma. The specification only discloses an aggregate analysis of mutation burden in a subject (e.g.: p.89-90 of the specification). Thus while the disclosure (p.109) asserts that “a novel association between lower risk of childhood asthma and a burden of rare pLOFs and deleterious variants was discovered in SLC27A3 (3,787 carriers; OR=0.65, 95% CI 0.55 to 0.76, P=8.2x10-8)” The disclosure does not teach which of the broadly encompassed mutations are in fact identified in case subjects with asthma or control individuals without asthma. Here it must also be noted the claims encompass a significantly large genus of any possible single or multiple nucleotide insertion, deletion or substitution in the coding or non-coding region of the SLC27A3 gene; and that the size of the genus is further compounded by the fact that the claims encompass detecting the SLC27A3 genetic variant in any subject, including non-human subjects. However, the specification does not describe in terms of its complete structure or other relevant identifying characteristics a representative number of SLC27A3 mutations that cause a LOF, which also have the functional attribute that they are associated with decreased risk of asthma. It is acknowledged that the specification teaches the general methodology for sequencing and performing association studies. However, possession may not be shown by merely describing how to obtain possession of members of the claimed genus or how to identify their common structural features. While the Federal Circuit has recognized that “the written description requirement can in some cases be satisfied by functional description,” it has made clear that “such functional description can be sufficient only if there is also a structure-function relationship known to those of ordinary skill in the art.” In re Wallach, 378 F.3d 1330, 1335 (Fed. Cir. 2004). Herein, the claims recite a functional description of the SLC27A3 genetic variants but do not identify a clear structure-function relationship – i.e., do not disclose a clear structure of SLC27A3 variants that perform a function that results in the decreased risk of asthma. With respect to the present invention, there is no record or description which would demonstrate conception of a representative number of SLC27A3variants that are associated with decreased risk of asthma. Therefore, the claims fail to meet the written description requirement because the claims encompass a significantly large genus of inhibitors and SLC27A3 variants which are not described in the specification. Response to Remarks Applicants have traversed the rejection of claims under 35 USC 112(a) as maintained above. Applicants’ arguments (p.8-10 of the Remarks of 12/05/2025) have been considered but are not persuasive to withdrawn the rejection. Relevant to the maintained rejection, Applicants have argued that the specification “discloses numerous SLC27A3 variant nucleic acid molecules encoding predicted loss-of-function variant polypeptides associated with a decreased risk of developing asthma.” This argument is not persuasive. The claims generically encompass any nucleic acid structures that are any variations in the SLC27A3 nucleic acid sequence. And while the specification teaches numerous particular mutations, the disclosure of these particular alterations is not informative of any other different variations that may be found in a sample for a subject. The nature of alleles is that they are variant structures occurring in genomes of individuals from a population; and in the present state of the art, the structure of one allele does not provide guidance to the existence or structure of any other alleles. Additionally, as noted above, the disclosure of the application is not a teaching of the association with asthma risk of any one individual allele. The teachings of the specification are related to an association with asthma (or lack of asthma) when considering the variants in aggregate between cases and control. Thus while the conclusion is that, broadly speaking, there is an association between SLC27A3 gene content and asthma risk, there is no teaching pertaining to risk associated with any individual mutation, variant, or allele. Conclusion Claims 17-26,28,35 and 42-46 remain rejected. Claims 1, 2 and 10 are allowed. The methods of the allowed claim are directed to the treatment of a subject having asthma, exercise-induced bronchoconstriction, or asthma-COPD asthma-chronic obstructive pulmonary disease (COPD) overlap syndrome (ACOS) or at risk of developing asthma, exercise-induced bronchoconstriction, or ACOS with an SLC27A3 inhibitor comprising an inhibitory nucleic acid molecule that hybridizes to an SLC27A3 nucleic acid molecule. The prior art does not teach or suggest treating a subject with the recited pathology using an inhibitory nucleic acid molecule that hybridizes to an SLC27A3 nucleic acid molecule. The teachings of the specification support the conclusion that SLC27A3 plays a role in the pathologies recited in the claims. THIS ACTION IS MADE FINAL. 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. Any inquiry concerning this communication or earlier communications from the examiner should be directed to STEPHEN THOMAS KAPUSHOC whose telephone number is (571)272-3312. The examiner can normally be reached M-F, 8am-5pm. Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Anne Gussow can be reached at 571-272-6047. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300. Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000. Stephen Kapushoc Primary Examiner Art Unit 1683 /STEPHEN T KAPUSHOC/Primary Examiner, Art Unit 1683
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Prosecution Timeline

Jun 30, 2022
Application Filed
Sep 06, 2025
Non-Final Rejection — §101, §112
Dec 05, 2025
Response Filed
Mar 05, 2026
Final Rejection — §101, §112 (current)

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Study what changed to get past this examiner. Based on 5 most recent grants.

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Prosecution Projections

3-4
Expected OA Rounds
47%
Grant Probability
99%
With Interview (+52.9%)
3y 11m
Median Time to Grant
Moderate
PTA Risk
Based on 728 resolved cases by this examiner. Grant probability derived from career allow rate.

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