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 .
Application Status
This action is written in response to applicant’s correspondence received 18 June 2026. Claims 1, 3-21, and 33-36 are currently pending. Accordingly, claims 1, 3-21, and 33-36 are examined herein.
Any rejection or objection not reiterated herein has been overcome by amendment.
Applicant' s amendments have been thoroughly reviewed, but are not persuasive to place the
claims in condition for allowance for the reasons that follow.
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.
Claim(s) 1, 3, 9, 11-16, 18-20, and 33-35 is/are rejected under 35 U.S.C. 103 as being unpatentable over Nelson (PG Pub No. US 2014/0080896 A1) in view of Yokota (Muscle Gene Therapy: Methods and Protocols. Totowa, NJ: Humana Press, 2010. 299-312) and Sazani (US Patent No. 9,234,198 B1).
Regarding claims 1, 3, and 33-35 Nelson is directed towards a study concerned with methods for enhancing exon skipping in a pre-mRNA of interest, comprising contacting the pre-mRNA with an effective amount of a small molecule (Abstract). Nelson teaches that DMD is primarily caused by out-of-frame multi-exon deletions in the DMD gene that ablate dystrophin protein production ([0004]). Nelson teaches that utilizing antisense oligonucleotides to promote DMD exon skipping can restore dystrophin protein expression in mice, dogs, and humans ([0004]). Nelson teaches the use of an antisense oligonucleotide that is complementary to a splicing sequence of interest ([0037]). Nelson teaches that Table 6 comprises suitable DMD exons that can be shipped via the use of an antisense oligonucleotide and that a person of ordinary skill in the art can “readily design AO's [(i.e., antisense oligonucleotides)] specific for blocking the relevant splice sites […] without undue experimentation” ([0037], [0056]). Nelson teaches the use of suitable exons that can have antisense oligonucleotides designed to be complementary to DMD exons selected from an exon 6 of a DMD gene that is 170 base pairs in length and comprises a sequence that is complementary to and comprises 100% identity to the claimed SEQ ID NO: 1 (see SEQ ID NO: 23 in previously attached sequence alignment), an exon 7 of a DMD gene that is 119 base pairs in length and comprises a sequence that has 100% identity to the claimed SEQ ID NO: 4 (see SEQ ID NO: 24 in previously attached sequence alignment), and an exon 8 of a DMD gene that is 182 base pairs in length and comprises 100% identity to the claimed SEQ ID NO: 10 (see SEQ ID NO: 25 in previously attached sequence alignment) ([0056]-[0057]; see Table 6). Nelson teaches that the antisense oligonucleotide can be 10-50 nucleotides in length, and that in one embodiment the antisense molecules are about 17 to about 30 nucleotides in length ([0050]). Nelson teaches that the term “about” encompasses plus 10% of the indicated value ([0045]).
Nelson does not specifically teach the use of a nucleotide sequence complementary to a nucleotide sequence comprising at least 80% identity to the claimed SEQ ID NOs: 1, 4, or 10 (Claim 1). Nelson does not teach or suggest that the nucleic acid comprises a combination of a nucleotide sequence that targets the human DMD gene at exons 6 and 7 (Claim 2) or a combination of exons 6-8 (Claim 3). Nelson does not specifically teach the use of a nucleotide sequence complementary to a nucleotide sequence comprising the claimed SEQ ID NOs: 1, 4, or 10 (Claims 33-35).
However, one of ordinary skill in the art would have considered the teachings of Yokota and Sazani as both references are common fields of endeavor pertaining to the use of antisense oligonucleotides that can skip exons in a DMD gene.
Yokota is directed towards a study concerned with antisense oligonucleotide mediated multiple exon skipping in a dog model (Abstract). Yokota teaches that skipping exons 6-8 in a DMD model via the use of antisense oligonucleotides restored functional dystrophin protein production (pg. 306; see Fig. 1).
Sazani is directed towards an invention concerned with antisense molecules capable of binding to a selected target site in the human dystrophin gene to induce exon skipping (Abstract). Sazani teaches that it is possible to combine two or more antisense oligonucleotides together to induce multiple exon skipping and that the combination of antisense oligonucleotides improves multiple exon skipping (Col. 3, lines 40-49).
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to try to create a nucleic acid comprising a nucleotide sequence that is complementary to the nucleotide sequence comprising at least 80% identity to the sequences set forth in the claimed SEQ ID NOs: 1, 4, or, 10, as described by Nelson. A person of ordinary skill in the art would have recognized that Nelson identified a need in the art to generate antisense oligonucleotides that target and allow for the skipping of DMD exons and Yokota teaches that skipping exons 6-8 is beneficial and results in the production of functional dystrophin proteins. A person of ordinary skill in the art would have recognized that Nelson taught that there had been a finite number of possible antisense oligonucleotides that could be generated that are complementary to exons present in DMD exons 6-8 because Nelson teaches that exon 6 of the DMD gene only comprises 170 base pairs, exon 7 only comprises 119 base pairs, and exon 8 only comprises 181 base pairs alongside an explicit disclosure that in one embodiment the antisense molecule is 10-50 nucleotides in length or about 17 to about 30 nucleotides in length, wherein the term “about” encompasses plus 10% of the indicated value. Therefore, the amount of experimentation required to arrive at a nucleotide sequence that is complementary to the nucleotide sequence comprising at least 80% identity to the claimed SEQ ID NOs: 1, 4, or 10 is not large because Nelson provides evidence that all three exons are less than 200 base pairs in length and that antisense oligonucleotides targeting the exons can be designed such that they are 10-50 base pairs, or about 17 base pairs to about 30 base pairs, in length and tested to ensure that the antisense oligonucleotides induce skipping of a targeted exon without undue experimentation. A person of ordinary skill in the art would have recognized that the known potential solutions could have been pursued because Nelson explicitly states that a person of ordinary skill in the art can readily design antisense oligonucleotides specific for blocking the relevant splice sites present in the exons of Table 6.
Additionally, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify the antisense oligonucleotides of Nelson in view of Yokota such that the nucleic acid comprised nucleotide sequences that targeted exons 6-8 of a human DMD gene, as described by Sazani. A person of ordinary skill in the art would have been motivated to do so in order to improve multiple exon skipping of exons 6-8 in a human DMD gene. A person of ordinary skill in the art would have had a reasonable expectation of success because both Sazani and Nelson in view of Yokota teach the use of antisense oligonucleotides that can target human DMD genes and induce exon skipping.
Regarding claim 9, Nelson teaches that a dosage comprising the therapeutic agent (i.e., the antisense oligonucleotide ([0065])) may comprise a pharmaceutically acceptable carrier ([0068]).
Regarding claim 11, Nelson teaches that the disclosed antisense oligonucleotides can be administered to a subject to treat muscular dystrophy ([0057]).
Regarding claims 12-13, Nelson teaches that the antisense oligonucleotides may be administered to a subject via subcutaneous injection ([0063]).
Regarding claim 14, Nelson teaches that the muscular dystrophy may be Duchenne Muscular Dystrophy (i.e., DMD) ([0055]).
Regarding claim 15, Nelson teaches that DMD is caused by multi-exon deletions in the DMD gene that ablate dystrophin protein production ([0004]). Nelson teaches that administering effective doses of the antisense oligonucleotides results in an inducing at least a detectable amount of dystrophin expression with targeted removal of a given exon (i.e., the introduction of the antisense oligonucleotide results in an increased level of functional dystrophin protein when compared to a level of functional dystrophin protein produced prior to the introduction) ([0046]).
Regarding claim 16, Nelson teaches that the level of dystrophin protein production following administration of the antisense oligonucleotide can be measured via the use of Western blot ([0009]; see FIG. 3).
Regarding claim 18, Nelson teaches that dantrolene can be utilized as a modulator of antisense-mediated exon skipping in DMD ([0007]); Nelson teaches that dantrolene, when administered to a synergistically with an antisense oligonucleotide, resulted in improved muscle strength in mice ([0027]).
Regarding claim 19, Nelson does not teach that a 6 minute walk test was utilized to measure improved muscle function in a subject (Claim 19).
However, Nelson further teaches that previous studies had utilized a 6 minute walk test to subjects who received antisense oligonucleotides directed against DMD exon 51 ([0005]). Nelson teaches that the subjects who received the antisense oligonucleotides showed a modest improvement in the test ([0005]).
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to utilize a 6 minute walk test as a measurement of muscular dystrophy progression, as described by Nelson. A person of ordinary skill in the art would have been motivated to do so in order to utilize a known method of determining if the antisense oligonucleotides successfully skipped exons in a subject such that their muscular dystrophy progression was able to be measured and ultimately reversed such that improvements in the test were demonstrated. A person of ordinary skill in the art would have had a reasonable expectation of success because Nelson in view of Yokota teach that it was known in the art that utilizing a 6 minute walk test to confirm the successful exon skipping, mediated by antisense oligonucleotides, in subjects of interest was a known method of measuring muscular dystrophy progression.
Regarding claim 20, Nelson teaches that a second combination therapeutic agent may be administered to a subject and present within a kit comprising the antisense oligonucleotide ([0086]).
Claim(s) 4 is/are rejected under 35 U.S.C. 103 as being unpatentable over Nelson (PG Pub No. US 2014/0080896 A1) in view of Yokota (Muscle Gene Therapy: Methods and Protocols. Totowa, NJ: Humana Press, 2010. 299-312) and Sazani (US Patent No. 9,234,198 B1) as applied to claims 1, 3, 9, 11-16, 18-20, and 33-35 above, and further in view of Flanigan (PG Pub No. US 2017/0218366 A1).
Regarding claims 4, Nelson in view of Yokota and Sazani renders obvious claims 1, 3, 9, 11-16, 18-20, and 33-35 as described above. Nelson further teaches that the antisense oligonucleotides can be administered via the use of an AAV expression vector ([0047]).
Nelson in view of Yokota and Sazani does not teach or suggest that the nucleic acid comprises a nucleotide sequence that is at least 70% identical to the claimed SEQ ID NO: 26 (Claim 4).
However, one of ordinary skill in the art would have considered the teachings of Flanigan as both references are common fields of endeavor pertaining to the use of AAV vectors to deliver antisense molecules to a cell of interest.
Flanigan is directed towards an invention concerned with methods for enhancing exon skipping in a pre-mRNA of interest, including methods that can treat DMD (Abstract). Flanigan teaches the use of an AAV vector that comprises a genome insert that comprises 83.6% identity to the claimed SEQ ID NO: 26 ([0037]-[0038]; see SEQ ID NO: 26 in attached sequence alignment).
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to substitute the AAV delivery vector rendered obvious by Nelson in view of Yokota and Sazani for an AAV vector comprising a nucleotide sequence that has at least 70% identity to the claimed SEQ ID NO: 26, as described by Flanigan. A person of ordinary skill in the art would have had a reasonable expectation of success because both Flanigan and Nelson and Sazani in view of Yokota teach the use of AAV vectors that can deliver antisense nucleic acid molecules.
Claim(s) 5-8 and 10 is/are rejected under 35 U.S.C. 103 as being unpatentable over Nelson (PG Pub No. US 2014/0080896 A1) in view of Yokota (Muscle Gene Therapy: Methods and Protocols. Totowa, NJ: Humana Press, 2010. 299-312) and Sazani (US Patent No. 9,234,198 B1) as applied to claims 1, 3, 9, 11-16, 18-20, and 33-35 above, and further in view of Kaspar (PG Pub No. WO 2019/236949 A1).
Regarding claims 5-8 and 10, Nelson in view of Yokota and Sazani renders obvious claims 1, 3, 9, 11-16, 18-20, and 33-35 as described above. Nelson further teaches that the antisense oligonucleotides can be administered via the use of an AAV expression vector ([0047]).
Nelson in view of Yokota and Sazani does not teach or suggest the use of an rAAV comprising the antisense oligonucleotide (Claims 5 and 10) selected from rAAV9 (Claims 6-7) that is self-complementary (Claim 8).
However, one of ordinary skill in the art would have considered the teachings of Kaspar as both references are common fields of endeavor pertaining to the use of vectors encoding antisense nucleic acids.
Kaspar is directed towards an invention concerned with transgene-expressing viral vector drug products (Abstract). Kaspar teaches the use of a vector comprising a rAAV9 genome to deliver nucleic acids of interest to a cell ([00126]). Kaspar teaches the use of a rAAV9 genome that can encode an antisense molecule ([00228]). Kaspar teaches that rAAV genome can be self-complementary ([00278]).
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to substitute the delivery vector rendered obvious by Nelson in view of Yokota and Sazani for an rAAV9 vector or a vector that is self-complementary, as described by Kaspar. A person of ordinary skill in the art would have had a reasonable expectation of success because both Kaspar and Nelson in view of Yokota and Sazani teach the use of vectors that can encode antisense oligonucleotides.
Claim(s) 17 is/are rejected under 35 U.S.C. 103 as being unpatentable over Nelson (PG Pub No. US 2014/0080896 A1) in view of Yokota (Muscle Gene Therapy: Methods and Protocols. Totowa, NJ: Humana Press, 2010. 299-312) and Sazani (US Patent No. 9,234,198 B1) as applied to claims 1, 3, 9, 11-16, 18-20, and 33-35 above, as evidenced Betorini (Official Journal of the American Association of Electrodiagnostic Medicine 14.6 (1991): 503-507).
Regarding claims 7, Nelson in view of Yokota and Sazani renders obvious claims 1, 3, 9, 11-16, 18-20, and 33-35 as described above. Nelson further teaches that dantrolene can be synergistically administered alongside the antisense oligonucleotide ([0007]).
Nelson in view of Yokota and Sazani does not teach or suggest that the level of serum creatine kinase is decreased after administration of a composition comprising the nucleic acid molecule (Claim 17).
However, one of ordinary skill in the art would have considered the teachings of Betorini as both references are common fields of endeavor pertaining to the study of dantrolene and its effects when administered to subjects who have DMD.
Betorini is directed towards a study concerned with the effect of dantrolene in DMD (Abstract). Betorini teaches that dantrolene reduces serum creatine kinase in subjects who have DMD (Abstract).
Therefore, as evidenced by Betorini, the composition comprising the nucleic acid molecule and dantrolene rendered obvious by Nelson in view of Yokota and Sazani would have resulted in the reduction of serum creatine kinase in a subject who was administered the composition, as evidenced by Betorini. A person of ordinary skill in the art would have recognized that Betorini teaches that dantrolene decreases the amount of serum creatine kinase in subjects who had DMD while Nelson in view of Yokota and Sazani renders obvious the administration of dantrolene to subjects who have DMD.
Claim(s) 21 is/are rejected under 35 U.S.C. 103 as being unpatentable over Nelson (PG Pub No. US 2014/0080896 A1) in view of Yokota (Muscle Gene Therapy: Methods and Protocols. Totowa, NJ: Humana Press, 2010. 299-312) and Sazani (US Patent No. 9,234,198 B1) as applied to claims 1, 3, 9, 11-16, 18-20, and 33-35 above, further in view of Manzur (Cochrane database of systematic reviews 1 (2008)).
Regarding claim 21, Nelson in view of Yokota and Sazani renders obvious claims 1, 3, 9, 11-16, 18-20, and 33-35 as described above.
Nelson in view of Yokota and Sazani does not teach or suggest that the method further comprises administering a glucocorticoid (Claim 21).
However, one of ordinary skill in the art would have considered the teachings of Manzur as both references are common fields of endeavor pertaining to the treatment of DMD.
Manzur is directed towards a study concerned with the use of glucocorticoid corticosteroids for the treatment of DMD (pf. 1). Manzur teaches that administering glucocorticoid corticosteroids improved muscle strength and function over six months (pg. 2). Manzur teaches that improvements were seen in time taken to rise from the floor (Gowers' time), nine meters walking time, four‐stair climbing time, ability to lift weights, leg function grade and forced vital capacity (pg. 2).
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify the method rendered obvious by Nelson in view of Yokota and Sazani such that it further comprised administering a glucocorticoid, as described by Manzur. A person of ordinary skill in the art would have been motivated to do so in order to improve muscle strength in a subject who had DMD. A person of ordinary skill in the art would have had a reasonable expectation of success because Nelson in view of Yokota and Sazani teaches that the antisense oligonucleotide can be utilized in a method of treating DMD while Manzur teaches that administering a glucocorticoid to a subject who had DMD was a known beneficial compound that aided in the treatment of the disease.
Response to Arguments
Applicant's arguments filed 18 June 2026 with respect to the previously pending claim 2 (i.e., a dependent claim that has been incorporated into the newly amended claim 1 wherein the rejection above has been maintained) have been fully considered but they are not persuasive.
Applicant alleges that the teachings of Sazani are drawn towards exons 44-55 of the human DMD gene, not exons 6-8, and provides antisense sequences for only exons 44-55 (Remarks; pg. 5). Applicant alleges that even assuming Sazani teaches combining antisense oligonucleotides generally, none of the cited references teach the specific combination of sequences targeting human exons 6-8 (Remarks; pg. 6).
In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
These arguments are not found persuasive because it is the combination of Nelson, Yokota, and Sazani that renders the claimed invention obvious. Sazani was merely relied upon for the teaching that it was known in the art that the delivery of multiple antisense molecules targeting different DMD exons was a known method of treating DMD.
Thus, one of ordinary skill in the art would have expected that skipping of exons 6-8 through the use of antisense molecules comprising the claimed SEQ ID NOs, as rendered obvious by the combination of Nelson and Yokota, would have also resulted in restored functional dystrophin protein production because both exons produce the same protein. The antisense molecules of Sazani similarly target DMD genes, so one of ordinary skill in the art would have expected targeting exons 6-8 of the DMD gene through the use of the AAV vector of Sazani would have predictably resulted in the silencing of exons 6-8 of human DMD genes. Thus, one of ordinary skill in the art would have expected that combining the teachings of Nelson, Yokota, and Sazani as described above would have rendered the claimed invention obvious.
Applicant alleges that Yokota’s teachings are directed towards canine DMD gene, and not a human DMD gene as required by the claims (Remarks; pg. 6).
This argument is not found persuasive because both Nelson and Yokota teach the targeting of exons 6-8 with antisense molecules, as discussed above. Because the exons are directed towards exons that encode the exact same proteins, one would have expected that targeting exons 6-8 within the human DMD gene of Nelson would have resulted in restored functional dystrophin protein production because they are the same exons described in Yokota. Thus, one of ordinary skill in the art would have expected that skipping the same exons within a human would have also resulted in restored functional dystrophin protein production because both exons produce the same protein.
Applicant alleges that none of the references demonstrate that the claimed nucleic acids restored the reading frame of the DMD gene and allowed for dystrophin expression both in vitro and in vivo (Remarks; pg. 6).
This argument is not found persuasive because Yokota teaches that skipping exons 6-8 in a DMD model via the use of antisense oligonucleotides restored functional dystrophin protein production and that the skipping was produced both in vivo and in vitro (Abstract). Thus, one of ordinary skill in the art would have expected that skipping exons 6-8 would have resulted in the restored functional dystrophin protein production (i.e., expression) both in vitro and in vivo.
Allowable Subject Matter
Claim 36 is objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims.
Regarding claim 36, the closest prior art is the combination of Nelson (PG Pub No. US 2014/0080896 A1), Yokota (Muscle Gene Therapy: Methods and Protocols. Totowa, NJ: Humana Press, 2010. 299-312), Sazani (US Patent No. 9,234,198 B1), and Flanigan as applied above to claim 4.
With respect to the claimed SEQ ID NOs, Flanigan teaches the use of an AAV vector that comprises a genome insert that comprises 83.6% identity to the claimed SEQ ID NOs: 26-29 described in Flanigan ([0037]-[0038]; see SEQ ID NO: 26 in previously attached sequence alignment).
Flanigan further teaches that the AAV vectors comprises three different antisense sequences located at base pairs 444-474, base pairs 888- 912, and base pairs 1324-1346 that do not share sequence identity with the claimed SEQ ID NO: 26 (see previously attached sequence alignment). If even, assuming arguendo, the claimed antisense sequences comprising the claimed SEQ ID NOs: 1, 4, or 10 rendered obvious above were integrated into the AAV vector, the AAV vector of Flanigan further comprises mismatches at positions 627-631 and 1060-1065 that were not identified in the disclosure of Flanigan as being directed towards any specific linker motif nor endonuclease restriction site. Thus, it would not have been obvious to a person of ordinary skill in the art to have modified the AAV vector of Flanigan such that the vector comprised the claimed SEQ ID NOs: 26-29 as claimed because even if the antisense sequences rendered obvious above were substituted into the AAV vector sequence of Flanigan, there would still remain non-obvious mismatches. Accordingly, the claimed 26-29 are both novel and nonobvious in view of the closest prior art.
Applicant has provided adequate written description for the claimed SEQ ID NOs: 26-29 and provides evidence that they are U7 sequences that can comprise multiple antisense sequences and be present within a vector such that the antisense molecules can be expressed within a cell of interest to silence DMD exons ([59-61]; see Tables 2-3).
Conclusion
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 KYLE T REGA whose telephone number is (571)272-2073. The examiner can normally be reached Mon-Fri, 9AM-5PM (EDT/EST).
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Neil Hammell can be reached at 571-270-5919. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/KYLE T REGA/Examiner, Art Unit 1636
/NEIL P HAMMELL/Supervisory Patent Examiner, Art Unit 1636
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