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 .
DETAILED ACTION
The amendment filed February 8, 2026 in response to the Office Action of November 7, 2025 is acknowledged and has been entered.
Claims 1, 7, 8, 13, and 15 have been amended.
Claims 11, 17-19, and 22 have been cancelled.
Claims 23-25 have been added.
Claims 1, 3, 7-10, 12-16, 21, and 23-25 are pending and under consideration.
In view of amendments on claims 13 and 15, the 112(b) rejection set forth in the previous Office Action of November 7, 2025 is hereby withdrawn.
In view of amendments on claims 1, 7 and 8, the 112(a) rejection set forth in the previous Office Action of November 7, 2025 is hereby withdrawn.
In view of abandonment of Appl. 17/760,322, the Double Patenting rejection over this application, set forth in the previous Office Action of November 7, 2025 is hereby withdrawn.
New Claim Objections
Claim 3 is objected to because of the following informalities: “The method according to claim 2” should be “The method according to claim 1”, because claim 1 is the only claim preceding claim 3. Appropriate correction is required.
NEW REJCTIONS
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, 3, 7-10, 12-16, 21, and 23-25 are rejected under 35 U.S.C. 103 as being unpatentable over Chi (Chi et al., J Clin Oncol, 36, 8539 (2018), Volume 36, Number 15 suppl, Publication Date: 06/01/2018, of record) in view of Dosset (Dousset et al., Annals of Oncology, Volume 30, Supplement 5, 1355P, Publication Date: October 2019), as evidenced by Drug_Toripalimab (downloaded from: https://go.drugbank.com/drugs/DB15043, on 11/4/2025, of record).
Chi teaches JS001, a humanized IgG4 antibody specific for human PD-1 (§ Background). As evidenced by Drug_Toripalimab, JS001 is the same as toripalimab.
As set forth above, toripalimab comprises a light chain of SEQ ID NO: 9 and a heavy chain of SEQ ID NO: 10. As shown below, SEQ ID NO: 9 and 10 of the instant application comprise SEQ ID NO: 7 and 8 of the instant application, respectively.
SEQ ID NO: 9 vs SEQ ID NO: 7:
Title: US-17-904-096-9
Perfect score: 1137
Sequence: 1 DVVMTQSPLSLPVTLGQPAS..........EVTHQGLSSPVTKSFNRGEC 219
Database : US-17-904-096-7.pep:*
SUMMARIES
%
Result Query
No. Score Match Length DB ID Description
----------------------------------------------------------------------------
1 584 51.4 112 1 US-17-904-096-7 USE OF ANTI-PD-1 A
ALIGNMENTS
RESULT 1
US-17-904-096-7
Query Match 51.4%; Score 584; DB 1; Length 112;
Best Local Similarity 100.0%;
Matches 112; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DVVMTQSPLSLPVTLGQPASISCRSSQSIVHSNGNTYLEWYLQKPGQSPQLLIYKVSNRF 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DVVMTQSPLSLPVTLGQPASISCRSSQSIVHSNGNTYLEWYLQKPGQSPQLLIYKVSNRF 60
Qy 61 SGVPDRFSGSGSGTDFTLKISRVEAEDVGVYYCFQGSHVPLTFGQGTKLEIK 112
||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 SGVPDRFSGSGSGTDFTLKISRVEAEDVGVYYCFQGSHVPLTFGQGTKLEIK 112
SEQ ID NO: 10 vs SEQ ID NO: 8:
Title: US-17-904-096-10
Perfect score: 2408
Sequence: 1 QGQLVQSGAEVKKPGASVKV..........MHEALHNHYTQKSLSLSLGK 452
Database : US-17-904-096-8.pep:*
SUMMARIES
%
Result Query
No. Score Match Length DB ID Description
----------------------------------------------------------------------------
1 662 27.5 125 1 US-17-904-096-8 USE OF ANTI-PD-1 A
ALIGNMENTS
RESULT 1
US-17-904-096-8
Query Match 27.5%; Score 662; DB 1; Length 125;
Best Local Similarity 100.0%;
Matches 125; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QGQLVQSGAEVKKPGASVKVSCKASGYTFTDYEMHWVRQAPIHGLEWIGVIESETGGTAY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QGQLVQSGAEVKKPGASVKVSCKASGYTFTDYEMHWVRQAPIHGLEWIGVIESETGGTAY 60
Qy 61 NQKFKGRVTITADKSTSTAYMELSSLRSEDTAVYYCAREGITTVATTYYWYFDVWGQGTT 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGRVTITADKSTSTAYMELSSLRSEDTAVYYCAREGITTVATTYYWYFDVWGQGTT 120
Qy 121 VTVSS 125
|||||
Db 121 VTVSS 125
Thus, toripalimab (JS001) reads on the anti-PD-1 antibody of the instant claims 1, 7-9 (see alignments above and paragraphs [0087] and [0161] of the instant publication US 2023/0082898).
Chi teaches treating advanced melanoma patients by administering JS001 at 3 mg/kg IV Q2W (§ Methods).
Chi teaches that patients with non-acral melanoma or with melanoma with indeterminate primary site (18 chronically sun-damaged (CSD), and 38 Non-CSD or origin unknown) have been treated with JS001 (§ Results).
Chi teaches that among all patients with advanced melanoma, ORR was lower in acral (14.3%) and mucosal (0%) subtypes when compared with CSD (35.3%) and non-CSD (33.3%) (§ Results).
Chi teaches that ORR was higher in PD-L1 positive population (45.8%) when compared with PD-L1 negative population (15%) (see Table on page 2).
Chi teaches that the anti-PD-1 mAb appears more efficacious for CSD (non-acral) and non-CSD than acral and mucosal subgroups (§ Conclusions).
Taken together, Chi teaches a method of treating a patient with non-acral melanoma (such as CSD) by administering JS001 antibody. Chi also teaches that JS001 is more efficacious for CSD than acral subgroup and PD-L1 positive subgroup achieve higher ORR than PD-L1 negative subgroup. However, Chi does not explicitly teach that the CSD patients are PD-L1 positive and a tumor mutation burden (TMB) of ≥ 3.6 Muts/Mb in peripheral blood or tumor tissue.
Dousset teaches that on the basis of emerging clinical evidence, increased TMB may be associated with higher sensitivity to immunotherapeutic agents (§ Background)
Dousset teaches that TMB was characterized as the number of somatic protein-coding base substitution or alteration mutations per megabase (Mb). DNA was extracted from sections of primary tumor or metastasis (tumor tissue). TMB was considered high if > 20 muts/Mb (§ Methods). It is noted that > 20 muts/Mb would read on the instantly claimed range ≥ 3.6 Muts/Mb.
Dousset teaches that complete and partial remission after 3 months of anti-PD-1 were more often observed in TMB high patients whereas in low and intermediate mutational patients, progression was found in respectively 62% and 53% (§ Results).
Dousset teaches that TMB is affected by a variety of causes, including ultraviolet light in melanoma. The study highlights the importance of TMB with higher response to PD-1 blockade (§ Conclusions).
It would have prima facie been obvious to one of ordinarily skilled in the art before the effective filing date of the claimed invention to combine teachings of Chi and Dousset to treat the CSD melanoma with JS001 antibody and to apply the treatment to patients with CSD melanoma having a positive PD-L1 expression and a high TMB (e.g. > 20 muts/Mb). One of ordinary skill in the art would have had a reasonable expectation that JS001 would also be efficacious to CSD melanoma having positive PD-L1 expression a high TMB (e.g. > 20 muts/Mb), because Chi teaches that among all melanoma subgroups, JS001 is most efficacious to CSD melanoma subgroup and among all melanoma patients (regardless of subgroups) JS001 is more efficacious to PD-L1 positive patients than to PD-L1 negative patients. In addition, Dousset teaches that melanoma patients with high TMB are more responsive to anti-PD-1 therapy. The motivation would have been to treat a suitable population with JS001 antibody.
Regarding claim 3, Chi teaches treating advanced melanoma patients by administering JS001 at 3 mg/kg IV Q2W (§ Methods).
Regarding claim 10, as evidenced by paragraph [0087] of the instant publication US 2023/0082898, JS001 (toripalimab) is a monoclonal antibody.
Regarding claims 12-15, 21 and 23-25, Chi teaches treating advanced melanoma patients by administering JS001 at 3 mg/kg IV Q2W (a liquid dosage), which reads on about 3 mg/kg body weight of claims 12; 3 mg/kg once every two weeks of claims 13 ,14 and 23; and parenteral intravenous infusion of claims 15, 21 and 24. The intravenous infusion would comprises an injection of claim 25. In addition, one of ordinary skill in the art could modify the dose, route of administration, and the like to reach the specific regimens as claimed through routine and conventional practices.
Regarding claim 16, Chi teaches administering JS001 once every two weeks. This would read on in cycles of two weeks.
Response to Arguments
For the 103 rejection, Applicant argues unexpected results as shown below:
As disclosed in Table 5 of this application, the anti-PD-I antibody in claim I was significantly more effective in treating non-acral melanoma or melanoma with indeterminate primary site with "TMB of ≥3.6 Muts/Mb" because of higher objective response rates (ORRs):
(1) 40.0% for non-acral melanoma with TMB of ≥ 3.6 Muts/Mb, compared to 27.8% for non-acral melanoma with TMB of <3.6 Muts/Mb;
(2) 50.0% for melanoma with indeterminate primary site with TMB of ≥ 3.6 Muts/Mb, compared to 17.6% for melanoma with indeterminate primary site with TMB of <3.6 Muts/Mb;
(3) 30.0% for melanoma with TMB of ≥3.6 Muts/Mb, compared to 12.8% for melanoma with TMB of <3.6 Muts/Mb.
Given the expected and superior therapeutic efficacy of the claimed anti-PD-I antibody or an antigen-binding fragment thereof or a pharmaceutical composition thereof, for the treatment of for non-acral melanoma or primary-site indeterminate melanoma characterized by either "TMB of ≥ 3 .6 Muts/Mb" alone or together with "positive PD-LI expression," these results could not have been predicted by a person having ordinary skill in the art in light of the teachings of Chi and Drug_ Toripalimab.
Applicant’s arguments have been fully considered but they are not persuasive. As set forth above, Dousset (new reference) teaches that increased TMB may be associated with higher sensitivity to immunotherapeutic agents and complete and partial remission after 3 months of anti-PD-1 were more often observed in TMB high patients (> 20 muts/Mb). Combining the teachings of Chi and Dousset, one of ordinary skill in the art would have reasonable expectation (not unexpected) that the non-acral melanoma patients with a positive PD-L1 expression and high TMB in peripheral blood or tumor tissue would respond to anti-PD-1 therapy (JS001 therapy) better. Because > 20 muts/Mb overlap with the claimed range, the methods taught by Chi and Dousset would read on the instant claims.
Regarding the results shown in Table 5, based on the P value (the bottom row of Table 5), the difference between the group with TMB ≥ 3.6 Muts/Mb or the group with TMB < 3.6 Muts/Mb was not statistically significant (
p
=
0.62
for Non-acral subtype;
p
=
0.23
for primary-site indeterminate subtype). Paragraph [0178] of the instant Publication (US 2023/0082898 A1, of record) states: “With 3.6 Muts/Mb as a cut-off value, patients with TMB ≥ 3.6 Muts/Mb (n=20) had a better response than patients with TMB < 3.6 Muts/Mb (n=78) (ORR 30.0% vs . 12.8%), but the difference was not statistically significant (
p
=
0.088
)….The group with TMB ≥ 3.6 Muts/Mb also had higher PFS and OS values, but the difference was not statistically significant either”. Thus, based on the results shown in the instant specification, one of ordinary skill in the art would not conclude that the anti-PD-1 antibody in claim 1 was significantly more effective in treating non-acral melanoma or menaloma with indeterminate primary site with “TMB of ≥ 3.6 Muts/Mb”, as applicant argued.
Thus, the 103 rejection is proper for the reasons of record.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Patent No. 10,066,013
Claims 1, 3, 7-10, 12-16, 21, and 23-25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-7 of U.S. Patent No. 10,066,013 B2 (hereinafter Pat. 013) in view of Chi (Chi et al., J Clin Oncol, 36, 8539 (2018), Volume 36, Number 15 suppl, Publication Date: 06/01/2018) and Dousset (Dousset et al., Annals of Oncology, Volume 30, Supplement 5, 1355P, Publication Date: October 2019), as evidenced by Drug_Toripalimab (downloaded from: https://go.drugbank.com/drugs/DB15043, on 11/4/2025).
The claims of Pat. 013 teach a monoclonal antibody or functional fragment thereof that binds to a programmed cell death 1 (PD-1) protein comprising the amino acid sequence of SEQ ID NO: 43, comprising a heavy chain variable region comprising SEQ ID NO: 33 and a light chain variable region comprising SEQ ID NO: 34 (claim 1). As shown below, SEQ ID NO: 33 and 34 of Pat. 013 are identical to SEQ ID NO: 8 and 7 of the instant application, respectively.
Alignment of SEQ ID NO: 33 of Pat. 013 to SEQ ID NO: 8 of the instant application:
Query Match 100.0%; Score 662; DB 1; Length 125;
Best Local Similarity 100.0%;
Matches 125; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QGQLVQSGAEVKKPGASVKVSCKASGYTFTDYEMHWVRQAPIHGLEWIGVIESETGGTAY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QGQLVQSGAEVKKPGASVKVSCKASGYTFTDYEMHWVRQAPIHGLEWIGVIESETGGTAY 60
Qy 61 NQKFKGRVTITADKSTSTAYMELSSLRSEDTAVYYCAREGITTVATTYYWYFDVWGQGTT 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGRVTITADKSTSTAYMELSSLRSEDTAVYYCAREGITTVATTYYWYFDVWGQGTT 120
Qy 121 VTVSS 125
|||||
Db 121 VTVSS 125
Alignment of SEQ ID NO: 34 of Pat. 013 to SEQ ID NO: 7 of the instant application:
Query Match 100.0%; Score 584; DB 1; Length 112;
Best Local Similarity 100.0%;
Matches 112; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DVVMTQSPLSLPVTLGQPASISCRSSQSIVHSNGNTYLEWYLQKPGQSPQLLIYKVSNRF 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DVVMTQSPLSLPVTLGQPASISCRSSQSIVHSNGNTYLEWYLQKPGQSPQLLIYKVSNRF 60
Qy 61 SGVPDRFSGSGSGTDFTLKISRVEAEDVGVYYCFQGSHVPLTFGQGTKLEIK 112
||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 SGVPDRFSGSGSGTDFTLKISRVEAEDVGVYYCFQGSHVPLTFGQGTKLEIK 112
Thus, the anti-PD-1 antibody of Pat. 013 read on the antibody of instant claim 1, 7 and 10.
The claims of Pat. 013 teach a pharmaceutical composition comprising the antibody or functional fragment thereof according to claim 1 and a pharmaceutical carrier (claim 7).
The claims of Pat. 013 teach an anti-PD-1 antibody or the antigen binding fragment thereof comprising a heavy chain variable region comprising SEQ ID NO: 33 and a light chain variable region comprising SEQ ID NO: 34. However, the claims of Pat. 013 do not teach treating non-acral melanoma or melanoma with indeterminate primary site, and wherein the patient has a positive PD-L1 expression and a TMB ≥ 3.6 Muts/Mb with the anti-PD-1 antibody, or the anti-PD-1 antibodies of instant claims 8 and 9; or administration regimens as instantly claimed.
Chi’s teachings, as evidenced by Drug_Toripalimab, are described above. In particular Chi teaches that JS001 (the same as toripalimab) treatment achieves higher ORR in advanced non-acral melanoma subgroup and PD-L1 positive subgroup. As set forth above, JS001 is a species reads on the antibody of claim 1 of Pat. 013 also the antibody of instant claims 8 and 9. Dousset teaches that increased TMB may be associated with higher sensitivity to immunotherapeutic agents and complete and partial remission after 3 months of anti-PD-1 were more often observed in TMB high patients.
It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to develop an anti-PD-1 antibody comprising a heavy chain variable region comprising SEQ ID NO: 33 and a light chain variable region comprising SEQ ID NO: 34, as taught by the claims of Pat. 013, and to choose a specific antibody JS001 (toripalimab) and to use JS001 for treating patients with advanced PD-L1 positive, a TMB > 20 Muts/Mb, and non-acral melanoma (e.g. CSD melanoma). One of ordinary skill in the art would have had a reasonable expectation that JS001 would be efficacious to advanced CSD melanoma having positive PD-L1 expression and with high TMB (e.g. > 20 Muts/Mb), because Chi teaches: 1) among all advanced melanoma subgroups, JS001 is most efficacious to CSD melanoma subgroup; 2) among all advanced melanoma patients (regardless of melanoma subtypes) JS001 is more efficacious to PD-L1 positive patients than to PD-L1 negative patients. In addition, Dousset teaches that melanoma patients with high TMB are more responsive to anti-PD-1 therapy. The motivation would have been to treat a suitable population with a well-tested anti-PD-1 antibody: JS001.
Regarding claims 12-15, 21, and 23-25, Chi teaches treating advanced melanoma patients by administering JS001 at 3 mg/kg IV Q2W, which reads on about 3 mg/kg body weight of claims 12; 3 mg/kg once every two weeks of claims 13 and 14; and intravenous infusion of claims 15 and 21. It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to use the administering regimens taught by Chi because the administration method are effective in treating patients with non-acral melanoma. In addition, one of ordinary skill in the art could modify the dose, route of administration, and the like to reach the specific regimens as claimed through routine and conventional practices.
Regarding claim 16, Chi teaches administering JS001 once every two weeks. This would read on in cycles of two weeks.
Response to Arguments
For the Double Patenting rejection, Applicant argues:
While claims 1-7 of Pat. 013 appear to be related to a monoclonal antibody or a fragment thereof that binds to PD-I, there is no teaching or suggestion in Pat. 013 of TMB in the context of non-acral melanoma or primary-site indeterminate melanoma that would have motivated a person having ordinary skill in the art to arrive at the claimed method with any reasonable expectation of success. Therefore, amended claim I is inventive in view of Pat. 013.
Applicant is iterating similar arguments as set forth in 103 rejection. Thus for the reasons set forth above the rejection is maintained.
Patent No. 10,815,302
Claims 1, 3, 7-10, 12-16, and 21 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-11 of U.S. Patent No. 10,815,302 B2 (hereinafter Pat. 302) in view of Chi (Chi et al., J Clin Oncol, 36, 8539 (2018), Volume 36, Number 15 suppl, Publication Date: 06/01/2018) and Dousset (Dousset et al., Annals of Oncology, Volume 30, Supplement 5, 1355P, Publication Date: October 2019),, as evidenced by Drug_Toripalimab (downloaded from: https://go.drugbank.com/drugs/DB15043, on 11/4/2025).
The claims of Pat. 302 teach antibody or a functional fragment thereof that can bind to the programmed cell death 1 (PD-1) protein having an amino acid sequence of SEQ ID NO: 43, wherein the antibody or a functional fragment thereof comprises:
i) a heavy chain CDR1 having the amino acid sequence of Asp Tyr Glu Met His (SEQ ID NO: 1), ii) a heavy chain CDR2 having the amino acid sequence of Val Ile Glu Ser Glu Thr Gly Gly Thr Ala Tyr Asn Gln Lys Phe Lys Gly (SEQ ID NO: 2), iii) a heavy chain CDR3 having the amino acid sequence of Glu Gly Ile Thr Thr Val Ala Thr Thr Tyr Tyr Trp Tyr Phe Asp Val (SEQ ID NO: 3), iv) a light chain CDR1 having the amino acid sequence of Arg Ser Ser Gln Ser Ile Val His Ser Asn Gly Asn Thr Tyr Leu Glu (SEQ ID NO: 10), v) a light chain CDR2 having the amino acid sequence of Lys Val Ser Asn Arg Phe Ser (SEQ ID NO: 11), and vi) a light chain CDR3 having the amino acid sequence of Phe Gln Gly Ser His Val Pro Leu Thr (SEQ ID NO: 12) (claim 1).
The claims of Pat. 302 teach a pharmaceutical composition comprising the antibody or functional fragment thereof of claim 1 and a pharmaceutical carrier (claim 11).
As shown below (CDR regions are underlined), toripalimab comprises the HCDRs 1-2-3 of SEQ ID NOs: 1-3 of Pat. 302 and LCDRs 1-2-3 of SEQ ID NOs: 10-12 of Pat. 302. Thus, toripalimab is a species of anti-PD-1 antibody encompassed by the claims of Pat. 302. It is also noted that the SEQ ID NOs: 1-3 and 10-12 of Pat. 302 are identical to SEQ ID NOs: 4-6 and 1-3 of instant application, respectively.
PNG
media_image1.png
656
888
media_image1.png
Greyscale
The claims of Pat. 302 teach an anti-PD-1 antibody or the antigen binding fragment thereof having the LCDR1, LCDR2, LCDR3 sequences respectively set forth in SEQ ID NOs: 10-12, and the HCDR1, HCDR2, HCDR3 sequences respectively set forth in SEQ ID NOs: 1-3. However, the claims of Pat. 302 do not teach treating non-acral melanoma or melanoma with indeterminate primary site, and wherein the patient has a positive PD-L1 expression and a TMB ≥ 3.6 Muts/Mb with the anti-PD-1 antibody, or the anti-PD-1 antibodies of instant claims 7-10; or administration regimens as instantly claimed.
Chi’s teachings, as evidenced by Drug_Toripalimab, are described above. In particular Chi teaches that JS001 (the same as toripalimab) treatment achieve higher ORR in advanced non-acral melanoma subgroup and PD-L1 positive subgroup. As set forth above, JS001 reads on the antibody of instant claims 7-10. Dousset teaches that increased TMB may be associated with higher sensitivity to immunotherapeutic agents and complete and partial remission after 3 months of anti-PD-1 were more often observed in TMB high patients.
It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to develop an anti-PD-1 antibody having the LCDR1, LCDR2, LCDR3 sequences respectively set forth in SEQ ID NOs: 10-12, and the HCDR1, HCDR2, HCDR3 sequences respectively set forth in SEQ ID NOs: 1-3, as taught by the claims of Pat. 302, and to choose a specific antibody JS001 (toripalimab) and to use JS001 for treating patients with advanced, PD-L1 positive, high TMB > 20 Muts/Mb non-acral melanoma (e.g. CSD melanoma). One of ordinary skill in the art would have had a reasonable expectation that JS001 would also be efficacious to advanced CSD melanoma having positive PD-L1 expression, because Chi teaches that among all advanced melanoma subgroups, JS001 is most efficacious to CSD melanoma subgroup and among all advanced melanoma patients (regardless of melanoma subtypes) JS001 is more efficacious to PD-L1 positive patients than to PD-L1 negative patients. In addition, Dousset teaches that melanoma patients with high TMB are more responsive to anti-PD-1 therapy. The motivation would have been to treat a suitable population with a well-tested anti-PD-1 antibody: JS001.
Regarding claim 10, as evidenced by paragraph [0087] of the instant publication US 2023/0082898, toripalimab is a monoclonal antibody.
Regarding claims 12-15, 21 and 23-25, Chi teaches treating advanced melanoma patients by administering JS001 at 3 mg/kg IV Q2W, which reads on about 3 mg/kg body weight of claims 12; 3 mg/kg once every two weeks of claims 13 and 14; and intravenous infusion of claims 15 and 21. It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to use the administering regimens taught by Chi because the administration method are effective in treating patients with non-acral melanoma. In addition, one of ordinary skill in the art could modify the dose, route of administration, and the like to reach the specific regimens as claimed through routine and conventional practices.
Regarding claim 16, Chi teaches administering JS001 once every two weeks. This would read on in cycles of two weeks.
Response to Arguments
For the Double Patenting rejection, Applicant argues:
Similar to Pat. 013, claims 1-11 of Pat. 302 also appear to be related to an antibody or a fragment thereof that binds to PD-1. However, there is no teaching or suggestion in Pat. 302 of TMB in the context of non-acral melanoma or primary-site indeterminate melanoma that would have motivated a person having ordinary skill in the art to arrive at the claimed method with any reasonable expectation of success. Therefore, amended claim I is inventive in view of Pat. 302.
Applicant is iterating similar arguments as set forth in 103 rejection. Thus for the reasons set forth above the rejection is maintained.
Application No. 18/282,856
Claims 1, 3, 7-10, 12-16, and 21 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 20-41 of copending Application No. 18/282,856 (hereinafter Appl. 856, US 2024/0254230 A1) in view of Chi (Chi et al., J Clin Oncol, 36, 8539 (2018), Volume 36, Number 15 suppl, Publication Date: 06/01/2018) and Dousset (Dousset et al., Annals of Oncology, Volume 30, Supplement 5, 1355P, Publication Date: October 2019), as evidenced by Drug_Toripalimab (downloaded from: https://go.drugbank.com/drugs/DB15043, on 11/4/2025).
The claims of Appl. 856 teach a composition comprising an inhibitor selected from anti-PD-1 antibody as the effective ingredient …and wherein the inhibitor is an anti-PD-1 antibody or the antigen binding fragment thereof having the LCDR1, LCDR2, LCDR3 sequences respectively set forth in SEQ ID NOs: 1-3, and the HCDR1, HCDR2, HCDR3 sequences respectively set forth in SEQ ID NOs: 4-6 (claim 32).
The claims of Appl. 856 teach a composition comprising an inhibitor selected from anti-PD-1 antibody as the effective ingredient for …, and wherein the inhibitor is an anti-PD-1 antibody or the antigen binding fragment thereof having the LCDR1, LCDR2, LCDR3 sequences respectively set forth in SEQ ID NOs: 1-3, and the HCDR1, HCDR2, HCDR3 sequences respectively set forth in SEQ ID NOs: 4-6 (claim 39). As shown below (CDR regions are underlined), toripalimab comprises the LCDRs 1-2-3 of SEQ ID NOs: 1-3 of Appl. 856 and HCDRs 1-2-3 of SEQ ID NOs: 4-6 of Appl. 856. Thus, toripalimab is a species of anti-PD-1 antibody encompassed by the claims of Appl. 856. It is also noted that the SEQ ID NOs: 1-6 of Appl. 856 are identical to SEQ ID NOs: 1-6 of instant application, respectively.
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The claims of Appl. 856 teach an anti-PD-1 antibody or the antigen binding fragment thereof having the LCDR1, LCDR2, LCDR3 sequences respectively set forth in SEQ ID NOs: 1-3, and the HCDR1, HCDR2, HCDR3 sequences respectively set forth in SEQ ID NOs: 4-6. However, the claims of Appl. 856 do not teach treating non-acral melanoma or melanoma with indeterminate primary site, and wherein the patient has a positive PD-L1 expression and a TMB ≥ 3.6 Muts/Mb with the anti-PD-1 antibody, or the anti-PD-1 antibodies of instant claims 7-10; or administration regimens as instantly claimed.
Chi’s teachings, as evidenced by Drug_Toripalimab, are described above. In particular Chi teaches that JS001 (the same as toripalimab) treatment achieve higher ORR in advanced non-acral melanoma subgroup. As set forth above, JS001 reads on the antibody of instant claims 7-10. Dousset teaches that increased TMB may be associated with higher sensitivity to immunotherapeutic agents and complete and partial remission after 3 months of anti-PD-1 were more often observed in TMB high patients.
It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to develop an anti-PD-1 antibody having the LCDR1, LCDR2, LCDR3 sequences respectively set forth in SEQ ID NOs: 1-3, and the HCDR1, HCDR2, HCDR3 sequences respectively set forth in SEQ ID NOs: 4-6, as taught by the claims of Appl. 856, and to choose a specific antibody JS001 (toripalimab) and to use JS001 for treating patients with advanced PD-L1 positive, a high TMB > 20 Muts/Mb non-acral melanoma (e.g. CSD melanoma). One of ordinary skill in the art would have had a reasonable expectation that JS001 would also be efficacious to advanced CSD melanoma having positive PD-L1 expression, because Chi teaches that among all advanced melanoma subgroups, JS001 is most efficacious to CSD melanoma subgroup. In addition, among all advanced melanoma patients (regardless of melanoma subtypes) JS001 is more efficacious to PD-L1 positive patients than to PD-L1 negative patients. In addition, Dousset teaches that melanoma patients with high TMB are more responsive to anti-PD-1 therapy. The motivation would have been to treat a suitable population with a well-tested anti-PD-1 antibody: JS001.
Regarding claim 10, as evidenced by paragraph [0087] of the instant publication US 2023/0082898, toripalimab is a monoclonal antibody.
Regarding claims 12-15, 21, and 23-25, Chi teaches treating advanced melanoma patients by administering JS001 at 3 mg/kg IV Q2W, which reads on about 3 mg/kg body weight of claims 12; 3 mg/kg once every two weeks of claims 13 and 14; and intravenous infusion of claims 15 and 21. It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to use the administering regimens taught by Chi because the administration method are effective in treating patients with non-acral melanoma. In addition, one of ordinary skill in the art could modify the dose, route of administration, and the like to reach the specific regimens as claimed through routine and conventional practices.
Regarding claim 16, Chi teaches administering JS001 once every two weeks. This would read on in cycles of two weeks.
This is a provisional nonstatutory double patenting rejection.
Response to Arguments
For the Double Patenting rejection, Applicant argues:
Claims 20-41 of Appl. 856 are related to PD-I antibody for treating urothelial carcinoma, which is different from the claimed non-acral melanoma or with melanoma with indeterminate primary site. There is no disclosure of non-acral melanoma or with melanoma with indeterminate primary in Appl. 856.
Additionally, the specific threshold of TMB is 3.6 Muts/Mb for determining different efficacy of claimed PD-1 antibody for non-acral melanoma or primary-site indeterminate melanoma, whereas the threshold of TMB is 10 Muts/Mb for urothelial carcinoma. Thus, a person having ordinary skill in the art could not have predicted the threshold of TMB in another tumor based on the teachings of Appl. 856 and would not have been motivated to arrive at the claimed method with any reasonable expectation of success. Therefore, amended claim I is inventive in view of Appl. 856.
Applicant’s arguments have been fully considered but they are not persuasive. As set forth above, the claims of Appl. 856 also drawn to pharmaceutical composition comprising an anti-PD-1 antibody encompassed by the instant claims. The pharmaceutical composition of Appl. 856 are not limited by the methods recited by claims of Aool. 856. Thus, in view of Chi and Dousset, one of ordinary skill in the art would have had a reasonable expectation of success that the pharmaceutical composition taught by the claims of Appl. 856 and Chi can be used in the instantly claimed method, as set forth in 103 rejection.
Application No. 18/291,935
Claims 1, 3, 7-10, 12-16, and 21 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of copending Application No. 18/291,935 (hereinafter Appl. 935, US 2024/0342083 A1) in view of Chi (Chi et al., J Clin Oncol, 36, 8539 (2018), Volume 36, Number 15 suppl, Publication Date: 06/01/2018) and Dousset (Dousset et al., Annals of Oncology, Volume 30, Supplement 5, 1355P, Publication Date: October 2019), as evidenced by Drug_Toripalimab (downloaded from: https://go.drugbank.com/drugs/DB15043, on 11/4/2025).
The claims of Appl. 935 teach that the pharmaceutical composition, comprising:
(1) a buffer; and (2) an anti-PD-1 antibody or an antigen-binding fragment thereof;
wherein the anti-PD-1 antibody or the antigen-binding fragment thereof comprises an LCDR1, an LCDR2 and an LCDR3 having amino acid sequences set forth in SEQ ID NO: 1, SEQ ID NO: 2 and SEQ ID NO: 3, respectively, and an HCDR1, an HCDR2 and an HCDR3 having amino acid sequences set forth in SEQ ID NO: 4, SEQ ID NO: 5 and SEQ ID NO: 6, respectively, wherein the anti-PD-1 antibody or the antigen-binding fragment thereof has a concentration of about 100-250 mg/mL (claim 1).
The claims of Appl. 935 teach that the pharmaceutical composition according to claim 1, wherein the anti-PD-1 antibody or the antigen-binding fragment thereof comprises a light chain variable region set forth in SEQ ID NO: 7 and a heavy chain variable region set forth in SEQ ID NO: 8 (claim 6); The pharmaceutical composition according to claim 6, wherein the anti-PD-1 antibody comprises a light chain amino acid sequence set forth in SEQ ID NO: 9 and a heavy chain amino acid sequence set forth in SEQ ID NO: 10 (claim 18). As shown below, SEQ ID NO: 9 and SEQ ID NO: 10 of Appl. 935 are the same as SEQ ID NO: 9 and SEQ ID NO: 10 of the instant application:
Alignment of SEQ ID NO:9:
US-18-291-935-9
Query Match 100.0%; Score 1137; DB 1; Length 219;
Best Local Similarity 100.0%;
Matches 219; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DVVMTQSPLSLPVTLGQPASISCRSSQSIVHSNGNTYLEWYLQKPGQSPQLLIYKVSNRF 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DVVMTQSPLSLPVTLGQPASISCRSSQSIVHSNGNTYLEWYLQKPGQSPQLLIYKVSNRF 60
Qy 61 SGVPDRFSGSGSGTDFTLKISRVEAEDVGVYYCFQGSHVPLTFGQGTKLEIKRTVAAPSV 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 SGVPDRFSGSGSGTDFTLKISRVEAEDVGVYYCFQGSHVPLTFGQGTKLEIKRTVAAPSV 120
Qy 121 FIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSL 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 FIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSL 180
Qy 181 SSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC 219
|||||||||||||||||||||||||||||||||||||||
Db 181 SSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC 219
Alignment of SEQ ID NO: 10:
US-18-291-935-10
Query Match 100.0%; Score 2408; DB 1; Length 452;
Best Local Similarity 100.0%;
Matches 452; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QGQLVQSGAEVKKPGASVKVSCKASGYTFTDYEMHWVRQAPIHGLEWIGVIESETGGTAY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QGQLVQSGAEVKKPGASVKVSCKASGYTFTDYEMHWVRQAPIHGLEWIGVIESETGGTAY 60
Qy 61 NQKFKGRVTITADKSTSTAYMELSSLRSEDTAVYYCAREGITTVATTYYWYFDVWGQGTT 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGRVTITADKSTSTAYMELSSLRSEDTAVYYCAREGITTVATTYYWYFDVWGQGTT 120
Qy 121 VTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPA 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 VTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPA 180
Qy 181 VLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFL 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 VLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFL 240
Qy 241 GGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQ 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 GGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQ 300
Qy 301 FNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQ 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 301 FNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQ 360
Qy 361 EEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKS 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 361 EEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKS 420
Qy 421 RWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK 452
||||||||||||||||||||||||||||||||
Db 421 RWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK 452
Thus, the antibody of Appl. 935 reads on the antibodies of instant claims 1, 7-8.
The claims of Appl. 935 teach a method for treating a disease or a disorder by eliminating, inhibiting or reducing PD-1 activity, which comprises administering to a subject in need thereof the pharmaceutical composition according to claim 1, wherein the disease or disorder is selected from cancer, infectious diseases and inflammatory diseases (claim 10).
The claims of Appl. 935 teach a method for treating a disease or a disorder by eliminating, inhibiting or reducing PD-1 activity, which comprises administering to a subject in need thereof the injection according to claim 8; wherein the disease or disorder is selected from cancer, infectious diseases and inflammatory diseases (claim 11)
Taken together, the claims of Appl. 935 teach treating a patient with cancer with anti-PD-1 antibody e.g. an anti-PD-1 antibody comprising SEQ ID NO: 9 and 10. However, the claims of Appl. 935 do not teach that malignancy is non-acral melanoma or melanoma with indeterminate primary site, and wherein the patient has a positive PD-L1 expression and a TMB ≥ 3.6 Muts/Mb, or the specific antibody toripalimab, or administration regimens as instantly claimed.
Chi’s teachings, as evidenced by Drug_Toripalimab, are described above. In particular Chi teaches that JS001 (the same as toripalimab) treatment achieve higher ORR in advanced non-acral melanoma subgroup and PD-L1 positive subgroup. Dousset teaches that increased TMB may be associated with higher sensitivity to immunotherapeutic agents and complete and partial remission after 3 months of anti-PD-1 were more often observed in TMB high patients.
It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to develop a method for treating cancer with an anti-PD-1 antibody comprising SEQ ID NO: 9 and 10, as taught by the claims of Appl. 935, and to choose toripalimab for treating patients with advanced PD-L1 positive and high HMB (> 20 Mut/Mb), non-acral melanoma (e.g. CSD melanoma). One of ordinary skill in the art would have had a reasonable expectation that JS001 would also be efficacious to advanced CSD melanoma having positive PD-L1 expression, because Chi teaches that among all advanced melanoma subgroups, JS001 is most efficacious to CSD melanoma subgroup and among all advanced melanoma patients (regardless of melanoma subtypes) JS001 is more efficacious to PD-L1 positive patients than to PD-L1 negative patients. In addition, Dousset teaches that melanoma patients with high TMB are more responsive to anti-PD-1 therapy. The motivation would have been to treat a suitable population with JS001 antibody.
Regarding claim 10, as evidenced by paragraph [0087] of the instant publication US 2023/0082898, toripalimab is a monoclonal antibody.
Regarding claims 12-15, 21 and 23-25, Chi teaches treating advanced melanoma patients by administering JS001 at 3 mg/kg IV Q2W, which reads on about 3 mg/kg body weight of claims 12; 3 mg/kg once every two weeks of claims 13 and 14; and intravenous infusion of claims 15 and 21. It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to use the administering regimens taught by Chi because the administration method are effective in treating patients with non-acral melanoma. In addition, one of ordinary skill in the art could modify the dose, route of administration, and the like to reach the specific regimens as claimed through routine and conventional practices.
Regarding claim 16, Chi teaches administering JS001 once every two weeks. This would read on in cycles of two weeks.
This is a provisional nonstatutory double patenting rejection.
Response to Arguments
For the Double Patenting rejection, Applicant argues:
Claims 1-20 of Appl. 935 appear to be related to a pharmaceutical compositions with an anti-PD-I antibody or a fragment thereof. However, there is no teaching or suggestion in Appl. 935 of TMB in the context of non-acral melanoma or primary-site indeterminate melanoma that would have motivated a person having ordinary skill in the art to arrive at the claimed method with any reasonable expectation of success. Therefore, amended claim I is inventive in view of Appl. 935.
Applicant’s arguments have been fully considered but they are not persuasive. Although the claims of Appl. 935 are drawn to a pharmaceutical composition, based on the teachings of Chi and Dousset, one of ordinary skill in the art would have been motivated to use the pharmaceutical composition in the instantly claimed method. Given the teachings of Chi and Dousset, one of ordinary skill in the art would have had a reasonable expectation that the pharmaceutical composition would be effective in the claimed method.
Conclusion
No claims are allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). 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 CHENG LU whose telephone number is (571)272-0334. The examiner can normally be reached Monday-Friday 8-5.
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, Samira Jean-Louis can be reached at (571)270-3503. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/CHENG LU/Examiner, Art Unit 1642
/PETER J REDDIG/Primary Examiner, Art Unit 1646
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