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 .
Claim Status
Claims 2-8 and 12-13 are cancelled. Claims 1, 9-11, and 14-42 as filed on 19 September 2025 are pending. Claims 9-11, 15, 18-22, and 24-28 are withdrawn. Claims 1, 14, 16-17, 23, and 29-42 are under examination.
Claim Objections
Claim 1 is objected to because of the following informalities: Claim 1 has been amended changing the location for the requirement of a hinge, a transmembrane domain, and a CD28 signaling domain. The claim require has subparts a and b in the alternative and the claim is written where it is unclear if the hinge, transmembrane domain, and CD28 signaling domain are required by both subparts or only subpart b. Appropriate correction is required.
For the purposes of prosecution the claim was examined as requiring all components in subparts a and b.
Rejections Amended – Amended as Necessitated by Applicant Amendment of Claims
Claim Rejections - 35 USC § 103
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.
Claims 1, 14, 16, 23, 31, and 39 are rejected under 35 U.S.C. 103 as being unpatentable over Galetto (WO 2015/150526 A2) (IDS), Wong (US 2018/0200366 A1) (Of Record), Asa (WO 2013/167756 A1) (Of Record), and Laszlo et. al. Blood Reviews. 28:143-153. (2014) (Of Record).
Regarding claims 1 and 31, Galetto teaches a CAR comprising a CD33 binding domain comprising a VH, linker, and VL domain, a hinge domain, a transmembrane domain, and intracellular T cell signaling domains as shown in Galetto’s Figure 3 and shown below. Galetto teaches the use of a CD3 zeta intracellular domain as required by claim 31. Galetto further teaches a number of co-stimulatory domains in the alternative including CD28 (page 19 in lines 16-28).
Regarding claim 14, Galetto teaches a CD8α transmembrane domain of SEQ ID NO: 6 which matches instant SEQ ID NO: 7, and a CD8α hinge of SEQ ID NO: 5 which matches instant SEQ ID NO: 6 (Table 1 in page 5).
Regarding claim 16, Galetto teaches the use of a linker between the extracellular ligand-binding domain and the transmembrane domain of the CAR (page 21 in lines 3-5). The specification states a linker sequence may be used as a spacer ([0036]) showing the linker of Galetto is teaching the spacer of the claim.
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Regarding claim 23, Galetto teaches the CAR in a composition with a pharmaceutically acceptable carrier (page 52 in lines 22-23).
Galetto teaches the use of these CARs for treating leukemia and lymphoma (abstract and claims 29-36). Galetto further teaches the use of multiple anti-CD33 binding domains in their CAR (page 74 in last paragraph onto page 75).
Galetto does not teach the binding domain of instant SEQ ID NO: 15 and 16, required by claims and elected by applicant with a CAR comprising instant SEQ ID NO: 23.
Regarding claims 35 and 39, Galetto teaches the CAR expressed in a T or NK cell (page 1 in lines 1-9) and further teaches T cells expressing the CAR in a pharmaceutically acceptable carrier (page 52 in lines 22-23).
This deficiency is filled by Wong, Asa, and Laszlo.
Wong teaches SEQ ID NO: 38 which comprises a signal peptide, a sequences that matches instant SEQ ID NO: 15, a linker comprising (G4S)3, a sequence that matches SEQ ID NO: 16, and then a human IL-15 ([0288]). This is taught as an anti-CD33 that binds a disease antigen (abstract and [0288]). SEQ ID NO: 38 is encoded by SEQ ID NO: 39 ([0289]) and Wong further teaches a method of treating diseases including lymphoma with a fusion protein with anti-CD33 binding moiety and IL-15 (claims 21-22). Wong teaches CD33 is a tumor antigen ([0108] in last 3 lines) and specifically a leukemia antigen ([0117]).
Asa teaches tissue-targeting complexes using tissue targeting moieties (Abstract). Instant SEQ ID NO: 15 matches SEQ ID NO: 1 (see alignment below) and instant SEQ ID NO: 16 matches SEQ ID NO: 2 (see alignment below). Asa teaches SEQ ID NO: 1 and SEQ ID NO: 2 as antibody AGC0700 (Table 2). Asa further teaches the antibodies as full antibodies, antibody fragments, and ScFv (claim 10). Asa teaches the binding to CD33 positive lymphoma cells HL-60 (Figure 2 and Example 8). Asa teaches CD33 positive HL-60 cells (Figure 2) which are lymphoma cells (Figure 4) (in particular the Brief Summary of the Figures on page 36) and Example 8.
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Laszlo teaches the treatment of leukemia using CD33 as it is broadly expressed on acute myeloid leukemia and is a known target for therapeutic antibodies (Abstract).
It would have been obvious at the time the application was filed to substitute the CD33 binding domain of Galetto with the anti-CD33 binding domains of Wong and Asa. Galetto teaches a CAR that binds CD33 for treatment of leukemia and lymphoma, Laszlo teaches CD33 is a known target for antibodies for treatment of leukemia, and Wong and Asa teach the CD33 binding domain of the claims for use in leukemia and lymphoma. The substitution of the CD33 binding domain of the therapeutic CAR of Galetto with the known therapeutic CD33 binding domain of Wong and Asa is a substitution of equivalent domains that can be used in lymphoma and leukemia patient populations. One of ordinary skill in the art would have been motivated to find explore alternative CD33 binding domains for the CAR of Galetto to provide an alternative effective CAR for treatment of leukemia and lymphoma. There would have been a reasonable expectation of success as Galetto teaches varying CD33 binding domains in the CARs of their invention.
Applicant Arguments
Applicant argues Galetto does not teach all of the requirements of the claims and specifically points to the binding domains of the claims and a CD28 signaling domain.
Applicant argues Galetto teaches away from substituting various combinations of signaling domains, transmembrane domains, transmembrane domains, and co-stimulatory domains pointing to the end of page 1 and 2 of Galetto.
Applicant argues regarding Wong that one of skill in the art would not have explored Wong in combination with Galetto as Wong is not presented in a CAR. Applicant argues one of skill in the art would not have removed the remainder of the fusion taught by Wong and used just the scAb of Wong which matches the linker and binding domain of the claims.
Regarding Asa, applicant argues the scFv of Asa is not taught in a CAR and one of skill in the art would not have been motivated to use the scFv of the antibody in a CAR and there would be no expectation of success.
Regarding Laszlo, applicant argues the CD33 binding CAR comprises different components from the claimed CAR and does not provide one with skill or motivation to make a CAR of the claims.
Response to Arguments
Applicant's arguments filed 18 September 2025 have been fully considered but they are not persuasive.
Galetto teaches multiple co-stimulatory domains including CD28 co-stimulatory domains as added to the amended rejection. Galetto further teaches a number of co-stimulatory domains in the alternative including CD28 (page 19 in lines 16-28). Additionally the cited writing of Galetto is referring to first generation CARs. Galetto is related to second generation CARs. Examiner points to Figure 2 of Galetto and the evidentiary reference of Chmielewski & Abken. Expert Opin. Biol. Ther. 15(8). (2015) (PTO-892) (Figure 1). Galetto is teaching the known in the art issues of first generation CARs which is why the field developed future generations of CARs. Galetto is making an argument for why their invention of second generation CARs are an improvement over previous CARs.
Galetto does contain the sentence cited by applicant but all art must be considered in its entirety and not sentence by sentence or even section by section.
Galetto teaches and one of skill in the art would have known that not all combinations of CAR components will work. CARs are broadly a fusion of an antigen binding domain, linker domains, a transmembrane domain, and signaling domains. Galetto specifically teaches in the abstract the broad framework of a CAR and specify their invention is a CAR comprising an extracellular ligand binding that is an scFv derived from a CD33 monoclonal antibody (abstract) and in their claims allows for large variation in the sequence of the anti-CD33 antibody including variation in sequence of the antibodies they specifically teach (all claims but specifically claims 1 and 11).
Galetto as noted by examiner teaches many alternative hinges, transmembrane domains, and signaling domains (exemplified in claim 1). While Galetto teaches that not all combinations of CAR components will work together they still claimed their invention as a CAR without a specific CD33 binding domain and variation in the additional CAR components.
One of skill in the art would have been directed to the art of Wong by the teaching of Galetto.
Galetto specifically teaches a CAR comprising an extracellular ligand binding that is an scFv derived from an anti-CD33 monoclonal antibody (abstract). One of skill in the art would have then been taught by Galetto to look at the art for an anti-CD33 antibody that can work as an extracellular ligand binding that binds CD33 for use in a CAR. Wong teaches that sequence.
This same teaching would direct one of skill in the art to Asa. Wong and Asa both teach anti-CD33 antibody that works in the form of a scAb and scFv and Asa provides the additional information that the scFv for use in the same patient population of lymphoma taught by Galetto (abstract).
The rejection relies upon Wong for its CD33 binding domain it is substituted with the generic CD33 binding domain of Galetto.
Laszlo is not relied upon to teach the component of the claimed CAR. Laszlo is relied upon for further teaching in the art showing the broader application of CD33 binding CARs for use in treatment of the patient population of leukemia.
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).
No single art relied upon the rejection teaches the entire CAR of the rejection. But in combination their render the CAR obvious.
Galetto provides on of skill in the art a the framework of a CD33 binding CAR used in lymphoma and leukemia.
Laszlo further supports the study of CD33 binding CARs for use in treating leukemia providing additional motivation.
Wong and Asa provides one of skill in the art the CD33 binding domain of the claims for use in treatment of the patient populations of Galetto and Laszlo.
Claims 1, 14, 16-17, 23, 29-38, and 40-42 are rejected under 35 U.S.C. 103 as being unpatentable over Brogdon (US 2014/0271635) (Of Record), Galetto (WO 2015/150526 A2) (IDS), Wong (US 2018/0200366 A1) (Of Record), Asa (WO 2013/167756 A1) (Of Record), Wang et. al. Experimental Hematology & Oncology. 1(36) (2012) (Of Record), Laszlo et. al. Blood Reviews. 28:143-153. (2014)) (Of Record), and Wiltzius (US 2017/0281766 A1) (Of Record) and Zhang (CN 107312098 A) (Of Record).
Applicant’s elected species in Remarks dated 04/11/2023 is instant SEQ ID NO: 23 which is required by claim 29. Instant SEQ ID NO: 23 is a CAR comprising a leader sequence of instant SEQ ID NO: 12, the anti-CD33 antigen binding domain comprising instant SEQ ID NO: 15, a linker domain of instant SEQ ID NO: 4, instant SEQ ID NO: 16, a spacer of Ser Gly, a CD28 hinge/transmembrane domain of instant SEQ ID NO: 10, a CD28 linker of instant SEQ ID NO: 37, and a CD3 zeta intracellular domain.
Regarding claims 1, Brogdon teaches a method of treating disease with a CAR that has a CD19 binding domain (Abstract). Brogdon teaches the treatment of lymphoma ([0036], [0318]). Brogdon teaches a CAR that comprises a VH, a linker sequence, a VL, a hinge/transmembrane domain, and an intracellular domain as shown in Figure 6A pasted below. Brogdon teaches the CD28 transmembrane domain ([0009], [0241]), a linker domain of Gly and Ser, and a CD3-zeta chain as an intracellular signaling domain ([0138]). Brogdon teaches instant SEQ ID NO: 37 in SEQ ID NO: 43 on page 100. Brogdon further teaches SEQ ID NO: 17 which comprises instant SEQ ID NO: 9.
Further Brogdon teaches VH to VL and VL to VH arrangements of their anti-CD19 CAR T in Figures 6A and 6B teaching them as equivalent alternatives of each other.
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Regarding claim 16, Brogdon teaches the presence of a spacer ([0198]).
Regarding claims 23, Brogdon teaches a pharmaceutical composition including a carrier ([0343]).
Brogdon teaches the linker sequence of instant SEQ ID NO: 4 in SEQ ID NO: 18 ([0383]). Brogdon teaches linker size did not impact function ([0407] in last 2 lines).
Brogdon does not teach the anti-CD33 VH and VLs of instant SEQ ID NO: 15 and 16 wherein they are SEQ ID NO: 15, linker, then SEQ ID NO: 16. Brogdon does not teach the specific leader sequence or CD3zeta extracellular domain of instant SEQ ID NO: 23; nor the CD28 hinge of SEQ ID NO: 10 as elected by applicant and required by claim 29.
Brogdon further teaches recombinant T cells that encode and comprise the CAR (abstract) and teaches the modified T cells administered as part of a pharmaceutical composition including ones comprising carriers ([0315] and [0343]-[0344]).
Brogdon does not teach the anti-CD33 VH and VLs of instant SEQ ID NO: 15 and 16 wherein they are SEQ ID NO: 15, linker, then SEQ ID NO: 16. Brogdon does not teach the specific leader sequence or CD3zeta extracellular domain of instant SEQ ID NO: 23; nor the CD28 hinge of SEQ ID NO: 10 as elected by applicant and required by claim 29.
These deficiencies are filled by Galetto, Asa, Wong, Wang, Laszlo, Wiltzius and Zhang.
The teachings of Galetto, Wong, Asa, and Laszlo from the previous 103 rejection are incorporated here in full. As previously described Galetto, Wong, Asa, and Laszlo teach a CAR comprising the unelected CD8α transmembrane and hinge domains.
Wang teaches that CD19 is a known target for treating leukemia and lymphoma. Wang further teaches there are anti-CD19 antibodies used in the treatment of both leukemia and lymphoma (Abstract and page 4 in col 1 “CD19 monoclonal antibodies for lymphoma and leukemia therapy”).
Wiltzius teaches chimeric antigen receptors and their use, particularly their use in T cell therapy (Abstract). Wiltziu teaches improved targeting of cancer cells for improved therapies with CAR T cells ([0004]-[0006]). Wiltzius teaches the leader sequence from positions 1 to 21 of instant SEQ ID NO: 23 of Wiltzius’s SEQ ID NO: 205. Wiltzius further teaches the CD28 transmembrane domain of instant SEQ ID NO: 10 and in instant SEQ ID NO: 23 from position 266 to 307, and the CD28 linker of instant SEQ ID NO: 37 and in instant SEQ ID NO: 23 from position 375 to 389, then the CD3zeta of instant SEQ ID NO: 23 from position 390 to 486. Wiltzius teaches the use of costimulatory molecules in a CAR including CD3zeta to mediate a costimulatory response ([007] and [0135]) . Wiltzius’s SEQ ID NO: 205 is an anti-CLL-1 CAR construct (page 180) which is used to treat lymphoma ([0048]).
Wiltzius teaches the CD28 hinge of instant SEQ ID NO: 10 in SEQ ID NO: 184 in Table 2 page 42 in col 2 in lines 6-7 and SEQ ID NO: 196 in page 2 col 2 in lines 16-17. Wiltzius teaches the use of CD28 transmembrane domains in ([0160] and [0161] on page 15 in col 1).
Zhang teaches an CD22 chimeric antigen receptor (abstract ) which comprises a hinge and transmembrane domain (page 2 in par 2 in lines 3-5). Zhang teaches the use of an anti-CD22 comprising instant SEQ ID NO: 10 and instant SEQ ID NO: 11 (SEQ ID NO: 2 (page 4). Zhang teaches the use of the CD22 CAR of SEQ ID NO: 2 in the treatment of leukemia and lymphoma (page 6 in second to last section labeled (2) and Figure 5).
It would have been obvious to one of ordinary skill in the art at the time the application was filed to substitute the binding moiety of the CAR of Brogdon with the anti-CD33 of Wong and Asa to form a CAR T comprising the anti-CD33 domain of Wong and Asa with a transmembrane domain, an intracellular T cell signaling domain, a linker, and a spacer of the elected instant SEQ ID NO: 23. Brogdon, Wong, and Asa all teach antigen binding domains that direct treatment of lymphoma and leukemia. As taught by Brogdon and Wang CD19 was known to one of ordinary skill in the art that targeting CD19 for the treatment of leukemia and lymphoma. Galetto teaches anti-CD33 CARs that can be used in the treatment of leukemia and lymphoma. Brogdon teaches the VH then VL and VL to VH arrangements of the antigen binding moieties in a CAR are equivalent configurations and without surprising results using an art taught CAR configuration would be obvious. Further, Wong and Asa teach an anti-CD33 domain that can be used in fusion proteins for treatment of lymphoma. The anti-CD33 domain taught by Wong and Asa was not a random binding moiety but a binding moiety that was taught for use in human lymphoma patients. Galetto teaches anti-CD33 CARs can be used in the treatment of leukemia and lymphoma. One of ordinary skill in the art would have known that CD19 and CD33 were targets for treatment of lymphoma and leukemia as taught by Wang and Galetto, Galetto teaches CD33 binding domains can be used in CARs, and Wong and Asa both teach a CD33 binding domain that can be used in therapeutics. One of ordinary skill in the art would have been motivated to substitute the CD19 binding domain of Brogdon with the CD33 binding domain of Wong and Asa as CD33 was a known in the art target for treating lymphoma and leukemia which are the same patient populations that CD19 CARs would be used in and the alternative target of CD33 would provide a new therapy that would provide profits when used. There would have been a reasonable expectation of success as binding domains for CD19 and CD33 were taught by Brogdon and Galetto for use in CARs and the art teaches both targets for use in lymphoma and leukemia patients.
It would have been obvious to one with ordinary skill in the art at the time the invention was filed to substitute the leader sequence, the CD28 domain, and CD3zeta sequence of the combined teachings of Brodgon and Asa’s anti-CD33 CAR comprising SEQ ID NOs: 1 and 2 (same as instant SEQ ID NOs:15 and 16) with the leader sequence and CD3zeta sequence of Wiltzius and the CD28 hinge and transmembrane domains of Zhang (instant SEQ ID NOs: 10 and 11) to produce an art equivalent CAR comprising the components of instant SEQ ID NO: 23. Brogdon and Asa, and Wiltzius and Zhang are teaching the use of CARs in the treatment of lymphoma. The art teaches CD33 as an immunotherapeutic target using antibodies and CARs (Asa, Wong, and Galetto) for patients with lymphoma and leukemia. One of ordinary skill in the art would have been motivated to use known working structures for CARs with known binding domains to develop new therapies for use in the patient populations. There would have been a reasonable expectation of success as they teachings in the same patient population the treatment of the same disease and showing improved outcomes. The combination of known in the art binding domains that have been shown to be effective for use in therapies with known CAR components is obvious without unexpected results.
Applicant Arguments
Applicant argues the arguments from the previous art rejection.
Applicant argues that Wang is to CD19 binding CARs and are not related to the claims which are anti-CD33 CARs.
Applicant argues Wiltzius is to anti-FLT3 CARs and anti-CLL-1 CARs and not anti-CD33 CARs as required by applicant’s claims.
Applicant repeats the arguments that Galetto teaches away from substitutions of CAR components.
Applicant argues there would be uncertainty in the art and cited Long et. al. 2015.
Regarding Zhang, applicant argues it teaches an anti-CD22 CAR and not an anti-CD33 CAR as required by the claims.
Applicant argues Galetto teaches away by stating work in CD19 directed CARs cannot be expanded to all antigens.
Applicant argues non-obvious in view of unexpected results in view of Table 6, Figure 1A, Applicant Specification ([0169]), and the attachment of clinical trial NCT03971799. Applicant notes clinical trials are expensive and the investment of performing a clinical trial is evidence.
Response to Arguments
Applicant's arguments filed 18 September 2025 have been fully considered but they are not persuasive.
Examiner directs applicant to response to arguments from the previous art rejection.
The cited writing of Galetto is referring to first generation CARs. Galetto is related to second generation CARs. Examiner points to Figure 2 of Galetto and the evidentiary reference of Chmielewski & Abken. Expert Opin. Biol. Ther. 15(8). (2015) (PTO-892) (Figure 1). Galetto is teaching the known in the art issues of first generation CARs which is why the field developed future generations of CARs. Galetto is making an argument for why their invention of second generation CARs are an improvement over previous CARs.
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).
Wang and Wiltzius are not relied upon for the binding domains of the claims.
The CARs of the art relied upon known components of CARs to produce the CARs of their teachings.
Wang and Wiltzius provide teaching of CARs that work in the same patient population of the anti-CD33 CARs taught by Galetto, Asa, and Laszlo.
Regarding unexpected results. Applicant has not provided how the combination of known components of a CAR with a known CD33 binding domain previously taught for use in therapeutics is unexpected.
Table 6 and Figure 1A are only recitations of the components of a CAR. They show possession of the recited claims but do not provide results, expected or otherwise.
Paragraph [0169] of the specification, pasted below, is a statement of an anti-CD33 being more effective than anti-CD19 or anti-CD22 CARs. Based on the language “Based on the above,” examiner reviewed Example 1 which is before this paragraph. Example 1 begins in [0140] and details first the generation of CD33 binding CARs from known in the art scFvs, then details the use in in vivo and in vitro experiments. Examiner did not identify any experiments that showed a comparison between effectiveness of anti-CD33 and anti-CD19 CARs or any experiment where anti-CD19 CARs were used by applicant in Example 1. A statement of improvement is not evidence.
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Regarding the clinical trial. The starting of a clinical trial is not evidence of unexpected results or effectiveness of a treatment as clinical trials do fail. The results of a clinical trial could be evidenced of unexpected results of a CAR if properly filed and presented.
Conclusion
No claims allowable.
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 FRANCESCA EDGINGTON-GIORDANO whose telephone number is (571)272-8232. The examiner can normally be reached Mon - Fri 8:00 - 5:00.
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/F.E./Examiner, Art Unit 1643
/Meera Natarajan/Primary Examiner, Art Unit 1643