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 .
This action is in response to the amendment filed 12/10/2025, in which claims 1, 6, 8, 11, 13, 15 and 20 were amended, claims 12, 14, 18, 19 and 22 were previously presented, claims 2-5, 7, 9, 16, 17 and 21 are canceled and claims 23 and 24 are newly added.
Claims 1, 6, 8, 10-15, 18-20 and 22-24 are currently pending.
Applicant’s arguments have been thoroughly reviewed, but are not persuasive for the
reasons that follow. Any rejection and objections not reiterated in this action have been
withdrawn. This action is FINAL.
Response to Amendments - Drawings
The previous objection to the drawings has been withdrawn in view of Applicant’s submission of new drawings filed on 12/10/2025.
Response to Amendments - Claim Objections
The previous objection of claims 2-5 and 7 are withdrawn in view of Applicant’s cancellation of the claims filed on 12/10/2025.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 6, 8, 15, 23 and 24 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claims 6 and 8 are incomplete in that the claims rely upon cancelled claims. See MPEP § 608.01(n)(V).
Claims 15 and 23 are vague and indefinite in that the metes and bounds of the phrase “gRNA having a sequence identity of” are unclear. The phrase is unclear in that the specification provides that the phrase “sequence identity of” refers to a percentage of identity to the original parent molecule (Page 17, Lines 1-9) however, the claim as currently written does not include a percent identity to the sequence provided in the SEQ ID NOs. It would be remedial to amend the claims to either include the percent identity to the SEQ ID NOs listed or to replace the phrase “gRNA having a sequence identity of” to recite “gRNA having the sequence of”.
Claim 24 is incomplete in that the claim relies upon itself. See MPEP § 608.01(n)(V).
Response to Amendments - Claim Rejections - 35 USC § 112
The previous rejection of claim 15 under 35 U.S.C. 112(b) has been withdrawn in view of Applicant’s amendments to the claim filed on 12/10/2025.
The previous rejections of claim 13 under 35 U.S.C. 112(a) has been withdrawn in view of Applicant’s amendments to the claim filed on 12/10/2025.
The previous rejection of claims 1-22 under 35 U.S.C. 112(a) has been withdrawn in view of Applicant’s amendments to the claim filed on 12/10/2025.
Response to Arguments - Claim Rejections - 35 USC § 102
The previous rejection of claims 1, 9-13 and 15-22 under 35 U.S.C. 102(a)(1)/(a)(2) as being anticipated by Bryson et al (WO 2019/217942 A1) has been withdrawn in view of Applicant’s amendments to the claims filed on 12/10/2025.
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 text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Claims 1, 10-15, 18-20 and 22 are rejected under 35 U.S.C. 103 as being unpatentable over Bryson et al (WO 2019/217942 A1) in view of Koblan et al (Nat Biotechnol 36, 843–846; 2018). This is a new rejection, necessitated by the amendment filed 12/10/2025.
Regarding claims 1, 12 and 14, Bryson teaches increased levels of fetal hemoglobin (HbF) can ameliorate the clinical course of inherited disorders of beta-globin gene expression, such as beta thalassemia and sickle cell anemia, and in a group of disorders called hereditary persistence of fetal hemoglobin (HPFH), the expression of one or both of the gamma globin genes (HBGJ/2) of HbF persists at high levels in adult erythroid cells. [0562]. Bryson teaches a method of editing an HBG1 or HBG2 gene loci using a targeted base editor and a guide RNA in CD34+ cells to increase expression of the gamma globin [0564-0565 and 0567]. Bryson teaches instant SEQ ID NOs: 49 and 50 as guide RNAs used within the system with 100% identity (See NEW Appendices V and VI) (Page 199, Table 4, Lines 44 and 51 and [0565] denoted as gRNA1). Bryson teaches that the multiplex editing can comprise one or more base editor system with a plurality of guide polynucleotides [0452].
Bryson does not teach base-editing enzyme is ABEmax, AncBE4max, or evoCDAI-BE4max-NG.
Koblan teaches the properties of optimized AncBE4max, BE4max, and ABEmax compared to those of BE4 and ABE7.10 specifically in HBG fetal hemoglobin promoter mutations (Page 845, Figure 2(e) and (f); and Figure 2 Description). Koblan teaches used ABEmax to install activating mutations in the promoters of HBG1 or HBG2 (γ-globin) that can rescue β-globin disorders with two sgRNAs: (1) −116 A→G and −113 A→G; and (2) −175 T →C (Page 846, Column 1). Koblan teaches BE4max, AncBE4max, and ABEmax thus offer increased editing in a variety of settings, especially under suboptimal conditions or at sites previously edited with modest efficiency (Page 846, Column 1).
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 teachings of Bryson to include the ABEmax base editor enzyme as taught by Koblan because Bryson teaches it is within the ordinary skill in the art to use a method of editing an HBG1 or HBG2 gene loci using a targeted base editor (APOBEC1) and a guide RNA in CD34+ cells to increase expression of the gamma globin and Koblan teaches BE4max, AncBE4max, and ABEmax thus offer increased editing in a variety of settings, especially under suboptimal conditions or at sites previously edited with modest efficiency.
One would have been motivated to make such a modification in order to receive the expected benefit of increased editing efficiency using BE4max in HBG promoter editing as taught by Koblan.
Regarding claims 10 and 11, Bryson teaches wildtype SpCas9 sequence [0174]. Bryson teaches the mutation of H840A (within the HNH domain) completely inactivates the nuclease activity of S. pyogenes Cas9 resulting in a nickase [0182 and 0224-0225]. Therefore, with the sequence provided by Bryson [0174] for the SpCas9 with a single H840A mutation shows 100% identity to instant SEQ ID NO: 33 (See NEW Appendix VII).
Regarding claim 13, Bryson teaches the suitable nucleic-acid editing domains, e.g., deaminases and deaminase domains, that can be fused to Cas9 domains, such as the Human AID sequences which is 100% identical to instant SEQ ID NO: 4 (See Appendix II; Cited in Previous Office Action) [0329].
Regarding claim 15, Bryson teaches increased levels of fetal hemoglobin (HbF) can ameliorate the clinical course of inherited disorders of beta-globin gene expression, such as beta thalassemia and sickle cell anemia, and in a group of disorders called hereditary persistence of fetal hemoglobin (HPFH), the expression of one or both of the gamma globin genes (HBGJ/2) of HbF persists at high levels in adult erythroid cells. [0562]. Bryson teaches a method of editing an HBG1 or HBG2 gene loci using a targeted base editor and a guide RNA in CD34+ cells to increase expression of the gamma globin [0564-0565 and 0567]. Bryson teaches instant SEQ ID NO: 50 as guide RNAs used within the system with 100% identity (See NEW Appendix VI) ([0565] denoted as gRNA1). Bryson teaches that the multiplex editing can comprise one or more base editor system with a plurality of guide polynucleotides [0452].
Bryson does not teach base-editing enzyme is ABEmax.
Koblan teaches the properties of optimized ABEmax compared to those of BE4 and ABE7.10 specifically in HBG fetal hemoglobin promoter mutations (Page 845, Figure 2(e) and (f); and Figure 2 Description). Koblan teaches used ABEmax to install activating mutations in the promoters of HBG1 or HBG2 (γ-globin) that can rescue β-globin disorders with two sgRNAs: (1) −116 A→G and −113 A→G; and (2) −175 T →C (Page 846, Column 1). Koblan teaches ABEmax thus offer increased editing in a variety of settings, especially under suboptimal conditions or at sites previously edited with modest efficiency (Page 846, Column 1).
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 teachings of Bryson to include the ABEmax base editor enzyme as taught by Koblan because Bryson teaches it is within the ordinary skill in the art to use a method of editing an HBG1 or HBG2 gene loci using a targeted base editor (APOBEC1) and a guide RNA in CD34+ cells to increase expression of the gamma globin and Koblan teaches ABEmax thus offer increased editing in a variety of settings, especially under suboptimal conditions or at sites previously edited with modest efficiency.
One would have been motivated to make such a modification in order to receive the expected benefit of increased editing efficiency using ABEmax in HBG promoter editing as taught by Koblan.
Regarding claims 18, 19 and 22, Bryson teaches increased levels of fetal hemoglobin (HbF) can ameliorate the clinical course of inherited disorders of beta-globin gene expression, such as beta thalassemia and sickle cell anemia, and in a group of disorders called hereditary persistence of fetal hemoglobin (HPFH), the expression of one or both of the gamma globin genes (HBGJ/2) of HbF persists at high levels in adult erythroid cells. [0562]. Bryson teaches a method of editing an HBG1 or HBG2 gene loci using a targeted base editor and a guide RNA in CD34+ cells to increase expression of the gamma globin [0564-0565 and 0567]. Bryson teaches a method of editing an HBB polynucleotide comprising a single nucleotide polymorphism (SNP) associated with sickle cell disease, the method comprising contacting the HBB polynucleotide with a base editor in complex with one or more guide polynucleotides, wherein the base editor comprises a polynucleotide programmable DNA binding domain and an adenosine deaminase domain, and wherein the one or more guide polynucleotides target the base editor to effect an A•T to G•C alteration of the SNP associated with sickle cell disease (Page 290, Claim 1).
Regarding claim 20, Bryson teaches a method of editing an HBG1 or HBG2 gene loci using a targeted base editor and a guide RNA in CD34+ cells to increase expression of the gamma globin [0564-0565 and 0567].
Claims 6, 8, 23 and 24 are rejected under 35 U.S.C. 103 as being unpatentable over Bryson et al (WO 2019/217942 A1) in view of Koblan et al (Nat Biotechnol 36, 843–846; 2018), as applied to claims 1, 10-15, 18-20 and 22 above, and further in view of Wienert et al (Trends in Genetics, December 2018, Vol. 34, No. 12). This is a new rejection, necessitated by the amendment filed 12/10/2025.
The teachings of Bryson and Koblan are described above and applied as before with regard to claims 1, 10-15, 18-20 and 22.
Regarding claim 6, the claim is interpreted as being relied on claim 1 instead of claim 5 which is a canceled claim.
Bryson does not specifically teach the point mutation at -200C>T allows the LRF repressor to bind to the promoter.
Wienert teaches a nuclease-dead Cas9 (dCas9) is can be coupled to a base editor, an enzyme that catalyzes nucleotide transitions (A>G, C>T, G>A and T>C) without making a DSB (Page 936 bridging Page 937). Wienert teaches Zinc Finger and BTB Domain Containing 7A (ZBTB7A, also known as LRF) was established as the second major fetal globin repressor by a knockout study in HUDEP-2 cells and transgenic mice (Page 931, Paragraph 2). Wienert teaches two clusters of mutations within the proximal promoter region have been identified, one at around -200 relative to the transcriptional start site, and another at around -115 (Page 932, Paragraph 3). Wienert teaches mutations in the -200 region (mutations between -201 to -195 including -200 C>T) HBG1/HBG2 promoter thereby disrupting a binding site for the ZBTB7A (Also known as LRF) repressor (Page 935, Figure 3B).
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 teachings of Bryson to include the specific point mutations at -200 C>T allowing LRF repressor to bind to the promoter as taught by Wienert because Bryson teaches it is within the ordinary skill in the art to use a method of editing an HBG1 or HBG2 gene loci using a targeted base editor and a guide RNA in CD34+ cells to increase expression of the gamma globin as well as the specific point mutations at -201 C>T, -197 C>T, -196 C>T and -195 C>T and Wienert teaches the -200 C>T mutation of the HBG1/HBG2 promoter of the gamma globin in order for LRF repressor to bind to the promoter.
One would have been motivated to make such a modification in order to receive the expected benefit of the point mutation disrupting the LRF repressor binding site on the promoter subsequently increasing the fetal hemoglobin levels as taught by Wienert.
Regarding claim 8, the claim is interpreted as being relied on claim 1 instead of claim 7 which is a canceled claim.
Bryson does not specifically teach the point mutation at -115 C>T that allows the BCL11A repressor to bind to the promoter.
Wienert teaches a nuclease-dead Cas9 (dCas9) is can be coupled to a base editor, an enzyme that catalyzes nucleotide transitions (A>G, C>T, G>A and T>C) without making a DSB (Page 936 bridging Page 937). Wienert teaches two clusters of mutations within the proximal promoter region have been identified, one at around -200 relative to the transcriptional start site, and another at around -115 (Page 932, Paragraph 3). Wienert teaches BCL11A as the repressor that binds to the -115 site and that HPFH mutations within the -115 region (-117 to -114, and the 13 bp deletion) impair BCL11A’s ability to directly bind to the promoter and therefore one strategy to elevate HbF levels is to target the fetal globin repressors BCL11A or ZBTB7A directly (Page 934, Paragraph 2 and 4). Wienert teaches a -115 C>T mutation in the HBG1/HBG2 promoter thereby disrupting a binding site for the BCL11A repressor (Page 935, Figure 3B).
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 teachings of Bryson to include the specific point mutation at -115 C>T allowing BCL11A repressor to bind to the promoter as taught by Wienert because Bryson teaches it is within the ordinary skill in the art to use a method of editing an HBG1 or HBG2 gene loci using a targeted base editor and a guide RNA in CD34+ cells to increase expression of the gamma globin as well as the specific point mutation at -114 C>T and Wienert teaches the -115 C>T mutation of the HBG1/HBG2 promoter of the gamma globin in order for BCL11A repressor to bind to the promoter.
One would have been motivated to make such a modification in order to receive the expected benefit of the point mutation disrupting the BCL11A repressor binding site on the promoter subsequently increasing the fetal hemoglobin levels as taught by Wienert.
Regarding claim 23, Bryson teaches increased levels of fetal hemoglobin (HbF) can ameliorate the clinical course of inherited disorders of beta-globin gene expression, such as beta thalassemia and sickle cell anemia, and in a group of disorders called hereditary persistence of fetal hemoglobin (HPFH), the expression of one or both of the gamma globin genes (HBGJ/2) of HbF persists at high levels in adult erythroid cells. [0562]. Bryson teaches a method of editing an HBG1 or HBG2 gene loci using a targeted base editor and a guide RNA in CD34+ cells to increase expression of the gamma globin [0564-0565 and 0567]. Bryson teaches instant SEQ ID NO: 50 as guide RNAs used within the system with 100% identity (See NEW Appendix VI) ([0565] denoted as gRNA1). Bryson teaches that the multiplex editing can comprise one or more base editor system with a plurality of guide polynucleotides [0452].
Bryson does not teach base-editing enzyme is ABEmax.
Koblan teaches the properties of optimized ABEmax compared to those of BE4 and ABE7.10 specifically in HBG fetal hemoglobin promoter mutations (Page 845, Figure 2(e) and (f); and Figure 2 Description). Koblan teaches used ABEmax to install activating mutations in the promoters of HBG1 or HBG2 (γ-globin) that can rescue β-globin disorders with two sgRNAs: (1) −116 A→G and −113 A→G; and (2) −175 T →C (Page 846, Column 1). Koblan teaches ABEmax thus offer increased editing in a variety of settings, especially under suboptimal conditions or at sites previously edited with modest efficiency (Page 846, Column 1).
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 teachings of Bryson to include the ABEmax base editor enzyme as taught by Koblan because Bryson teaches it is within the ordinary skill in the art to use a method of editing an HBG1 or HBG2 gene loci using a targeted base editor (APOBEC1) and a guide RNA in CD34+ cells to increase expression of the gamma globin and Koblan teaches ABEmax thus offer increased editing in a variety of settings, especially under suboptimal conditions or at sites previously edited with modest efficiency.
One would have been motivated to make such a modification in order to receive the expected benefit of increased editing efficiency using ABEmax in HBG promoter editing as taught by Koblan.
Bryson does not specifically teach the point mutation at -115 C>T that allows the BCL11A repressor to bind to the promoter. Bryson does not specifically teach the point mutation at -200C>T allows the LRF repressor to bind to the promoter.
Wienert teaches a nuclease-dead Cas9 (dCas9) is can be coupled to a base editor, an enzyme that catalyzes nucleotide transitions (A>G, C>T, G>A and T>C) without making a DSB (Page 936 bridging Page 937). Wienert teaches Zinc Finger and BTB Domain Containing 7A (ZBTB7A, also known as LRF) was established as the second major fetal globin repressor by a knockout study in HUDEP-2 cells and transgenic mice (Page 931, Paragraph 2). Wienert teaches two clusters of mutations within the proximal promoter region have been identified, one at around -200 relative to the transcriptional start site, and another at around -115 (Page 932, Paragraph 3). Wienert teaches mutations in the -200 region (mutations between -201 to -195 including -200 C>T) HBG1/HBG2 promoter thereby disrupting a binding site for the ZBTB7A (Also known as LRF) repressor (Page 935, Figure 3B). Wienert teaches BCL11A as the repressor that binds to the -115 site and that HPFH mutations within the -115 region (-117 to -114, and the 13 bp deletion) impair BCL11A’s ability to directly bind to the promoter and therefore one strategy to elevate HbF levels is to target the fetal globin repressors BCL11A or ZBTB7A directly (Page 934, Paragraph 2 and 4). Wienert teaches a -115 C>T mutation in the HBG1/HBG2 promoter thereby disrupting a binding site for the BCL11A repressor (Page 935, Figure 3B).
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 teachings of Bryson to include the specific point mutations at -200 C>T allowing LRF repressor to bind to the promoter as taught by Wienert because Bryson teaches it is within the ordinary skill in the art to use a method of editing an HBG1 or HBG2 gene loci using a targeted base editor and a guide RNA in CD34+ cells to increase expression of the gamma globin as well as the specific point mutations at -201 C>T, -197 C>T, -196 C>T and -195 C>T and Wienert teaches the -200 C>T mutation of the HBG1/HBG2 promoter of the gamma globin in order for LRF repressor to bind to the promoter.
One would have been motivated to make such a modification in order to receive the expected benefit of the point mutation disrupting the LRF repressor binding site on the promoter subsequently increasing the fetal hemoglobin levels as taught by Wienert.
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 teachings of Bryson to include the specific point mutation at -115 C>T allowing BCL11A repressor to bind to the promoter as taught by Wienert because Bryson teaches it is within the ordinary skill in the art to use a method of editing an HBG1 or HBG2 gene loci using a targeted base editor and a guide RNA in CD34+ cells to increase expression of the gamma globin as well as the specific point mutation at -114 C>T and Wienert teaches the -115 C>T mutation of the HBG1/HBG2 promoter of the gamma globin in order for BCL11A repressor to bind to the promoter.
One would have been motivated to make such a modification in order to receive the expected benefit of the point mutation disrupting the BCL11A repressor binding site on the promoter subsequently increasing the fetal hemoglobin levels as taught by Wienert.
Regarding claim 24, Bryson teaches increased levels of fetal hemoglobin (HbF) can ameliorate the clinical course of inherited disorders of beta-globin gene expression, such as beta thalassemia and sickle cell anemia, and in a group of disorders called hereditary persistence of fetal hemoglobin (HPFH), the expression of one or both of the gamma globin genes (HBGJ/2) of HbF persists at high levels in adult erythroid cells. [0562]. Bryson teaches a method of editing an HBG1 or HBG2 gene loci using a targeted base editor and a guide RNA in CD34+ cells to increase expression of the gamma globin [0564-0565 and 0567]. Bryson teaches a method of editing an HBB polynucleotide comprising a single nucleotide polymorphism (SNP) associated with sickle cell disease, the method comprising contacting the HBB polynucleotide with a base editor in complex with one or more guide polynucleotides, wherein the base editor comprises a polynucleotide programmable DNA binding domain and an adenosine deaminase domain, and wherein the one or more guide polynucleotides target the base editor to effect an A•T to G•C alteration of the SNP associated with sickle cell disease (Page 290, Claim 1).
Response to Arguments - Claim Rejections - 35 USC § 103
The previous rejection of claims 1-3 and 5-8 under 35 U.S.C. 103 as being unpatentable over Bryson et al (WO 2019/217942 A1) in view of Wienert et al (Trends in Genetics, December 2018, Vol. 34, No. 12) has been withdrawn in view of Applicant’s amendments to the claims filed on 12/10/2025.
The previous rejection of claim 4 under 35 U.S.C. 103 as being unpatentable over Bryson et al (WO 2019/217942 A1) in view of Martyn et al (Blood, 133(8), 852–856; 2019) has been withdrawn in view of Applicant’s cancellation of the claim filed on 12/10/2025.
The previous rejection of claim 14 under 35 U.S.C. 103 as being unpatentable over Bryson et al (WO 2019/217942 A1) in view of Koblan et al (Nat Biotechnol 36, 843–846; 2018) has been withdrawn in view of Applicant’s amendments to the claims filed on 12/10/2025.
Conclusion
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 ALEXANDRA ROSE LIPPOLIS whose telephone number is (703)756-5450. The examiner can normally be reached Monday-Friday, 8:00am to 5:00pm EST.
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/ALEXANDRA ROSE LIPPOLIS/Examiner, Art Unit 1637
/CELINE X QIAN/Primary Examiner, Art Unit 1637