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
Election/Restriction
Applicant’s election, without traverse, of Group I, claims 1-3, 8-11, 15, 18, 21, 23-25, 28, 32-33, 36, 38-41, 46-48, 87-89, 93-94, 102 and 104-106, drawn to an engineered T cell comprising a modified T cell stimulation-associated locus, in the reply filed on 11/24/2025 is acknowledged.
Claims 62, 66-68, 70-72, 75, 80, 95-100 and 107 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim.
Applicant further elects Nur77 as species of endogenous T cell stimulation-associated locus in claims 8, 25 and 39, and elects CAR as species of recombinant receptor in claim 15.
Claims 18, 23-24, 40-41 and 106 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected species, there being no allowable generic or linking claim.
Rejoinder
The species election requirement for species of endogenous T cell stimulation-associated locus as set forth in the Office action mailed on 08/26/2025 has been reconsidered in view of the prior art. FoxP3 is rejoined as an endogenous T cell stimulation-associated locus in claims 8 and 39.
Claim Status
Claims 1-3, 8-11, 15, 18, 21, 23-25, 28, 32-33, 36, 38-41, 46-48, 62, 66-68, 70-72, 75, 80, 87-89, 93-100, 102 and 104-107 are pending.
Claims 18, 23-24, 40-41, 62, 66-68, 70-72, 75, 80, 95-100 and 106-107 are withdrawn.
claims 1-3, 8-11, 15, 21, 25, 28, 32-33, 36, 38-39, 46-48, 87-89, 93-94, 102 and 104-105 are considered on the merits.
Priority
This application is a 371 of PCT/EP2021/067505 (filed on 06/25/2021), which claims benefit from Application 63/044,984 (filed on 06/26/2020). The priority claim of the instant application has been granted and the earliest benefit date is 06/26/2020 from the application 63/044,984.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 07/19/2023 and 11/24/2025 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements are being considered by the examiner. The corresponding signed and initialed PTO forms 1449 have been mailed with this action.
Specification Objections
The disclosure is objected to because it contains an embedded hyperlink and/or other form of browser-executable code (e.g., p. 167, 172, 176). Applicant is required to amend or delete the embedded hyperlink and/or other form of browser-executable code. For example, “www” can be replaced with “world wide web” and “http” can be replaced with “hypertext transfer protocol” as the URL code. See MPEP § 608.01.
Claim Objections
Claim 102 is objected to because of the following informalities:
Claim 102 recites “a target site within a T cell stimulation-associated locus”. Since base claim 33 has recited a target site within an endogenous T cell stimulation-associated locus, it is recommended to change the phrase in claim 102 to “the target site within the T cell stimulation-associated locus”.
Appropriate correction is required.
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 2, 10, 21, 47, 87 and 89 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.
Claim 2 recites the limitation “the recombinant receptor or a portion thereof” in line 2. There is insufficient antecedent basis for this limitation because base claim 1 only recites a recombinant receptor but is silent on “a portion thereof”. It is recommended to remove the limitation “or a portion thereof”.
Claim 10 and claim 47 recite the limitation “the T cell receptor (TCR) complex”. There is insufficient antecedent basis for this limitation because base claims 1 and 33 are silent on a T cell receptor (TCR) complex. It is recommended to change the limitation to “a T cell receptor (TCR) complex”.
Claim 21 recites the limitation “the target site” at the end of (a). There is insufficient antecedent basis for this limitation because base claim 1 is silent on a target site. It is recommended to change to “a target site”.
Claim 87 is dependent on withdrawn Claim 62. Instant Claim 87 is indefinite because it refers to the limitations of the withdrawn claim, thus lacks antecedent basis. Examiner suggests to make claim 87 independent by listing all the limitations of the withdrawn claim. Claim 89 is rejected as being dependent from claim 87.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Rejection over FoxP3 locus
Claims 1-3, 8-9, 21, 33, 36, 39, 46, 87-89 and 93-94 are rejected under 35 U.S.C. 102 (a)(1) as being anticipated by Kim et al., (Nature Immunology. 2007;8:191-197. Prior art of record) as evidenced by Pillai et al., (Clinical Immunology. 2007; 123: 18-29).
With respect to claim 1, Kim teaches a knock-in mouse line (i.e., an engineered mouse line) comprising T cells (i.e., an engineered T cell) in which the endogenous Foxp3 locus is engineered (i.e., a modified T cell stimulation-associated locus, also see instant claim 8 reciting FoxP3 locus as an endogenous T cell-stimulation-associated locus) by targeted insertion of a human diphtheria toxin receptor (i.e., a transgene encoding a recombinant receptor) into the 3ʹ untranslated region of Foxp3 linked by an IRES (i.e., the transgene being operably linked to and being driven by the endogenous transcriptional regulatory element of the Foxp3 locus) (see abstract, see p. 191, last para – p. 192, 1st para, also see p. 196, right col, section “Methods”, para “Mice”, and see Supplementary Figure 1 in the last page).
Regarding the limitation in the last wherein clause, it is noted that this is a contingent limitation and thus is examined as the endogenous transcriptional regulatory element is capable of inducing or upregulating the expression of the operably linked transgene following an activation signal in the T cell. Pillai evidences that virtually all activated CD4+ and CD8+ T-cells transiently upregulate FOXP3 and this activation-induced FOXP3 expression is a broad T cell phenomenon (e.g., abstract and p. 27, right col.). Accordingly, Pillai evidences that the endogenous FoxP3 transcriptional regulatory element is capable of inducing or upregulating the expression of the operably linked FoxP3 and the transgene DTR following an activation signal in the T cell of Kim.
With respect to claim 2, as stated supra, Kim teaches the transgene is inserted into the 3ʹ untranslated region of Foxp3 gene linked by an IRES, such that the transgene is regulated by the endogenous Foxp3 promoter and enhancers (see e.g., p. 192, para 1 and see Supplementary Figure 1 in the last page), thus teaches the endogenous transcriptional regulatory element is a promoter of the endogenous gene locus, and the transgene is present downstream of the promoter.
With respect to claim 3, as stated supra, Pillai evidences that virtually all activated CD4+ and CD8+ T-cells transiently upregulate FOXP3 and this activation-induced FOXP3 expression is a broad T cell phenomenon (e.g., abstract and p. 27, right col.). Accordingly, Pillai evidences that the endogenous FOXP3 transcriptional regulatory element inherently comprises a response element recognized by a transcription factor that is activated following the activation signal.
With respect to claim 8, as stated supra, Kim teaches the endogenous T cell stimulation-associated locus is FoxP3 locus.
With respect to claim 9, Kim teaches the recombinant receptor being a human diphtheria toxin receptor, which comprises an extracellular binding domain.
With respect to claim 21, it is noted that this claim is directed to a product-by-process claim. The applicant is reminded that “even though product-by-process claims are limited by and defined by the process, determination of patentability is based on the product itself. The patentability of a product does not depend on its method of production. If the product in the product-by-process claim is the same as or obvious from a product of the prior art, the claim is unpatentable even though the prior product was made by a different process.” See MPEP § 2113. In the instant case, the claimed product itself, an engineered T cell comprising a transgene integrated into the FoxP3 locus, is the same as the product of the prior art of Kim as evidenced by Pillai, thus the claim is unpatentable even though the prior product was made by a different process.
With respect to claim 33, Kim teaches a targeting vector (i.e., a polynucleotide) comprising (a) a transgene encoding a human diphtheria toxin receptor (i.e., a recombinant receptor), and (b) a 5’ homology arm and a 3’ homology arm linked to the transgene that comprise a nucleic acid sequence homologous to a target site within FoxP3 locus in a T cell (see Supplementary Figure 1 in the last page, homology arms are labeled with an “X”).
With respect to claim 36, as stated supra, Kim teaches the transgene is inserted into the 3ʹ untranslated region of Foxp3 gene linked by an IRES (see Supplementary Figure 1 in the last page), thus teaches the target site is downstream of the endogenous transcriptional regulatory element of FoxP3 locus.
With respect to claim 39, as stated supra, Kim teaches the endogenous T cell stimulation-associated locus is FoxP3 locus.
With respect to claim 46, Kim teaches the recombinant receptor being a human diphtheria toxin receptor, which comprises an extracellular binding domain.
With respect to claim 87, it is noted that this claim is directed to a product-by-process claim. In the instant case, the claimed product itself, an engineered T cell comprising a transgene integrated into the FoxP3 locus, is the same as the product of the prior art of Kim as evidenced by Pillai, thus the claim is unpatentable even though the prior product was made by a different process. See MPEP § 2113.
With respect to claim 88 and claim 89, Kim teaches obtaining single-cell suspensions from lymph nodes, spleen and thymus (p. 196, right col, para “Cell isolation”), thus teaches a composition comprising the engineered T cell of claim 1 in claim 88. As stated supra, the claimed product itself in claim 87 is the same as the product of the prior art of Kim as evidenced by Pillai, thus Kim teaches a composition comprising the engineered T cell of claim 87 in claim 89.
With respect to claim 93 and claim 94, as stated supra, Kim teaches obtaining single-cell suspensions from lymph nodes and spleen and teaches analysis of the cell subsets in those tissues in which the number of CD4+ T cells in DTR knock-in lymph node is 7.97 x 107 and CD8+ T cells 6.45 x 107 (see p. 195, Table 1, row 2 and row 3), thus teaches the composition comprises CD4+ T cells and CD8+ T cells in claims 93-94, and the ratio of CD4+ to CD8+ T cells is 1:3 to 3:1 in claim 94.
Accordingly, Kim, as evidenced by Pillai, anticipates instant claims.
Rejection over a CAR in a T cell stimulation-associated locus
Claims 1-3, 9-11, 15, 21, 28, 32-33, 36, 46-48, 87-89, 93 and 104-105 are rejected under 35 U.S.C. 102 (a)(1) as being anticipated by Busser et al., (WO 2018/073391. Cited in IDS 07/19/2023).
With respect to claim 1, Busser teaches targeted gene insertion for improved immune cells therapy, such as CAR-T cells (e.g., abstract and p. 5, line 13), thus teaches an engineered T cell comprising a transgene encoding a recombinant receptor (i.e., a CAR). Busser teaches the invention relies on expressing a chimeric antigen receptor (CAR) at selected gene loci that are upregulated upon immune cells activation (i.e., a modified T cell stimulation-associated locus comprising the transgene, p. 5, last full para.). Busser teaches genetic insertion of exogenous coding sequence(s) under the transcriptional control of endogenous gene promoters that are sensitive to immune cells activation allows the production of safer immune primary cells of higher therapeutic potential (i.e., the transgene is operably linked to an endogenous transcriptional regulatory element of the locus, wherein the endogenous transcription regulatory element induces or upregulates the expression of the transgene following an activation signal in the T cell, see e.g., abstract).
With respect to claim 2, as stated supra, Busser teaches genetic insertion of exogenous coding sequence(s) under the transcriptional control of endogenous gene promoters (see e.g., abstract and p. 5, last full para.), thus teaches the endogenous transcriptional regulatory element is a promoter, and the transgene is present downstream of the promoter.
With respect to claim 3, as stated supra, Busser teaches genetic insertion of exogenous coding sequence(s) under the transcriptional control of endogenous gene promoters that are upregulated upon immune cells activation (see e.g., abstract and p. 5, last full para.), thus teaches the endogenous transcriptional regulatory element inherently comprises a response element recognized by a transcription factor that is activated following the activation signal.
With respect to claim 9, Busser teaches CARs comprise a targeting moiety, such as an antigen-binding domain of a single-chain antibody (p. 3, lines 11-14), thus teaches the CAR comprises an extracellular binding domain.
With respect to claim 10 and claim 11, Busser teaches the signaling domains for the CARs are derived from the cytoplasmic region of the CD3zeta (p. 3, lines 16-23), thus teaches the CAR comprises an intracellular region comprising an intracellular signaling domain of a component of a TCR complex, such as a CD3 chain.
With respect to claim 15, as stated supra, Busser teaches CAR-T cells (e.g., p. 5, line 13), thus teaches the recombinant receptor is a CAR.
With respect to claim 21, Busser teaches the method of the invention comprises the step of generating a double-strand break (i.e., a genetic disruption) at a locus by expressing sequence-specific nuclease reagents, such as TALEN, ZFN or RNA-guided endonucleases in the presence of a DNA repair matrix set into an AAV6 based vector comprising DNA donor template including two homology arms embedding the exogenous coding sequences (p. 6, para 2).
With respect to claim 28, Busser teaches the immune cells are further made [TCR]negative for allogeneic transplantation. This can be achieved especially by genetic disruption of at least one endogenous sequence encoding at least one component of TCR, such as TRAC (locus encoding TCRalpha) (p. 7, para 1), thus teaches the T cell further comprises a genetic disruption at an endogenous TRAC gene.
With respect to claim 32, Busser teaches one aspect of the present invention is the transduction of AAV vectors in human primary immune cells (e.g., p. 32, lines 28-29), thus teaches the engineered CAR-T cell is a T cell derived from a human subject.
With respect to claim 33, as stated supra, Busser teaches generating a double-strand break at a locus (i.e., a target site within the locus) and a DNA repair matrix comprising a DNA donor template (i.e., a polynucleotide) including two homology arms (i.e., (b) a 5’ homology arm and a 3’ homology arm comprising sequence homologous to a target site within the locus) embedding the exogenous coding sequences (i.e., (a) a transgene encoding the CAR, p. 6, para 2).
With respect to claim 36, as stated supra, Busser teaches genetic insertion of exogenous coding sequence(s) under the transcriptional control of endogenous gene promoters (see e.g., abstract and p. 5, last full para.), thus teaches the target site is downstream of an endogenous transcriptional regulatory element of the locus.
With respect to claim 46, Busser teaches CARs comprise a targeting moiety, such as an antigen-binding domain of a single-chain antibody (p. 3, lines 11-14), thus teaches the CAR comprises an extracellular binding domain.
With respect to claim 47 and claim 48, Busser teaches the signaling domains for the CARs are derived from the cytoplasmic region of the CD3zeta (p. 3, lines 16-23), thus teaches the CAR comprises an intracellular region comprising an intracellular signaling domain of a component of a TCR complex, such as a CD3 chain.
With respect to claim 87, directed to an engineered T cell generated using the method of claim 62, as stated supra, Busser teaches the method of the invention comprises the step of generating a double-strand break at a locus by expressing sequence-specific nuclease reagents, such as TALEN, ZFN or RNA-guided endonucleases (i.e., introducing into a T cell one or more agents that induces a genetic disruption at a target site within the locus) in the presence of a DNA repair matrix set into an AAV6 based vector comprising DNA donor template including two homology arms embedding the exogenous coding sequences (i.e., the polynucleotide of claim 33 for homology directed repair) (p. 6, para 2).
With respect to claim 88 and claim 89, Busser teaches a pharmaceutical composition comprising an engineered primary immune cell (e.g., T cell, p. 48, last line) or immune cell population as previously described (e.g., p. 49, lines 18-19).
With respect to claim 93, Busser teaches the populations of cells mainly comprises CD4 and CD8 positive T-cells (e.g., p. 52, lines 6-7).
With respect to claim 104, Busser teaches integrating exogenous coding sequence at loci, which are specifically transcribed during T-cells activation on a CAR dependent fashion (p. 5, lines 22-24), thus teaches binding of an agent to the extracellular binding domain of the CAR (i.e., CAR-dependent T-cells activation) results in the inducing or transmitting of the activation signal in the cell (such that the loci are specifically transcribed during T-cells activation).
With respect to claim 105, as stated supra, Busser teaches the signaling domains for the CARs are derived from the cytoplasmic region of the CD3zeta (p. 3, lines 16-23), which comprises an ITAM.
Accordingly, Busser anticipates instant 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.
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, 9-11, 15, 21, 28, 32-33, 36, 46-48, 87-89, 93, 102 and 104-105 are rejected under 35 U.S.C. 103 as being unpatentable over Busser et al., (WO 2018/073391. Cited in IDS 07/19/2023).
Claims 1-3, 9-11, 15, 21, 28, 32-33, 36, 46-48, 87-89, 93 and 104-105 are anticipated by Busser as discussed above, thus Busser makes obvious instant claims.
Claim 102 is directed to a kit comprising one or more agents capable of inducing a genetic disruption at the target site and the polynucleotide of claim 33.
As stated supra, Busser teaches generating a double-strand break at a locus by expressing sequence-specific nuclease reagents, such as TALEN, ZFN or RNA-guided endonucleases (i.e., one or more agents capable of inducing a genetic disruption at a target site within the locus) in the presence of a DNA repair matrix comprising DNA donor template including two homology arms embedding the exogenous coding sequences (i.e., the polynucleotide of claim 33) (p. 6, para 2).
Although Busser does not specifically recite a kit, it would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to have combined said components disclosed by Busser into a kit with a reasonable expectation of success. One of ordinary skill in the art would have had a reason to do so for the purposes of convenience and economy.
Hence, the claimed invention as a whole was prima facie obvious to a person of ordinary skill before the effective filing date of the claimed invention in the absence of evidence to the contrary.
Rejection over CAR integrated into Nur77 locus
Claims 1-3, 8-11, 15, 21, 25, 28, 32-33, 36, 38-39, 46-48, 87-89, 93 and 104-105 are rejected under 35 U.S.C. 103 as being unpatentable over Busser et al., (WO 2018/073391. Cited in IDS 07/19/2023) in view of Amin et al., (WO 2019/089982, published 2019 May. Cited in IDS 07/19/2023).
Claims 1-3, 9-11, 15, 21, 28, 32-33, 36, 46-48, 87-89, 93 and 104-105 are anticipated by Busser as discussed above, thus Busser makes obvious instant claims.
Claims 8, 25 and 39 are directed to the T cell stimulation-associated locus being Nur77. Claim 25 is also directed to the genetic disruption being effected by CRISPR-Cas9 using a gRNA that has a targeting domain in a Nur77 gene. Claim 38 is directed to the homology arms being between 50 and 750 nucleotides.
As states supra, Busser teaches the invention relies on expressing a chimeric antigen receptor (CAR) at selected gene loci that are upregulated upon immune cells activation (i.e., a T cell stimulation-associated locus, p. 5, last full para.). Busser further teaches, for instance, the exogenous sequences encoding a CAR can be placed under transcriptional control of the promoter of endogenous genes that are activated by the tumor microenvironment, such as HIF1a, transcription factor hypoxia inducible factor (p. 5, last full para.).
Regarding the locus being Nur77 gene, Busser teaches the inventors have established a first list of endogenous genes (Table 6) which have been found to be particularly appropriate for applying the targeted gene recombination as per the present invention, and the selected loci are particularly relevant for the insertion of sequences encoding CARs (p. 35, 1st para. after the bullet points). In the first page of Table 6, Nr4a1 (also known as Nur77) is listed in row 14 (see p. 100). Furthermore, Busser lists gene loci upregulated in hypoxic tumor conditions useful for gene integration of exogenous coding sequences as per the present invention in Table 13, in which NR4A1 (i.e., Nur77) is listed as a HIF target (see p. 118).
Amin teaches a reporter T-cell in which the reporter is operably linked to a transcriptional regulatory element within the endogenous Nur77 locus and the reporter T cell further contains a chimeric antigen receptor (CAR) for screening the activity of the CAR (e.g., abstract and [0005]). Amin teaches the reporter molecule is integrated by (a) inducing a genetic disruption at a target site at the endogenous locus of Nur77 effected by a CRISPR-Cas9 combination including a guide RNA (gRNA) having a targeting domain that is complementary to the target site, and (b) introducing a template polynucleotide for homology directed repair comprising a 5’ homology arm and a 3’ homology arm that are independently between about 50 and 100, 100 and 250, 250 and 500, 500 and 750 base pairs in length (e.g., [0007]-[0008]). Amin teaches Nur77 expression is sensitive to a primary activation signal in a T cell, signals from a signaling domain of a T cell receptor (TCR) component, and/or a signaling domain comprising an immunoreceptor tyrosine-based activation motif (ITAM) (e.g., [0074]), thus teaches Nur77 locus is a T cell stimulation-associated locus.
Therefore, it would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to have chosen Nur77 gene locus as the T cell stimulation-associated locus for CAR integration as suggested by Busser and Amin with a reasonable expectation of success. Since Busser teaches expressing a CAR at selected gene loci that are upregulated upon immune cells activation or that are activated by the tumor microenvironment (p. 5, last full para.), and suggests a list of selected loci, including Nur77 locus, that are particularly relevant for the insertion of CARs in Table 6 (p. 35, 1st para. after the bullet points, see Table 6 in p. 100), and a list of gene loci, including Nur77 locus, that are upregulated in hypoxic tumor conditions useful for gene integration (see Table 13 in p. 118), and since Amin teaches Nur77 expression is sensitive to activation signals in a T cell and reduces to practice a method for integrating a transgene operably linked within the endogenous Nur77 locus (e.g., [0074], [0005), one of ordinary skill in the art would have had a reason to choose Nur77 gene locus as the T cell stimulation-associated locus for CAR integration in order to obtain controlled CAR expression upon T cell activation and in the tumor microenvironment (Busser, p. 5, last full para.). Furthermore, one of ordinary skill in the art would have had a reason to choose the method of Amin to use CRISPR-Cas9 including a gRNA that has a targeting domain complementary to a target site in the Nur77 gene and to use a template having 5’ and 3’ homology arms being between 50 and 750 nucleotides since Amin has reduced to practice the method for targeted integration of a transgene into the Nur77 locus.
Hence, the claimed invention as a whole was prima facie obvious to a person of ordinary skill before the effective filing date of the claimed invention in the absence of evidence to the contrary.
Conclusion
No claims are allowed.
Examiner Contact Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Jianjian Zhu whose telephone number is (571)272-0956. The examiner can normally be reached M - F 8:30AM - 4PM (EST).
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/JIANJIAN ZHU/Examiner, Art Unit 1631