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 .
Claims Status
The Amendment filed on 08May2024 is acknowledged in which claim(s) 3, 5-7, 9-42, 44, 48-53, 55, 57-58, 63-68, 70-71, 73-88, 91-134, and 137-140 were canceled by Applicant.
Claim(s) 1-2, 4, 8, 43, 45-47, 54, 56, 59-62, 69, 72, 89-90, and 135-136 is/are currently pending and presented for examination on the merits.
Specification
The use of trade name(s) or mark(s) used in commerce (e.g., Cryostor, Nanomab, Genentech, Merck, Pfizer, Lilly, Zymworks, GSK, Medimmune, Celldex, BeiGene, BioNTech, BMS, Amgen, etcetera), has been noted in this application. The term should be accompanied by the generic terminology; furthermore the term should be capitalized wherever it appears or, where appropriate, include a proper symbol indicating use in commerce such as ™, SM , or ® following the term.
Although the use of trade names and marks used in commerce (i.e., trademarks, service marks, certification marks, and collective marks) are permissible in patent applications, the proprietary nature of the marks should be respected and every effort made to prevent their use in any manner which might adversely affect their validity as commercial marks.
Claim Objections
Claim 2 is objected to because of the following informalities: “(CDRH1 comprising” in line 6 should be “(CDRH1) comprising”. Appropriate correction is required.
Claim Rejections - 35 USC § 112(b)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
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(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claim(s) 89 is/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.
Regarding claim(s) 89, recites the phrase "A frozen vial comprising the composition of claim 72.", rendering the claim indefinite. Specifically, it is unclear if the phrase "A frozen vial comprising the composition.." means that the instant invention is (a) a frozen vial comprising a composition, (b) the composition, wherein the composition is cryopreserved, or (c) something else. For the purposes of compact prosecution, the phrase "A frozen vial comprising the composition of claim 72." is considered to mean “The composition of claim 72, wherein the composition is cryopreserved.”. This rejection may be overcome by amending claim 89 as recited above.
Claim Rejections - 35 USC § 102
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 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.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Claim(s) 1, 8, 47, 56, 59-62, 69, 72, 90, and 135-136 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by US 2020/0308541 A1 (hereinafter “US541”).
Regarding instant claim(s) 1, 8, 47, US541 teaches (1) a CAR comprising (a) an antigen recognition domain, (b) a hinge region, (c) a transmembrane domain, (d) a costimulatory domain, and (c) a signaling domain, (2) an IL15, and (3) a polynucleotide encoding said CAR and IL15 polypeptides joined by a cleavable linker (e.g., T2A) [e.g., title; abstract; ¶ 0047, 0237-0240; figs. 53A-B]. US541 further teaches the antigen recognition domain is an scFv [e.g., ¶ 0007-0009; fig. 53A-B] and that the cancer associated target antigen is ERBB2 (e.g., HER2) [e.g., ¶ 015, 0237, 0300, 0302, 0326, 0537, 0545, 0555].
Regarding instant claim(s) 56, 59, US541 further teaches a host cell comprising an expression vector comprising a recombinant polynucleotide encoding the invention (e.g., CAR/IL15 construct) [e.g., ¶ 0247, 0251].
Regarding instant claim(s) 60-62, US541 further teaches engineered (e.g., CAR/IL15-expressing) NK cells [e.g., ¶ 0261-0264, 0278, 0586, 0752, 0763; fig. 50C].
Regarding instant claim(s) 69, 72, 90, 135-136, US541 further teaches a method of treating cancer comprising administering a therapeutically effective amount of engineered cells (e.g., a pharmaceutical composition) to a subject in need thereof [e.g., ¶ 0588, 0591, 0301]. US541 further teaches the disease or condition is associated with the cancer antigen ERBB (e.g., HER2) [e.g., ¶ 301], and provides methods for treating breast cancer (e.g., HER2 associated) [e.g., ¶ 0016]. US541 also teaches combination therapy wherein the CAR/IL15 NK cells of the invention are combined with additional agents including chemotherapy (e.g., lymphodepleting) [e.g., ¶ 0583].
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claim(s) 2 and 4 is/are rejected under 35 U.S.C. 103 as being unpatentable over US 2020/0308541 A1 (hereinafter “US541”) as applied to claim(s) 1 above, and further in view of WO 2019/098682 A1 (Google Translation relied upon below; hereinafter “WO682”).
The teachings of US541 as recited above apply for claim(s) 1.
US541 does not expressly teach the polynucleotide encodes an hz39D2 (e.g., anti-HER2) CAR/IL15 construct.
Regarding instant claims 2, 4, WO682 teaches a CAR expressing the anti-HER2 hz39D2 clone is effective in treating breast cancer [e.g., ¶ 14, 117, 149-158, 53, 57, 84-85]. WO682 further teaches the hz39D2 clone comprises a VH domain of SEQ ID NO: 39, and a VL of SEQ ID NO: 43 [e.g., ¶ 84-85], which are the same as the instant claimed anti-HER2 VH and VL domains (SEQ ID NOs: 42 and 32; see alignment below), which comprise the instant claimed CDRH1-3 (SEQ ID NOs: 44, 46, 48) and CDRL1-3 (SEQ ID NOs: 34, 36, 38). WO682 also teaches delivery and expression vector comprising polynucleotide(s) encoding the CAR construct [e.g., ¶ 137-138].
Alignment of instant anti-HER2 VH (SEQ ID NO: 42) with WO682 (Anti-HER2 humAb hz39D2 VH protein, SEQ ID 39):
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232
619
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Alignment of instant anti-HER2 VL (SEQ ID NO: 32) with WO682 (Anti-HER2 humAb hz39D2 VL protein, SEQ ID 43):
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236
616
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It would have been prima facie obvious to a person having ordinary skill in the art (PHOSITA) before the effective filing date of the claimed invention to substitute the general HER2 binding domain of the polynucleotide encoding an anti-HER2 CAR/IL15 construct as taught by US541, with the hz39D2 anti-HER2 clone taught by WO682, in the context of designing and developing a polynucleotide encoding a HER2 directed, IL15 expressing CAR for cancer therapy. A PHOSITA would have been motivated to substitute the general HER2 binding domain taught by US541 with the hz39D2 taught by WO682, because US541 teaches a polynucleotide encoding both the CAR and IL15, US541 and WO682 teach the overlapping subject matter of anti-cancer CAR therapy and teach the HER2 antigen as a target, and WO682 teaches the specific anti-HER2 antigen binding domain sequence (e.g., hz39D2 clone). Additionally, US541 taught that IL15 CAR Co-expression is important for the longer persistence and enhanced activity of CAR NK cells [e.g., ¶ 0522-0523], which is why a PHOSITA would have been motivated to utilize the polynucleotide encoding the anti-HER2 CAR/IL15 construct base structure taught by US541 rather than the engineered CAR construct of WO682, which lacks the beneficial IL15 co-expression. There would have been a reasonable expectation of success for a PHOSITA to substitute the general HER2 binding domain of the polynucleotide encoding an anti-HER2 CAR/IL15 construct as taught by US541 taught by US541with the hz39D2 anti-HER2 clone taught by WO682, because US541 teaches the base structure comprises a readily substitutable scFv antigen binding domain, US541 and WO682 teach HER2 directed CAR constructs as well as uses in cancer therapy, and WO682 teaches a specific anti-HER2 antigen binding domain (e.g., hz39D2) that treats cancer. This rationale aligns with the principle of simple substitution of one known element for another to obtain predictable results, supporting a conclusion of obviousness (see MPEP § 2141).
Thus, the invention as a whole is prima facie obvious over the references, especially in the absence of evidence to the contrary.
Claim(s) 43 is/are rejected under 35 U.S.C. 103 as being unpatentable over US 2020/0308541 A1 (hereinafter “US541”) as applied to claim(s) 1 above, and further in view WO 2019/098682 A1 (Google Translation relied upon below; hereinafter “WO682”), and US 2019/0336533 A1 (hereinafter “US533”).
The teachings of US451 as recited above apply for claim(s) 1.
US541 does not expressly teach that the polynucleotide encodes an anti-HER2 CAR/IL15 construct, wherein the CAR construct comprises instant SEQ ID NO: 56.
Regarding instant claim 43, WO682 teaches a CAR expressing the anti-HER2 hz39D2 clone is effective in treating breast cancer [e.g., ¶ 14, 117, 149-158, 53, 57, 84-85]. WO682 further teaches the hz39D2 clone comprises a VH domain of SEQ ID NO: 39, and a VL of SEQ ID NO: 43 [e.g., ¶ 84-85], which are the same as the instant claimed anti-HER2 VH and VL domains (SEQ ID NOs: 42 and 32; see alignments in rejection above), which comprise the instant claimed CDRH1-3 (SEQ ID NOs: 44, 46, 48) and CDRL1-3 (SEQ ID NOs: 34, 36, 38). WO682 teaches the hz39D2 VH and VL domains are joined by a (G4S)3 linker (e.g., forming an scFv) [e.g., ¶ 96-102].
Alignment of the instant claimed anti-HER2 CAR (SEQ ID NO: 56) with WO682 anti-HER2 hz39D2 clone (SEQ ID NO: 43 – (G4S)3 Linker – SEQ ID NO: 39):
CLUSTAL O(1.2.4) multiple sequence alignment
VL(instant SEQ ID NOs: 32); LCDRs(instant SEQ ID NOs: 34,36,38); (G4S)X3 Linker; VH(instant SEQ ID NO: 42); HCDRs(instant SEQ ID NOs: 44, 46, 48)
CAR_56 MALPVTALLLPLALLLHAARPDIQMTQSPSSLSASVGDRVTITCKASQDINSYLSWFQQK 60
WO682_Seq43.L.39 ---------------------DIQMTQSPSSLSASVGDRVTITCKASQDINSYLSWFQQK 39
***************************************
CAR_56 PGKAPKTLIYRANRLVDGVPSRFSGSGSGQDYTLTISSLQPEDFATYYCLQYDEFPWTFG 120
WO682_Seq43.L.39 PGKAPKTLIYRANRLVDGVPSRFSGSGSGQDYTLTISSLQPEDFATYYCLQYDEFPWTFG 99
************************************************************
CAR_56 QGTKVEIKGGGGSGGGGSGGGGSQVQLVQSGSELKKPGASVKVSCKASGYTFTNYGVNWV 180
WO682_Seq43.L.39 QGTKVEIKGGGGSGGGGSGGGGSQVQLVQSGSELKKPGASVKVSCKASGYTFTNYGVNWV 159
************************************************************
CAR_56 RQAPGQGLEWMGWINTHTGEPTYAEEFKGRFVFSLDTSVSTAYLQISSLKAEDTAVYYCA 240
WO682_Seq43.L.39 RQAPGQGLEWMGWINTHTGEPTYAEEFKGRFVFSLDTSVSTAYLQISSLKAEDTAVYYCA 219
************************************************************
CAR_56 RDDYYVRVDYWGQGTTVTVSSAKPTTTPAPRPPTPAPTIASQPLSLRPEACRPAAGGAVH 300
WO682_Seq43.L.39 RDDYYVRVDYWGQGTTVTVSS--------------------------------------- 240
*********************
CAR_56 TRGLDFACDFWVLVVVGGVLACYSLLVTVAFIIFWVRSKRSRLLHSDYMNMTPRRPGPTR 360
WO682_Seq43.L.39 ------------------------------------------------------------ 240
CAR_56 KHYQPYAPPRDFAAYRSERVQPLEENVGNAARPRFERNKRVKFSRSADAPAYQQGQNQLY 420
WO682_Seq43.L.39 ------------------------------------------------------------ 240
CAR_56 NELNLGRREEYDVLDKRRGRDPEMGGKPRRKNPQEGLYNELQKDKMAEAYSEIGMKGERR 480
WO682_Seq43.L.39 ------------------------------------------------------------ 240
CAR_56 RGKGHDGLYQGLSTATKDTYDALHMQALPPR 511
WO682_Seq43.L.39 ------------------------------- 240
Regarding instant claim 43, US533 teaches nucleic acids encoding CARs comprising an OX40L (CD252) intracellular signaling domain increase anti-cancer activity of the CAR expressing immune cell [e.g., title, abstract; ¶ 0040-0041, 0098]. US533 teaches the CAR comprises a signal peptide, an extracellular antigen binding domain, CD8a hinge domain, a CD28 transmembrane domain, a CD28 costimulatory signaling domain, an OX40L signaling domain , and a CD3z signaling domain (e.g., SEQ ID NO: 85, see alignment below) [e.g., tbl. 1, “serial no. C12” ], which is the same as instant claimed CAR comprising SEQ ID NO: 56 in all aspects except for the scFv. US533 teaches the CAR extracellular antigen binding domain can be substituted with an antibody or antigen binding fragment thereof (e.g., scFv) that recognizes the target antigen (e.g., expressed on cancer) [e.g., ¶ 0019, 0076-0077, 0088-0089], and teaches that the cancer is breast cancer [e.g., ¶ 0106, 109; example 3].
Alignment of the instant claimed anti-HER2 CAR (SEQ ID NO: 56) with US533 (SEQ ID NO: 85):
CLUSTAL O(1.2.4) multiple sequence alignment
Signal Seq; scFv; CD8a-Hinge/CD28-TM/CD28-COSTIM/OX40L/CD3z DOMAINS
CAR_56 MALPVTALLLPLALLLHAARPDIQMTQSPSSLSASVGDRVTITCKASQDINSYLSWFQQK 60
US533_Seq85 MALPVTALLLPLALLLHAARPLFNQEVQIPLTESY--------C---------------- 36
*********************
CAR_56 PGKAPKTLIYRANRLVDGVPSRFSGSGSGQDYTLTISSLQPEDFATYYCLQY--DEFPWT 118
US533_Seq85 -GPCPKNWICYKNN----------------------------------CYQFFDESKNWY 61
CAR_56 FGQGTKVEIKGGGGSGGGGSGGGGSQVQLVQSGSELKKPGASVKVSCKASGYTFTNYGVN 178
US533_Seq85 ESQASCMS----------------------QNAS-------LLKVYSKED--------QD 84
CAR_56 WVRQAPGQGLEWMGWINTHTGEPTYAEEFKGRFVFSLDTSVSTAYLQISSLKAEDTAVYY 238
US533_Seq85 L--LKLVKSYHWMGLVHIPTN---------GSWQWEDGSILSPNLLTIIEMQKGDCALYA 133
CAR_56 CARDDYYVRVDYWGQGTTVTVSSAKPTTTPAPRPPTPAPTIASQPLSLRPEACRPAAGGA 298
US533_Seq85 SSFKGYIENCSTPNTYICMQRTVAKPTTTPAPRPPTPAPTIASQPLSLRPEACRPAAGGA 193
*************************************
CAR_56 VHTRGLDFACDFWVLVVVGGVLACYSLLVTVAFIIFWVRSKRSRLLHSDYMNMTPRRPGP 358
US533_Seq85 VHTRGLDFACDFWVLVVVGGVLACYSLLVTVAFIIFWVRSKRSRLLHSDYMNMTPRRPGP 253
************************************************************
CAR_56 TRKHYQPYAPPRDFAAYRSERVQPLEENVGNAARPRFERNKRVKFSRSADAPAYQQGQNQ 418
US533_Seq85 TRKHYQPYAPPRDFAAYRSERVQPLEENVGNAARPRFERNKRVKFSRSADAPAYQQGQNQ 313
************************************************************
CAR_56 LYNELNLGRREEYDVLDKRRGRDPEMGGKPRRKNPQEGLYNELQKDKMAEAYSEIGMKGE 478
US533_Seq85 LYNELNLGRREEYDVLDKRRGRDPEMGGKPRRKNPQEGLYNELQKDKMAEAYSEIGMKGE 373
************************************************************
CAR_56 RRRGKGHDGLYQGLSTATKDTYDALHMQALPPR 511
US533_Seq85 RRRGKGHDGLYQGLSTATKDTYDALHMQALPPR 406
*********************************
It would have been prima facie obvious to a person having ordinary skill in the art (PHOSITA) before the effective filing date of the claimed invention to substitute the CAR and antigen binding domain thereof of the polynucleotide encoding an anti-HER2 CAR/IL15 construct as taught by US541, with the CAR comprising OX40L taught by US533 and the hz39D2 anti-HER2 clone taught by WO682, in the context of designing and developing a polynucleotide encoding an anti-HER2 CAR/IL15 construct for breast cancer therapy. A PHOSITA would have been motivated to substitute the general HER2 antigen binding domain taught by US541 with the hz39D2 taught by WO682 and the CAR comprising OX40L as taught by US533, because US541 teaches a polynucleotide encoding both the CAR and IL15; US541, WO682, and US533 teach the overlapping subject matter of anti-cancer CAR therapy; US541 and WO682 teach the HER2 antigen as a target antigen; WO682 teaches the specific anti-HER2 antigen binding domain sequence (e.g., hz39D2 clone) as a breast cancer therapy; and US533 teaches that including an OX40L intracellular domain increases anti-cancer activity. Additionally, US541 taught that IL15 CAR Co-expression is important for the longer persistence and enhanced activity of CAR NK cells [e.g., ¶ 0522-0523]. Therefore, a PHOSITA would have been motivated to utilize the polynucleotide encoding the anti-HER2 CAR/IL15 construct base structure taught by US541 substituted with the CAR having increased anticancer activity of US533, rather than the engineered CAR construct of US533 alone, which lacks the IL15 co-expression which is beneficial for CAR cell persistence. There would have been a reasonable expectation of success for a PHOSITA to substitute the general HER2 antigen binding domain of the polynucleotide encoding an anti-HER2 CAR/IL15 construct as taught by US541 with the hz39D2 taught by WO682 and the CAR comprising OX40L as taught by US533, because US541 teaches the base structure (e.g., CAR– P2A – IL15 construct) wherein the CAR structure comprises a readily substitutable scFv antigen binding domain, US541, US533, and WO682 teach CAR mediated cancer therapy; US541 and WO682 teach anti-HER2 CARs; WO682 teaches a specific anti-HER2 antigen binding domain (e.g., hz39D2) that treats cancer; and US533 teaches a CAR construct comprising an OX40L that increased anticancer activity. This rationale aligns with the principle of simple substitution of one known element for another to obtain predictable results, supporting a conclusion of obviousness (see MPEP § 2141).
Thus, the invention as a whole is prima facie obvious over the references, especially in the absence of evidence to the contrary.
Claim(s) 45 is/are rejected under 35 U.S.C. 103 as being unpatentable over US 2020/0308541 A1 (hereinafter “US541”) as applied to claim(s) 1 above, and further in view of US 2015/0359853 A1 (hereinafter “US853”).
The teachings of US451 as recited above apply for claim(s) 1.
US541 does not expressly teach that the IL15 comprises instant SEQ ID NO: 22.
Regarding instant claim 45, US853 teaches IL15 and methods of increasing anti-cancer immune cell therapy function [e.g., title, abstract]. US853 teaches IL15 enhances function of immune cells and immune cells expressing CAR(s) [e.g., ¶ 0004, 0019-0020, 0182, 0376]. US853 further teaches native (e.g., wild-type) human IL15 comprising SEQ ID NO: 1 [e.g., ¶ 0059-0060, 0062], which is the same as the instant claimed IL15 sequence (SEQ ID NO: 22).
Alignment of IL15 instant SEQ ID NO: 22 with US853 (Human interleukin-15 (IL-15) polypeptide, SEQ ID 1):
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311
620
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It would have been prima facie obvious to a person having ordinary skill in the art (PHOSITA) before the effective filing date of the claimed invention to substitute the general IL15 of the polynucleotide encoding anti-HER2 CAR/IL15 construct as taught by US541, with the wild-type IL15 construct taught by US853, in the context of designing and developing an anti-HER2 CAR/IL15 cancer therapeutic. A PHOSITA would have been motivated to substitute the general IL15 of the polynucleotide encoding anti-HER2 CAR/IL15 construct as taught by US541 with the wild-type IL15 construct taught by US853, because US541 and US853 both teach IL15 enhances CAR immune cell therapy for cancer; US541 teaches the CAR/IL15 construct structure, and US853 teaches the wild-type IL15 sequence. A PHOSITA would have understood it is ordinary practice in the art to search for widely known sequences (e.g., IL15) rather than creating a sequence de novo. There would have been a reasonable expectation of success for a PHOSITA to substitute the general IL15 of the polynucleotide encoding anti-HER2 CAR/IL15 construct as taught by US541 with the wild-type IL15 construct taught by US853, because US541 teaches the CAR/IL15 construct structure, both US541 and US853 teach the overlapping subject matter of IL15 enhanced function of CAR expressing immune cells, and US853 teaches the wild-type IL15 sequence as an enhancer of said immune cell function. This rationale aligns with the principle of simple substitution of one known element for another to obtain predictable results, supporting a conclusion of obviousness (see MPEP § 2141).
Thus, the invention as a whole is prima facie obvious over the references, especially in the absence of evidence to the contrary.
Claim(s) 54 is/are rejected under 35 U.S.C. 103 as being unpatentable over US 2020/0308541 A1 (hereinafter “US541”), as applied to claim(s) 1 above, and further in view WO 2019/098682 A1 (Google Translation relied upon below; hereinafter “WO682”), US 2019/0336533 A1 (hereinafter “US533”), and US 2015/0359853 A1 (hereinafter “US853”).
The teachings of US451 as recited above apply for claim(s) 1.
US541 does not expressly teach that the polynucleotide encodes an anti-HER2 CAR/IL15 construct comprising instant SEQ ID NO: 59.
The teachings of US451, WO682, and US533 from previous art rejections (claim 43, see above) are incorporated here in full.
The teachings of US541 and US853 from previous art rejections (claim 45, see above) are incorporated here in full.
For clarity of the record, it is noted that the claimed instant SEQ ID NOs: 56 and 59 differ in that the latter additionally comprises T2A and IL15 domains (see alignment below).
Alignment of CAR instant SEQ ID N)s: 56 and 59:
CLUSTAL O(1.2.4) multiple sequence alignment
Anti-HER2 CAR; T2A; IL15
CAR_SeqID56 MALPVTALLLPLALLLHAARPDIQMTQSPSSLSASVGDRVTITCKASQDINSYLSWFQQK 60
CAR.IL15_SeqID59 MALPVTALLLPLALLLHAARPDIQMTQSPSSLSASVGDRVTITCKASQDINSYLSWFQQK 60
************************************************************
CAR_SeqID56 PGKAPKTLIYRANRLVDGVPSRFSGSGSGQDYTLTISSLQPEDFATYYCLQYDEFPWTFG 120
CAR.IL15_SeqID59 PGKAPKTLIYRANRLVDGVPSRFSGSGSGQDYTLTISSLQPEDFATYYCLQYDEFPWTFG 120
************************************************************
CAR_SeqID56 QGTKVEIKGGGGSGGGGSGGGGSQVQLVQSGSELKKPGASVKVSCKASGYTFTNYGVNWV 180
CAR.IL15_SeqID59 QGTKVEIKGGGGSGGGGSGGGGSQVQLVQSGSELKKPGASVKVSCKASGYTFTNYGVNWV 180
************************************************************
CAR_SeqID56 RQAPGQGLEWMGWINTHTGEPTYAEEFKGRFVFSLDTSVSTAYLQISSLKAEDTAVYYCA 240
CAR.IL15_SeqID59 RQAPGQGLEWMGWINTHTGEPTYAEEFKGRFVFSLDTSVSTAYLQISSLKAEDTAVYYCA 240
************************************************************
CAR_SeqID56 RDDYYVRVDYWGQGTTVTVSSAKPTTTPAPRPPTPAPTIASQPLSLRPEACRPAAGGAVH 300
CAR.IL15_SeqID59 RDDYYVRVDYWGQGTTVTVSSAKPTTTPAPRPPTPAPTIASQPLSLRPEACRPAAGGAVH 300
************************************************************
CAR_SeqID56 TRGLDFACDFWVLVVVGGVLACYSLLVTVAFIIFWVRSKRSRLLHSDYMNMTPRRPGPTR 360
CAR.IL15_SeqID59 TRGLDFACDFWVLVVVGGVLACYSLLVTVAFIIFWVRSKRSRLLHSDYMNMTPRRPGPTR 360
************************************************************
CAR_SeqID56 KHYQPYAPPRDFAAYRSERVQPLEENVGNAARPRFERNKRVKFSRSADAPAYQQGQNQLY 420
CAR.IL15_SeqID59 KHYQPYAPPRDFAAYRSERVQPLEENVGNAARPRFERNKRVKFSRSADAPAYQQGQNQLY 420
************************************************************
CAR_SeqID56 NELNLGRREEYDVLDKRRGRDPEMGGKPRRKNPQEGLYNELQKDKMAEAYSEIGMKGERR 480
CAR.IL15_SeqID59 NELNLGRREEYDVLDKRRGRDPEMGGKPRRKNPQEGLYNELQKDKMAEAYSEIGMKGERR 480
************************************************************
CAR_SeqID56 RGKGHDGLYQGLSTATKDTYDALHMQALPPR----------------------------- 511
CAR.IL15_SeqID59 RGKGHDGLYQGLSTATKDTYDALHMQALPPRGSGEGRGSLLTCGDVEENPGPMRISKPHL 540
*******************************
CAR_SeqID56 ------------------------------------------------------------ 511
CAR.IL15_SeqID59 RSISIQCYLCLLLNSHFLTEAGIHVFILGCFSAGLPKTEANWVNVISDLKKIEDLIQSMH 600
CAR_SeqID56 ------------------------------------------------------------ 511
CAR.IL15_SeqID59 IDATLYTESDVHPSCKVTAMKCFLLELQVISLESGDASIHDTVENLIILANNSLSSNGNV 660
CAR_SeqID56 ---------------------------------- 511
CAR.IL15_SeqID59 TESGCKECEELEEKNIKEFLQSFVHIVQMFINTS 694
It would have been prima facie obvious to a person having ordinary skill in the art (PHOSITA) before the effective filing date of the claimed invention to substitute the CAR and antigen binding domain thereof of the polynucleotide encoding an anti-HER2 CAR/IL15 construct as taught by US541, with the CAR comprising OX40L taught by US533 and the hz39D2 anti-HER2 clone taught by WO682, in the context of designing and developing a polynucleotide encoding an anti-HER2 CAR/IL15 construct for breast cancer therapy. A PHOSITA would have been motivated to substitute the general HER2 antigen binding domain taught by US541 with the hz39D2 taught by WO682 and the CAR comprising OX40L as taught by US533, because US541 teaches a polynucleotide encoding both the CAR and IL15; US541, WO682, and US533 teach the overlapping subject matter of anti-cancer CAR therapy; US541 and WO682 teach the HER2 antigen as a target antigen; WO682 teaches the specific anti-HER2 antigen binding domain sequence (e.g., hz39D2 clone) as a breast cancer therapy; and US533 teaches that including an OX40L intracellular domain increases anti-cancer activity. Additionally, US541 taught that IL15 CAR Co-expression is important for the longer persistence and enhanced activity of CAR NK cells [e.g., ¶ 0522-0523]. Therefore, a PHOSITA would have been motivated to utilize the polynucleotide encoding the anti-HER2 CAR/IL15 construct base structure taught by US541 substituted with the CAR having increased anticancer activity of US533, rather than the engineered CAR construct of US533 alone, which lacks the IL15 co-expression which is beneficial for CAR cell persistence. There would have been a reasonable expectation of success for a PHOSITA to substitute the general HER2 antigen binding domain of the polynucleotide encoding an anti-HER2 CAR/IL15 construct as taught by US541 with the hz39D2 taught by WO682 and the CAR comprising OX40L as taught by US533, because US541 teaches the base structure (e.g., CAR– P2A – IL15 construct) wherein the CAR structure comprises a readily substitutable scFv antigen binding domain, US541, US533, and WO682 teach CAR mediated cancer therapy; US541 and WO682 teach anti-HER2 CARs; WO682 teaches a specific anti-HER2 antigen binding domain (e.g., hz39D2) that treats cancer; and US533 teaches a CAR construct comprising an OX40L that increased anticancer activity. This rationale aligns with the principle of simple substitution of one known element for another to obtain predictable results, supporting a conclusion of obviousness (see MPEP § 2141).
Further, it would have been obvious to a PHOSITA to modify the modified polynucleotide encoding hz39D2 CAR/IL15 construct as taught by US541, WO682, and US533 (see above) to include the that the IL15 comprises the human WT IL15 sequence as taught by US853, because US541, WO682 and US533 teach the polynucleotide encoding hz39D2 CAR/IL15 construct structure; US541, WO682, US533, and US853 teach CAR mediated cancer therapy; US541 and US583 teach IL15 co-expression enhances CAR immune cell function; and US583 teaches the WT human IL15 sequence shown in the art to increase immune cell function. There is an expectation of success for a PHOPSITA to substitute the general IL15 of the modified polynucleotide encoding hz39D2 CAR/IL15 construct as taught by US541, WO682, and US533 (see above) with the WT human IL15 sequence taught by US583, because US541, WO682 and US533 teach the polynucleotide encoding hz39D2 CAR/IL15 construct structure; S541 and US583 teach IL15 co-expression enhances CAR immune cell function, and US853 teaches the WT IL15 sequence and that it enhances CAR immune cell function. This rationale aligns with the principle of simple substitution of one known element for another to obtain predictable results, supporting a conclusion of obviousness (see MPEP § 2141).
Thus, the invention as a whole is prima facie obvious over the references, especially in the absence of evidence to the contrary.
Claim(s) 89 is/are rejected under 35 U.S.C. 103 as being unpatentable over US 2020/0308541 A1 (hereinafter “US541”) as applied to claim(s) 1, 60, 69, 72 above, and further in view of Panch et al. ((Molecular Therapy Vol. 27 No 7 July 2019; hereinafter “Panch”).
The teachings of US541as recited above apply for claim(s) ) 1, 60, 69, and 72.
US541 does not expressly teach that the pharmaceutical composition comprising the CAR expressing immune cells (e.g., CAR product) is cryopreserved.
Regarding instant claim(s) 84, Panch teaches that the final CAR expressing immune cell product (e.g., pharmaceutical composition) is cryopreserved by “most commercial manufacturers”, suggesting cryopreservation of CAR cell product is common practice in the art [e.g., pg. 1275, col. 2, ¶ 2-3; fig. 1].
Further, it would have been obvious to a PHOSITA to modify the modified This rationale aligns with the principle of simple substitution of one known element for another to obtain predictable results, supporting a conclusion of obviousness (see MPEP § 2141).
It would have been prima facie obvious to a person having ordinary skill in the art (PHOSITA) before the effective filing date of the claimed invention to combine the anti-HER2 CAR/IL15 cell product taught by US541, with Panch’s teachings of cryopreserving CAR cell products, in the context of designing and developing anti-HER2 CAR/IL15 engineered cells for cancer therapy. A PHOSITA would have been motivated to combine the anti-HER2 CAR/IL15 cell product as taught by US541 with the CAR product cryopreservation as taught by Panch, because US541 teaches the anti-HER2 CAR/IL15 cell product, and Panch teaches it is common practice in the art for manufacturers to cryopreserve the CAR product. There is an expectation of success for a PHOPSITA to cryopreserve the anti-HER2 CAR/IL15 cell product of US541, because Panch teaches it is common practice in the art for manufacturers to cryopreserve the CAR product. This rationale aligns with the principle of applying a known technique to a known method to yield predictable results, supporting a conclusion of obviousness (see MPEP § 2143).
Thus, the invention as a whole is prima facie obvious over the references, especially in the absence of evidence to the contrary.
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.
Claim(s) 1, 45, 47, 56, 59-62, 69, 72, and 89-90 is/are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim(s) 1, 14-15, 17, 39, 42-45, 52, 55, and 73-74 of copending Application No. 18/285,631 (reference application; hereinafter “A631”). Although the claims at issue are not identical, they are not patentably distinct from each other.
Regarding instant claim(s) 1, A631 claim 1 teaches the genus, the instant application teaches a species thereof, and per MPEP2131.02(I) “A species will anticipate a claim to a genus”.
Regarding instant claim(s) 45, A631 claims 14-15 teach that IL15 comprises SEQ ID NO: 22, which is the same as instant IL15 SEQ ID NO: 22.
Alignment of instant IL15 SEQ ID NO: 22 with A631 IL15 SEQ ID NO: 22:
CLUSTAL O(1.2.4) multiple sequence alignment
Instant_SeqID22 MRISKPHLRSISIQCYLCLLLNSHFLTEAGIHVFILGCFSAGLPKTEANWVNVISDLKKI 60
A631_SeqID22 MRISKPHLRSISIQCYLCLLLNSHFLTEAGIHVFILGCFSAGLPKTEANWVNVISDLKKI 60
************************************************************
Instant_SeqID22 EDLIQSMHIDATLYTESDVHPSCKVTAMKCFLLELQVISLESGDASIHDTVENLIILANN 120
A631_SeqID22 EDLIQSMHIDATLYTESDVHPSCKVTAMKCFLLELQVISLESGDASIHDTVENLIILANN 120
************************************************************
Instant_SeqID22 SLSSNGNVTESGCKECEELEEKNIKEFLQSFVHIVQMFINTS 162
A631_SeqID22 SLSSNGNVTESGCKECEELEEKNIKEFLQSFVHIVQMFINTS 162
******************************************
Regarding instant claim(s) 47, A631 claim 17 teaches the polynucleotide encodes a polyprotein comprising the CAR and the IL15.
Regarding instant claim(s) 56, A631 claim 39 teaches a vector comprising the polynucleotide of claim 1.
Regarding instant claim(s) 59, A631 claim 42 teaches a cell comprising the polynucleotide of claim 1.
Regarding instant claim(s) 60, A631 claim 43 teaches a cell expressing the chimeric antigen receptor and the IL15 encoded by the polynucleotide of claim 1.
Regarding instant claim(s) 61, A631 claim 44 teaches the cell of claim 42 is a lymphocyte.
Regarding instant claim(s) 62, A631 claim 45 teaches the lymphocyte of claim 44 is a NK cell.
Regarding instant claim(s) 69, A631 claim 52 teaches a population of cells comprising a plurality of cells of claim 42; the species of instant claim 69 anticipates the species of A631 claim 52.
Regarding instant claim(s) 72, A631 claim 55 teaches a pharmaceutical composition comprising the population of cells of claim 52.
Regarding instant claim(s) 89, A631 claim 73 teaches a frozen vial comprising the composition of claim 55.
Regarding instant claim(s) 90, A631 claim 74 teaches a method of treatment comprising administering the cell of claim 42 to a subject having a disease or condition.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Allowable Subject Matter
Claim 46 is objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims.
Briefly, the polynucleotide(s) encoding IL15 comprising (1) SEQ ID NO: 23; or (2) SEQ ID NO: 24, were found to be nonobvious over the prior art. Briefly, a sequence search of the prior art returned no 100% matches to either of the instant claimed polynucleotide sequences (see closest prior art alignments below). Further, the IL15 polypeptide sequence (SEQ ID NO: 22) was reverse translated into DNA and codon optimized, and neither the non-optimized, nor the optimized DNA sequences resulted in a 100% matched to either of SEQ ID NOs: 23-24. Each of the instant claimed polynucleotide sequences were translated into polypeptide sequences and were confirmed to encode IL15 (e.g., 100% sequence identity match to instant SEQ ID NO: 22).
Alignment of IL15 SEQ ID NO: 23 with Strausberg et al. (Proc. Natl. Acad. Sci. U.S.A. 99 (26), 16899-16903 (2002); PubMedID: 12477932; “Homo sapiens interleukin 15, mRNA (cDNA clone MGC:119225), complete cds.”).
Query Match 59.8%; Score 292.2; Length 1065;
Best Local Similarity 74.8%;
Matches 366; Conservative 0; Mismatches 123; Indels 0; Gaps 0;
Qy 1 ATGAGAATCAGCAAACCACACCTCCGGAGCATATCAATCCAGTGTTACTTGTGCCTTCTT 60
|||||||| |||||||| | | || || || |||||||| |||||||| | |||
Db 81 ATGAGAATTTCGAAACCACATTTGAGAAGTATTTCCATCCAGTGCTACTTGTGTTTACTT 140
Qy 61 TTGAACTCCCATTTCCTCACCGAGGCAGGCATTCATGTGTTCATATTGGGGTGCTTTAGT 120
| ||| ||||| || || || || ||||||||||| ||||| ||||| || || |||
Db 141 CTAAACAGTCATTTTCTAACTGAAGCTGGCATTCATGTCTTCATTTTGGGCTGTTTCAGT 200
Qy 121 GCTGGGCTTCCGAAAACGGAAGCTAACTGGGTAAACGTCATCAGTGACCTTAAAAAAATT 180
|| |||||||| ||||| ||||| |||||||| || || || ||||| | |||||||||
Db 201 GCAGGGCTTCCTAAAACAGAAGCCAACTGGGTGAATGTAATAAGTGATTTGAAAAAAATT 260
Qy 181 GAGGATCTTATCCAATCAATGCACATCGACGCGACTCTCTACACAGAATCTGACGTACAC 240
|| |||||||| ||||| ||||| || || || ||| | || || ||| ||| || |||
Db 261 GAAGATCTTATTCAATCTATGCATATTGATGCTACTTTATATACGGAAAGTGATGTTCAC 320
Qy 241 CCGTCATGCAAAGTCACGGCAATGAAGTGTTTTCTTCTCGAGCTCCAAGTAATTTCCCTG 300
|| |||||||| || ||||||||||| ||||| | ||| | ||||| ||||| ||
Db 321 CCCAGTTGCAAAGTAACAGCAATGAAGTGCTTTCTCTTGGAGTTACAAGTTATTTCACTT 380
Qy 301 GAGTCTGGCGATGCCTCCATCCACGATACGGTTGAAAATCTGATTATATTGGCCAACAAT 360
||||| || ||||| || || ||||| || ||||||||||| || | || |||||
Db 381 GAGTCCGGAGATGCAAGTATTCATGATACAGTAGAAAATCTGATCATCCTAGCAAACAAC 440
Qy 361 AGCCTCAGTTCTAACGGTAACGTGACTGAAAGTGGCTGCAAAGAGTGCGAAGAGCTCGAA 420
|| | |||||| || || || || ||| ||| |||||||| || || || || ||
Db 441 AGTTTGTCTTCTAATGGGAATGTAACAGAATCTGGATGCAAAGAATGTGAGGAACTGGAG 500
Qy 421 GAAAAGAATATCAAGGAGTTCCTCCAATCATTTGTTCACATTGTGCAAATGTTTATCAAC 480
||||| ||||| || || || | || ||||| || ||||| |||||||| ||||||
Db 501 GAAAAAAATATTAAAGAATTTTTGCAGAGTTTTGTACATATTGTCCAAATGTTCATCAAC 560
Qy 481 ACCTCTTGA 489
|| ||||||
Db 561 ACTTCTTGA 569
Alignment of IL15 SEQ ID NO: 24 with Strausberg et al. (Proc. Natl. Acad. Sci. U.S.A. 99 (26), 16899-16903 (2002); PubMedID: 12477932; “Homo sapiens interleukin 15, mRNA (cDNA clone MGC:119225), complete cds.”):
Query Match 59.8%; Score 292.2; Length 1065;
Best Local Similarity 74.8%;
Matches 366; Conservative 0; Mismatches 123; Indels 0; Gaps 0;
Qy 1 ATGCGCATAAGTAAGCCTCATCTGCGGTCCATTTCTATACAATGTTATCTGTGCTTGCTT 60
||| | || || || ||| || | ||||| || || || || |||| || |||
Db 81 ATGAGAATTTCGAAACCACATTTGAGAAGTATTTCCATCCAGTGCTACTTGTGTTTACTT 140
Qy 61 TTGAACTCCCACTTTCTTACGGAAGCAGGCATTCATGTGTTCATTCTGGGTTGTTTTTCT 120
| ||| || ||||| || ||||| ||||||||||| |||||| |||| ||||| |
Db 141 CTAAACAGTCATTTTCTAACTGAAGCTGGCATTCATGTCTTCATTTTGGGCTGTTTCAGT 200
Qy 121 GCCGGGCTGCCCAAAACCGAGGCCAACTGGGTCAACGTGATCAGCGACCTCAAGAAGATC 180
|| ||||| || ||||| || ||||||||||| || || || || || | || || ||
Db 201 GCAGGGCTTCCTAAAACAGAAGCCAACTGGGTGAATGTAATAAGTGATTTGAAAAAAATT 260
Qy 181 GAGGATTTGATTCAAAGTATGCATATAGACGCCACACTCTATACTGAGTCCGACGTTCAC 240
|| ||| | |||||| ||||||||| || || || | ||||| || || ||||||
Db 261 GAAGATCTTATTCAATCTATGCATATTGATGCTACTTTATATACGGAAAGTGATGTTCAC 320
Qy 241 CCGAGTTGTAAAGTTACGGCTATGAAGTGCTTTTTGTTGGAACTCCAGGTGATTTCCCTT 300
|| ||||| ||||| || || |||||||||||| | ||||| | || || ||||| |||
Db 321 CCCAGTTGCAAAGTAACAGCAATGAAGTGCTTTCTCTTGGAGTTACAAGTTATTTCACTT 380
Qy 301 GAATCCGGCGATGCGAGCATCCACGATACGGTAGAGAATCTTATTATTCTGGCGAATAAT 360
|| ||||| ||||| || || || ||||| ||||| ||||| || || || || || ||
Db 381 GAGTCCGGAGATGCAAGTATTCATGATACAGTAGAAAATCTGATCATCCTAGCAAACAAC 440
Qy 361 TCTCTGTCTTCAAATGGGAATGTAACTGAGAGCGGTTGTAAAGAATGCGAAGAACTTGAA 420
| ||||||| |||||||||||||| || || || |||||||| || ||||| ||
Db 441 AGTTTGTCTTCTAATGGGAATGTAACAGAATCTGGATGCAAAGAATGTGAGGAACTGGAG 500
Qy 421 GAAAAGAATATCAAGGAATTTCTTCAGAGTTTCGTGCATATTGTTCAAATGTTCATCAAC 480
||||| ||||| || |||||| | |||||||| || |||||||| |||||||||||||||
Db 501 GAAAAAAATATTAAAGAATTTTTGCAGAGTTTTGTACATATTGTCCAAATGTTCATCAAC 560
Qy 481 ACATCCTGA 489
|| || |||
Db 561 ACTTCTTGA 569
Conclusion
No claims are currently allowed.
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/AMY M. CHATTIN/Examiner, Art Unit 1643
/JULIE WU/Supervisory Patent Examiner, Art Unit 1643