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
Claims 1-10 and 12-17 are pending in the instant application.
Claim Rejections Withdrawn
The rejections to claims 5-6 under 35 USC §112(b) are withdrawn in view of claim amendment.
The rejections to claims 1-10, 12-13, and 15-17 under 35 USC §103 are withdrawn in view of claim amendment.
New Claim Rejections Necessitated by Amendment
Claims 1-10 and 12-17 are objected to because of the following informalities:
Regarding instant claim 1 a conjunction of “and” is missing following “SEQ ID NO:7; “ in line 8. Instant claims 2-4, 7-10 and 12-17 are dependent on instant claim 1 and further include the claimed subject matter.
Regarding instant claim 5 a conjunction of “and” is missing following “SEQ ID NO:7; “ in line 9.
Regarding instant claim 6, a conjunction of “and” is missing following “SEQ ID NO:7; “ in line 10.
Appropriate correction is required.
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.
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 1, 4, 6-10, 12-13, and 15-17 are rejected under 35 U.S.C. 103 as being unpatentable over US 20160136287 (Toellner KM et al. reference of record), US 5,843,462 (Conti-Fine BM et al.), Slingluff CL et al. (Cancer J 2011 17(5):343-50 reference of record), and Sercarz EE et al. (Nature Reviews Immunology 2003 3 621–629 reference of record).
Regarding instant claims 1-2, 4, 7-10, and 13, Toellner taught administration of a composition for provoking an immune memory response in a patient to an autoantigen target, wherein the patient is: 1) pre-exposed to at least one carrier epitope wherein the carrier protein will itself elicit an immune memory response; and 2) upon re-administration of the carrier protein, this time conjugated to the target, the immune memory response to the carrier is again elicited (page 1, paragraphs 5-6). Toellner taught diphtheria toxoid or the non-toxic fragment C of tetanus toxin (FrC) as carrier proteins (page 1, paragraph 7). Toellner taught the amino acid sequence of Diphtheria toxoid in SEQ ID NO:1 and fragments of SEQ ID NO:1 as the carrier protein (page 2, paragraph 7). Regarding instant claims 1-2, 4, 7-10, and 13, Toellner taught a method of treating mammalian mouse subjects with cancer wherein the subjects were primed with a tumor immune enhancer comprising fragment C of tetanus toxin (FrC) in alum, wherein alum is a DC activator (instant claim 9), then administered a tumor vaccine pharmaceutical composition (instant claim 10) of murine CLEC14a-fragment C of tetanus toxin (muCLEC14a-FrC) which would be a tumor-treating drug, with the pharmaceutically acceptable excipient PBS as a tumor immune enhancer drug wherein an enhanced immune response was induced that had better survival after tumor implantation and vaccination than subjects non-primed and non-vaccinated (page 6, [0065] and Fig. 5), wherein CLEC14a is a tumor endothelial cell antigen (page 3, [0073]) (instant claim 8)(instant claims 4, 7, and 13). Thus, priming with a tumor immune enhancer then administering a vaccine composition conjugated to the tumor immune enhancer is effective. Toellner taught the protein sequence of FrC as SEQ ID NO:2 (page 2, [0016]) and Clec14a-FrC as SEQ ID NO:22 (page 17). Regarding instant claim 6, Toellner taught a lentiviral expression vector of mouse CLEC14a linked to non-toxic fragment C of tetanus toxin (FrC) (page 6, [0060] and Fig. 3.), which is an isolated nucleic acid molecule which encodes for a polypeptide. Regarding instant claim 12, Toellner taught a kit comprising the composition as defined herein for a disease condition to be treated in a patient wherein, the kit further comprises instructions for use (page 3, [0030].
Toellner does not teach a tumor immune enhancer with the sequence of ITAENTPLPIAGVLLPTIPGKLD, but this is obvious in view of Conti-Fine, Slingluff, and Sercarz.
Conti-Fine taught administration of the diphtheria peptide ‘462 SEQ ID NO: 4 TAENTPLPIAGVLLPTIPGK containing amino acids 421-440 effectively induced proliferaton of CD4+ enriched PBMC cells (Fig. 3A). Conti-Fine taught: i) if a CD4+ cell possesses receptors or a receptor complex which enables it to recognize a given MHC class II product-antigen complex, it becomes activated, proliferates and generates lymphokines, such as interleukin 2 (IL-2); ii) the lymphokines in turn cause the proliferation of several types of "killer" cells, including Tc cells and macrophages, which can exhibit antimicrobial and tumoricidal activity; and ii) after stimulation subsides, survivors of the expanded CD4+ cells remain as member cells in the body, and can expand rapidly again when the same antigen is presented (column 8, lines 28-37)
Slingluff taught recent work with long peptides that encompass short minimal epitopes suggests that these longer peptides as more effective immunogens than the minimal peptides (page 8, first paragraph). Slingluff taught the extra length contributes to a tertiary structure that may protect from exopeptidase-mediated degradation, and they are too long to be presented directly on MHC; so they must be internalized by professional APC and processed for presentation (e.g. CD11c+ DC) (page 8, first paragraph). Slingluff taught unlike short peptides, long peptides induce memory CD8+ T cell responses that are boosted dramatically on repeat vaccination in mice, and induce substantially improved tumor control compared to vaccination with short peptides (page 8, first paragraph). Slingluff taught induction of helper T cells reactive to epitopes within the long peptide have been implicated as necessary for long term T cell memory (page 8, first paragraph). Slingluff taught this is supported by the finding that the improved immunologic responses and tumor control are blocked in mice knocked out for CD4 or for CD40 (page 8, first paragraph). Slingluff taught a vaccine using long peptides from HPV-16 for squamous vulvar neoplasia has induced clinical regressions in most patients, supporting clinical activity of long peptide vaccines (page 8, first paragraph). Slingluff taught using these long peptides promises to induce a broad and more durable adaptive immune responses against multiple antigens (page 8, first paragraph).
Sercarz taught rather than the shorter MHC class II peptides being optimal for binding, inducing or recalling responses to them, the opposite was true wherein longer peptides were much better, wherein a 23-mer peptide was more than 32 times better than the 10-mer cytochrome c peptide (pages 622 to 623 bridging paragraph). Thus, peptides lengthened to lengths of about 20 amino acids and longer are expected to be better.
Regarding instant claims 1, 4, 6-10, 13, and 15-17, it would have been obvious for a person having ordinary skill in the art to take the method of Toellner of effectively treating mammalian subjects with cancer wherein the subjects were: A) primed with a tumor immune enhancer pharmaceutical composition comprising fragment C of tetanus toxin (FrC) in alum; then B) administered a tumor vaccine pharmaceutical composition of murine CLEC14a-fragment C of tetanus toxin (muCLEC14a-FrC), with the pharmaceutically acceptable excipient PBS as a tumor immune enhancer drug wherein an enhanced immune response was induced that had better survival after tumor implantation and vaccination than subjects non-primed and non-vaccinated – and: 1) exchange the tumor immune enhancer of FrC for a diphtheria toxoid fragment as taught by Toellner; 2) produce the tumor immune enhancer polypeptide by lentiviral expression which contains an isolated nucleic acid molecule which encodes for the polypeptide as taught by Toellner; and 3) use the diphtheria peptide immune enhancer as TAENTPLPIAGVLLPTIPGK and further extend the fragment to include a longer peptide which would include the peptide sequence ITAENTPLPIAGVLLPTIPGKLD in view of Conti-Fine, Slingluff , and Sercarz.
This is obvious because: 1) Toellner taught diphtheria toxoid or the non-toxic fragment C of tetanus toxin (FrC) as carrier proteins for provoking an immune memory response; 2) Toellner taught a lentiviral expression vector of mouse CLEC14a linked to non-toxic fragment C of tetanus toxin (FrC), which is an isolated nucleic acid molecule which encodes for a polypeptide tumor immune enhancer; 3a) Conti-Fine taught administration of the diphtheria peptide ‘462 SEQ ID NO: 4 TAENTPLPIAGVLLPTIPGK containing amino acids 421-440 effectively induced proliferaton of CD4+ enriched PBMC cells and i) if a CD4+ cell possesses receptors or a receptor complex which enables it to recognize a given MHC class II product-antigen complex, it becomes activated, proliferates and generates lymphokines, such as interleukin 2 (IL-2); ii) the lymphokines in turn cause the proliferation of several types of "killer" cells, including Tc cells and macrophages, which can exhibit antimicrobial and tumoricidal activity; and ii) after stimulation subsides, survivors of the expanded CD4+ cells remain as member cells in the body, and can expand rapidly again when the same antigen is presented; 3b) Slingluff taught: i) longer peptides as more effective immunogens than the minimal peptides; ii) long peptides induce memory CD8+ T cell responses that are boosted dramatically on repeat vaccination in mice, and induce substantially improved tumor control compared to vaccination with short peptides; iii) induction of helper T cells reactive to epitopes within the long peptide have been implicated as necessary for long term T cell memory; iv) long peptides promises to induce a broad and more durable adaptive immune responses against multiple antigens; and 3c) Sercarz taught rather than the shorter MHC class II peptides being optimal for binding, inducing or recalling responses to them, the opposite was true wherein longer peptides were much better, wherein a 23-mer peptide was more than 32 times better than the 10-mer cytochrome c peptide. Thus, extending the TAENTPLPIAGVLLPTIPGK diphtheria peptide to a longer length would encompass the obvious variant of ITAENTPLPIAGVLLPTIPGKLD.
There is a reasonable expectation of success because: 1) Toellner taught priming with a tumor immune enhancer then administering a vaccine composition conjugated to the tumor immune enhancer is effective; 2) Toellner taught a lentiviral expression vector of mouse CLEC14a linked to non-toxic fragment C of tetanus toxin (FrC), which is an isolated nucleic acid molecule which encodes for the polypeptide tumor immune enhancer; 3a) Conti-Fine taught administration of the diphtheria peptide ‘462 SEQ ID NO: 4 TAENTPLPIAGVLLPTIPGK containing amino acids 421-440 effectively induced proliferaton of CD4+ enriched PBMC cells and i) if a CD4+ cell possesses receptors or a receptor complex which enables it to recognize a given MHC class II product-antigen complex, it becomes activated, proliferates and generates lymphokines, such as interleukin 2 (IL-2); ii) the lymphokines in turn cause the proliferation of several types of "killer" cells, including Tc cells and macrophages, which can exhibit antimicrobial and tumoricidal activity; and ii) after stimulation subsides, survivors of the expanded CD4+ cells remain as member cells in the body, and can expand rapidly again when the same antigen is presented; 3b) Slingluff taught: i) longer peptides may be more effective immunogens than the minimal peptides; ii) long peptides induce memory CD8+ T cell responses that are boosted dramatically on repeat vaccination in mice, and induce substantially improved tumor control compared to vaccination with short peptides; iii) induction of helper T cells reactive to epitopes within the long peptide have been implicated as necessary for long term T cell memory; iv) long peptides promises to induce a broad and more durable adaptive immune responses against multiple antigens; and 3c) Sercarz taught rather than the shorter MHC class II peptides being optimal for binding, inducing or recalling responses to them, the opposite was true wherein longer peptides were much better, wherein a 23-mer peptide was more than 32 times better than the 10-mer cytochrome c peptide. Thus, peptides with an extension of 23 or more would be expected to be effective. Thus, extending the TAENTPLPIAGVLLPTIPGK diphtheria peptide to a longer length would encompass the obvious variant of ITAENTPLPIAGVLLPTIPGKLD.
This would produce a method of Toellner, Conti-Fine, Slingluff, and Sercarz of treating mammalian subjects with cancer wherein the subjects are: A) primed with a tumor immune enhancer composition comprising the diphtheria fragment ITAENTPLPIAGVLLPTIPGKLD, which is identical to instant SEQ ID NO:4 wherein Z0 and Z2 are none (instant claim 1), in alum, wherein alum is a DC activator (instant claim 9); then B) administered a tumor vaccine pharmaceutical composition (instant claim 10) of murine CLEC14a-diphtheria fragment ITAENTPLPIAGVLLPTIPGKLD (muCLEC14a- ITAENTPLPIAGVLLPTIPGKLD) which would be a tumor-treating drug, with the pharmaceutically acceptable excipient PBS as a tumor immune enhancer drug wherein an enhanced immune response is produced that enhances tumor immunity, wherein a CD8+ T cell response is naturally induced (instant claim 4), wherein CLEC14a is a tumor endothelial cell antigen (instant claim 8), and wherein the tumor immune enhancer and murine CLEC14a-diphtheria fragment ITAENTPLPIAGVLLPTIPGKLD are produced with an isolated nucleic acid molecule in a lentivirus (instant claim 6) (instant claims 7, 13, and 15-17).
Regarding instant claim 12, it would have been obvious for a person having ordinary skill in the art to take compositions A) and B) above in the combined method of Toellner, Conti-Fine, Slingluff, and Sercarz – and: 1) include the compositions in a kit in separate containers with instructions for use as taught by Toellner.
This is obvious because: a1) Toellner taught a kit comprising the composition as defined herein for a disease condition to be treated in a patient wherein, the kit further comprises instructions for use; and 1b) the compositions of A) and B) are administered separately so they would need separate containers in the kit.
There is a reasonable expectation of success because: 1) a kit was taught by Toellner and would allow a single kit that contained all necessary components to be together for patients.
Response to Arguments
Applicant amended the independent claim 1 and 5-6.
The updated rejection is above.
Claims 1-4, 6-10, 12-13, and 15-17 are rejected under 35 U.S.C. 103 as being unpatentable over US 20160136287 (Toellner KM et al. reference of record), US 5,843,462 (Conti-Fine BM et al.), Slingluff CL et al. (Cancer J 2011 17(5):343-50 reference of record), and Sercarz EE et al. (Nature Reviews Immunology 2003 3 621–629 reference of record) as applied to claims 1, 4, 6-10, 12-13, and 15-17 above, and further in view of Oh D et al. (Mol. Pharmaceutics 2014, 11, 8, 2845–2854 reference of record) and Grau M et al. (Cell Mol Life Sci. 2018 75(16):2887-2896 reference of record).
Toellner, Conti-Fine, Slingluff, and Sercarz are described above.
Toellner does not teach a tumor immune enhancer wherein at least one of Z0 and Z2 contains (Arg)n structure, and wherein n is a positive integer of 3-6, but this is obvious in view of Oh and Grau.
Oh taught fluorescence-labeled acylated cyclic peptide dodecanoyl-[R5] and linear peptide dodecanoyl-(R5) showed higher cellular uptake than that of control 5,6-carboxyfluorescein, respectively via a mechanism of peptide internalization of energy-dependent endocytosis (abstract). Oh taught dodecanoyl-[R5] and dodecanoyl-[R6], which comprised (Arg)5 and (Arg)6, enhanced the intracellular uptake of a fluorescence-labeled cell-impermeable negatively charged phosphopeptide (abstract).
Grau taught cell penetrating peptides (CPPs) efficiently penetrate cell membranes, even when linked to antigenic cargos, which can induce both CD8 and CD4 T-cell responses (abstract). Grau taught CPP-based cancer vaccines represent a flexible and powerful means to extend therapeutic vaccination to many cancer indications (abstract). Grau taught dendritic cells (DCs) are professional antigen presenting cells (APCs) able to activate both CD8 and CD4 T cells by presenting captured-Ag in association with MHC-I or MHC-II molecules, respectively; and CPPs can facilitate this key immunological mechanism (page 2888, left column, second paragraph).
Regarding instant claims 2-3, it would have been obvious for a person having ordinary skill in the art to take the tumor immune enhancer of Toellner, Conti-Fine, Slingluff, and Sercarz above – and: 1) include a (Arg)n structure in Z0 wherein n is 5 or 6 in view of Oh and Grau.
This is obvious because: 1a) Oh taught dodecanoyl-[R5] and dodecanoyl-[R6], which comprised (Arg)5 and (Arg)6, enhanced the intracellular uptake of a fluorescence-labeled cell-impermeable negatively charged phosphopeptide; and 1b) Grau taught: i) cell penetrating peptides (CPPs) efficiently penetrate cell membranes, even when linked to antigenic cargos, which can induce both CD8 and CD4 T-cell responses; ii) CPP-based cancer vaccines represent a flexible and powerful means to extend therapeutic vaccination to many cancer indications; and iii) dendritic cells (DCs) are professional antigen presenting cells (APCs) able to activate both CD8 and CD4 T cells by presenting captured-Ag in association with MHC-I or MHC-II molecules, respectively; and CPPs can facilitate this key immunological mechanism.
There is a reasonable expectation of success because: 1a) inclusion of a dodecanoyl-[R5] or dodecanoyl-[R6] cell penetrating peptide would increase uptake of the immune enhancing polypeptide comprising ITAENTPLPIAGVLLPTIPGKLD; and 1b) Grau taught: i) cell penetrating peptides (CPPs) efficiently penetrate cell membranes, even when linked to antigenic cargos, which can induce both CD8 and CD4 T-cell responses; ii) CPP-based cancer vaccines represent a flexible and powerful means to extend therapeutic vaccination to many cancer indications; and iii) dendritic cells (DCs) are professional antigen presenting cells (APCs) able to activate both CD8 and CD4 T cells by presenting captured-Ag in association with MHC-I or MHC-II molecules, respectively; and CPPs can facilitate this key immunological mechanism.
Response to Arguments
Applicant amended the independent claim 1 and 5-6.
The updated rejection is above.
Claims 1, 4-10, 12-13, and 15-17 are rejected under 35 U.S.C. 103 as being unpatentable over US 20160136287 (Toellner KM et al. reference of record), US 5,843,462 (Conti-Fine BM et al.), Slingluff CL et al. (Cancer J 2011 17(5):343-50 reference of record), and Sercarz EE et al. (Nature Reviews Immunology 2003 3 621–629 reference of record) as applied to claims 1, 4, 6-10, 12-13, and 15-17 above, and further in view of Falugi F et al. (Euro J Immunology 2001 31(12) 3816-3824 reference of record) and Diethelm-Okita BM et al. (The Journal of Infectious Diseases 2000;181:1001–9 reference of record).
Toellner, Conti-Fine, Slingluff, and Sercarz are described above.
Toellner does not teach a multimer, which is composed of m monomers in series connection, and has a function of enhancing tumor immunity, wherein, m is a positive integer ≥ 2, and each monomer independently has the structure of formula I, but this is obvious in view of Falugi.
Falugi taught carrier proteins constituted by multimeric strings in series of human CD4+ T cell epitopes from pathogen-derived antigens comprising tetanus toxin, wherein each of these epitopes is defined as universal in that it binds to many human MHC class II molecules, and wherein when conjugated to an antigen, these carriers elicit a potent anti-antigen antibody response in vivo (abstract). Falugi taught the multimers in series of CD4+ T cell epitopes fused to an antigen caused a greater immune response to the antigen (Fig. 2)
Diethelm-Okita taught diphtheria toxoid contains the CD4 universal epitope of diphtheria toxoid 271-290, which is recognized in more than 80% of subjects studied (abstract). This corresponds to a sequence of PVFAGANYAAWAVNVAQVID.
Regarding instant claim 5, it would have been obvious for a person having ordinary skill in the art to take the tumor immune enhancer of Toellner, Conti-Fine, Slingluff, and Sercarz above – and: 1) include a multimeric string in series of the tumor immune enhancer of Toellner above wherein the m monomers is a positive integer ≥ 2; 2) further include the CD4 universal epitope of diphtheria toxoid 271-290 of sequence of PVFAGANYAAWAVNVAQVID as a tumor immune enhancer in the multimer; and 3) further extend the fragment to include a longer peptide which would include the peptide sequence TGTNPVFAGANYAAWAVNVAQVID in the multimer view of Conti-Fine, Slingluff , and Sercarz.
This is obvious because: 1) Falugi taught carrier proteins constituted by multimeric strings in series of human CD4+ T cell epitopes from pathogen-derived antigens comprising elicit a potent anti-antigen antibody response in vivo and a greater immune response to the antigen; 2) diphtheria toxoid 271-290 is a CD4 universal epitope which is recognized in more than 80% of subjects studied and corresponds to a sequence of PVFAGANYAAWAVNVAQVID; 3a) Slingluff taught: i) longer peptides as more effective immunogens than the minimal peptides; ii) long peptides induce memory CD8+ T cell responses that are boosted dramatically on repeat vaccination in mice, and induce substantially improved tumor control compared to vaccination with short peptides; iii) induction of helper T cells reactive to epitopes within the long peptide have been implicated as necessary for long term T cell memory; iv) long peptides promises to induce a broad and more durable adaptive immune responses against multiple antigens; and 3c) Sercarz taught rather than the shorter MHC class II peptides being optimal for binding, inducing or recalling responses to them, the opposite was true wherein longer peptides were much better, wherein a 23-mer peptide was more than 32 times better than the 10-mer cytochrome c peptide. Thus, extending the PVFAGANYAAWAVNVAQVID diphtheria peptide to a longer length would encompass the obvious variant of TGTNPVFAGANYAAWAVNVAQVID.
There is a reasonable expectation of success because: 1) the multimer comprising multiple CD4+ T cell epitopes fused to the antigen would be expected to elicit a potent anti-antigen antibody response in vivo and a greater immune response to the antigen as a multimer; 2) diphtheria toxoid 271-290 is a CD4 universal epitope which is recognized in more than 80% of subjects studied and corresponds to a sequence of PVFAGANYAAWAVNVAQVID; 3a) Slingluff taught: i) longer peptides may be more effective immunogens than the minimal peptides; ii) long peptides induce memory CD8+ T cell responses that are boosted dramatically on repeat vaccination in mice, and induce substantially improved tumor control compared to vaccination with short peptides; iii) induction of helper T cells reactive to epitopes within the long peptide have been implicated as necessary for long term T cell memory; iv) long peptides promises to induce a broad and more durable adaptive immune responses against multiple antigens; and 3b) Sercarz taught rather than the shorter MHC class II peptides being optimal for binding, inducing or recalling responses to them, the opposite was true wherein longer peptides were much better, wherein a 23-mer peptide was more than 32 times better than the 10-mer cytochrome c peptide. Thus, peptides with an extension of 23 or more would be expected to be effective. Thus, extending the PVFAGANYAAWAVNVAQVID diphtheria peptide to a longer length would encompass the obvious variant of TGTNPVFAGANYAAWAVNVAQVID.
This would produce a tumor immune enhancer of Toellner, Conti-Fine, Slingluff, Sercarz, Falugi, and Diethelm-Okita of a multimeric string of the tumor immune enhancer of ITAENTPLPIAGVLLPTIPGKLD, which is instant SEQ ID NO:4, and TGTNPVFAGANYAAWAVNVAQVID, which is identical to instant SEQ ID NO: 2 wherein the m monomers is a positive integer ≥ 2.
Response to Arguments
Applicant amended the independent claim 1 and 5-6.
The updated rejection is above.
Allowable Subject Matter
Claim 14 is objected to as being dependent upon a rejected base claim, but would be allowable is rewritten in independent form, including all of the limitations of the base claim and any intervening claims.
Conclusion
Instant claims 1-10 and 12-13, and 15-17 are rejected. Instant claim 14 is objected to.
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/J.J.S./ Examiner, Art Unit 1643
/JULIE WU/ Supervisory Patent Examiner, Art Unit 1643
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