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 .
Restrictions/Elections
Applicant’s election of the following invention/species without traverse, as set forth in the Reply filed 13 August 2025, is acknowledged:
An antigen binding domain that specifically binds HLA-A*02 having CDRs SEQ ID NOs: 22-27 (as in claim 107)
A hinge domain according to SEQ ID NO. 19 (claim 96 and new claim 129)
An inhibitory receptor according to SEQ ID NO: 122 (claims 109-111), encoded by SEQ ID NO: 123 (claim 113)
An immunoreceptor tyrosine-based inhibitory motif according to SEQ ID NO: 8 (claim 91).
Claims 91-101, 103-131 read on the elected species.
Status of the Claims
Claims 91-134 are currently pending. Claims 102 and 132-134 are withdrawn. Claims 91-101, 103-131 are the subject of this Office Action. This is the first Office Action on the merits of the claims.
Information Disclosure Statement
The references cited on the information disclosure statement(s) were considered and have been made of record.
Claim Rejections - 35 USC § 112
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 the first paragraph of pre-AIA 35 U.S.C. 112:
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 of carrying out his invention.
Claims 91-101, 103-131 are rejected under 35 U.S.C. 112(a) as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Regarding claim 92, applicant claims a chimeric receptor polypeptide with an antigen binding domain. Antigen binding domains within the scope of the claim therefore would encompass not only a wide variety of antibody-based variants and molecules, but also as is claimed other types of antigen binding polypeptides such as a TCR construct or for instance any type of ligand which may bind to another protein, the basis for which resides most if not all inter-cellular interactions. Looking to the specification, the applicant has disclosed with respect to LILRB1 inhibitory receptors, Ligand binding domains that comprise scFv molecules which bind to antigens HLA-A*02 and NY-ESO-1 in one instance and a modified TCR alpha-beta complex which binds to antigen as a MHC-peptide complex (Fig 1-3). As the TCR alpha TCR beta constructs appear to comprise two separate polypeptides this does not satisfy the requirements of “a polypeptide” CAR as described in the claims. It is therefore found that the applicant has described one species of “antigen binding domain” embodied as three scFv (two of which bind to HLA-A*02 one binds NY-ESO-1). One would therefore conclude that the applicant has not disclosed a representative number of species of the broad genus of “antigen binding domain” to satisfy the written description requirement (see MPEP 2163 3(a) (ii)).
Similarly in 91(a) and (b), (from which all claims depend) applicant has claimed “an LILRB1 hinge domain” and “a transmembrane domain”. With respect to LILRB1 hinge domains applicant has disclosed, 8 sequences which are derived from LILRB1 and function as “an LILRB1” hinge domain. It appears that SEQ ID NO: 4 is the unmodified LILRB1 hinge domain, SEQ ID NO: 80 appears identical with the addition of a single extra V amino acid at the C terminus. Applicant appears to include SEQ ID NOs: 82-84 as sequences satisfying the requirements of claim 91 (a), sequences which have very low aggregate sequence identity with the base LILRB1 sequences. The applicant has at most therefore disclosed 8 sequences which are fragments of the LILRB1 hinge domain while claiming the large genus of sequences that may be interpreted to contain any sequence greater than one amino acid of the naturally occurring LILRB1 hinge domain, or in fact as almost any sequence at all that functions as a hinge domain, as evidenced by the low amount of sequence homology of the SEQ ID NOs: 82-84 to the SEQ ID Nos 4 and 80. Therefore one can see that 91(a) encompasses a broad genus of amino acid sequences which may as defined be only 2 amino acids in length, and any combination of the amino acids of the defined hinge sequence. The applicant has therefore disclosed a small number of species of the broad claimed genus of defined LILRB1 derived hinge molecules which might satisfy the functional requirement as a hinge molecule.
Further, applicant has not in the specification disclosed structural characteristics to guide one of ordinary skill in the art as to what constitutes an appropriate hinge molecule to allow one to recognize that the applicant was in possession of the claimed genus. With respect to the transmembrane domain, an identical issue exists with the applicant singularly disclosing SEQ ID NO: 5 as a derived LILRB1 transmembrane domain.
Additional description issues arise with respect to claims 93, 95-99, 108-109, and 131, as applicant claims sequences that are 95% identical to the referenced sequences which function as described in the claims. As described above for claim 91, applicant has therefore claimed a broad genus of molecules, while particularly disclosing a small, or singular number of species of this genus which satisfy the claim. One may hypothetically mutate any of the amino acids or utilize truncated mutants, or mutants with small fragments that are 95% identical to the claimed sequences and still comply with the claims as written. Applicant does not however disclose in the specification particularly which structural amino acids may be changed, or in fact omitted completely and still satisfy the claimed function. This is of particular concern with respect to claims 108-109, where it appears that the mutations or substitutions may occur in the CDR regions of antibody or antigen binding domains, regions that are particularly sensitive to the specific amino acid sequence of the combined fragments.
With respect to claims 104 and 105, applicant has similarly claimed antigen binding molecules which are specific for the highly variable MHC Class I genetic locus which is highly variable within the human gene pool. Applicant however has disclosed two basic scFv based antigen binding molecules which satisfy the claims as written. Once again this is not sufficient to provide one of ordinary skill in the art evidence that the applicant was in possession of the broad genus of structurally diverse antigen binding polypeptide fragments which would satisfy the claimed function of binding diverse class I MHC molecules and HLA-A subsets of this genus. Note the following Court Decisions regarding the written description of antibodies in the context of the current claims. Given the broadly claimed class of antibodies, in the absence of sufficient disclosure of relevant identifying characteristics, the patentee must establish “a reasonable structure-function correlation” either within the specification or by reference to the knowledge of one skilled in the art with functional claims. AbbVie Deutschland GmbH & Co. v. Janssen Biotech, Inc. (Fed. Cir. 2014) and the specification at best describes plan for making antibodies with the “limitations above” (for example binding to MHC class I molecules) and then identifying those that satisfy claim limitations, but mere “wish or plan” for obtaining claimed invention is not sufficient. Centocor Ortho Biotech Inc. v. Abbott Laboratories, 97 USPQ2d 1870 (Fed. Cir. 2011). There is insufficient written description of the required kind of structure-identifying information about the corresponding makeup of the claimed antibodies to demonstrate possession. Also, see Amgen Inc. v. Sanofi, Aventisub LLC, No. 2017-1480 (Fed. Cir. 2017). Thus, one of skill in the art would conclude that the specification fails to provide adequate written description to demonstrate that Applicant was in possession of the claimed genus. See Eli Lilly, 119 F. 3d 1559, 43, USPQ2d 1398.
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 93, 95-99, 108-113, 131 are rejected under 35 U.S.C. 112(b) as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor, regards as the invention.
Claims 93, 95-99, 108-113, 131 utilize terminology referencing chimeric sequences and scFV molecules which comprise “a sequence” or “an amino acid sequence” that is of variable homology to the reference sequence. For example in claim 109 the SEQ ID NO: 48 “C1759 chimeric antigen receptor construct “ appears to comprise a scFv antigen binding domain N (terminal) linked (C terminal) to a KIR3DL2 receptor derived domain (100% homology). This is not a LILRB1 hinge. Therefore when the “hinge-TM-Intracellular domain” of the SEQ ID NO: 48 is aligned to the LIRB1 Hinge-TM-intracellular domain as SEQ ID NO:2 for example one finds that sequence has very little sequence homology over the entire length. However applicant includes this as a claim dependent on the claim 91 which describes sequences derived from the LILRB1 hinge domain or functional fragment or variant thereof.
Therefore considering Applicant’s inclusion of sequences with minimal sequence homology (and much less than 95%), Examiner will interpret for purposes of examination that as defined in claim 91, it appears that in light of the inclusion of sequences of minimal homology in the dependent claim set that for example “an LILRB1 hinge domain or functional fragment or variant thereof” as well as other locations of similar terminology allow for inclusion of sequences of similar minimal homology in the transmembrane and intracellular domain of the claimed chimeric molecules.
Appropriate correction and/or clarification is required.
Priority
The earliest effective U.S. filing date afforded the instantly claimed invention has been
determined to be 11 December 2019, the filing date of Provisional Application No. 62/946,888, to which Int. Application No. PCT/US2021/012977 claims priority to.
Claim Rejections - 35 USC § 101
35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Claims 91-101, 103-105, and 126-127 are rejected under 35 U.S.C. 101 because
the claimed invention is directed to a natural phenomenon (product of nature) without significantly more. The claims recite a receptor which may be identical to the naturally occurring LILRB1 receptor. As support of the further functional requirements added in dependent claims rejected the disclosure of Brown (“The LILR Family: Modulators of Innate and Adaptive Immune Pathways in Health and Disease”, Tissue Antigens 2004: 64: 215–225; cited on the IDS) describes that LILRB1 is an inhibitory receptor which binds to a wide variety of HLA molecules “antigen” on target cells(table 2) and is present on subsets of T cells for example (p222 last paragraph). As such with regards to claims 127 for example a T cell which comprises the LILRB1 receptor also comprises an “activating receptor” as for example one would expect a CD8+ T to comprise a T cell receptor molecule/s on the surface which are activated in response to engagement of cognate MHC-peptide complexes. The claims do not include additional elements that are sufficient to amount to significantly more than the judicial exception because all of the presented elements in rejected dependent claims recite function which are substantially identical to the functioning of the native LILRB1 receptor as indicated above and verified by the disclosure of Brown.
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.
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 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.
Claims 91-101, 103-105 126-128 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Brown (supra).
As indicated above the rejected claims describe a receptor molecule which is in embodiment identical to the native LILRB1 receptor molecule. With regards to the instant claim 91-101 and 126-127, the disclosure of Brown as described above indicates that the native LILRB1 molecule is found on a subset of T cells and therefore is found on an immune T cell which comprises an activator receptor as a TCR. In anticipation of the claims 92, 101, 103-105, the disclosure of Brown (table 2) indicates that the LILRB1 receptor molecule is capable of binding to a variety of HLA-A molecules as well as HLA-G molecules for example. The claims 93-101 recite sequences identical to particular subsequences of the native LILRB1 and are therefore necessarily anticipated by the disclosure of Brown which provides for a T cell which incorporate the LILRB1 molecule and comprise identical sequences to the claimed molecules.
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.
Claims 91-92, 101, 103-106, 114-118, 123-128 and 130 are rejected under 35 U.S.C. 103 as being unpatentable over Beiman (WO2019068007A1; cited on the IDS) in view of Pule (WO2015075468A1; cited on the IDS)
Claims 91-92 indicate in embodiments a receptor molecule with an antigen binding domain which may be equivalent to (see above) the LILRB1 receptor molecule or in embodiments a chimeric receptor which is directed to for example an HLA-A02 class I molecule through incorporation of a scFv molecule or CDR derived from said scFv molecule into a chimeric molecule. Claims 103-105 describe that the potential antigen binding molecule of the chimeric molecule binds terminally to an HLA-A *02 molecule. Claim 101 indicates that the antigen binding domain is specific for an antigen potentially lost in cancer through loss of heterozygosity. With regards to the instant claims 91-92, 101, and 103-106, the disclosure of Beiman describes inhibitory chimeric antigen receptors (iCAR) which may bind to the HLA-A2 molecules (0020,0095,Figure 19,figure 15, 00328) and potentially comprise intracellular inhibitory sequences derived from the LIR1 molecule (LIR1B1)(00148) ITIM domains.
The SEQ ID NO: 10 of Beiman does not utilize the particular ITIM intracellular domain derived from the LIR1 molecule as described or a sequence derived from LILRB1 hinge . However, congruent with the Applicant definition of LILRB1 hinge and as detailed in the section 112 indefinite rejection above, the disclosure of Beiman describes the SEQ ID NO:10. Alignment of the extracellular membrane proximal domain of SEQ ID NO:10 with instant application LILRB1 hinge domain as SEQ ID NO: 2 for instance reveals a sequence as at least 100% homologous to the hinge domain portion of SEQ ID NO:2 of LILRB1 over the “PT” two amino acid length of the LILRB1 hinge region. A transmembrane domain is included in the SEQ ID NO:10 of Beiman.
Additionally with regards to the specific ITIM domains of the claimed molecule the disclosure of Pule describes inhibitory CAR systems and molecules of which, homologous to Beiman, describes the use of inhibitory intracellular (ITIM) signaling domains derived from the inhibitory receptor molecules such as the LILRB1 molecule (SEQ ID NO:24, p44 30-35). As such, the SEQ ID NO:24 of Pule comprises the ITIM domains such as NYLAAV (instant SEQ ID NO:8). Beiman further discloses incorporation of a promoter, including those set forth in instant claims 115-118, operably linked to the polynucleotide as a control element (p18 67-69). It would thus be obvious considering the disclosure of Beiman and Pule to create an inhibitory CAR molecule directed to the HLA-A2 molecule, as a typical loss of heterozygosity receptor in particular cancers, as such comprised of the particular sequences as are jointly disclosed as functional components of iCAR molecules for the purposes of utilizing such molecules in a dual CAR system (iCAR/activating-CAR) which selectively “recognizes” potential cancer cells which may have lost expression of the iCAR molecular target (HLA-A). The effector cells which comprised in such a dual CAR system would preferentially be activated to kill cancer cells which may not express a Class I MHC A*02 molecule through loss of heterozygosity while likewise being activation inhibited by contact with normal cells expressing Class I MHC (HLA-A2 for example) through functioning of the engaged inhibitory receptor (for instance see Beiman 00134). Therefore with regards to the claims 125-128, the disclosure of Beiman indicates that chimeric molecules, both inhibitory and activating chimeric fusion proteins, may be comprised in a single vector or separate nucleic acid vector which encode the chimeric molecules (00260). The vector may then be utilized for engineering a T cell for example or a natural killer (NK) cell (00296). It would be obvious to engineer immune cells as described in Beiman with nucleic acid encoding the chimeric fusion protein/s for the purposes of arriving at an engineered T cell for example that may advantageously function to selectively target cancer cells which may have lost expression of a Class I MHC molecule for example for the purposes of selectively eliminating said cancer cells while normal cells which express the ligand of the inhibitory CAR molecule are not actively engaged.
Claims 93-95, 98-100 are rejected under 35 U.S.C. 103 as being unpatentable over Beiman and Pule as applied to the claims listed above, and further in view of Duchateau (WO2016097231A2; cited on the IDS).
Claims 93-98 describe various permutations of hinge-transmembrane-intracellular domain and combinations thereof. Regarding Claim 93, SEQ ID NO:34 (encodes the polypeptide comprising instant SEQ ID NO: 7) indicates the complete intracellular domain derived from the LILRB1 molecule. Regarding claims 94-95, SEQ ID NO: 5 encompasses the complete annotated transmembrane domain of the LILRB1 molecule. Claim 96 comprises a number of unrelated hinge domains and designates a number of unrelated extracellular hinge/spacer domains that are designated in sequence listing as “laboratory” manufactured. Regarding Claim 97, SEQ ID NO 20 is identical to contiguous extracellular -transmembrane derived from LILRB1. Regarding claim 98, SEQ ID NO 21 is derived from the contiguous LILRB1 transmembrane and intracellular domain (contiguous). Regarding claims 99-100 and 130, SEQ ID NO: 2-3 (encoded by SEQ ID NO: 126 and 18 respectively) are contiguous N-C sequences derived from the LILRB1 sequence extracellular domain-transmembrane-intracellular domain. Thus SEQ ID NO: 2 is identical with SEQ ID NO: 2 comprising an extra 20 amino acid of the native LILRB1 protein (N-terminal). All sequences are identical to the native LILRB1 protein.
With respect to the instant claims 93-95 and 98, the disclosure of Beiman and Pule make obvious the utilization of an intracellular domain derived from the LILRB1 molecule or a sequence 95% identical to said sequence. The disclosure of Beiman and Pule do not particularly describe that the transmembrane domain is 95% identical to the SEQ ID NO: 5. SEQ NO:5 appears to be the transmembrane domain derived from the LILR1B protein sequence. The disclosure of Duchateau describes inhibitory CAR molecules (not-CAR, N-CAR) which are created by adding a scFv molecule to the transmembrane and intracellular components of an inhibitory receptor molecule. One such molecule is described as a LIR (LILR) molecule such as LILRB4 molecule, SEQ ID NO:10 and the derived intracellular and transmembrane domain as comprised in a CAR molecule (N-CAR) SEQ ID NO:151 (subsequence of SEQ ID NO:10, residues 219-448)(p105,25-35 p99; Table 1). This sequence comprises a transmembrane domain that is 95.7% identical to the claimed sequence. It would therefore be obvious to utilize a transmembrane sequence that is 95% identical to the sequence as in SEQ ID NO:5 or greater as a choice of transmembrane already disclosed as functional in an inhibitory chimeric antigen receptor molecule.
Claims 96-97, 119-122 and 129 are rejected under 35 U.S.C. 103 as being unpatentable over the combined teachings of Beiman and Pule, as applied to the claims listed above, and in further in view of Sadelain (US20040043401A1; cited on the IDS) and Maute (US20180251558A1; cited on the IDS) .
The disclosure of Beiman , Pule and Duchateau account for the use of the transmembrane and intracellular domain of the LILR1B molecule in an inhibitory chimeric antigen receptor as described above, but do not explicitly incorporate the LILRB1 “hinge” or stalk/ extracellular spacer region in an inhibitory chimeric antigen receptor. For reference to the entire amino acid sequences of the LILRB1 complete isoform sets the reference of Maute is provided as SEQ ID NOs: 1-6. The specific instant sequences that are claimed as LILRB1 hinge portion are the SEQ ID NO: 4 as “hinge” in the instant specification and SEQ ID NO: 20 as the “long hinge” (claim 97) derived from LILRB1 and incorporated into the N terminal sequence of SEQ ID NO: 2 (claims 97). With regards to the native LILRB1 sequences of the instant application and the sequence reference of Maute the SEQ ID NO:4 (and hinge sequences of instant SEQ ID NO:19 and 2) are identical match to the “hinge” residues of the native LILRB1 isoform 1 (SEQ ID NO: 1) of the disclosure of Maute. This established, along with the disclosure of Duchateau, describes creating inhibitory chimeric receptors (i-CAR or N-CAR) through removal of N terminal extracellular topological domain amino acids of naturally occurring inhibitory receptors (as LILRB1 is a type), retaining the stalk (“hinge”), transmembrane and intracellular signaling domain which is then fused to a redirecting scFv antigen targeting domain (see figure 2). Likewise, the disclosure of Sadelain describes the construction of chimeric antigen receptor molecules comprising CD28 stalk (hinge) transmembrane and intracellular signaling domain fused to an additional CD3 zeta intracellular signaling domain which function better by providing costimulatory signal to T cell transduced with the CAR molecules engaged through the antigen binding domain when compared to those with CD28 signaling components arranged in a different order (0030). The disclosure of Sadelain thus describes that utilization of complete native protein sequences retains the conformational integrity of the native receptor which allows for construction of a CAR molecule that signals as expected and desired relative to the native protein (0031). Thus, considering the disclosure of Duchateau and Sadelain, one would initially construct an inhibitory chimeric antigen receptor utilizing inhibitory receptor sequences (stalk/hinge-transmembrane-intracellular signaling domain) derived exactly as arranged in the native LILRB1 inhibitory receptor (as in instant SEQ ID NO:3 or SEQ ID NO 2 for example). One would do this with a reasonable expectation of success that the receptor would be functional and useful when paired with (fused) to an scFv which binds to the HLA-A molecule as is instantly claimed and made obvious by Beiman and Pule.
Additionally, there would be a reasonable expectation of success because the prior art is presumed fully enabled (see, e.g., MPEP § 2121(I)) for all that it discloses (see, e.g., MPEP §§ 2123(I)-(II)).
Accordingly, claims 91-101, 103-106, 114-130 are rejected.
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.
Patent No. 11,254,726
Claims 91-101, 103-131 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-16 of U.S. Patent No 11,254,726 (reference patent). Although the claims at issue are not identical, they are not patentably distinct from each other as described below.
MPEP § 804(II)(B)(2)-(3) identifies that a Nonstatutory Double Patenting Rejection may be appropriate based upon either an anticipation analysis or an obviousness analysis (see, e.g., MPEP § 804(II)(B)(2)-(3)). The following rejection is based upon both anticipation and obviousness analyses.
Anticipation Analysis: Regarding claims 91-100, 103-111, 113, 119, 123-131, the reference patent claims a polynucleotide, vector, and T cell encoding/comprising a chimeric antigen receptor comprising a polypeptide having an LILRBI hinge domain, a transmembrane domain, a LILRBI intracellular domain comprising at least one immunoreceptor tyrosine-based inhibitory motif (ITIM) of NLYAAV (SEQ ID NO: 8; compare id. with instant SEQ ID NO: 8), and an antigen binding domain having the CDRs set forth in SEQ ID NOs: 22-27 (compare id. to instant SEQ ID NOs: 22-27, as presently claimed) wherein the receptor comprises an amino acid sequence SEQ ID NO: 122 (compare id. to instant SEQ ID NO: 122, which comprises or is encoded by sequences identical to instantly claimed SEQ ID NOs: 2-3, 8, 19, 22-27, 34, 123, and 125), wherein the antigen binding domain specifically binds a HLA-A*02 allele of HLA-A, and wherein the polynucleotide comprises an activating receptor (see reference claims 1-16; reads on instant claims 91-100, 103-111, 113, 119, 123-124, 126-131).
Obviousness Analysis: Although the reference patent doesn’t expressly claim the limitations set forth in instant claims 101, 114-118, 120-122, 125 these limitations are set forth in the reference specification (see, e.g., col. 40, 34, 13, 75, 31-33, and 61), and therefore, are obvious variants1 of the claimed invention. Accordingly, a skilled artisan would readily appreciate the limitations set forth in the reference patent, as the they are obvious variations described in the specification of the reference patent (see, e.g., MPEP § 804(II)(B)(1), regarding construing the claim using the reference patent disclosure).
Accordingly, instant claims 91-101, 103-131 are not patentably distinct relative to the reference claims.
Patent No. 12,187,775
Claims 91-101, 103-131 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-38 of U.S. Patent No 12,187,775 (reference patent). Although the claims at issue are not identical, they are not patentably distinct from each other as described below.
MPEP § 804(II)(B)(2)-(3) identifies that a Nonstatutory Double Patenting Rejection may be appropriate based upon either an anticipation analysis or an obviousness analysis (see, e.g., MPEP § 804(II)(B)(2)-(3)). The following rejection is based upon both anticipation and obviousness analyses.
Anticipation Analysis: Regarding claims 91-100, 103-111, 113, 119, 123-124, 126-131, the reference patent claims a polynucleotide, vector, and T cell encoding/comprising a chimeric antigen receptor comprising a polypeptide having an LILRBI hinge domain, a transmembrane domain, a LILRBI intracellular domain comprising at least one immunoreceptor tyrosine-based inhibitory motif (ITIM) of NLYAAV (SEQ ID NO: 8; compare id. with instant SEQ ID NO: 8), and an antigen binding domain having the CDRs set forth in SEQ ID NOs: 22-27 (compare id. to instant SEQ ID NOs: 22-27, as presently claimed) wherein the receptor comprises an amino acid sequence SEQ ID NO: 122 (compare id. to instant SEQ ID NO: 122, which comprises or is encoded by sequences identical to instantly claimed SEQ ID NOs: 2-3, 8, 19, 22-27, 34, 123, and 125), wherein the antigen binding domain specifically binds a HLA-A*02 allele of HLA-A, and wherein the polynucleotide comprises an activating receptor (see reference claims 1-38; reads on instant claims 91-100, 103-111, 113, 119, 123-124, 126-131).
Obviousness Analysis: Although the reference patent doesn’t expressly claim the limitations set forth in instant claims 101, 114-118, 120-122, 125 these limitations are set forth in the reference specification (see, e.g., col. 41-42, 34, 13, 75, 31-33, and 61), and therefore, are obvious variants2 of the claimed invention. Accordingly, a skilled artisan would readily appreciate the limitations set forth in the reference patent, as the they are obvious variations described in the specification of the reference patent (see, e.g., MPEP § 804(II)(B)(1), regarding construing the claim using the reference patent disclosure).
Accordingly, instant claims 91-101, 103-131 are not patentably distinct relative to the reference claims.
Patent No. 12,195,513
Claims 91-101, 103-131 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-18 of U.S. Patent No 12,195,513 (reference patent). Although the claims at issue are not identical, they are not patentably distinct from each other as described below.
MPEP § 804(II)(B)(2)-(3) identifies that a Nonstatutory Double Patenting Rejection may be appropriate based upon either an anticipation analysis or an obviousness analysis (see, e.g., MPEP § 804(II)(B)(2)-(3)). The following rejection is based upon an obviousness analysis.
Obviousness Analysis: Regarding claims 91-101, 103-131, the reference patent explicitly claim methods that expressly recite and require products as instantly claimed (compare instant claims 1 with reference claims 1-18), and therefore in view of the reference claims, an artisan would at once envisage the products having the structures of the polynucleotide, vector, and T cell encoding/comprising a chimeric antigen receptor comprising a polypeptide having an LILRBI hinge domain, a transmembrane domain, a LILRBI intracellular domain comprising at least one immunoreceptor tyrosine-based inhibitory motif (ITIM) of NLYAAV (SEQ ID NO: 8; compare id. with instant SEQ ID NO: 8), and an antigen binding domain having the CDRs set forth in SEQ ID NOs: 22-27 (compare id. to instant SEQ ID NOs: 22-27, as presently claimed) wherein the receptor comprises an amino acid sequence SEQ ID NO: 122 (compare id. to instant SEQ ID NO: 122, which comprises or is encoded by sequences identical to instantly claimed SEQ ID NOs: 2-3, 8, 19, 22-27, 34, 123, and 125), wherein the antigen binding domain specifically binds a HLA-A*02 allele of HLA-A, and wherein the polynucleotide comprises an activating receptor (see reference claims 1-18; reads on instant claims 91-100, 103-111, 113, 119, 123-124, 126-131).
Although the reference patent doesn’t expressly claim the limitations set forth in instant claims 101, 114-118, 120-122, 125 these limitations are set forth in the reference specification (see, e.g., col. 39, 34, 13, 75, 31-33, and 62), and therefore, are obvious variants3 of the claimed invention. Accordingly, a skilled artisan would readily appreciate the limitations set forth in the reference patent, as the they are obvious variations described in the specification of the reference patent (see, e.g., MPEP § 804(II)(B)(1), regarding construing the claim using the reference patent disclosure).
Accordingly, instant claims 91-101, 103-131 are not patentably distinct relative to the reference claims.
Conclusion
No claims are allowed.
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/LEA S O'BRIEN/Examiner, Art Unit 1646
/MARK HALVORSON/Primary Examiner, Art Unit 1646
1 See, e.g., MPEP § 804(II)(B)(1), “those portions of the specification which provide support for the reference claims may also be examined and considered when addressing the issue of whether a claim in the application defines an obvious variation of an invention claimed in the reference patent or application”
2 See, e.g., MPEP § 804(II)(B)(1), “those portions of the specification which provide support for the reference claims may also be examined and considered when addressing the issue of whether a claim in the application defines an obvious variation of an invention claimed in the reference patent or application”
3 See, e.g., MPEP § 804(II)(B)(1), “those portions of the specification which provide support for the reference claims may also be examined and considered when addressing the issue of whether a claim in the application defines an obvious variation of an invention claimed in the reference patent or application”