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
Status of the Claims
1. Claims 1-20 are the original claims filed 8/15/2022. Claims 1-20 are refiled in the Response of 7/3/2023. In the Preliminary Amendment of 6/25/2024, Claims 1-16 and 18-20 are amended. In the Response of 1/24/2025, Claims 1, 8 and 15 are amended. In the Response of 9/11/2025, claims 2-3 and 5-14 are amended and claims 1 and 15-20 are cancelled.
Claims 2-14 are all the claims.
The amendments to the claims raise new grounds for objection and rejection. The Office Action is final.
Priority
2. USAN 17/590,983, filed 02/02/2022, is a Continuation of 16/061,987, filed 06/13/2018, now abandoned 16/061,987 is a National Stage entry of PCT/US2016/068353, International Filing Date: 12/22/2016, PCT/US2016/ 068353 Claims Priority from Provisional Application 62/270,657, filed 12/22/2015.
Information Disclosure Statement
3. As of 10/16/2025, a total of three (3) IDS are filed: 2/9/2022; 1/24/2025; and 1/24/2025. The corresponding initialed and dated 1449 form is considered and of record.
Withdrawal of Objections
Claim Objections
4. The objection to Claims 7-8 and 10 because of informalities is withdrawn.
a) Claim 7 is amended to recite “wherein the first signal peptide and second signal peptide independently comprise the signal peptide of CD8, CD45, or CSF.”
b) Claim 8 is amended to recite “the hinge region from [CD8a] CD8 alpha.”
c) Claim 10 is amended to recite “…independently comprise the transmembrane domain of CD3 epsilon,…”
Withdrawal of Rejections
Double Patenting
5. The provisional Claims 1-14 and 17-20 on the ground of nonstatutory double patenting as being unpatentable over claims of copending Application No. 18/520,972 (reference application US20240350632) is moot for the canceled claims and withdrawn for the pending claims.
The terminal disclaimer filed on 9/11/2025 disclaiming the terminal portion of any patent granted on this application which would extend beyond the expiration date of Application No. 18/520,972 has been reviewed and is accepted. The terminal disclaimer has been recorded.
6. The rejection of Claims 1-14 and 17-20 on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. 10273280 is moot for the canceled claims and withdrawn for the pending claims.
The terminal disclaimer filed on 9/11/2025 disclaiming the terminal portion of any patent granted on this application which would extend beyond the expiration date of U.S. Patent No. 10273280 has been reviewed and is accepted. The terminal disclaimer has been recorded.
7. The provisional rejection of Claims 1-14 and 17-20 on the ground of nonstatutory double patenting as being unpatentable over claims 1-17 of copending Application No. 17/994,883 (reference application US 20230302051) is moot for the canceled claims and withdrawn for the pending claims.
The terminal disclaimer filed on 9/11/2025 disclaiming the terminal portion of any patent granted on this application which would extend beyond the expiration date of Application No. 17/994,883 has been reviewed and is accepted. The terminal disclaimer has been recorded.
8. Claims 1-14 and 17-20 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 108-110 of copending Application No. 18/121,101 (reference application US 20240124547) is moot for the canceled claims and withdrawn for the pending claims.
The terminal disclaimer filed on 9/11/2025 disclaiming the terminal portion of any patent granted on this application which would extend beyond the expiration date of Application No. 18/121,101 has been reviewed and is accepted. The terminal disclaimer has been recorded.
Claim Rejections - 35 USC § 103
9. The rejection of Claim(s) 1, 5-6, 8-12, 14, and 17-20 under 35 U.S.C. 103 as being unpatentable over Powell et al (US 20140099309; published 2014-04-10; priority 2012-10-05 (IDS 2/9/2022, ref 7) is moot for the canceled claims and withdrawn for the pending claims. Applicants allege amending claim 7 into original claim 1 (because claim 7 was not rejected) overcomes the rejection.
10. The rejection of Claim(s) 1-2 and 13 under 35 U.S.C. 103 as being unpatentable over Powell et al (US 20140099309; published 2014-04-10; priority 2012-10-05 (IDS 2/9/2022, ref 7) as applied to claim 1 above, and further in view of Penney et al (IDS 1/24/2025, ref 17) is moot for the canceled claims and withdrawn for the pending claims. Applicants allege amending claim 7 into original claim 1 (because claim 7 was not rejected) overcomes the rejection.
11. The rejection of Claim(s) 1 and 3-4 under 35 U.S.C. 103 as being unpatentable over Powell et al (US 20140099309; published 2014-04-10; priority 2012-10-05 (IDS 2/9/2022, ref 7) as applied to claim 1 above, and further in view of Mamonkin et al (Blood, 20 August 2015 volume 126, number 8) is moot for the canceled claims and withdrawn for the pending claims. Applicants allege amending claim 7 into original claim 1 (because claim 7 was not rejected) overcomes the rejection.
Objections Maintained
Specification
12. The objection to the disclosure because of informalities is maintained.
The amended paragraphs for the specification filed in the Response of 9/11/2025 do not correspond with the respective paragraphs from the most recent version of the specification (7/3/2023). Most notably, the paragraphs from 7/3/2023 contain proper trademarks for some terms (i.e., RetroNectin™) that are not present (i.e., RetroNectin) in the amended version from 9/11/2025. Most notably, the paragraph from 7/3/2023 that includes sequence identifiers on page 39, line 26 are in fact altogether missing from the same amended paragraph of the version from 9/11/2025.
Applicants are advised that amending the specification requires continuity with all of the past amended versions of the specification in the file history.
Applicants’ response is incomplete.
a) The use of the term, e.g., Tween, Alexa Fluor, ATCC, ProBond, which is a trade name or a mark used in commerce, 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.
Appropriate correction is required.
Rejections Maintained
Claim Rejections - 35 USC § 112(b)
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.
13. The rejection of Claim 8 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite is maintained.
a) Claim 8 is amended to delete the phrase “are recruited to cancer cells” but retains the phrase “the hinge region…or IgD innate immune cells comprising at least one of CD2, CD3, CD4, CD5, CD7, or CD8.” The meaning of the claim is incomprehensible. It is not clear or concise how the hinge region relates to the CD markers and whether both are expressed on an innate immune cell. It is not clear how an innate immune cell corresponds to the engineered cell. The claim is narrative and indefinite, failing to conform with current U.S. practice. It appears to be a literal translation into English from a foreign document and contains grammatical and idiomatic errors.
The rejection is maintained.
New Grounds for Objection
Claim Objections
14. Claims 2-14 are objected to because of the following informalities:
-) The claims are objected to for being out of order with respect to the claim numbering for the most generic claim 7. The numbering of claims 2-6 is not in accordance with 37 CFR 1.126 in order to be re-written as new claims 21-25, respectively, that depend from claim 7.
Appropriate correction is required.
New Grounds for Rejection
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.
Written Description
15. Claims 2-14 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, 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.
Claim interpretation
Generic claim 7 is construed as a 1st polypeptide comprising a CAR polypeptide comprising from N- to C-terminus a first antigen recognition domain, a first signal peptide, a first hinge region, a first transmembrane domain, a co-stimulatory domain, and a signaling domain; and a 2nd polypeptide comprising from N- to C-terminus a second antigen recognition domain, a second signal peptide, a second hinge region, and a second transmembrane domain, wherein the second polypeptide does not comprise a co-stimulatory domain or a signaling domain.
Generic claim 7 further requires the first signal peptide and second signal peptide independently comprise the signal peptide of CD8, CD45, or CSF.
Disclosure in the Specification
a) The specification teaches constructs for the 1st polypeptide and 2nd polypeptides comprising a “leader sequence” as in Figure 1:
Figure 1: Leader sequence, the anti-CD5 extracellular single chain variable fragment (Anti-CD5 scFv), the hinge region, the trans-membrane region, and the three intracellular signaling domains that define this construct as a 3rd generation car; CD28, 4-1BB and CD3ζ. The DNA construct of the anchored CD5 scFv antibody is the same as the CDSCAR construct without the intracellular signaling domains, as is the translated protein product for anchored CD5 scFv antibody.
“leader sequence”: an example of a leader sequence is of CD8 as in
[0372] “…Leader sequence, the anti-CD5 extracellular single chain variable fragment (Anti-CD5 scFv), the hinge region, the trans-membrane region, and the three intracellular signaling domains that define this construct as a 3rd generation car; CD28, 4-1BB and CD3ζ. The DNA construct of the anchored CD5 scFv antibody is the same as the CDSCAR construct without the intracellular signaling domains, as is the translated protein product for anchored CD5 scFv antibody.
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The translated protein construct of Figure 1 does not show a peptide signal interposed between the 1st antigen binding domain and 1st hinge region nor between the 2nd antigen binding domain and 2nd hinge region.
b) The specification teaches constructs for the 1st polypeptide and 2nd polypeptides comprising a “leader sequence” as in Figures 13, 14A. Neither figure comprises a signal peptide interposed between the 1st antigen binding domain and 1st hinge region nor between the 2nd antigen binding domain and 2nd hinge region. Instead, the specification teaches constructs for the 1st polypeptide and 2nd polypeptides comprising a “leader sequence” as in Figures 13, 14A.
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The translated protein construct of Figure 13 and 14A does not show a peptide signal interposed between the 1st antigen binding domain and 1st hinge region nor between the 2nd antigen binding domain and 2nd hinge region. P2A is defined as cleavable linking peptide [0063; 0148; 0301] with no reference or comparison to a signal peptide.
c) The specification teaches constructs for the 1st polypeptide and 2nd polypeptides comprising a signal and a spacer as in Figure 21. The figure does not comprise a signal peptide interposed between the 1st antigen binding domain and 1st hinge region nor between the 2nd antigen binding domain and 2nd hinge region. Instead, the specification teaches constructs for the 1st polypeptide and 2nd polypeptides comprising an N-terminal signal for both the 1st and 2nd polypeptides and a spacer for the 2nd polypeptide.
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Accordingly, the meaning of a leader sequence versus a signal peptide versus a spacer is unclear and ambiguous. A 1st and 2nd signal peptide much less of CD8, CD45 or CSF finds no support in the disclosed figures for the prototypes of the constructs much less in the examples. The only disclosure for a signal peptide comprising CD8, CD45 or CSF is found in claim 7 where the meaning of a signal peptide is unclear and ambiguous. See Mølhøj et asl (Nature Biotechnology volume 22, page1502 (2004); PTO 892).
It is unclear and ambiguous whether/how a signal peptide, a leader sequence and/or a peptide linker are associated with the constructs of the claimed invention.
The breadth and scope of the construct as interpretated from the instant claims does not find original description support in the specification as filed.
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.
16. Claim(s) 5-6, 7-12, and 14 is/are rejected under 35 U.S.C. 103 as being unpatentable over Powell et al (US 20140099309; published 2014-04-10; priority 2012-10-05 (IDS 2/9/2022, ref 7).
Generic claim 7 is construed as a 1st polypeptide comprising a CAR polypeptide comprising from N- to C-terminus a first antigen recognition domain, a first signal peptide, a first hinge region, a first transmembrane domain, a co-stimulatory domain, and a signaling domain; and a 2nd polypeptide comprising from N- to C-terminus a second antigen recognition domain, a second signal peptide, a second hinge region, and a second transmembrane domain, wherein the second polypeptide does not comprise a co-stimulatory domain or a signaling domain.
Generic claim 7 further requires the first signal peptide and second signal peptide independently comprise the signal peptide of CD8, CD45, or CSF.
The meaning of a signal peptide is unclear and ambiguous as discussed herein above.
The claims are read under the BRI standard where no specific order is implied to the members or elements for either the 1st and/or 2nd polypeptide of claim 7, where the meaning of a leader sequence, a signal peptide and/or a linker peptide is interchangeable.
The claims are prima facie obvious over Powell.
As regards Claim 7, Powell teaches a dual polypeptide construct comprising the 1st and 2nd polypeptides shown in Figure 1:
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. The costimulatory CAR of Powell corresponds to the first polypeptide of Claim 7 comprising a first leader sequence, a first antigen binding domain (VH-L-VL), a first hinge (CD8a), a first transmembrane (CD8a), a first intracellular domain (CD28). The truncated CAR (no signaling domains) of Powell corresponds to the second polypeptide of Claim 1 comprising a first leader sequence, a second antigen binding domain (VH-L-VL (Claim 1)), a second hinge (CD8a), and a second transmembrane (CD8a).
AS regards Claim 12, Powell teaches modified or engineered T-cells comprising the dual polypeptide construct at [0028, 0137, 0154-0163, 0218].
AS regards Claims 7, Powell teaches inclusion of a “signal module” in the construct polypeptides at [0030]
In one embodiment, the trans-signaling CAR cells comprise a first signal module and a distinct second signal module which are incorporated into two distinct CARs, a first CAR and a second CAR, respectively, each with a different antigen specificity.
The “signal peptide” is not defined for Claim 7 but for being CD8, CD45 or CSF. Under the BRI standard, the POSA could reasonably envisage the “signal module” of Powell corresponding to a signal peptide of the invention.
AS regards Claims 7, 8, and 9, Powell teaches hinges for CD8 [0017] and CD8 alpha [0107].
AS regards Claims 7, 10, and 11, Powell teaches transmembrane domains at [0122], e.g., CD28, CD3 epsilon, CD45, CD4, CD5, CD8, CD9, CD16, CD22, CD33, CD37, CD64, CD80, CD86, CD134, CD137, CD154, ICOS.
AS regards Claims 7 and 5-6, Powell teaches antigens recognized by the antigen recognition domains at [0114-0115; 0117], e.g., CD19, CD20, CD22 and CD33.
AS regards Claim 14, Powell teaches IL-15 and Il-12 being factors necessary for proliferation of engineered T cells at [0171], where the POSA would recognize recombinant cytokines in the engineered T cell would provide the factors.
Powell teaches the enhanced potency of CARs can be associated with autoimmunity due to on-target toxicities against normal tissues expressing the lower levels of the tumor associated antigens, with two serious adverse events (SAEs) reported so far. [0004] The first SAE occurred in a clinical trial where administration of anti-ErbB2 CART cells containing the CD28 and 4-1BB costimulatory signaling regions into a patient with refractory colon cancer with metastatic sites in lung and liver led to development of dramatic pulmonary toxicity with lung infiltrates and a cytokine storm followed by cardiac arrest and patient death (Morgan et al., 2010, Cancer J. 16:336-341). In the second report, a lymphodepleted patient with bulky chronic lymphocytic leukemia received autologous T cells engineered with an anti-CD 19 second-generation CAR containing the CD28 domain at a total dose of 3.times.10.sup.7 T cells/kg. This patient developed fever, hypotension, and dyspnea 20 hours after infusion, which rapidly progressed. Low grade sepsis was the most likely reason of the patient’s death, however the possibility that a cyclophosphamide-induced “cytokine storm” may have enhanced the in vivo activation of modified T cells is well considered (Brentjens et al., 2010, Mol. Ther. 18:666-668). It is therefore clear that the development of strategies limiting potential early or late toxicity is mandatory.
Powell provides a solution and the motivation to construct two CARs, one of which transmits a T cell activation signal and the other truncated in its intercellular signaling mechanism on the same engineered T cell, but antigen-specific for bispecific targeting of the same engineered T cell (Claim 1) and useful as a tag reporter for, example, examining CAR-T cell trafficking of the same engineered T cell (Claim 17).
17. Claim(s) 7, 2 and 13 is/are rejected under 35 U.S.C. 103 as being unpatentable over Powell et al (US 20140099309; published 2014-04-10; priority 2012-10-05 (IDS 2/9/2022, ref 7) as applied to claim 7 above, and further in view of Penney et al (IDS 1/24/2025, ref 17).
Claim 2 depends from Claim 7 and is drawn the engineered T cell being CD5 deficient.
Claim 13 depends from Claim 7 and is drawn the engineered T cell being CD5 deficient.
Claims 7, 2 and 13 are prima facie obvious over Powell in view of Penney.
The rejection of Claim 7 over Powell from section 16 supra is incorporated herein by reference.
Powell teaches CD5 expression is inherent to T cells in the capacity of an activation signal in [0127-0128]. Powell recognizes and emphasizes the need for attenuating T cell-mediated adverse events associated with the 1st and 2nd generation CAR, as well as CAR T cell dysfunction and lack of expansion and/or persistence after infusion. Powell suggests multiple CARs being present in engineered T cells.
Penney teaches the availability of CD5 deficient T cells (pg 5 col 1 para 3; “variant CD5-negative T cell clones"). The POSA would recognize that CD5+ marker is expressed abundantly on various T-cell lymphomas and leukemias (e.g. T-ALLs), and to a lesser degree on regular T-cells, and that to provide a therapeutic CAR directed against cancer cells expressing the marker, T-cells deficient in CD5 marker would have been suitable host cells for said CAR construct.
Powell and Penney provide the motivation to include a CD5 deficient CAR engineered T-cell that would lessen dysfunction and/or increase longevity of the engineered T cell that otherwise expresses endogenous CD5.
18. Claim(s) 7 and 3-4 is/are rejected under 35 U.S.C. 103 as being unpatentable over Powell et al (US 20140099309; published 2014-04-10; priority 2012-10-05 (IDS 2/9/2022, ref 7) as applied to claim 7 above, and further in view of Mamonkin et al (Blood, 20 August 2015 volume 126, number 8).
Claim 3 depends from Claim 7 and is drawn to a 3rd polypeptide comprising an CD5 recognition polypeptide where the structure is not defined much less as corresponding to the 1st or 2nd polypeptide of Claim 1 but that engineered T cell expresses the CD5 recognition polypeptide.
Claim 4 depends from Claim 3 and requires that the CD5 recognition polypeptide comprise a scfv.
Claims 7 and 3-4 are prima facie obvious over Powell in view of Mamonkin.
The rejection of Claim 7 over Powell from section 16 supra is incorporated herein by reference.
Powell teaches CD5 expression is inherent to T cells in the capacity of an activation signal in [0127-0128]. Powell recognizes and emphasizes the need for attenuating T cell-mediated adverse events associated with the 1st and 2nd generation CAR, as well as CAR T cell dysfunction and lack of expansion and/or persistence after infusion. Powell suggests multiple CARs being present in engineered T cells.
As regards Claim 3, Mamonkin teaches clinical trials demonstrated that chimeric antigen receptors (CARs) can effectively redirect T lymphocytes to eradicate lymphoid malignancies of B-cell origin. However, T-lineage neoplasms remain a more challenging task for CAR T cells due to shared expression of most targetable surface antigens between normal and malignant T cells, potentially leading to fratricide of CAR T cells or profound immunodeficiency. T cells transduced with a CAR targeting CD5, a common surface marker of normal and neoplastic T cells, undergo only limited fratricide and can be expanded long-term ex vivo. These CD5 CAR T cells effectively eliminate malignant T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoma lines in vitro and significantly inhibit disease progression in xenograft mouse models of T-ALL.
AS regards Claim 4, Mamonkin teaches the anti-CD5 single chain variable fragment (scFv) was created using commercial gene synthesis and cloned into a backbone of a 2nd generation (k chain-specific) CAR; that for the in vivo studies, the CH2 portion of the immunoglobulin (Ig)G Fc spacer was removed to create a truncated version of CD5 CAR (DCD5 CAR) by deleting cytoplasmic domains.
Powell and Mamonkin provide the motivation to include a CD5 regulatory molecule that would lessen dysfunction and/or increases longevity of the engineered T cell that otherwise expresses endogenous CD5.
Conclusion
19. No claims are allowed.
20. Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
21. Any inquiry concerning this communication or earlier communications from the examiner should be directed to LYNN A. BRISTOL whose telephone number is (571)272-6883. The examiner can normally be reached on Mon-Fri 9 AM-5 PM.
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/LYNN A BRISTOL/Primary Examiner, Art Unit 1643