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 .
Change in Examiner
The examiner of your application in the PTO has changed. To aid in correlating any papers for this application, all further correspondence regarding this application should be directed to Stephanie Sullivan, Art Unit 1635.
Election/Restrictions
Applicant’s election without traverse of Group I (claims 1,6,7,12,16,17,20 and 35-37), and as species, a glial cell marker in claim 12, and macrophages as the cell type in claim 16, in the reply filed on 02/17/2026 is acknowledged.
Applicant canceled claims 38 and 43-45 drawn to Group 2.
Claims 1,2,6,7,12,16,17,20 and 35-37 are pending and under examination.
Priority
This application is a 371 of PCT/US2021/028808, filed 04/23/2021 which claims benefit of 63/014,344, filed 04/23/2020 as reflected by the most recent filing receipt.
Claim Rejections - 35 USC § 101
Section 33(a) of the America Invents Act reads as follows:
Notwithstanding any other provision of law, no patent may issue on a claim directed to or encompassing a human organism.
Claims 20 and 35-37 are rejected under 35 U.S.C. 101 and section 33(a) of the America Invents Act as being directed to or encompassing a human organism. See also Animals - Patentability, 1077 Off. Gaz. Pat. Office 24 (April 21, 1987) (indicating that human organisms are excluded from the scope of patentable subject matter under 35 U.S.C. 101).
Claim 20 recites “an engineered cell transduced with the vector of claim 1”, and claims 35-37 recite the engineered cell is a stem cell, a lymphocyte, a Treg, or derived from a donor for allogenic transplant in a subject. As the claimed engineered cell is not recited as being isolated, claims 20 and 35-37 encompass that the recited engineered cell is within a human organism, and therefore these claims encompass a human organism comprising an engineered cell transduced with the vector of claim 1 which is not patentable subject matter. The rejection may be overcome by reciting, “an isolated, engineered cell…”.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claim 7 is rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Claim 7 recites, “The vector of claim 1, operable to knock-down B2M expression in transduced cell by at least 75% compared to wild type”. Claim 7 does not further limit the structure of the vector, and merely recites a function of the recited vector that would be carried out by the structure of the vector of claim 1. Therefore, claim 7 does not further limit the subject matter of the claim upon which it depends, claim 1.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 1,2,7,17,20 and 35 are rejected under 35 U.S.C. 103 as being unpatentable over Martin (WO 2020206248, effectively filed 03 April 2019), cited on an IDS, in view of Bear (WO 2004022722, Published 18 March 2004).
Regarding claim 1, Martin teaches it would be advantageous to develop “off the shelf” CAR T cells, prepared using T cells from a third party, healthy donor that have reduced expression or no detectable cell-surface expression of an endogenous T cell receptor and do not initiate GVHD upon administration (page 2, liens 11-14). Martin teaches that beta-2 microglobulin is a component of the MHC class I molecule which will not assemble on the cell surface without B2M present, and therefore knocking out B2M is a means for eliminating MHC class I molecules which should reduce GVHD when CAR T cells are administered to allogenic patients (page 2, lines 21-24). Martin teaches the need for CAR T cells that can maintain stable knockdown of endogenous proteins such as B2M (page 3, lines 9-10).
Martin teaches cassettes comprising a nucleic acid sequence encoding an shRNAmiR that reduces expression of B2M (page 11, lines 16-18), and that the nucleic acid sequence encoding the shRNAmiR and the nucleic acid sequence encoding the CAR can be located in the same gene (page 11, lines 19-20). Regarding the vector, Martin teaches the template nucleic acid is introduced into the immune cell using a viral vector (page 22 lines 28-29, page 23 line 13). Martin teaches an shRNAmiR wherein the passenger strand comprises the nucleic acid sequence of SEQ ID NO: 13 (page 18, lines 12,19,20 and page 37, lines 30-31). SEQ ID NO: 13 (Db) of Martin is 22 nucleotides in length and nucleotides 2-22 of SEQ ID NO: 13 have 100% identity to nucleotides 1-21 of instant SEQ ID NO: 1 (Qy). See alignment below:
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Martin does not teach a hairpin loop encoded by the nucleotide sequence set forth in SEQ ID NO: 6.
Before the effective filing date, Bear taught lentiviral vectors whose presence within a cell results in transcription of one or more RNAs that self-hybridized to each other to form short hairpin RNA (shRNA) or short interfering RNA (siRNA) that inhibits expression of at least one target transcript in the cell (paragraph 0014). Bear taught the term short hairpin RNA refers to an RNA molecule comprising at least two complementary portions hybridized or capable of hybridizing to form a double-stranded structure sufficiently long to mediate RNAi (typically at least 19 base pairs in length), and at least one single-stranded portion, typically between approximately 1 and 10 nucleotides in length that forms a loop, and that shRNAs are precursors of siRNAs and are similarly capable of inhibiting expression of a target transcript (paragraph 0073).
Bear taught embodiments of the invention wherein the sequence TTCAAGAGA (SEQ ID NO: 10) is selected for the loop, and that a loop sequence is added at the 3’ end of the 19 or 21 nt sequence, and that any of a variety of other sequences may be selected for the loop including, but not limited to loops used in the shRNAs described in Brummelkamp et al. (paragraph 00180). Bear also exemplifies using this loop sequence of SEQ ID NO: 10 in making an shRNA which is inserted into lentiviral plasmids (Example 3, pages 85-86).
As shown in the alignment below the loop sequence of SEQ ID NO: 10 (Db) used in the shRNA of Bear has 100% identity to nucleotides 1-7 of instant SEQ ID NO: 6 (Qy).
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Regarding claim 2, Martin teaches the viral vector may be a lentiviral vector (page 22, line 30).
Regarding claim 7, the function “operable to knock-down B2M expression in transduced cells by at least 75% compared to wild type”, is a function that would result from the structure of the vector. Nevertheless, Martin teaches that when the target protein is B2M, cell surface expression of B2M is reduced by at least 10%......or up to about 99% compared to a control cell (page 37, lines 13-17).
Regarding claim 17, Martin teaches genetically modified immune cells of the invention can be further modified to express one or more inducible suicide genes, which provokes cell death and allows for selective destruction of the cells in vitro or in vivo (page 117, lines 5-7), and suicide genes can encode a polypeptide that is expressed at the surface of the cell that makes the cells sensitive to a therapeutic and/or cytotoxic monoclonal antibodies (page 117, lines 17-18).
Regarding claims 20 and 35, Martin teaches an immune cell made by any of the methods described herein, and wherein the target protein is B2M and the immune cell made by the method has reduced cell-surface expression of B2M and/or MHC class I proteins (page 42, lines 1-4). Martin teaches the immune cell is a T cell, NK cell, or B cell, which are lymphocytes (page 22, lines 22-24).
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention, to have modified the lentiviral vector encoding the B2M shRNA and CAR of Martin and the immune cell comprising the vector of Martin to comprise the hairpin loop sequence of Bear of SEQ ID NO: 10 in the B2M shRNA of Martin with a reasonable expectation of success. There would be a reasonable expectation of success, as both Martin and Bear pertain to shRNA molecules, and would amount to substituting the loop of the shRNA of Martin with the loop sequence of Bear to obtain predictable results. One of ordinary skill in the art would have been motivated to do so because Bear taught that shRNAs contain typically between approximately 1 and 10 nucleotides in length that forms a loop and taught a specific loop sequence as TTCAAGAGA (SEQ ID NO: 10) that is added at the 3’ end of the 19 or 21 nt sequence. Regarding loop sequences, Bear taught that any of a variety of other sequences may be selected for the loop including, but not limited to loops used in the shRNAs described in Brummelkamp et al. (paragraph 00180), and therefore are loop sequences well known in the art, and also exemplifies using this loop sequence of SEQ ID NO: 10 in making an shRNA which is inserted into lentiviral plasmids (Example 3, pages 85-86).
Accordingly, the limitations of claims 1,2,7,17,20 and 35 would have been prima facie obvious to one of ordinary skill in the art before the effective filing date.
Claim 6 is rejected under 35 U.S.C. 103 as being unpatentable over Martin in view of Bear as applied to claims 1,2,7,17,20 and 35 above, and further in view of He et al. (Cell Biosci, 2015, 5:67).
The teachings of Martin and Bear as applicable to claims 1,2,7,17,20 and 35 have been described above.
In addition, Martin teaches the template nucleic acid can comprise two or more nucleic acids encoding shRNAmiRs and can encode the same shRNAmiR (page 35, lines 24-26).
Martin and Bear do not teach the B2M shRNA comprises a second hairpin loop encoded by the nucleotide sequence set forth in SEQ ID NO: 7.
Before the effective filing date, He et al. taught designing shRNA vectors targeting the EGFP reporter gene and evaluation of the effects of various factors on silencing efficiency including stem length, loop sequence, antisense location and the ratio between AGO2 and shRNA, and found that a 19~21 bp stem and a 6 or 9 nt loop structure in the sense-loop, antisense orientation was the optimal design in the AGO2-shRNA system and constructed a lentiviral vector expressing the shRNA (Abstract).
He et al. taught design of shRNA with different loop sizes, include 4-nt, 6-nt and 9-nt long sequences, wherein the 6-nt long sequence was “CTCGAG” which is the same sequence as instant SEQ ID NO: 7, and also taught the 9-nt sequence as “TTCAAGAGA”, and that the silencing efficiency of the shRNA with the 6-nt CTCGAG loop was comparable to the 9-nt TTCAAGAGA loop (>75%) and the 4-nt loop showed much less inhibition (page 3, bottom).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the shRNA of Martin and Bear to include a second hairpin loop of “CTCGAG” of He et al. with a reasonable expectation of success. There would be a reasonable expectation of success as this would amount to combining prior art elements according to known methods to yield predictable results, and because Martin suggests that there can be multiple nucleic acids encoding the shRNAs. One of ordinary skill in the art would be motivated to do so because He et al. taught design of shRNA with different loop sizes, include 4-nt, 6-nt and 9-nt long sequences, wherein the 6-nt long sequence was “CTCGAG” which is the same sequence as instant SEQ ID NO: 7, and also taught the 9-nt sequence as “TTCAAGAGA”, which has 100% identity to instant SEQ ID NO: 6 (TCAAGAG), and that the silencing efficiency of the shRNA with the 6-nt CTCGAG loop was comparable to the 9-nt TTCAAGAGA loop (>75%). Therefore, an ordinary artisan would have been motivated to provide multiple loop sequences including CTCGAG and TTCAAGAGA for the shRNA of Martin and Bear to provide enhanced silencing efficiency.
Accordingly, the limitations of claims 6 would have been prima facie obvious to one of ordinary skill in the art before the effective filing date.
Claims 12 and 36 are rejected under 35 U.S.C. 103 as being unpatentable over Martin in view of Bear as applied to claims 1,2,7,17,20 and 35 above, and further in view of Smith (WO 2019190879, Published 03 Oct 2019), cited on an IDS.
The teachings of Martin and Bear as applicable to claims 1,2,7,17,20 and 35 have been described above.
Martin and Bear do not teach wherein the CAR specifically binds a glial cell marker, or an engineered cell which is a regulatory T cell (Treg) transduced with the vector of claim 1.
Before the effective filing date, Smith taught compositions that use T regulatory lymphocytes (Tregs) to modulate neurodegenerative immune responses targeting glial cells in the central nervous system, and that by coupling either Tregs or immunosuppressive proteins to a chimeric antigen receptor (CAR) or a single-chain variable fragment that specifically recognizes and binds glial cell markers, the immunosuppressive Tregs are drawn to glial cells of the CNS to reduce inflammation and protect the CNS from autoimmune attack (Summary, page 2, lines 6-13). Smith taught engineered Tregs expressing a CAR that specifically binds to a glial cell marker including myelin oligodendrocytes glycoprotein, oligodendrocyte marker 01, oligodendrocyte marker 04, neural/glial marker 2, A2B5, galactosylceramidase, myelin basic protein, glial fibrillary acidic protein, or myelin oligodendrocyte specific protein, and which protects neural tissue and reduces inflammation thereby treating the neurodegenerative disease (page 3, lines 1-4 and 16-23).
It would have been obvious to one of ordinary skill in the art before the effective filing date, to substitute the CAR of Martin used in the vector and cells engineered with the vector comprising the CAR and shRNA of Martin and Bear, with the CAR and Treg cells of Smith to arrive at the instant claims with a reasonable expectation of success as this would amount to simple substitution of one known element for another to obtain predictable results. One of ordinary skill in the art would have been motivated to do so because Smith taught compositions that use T regulatory lymphocytes (Tregs) to modulate neurodegenerative immune responses targeting glial cells in the central nervous system, and that by coupling either Tregs or immunosuppressive proteins to a chimeric antigen receptor (CAR) or a single-chain variable fragment that specifically recognizes and binds glial cell markers, the immunosuppressive Tregs are drawn to glial cells of the CNS to reduce inflammation and protect the CNS from autoimmune attack and taught engineered Tregs expressing a CAR that specifically binds to a glial cell marker including myelin oligodendrocytes glycoprotein, oligodendrocyte marker 01, oligodendrocyte marker 04, neural/glial marker 2, A2B5, galactosylceramidase, myelin basic protein, glial fibrillary acidic protein, or myelin oligodendrocyte specific protein, and which protects neural tissue and reduces inflammation thereby treating the neurodegenerative disease.
Accordingly, the limitations of claims 12 and 36 would have been prima facie obvious to one of ordinary skill in the art before the effective filing date.
Claim 16 is rejected under 35 U.S.C. 103 as being unpatentable over Martin in view of Bear as applied to claims 1,2,7,17,20 and 35 above, and further in view of Haque et al. (Scientific Reports, Published 10 Oct 2019, 9:14611, pages 1-10) and Juillerat et al. (US 20170296623, Published 19 Oct 2017).
The teachings of Martin and Bear as applicable to claims 1,2,7,17,20 and 35 have been described above.
Martin and Bear do not teach wherein the CAR specifically binds to a marker specific to macrophages.
Before the effective filing date, Haque et al. taught that CD163-, CD204- and CD206- positive macrophages are significantly associated with poor prognosis, pTNM staging and lymph node metastasis in lung cancer, and thus CD163, CD204 and CD206 are considered as useful markers for activation of tumor-associated macrophages (TAM) (page 1, 2nd paragraph). Haque et al. taught that CD204 is a Class A scavenger receptor involved in pathogenesis of atherosclerosis and pattern recognition of pathogen infection; CD206 is a macrophage mannose receptor 1 that is strongly expressed in prostate adenocarcinoma and the number of CD206-positive tumor-associated macrophages was correlated with poor prognosis of the disease (pages 1-2, 2nd paragraph). Haque et al. taught a study examining the expression of TAM subsets in OSCC tissues and the relationship between the expression of TAM markers and EGF production and tumor progression and results suggest that CD206+ TAMs might play an important role in the proliferation and invasion of OSCC via EGF secretion, and the numbers of CD206+ TAMs in OSCCs were positively correlated with several clinicopathologic factors including clinical stage, clinical T classification, mode of invasion, and cervical nodal metastasis. Notably, a high number of CD206+ TAMs was significantly correlated with poor prognosis (Discussion pages 8-9).
Juillerat et al. recited and taught an inhibitory chimeric antigen receptor (N-CAR) comprising an extracellular domain comprising an antigen binding domain, which binds to a cell surface antigen and which is CD206 (claim 7; paragraphs 0040,0053,0184,0185,0432,0436). Juillerat et al. taught for treatment of multiple myeloma, the extracellular binding domain of the N-CAR binds to at least one “off-target” antigen expressed on healthy cells and may be CD206 antigen (expressed on the surface of macrophages) (paragraphs 0429,0430).
It would have been obvious to one of ordinary skill in the art before the effective filing date, to substitute the CAR of Martin used in the vector and cells engineered with the vector comprising the CAR and shRNA of Martin and Bear, with a CAR that binds a marker specific to macrophages based on the teachings of Haque et al. and Juillerat et al. with a reasonable expectation of success, as this would amount to simple substitution of one known element for another to obtain predictable results. One of ordinary skill in the art would have been motivated to do so because Haque et al. taught that CD163-, CD204- and CD206- positive macrophages are significantly associated with poor prognosis, pTNM staging and lymph node metastasis in lung cancer, and thus CD163, CD204 and CD206 are considered as useful markers for activation of tumor-associated macrophages (TAM), that CD206+ TAMs might play an important role in the proliferation and invasion of OSCC via EGF secretion, and the numbers of CD206+ TAMs in OSCCs were positively correlated with several clinicopathologic factors including clinical stage, clinical T classification, mode of invasion, and cervical nodal metastasis and a high number of CD206+ TAMs was significantly correlated with poor prognosis. In addition, Juillerat et al. taught an inhibitory chimeric antigen receptor (N-CAR) comprising an extracellular domain comprising an antigen binding domain, which binds to a cell surface antigen and which is CD206 (claim 7; paragraphs 0040,0053,0184,0185,0432,0436) and taught for treatment of multiple myeloma, the extracellular binding domain of the N-CAR binds to at least one “off-target” antigen expressed on healthy cells and may be CD206 antigen (expressed on the surface of macrophages). Therefore, both Haque et al. and Juillerat et al. teach markers associated with macrophages, including CD206 and provide motivation for why one of ordinary skill in the art would want to target those markers including CD206 that are associated with poor prognosis of OSCC, using a CAR as taught by Juillerat et al.
Accordingly, the limitations of claim 16 would have been prima facie obvious to one of ordinary skill in the art before the effective filing date.
Claim 37 is rejected under 35 U.S.C. 103 as being unpatentable over Martin in view of Bear as applied to claims 1,2,7,17,20 and 35 above, and further in view of Poirot et al. (US 20170016025, Published 19 Jan 2017), cited on an IDS.
The teachings of Martin and Bear as applicable to claims 1,2,7,17,20 and 35 have been described above.
Martin and Bear do not teach wherein the engineered cell is derived from a donor for allogenic transplant in a subject.
Before the effective filing date, Poirot et al. taught engineered T cells for immunotherapy, and which are characterized in that expression of beta 2-microglobulin is inhibited and which modified T cells are suitable for allogenic transplantations, because it reduces the risk of rejection by the host’s immune system and the risk of developing graft versus host disease (paragraph 0001). Poirot et al. taught the current protocol for treatment of patients using adoptive immunotherapy is based on autologous cell transfer and that autologous therapies face substantial technical and logistic hurdles to practical application, their generation requires expensive dedicated facilities and expert personnel, they must be generated in a short time following a patient's diagnosis, and in many cases, pretreatment of the patient has resulted in degraded immune function, such that the patient's lymphocytes may be poorly functional and present in very low numbers (paragraph 0004).
Poirot et al. taught ideally, one would like to use a standardized therapy in which allogeneic therapeutic cells could be pre-manufactured, characterized in detail, and available for immediate administration to patients (paragraph 0005) and provides strategies for immunotherapy by which T-cells, especially allogeneic T-cells, are made particular suitable for allogeneic transplantations, reducing the risk for host versus graft rejections and for developing graft versus host disease and to render the T cells “stealthy” (paragraph 0011). Poirot et al. taught a method of preparing allogenic T-cell from a donor to make them suitable for immunotherapy purposes, comprising providing a T-cell, preferably an allogenic T cell obtained from a donor and inhibiting the expression of beta 2-microglobulin in said T-cell (paragraphs 0012-0013), and the inhibition of expression of B2M is achieved using a nucleic acid molecule that specifically hybridizes under cellular conditions with the cellular mRNA and/or genomic DNA encoding B2M (paragraph 0017), and includes shRNA as the nucleic acid inhibiting the expression of B2M (paragraph 0074).
Poirot et al. further teaches the engineered T cell further expresses a CAR directed against an antigen expressed on the surface of a malignant or infected cell (paragraph 0090).
It would have been obvious to one of ordinary skill in the art before the effective filing date, to provide the vector comprising the CAR and shRNA of Martin and Bear, in a cell derived from a donor for allogenic transplant in a subject based on the teachings of Poirot et al. to arrive at the instant claims with a reasonable expectation of success. There would be a reasonable expectation of success because Poirot et al. also pertains to engineered T cells for immunotherapy, and which are characterized in that expression of beta 2-microglobulin is inhibited, including using shRNA, and also teaches the T cell as further expressing a CAR. One of ordinary skill in the art would have been motivated to do so because Poirot et al. taught problems for treatment of patients using adoptive immunotherapy based on autologous cell transfer including that their generation requires expensive dedicated facilities and expert personnel, they must be generated in a short time following a patient's diagnosis, and in many cases, pretreatment of the patient has resulted in degraded immune function, such that the patient's lymphocytes may be poorly functional and present in very low numbers, and suggested a standardized therapy in which allogeneic therapeutic cells could be pre-manufactured and are made particular suitable for allogeneic transplantations, reducing the risk for host versus graft rejections and for developing graft versus host disease, and Poirot et al. taught a method of preparing allogenic T-cell from a donor to make them suitable for immunotherapy purposes, comprising providing a T-cell, preferably an allogenic T cell obtained from a donor and inhibiting the expression of beta 2-microglobulin in said T-cell (paragraphs 0012-0013), and the inhibition of expression of B2M is achieved using a nucleic acid molecule that specifically hybridizes under cellular conditions with the cellular mRNA and/or genomic DNA encoding B2M (paragraph 0017), and includes shRNA as the nucleic acid inhibiting the expression of B2M (paragraph 0074).
Accordingly, the limitations of claim 37 would have been prima facie obvious to one of ordinary skill in the art before the effective filing date.
Conclusion
Claims 1,2,6,7,12,16,17,20 and 35-37 are rejected.
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/STEPHANIE L SULLIVAN/Examiner, Art Unit 1635
/ABIGAIL VANHORN/Primary Examiner, Art Unit 1636
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