DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claims 2, 3, 5, 7, 9, 11-19, 21-26, 30, 33, 34, 40, 43 have been canceled. Claims 1, 4, 6, 8, 10, 20, 27-29, 31, 32, 35-39, 41, 42 are pending.
Election/Restrictions
Applicants elected Group I, claims 1, 4, 6, 8-10, 19, 20, 27-29, 31; PDL1; SEQ ID NO: 1; CTL; CAR; SEQ ID NO: 12 without traverse in the reply filed on 9-3-25.
Claims 32, 35-39, 41, 42 remain withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected inventions, there being no allowable generic or linking claim.
Claims 1, 4, 6, 8, 10, 20, 27-29, 31 remain under consideration.
Applicant's arguments filed 5-13-26 have been fully considered but they are not persuasive.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Claim objections
Claim 1 can be written more simply and accurately as ---An isolated mammalian T-cell, natural killer cell, dendritic cell, or peripheral blood mononuclear cell (PBMC) comprising an exogenous nucleic acid sequence encoding an immune checkpoint ligand and an exogenous nucleic acid sequence encoding an engineered receptor---.
Claim Rejections - 35 USC § 112
Written Description
Claims 1, 4, 6, 8, 10, 20, 27-29, 31 remain rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for an isolated mammalian cytotoxic T-cell comprising an exogenous nucleic acid sequence encoding PDL1 that expresses the PDL1 and an MHC molecule, does not reasonably provide enablement for the claims as broadly written. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make/use the invention commensurate in scope with these claims.
Withdrawn rejection
The rejection regarding making/using a modified therapeutic cell comprising a first heterologous nucleic acid sequence encoding PDL1, wherein the therapeutic cell expresses a Major Histocompatibility Complex (MHC) molecule as being examined in claim 1 other than an isolated mammalian cell comprising an exogenous nucleic acid sequence encoding PDL1 has been withdrawn in view of the rejection.
Pending rejection
A) The specification lacks written description for a mammalian immune cell comprising exogenous nucleic acid sequences encoding PDL1 and a chimeric antigen receptor (CAR) as encompassed by claim 1 (elected in original claims 19, 20), that are “present in a vector” as required in claim 27, “fused” “via a third nucleic acid sequence encoding a self-cleavable linker” as required in claim 28, or a first heterologous nucleic acid sequence encoding PDL1 and a second heterologous nucleic acid sequence encoding the amino acid sequence of SEQ ID NO: 12 as required in claim 29.
SEQ ID NO: 12 was the elected species in claim 29.
The art at the time of filing taught isolated mammalian T-cells and NK comprising a nucleic acid sequence encoding a CAR that targets PDL1 (CN 109161532; CN 109576307; CN 110079502), but SEQ ID NO: 12 encodes PDL1.
Fig. 1A shows a vector comprising a first heterologous nucleic acid sequence encoding an “ICP ligand” which can be PDL1.
Fig. 1B shows a vector encoding a CAR (“antigen-binding domain; hinge + transmembrane; costimulatory; CD3z”) and an ICP ligand (which can be PDL1 – pg 6, para 26).
SEQ ID NO: 12 comprises SEQ ID NO: 1 (amino acids 1-209) which encodes PLD1 (pg 37, para 131) plus amino acids 210-798 of a non-disclosed structure. Pg 69, lines 4-8, contemplates using SEQ ID NO: 12; however, the function of SEQ ID NO: 12 is not disclosed.
The specification does not teach how to use a cell that encodes PDL1 (SEQ ID NO: 1) and a CAR (SEQ ID NO: 12) that encodes PDL1 as required in claims 1, 20, 27, 28, 29. The specification does not teach SEQ ID NO: 12 is a CAR. Assuming it IS a CAR, the function of a CAR encoding PDL1 cannot be determined, and the function of expressing PDL1 along with a CAR encoding PDL1 is not disclosed and cannot be envisioned from the specification or the art at the time of filing. The specification does not correlate the function of SEQ ID NO: 12 to any other CARs as broadly encompassed by claims 12, 20, 27-29. The specification does not correlate the function of SEQ ID NO: 12 to SEQ ID NO: 12-27 in claim 29.
The specification does not teach how to use an immune cell encoding PDL1 and a CAR as required in claims 1, 20, 27-29. The specification does not teach the structure of the CAR to use in combination with PDL1. The specification does not correlate a T-cell, natural killer cell, dendritic cell, or peripheral blood mononuclear cell (PBMC) to any red blood cells, B-cells, thymus, spleen, pituitary, blood vessel, et al. cells of the immune system as broadly encompassed by “immune cell” in claims 1, 20, 27-29.
Accordingly the specification lacks written description for a mammalian immune cell comprising exogenous sequences encoding PDL1 and a CAR as required in claims 1, 20, 27-29.
Response to arguments
Applicants argue Fig. 1B shows a vector encoding a CAR (“antigen-binding domain; hinge + transmembrane; costimulatory; CD3z”) and an ICP ligand (which can be PDL1 – pg 6, para 26). Applicants’ argument is not persuasive. The specification does not teach how to use an immune cell encoding PDL1 and a CAR as required in claims 1, 20, 27-29. The specification does not teach the structure of the CAR to use in combination with PDL1. The specification does not correlate a T-cell, natural killer cell, dendritic cell, or peripheral blood mononuclear cell (PBMC) to any red blood cells, B-cells, thymus, spleen, pituitary, blood vessel, et al. cells of the immune system as broadly encompassed by “immune cell” in claims 1, 20, 27-29.
B) The specification lacks written description for any “variant thereof” of SEQ ID NO: 1 having at least about 95% identity to SEQ ID NO: 1 as broadly encompassed by claim 8 other than SEQ ID NO: 1.
SEQ ID NO: 1 was the species of PDL1 elected by applicants.
Claim 8 requires the “ICL comprises an amino acid sequence selected from the group consisting of SEQ ID NO: 1-8 or variants thereof comprising an amino acid sequence that is at least about 95% identical to an amino acid sequence selected from the group consisting of SEQ ID NO: 1-8”.
The specification does not teach any assay to determine whether any fragment of SEQ ID NO: 1 is a functional variant of SEQ ID NO: 1. The specification does not teach any assay to determine whether any fragment of SEQ ID NO: 1 that shares at least about 95% identity to SEQ ID NO: 1 is a functional variant of SEQ ID NO: 1. The specification does not teach how to use any fragment of SEQ ID NO: 1 is not functional in a “modified therapeutic cells” as encompassed by claim 8. Accordingly, claim 8 lacks written description other than SEQ ID NO: 1.
Response to argument
Applicants argue the amendment overcomes the rejection. Applicants’ argument is not persuasive for reasons set forth above.
C) The specification lacks written description for a cell comprising exogenous nucleic acid sequences encoding PDL1 and a CAR that are “present in a vector” as required in claim 27, “fused” “via a third nucleic acid sequence encoding a self-cleavable linker” as required in claim 28, or a first heterologous nucleic acid sequence encoding PDL1 and a second heterologous nucleic acid sequence encoding the amino acid sequence of SEQ ID NO: 12 as required in claim 29.
SEQ ID NO: 12 was the elected species in claim 29.
The art at the time of filing taught isolated mammalian T-cells and NK comprising a nucleic acid sequence encoding a CAR that targets PDL1 (CN 109161532; CN 109576307; CN 110079502), but SEQ ID NO: 12 encodes PDL1.
Fig. 1A shows a vector comprising a first heterologous nucleic acid sequence encoding an “ICP ligand” which can be PDL1.
Fig. 1B shows a vector encoding a CAR (“antigen-binding domain; hinge + transmembrane; costimulatory; CD3z”) and an ICP ligand (which can be PDL1 – pg 6, para 26).
SEQ ID NO: 12 comprises SEQ ID NO: 1 (amino acids 1-209) which encodes PLD1 (pg 37, para 131) plus amino acids 210-798 of a non-disclosed structure. Pg 69, lines 4-8, contemplates using SEQ ID NO: 12; however, the function of SEQ ID NO: 12 is not disclosed.
The specification does not teach exogenous sequences encoding PDL1 and a CAR are “in a vector” as required in claim 27. The specification does not teach the structure/function of the “self-cleavable linker” in claim 28. The specification does not teach how to use a cell comprising a vector comprising SEQ ID NO: 12 as required in claim 29. Applicants’ arguments filed 5-13-26 say SEQ ID NO: 12 encodes PDL1 (SEQ ID NO: 1) and anti-CD19 CAR CTL-109 (SEQ ID NO: 9) via a P2A linker (SEQ ID NO: 11). However, the function of an anti-CD19 CAR CTL-109 is not disclosed in the specification or the art at the time of filing. The function of SEQ ID NO: 12 encoding PDL1 and an anti-CD19 CAR CTL-109 is disclosed. The function of SEQ ID NO: 12 is not disclosed in the specification or the art at the time of filing. The specification does not correlate the function of SEQ ID NO: 12 to SEQ ID NO: 13-27 in claim 29.
Given the lack of guidance in the specification taken with the art at the time of filing, the concepts in claims 27-29 lack written description.
Response to arguments
Applicants point to Fig. 1B. Applicants’ argument is not persuasive. The specification does not teach exogenous sequences encoding PDL1 and a CAR are “in a vector” as required in claim 27. The specification does not teach the structure/function of the “self-cleavable linker” in claim 28. The specification does not teach how to use a cell comprising a vector comprising SEQ ID NO: 12 as required in claim 29.
Applicants’ arguments filed 5-13-26 say SEQ ID NO: 12 encodes PDL1 (SEQ ID NO: 1) and anti-CD19 CAR CTL-109 (SEQ ID NO: 9) via a P2A linker (SEQ ID NO: 11). However, the function of an anti-CD19 CAR CTL-109 is not disclosed in the specification or the art at the time of filing. The function of SEQ ID NO: 12 encoding PDL1 and an anti-CD19 CAR CTL-109 is disclosed. The function of SEQ ID NO: 12 is not disclosed in the specification or the art at the time of filing. The specification does not correlate the function of SEQ ID NO: 12 to SEQ ID NO: 13-27 in claim 29.
Enablement
Claims 1, 4, 6, 8, 10, 20, 27-29, 31 remain rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for an isolated mammalian cell comprising an exogenous nucleic acid sequence encoding PDL1, does not reasonably provide enablement for the claims as broadly written. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make/use the invention commensurate in scope with these claims.
Withdrawn rejection
The rejection regarding making/using a modified therapeutic cell comprising a first heterologous nucleic acid sequence encoding PDL1, wherein the therapeutic cell expresses a Major Histocompatibility Complex (MHC) molecule as being examined in claim 1 other than an isolated mammalian cell comprising an exogenous nucleic acid sequence encoding PDL1 has been withdrawn in view of the rejection.
Pending rejection
A) The specification does not enable making/using an immune cell comprising a first heterologous nucleic acid sequence encoding PDL1 and a second heterologous nucleic acid sequence encoding a chimeric antigen receptor (CAR) as encompassed by claim 1 (elected in original claims 19, 20), that are “present in a vector” as required in claim 27, “fused” “via a third nucleic acid sequence encoding a self-cleavable linker” as required in claim 28, or a first heterologous nucleic acid sequence encoding PDL1 and a second heterologous nucleic acid sequence encoding the amino acid sequence of SEQ ID NO: 12 as required in claim 29.
SEQ ID NO: 12 was the elected species in claim 29.
The art at the time of filing taught isolated mammalian T-cells and NK comprising a nucleic acid sequence encoding a CAR that targets PDL1 (CN 109161532; CN 109576307; CN 110079502), but SEQ ID NO: 12 encodes PDL1.
Fig. 1A shows a vector comprising a first heterologous nucleic acid sequence encoding an “ICP ligand” which can be PDL1.
Fig. 1B shows a vector encoding a CAR (“antigen-binding domain; hinge + transmembrane; costimulatory; CD3z”) and an ICP ligand (which can be PDL1 – pg 6, para 26).
SEQ ID NO: 12 comprises SEQ ID NO: 1 (amino acids 1-209) which encodes PLD1 (pg 37, para 131) plus amino acids 210-798 of a non-disclosed structure. Pg 69, lines 4-8, contemplates using SEQ ID NO: 12; however, the function of SEQ ID NO: 12 is not disclosed.
The specification does not teach how to use a cell that encodes PDL1 (SEQ ID NO: 1) and a CAR (SEQ ID NO: 12) that encodes PDL1 as required in claims 1, 20, 27, 28, 29. The specification does not teach SEQ ID NO: 12 is a CAR. Assuming it IS a CAR, the function of a CAR encoding PDL1 cannot be determined, and the function of expressing PDL1 along with a CAR encoding PDL1 is not disclosed and cannot be envisioned from the specification or the art at the time of filing. The specification does not correlate the function of SEQ ID NO: 12 to any other CARs as broadly encompassed by claims 12, 20, 27-29. The specification does not correlate the function of SEQ ID NO: 12 to SEQ ID NO: 12-27 in claim 29.
The specification does not teach how to use an immune cell encoding PDL1 and a CAR as required in claims 1, 20, 27-29. The specification does not teach the structure of the CAR to use in combination with PDL1. The specification does not correlate a T-cell, natural killer cell, dendritic cell, or peripheral blood mononuclear cell (PBMC) to any red blood cells, B-cells, thymus, spleen, pituitary, blood vessel, et al. cells of the immune system as broadly encompassed by “immune cell” in claims 1, 20, 27-29.
Given the lack of guidance in the specification taken with the art at the time of filing, it would have required those of skill undue experimentation to determine how to make/use any cell as required in claims 1, 20, 27-29.
Response to arguments
Applicants argue Fig. 1B shows a vector encoding a CAR (“antigen-binding domain; hinge + transmembrane; costimulatory; CD3z”) and an ICP ligand (which can be PDL1 – pg 6, para 26). Applicants’ argument is not persuasive. The specification does not teach how to use an immune cell encoding PDL1 and a CAR as required in claims 1, 20, 27-29. The specification does not teach the structure of the CAR to use in combination with PDL1. The specification does not correlate a T-cell, natural killer cell, dendritic cell, or peripheral blood mononuclear cell (PBMC) to any red blood cells, B-cells, thymus, spleen, pituitary, blood vessel, et al. cells of the immune system as broadly encompassed by “immune cell” in claims 1, 20, 27-29. .
Indefiniteness
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 1, 4, 6, 8, 10, 20, 27-29, 31 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
A) The metes and bounds of a “primary immune” cell in claim 1 cannot be determined. It cannot be determined if the phrase is limited to “fresh” cells taken directly from an organism. If so, how fresh must they be to be considered “primary” cells. It cannot be determined if the phrase encompasses any cell taken from tissue of any organism and maintained for growth in culture medium. The line at which “fresh” cells are no longer “primary” cells is not defined in the specification or the art at the time of filing. The number of passages that define when cells are/are not “primary” is not described by applicants or the art. The time in culture that defines when cells are/are not “primary” is not described by applicants or the art.
It is unclear whether “primary” cells are limited to cells isolated directly from tissue before being placed in culture or if they encompass cells removed from tissue and placed into a culture dish. If the phrase encompasses cells removed from tissue and placed into a culture dish, it is unclear whether the phrase is limited to cells placed into culture for a limited number of seconds, or if it encompasses cells placed into culture for minutes, hours, days, weeks, months, etc. If the phrase encompasses cells removed from tissue and placed into a culture dish for a limited number of minutes, hours, days, weeks, months, etc., it is unclear when the cells are/are not “primary”. It is unclear whether “primary” cells are limited to cells that have undergone no changes in media in culture or if the phrase encompasses any number of changes in media in culture. If the phrase encompasses any number of changes in media in culture, it is unclear whether “primary” cells are limited to cells that have undergone a particular number of changes in media or if the phrase encompasses an unlimited number of changes in media. If the phrase encompasses an unlimited number of changes in media, then it is unclear how the “primary” further limits the term “cells” at all.
Accordingly, it cannot be determined if the term “primary” is limiting in any way, and if so how. The metes and bounds of “primary cells” are not defined in the specification or the art at the time of filing. It is unclear when cells are “primary” and when they are no longer “primary” and become a “cell line”. Therefore, those of skill would not be able to determine when they were infringing on the claim.
B) It is unclear whether an “immune cell” in claim 1 is limited to white blood cells or whether it encompasses red blood cells. It is also unclear whether spleen, thymus, thyroid, pituitary, blood vessel, et al. cells are encompassed by the phrase because of their role in the immune system.
Claim Rejections - 35 USC § 102
A) Claims 1, 4, 6, 10, 20, 27, 28, 31 remain rejected under 35 U.S.C. 102a1 as being anticipated by Nagy (CN 110869494).
Nagy taught isolated mouse ES cells comprising an exogenous nucleic acid sequence encoding PDL1 (para 19); the cells inherently MUST express MHC as required in claim 1 because they are nucleated cells. PDL1 is the immune checkpoint ligand in claim 1. The cells are also immune cells, e.g. T-cells, B-cells, natural killer cells, dendritic cells, peripheral blood lymphocytes (para 28 et al), as required in claim 1. Mice made from the ES cells inherently MUST have immune cells having the genetic modification claimed as well. Nagy taught the cell further comprised an exogenous nucleic acid sequence encoding an engineered receptor (para 353, 397, 403) as required in claim 1.
Nagy did not teach modifying the B2M gene as required in claim 4.
Nagy taught PDL1 as required in claim 6.
The cells are immune cells, e.g. T-cells, B-cells, natural killer cells, dendritic cells, peripheral blood lymphocytes (para 28 et al), as required in claims 9 and 10.
Nagy taught the receptor was an Fc-receptor fusion protein (para 403) which is a “chimeric antigen receptor” (CAR) as required in claim 20.
The exogenous sequence encoding the receptor can be operably linked to the first exogenous sequence in a vector (para 353) as required in claims 27, 28.
The cell is a pharmaceutically composition as required in claim 31 because it is in pH balanced culture medium.
Response to arguments
Applicants argue Nagy is limited to ES cells. Applicants’ argument is not persuasive. The cells were also immune cells, e.g. T-cells, B-cells, natural killer cells, dendritic cells, peripheral blood lymphocytes (para 28 et al), as required in claim 1. Furthermore, mice made from the ES cells inherently MUST have immune cells having the genetic modification claimed as well.
Applicants argue Nagy did not teach a second nucleic acid encoding an engineered receptor as required in claim 1. Applicants’ argument is not persuasive. Nagy taught the cell further comprised an exogenous nucleic acid sequence encoding an engineered receptor (para 353, 397, 403).
B) Claims 1, 4, 6, 10, 20, 27, 28, 31 remain rejected under 35 U.S.C. 102a1 as being anticipated by Themeli (AU 20140248119).
Themeli taught isolated cells transfected with a vector comprising an exogenous nucleic acid sequence encoding PDL1 and a CAR (claim 29). The cells inherently MUST express MHC as required in claim 1 because they are nucleated cells. PDL1 is the immune checkpoint ligand in claim 1. The cells are immune cells, e.g. T-cells, B-cells, natural killer cells, dendritic cells, peripheral blood lymphocytes (claim 16), as required in claim 1. Themeli taught the cell further comprised an exogenous nucleic acid sequence encoding an engineered receptor (claim 1) as required in claim 19.
Themeli taught modifying or not modifying the B2M gene (claim 1 vs. 15). Not modifying the B2M gene as encompassed by Themeli is equivalent to claim 4.
Themeli taught PDL1 (claim 29) as required in claim 6.
The cells are immune cells, e.g. T-cells, B-cells, natural killer cells, dendritic cells, peripheral blood lymphocytes (claim 16), as required in claims 9 and 10.
Themeli taught the receptor was an (CAR) (claim 1) as required in claim 20.
Themeli taught exogenous sequence encoding the CAR can be operably linked to another exogenous coding sequence in a vector (Fig. 4) as required in claims 27, 28.
The cell is a pharmaceutically composition as required in claim 31 because it is in pH balanced culture medium.
Response to arguments
Applicants argue Themeli is limited to ES cells. Applicants’ argument is not persuasive. The cells are immune cells, e.g. T-cells, B-cells, natural killer cells, dendritic cells, peripheral blood lymphocytes (claim 16), as required in claim 1. Furthermore, mice made from the ES cells inherently MUST have immune cells having the genetic modification claimed as well.
Claim Rejections - 35 USC § 103
A) Claims 1, 4, 6, 8, 10, 20, 27, 28, 31 remain rejected under 35 U.S.C. 102a1 as being unpatentable over Nagy (CN 110869494) in view of Freeman (J. Exp. Med., 2000. Vol. 192, pg 1027-1034).
Nagy taught ES cells comprising an exogenous nucleic acid sequence encoding PDL1 (para 19); the cells inherently MUST express MHC as required in claim 1 because they are nucleated cells. PDL1 is the immune checkpoint ligand in claim 1.
Nagy did not teach the PDL1 had an amino acid sequence that is at least 85% identical to SEQ ID NO: 1 as required in claim 8.
However, Freeman taught an amino acid sequence encoding human PDL1 that is at least 85% identical to SEQ ID NO: 1 (Fig. 1).
Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to make cells comprising an exogenous nucleic acid sequence encoding PDL1 that inherently express endogenous MHC as described by Nagy wherein the PDL1 was human and had an amino acid sequence that is at least 85% identical to SEQ ID NO: 1 as described by Freeman. Those of ordinary skill in the art at the time of filing would have been motivated to express human PDL1 to humanize the mouse cell, to study “negative regulation of lymphocyte activation” in vitro as described by Freeman (title; pg 1028, 1st full paragraph).
Claims 1, 4, 6, 10, 20, 27, 28, 31 have been included for reasons set forth above under anticipation.
Response to arguments
Applicants argue Nagy is limited to ES cells. Applicants’ argument is not persuasive. The cells were also immune cells, e.g. T-cells, B-cells, natural killer cells, dendritic cells, peripheral blood lymphocytes (para 28 et al), as required in claim 1. Furthermore, mice made from the ES cells inherently MUST have immune cells having the genetic modification claimed as well.
Applicants argue Nagy did not teach a second nucleic acid encoding an engineered receptor as required in claim 1. Applicants’ argument is not persuasive. Nagy taught the cell further comprised an exogenous nucleic acid sequence encoding an engineered receptor (para 353, 397, 403).
B) Claims 1, 4, 6, 8, 10, 20, 27, 28, 31 remain rejected under 35 U.S.C. 102a1 as being unpatentable over Themeli (AU 20140248119) in view of Freeman (J. Exp. Med., 2000. Vol. 192, pg 1027-1034).
Themeli taught cells transfected with a vector comprising an exogenous nucleic acid sequence encoding PDL1 and a CAR (claim 29). The cells inherently MUST express MHC as required in claim 1 because they are nucleated cells. PDL1 is the immune checkpoint ligand in claim 1.
Themeli did not teach the PDL1 had an amino acid sequence that is at least 85% identical to SEQ ID NO: 1 as required in claim 8.
However, Freeman taught an amino acid sequence encoding human PDL1 that is at least 85% identical to SEQ ID NO: 1 (Fig. 1).
Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to make cells comprising an exogenous nucleic acid sequence encoding PDL1 that inherently express endogenous MHC as described by Nagy wherein the PDL1 was human and had an amino acid sequence that is at least 85% identical to SEQ ID NO: 1 as described by Themeli. Those of ordinary skill in the art at the time of filing would have been motivated to express human PDL1 to humanize the mouse cell, to study “negative regulation of lymphocyte activation” in vitro as described by Freeman (title; pg 1028, 1st full paragraph).
Claims 1, 4, 6, 10, 20, 27, 28, 31 have been included for reasons set forth above under anticipation.
Response to arguments
Applicants argue Themeli is limited to ES cells. Applicants’ argument is not persuasive. The cells are immune cells, e.g. T-cells, B-cells, natural killer cells, dendritic cells, peripheral blood lymphocytes (claim 16), as required in claim 1. Furthermore, mice made from the ES cells inherently MUST have immune cells having the genetic modification claimed as well.
Conclusion
No claim is allowed.
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.
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Michael C. Wilson
/MICHAEL C WILSON/ Primary Examiner, Art Unit 1638
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