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 .
Withdrawal of Rejections
Applicant’s arguments, pages 8-9, “III Issue under 35 U.S.C § 112(b)”, filed regarding claims 18,21, 24,27,29, and 32 deemed indefinite, the arguments were fully considered and are persuasive. The 35 U.S.C 112(b) rejection of the claims 18,21,24,27,29, and 32 has been withdrawn. Applicant has provided compliance with the requirements.
Election/Restrictions
Election of Species
Claim 37, 41, and 45 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the interview on 8/4/2025.
Claims 16-32, 34-36, 38-40, and 42-44 remain pending and are being considered on their merits.
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.
Claims 16-32, 34-36, 38-40, 42-44 are rejected under 35 U.S.C. 103 as being unpatentable over Rafiq et al (2020, Nature Reviews Clinical Oncology, 17: 147–167; reference U) in view of Kjellman et al (U.S. PGPUB 20180023070).
Regarding claims 16, 18, 22, 24 and 28-29, Rafiq teaches T cells genetically engineered to express chimeric antigen receptors (CAR T cells) are a useful cell therapy for treatment of cancers (see page 147); reads on “adoptive cell transfer immunotherapy”. Regarding claims 16, 22 and 28, Rafiq teaches that relying only on autologous CAR T cells causes manufacturing issues of inadequate cell numbers, suboptimal T cell states and delays in treatment, and that using CAR T cells engineered from allogeneic donor T cells is an alternative to autologous CAR T cells that could circumvent these issues (col. 1 on page 161). Regarding claims 16, 22 and 28, Rafiq teaches that a there are problems as that the engrafted allogeneic donor T cells can become reactive to cells of the recipient, resulting in GVHD, as the host immune cells can also recognize and eliminate the donor T cells (col. 2 on page 161). Regarding claims 16, 22 and 28, Rafiq teaches T cells of the recipient recognize the MHC in the treatment cells and thus cause rejection of the graft (paraphrase col. 2 on page 161).
Rafiq does not teach the cell immunotherapy of CAR T cells also comprises administering an IgG cysteine protease to reduce the antibody-mediated rejection of the grafted treatment cells.
Regarding claims 16, 20, 22, 26, 28 and 31, Kjellman teaches a method of administering to the subject an enzyme which inactivates serum IgG molecules just prior to transplantation of cells, wherein the enzyme which inactivates serum IgG molecules has the capacity to effectively desensitize a sensitized or highly sensitized patient, thereby allowing transplantation and avoiding acute antibody-mediated rejection (see paragraphs 22-25 and 124); reads on “improving the benefit to a patient” of a cell transfer. Regarding claims 22 and 28, Kjellman teaches the method is a useful treatment for both cancers and autoimmune conditions (see paragraphs 104 and 107-110).
Regarding claims 16, 21-22, 27-28,32,34,35,36, and 38-44, Kjellman teaches the enzyme is an IgG cysteine protease, from Streptococcus pyogenes, that is IdeS (imlifidase), having a sequence that is at least 85% identical to SEQ ID NO: 2, and wherein the sequence includes an additional methionine at the N terminus and/or a histidine tag at the C terminus (see paragraphs 7-8 & 59-60, and at least SEQ ID NOs: 2-5 and 9-17).
Regarding claims 16, 22 and 28, Kjellman teaches that the IgG cysteine protease is useful for various conditions wherein there antibody mediated rejection is a concern, as antibodies against MHC antigens of the potential donor, and the donor specific antibodies is a direct contraindication to transplantation because of the risk of acute antibody-mediated rejection, and that the IgG cysteine protease treatment allows for allows the rapid, temporary and safe removal of donor specific antibodies in a potential transplant recipient (see paragraphs 20-21 and 122-124).
Regarding claims 16-17, 19-20, 22-23, 25-26, 28,30, and 31, Kjellman teaches the sensitized or highly sensitized patient, may be a subject that has developed antibodies to human leukocyte antigens (HLA), and that the anti-HLA antibodies originate from allogenically sensitized B-cells and are usually present in patients that have previously been sensitized by blood transfusion, previous transplantation or pregnancy, and that the administering the an IgG cysteine protease just prior to transplantation has the capacity to effectively desensitize a highly sensitized patient, thereby allowing transplantation and avoiding acute antibody-mediated rejection (paragraphs 120 and 124); reads on increases survival of transplanted cells, reduced antibody dependent cellular cytotoxicity and receptor activated cell death of cells administered. Regarding claims 16, 22 and 28, Kjellman teaches their method can be used to improve the benefit to patient of another therapy or a therapeutic agent, such that the method comprises administering the treatment to the subject in combination with another therapy or therapeutic agent (paragraphs 105-106, 117-118, 124, 128).
It would have been obvious to combine Rafiq and Kjellman to also administering an IgG cysteine protease to reduce the antibody-mediated rejection of grafted allogeneic CAR T cells. A person of ordinary skill in the art would have had a reasonable expectation of success in also administering an IgG cysteine protease to reduce the antibody-mediated rejection of grafted allogeneic CAR T cells because Kjellman teaches that the method can be combined with other treatments, including cell therapy, and that the IgG cysteine protease treatment avoids antibody-mediated rejection in transplant recipient. Additionally, there is a reasonable expectation of success because both references teach that their treatments are useful for treating cancer, and both references teach that their treatments can be combined with other treatments. The skilled artisan would have been motivated to also administering an IgG cysteine protease to reduce the antibody-mediated rejection of grafted allogeneic CAR T cells because Rafiq recognizes that while allogeneic CAR T cells can solve problems of low available cell numbers for treatment, that there are concerns with antibody mediated rejection of the transplanted cells and Kjellman also teaches that the IgG cysteine protease treatment allows for allows the rapid, temporary and safe removal of donor specific antibodies in a potential transplant recipient.
Therefore, the invention as a whole would have been prima facie obvious to a person of ordinary skill at the time the invention was made.
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.
Claims 16, 21-22, 27-28,32,34,35,36, and 38-44 are rejected on the ground of nonstatutory double patenting as being unpatentable over:
claims 1-5 of U.S. Patent No. 10696959 (corresponds to Kjellman et al, USPGPUB 20180023070 above), limiting to a product of IgG cysteine protease activity wherein said sequence comprises or consists of SEQ ID NOs: 3, 4, 5, 9, 10, 11, 12, 13, 14, 15, or 16 and includes an additional methionine at the N terminus and/or a histidine tag at the C terminus;
claims 1-7 of U.S. Patent No. 10758597, limiting to a product of IgG cysteine protease activity wherein said sequence is at least 95% identical to SEQ ID NO: 14 and includes an additional methionine at the N terminus and/or a histidine tag at the C terminus;
claims 1-9 of U.S. Patent No.11524057, limiting to a product of IgG cysteine protease activity wherein said sequence is at least 95% identical to SEQ ID NOs: 4 or 17, and includes an additional methionine at the N terminus and/or a histidine tag at the C terminus;
claims 1-10 of U.S. Patent No. 11214784, limiting to a method of treatment comprising administering IgG cysteine protease activity wherein said sequence is at least 80% identical to SEQ ID NOs: 2, and wherein the IgG cysteine protease includes an additional methionine at the N terminus and/or a histidine tag at the C terminus;
claims 1-21 of U.S. Patent No. 11667905, limiting to a method of treatment comprising administering IgG cysteine protease activity wherein said sequence is at least 80% identical to SEQ ID NOs: 2, and wherein the IgG cysteine protease includes an additional methionine at the N terminus and/or a histidine tag at the C terminus, and of said IgG cysteine protease; or
claims 1-5 of U.S. Patent No. 12359183, limiting to a product of IgG cysteine protease activity wherein said sequence is at least 95% identical to SEQ ID NO: 14 and includes an additional methionine at the N terminus and/or a histidine tag at the C terminus; when any are taken in view of Rafiq et al (2020, Nature Reviews Clinical Oncology, 17: 147–167) and Kjellman et al (U.S. PGPUB 20180023070).
Although the claims at issue are not identical, they are not patentably distinct from each other because each of the patents disclose a product of an IgG cysteine protease that is identical to the IgG cysteine protease used in the instantly claimed method, and/or a method of using said IgG cysteine protease. While none of the conflicting patents limit to all of the features of the instantly pending claims, Kjellman et al, USPGPUB 20180023070, which corresponds to Patent 10696959, discloses a method of administering to the subject an enzyme which inactivates serum IgG molecules just prior to transplantation of cells, wherein the enzyme which inactivates serum IgG molecules has the capacity to effectively desensitize a sensitized or highly sensitized patient, thereby allowing transplantation and avoiding acute antibody-mediated rejection (see paragraphs 22-25 and 124) reads on “improving the benefit to a patient” of a cell transfer. Kjellman teaches the method is a useful treatment for both cancers and autoimmune conditions (see paragraphs 104 and 107-110). Kjellman teaches the sensitized or highly sensitized patient, may be a subject that has developed antibodies to human leukocyte antigens (HLA), and that the anti-HLA antibodies originate from allogenically sensitized B-cells and are usually present in patients that have previously been sensitized by blood transfusion, previous transplantation or pregnancy, and that the administering the an IgG cysteine protease just prior to transplantation has the capacity to effectively desensitize a highly sensitized patient, thereby allowing transplantation and avoiding acute antibody-mediated rejection (paragraphs 120 and 124); reads on increases survival of transplanted cells, reduced antibody dependent cellular cytotoxicity and receptor activated cell death of cells administered. Kjellman teaches their method can be used to improve the benefit to patient of another therapy or a therapeutic agent, such that the method comprises administering the treatment to the subject in combination with another therapy or therapeutic agent (paragraphs 105-106, 117-118, 124, 128).
Rafiq teaches T cells genetically engineered to express chimeric antigen receptors (CAR T cells) are a useful cell therapy for treatment of cancers (see page 147); reads on “adoptive cell transfer” immunotherapy. Rafiq teaches that relying only on autologous CAR T cells causes manufacturing issues of inadequate cell numbers, suboptimal T cell states and delays in treatment, and that using CAR T cells engineered from allogeneic donor T cells is an alternative to autologous CAR T cells that could circumvent these issues (col. 1 on page 161). Rafiq teaches that a there are problems as that the engrafted allogeneic donor T cells can become reactive to cells of the recipient, resulting in GVHD, as the host immune cells can also recognize and eliminate the donor T cells (col. 2 on page 161). Rafiq teaches T cells of the recipient recognize the MHC in the treatment cells and thus cause rejection of the graft (paraphrase col. 2 on page 161).
Therefore, in view of the teachings in the disclosure of Kjellman and Rafiq, it would have been obvious to use the IgG cysteine protease of any of the Patents in the method of the instant claims as Kjellman specifically teaches that the same IgG cysteine protease can be beneficially used in methods of treating cancers and treatments of cell therapy, and Rafiq teaches that CAR T cell therapy is also a beneficial cancer treatment. Therefore, Kjellman provides both motivation and a reasonable expectation of success for using the IgG cysteine protease of any of the Patents treatment methods of cancer, cell therapy, and methods wherein antibody dependent rejection is a concern, while Rafiq teaches cell therapy of CAR T cells is also a useful treatment for cancer but that antibody dependent rejection is a concern.
Claims 16-32 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 21, 27, 28,34,35,38-40, 42-44 and 18, 19, 21, 22, 31, 34- 37 of copending Application No.17909040 (reference application) in view of Rafiq et al (2020, Nature Reviews Clinical Oncology, 17: 147–167).
Although the claims at issue are not identical, they are not patentably distinct from each other because both limit to a method of administering the same IgG cysteine protease, that is IdeS which was identified and isolated from the organism, Streptococcus pyogenes, with a cell transplant.
Rafiq teaches T cells genetically engineered to express chimeric antigen receptors (CAR T cells) are a useful cell therapy for treatment of cancers (see page 147); reads on “adoptive cell transfer” immunotherapy. Rafiq teaches that relying only on autologous CAR T cells causes manufacturing issues of inadequate cell numbers, suboptimal T cell states and delays in treatment, and that using CAR T cells engineered from allogeneic donor T cells is an alternative to autologous CAR T cells that could circumvent these issues (col. 1 on page 161). Rafiq teaches that a there are problems as that the engrafted allogeneic donor T cells can become reactive to cells of the recipient, resulting in GVHD, as the host immune cells can also recognize and eliminate the donor T cells (col. 2 on page 161). Rafiq teaches T cells of the recipient recognize the MHC in the treatment cells and thus cause rejection of the graft (paraphrase col. 2 on page 161).
It would have been obvious to combine the copending application with Rafiq to use a cell therapy that is a transplant of allogeneic CAR T cells for cancer treatment. A person of ordinary skill in the art would have had a reasonable expectation of success in use a cell therapy that is a transplant of allogeneic CAR T cells for cancer treatment because copending application teaches including cell therapy, and Rafiq teaches that CAR T cell therapy is a beneficial cancer treatment. The skilled artisan would have been motivated use a cell therapy that is a transplant of allogeneic CAR T cells for cancer treatment in because Rafiq teaches that CAR T cell therapy is also a beneficial cancer treatment and copending application teaches IgG cysteine protease treatment, which is isolated from Streptococcus pyogenes and is the protein identified as IdeS, combined with cell therapy.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Response to Argument
Applicant’s arguments: pages 9-10 “IV Issue under 35 U.S.C. § 103”, filed regarding claims 16-32 .
The applicant argues the following:
Argument: The inventors were the first to recognize that the combination of adoptive cell transfer (ACT) immunotherapy with a protein having IgG cysteine protease or IgG endoglycosidase activity improves the benefit of the adoptive cell transfer immunotherapy. In particular, the inventors have shown that proteins with IgG cysteine protease or IgG endoglycosidase activity may protect transferred cells from surface receptor-specific antibodies that would otherwise attack the cells, and therefore the methods of the currently claimed invention increase the survival and activity of the transferred cells.
Response: Applicants assertion of the inventors as the first to recognize a benefit, does not overcome the current rejection where the claimed combination presents an establishment of function(s), and according to previously established biology, and was well within the ordinary skill level in the art, as further discussed below.
The historical background of IdeS (also referenced in Seq ID NO. 2 of instant application) illustrates that IdeS,, produced naturally by Streptococcus pyogenes, and its function and structure as a cysteine protease able to cleave IgG, were well-established and in seminal studies in the early 2000s. These foundational studies illustrate IdeS destroying surface bound IgG-Fc and all four subclasses of human IgG. By cleaving IgG, IdeS removes functional Fc regions that do not compete with intact IgG, which would otherwise allow resistance to specific antibodies- even in the presence of non-specific IgG. The generated fragments trigger immune responses away from a localized site, and disrupt host defense mechanisms. These events are known to prevent phagocytic cell recruitment and further downstream cell-mediated immune response(s). Consequently, the next stages of these foundational studies spurred innovation in disease prevention, wherein IdeS was used to cleave pathogenic IgG autoantibodies into non-pathogenic fragment(s). This resulted in therapeutic efficacy in antibody-mediated autoimmune pathologies, which was carried even further with pre-treatment of IdeS to eliminate hyperacute rejection.
Accordingly, despite the Applicant’s statement that they are the first to recognize the combination, the foundational knowledge was laid well in advance, and the application of this foundational knowledge (the use of ACT in combination with IgG cysteine protease or IgG endoglycosidase activity), as exemplified by the cited references, in combination with the ordinary skill level in the art, would have been obvious.
Applicant argues that Rafiq et al., in view of Kjellman et al., does not recognize the specific problems associated with adoptive cell transfer (ACT). However, obviousness does not require that a reference recognize the identical problem addressed by applicant. It is sufficient that the prior art and seminal studies established regarding the fundamental biology of the cysteine protease, teaches the claimed elements and that a person of ordinary skill would have had reason to combine them to obtain the predictable benefits of the combination. Accordingly, as the established science regarding IdeS structure and function, along with the teaching of Rafiq et al., on adoptive cell therapy, transplanted immune cells, and immune rejection limits combined with the teachings of Kjellman et al., regarding IgG cysteine protease administration to subjects to prevent antibody mediated injury of tissues, meet the obviousness of the claims.
By focusing the argument on Kjellman, the Applicant is not considering the combination set forth by the examiner in the office action. In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
Argument: The skilled artisan would have no guidance to select the embodiments of the current invention, when other known factors to reduce deleterious immune reaction for ACT were known, as per examples provided.
Response: Applicant’s acknowledgement that numerous methods for reducing immune-mediated injury were known further supports that immune-rejection was a poignant and recognized objective within the art. Therefore, an artisan skilled in the art would have reasonably considered the known IgG cleaving approach taught by Kjellman et al., along with seminal studies prior-to as discussed previously, as another method for reducing antibody-mediated immune response/rejection.
- Argument: A skilled person could not have expected that the claimed method would work, given that ACT provides unique challenges different than those of transplanted solid organs as discussed in Kjellman et al.
Response: A person of ordinary skill in the art would have recognized that the fundamental biology – as previously discussed above, regarding IdeS and antibody cleavage, is the same fundamental biology and does not deviate from the activity/function of IdeS. IdeS cleaves circulating IgG, whether it is used with ACT or other comparable scenarios in which non-host cells may interact with host immune response Therefore, the teachings apply regardless of whether it is cells of a transplanted organ, CAR-T cells, and/or other forms of ACT.
Rafiq et al. teaches immune barriers to CAR-T cell therapy and Kjellman et al., teaches removing said barriers. The fundamental biology of IdeS as a cysteine protease able to cleave IgG were seminal studies which led to expansive growth regarding improvements to auto-immune disease and other antibody mediated host-rejection studies resulting in removing pathogenic IgG. Therefore, the combination of two immune therapies, with the established knowledge of host-rejection, to then further reduce immune-mediated destruction of ACTwould have been obvious.
Argument: Applicant also states that in ACT methods the population of cells is lower than in methods in which a solid organ is transplanted, and thereby ACT cells are targets by more donor specific antibodies (DSAs) and therefore a skilled person would not have considered the combination of Kjellman et al and Rafiq et al, as the combination does not provide indication that the method would work with cell transplants.
Response: Applicants’ assertion, that circulating antibodies affect ACT with unexpected susceptibilities relative to transplanted tissues, lacks objective evidence sufficient to overcome the current rejection for obviousness. Mechanistically, T-cells can downregulate the surface expression of targeted antigens, including human leukocyte antigens (HLAs), further minimizing and/or neutralizing antibody-mediated neutralization, as compared with solid organs. Studies also demonstrate that DSAs impact on CAR-T therapy is dependent on allogeneic versus autologous cells. Additionally, a summation of studies teaches solid organs, which contain vascular endothelial cells that are highly susceptible to DSA binding and can trigger complement-dependent cytotoxicity and antibody-mediated rejection.
Applicant’s comparison of ACT to kidney (and/or solid organ) transplantation and acceptable cutoffs for DSAs relies on biological differences that are not without circumstantial consideration: The instant claims are directed to administering an IgG-cleaving cysteine protease in conjunction with ACT, and are not limited to any particular antibody concentration, DSA threshold, mechanism(s) of antibody-based injury, or protocol(s) for transplantation. Accordingly, Kjellman et al., teaches an IgG -cleaving cysteine protease to minimize and/or eliminate pathogenic antibodies directed to transplantation. Rafiq et al., teaches ACT (CAR-T cell) therapies, in both the survival of transferred cells (or tissues) depend upon the efficacy of an inhibitor, in this case administering said IgG cysteine protease (IdeS). As it was known in the art that ACT experience immune-mediated inactivation, a person of ordinary skill in the art would have reasonably expected a reduction in circulating IgG as taught by Kjellman et al., thus improving therapeutic efficacy.
Applicant’s arguments, pages 10-13 “V Double Patenting” :
The applicant’s arguments regarding the double patenting rejection, which are similar to those discussed above, are not persuasive for the same reasons as those discussed above.
Conclusion
No claims are free of the art. No claims are allowed.
THIS ACTION IS MADE FINAL. 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.
Correspondence Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ENUSHA KARUNASENA whose telephone number is (571)272-3972. The examiner can normally be reached Monday-Friday 7:30am-5pm.
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/ENUSHA KARUNASENA/Examiner, Art Unit 1653
/SHARMILA G LANDAU/Supervisory Patent Examiner, Art Unit 1653
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