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 .
This action is in response to the papers filed 03/02/2026.
Claims 1, 38, 40, 55 and 61 have been amended, no claims have been canceled, and no new claims have been added as set forth in the claim set filed 03/02/2026. Claims 1, 22, 31, 33, and 58 are independent claims.
Claims 1, 22, 31-33, 37-40, 55-56, and 58-63 are examined on the merits.
Response to arguments
Withdrawn objections/ Rejections in response to Applicants’ arguments or amendments
Claim objections
The claim objections previously set forth in the office action filed 09/10/2025 is withdrawn in light of the amendments made to add the article “a” in claim 1 in line 2.
Claim Rejections - 35 USC § 112
The rejection of claims 38, 40, 55 and 61 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite is withdrawn.
Applicant’s arguments and amendments filed 03/02/2026 have been considered and are persuasive. Particularly, the amendments correcting antecedent basis and the removal of the term “and/or” from the indicated claims.
Maintained Rejections in response to Applicants’ arguments or amendments
Claim Rejections - 35 USC § 103
Claim 1, 22, 58, and 61-62 remain rejected under 35 U.S.C. 103 as being unpatentable over Haverkamp (IDS reference filed 07/17/2019, Immunity; new version with Supplementary material) as evidenced by Veglia (Nat Rev Immunol 21, 485–498 (2021); previously cited) in view of Seal (Experimental Hematology 2008; 36:1660–1672)
Regarding claim 1, 58, and 61, Haverkamp teaches mouse MDSCs which comprise heterogeneous mixtures of mature and immature granulocytes and monocyte-macrophages (p. 948, 2nd column; p. 947-948, bridging paragraph). Particularly Haverkamp teaches obtaining monocytic myeloid derived suppressor cells (Mo-MS) via in vitro differentiation of bone marrow precursor cells (p. 948, 2nd column). As evidenced by Veglia, neutrophils and monocytes with potent immunosuppressive activity were first reported around 30 years ago and later named myeloid-derived suppressor cells (MDSCs) (p.485). Therefore, the MDSCs comprise monocytes.
Although Haverkamp does not teach explicitly that human CD14+ MDSCs are utilized in their in vitro culture, Haverkamp states that the MDSCs utilized in the experiments are counterparts to human MDSCs and that human counterparts are readily available for gene expression studies (p. 948, 1st column; p. 951, 1st column). Haverkamp teaches that the MDSCs isolated from humans in their other gene expression experiments are CD14+ HLA-DR-/low (Supplemental Material, p. 9).
Therefore, it would have been obvious to one of ordinary skill in the art to utilize human CD14+ MDSC counterparts which comprise CD14+ monocytes in place of the mouse MDSCs utilized in the in vitro culture method to obtain CD14+ monocytes that when treated with TNF and GM-CSF have increased expression of cFLIP (p. 951). Therefore, the population of CD14+ monocytes are engineered to have increased expression of Cellular Flice Inhibitory Protein (cFLIP) and Haverkamp reads on the CD14 monocyte limitation of the independent claim. Moreover, Haverkamp teaches that the presence of cFLIP in the MDSCs is constitutively required for development as the continuous c-FLIP expression prevents caspase-8-dependent, RIPK3-independent cell death. Further enforcement of c-FLIP expression increases viability (p. 948, 1st column, Abstract).
However, Haverkamp does not teach that the cFLIP is increased by providing a nucleic acid, transfection nor that the transfection is stable or with the long or short version of the cFLIP protein (cFLIPs or cFLIPl).
Seal teaches utilizing lentiviral vectors to highly express cFLIPs or cFLIPl in myeloid cells such as ML-1 (p. 1663, Figure 2B). Seal teaches that this is a stable transfection step to constitutively overexpress C-FLICE inhibitory protein (C-flip) (Figure 32). Seal teaches that such an overexpression reduced TRAIL and TNF-a induced apoptosis (Abstract, results).
It would have been obvious to one of ordinary skill in the art to increase the cFLIP in the population of MDSCs (i.e. CD14 monocytes) as taught by Haverkamp with transduction via lentiviral vectors encoding cFLIPs or cFLIPlong as taught by Seal with a reasonable expectation of success. An artisan would be motivated to overexpress cFLIP or cFLIPl via lentiviral vector as it results in a constitutive and stable expression of cFLIP or cFLIPl and reduced TRAIL and TNF-a induced apoptosis (Abstract, results). Additionally, Haverkamp teaches that the presence of cFLIP in the MDSCs is constitutively required for development as the continuous c-FLIP expression prevents caspase-8-dependent, RIPK3-independent cell death. Further enforcement of c-FLIP expression increases viability (p. 948, 1st column, Abstract).
Regarding the limitation of increased expression of IDO1 in addition to the increased cFLIP, as each and every structural limitation is taught by the combination of Haverkamp and Seal, the increased expression of IDO1 would also occur with a reasonable expectation of success.
Regarding claim 22, the combined teachings of Haverkamp and Seal render obvious claim 1. Moreover, Haverkamp teaches MDSCs are diluted and then plated (p. 957, 2nd paragraph) as dilutions comprise either water or buffer as known in the art, with no evidence to the contrary in the reference, this reads on the claim of pharmaceutical composition as the composition would contain a pharmaceutically acceptable carrier such as buffer or water.
Regarding claim 62, the combined teachings of Haverkamp and Seal render obvious claim 1. Moreover, Haverkamp teaches that MDSCs are obtained via in vitro differentiation from bone marrow cells via inflammatory stress and that the MSs (in vitro obtained MDSCs) are obtained via culture with GM-CSF (p. 948, 2nd column). Haverkamp teaches that MDSC expansion also related to response to G-CSF in addition to GM-CSF (p. 947, 2nd column). Therefore, it would be obvious to one of ordinary skill in the art to combine both GM-CSF and G-CSF to obtain MDSCs with a reasonable expectation of success.
Therefore, the invention would have been prima facie obvious to one of ordinary skill in the art at the time of the effective filing date.
Claim 31 remains rejected under 35 U.S.C. 103 as being unpatentable over Haverkamp (supra) as evidenced by Veglia (Nat Rev Immunol 21, 485–498 (2021); previously cited) in view of Seal (supra) as applied to claim 1, and in further view of Messmann (2015. BLOOD, 25, VOLUME 126, NUMBER 9; previously cited)
Haverkamp and Seal make obvious a population of human CD14+ monocyte cells transfected with a nucleic acid encoding cFLIP short or cFlip long, resulting in the increased expression of cellular FLIP and IDO1 as iterated above in the 103 rejection the content of which is incorporated herein, in its entirety.
However, Haverkamp and Seal do not teach that the MDSCs are administered to a patient in need of immunosuppression in order to inhibit or reduce an immune response.
Messmann teaches administering MDSCs created via culture with G-CSF to subjects in need of immunosuppression as the subjects needed to prevent GVHD via immunosuppression (p. 1138-1139).
It would have been obvious to one of ordinary skill in the art to utilize the cells of Haverkamp in a method for reducing an immune response in an individual in need of immunosuppression as taught by Messmann with a reasonable expectation of success. An artisan would be motivated to utilize MDSCs to inhibit or reduce an immune response in a subject in need thereof as Messmann teaches that MDSCs are effective in helping to prevent immune responses/GvHD (p. 1138-1139).
It would have been prima facie obvious to one of ordinary skill in the art at the time of the effective filing date.
Claim 32 remains rejected under 35 U.S.C. 103 as being unpatentable over Haverkamp (IDS reference filed 07/17/2019) as evidenced by Veglia (Nat Rev Immunol 21, 485–498 (2021); previously cited) in view of Messmann (2015. BLOOD, 25, VOLUME 126, NUMBER 9) as applied to claims 1 and 31 above, and in further view of Nash (2000. Journal of Clinical Immunology 20(1): 38-45); previously cited in PTO892).
Haverkamp, Seal and Messman make obvious a method of reducing or inhibiting an adverse immune response in a patient in need of immunosuppression comprising administering to the patient an effective amount of MDSCs which have an increased expression of cFLIP and IDO1 via administration of a nucleic acid encoding cFLIP as iterated above in the 103 rejection the content of which is incorporated herein, in its entirety.
Regarding claim 32, Haverkamp and Messman do not teach wherein the cells are autologous.
Nash teaches allogeneic cell transplantation should only be considered in highly selected cases of severe autoimmune diseases because of the increased risk of transplant-related complications including graft-versus-host disease (GVHD) and graft rejection (p. 38, 2nd column).
Based on these teachings, it would be obvious to one of ordinary skill in the art to utilize autologous MDSCs in the method of administering MDSCs to a subject in need of immunosuppression with a reasonable expectation of success. It would be beneficial to utilize autologous cells in transplants of autoimmune diseases as allogeneic cell transplantation should only be considered in highly selected cases of severe autoimmune diseases because of the increased risk of transplant-related complications including graft-versus-host disease (GVHD) and graft rejection (Nash; p. 38, 2nd column).
Therefor the invention would have been prima facie obvious to one of ordinary skill in the art at the time of the effective filing date.
Claims 33, 37, 38, 40, and 55 remains rejected under 35 U.S.C. 103 as being unpatentable over Messman et al (2015. BLOOD, 25, VOLUME 126, NUMBER 9) in view of Haverkamp et al (IDS reference filed 07/17/2019) and Seal (Experimental Hematology 2008; 36:1660–1672).
Regarding claim 33, 37, 38 and 55, Messmann teaches a method of delivering in vitro generated myeloid cells (p. 1139, 2nd column) to murine patients to reduce GVHD (graft versus host disease) as shown in Figure 3. The administration of the MDSC (myeloid cells) was immunosuppression to reduce the immune response against the graft thus resulting in immunosuppression (p. 1141, bridging paragraph of col 1-2). Messmann teaches that the MDSCs created via culture with G-CSF (p. 1138).
Haverkamp developed a subset of myeloid cells by continuous expression of C-FLICE inhibitory protein (c-Flip) that led to production of a subpopulation of monocytic suppressor cells with immunosuppressive effects such as suppression of T cell proliferation (Abstract). These steps resolve issue of a heterogenous population of myeloid suppressor cells thus improving immunosuppression (p. 947) wherein the cells were made by treatment with TNF and GM-CSF (p. 948, 2nd column). Haverkamp teaches mouse MDSCs which comprise heterogeneous mixtures of mature and immature granulocytes and monocyte-macrophages (p. 947-948; bridging paragraph). Particularly Haverkamp teaches obtaining monocytic myeloid derived suppressor cells (Mo-MS) via in vitro differentiation of bone marrow precursor cells (p. 947; p. 948, 2nd column).
Although Haverkamp does not teach explicitly that human CD14+ MDSCs are utilized in their in vitro culture, Haverkamp states that the MDSCs utilized in the experiments are counterparts to human MDSCs (p. 948, 1st column). Haverkamp teaches that the MDSCs isolated from humans in their other gene expression experiments are CD14+ HLA-DR-/low (Supplemental Material, p. 9). Therefore, it would have been obvious to one of ordinary skill in the art to utilize human CD14+ MDSC counterparts which comprise CD14+ monocytes in place of the mouse MDSCs utilized in the in vitro culture method to obtain CD14+ monocytes that when treated with TNF and GM-CSF have increased expression of cFLIP (p. 951). Therefore, the population of CD14+ monocytes are engineered to have increased expression of cFLIP and Haverkamp reads on the CD14 monocyte limitation of the independent claim. Moreover, Haverkamp teaches that the presence of cFLIP in the MDSCs is constitutively required for development as the continuous c-FLIP expression prevents caspase-8-dependent, RIPK3-independent cell death. Further enforcement of c-FLIP expression increases viability (p. 948, 1st column, Abstract).
However, Messman and Haverkamp do not teach stable transfection, nor that cFlip is provided in a nucleic acid.
Seal teaches production of myeloid cells using lentivirus (i.e. viral vector) which is a stable transfection step to constitutively overexpress C-FLICE inhibitory protein (C-flip) (Figure 32). This is an improvement on producing these cells so that they could continuously express C-FLICE inhibitory protein in vivo is provided in the art.
Based on such teachings, it would have prima facie been obvious to one of ordinary skill in the art to use lentivirus to overexpress C-FLICE inhibitory protein to produce a subpopulation of myeloid suppressor cells that have improved T-cell suppressive activity in order to deliver an immunosuppressive agent for treatment of GVHD. Doing so would have led to a method as claimed in claim 33. As noted in the teachings above: Messman teaches that myeloid cells can be administered to mice to mediate immunosuppression of GVHD (p. 1141, bridging paragraph) while Haverkamp teaches that improved cell types with immunosuppressive properties are produced by inducing C-FLICE inhibitory protein. Additionally, Seal taught that overexpression myeloid cells for delivery to subjects could be improved by using lentivirus for stable transfection of the cells to produce a system for continuous expression of C-FLICE inhibitory protein (Figure 32). Thus, a person of ordinary skill in the art would have a reasonable expectation of success that the method would allow improved treatment.
Regarding claim 40, Seal teaches utilizing lentiviral vectors with cDNA to highly express cFLIPs or cFLIPl in myeloid cells such as ML-1 (p. 1663, Figure 2B). Therefore the combination of Messman and Seal above would read on cFLIPs or cFLIPl being stably transfected with lentiviral vectors.
It would have been prima facie obvious to one of ordinary skill in the art at the time of the effective filing date.
Claim 39 remains rejected under 35 U.S.C. 103 as being unpatentable over Messmann (supra) in view of Haverkamp (supra) and Seal (supra) as applied to claim 33 above, and in further view of Markovic (J Tranlsational Medicine, 2006, pages 1-13)
As discussed in the above 103 rejection, Messman Haverkamp provide teachings which read on administering autologous MDSCs which comprise CD14 monocytes which have been engineered to overexpress an increase in c-FLIP via a lentiviral vector with cDNA as a nucleic acid, as iterated above in the 103 rejection the content of which is incorporated herein, in its entirety.
Regarding claim 39, however, these references do not teach that the nucleic acid is RNA.
Markovic teaches a method of electrotransfecting RNA into a dendritic (myeloid) cell in order to obtain clinical grade cells (p. 2, 2nd column). Markovic further teaches that the delivery of RNA containing entire protein coding sequences eliminates the need to select patients on the basis of their HLA antigens (p. 2, 1st column).
Based on these teachings, it would be prima facie obvious to one of ordinary skill in the art to electrotransfect RNA into the myeloid cells of Messman in order to obtain a cell which overexpresses cFLIP with a reasonable expectation of success. An artisan would find this beneficial over other nucleic acid transfection methods including lentiviral means of Seal as the method would obtain clinical grade cells in that that the delivery of RNA containing entire protein coding sequences eliminates the need to select patients on the basis of their HLA antigens (Markovic, p. 2, 1st column).
Therefore it would have been prima facie obvious to one of ordinary skill in the art at the time of the effective filing date.
Claims 56 remains rejected under 35 U.S.C. 103 as being unpatentable over Messmann (supra) in view of Haverkamp (supra) as evidenced by Veglia (Nat Rev Immunol 21, 485–498 (2021); previously cited) and Seal (supra) as applied to 33, and in further view of Shin (US Patent 11,464,832; US Application No. 16321409; effectively filed 07/29/2016).
As discussed in the above 103 rejection, Messman Haverkamp and Seal provide teachings which read on administering autologous MDSCs which comprise CD14 monocytes which have been engineered to overexpress an increase in c-FLIP via a lentiviral vector with cDNA as a nucleic acid encoding c-FLIP long or c-FLIP short, as iterated above in the 103 rejection the content of which is incorporated herein, in its entirety.
However, these references do not teach that the nucleic acid sequence of c-FLIP short is SEQ ID NO: 4.
The RNI search of SEQ ID NO: 4 yields results for Shin which teaches a SEQ ID NO: 8 (a CFLAR/cFLIP variant) which has 100% sequence identity to and is the same length as SEQ ID NO: 4 of the present application, as seen below. Therefore, the sequence is known in the art.
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It would have been obvious to one of ordinary skill in the art at the time of the effective filing date to utilize the known sequence detailed in Shin for a c-flip/cflar variant for the c-flip variant made obvious by the combination of Messman, Haverkamp and Seal with a reasonable expectation of success. An artisan would substitute the sequence as it is a known equivalent sequence which encodes for the same c-FLIP/cFLAR protein.
Therefore, it would have been prima facie obvious to one of ordinary skill in the art at the time of the effective filing date.
Claim 59 remains rejected under 35 U.S.C. 103 as being unpatentable over Haverkamp (supra) as evidenced by Veglia (supra) in view of Seal (supra) as applied to claims 1, and in further view of Markovic (J Tranlsational Medicine, 2006, pages 1-13)
Haverkamp and Seal make obvious a population of human CD14+ monocyte cells transfected with a nucleic acid encoding cFLIP short or cFlip long wherein the nucleic acid is cDNA, resulting in the increased expression of cellular FLIP and IDO1 as iterated above in the 103 rejection the content of which is incorporated herein, in its entirety.
Regarding claim 59, however, these references do not teach that the nucleic acid is RNA.
Markovic teaches a method of electrotransfecting RNA into a dendritic (myeloid) cell in order to obtain clinical grade cells (p. 2, 2nd column). Markovic further teaches that the delivery of RNA containing entire protein coding sequences eliminates the need to select patients on the basis of their HLA antigens (p. 2, 1st column).
Based on these teachings, it would be prima facie obvious to one of ordinary skill in the art to electrotransfect RNA into the myeloid cells of Messman in order to obtain a cell which overexpresses cFLIP with a reasonable expectation of success. An artisan would find this beneficial over the lentiviral means of Seal as the method would obtain clinical grade cells in that that the delivery of RNA containing entire protein coding sequences eliminates the need to select patients on the basis of their HLA antigens (Markovic, p. 2, 1st column).
Therefore, it would have been prima facie obvious to one of ordinary skill in the art at the time of the effective filing date.
Claim 60 and 63 remains rejected under 35 U.S.C. 103 as being unpatentable over Haverkamp (supra) in view of Seal (supra) as applied to claim 1, and further in view of Shin (US Patent 11,464,832; US Application No. 16321409; effectively filed 07/29/2016).
Haverkamp and Seal make obvious a population of human CD14+ monocyte cells transfected with a nucleic acid encoding cFLIP short or cFlip long, resulting in the increased expression of cellular FLIP and IDO1 as iterated above in the 103 rejection the content of which is incorporated herein, in its entirety.
However, these references do not teach that the nucleic acid sequence of c-FLIP short is SEQ ID NO: 4.
The RNI search of SEQ ID NO: 4 yields results for Shin which teaches a SEQ ID NO: 8 (a CFLAR/cFLIP variant) which has 100% sequence identity to and is the same length as SEQ ID NO: 4 of the present application, as seen below. Therefore, the sequence is known in the art.
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It would have been obvious to one of ordinary skill in the art at the time of the effective filing date to utilize the known sequence detailed in Shin for a c-flip/cflar variant for the c-flip variant made obvious by the combination of Messman, Haverkamp and Seal with a reasonable expectation of success. An artisan would substitute the sequence as it is a known equivalent sequence which encodes for the same c-FLIP/cFLAR protein.
Regarding claim 63, the combination of Haverkamp, Seal and Shin above make obvious claims 1 and 60. Moreover, it would be obvious to one of ordinary skill in the art that the nucleic acid SEQ ID NO: 4 would encode for amino acid SEQ ID NO: 3 as a protein. As evidenced by the instant specification SEQ ID NO: 4 encodes for amino acid SEQ ID NO: 3 (instant specification; p. 37-38, bridging paragraph). Therefore, the combination of references would encode for SEQ ID NO: 3 with a reasonable expectation of success.
Therefore, it would have been prima facie obvious to one of ordinary skill in the art at the time of the effective filing date.
In response to Applicant’s arguments and amendments filed 03/02/2026 regarding the 103 rejections,
Applicant’s arguments and amendments filed 03/02/2026 have been considered, however they are not persuasive.
Applicant argues that no references alone or in combination teach the increase in IDO1 found in the present invention or the use of primary cells which resulted in the increase in IDO1 and CFLAR. Applicant further argues that Haverkamp does not teach that the MDSCs in their invention are counterparts to the human MDSCs and that Haverkamp specifically creates cells with specific gene deletions, therefore, there is not a showing of primary cells with an increased expression of c-FLIP. Applicant argues that there is no reasonable expectation of success and the reliance of inherency is improper with no one reference saying a gene inserted into a primary monocyte and that no cells are human cells.
In response to applicant's argument that no reference in combination or alone suggests the invention, the test for obviousness is not whether the features of a secondary reference may be bodily incorporated into the structure of the primary reference; nor is it that the claimed invention must be expressly suggested in any one or all of the references. Rather, the test is what the combined teachings of the references would have suggested to those of ordinary skill in the art. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981). The combination of references, while not having explicit instructions on active steps to achieve the present invention of a population of primary CD14+ or CD34+ stem cells with increased expression of CFLIP and IDO1 within each reference, as a whole teaches an artisan to arrive at the present invention with a reasonable expectation of success. Regarding the argument of Haverkamp not disclosing primary cells, Haverkamp utilizes isolated MDSCs from tissue (i.e. primary cells) which are genetically modified. Therefore, the cells are primary cells. While Haverkamp does not explicitly teach IDO1 expression, as the method of increasing CFLIP in the primary cells, increases IDO1 in the present invention, the same can be expected with a reasonable expectation of success. Regarding the argument of not stating the cells are the mouse counterpart to human MDSCs, the paragraph which is cited by Applicant in their remarks does indicate that the human MDSC counterparts are counterparts to mice MDSCs. Moreover, p. 951 in column 1, shows that Haverkamp utilizes both human and mouse MDSCs in experiments of gene expression.
Applicant further argues that Haverkamp deletes genes in their study and their Exhibit A shows that the deletion of even a single gene in a cell can have genome wide consequences.
Examiner agrees that the deletion of a gene can have genome wide consequences, however Haverkamp and Seal are utilized together, which rescues the gene expression and increases the gene expression when considered as a whole. Therefore, there would still be a reasonable expectation of success in achieving increased cFLIP and increase IDO1.
Applicant argues that Seal does not overcome the deficiencies within Haverkamp and points to Exhibit B shows that gene expression differs significantly from normal cells to cancer cells therefore one would not expect IDO1 increase. Moreover, all other references do not cure this deficiency.
Examiner agrees that Exhibit B shows that gene expression is different in normal and cancer cells. However, Seal is not utilized for teachings on cancer cells. The normal primary cell limitation is met by the primary reference of Haverkamp, Seal is utilized for the teaching of introducing lentiviral vectors into monocytes in general, whether cancerous or normal.
Conclusion
Claims 1, 22, 31-33, 37-40, 55-56, and 58-63 are rejected.
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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/ALEXANDRA F CONNORS/Examiner, Art Unit 1634
/MARIA G LEAVITT/Supervisory Patent Examiner, Art Unit 1634
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