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 June 25, 2026.
Claims 111-119, 131, and 134-156 are pending in the application. Claims 111-113, 115, 119 and 131 are amended, claims 120-130 and 132-133 are canceled, and claims 134-156 are newly added as set forth in the claim set filed 06/25/26.
Applicant’s election without traverse of Group I (111-119 and 131) in the reply filed on 06/25/2026 is acknowledged.
Applicant has canceled all withdrawn claims.
Therefore, claims 111-119, 131, and 134-156 are examined on the merits.
Priority
Applicant’s claim for the benefit of a prior-filed parent provisional applications 63/390,513 filed 07/19/2022 under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) is acknowledged.
Thus, the earliest possible priority for the instant application is July 19, 2022.
Claim Rejections - 35 USC § 112
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 139 and 151 is 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.
Claim 139 is indefinite in its recitation of “an extracellular portion of a human SIRPA polypeptide” and “an intracellular portion of a non-human animal Sirpa Polypeptide”. The term "portion" is not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention. Appropriate action is required.
Claim 151 recites the limitation "the inactivated endogenous Fah" in line 2. Claim 151 depends on claim 149 which does not recite “inactivated endogenous Fah.” Therefore, there is insufficient antecedent basis for this limitation in the claim.
Therefore, claim 151 is rejected as being indefinite.
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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 111-112, 114-119, 131, 134, 138-143, 145-150, 152-153, and 155-156 are rejected under 35 U.S.C. 103 as being unpatentable over Murphy (US20200060244A1) in view of Kovtunovych (2010, Blood 116, 26: 6054-6062; IDS Reference).
Regarding claims 111 and 119, Murphy teaches creating a genetically modified rodent which is a Rag2−/−Il2rgnull Tpoh/h Il3h/h Gmcsfh/h Epoh/m SIRPαh/h mouse and expresses human EPO operably linked to a human EPO gene promoter (Claim 1, para. 0016-0017). These are immunodeficient mice. Moreover, Murphy states that the non-human genes are homozygous null (i.e. Rag2 and IL2rg) (para. 0011). Murphy aims to study diseases such as malaria (para. 0005). The nucleic acids are provided into an animal cell to produce the genetically modified animal, therefore, Murphy teaches on the animal cell of independent claim 111.
However, Murphy does not teach that the animal cell or the genetically modified rodent are homozygous null for non-human Heme oxygenase (Hmox-1) gene.
Kovtunovych teaches that in Heme oxygenase (HO-1) null animals splenic and liver macrophages are mostly absent (Abstract). Moreover, in the kidney, the team observed a distinct pattern of increased iron staining in epithelial cells of the proximal tubules and some glomeruli (Figure 5A). The phenomenon of significant iron increase in kidney is usually associated with diseases that increase intravascular hemolysis, such as sickle cell disease, malaria, and artificially induced intravascular hemolysis.
It would have been obvious to one of ordinary skill in the art at the time of the effective filing date to additionally include a Hmox-1 null mutation in the animal models and cells of Murphy with a reasonable expectation of success. An artisan would be motivated to do so as Murphy demonstrates animal models with immunodeficient mice which are depleted of in vivo phagocytotic cells prior to and during infection (para. 0092). Kovtunovych demonstrates an animal model which additionally eliminates macrophages in liver and spleen and resulting in RBCs not subjected to phagocytosis and both Murphy and Kovtunovych demonstrate animal models which resemble symptoms consistent with malaria.
Regarding claim 112, Murphy and Kovtunovych make obvious the cells of claim 111. Moreover, Murphy teaches that deficiencies such as Rag1 and Rag2 may be utilized to achieve immunodeficiency in the animal models and cells (para. 0064).
Regarding claim 114, Murphy and Kovtunovych make obvious the cells of claim 111. Moreover, Murphy teaches that the mice and therefore the cells of the mice, bear a humanized SIRPA polypeptide encoded by a nucleic acid construct operably linked to a Sirpa promoter (para. 0011, 0034, 0144).
Regarding claim 115, Murphy and Kovtunovych make obvious the cells of claims 111 and 114. Moreover, Murphy teaches a human EPO protein encoded by a nucleic acid operably linked to an EPO promoter, human TPO with TPO promoter, human GM-CSF with GM-CSF promoter, and human IL-3 with IL-3 promoter (para 0011).
Regarding claims 116-117, Murphy and Kovtunovych make obvious the cells of claim 111. Moreover, Murphy teaches that the animal and thereby animal cells are rodent/mouse cells and models (para. 0025).
Regarding claim 118, Murphy and Kovtunovych make obvious the cells of claim 111. Moreover, Murphy teaches that the animal cells are pluripotent mouse cells such as ES cells (para. 0027).
Regarding claim 131, Murphy and Kovtunovych make obvious the cells of claim 111 and 118. Moreover, Murphy teaches genetically modified animals can be created by microinjection, embryo transfer, and introducing cells into preimplantation embryos. Therefore, Murphy makes obvious an embryo comprising the stem cell of 118 in order to produce the animal model described.
Regarding claim 134, Murphy and Kovtunovych make obvious the animal model of claim 119. Moreover, Murphy teaches that deficiencies such as Rag1 and Rag2 may be utilized to achieve immunodeficiency in the animal models and cells (para. 0064).
Regarding claim 138, Murphy and Kovtunovych make obvious the animal model of claim 119. Moreover, Murphy teaches that the mice and therefore the cells of the mice, bear a humanized SIRPA polypeptide encoded by a nucleic acid construct operably linked to a Sirpa promoter (para. 0011, 0034, 0144).
Regarding claim 139, Murphy and Kovtunovych make obvious the animal model of claim 119 and 138. Moreover, Murphy teaches the genetically modified non-human animal expresses a humanized SIRPA polypeptide comprising an extracellular portion of a human SIRPA polypeptide and an intracellular portion of a non-human animal Sirpa polypeptide (para. 0052).
Regarding claim 140, Murphy and Kovtunovych make obvious the animal model of claim 119 and 138. Moreover, Murphy teaches a human EPO protein encoded by a nucleic acid operably linked to an EPO promoter, human TPO with TPO promoter, human GM-CSF with GM-CSF promoter, and human IL-3 with IL-3 promoter (para 0011).
Regarding claim 141, Murphy and Kovtunovych make obvious the animal model of claim 119 and 140. Moreover, Murphy teaches the nucleic acid encoding the human EPO protein is operably linked to endogenous non-human EPO promoter (para. 0055)
Regarding claims 142-143, Murphy and Kovtunovych make obvious the animal model of claim 119 and 140. Moreover, Murphy teaches the endogenous non-human animal EPO promoter is at the corresponding non-human animal EPO gene locus and in some such embodiments, the operable linkage results in a null mutation in the non-human EPO gene at the non-human EPO gene locus. (para. 0008).
Regarding claims 146, Murphy and Kovtunovych make obvious the animal model of claim 119 and 138. Moreover, Murphy teaches a human EPO protein encoded by a nucleic acid operably linked to an EPO promoter (para 0011).
Regarding claims 147, Murphy and Kovtunovych make obvious the animal model of claim 119 and 138. Moreover, Murphy teaches the animal model further comprising an engraftment of human hematopoietic cells (Claim 63).
Regarding claims 148, Murphy and Kovtunovych make obvious the animal model of claim 119 and 147. Moreover, Murphy teaches wherein the human hematopoietic cells comprise one or more cells selected from the group consisting of a human CD34-positive cell, a human hematopoietic stem cell, a human hematopoietic progenitor cell, a human erythroid precursor cell, and a human erythrocyte (Claim 64).
Regarding claims 149, Murphy and Kovtunovych make obvious the animal model of claim 119 and 148. Moreover, Murphy teaches wherein the non-human animal comprises human cells of erythroid lineage (para. 0067-0069).
Regarding claims 150, Murphy and Kovtunovych make obvious the animal model of claim 119 and 149. Moreover, Murphy teaches wherein the non-human animal further comprises an infection with a pathogen that targets human cells of the erythroid lineage (para. 0022).
Regarding claim 152-153, Murphy and Kovtunovych make obvious the animal model of claim 119 and 150. Moreover, Murphy teaches wherein the pathogen can cause malaria in a human and is selected from a Plasmodium sp., a Babesia sp., and a Theileria sp. (para. 0091).
Regarding claims 155-156, Murphy and Kovtunovych make obvious the animal model of claim 119. Moreover, Murphy teaches that the animals are rodents/mice (para. 0025).
Therefore, the invention would have been obvious to one of ordinary skill in the art at the time of the effective filing date.
Claims 113, 137 and 151 are rejected under 35 U.S.C. 103 as being unpatentable over Murphy (US20200060244A1) in view of Kovtunovych (2010, Blood 116, 26: 6054-6062; IDS Reference) as applied to 111, 119, and 147, and in further view of Bial (US20160249591A1; IDS Reference)
Murphy and Kovtunovych make obvious animal models which are homozygous null for Rag2, Rag1, Hmox-1 and Il2rg and cells utilized to create said models as discussed above and incorporated herein in its entirety.
However, these references do not teach a homozygous null mutation in a Fah gene.
Bial teaches a Fah deficient rat which is homozygous null for Fah and inactivated and isolated embryonic stem cells therefrom (para. 0014-0015). In some embodiments, an “immunodeficient rat” comprises one or more of the following genetic alterations: Rag1−/−, Rag2−/−, Il2rg−/−, Il2rg−/y, SCID, SIRP-alpha genotype, perforin−/−, and/or nude. Immunodeficient animal strains are well known in the art and are commercially available, such as from The Jackson Laboratory (Bar Harbor, Me.) or Taconic (Hudson, N.Y.). In some embodiments, the rat is a Fah−/−/Rag2−/−/Il2rg−/−/Il1r1−/− rat, a Fah−/−/Rag1−/−/Il2rg−/−/Il1r1−/− rat, a Fah−/−/Rag2−/−/Il2rg−/−/Il1r1−/− rat, or a Fah−/−/Rag1−/−/Il2rg−/−/Il1r1−/− rat (para. 0065). These models are administered hepatocytes (para. 0079).
It would have been obvious to one of ordinary skill in the art to additionally make the animal model and cells thereof have a homozygous null mutation in the Fah gene as taught by Bial with a reasonable expectation of success. An artisan would have been motivated to modify the Hmox1−/−/Rag2−/−/Il2rg−/− model as Bial teaches that it is known in the art to make animal models which are Fah−/−/Rag2−/−/Il2rg−/−.
Therefore, the invention would have been obvious to one of ordinary skill in the art at the time of the effective filing date
Claims 135-136 are rejected under 35 U.S.C. 103 as being unpatentable over Murphy (US20200060244A1) in view of Kovtunovych (2010, Blood 116, 26: 6054-6062; IDS Reference) as applied to 111, 119, and 147, and in further view of Poss (Proc. Natl. Acad. Sci. USA 94 (1997); IDS Reference)
Murphy and Kovtunovych make obvious animal models which are homozygous null for Rag2, Rag1, Hmox-1 and Il2rg and cells utilized to create said models as discussed above and incorporated herein in its entirety.
However, these references do not teach the specific deletion of exons which result in the Hmox-1 mutation.
Poss teaches the generation of Hmox1-/- mice comprising a construct designed to replace 85% of the coding locus (exons 3-5) (p. 10921, 1st column; Figure 1).
It would have been obvious to one of ordinary skill in the art at the time of the effective filing date to delete exons 3-5 to produce the null mutation in the Hmox-1 gene of Murphy and Kovyunovych as Poss teaches it is known in the art to make Hmox1 null mice by modifying/deleting exons 3-5. Regarding the limitation of deleting all of the endogenous coding sequence, it would be obvious to try as there are only 5 exons in the coding sequence, therefore an artisan would try 4 instead of 3 or all 5, and it is known in the art that deleting coding sequences would delete genes with a reasonable expectation of success.
Therefore, the invention would have been obvious to one of ordinary skill in the art at the time of the effective filing date
Claims 144-145 are rejected under 35 U.S.C. 103 as being unpatentable over Murphy (US20200060244A1) in view of Kovtunovych (2010, Blood 116, 26: 6054-6062; IDS Reference) as applied to 111, 119, 138 and 140, and in further view of Gurer (US2021/0161112; IDS Reference)
Murphy and Kovtunovych make obvious animal models which are homozygous null for Rag2, Rag1, Hmox-1 and Il2rg and cells utilized to create said models which can comprise a human or humanized SIRPA polypeptide encoded by a nucleic acid operably linked to a Sirpa promoter; and (ii) a human M-CSF protein encoded by a nucleic acid operably linked to an M-CSF promoter as discussed above and incorporated herein in its entirety.
However, these reference do not teach wherein the genetically modified non-human animal expresses a humanized CD47 protein, and the humanized CD47 protein comprises an extracellular portion of a human CD47 protein and an intracellular portion of an endogenous non-human animal CD47 protein operably linked to a CD47 promoter.
Gurer teaches non-human animals which comprise a humanized CD47 polypeptide and are operably linked to a CD47 promoter (Abstract, Claim 1). Gurer teaches that it is desirable to do so in order to identify new therapies for diseases such as cancer which overcome systemic toxicity and provide a more efficient in vivo system for engraftment of human hematopoietic stem cells (para. 0004). CD47 polypeptide comprises an extracellular portion of a human CD47 polypeptide and an intracellular portion of an endogenous CD47 polypeptide (para. 0010).
It would have been obvious to one of ordinary skill in the art at the time of the effective filing date to have a humanized CD47 polypeptide in the animal model of Murphy and Kovtunovych as taught by Gurer with a reasonable expectation of success. An artisan would be motivated to do so as Gurer teaches that the humanized CD47 polypeptide provides a more efficient in vivo system for engraftment.
Therefore, the invention would have been obvious to one of ordinary skill in the art at the time of the effective filing date.
Claims 154 are rejected under 35 U.S.C. 103 as being unpatentable over Murphy (US20200060244A1) in view of Kovtunovych (2010, Blood 116, 26: 6054-6062; IDS Reference) and Bial (US20160249591A1) as applied to 111, 119, and 147, and in further view of Song (Science 371 (2021): 1019-1025; IDS Reference).
Murphy, Kovtunovych and Bial make obvious animal models which are homozygous null for Rag2, Rag1, Hmox-1, Fah, and Il2rg and cells utilized to create said models which can comprise engrafted human HSCs discussed above and incorporated herein in its entirety.
However, these references do not teach wherein the HSCs comprise a mutation in the beta globin gene which leads to sickle cell disease.
Song teaches engraftment of human sickle cell disease (SCD) derived HSCs in huHepMISTRGFah−/− mice, which carry knock-ins for the human cytokines granulocyte-monocyte and macrophage colony-stimulating factor (M-CSF), interleukin-3 (I), thrombopoietin (T), and for signal regulatory protein alpha (S), the receptor for the “don’t eat me” signal regulatory protein CD47, in the Rag2−/−Il2rg−/− (RG) background, and a deletion of the Fah gene (Abstract; p. 1, 2nd column). Song teaches single nucleotide point mutation in the beta globin gene causes SCD and engrafting SCD HSPCs in the mice to establish SCD mouse models (p. 7, 1st column).
It would have been obvious to one of ordinary skill in the art at the time of the effective filing date to engraft HPSCs with mutations in the beta globin gene which cause SCD as taught by Song into the immunodeficient animal models taught by the combination of Murphy, Kovtunovych and Bial with a reasonable expectation of success. An artisan would be motivated to do so as Song shows engrafting HPSCs with such mutations provide a SCD animal model in immunodeficient mice.
Therefore, the invention would have been obvious to one of ordinary skill in the art at the time of the effective filing date.
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 111-119, 131, 134-156 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 19, and 20 of U.S. Patent No. 10123518 in view of Kovtunovych (2010, Blood 116, 26: 6054-6062; IDS Reference).
While the claims are not identical, they overlap in subject matter such as rodent animal models genetically modified to have Rag2 and IL2rg knockout mutations and IL-15 and SIRPA proteins (See instant claims 114-115).
However, Patent ‘518 does not recite a Hmox-1 null mutation.
Kovtunovych teaches that in Heme oxygenase (HO-1) null animals splenic and liver macrophages are mostly absent (Abstract). Moreover, in the kidney, the team observed a distinct pattern of increased iron staining in epithelial cells of the proximal tubules and some glomeruli (Figure 5A). The phenomenon of significant iron increase in kidney is usually associated with diseases that increase intravascular hemolysis, such as sickle cell disease, malaria, and artificially induced intravascular hemolysis.
It would have been obvious to one of ordinary skill in the art at the time of the effective filing date to additionally include a Hmox-1 null mutation in the animal models and cells of Patent ‘518 with a reasonable expectation of success. An artisan would be motivated to do so as Patent ‘518 demonstrates animal models with immunodeficient mice which are depleted of in vivo phagocytotic cells prior to and during infection and Kovtunovych demonstrates an animal model which additionally eliminates macrophages in liver and spleen and resulting in RBCs not subjected to phagocytosis.
Therefore, Patent ‘518 is rejected under obviousness type double patenting.
Claims 111-119, 131, 134-156 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 68 of U.S. Patent No. 11576356 in view of Kovtunovych (2010, Blood 116, 26: 6054-6062; IDS Reference).
While the claims are not identical, they overlap in subject matter such as rodent animal models genetically modified to have Rag2 and IL2rg knockout mutations and IL-15 and SIRPA proteins (See instant claims 114-115).
However, Patent ‘356 does not recite a Hmox-1 null mutation.
Kovtunovych teaches that in Heme oxygenase (HO-1) null animals splenic and liver macrophages are mostly absent (Abstract). Moreover, in the kidney, the team observed a distinct pattern of increased iron staining in epithelial cells of the proximal tubules and some glomeruli (Figure 5A). The phenomenon of significant iron increase in kidney is usually associated with diseases that increase intravascular hemolysis, such as sickle cell disease, malaria, and artificially induced intravascular hemolysis.
It would have been obvious to one of ordinary skill in the art at the time of the effective filing date to additionally include a Hmox-1 null mutation in the animal models and cells of Patent ‘356 with a reasonable expectation of success. An artisan would be motivated to do so as Patent ‘356 demonstrates animal models with immunodeficient mice which are depleted of in vivo phagocytotic cells prior to and during infection and Kovtunovych demonstrates an animal model which additionally eliminates macrophages in liver and spleen and resulting in RBCs not subjected to phagocytosis.
Therefore, Patent ‘356 is rejected under obviousness type double patenting.
Conclusion
No claims are allowed.
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/ALEXANDRA F CONNORS/Examiner, Art Unit 1634
/MARIA G LEAVITT/Supervisory Patent Examiner, Art Unit 1634
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