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 1-17 are pending and under consideration.
The office action sent 5-9-25 has been vacated in favor of the following office action in order to clarify the “McGregor” citation on pg 15 and pg 17. The “Feng” reference has also been provided because it does not appear to have been mailed with the office action send 5-9-25.
Request for Information under 37 CFR § 1.105
Applicants and the Assignee of this application are required under 37 CFR 1.105 to provide the following information that the examiner has determined is reasonably necessary to the examination of this application:
The disclosure does not provide any information about what was known about using a genetically modified animal whose genome comprises a knocked out Gal gene as a recipient of a transplant as broadly encompassed by claim 1. For example, Denning (Nature Biotech, 2001, Vol. 19, pg 559-561) taught a sheep with a knockout of the α1, 3 galactosyltransferase gene and that the sheep can be used to determine the importance of Gal in graft rejection, to develop immunosuppression regimes, and to make tissue for xenotransplantation (pg 560, col 2, 2nd full para). However, the search terms related to Gal knockouts, “transplant” or “xenotransplant”, and “recipient” or “donor” makes it virtually impossible to determine whether Gal KO animals had been used as transplant recipients. Applicants must disclose any references that teach or suggest using a genetically modified animal whose genome comprises a knocked out Gal gene as a recipient of a transplant. It is incumbent upon applicants to provide such information.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Enablement
Claims 1-17 are 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 a genetically modified sheep whose genome comprises a homozygous inactivation of an alpha-1,3-galactosyltransferase (GGTA1) gene, wherein the sheep does not express functional GGTA1 and is capable of producing an antibody that binds galactose alpha 1,3 galactose carbohydrate (Gal) upon administration of Gal, wherein the genetically modified sheep is produced using Cas9 and a guide RNA (gRNA) comprising the nucleic acid sequence of SEQ ID NO: 7, does not reasonably provide enablement for obtaining any “recipient gal knockout animal” as broadly encompassed by claim 1 other than the sheep above, using the sheep or other Gal knockout animal to screen any “biological implant for stimulation of an antibody-mediated inflammatory response to Gal antigen” as required in claim 1, obtaining any implant from a gal knockout animal as broadly encompassed by claims 6 & 8 other than the sheep above, or using any implant in a human after being screened in the Gal KO animal as required in claim 13. 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.
A) The specification does not enable making/using any Gal knockout animal as broadly encompassed by claim 1 other than a genetically modified mouse, pig, or sheep whose genome comprises an inactivated alpha-1,3-galactosyltransferase (GGTA1) gene, wherein the mouse, pig, or sheep does not express functional GGTA1.
Fang (Xenotransplantation, 2012, Vol. 19, No. 5, pg 305-310) taught humans, apes, and old world monkeys do NOT express GGTA1, but all other mammals DO express GGTA1 (2nd paragraph). Fang taught genetically modified GGTA1-knockout mice and pigs were well-known that lack Gal and are capable of making anti-Gal antibodies upon administration of Gal (because it is no longer recognized as a “self-antigen” after being knocked out) (pg 306, 1st paragraph; see citations 21-26).
Chtourou (2009/0311239) taught a sheep with a knockout of the α1, 3 galactosyltransferase gene (para 33).
Denning (Nature Biotech, 2001, Vol. 19, pg 559-561) taught a sheep with a knockout of the α1, 3 galactosyltransferase gene (pg 560, col 2, 2nd full para).
McGregor (J. Heart Valve Dis., 2013, Vol. 35, pg 17-23) implanted either wild-type or GTKO pig valves into the mitral position in non-human primates. Over a period of 1 year, anti-Gal IgG levels rose significantly higher in the wild-type recipients compared to the GTKO recipients. (Manji, International J. of Surgery, 2015, Vol. 23, pg 280-284; paragraph bridging pg 281-282; Manji’s “[26]” is McGregor.
The specification teaches making a genetically modified sheep whose genome comprises a homozygous inactivation of a GGTA1 gene, wherein the sheep does not express functional GGTA1 and is capable of producing an antibody that binds Gal upon administration of Gal, wherein the genetically modified sheep is produced using Cas9 and a gRNA comprising the nucleic acid sequence of SEQ ID NO: 7 (Example 1).
Specifically, applicants transfected sheep fetal fibroblasts with gRNA that targeted exon 4 of a sheep GGTA1 gene and [a nucleic acid sequence encoding] Cas9 (pg 17-18). “Targeted biallelic disruption of GGTA1 was achieved in 10/26 colonies” (pg 18, line 7). Four GGAT1-/- male colonies were used for nuclear transfer. Two lambs with the same mutations were successfully produced, and they showed a “complete loss of Gal expression” (pg 18, lines 14-19). It is assumed this is limited to a complete loss of GGTA1 expression since no other galactosyltransferase genes were modified:
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The claim encompasses any modification that is an insertion, deletion, or substitution that causes the GGTA1 gene to be “knocked out”. The specification does not correlate the GGTA1 inactivations known in the art or taught in the specification to any insertion or substitution that causes the GGTA1 gene to be “knocked out”.
The claim encompasses any genetically modified invertebrate, crustacean, insect, fish, amphibian, reptile, bird, or mammal. Mammals include rodents such as mouse, rat, beaver, squirrel, groundhog, muskrat, hamster, capybara, chinchilla, porcupine, mole, vole, otter, gerbil. Mammals include humans and other primates. Mammals include pig, rabbit, sheep, goat, cat, dog, cattle, elephant, gazelle, deer, antelope, elk, whale, dolphin, tiger, leopard, cheetah, dingo, wolf, etc. Claim 2 requires the animal is an ovine (sheep), porcine, bovine, equine, canine, feline, or camelid. The specification does not correlate the well-known Gal KO mouse, pig, or sheep to any other invertebrate, crustacean, insect, fish, amphibian, reptile, bird, rat, beaver, squirrel, groundhog, muskrat, hamster, capybara, chinchilla, porcupine, mole, vole, otter, gerbil, rabbit, goat, cat, dog, cattle, elephant, gazelle, deer, antelope, elk, whale, dolphin, tiger, leopard, cheetah, dingo, wolf, etc.
The specification does not correlate the limited enabled embodiments to bovine, equine, canine, feline, or camelid embodiments in claim 2.
The claims encompass using humans, apes, and old world monkeys that naturally do not express Gal as the donor for the biological implant, but the specification does not teach how to make/use such an animal.
The claims encompass using humans, apes, and old world monkeys that naturally do not express Gal as the “Gal knockout animal” receiving the biological implant, but the specification does not teach how to make/use such an animal.
The claim encompasses an animal with an inactivated exogenous or endogenous GGTA1 gene having any phenotype including expression of a GGTA1 protein from an endogenous or exogenous source. The specification discusses “Commercial Valve Antigenicity and Gal Antibody-Induced Calcification” on pg 18 and says:
“In the rat and rabbit subcutaneous implant models, the human anti-Gal IgG increases calcification of standard, but not GalKO pig, pericardium (FIG. 2A). Anti-calcification treatment reduced calcification levels in standard and GalKO pericardium as expected (FIG. 2B) but did not prevent anti-Gal Ab induced calcification (FIG. 2C), showing that passive physiochemical tissue calcification and immune-mediated calcification are independent processes. This was the first experimental identification of a clinically plausible source of BHV-specific Ab that could initiate an immune-mediated inflammatory response to promote calcification and SVD” (paragraph bridging pg 18-19).
A number of sentences in the paragraph are indecipherable for various reasons. The “rat and rabbit subcutaneous implant models” are not disclosed and cannot be found in the art at the time of filing. The meaning of an antibody increasing “calcification of standard, but not GalKO pig, pericardium” cannot be determined. “BHV” appears to relate to “Bioprosthetic Heart Valve” (pg 24, line 28), and “SVD” appears to be structural valve deterioration (pg 1, line 29). However, it is unclear how any conclusion about BHVs can be made by administering anti-GAL IgG in sheep or pigs. Therefore, it is unclear why the IgGs are “BHV-specific Ab that could initiate an immune-mediated inflammatory response to promote calcification and SVD”. It is also unclear why one would want to promote valve deterioration. If the sheep are models of valve disease, it is wholly unclear how to make such a sheep or what specific valve disease applicants are attempting to model. It is also unclear what applicants consider a “Bioprosthetic Heart Valve”. While sheep lacking GGTA1 expression can be used to investigate the role of GGTA1 in heart disease, the specification does not teach the sheep are models of disease. Regardless, the specification is limited to a genetically modified animal whose genome comprises an inactivated endogenous GGTA1 gene, wherein the animal does not express functional GGTA1 (see above).
The claim encompass knocking out any Gal gene (see above). However, the specification does not correlate the GGTA1 gene (see MGI description of GGTA1, 2023) to any other GAL gene.
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 Gal knockout animal as broadly encompassed by claim 1 other than a genetically modified mouse, pig, or sheep whose genome comprises an inactivated GGTA1 gene, wherein the sheep does not express any GGTA1.
B) The specification does not enable detecting any “signs” of an “antibody-mediated inflammatory response” as broadly encompassed by claim 1 other than detecting whether anti-GTTA1 antibodies occur after implanting the implant. The phrase encompasses detecting any antibody mediated inflammatory response or cytokines, markers, or symptoms associated with such a response. The phrase encompasses detecting antibodies against any Gal protein. However, the specification is limited to detecting whether anti-GTTA1 antibodies occur.
C) The specification does not enable using a Gal knockout animal for screening implants.
The specification contemplates using a sheep that does not express any Gal antigen to determine whether an implant causes an antibody-mediated inflammatory response against Gal. For this to work, the animal cannot express ANY Gal proteins which is missing from the claim. Even in the limited embodiment of a determining whether an implant causes antibodies against GGTA1, the animal cannot express ANY GGTA1 which is missing from the claim. The implant must also be cells or tissue and exclude stents, metal, plastic, silicone, or other implants because they do not and cannot comprise GAL antigens. The implants must be cells/tissues capable of GAL expression which is missing from the claims.
The method requires determining whether antibodies that bind GAL are obtained after implant; however, the specification does not teach how to make any determination once that has been performed. It is unclear what that means about the implant or how to interpret the results. This is missing from the specification and is not readily apparent from the art. It is unclear if the “implant” is the reimplanted into another subject or if there is something to be said about the source of the “implant” for use in other animals. If no antibodies are detected in the animal after transplant, it is unclear what is to be said about the source of the “implant”.
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 perform the method of claim 1 and make any determination about the animal or the implant based on whether anti-Gal antibodies occur.
D) The specification does not enable screening an implant using a GAL knockout animal, detecting whether antibodies against a Gal protein are produced, and implanting any second implant into a human as required in claim 13. Claim 13 is limited for reasons A) and B) above. In addition, it is unclear what applicants are attempting to do here because the second implant in the third step has no nexus with the implant put into the Gal knockout animal in the first step or the detection of anti-Gal antibodies in the second step. It is unclear whether some decision about the type of implant, i.e. cartilage, cardiac, muscle, that can be used is being made. It is unclear whether some decision about the source of the implant is being made. It is unclear whether some decision about the amount of anti-Gal antibody response is being. If some amount of anti-Gal antibody response IS desired, then that amount is not disclosed in the specification or the art at the time of filing. Nor is it in the claim. If no anti-Gal antibody response is desired, then that concept is missing from the specification, the art at the time of filing, and the claim. 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 any decisions about what “second implant” to put into a human after putting a first implant into the Gal KO animal and screening for anti-Gal antibodies.
Indefiniteness
Claims 1-17 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 preamble of claim 1 requires screening for “stimulation of an antibody-mediated inflammatory response to a Gal antigen” by “detecting signs of antibody-mediated inflammatory response” in the recipient Gal KO animal. However, the preamble and step c) do not have a nexus because they have different scopes and because step c) never requires detecting anti-Gal antibodies in the recipient Gal KO animal. Therefore, it is unclear whether the claim requires detecting anti-Gal antibodies in the recipient Gal KO or whether it encompasses detecting any “sign” of any “antibody-mediated inflammatory response” against anything as broadly encompassed by step c).
B) The metes and bounds of a “conduit” in claim 3 cannot be determined. It is unclear whether this is limited to a cellular tissue that is a conduit or if it encompasses any plastic, metal, etc. “conduit”.
C) The metes and bounds of “tissue mesh” in claim 3 cannot be determined. It is unclear whether it encompasses any “tissue” or if it is limited to “tissue” that has the structure or function of “mesh”. If the phrase is limited to “tissue” that is has the structure or function of “mesh”, then the structures/functions that define when “tissue” is “mesh” are not defined in the specification or the art at the time of filing.
D) The metes and bounds of “decellularized tissue” in claim 3 cannot be determined. It is unclear how an implant that is “decellularize”, i.e. without cells, is “tissue”. The specification and the art at the time of filing do not define the phrase. Therefore, those of skill would not be able to determine when they were infringing on the claim.
E) The metes and bounds of “engineered tissue produced form [sic] in vitro cell culture” in claim 3 cannot be determined. It is unclear whether the claim encompasses any cells in vitro or if the phrase is limited to cells in vitro that have certain structures or functions. If the phrase is limited to cells in vitro that have certain structures or functions, then the structures/functions that define when cells in vitro are “engineered tissue” cannot be determined.
F) Claim 5 does not further limit claim 1 because all “implants” are derived from a donor animal.
G) The phrase “wherein the detection step comprises a radiologic, immunologic, or histologic evaluation of the implanted biological implant” in claim 9 does not have a nexus with detecting whether an anti-Gal antibody response occurs in claim 1. Therefore, it is unclear how claim 9 further limits the “detecting” in claim 1.
H) The phrase “wherein the detecting comprises testing the performance of the implant and/or evaluating implant calcification” in claim 11 does not have a nexus with detecting whether an anti-Gal antibody response occurs in claim 1. Therefore, it is unclear how claim 11 further limits the “detecting” in claim 1.
I) The second implant in the third step of claim 13 has no nexus with the implant put into the Gal knockout animal in the first step or the detection of anti-Gal antibodies in the second step. This makes the claim indefinite. It is unclear whether some decision about the type of implant, i.e. cartilage, cardiac, muscle, that can be used is being made. It is unclear whether some decision about the source of the implant is being made. It is unclear whether some decision about the amount of anti-Gal antibody response is being. If some amount of anti-Gal antibody response IS desired, then that amount is not in the claim. If no anti-Gal antibody response is desired, then that concept is missing from the claim. It is unclear how to make any decisions about what “second implant” to put into a human after putting a first implant into the Gal KO animal and screening for anti-Gal antibodies.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 1, 3, 5, 6, 9-12 are rejected under 35 U.S.C. 102a1 as being anticipated by Weiner (Xenotransplantation, 2010, Vol. 17, No. 2, pg 147-152).
Weiner transplanted GalTKO pig skin on to baboon skin (materials and methods). The baboon is a “recipient Gal knockout animal” as required in claim 1 because it does not express Gal. Weiner detected the amount of antibodies against Gal expressed by the baboon (materials and methods) which is equivalent to step c) of claim 1.
The skin used by Weiner includes “a blood vessel”, “a conduit”, a “tissue mesh” as required in claim 3.
The skin used by Weiner is from a GalTKO pig is “from a donor animal” as required in claim 5.
The skin used by Weiner is from a GalTKO pig is “from a donor Gal knockout animal” as required in claim 6.
The detection of Gal antibodies described by Weiner is an “immunological” or “histological” evaluation (pg 3, Histology) as required in claim 9.
The detection of Gal antibodies described by Weiner is “measuring Gal antibodies in a biological sample from the recipient” as required in claim 10.
Weiner observed the survival of the skin and the presence of anti-Gal antibodies over time (pg 3-4 results) which is testing the performance of the implant as required in claim 11.
Claim 12 has been included because it further limits the “implant calcification” in claim 11 without limiting the claim to evaluating implant calcification. Although Weiner observed the survival of the skin over time which can be considered a version of observing whether the skin calcified.
B) Claims 1, 3-6, 9-12 are rejected under 35 U.S.C. 102a1 as being anticipated by McGregor (J. Heart Valve Dis., 2013, Vol. 22, pg 1-8).
McGregor implanted either wild-type or GTKO pig valves into the mitral position in non-human primates that do not endogenously express Gal and detected anti-Gal IgG levels for over a year (materials and methods). The non-human primates area “recipient Gal knockout animal” as required in claim 1 because they do not express Gal.
McGregor taught a heart valve as required in claims 3 and 4.
McGregor taught a heart valve from a donor as required in claim 5.
McGregor taught a heart valve from a Gal KO donor as required in claim 6.
McGregor tested calcification and function of the implant (Materials and Methods) as required in claim 9.
McGregor tested anti-Gal antibody levels in the recipient following implantation (Materials and Methods) as required in claim 10.
McGregor tested calcification of the implant (Materials and Methods) as required in claim 11.
Claim 12 has been included because it further limits the “implant calcification” in claim 11 without limiting the claim to evaluating implant calcification. Although McGregor observed the survival of the implant over time which can be considered a version of observing whether the implant calcified.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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 1-17 are rejected under 35 U.S.C. 103 as being unpatentable over McGregor (J. Heart Valve Dis., 2013, Vol. 22, pg 1-8) in view of Denning (Nature Biotech, 2001, Vol. 19, pg 559-561) and Goldstein (Ann. Thoracic Surg., 2000, Vol. 70, pg 1962-1969).
McGregor implanted either wild-type or GTKO pig valves into the mitral position in non-human primates that do not endogenously express Gal and detected anti-Gal IgG levels for over a year (materials and methods).
McGregor did not teach the recipient was a Gal knockout animal as required in claim 1.
However, Denning taught a sheep with a knockout of the α1, 3 galactosyltransferase gene (abstract; materials and methods).
Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to implant pig valves into an animal that does not endogenously express Gal and detect anti-Gal antibodies over time as described by McGregor using the Gal KO sheep described by Denning. Those of ordinary skill in the art at the time of filing would have been motivated to replace the non-human primate with the Gal KO sheep because Denning taught the sheep can be used to determine the importance of Gal in graft rejection, to develop immunosuppression regimes, and to make tissue for xenotransplantation (pg 560, col 2, 2nd full para). It was well known to put pig heart valves into sheep as described by Goldstein (Materials and Methods).
Denning taught a sheep, i. e. ovine, as required in claim 2.
McGregor taught a heart valve as required in claims 3 and 4.
McGregor taught a heart valve from a donor as required in claim 5.
McGregor taught a heart valve from a Gal KO donor as required in claim 6.
Denning taught a Gal KO sheep recipient and McGregor taught a Gal KO pig donor as required in claim 7.
Denning taught a Gal KO sheep recipient and McGregor taught a Gal KO pig donor as required in claim 8.
McGregor tested calcification and function of the implant (Materials and Methods) as required in claim 9.
McGregor tested anti-Gal antibody levels in the recipient following implantation (Materials and Methods) as required in claim 10.
McGregor tested calcification of the implant (Materials and Methods) as required in claim 11.
Claim 12 has been included because it further limits the “implant calcification” in claim 11 without limiting the claim to evaluating implant calcification. Although McGregor observed the survival of the implant over time which can be considered a version of observing whether the implant calcified.
Claim 13 has been included because it would have been obvious to put a Gal KO pig valve from the same lineage into a human. Those of ordinary skill in the art at the time of filing would have been motivated to do so because screening the Gal KO pig valve in vivo is a model for humans.
Claims 14-17 have been included because they further limit the recipient and donor tissue using the same language in claims discussed above.
Thus, Applicants' claimed invention as a whole is prima facie obvious in the absence of evidence to the contrary.
Conclusion
The prior art made of record and not relied upon is considered pertinent to applicant's disclosure:
McGregor (J. Thoracic and Cardiovascular Surg., 2023, Vol. 166, e142-152).
No claim is allowed.
Inquiry concerning this communication or earlier communications from the examiner should be directed to Michael C. Wilson who can normally be reached at the office on Monday through Friday from 9:30 am to 6:00 pm at 571-272-0738.
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Michael C. Wilson
/MICHAEL C WILSON/
Primary Examiner, Art Unit 1638
/Tracy Vivlemore/Supervisory Primary Examiner, Art Unit 1638