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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 12-19-25 has been entered.
Claims 1, 3-19, 24-91, 97 have been canceled. Claims 2, 20-23, 92-96, 98, 99 remain pending.
Applicant's arguments filed 12-19-25 have been fully considered but they are not persuasive.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Election/Restrictions
Applicants elected Group I, claims 2, 3, 17, 20-25, 28, with traverse on 7-27-21. The examiner required restriction between product claims and process claims. Where applicant elect claims directed to the product/apparatus, and all product/apparatus claims are subsequently found allowable, withdrawn process claims that include all the limitations of the allowable product/apparatus claims should be considered for rejoinder.
Claims 2, 20-23, 92-96, 98, 99 remain under consideration.
Claim Objections
The concept of a) b) c) and d) being “capable of rearranging in a B-cell of a mouse” in claim 2 is missing element e). The endogenous mouse IgM gene is technically part of rearrangement in B-cells because it is being operably linked to VH, DH, and JH gene segments.
Claim 2 requires “wherein (a) the at least one human Ig VH gene segment, (b) the at least one human Ig DH gene segment, (c) the at least one modified human Ig DH gene segment, and (d) the at least one human Ig JH gene segment are capable of rearranging in a B-cell of a mouse whose genome comprises the nucleotide molecule to form a nucleotide sequence encoding a human Ig heavy chain variable domain that, in combination with (e) the mouse IgM gene, encodes a functional humanized IgM molecule comprising the human Ig heavy chain variable domain fused to a mouse IgM domain”, but it is confusing.
The phrase “to form a nucleotide sequence encoding a human Ig heavy chain variable domain that, in combination with (e) the mouse IgM gene, encodes a functional humanized IgM molecule” in claim 2 is an intended use that does not have to occur. The phrase does not say items a), b), c), d), and e) are capable of rearranging and encoding a functional humanized IgM. Therefore a)-c) must be capable of rearranging but they are not necessarily capable of encoding a functional humanized IgM comprising a human Ig VH domain.
The phrase “the human Ig heavy chain variable domain” in the last two lines of claim 2 lacks antecedent basis. Perhaps it would be sufficient to say ---a human Ig VH domain”. Perhaps it would be more accurate to say ---a human Ig VH domain encoded by the at least one human Ig VH gene segment”.
Claim 2 does not require the “mouse IgM domain” in the last line is encoded by the “mouse IgM gene”. Perhaps this is sufficient. Or perhaps it would be more accurate to say ---a mouse IgM domain encoded by the mouse IgM gene”.
It may be simpler to describe the “capability” of the nucleotide molecule in claim 2 as --- capable of encoding a functional humanized IgM comprising a human VH domain and a mouse IgM domain upon rearrangement in an B-cell of a mouse whose genome comprises the nucleotide molecule---.
Claims 94-96 can be written more clearly as ---wherein the heptamer consists of the nucleic acid sequence of SEQ ID NO: 144 or 145---.
Claim Rejections - 35 USC § 112
Enablement
Claims 2, 20-23, 92-96, 98, 99 remain rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
Withdrawn rejections
The rejection regarding making a VH gene segment “flanked” by “a first recombinant signal sequence (RSS)” (singular) as broadly encompassed by claim 2 has been withdrawn because claim 2 has been limited to a hVH gene segment flanked by an RSS on its 3’ end.
The rejection regarding making a JH gene segment “flanked” by “a first recombinant signal sequence (RSS)” (singular) as broadly encompassed by claim 2 has been withdrawn because claim 2 has been limited to a hVH gene segment flanked by an RSS on its 5’ end.
The rejection regarding making “a JH gene segment” (singular) comprising unrearranged JH1, JH2, JH3, JH4, JH5, and JH6 gene segments (plural) in claim 23 has been withdrawn because the claim has been amended to ---at least one human Ig JH gene segment”.
The rejection regarding JH1-6 gene segments “in germline configuration” in claim 97 has been withdrawn because the claim has been canceled.
Pending rejections
A) The specification does not enable making/using a nucleotide molecule comprising a hVH gene segment flanked at its 3’ end to a single naturally occurring RSS, a hDH gene segment flanked on both sides by genetically modified RSSs, a hDH gene segment flanked on both sides by naturally occurring RSSs, a hJH gene segment flanked on its 5’ side by a naturally occurring RSS, and a mouse IgM gene segment as broadly encompassed by claim 2.
Claim 2 is drawn to:
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Paragraph 270, pg 95-96, describes a “23:DH3-3:12/JH6 targeting vector”, a “23:DH3-3:12/JH4-6 targeting vector”, and a “12:DH2-2:23|12DH2-8:23|12:DH2-15:23/JH6 targeting vector” in Fig. 2.
Paragraph 271, pg 96-97, describes the “23:DH3-3:12/JH6 targeting vector”, and paragraphs 272-273 (pg 97-99) describe the “23:DH3-3:12/JH4-6 targeting vector”. It is assumed the DH gene segments with the “hash marks” (“\\”) in these two vectors in the top two panels of Fig. 2 are naturally occurring hDH gene segments.
Para 274 (pg 99-106) “12:DH2-2:23|12DH2-8:23|12:DH2-15:23/JH6 targeting vector” in Fig. 2. It is assumed the DH2-2, DH2-8, and DH2-15 gene segments with the label “23mer” below them are genetically modified because they are labeled “12:DH2-2:23”, “12DH2-8:23” and “12:DH2-15:23” in the name of the vector. It is assumed the triangles in between them are naturally occurring DH gene segments.
The specification does not teach how the 2 DH gene segments flanked with RSSs having the specific structures set forth in claim 2 are operably linked to each other and to the unrearranged human VH and JH gene segments. The specification does not teach the structure of the “μ0pro” in the top two panels of Fig. 2. Pg 29, line 1, and pg 54, line 11, use the term “μ0pro” without defining the structure/function.
The specification does not provide adequate guidance to use the construct. The sole disclosed purpose for the molecule is to encode a functional IgM comprising a human VH domain and a mouse IgM domain upon rearrangement in an B-cell of a mouse whose genome comprises the nucleotide molecule and for the “engineered” [human] DH gene segment causing “increased expression of antibodies containing [CDR3s with] longer amino acid length as compared to wild-type [ ] and by diversity that, in some embodiments, directs binding to particular antigens” (pg 2, para 4). It is unclear how the vectors in Fig. 1 and 2 lengthen the amino acid length because Fig. 1 and 2 appear to replace some endogenous DH gene segments with the human DH gene segment, thereby decreasing the DH gene segments. It is unclear how adding DH gene segments increases antibody length or directs the antibody to “particular” antigens. If the genetic modification is intended to lengthen the Ig to bind “particular” antigens, the specification fails to correlate any specific DH genetic modification to a longer antibody or any “particular” antigen.
The specification says the DH-DH recombination results in “antibodies containing CDR3s generated [ ] characterized as having increased diversity resulting from longer amino acid length to direct binding to particular antigens (e.g., viruses, membrane channels, etc.)” (pg 50, lines 9-11). However, it is unclear what this means or how those of skill would test whether an antibody had “increased diversity”. It is unclear whether the “increased diversity” means the VH domain is no longer categorized by well-known VH names, e.g. VH6-1, to create novel VH domains. It is unclear whether the “increased diversity” is simply a matter of having longer amino acid length. The specification does not provide any guidance regarding the specific goal for any type of “increased diversity”, why longer amino acid length has anything to do with “increased diversity”, or how the modified 23:DH3-3:12 gene segment is operably linked to the naturally occurring hDH, hVH, and hJH gene segments such that “longer amino acid length” or increased diversity is obtained. The specification does not correlate the modified 23:DH3-3:12 gene segment operably linked to the naturally occurring hDH, hVH, and hJH gene segments to any other modified DH gene segment such that “longer amino acid length” or “increased diversity” is obtained. If the phrase “increased diversity” on pg 50 refers to making new VH gene segments, then the specification does not teach how to use the sequence in claim 2 to obtain “increased diversity” with just one hVH gene segment. A diverse VH gene segment repertoire occurs only in the presence of a plurality of varied VH gene segments which are missing from 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 use the nucleotide of claim 2 because applicants did not teach how to operably link the elements claimed for the sole disclosed purpose, i.e. “increased diversity” or “longer amino acid length” as described on pg 50, lines 9-11.
Response to arguments
Applicants argue they are not obligated to provide enablement for something that is not claimed. Applicants’ argument is not persuasive. The sole disclosed purpose for using the nucleic acid is for the “engineered” [human] DH gene segment causing “increased expression of antibodies containing [CDR3s with] longer amino acid length as compared to wild-type [ ] and by diversity that, in some embodiments, directs binding to particular antigens” (pg 2, para 4).
B) The specification does not enable using a “mouse whose genome comprises the nucleotide molecule” in the absence of a full repertoire of hVH gene segments as broadly encompassed by claim 2.
The rejection regarding using a vector with only one human Ig VH gene segment has been withdrawn in view of MacDonald (10246509) and applicants argument on pg 11 of the response filed 12-19-25.
The rejection regarding using a vector with only one human Ig JH gene segment has been withdrawn. Example 1A taught a nucleotide comprising a single hJH6 and Example 4 shows using it to make humanized Ig from the mice. Pg 114, para 300, discusses the mouse made with “23:DH3-3:12/JH6” which has single hJH6 and is shown in Fig. 2.
Claim 2 is recited above.
Jung (Cell, 2004, Vol. 116, No. 2, pg 299-311) taught “RSs consist of a relatively conserved heptamer and nonamer, with respective consensus sequences of CACAGTG and ACAAAAACC, separated by a nonconserved spacer of either 12 or 23 base pairs (Figure 2; Max et al., 1979; Sakano et al., 1979), which we will refer to as a ‘12RS’ or a ‘23RS’” (pg 300, col. 2, line 10). Fig. 2 (pg 301) of Jung taught DH gene segments flanked by a 12 bp spacers:
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Claim 2 encompasses the vector once it has integrated into the “mouse whose genome comprises the nucleotide molecule” because the “Targeted ES cell genomes” in the bottom panel of Fig. 3 has a plurality of hVH gene segments, a plurality of naturally occurring hDH gene segments, a modified DH3-3 gene segment, a hJH gene segment, and a mouse IgM gene.
“23:DH3-3:12/JH6 Targeting vector” in the top panel of Fig. 2 and the middle panel of Fig. 3 has the structure claimed but is not capable of rearranging until it is integrated into the genome of a mouse.
The “23:DH3-3:12/JH4-6 Targeting vector” in the middle panel of Fig. 2 and the middle panel of Fig. 5 has one hVH gene segment but is not capable of rearranging until it is integrated into the genome of a mouse.
The “23:DH3-3:12|12:DH2-8:23|12:DH2-15:23/JH1-6 Targeting vector” in the bottom panel of Fig. 2 and the middle panel of Fig. 7 has three hVH gene segments but is not capable of rearranging. The term “23mer” underneath each DH2-2, DH2-8, and DH2-15 in Figures 2 and 7 appears to be merely a notation for a DH gene segment that has had one RSS modified to have a 23mer spacer (and retain one naturally occurring RSs with a 12mer spacer)
The top two Targeting Vectors in Fig. 2 have one hVH gene segment and a plurality of hJH gene segments, but they are not capable of rearrangement until they are inserted into the genome of a genetically modified mouse with a full repertoire of human VH gene segments (see bottom panel of Fig. 3 “Targeted ES cell genome (6394het/6799het/1293HO)”. The “Targeting vectors” with one hVH gene segment and multiple hJH gene segments are not capable of rearrangement until they are integrated into the genome of a mouse with a plurality of hVH gene segments.
While the targeting vector may be inserted into the genome of a mouse, the “mouse whose genome comprises the nucleotide molecule” in the last 5 lines of claim 2 must have a full repertoire of hVH gene segments and a plurality of hJH gene segments. The full repertoire of hVH gene segments is missing from the “mouse whose genome comprises the nucleotide molecule” in claim 2.
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 use a vector in a “mouse whose genome comprises the nucleotide molecule” in the absence of a full repertoire of hVH gene segments as broadly encompassed by claim 2.
Response to arguments
Applicants’ arguments do not address this aspect of the rejection.
Written Description
Claims 2, 20-23, 92-96, 98, 99 remain rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Withdrawn rejections
The rejection regarding making a VH gene segment “flanked” by “a first recombinant signal sequence (RSS)” (singular) as broadly encompassed by claim 2 has been withdrawn because claim 2 has been limited to a hVH gene segment flanked by an RSS on its 3’ end.
The rejection regarding making a JH gene segment “flanked” by “a first recombinant signal sequence (RSS)” (singular) as broadly encompassed by claim 2 has been withdrawn because claim 2 has been limited to a hVH gene segment flanked by an RSS on its 5’ end.
The rejection regarding making “a JH gene segment” (singular) comprising unrearranged JH1, JH2, JH3, JH4, JH5, and JH6 gene segments (plural) in claim 23 has been withdrawn because the claim has been amended to ---at least one human Ig JH gene segment”.
The rejection regarding JH1-6 gene segments “in germline configuration” in claim 97 has been withdrawn because the claim has been canceled.
Pending rejections
A) The specification lacks written description for making the nucleotide molecule of claim 2 or for using it for its sole disclosed purpose, i.e. “increased diversity” or “longer amino acid length” as described on pg 50, lines 9-11 as broadly encompassed by claim 2.
Claim 2 and its scope are recited above.
Paragraph 270-274 are discussed above.
The specification does not teach how the 2 DH gene segments flanked with RSSs having the specific structures set forth in claim 2 are operably linked to each other and to the unrearranged human VH and JH gene segments. The specification does not teach the structure of the “μ0pro” in the top two panels of Fig. 2. Pg 29, line 1, and pg 54, line 11, use the term “μ0pro” without defining the structure/function.
The specification does not provide written description for how to use the construct for the sole disclosed purpose for the molecule is to encode a functional IgM comprising a human VH domain and a mouse IgM domain upon rearrangement in an B-cell of a mouse whose genome comprises the nucleotide molecule and for the “engineered” [human] DH gene segment causing “increased expression of antibodies containing [CDR3s with] longer amino acid length as compared to wild-type [ ] and by diversity that, in some embodiments, directs binding to particular antigens” (pg 2, para 4). It is unclear how the vectors in Fig. 1 and 2 lengthen the amino acid length because Fig. 1 and 2 appear to replace some endogenous DH gene segments with the human DH gene segment, thereby decreasing the DH gene segments. It is unclear how adding DH gene segments increases antibody length or directs the antibody to “particular” antigens. If the genetic modification is intended to lengthen the Ig to bind “particular” antigens, the specification fails to correlate any specific DH genetic modification to a longer antibody or any “particular” antigen.
The specification says the DH-DH recombination results in “antibodies containing CDR3s generated [ ] characterized as having increased diversity resulting from longer amino acid length to direct binding to particular antigens (e.g., viruses, membrane channels, etc.)” (pg 50, lines 9-11). However, it is unclear what this means or how those of skill would test whether an antibody had “increased diversity”. It is unclear whether the “increased diversity” means the VH domain is no longer categorized by well-known VH names, e.g. VH6-1, to create novel VH domains. It is unclear whether the “increased diversity” is simply a matter of having longer amino acid length. The specification does not provide any guidance regarding the specific goal for any type of “increased diversity”, why longer amino acid length has anything to do with “increased diversity”, or how the modified 23:DH3-3:12 gene segment is operably linked to the naturally occurring hDH, hVH, and hJH gene segments such that “longer amino acid length” or increased diversity is obtained. The specification does not correlate the modified 23:DH3-3:12 gene segment operably linked to the naturally occurring hDH, hVH, and hJH gene segments to any other modified DH gene segment such that “longer amino acid length” or “increased diversity” is obtained. If the phrase “increased diversity” on pg 50 refers to making new VH gene segments, then the specification does not teach how to use the sequence in claim 2 to obtain “increased diversity” with just one hVH gene segment. A diverse VH gene segment repertoire occurs only in the presence of a plurality of varied VH gene segments which are missing from the claim.
Accordingly, the specification lacks written description for making the nucleotide molecule of claim 2 or for using it for its sole disclosed purpose, i.e. “increased diversity” or “longer amino acid length” as described on pg 50, lines 9-11 as broadly encompassed by claim 2.
Response to arguments
Applicants argue they are not obligated to provide enablement for something that is not claimed. Applicants’ argument is not persuasive.
The specification does not teach how the 2 DH gene segments flanked with RSSs having the specific structures set forth in claim 2 are operably linked to each other and to the unrearranged human VH and JH gene segments. The specification does not teach the structure of the “μ0pro” in the top two panels of Fig. 2. Pg 29, line 1, and pg 54, line 11, use the term “μ0pro” without defining the structure/function. So applicants do not provide adequate written description for making the nucleotide molecule.
The sole disclosed purpose for using the nucleic acid is for the “engineered” [human] DH gene segment causing “increased expression of antibodies containing [CDR3s with] longer amino acid length as compared to wild-type [ ] and by diversity that, in some embodiments, directs binding to particular antigens” (pg 2, para 4). So applicants do not provide adequate written description for using the nucleotide molecule for its sole disclosed purpose.
B) The specification lacks written description for a vector capable of being used in a “mouse whose genome comprises the nucleotide molecule” in the absence of a full repertoire of hVH gene segments as broadly encompassed by claim 2.
The rejection regarding using a vector with only one human Ig VH gene segment has been withdrawn in view of MacDonald (10246509) and applicants argument on pg 11 of the response filed 12-19-25.
The rejection regarding using a vector with only one human Ig JH gene segment has been withdrawn. Example 1A taught a nucleotide comprising a single hJH6 and Example 4 shows using it to make humanized Ig from the mice. Pg 114, para 300, discusses the mouse made with “23:DH3-3:12/JH6” which has single hJH6 and is shown in Fig. 2.
Claim 2 is recited above.
Jung (Cell, 2004, Vol. 116, No. 2, pg 299-311) taught “RSs consist of a relatively conserved heptamer and nonamer, with respective consensus sequences of CACAGTG and ACAAAAACC, separated by a nonconserved spacer of either 12 or 23 base pairs (Figure 2; Max et al., 1979; Sakano et al., 1979), which we will refer to as a ‘12RS’ or a ‘23RS’” (pg 300, col. 2, line 10). Fig. 2 (pg 301) of Jung taught DH gene segments flanked by a 12 bp spacers:
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Claim 2 encompasses the vector once it has integrated into the “mouse whose genome comprises the nucleotide molecule” because the “Targeted ES cell genomes” in the bottom panel of Fig. 3 has a plurality of hVH gene segments, a plurality of naturally occurring hDH gene segments, a modified DH3-3 gene segment, a hJH gene segment, and a mouse IgM gene.
“23:DH3-3:12/JH6 Targeting vector” in the top panel of Fig. 2 and the middle panel of Fig. 3 has the structure claimed but is not capable of rearranging until it is integrated into the genome of a mouse.
The “23:DH3-3:12/JH4-6 Targeting vector” in the middle panel of Fig. 2 and the middle panel of Fig. 5 has one hVH gene segment but is not capable of rearranging until it is integrated into the genome of a mouse.
The “23:DH3-3:12|12:DH2-8:23|12:DH2-15:23/JH1-6 Targeting vector” in the bottom panel of Fig. 2 and the middle panel of Fig. 7 has three hVH gene segments but is not capable of rearranging. The term “23mer” underneath each DH2-2, DH2-8, and DH2-15 in Figures 2 and 7 appears to be merely a notation for a DH gene segment that has had one RSS modified to have a 23mer spacer (and retain one naturally occurring RSs with a 12mer spacer)
The top two Targeting Vectors in Fig. 2 have one hVH gene segment and a plurality of hJH gene segments, but they are not capable of rearrangement until they are inserted into the genome of a genetically modified mouse with a full repertoire of human VH gene segments (see bottom panel of Fig. 3 “Targeted ES cell genome (6394het/6799het/1293HO)”. The “Targeting vectors” with one hVH gene segment and multiple hJH gene segments are not capable of rearrangement until they are integrated into the genome of a mouse with a plurality of hVH gene segments.
While the targeting vector may be inserted into the genome of a mouse, the “mouse whose genome comprises the nucleotide molecule” in the last 5 lines of claim 2 must have a full repertoire of hVH gene segments and a plurality of hJH gene segments. The full repertoire of hVH gene segments is missing from the “mouse whose genome comprises the nucleotide molecule” in claim 2.
Accordingly, the specification lacks written description for a vector capable of being used in a “mouse whose genome comprises the nucleotide molecule” in the absence of a full repertoire of hVH gene segments as broadly encompassed by claim 2.
Response to arguments
Applicants’ arguments do not address this aspect of the rejection.
Indefiniteness
The rejection of claims 2, 20-23, 92-96, 98, 99 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, has been withdrawn in view of the amendment.
Claim interpretation
Jung (Cell, 2004, Vol. 116, No. 2, pg 299-311) taught “RSs consist of a relatively conserved heptamer and nonamer, with respective consensus sequences of CACAGTG and ACAAAAACC, separated by a nonconserved spacer of either 12 or 23 base pairs (Figure 2; Max et al., 1979; Sakano et al., 1979), which we will refer to as a ‘12RS’ or a ‘23RS’” (pg 300, col. 2, line 10). Fig. 2 (pg 301) of Jung taught DH gene segments flanked by a 12 bp spacers. The 1st DH gene segment in claim 2 is a naturally occurring DH gene segment because it has 12 bp spacers. The 2nd DH gene segment in claim 2 is a genetically DH gene segment because it has one naturally occurring 12 bp spacer and one non-natural 23 bp spacer.
Withdrawn rejections
The rejection regarding the phrase “wherein the human Ig VH gene segment [singular] comprises a complete repertoire of functional unrearranged human Ig VH gene segments [plural]” in claim 20 has been withdrawn in view of the amendment.
The rejection regarding the phrase “wherein the human Ig JH gene segment [singular] comprises an unrearranged human Ig JH4 gene segment, an unrearranged human Ig JH5 gene segment, and an unrearranged human Ig JH6 gene segment [plural]” in claim 22 has been withdrawn in view of the amendment.
The rejection regarding the phrase “wherein the second human Ig DH gene segment [singular] is a human DH2-2 gene segment,… and/or a DH2-15 gene segment [plural]” in claim 93 has been withdrawn in view of the amendment.
The rejection regarding the metes and bounds of when JH1-6 gene segments are “in germline formation” as required in claim 97 has been withdrawn because the claim has been canceled.
The art at the time of filing did not teach or suggest a nucleotide molecule comprising a 1st naturally occurring hDH gene segment and 2nd genetically modified human DH gene segments specifically set forth in claim 2.
Conclusion
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 1632