DETAILED ACTION
Status of Application, Amendments and/or Claims
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA . Claims 139-158 are pending.
In the Office action mailed on 2/19/26, four elections of species were required. In the reply filed on 2/24/26, Applicants elect the following species without traverse: (1) SEQ ID NO: 13 as the species of engineered estrogen binding domain (EBD); (2) 4-1BB as the species of fusion partner (co-stimulatory or inhibitor immune molecule); (3) a ligand binding domain (LBD) binding a cancer antigen as the species of LBD; and (4) cancer as the species of disease. Claim 153 is withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected species, there being no allowable generic or linking claim.
Claims 139-152 and 154-158 are under consideration, as they read upon the elected species.
Drawings
Corrected drawings in compliance with 37 CFR 1.121(d) are required because:
---The drawings do not comply with 37 C.F.R. 1.84(u)(1), which states that partial views of a drawing which are intended to form one complete view, whether contained on one or several sheets, must be identified by the same number followed by a capital letter. Specifically, certain sheets are labeled as “continuations” rather being given a separate letter. For example, the three views of Figure 10 are labeled, “FIG. 10”, “FIG. 10 (cont’d)” and “FIG. 10 (cont’d)” instead of Figures 10A, 10B and 10C. Similar corrections should be made to each other figure with sheets labeled as “continuations”, including at least Figures 13, 15, 17-20, 22-25, 28, 29, 31 and 33.
Applicants are reminded that once the drawings are changed to meet the separate numbering requirement of 37 C.F.R. 1.84(u)(1), Applicants are required to file an amendment to change the Brief Description of the Drawings and the rest of the specification accordingly. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). Applicants are advised to employ the services of a competent patent draftsperson outside the Office, as the USPTO no longer prepares new drawings. The corrected drawings are required in reply to the Office action to avoid abandonment of the application. The requirement for corrected drawings will not be held in abeyance.
Specification
The disclosure is objected to because of the following informalities:
---At each of page 87 (element 24) and page 90 (element 75), “1 Gly” and “2 Gly” should be “1Gly” and “2Gly”.
---The specification at ¶ 51 (published application) teaches that SEQ ID NO: 7 is the coding sequence of an EBD having an E353A mutation, but at ¶ 72 teaches that SEQ ID NO: 7 has mutations G440V, M543A and L544A.
Appropriate correction is required.
Claim Objections
Claims 139-152 and 154-158 are objected to for the following informalities:
In each of independent claims 139, 154 and 157, the abbreviation “hsp90” should be accompanied by the full terminology the first time it is used in a series of claims; i.e., “heat shock protein 90 (hsp90)”.
In claim 146, the abbreviation “4-OHT” should be accompanied by the full terminology the first time it is used, e.g., “4-hydroxytamoxifen (4-OHT)”.
In claim 150, lines 1-2, “1 Gly” and “2 Gly” should be written in the same manner as “3Gly”, i.e., “1Gly” and “2Gly”.
The remaining claims are objected to for depending from an objected claim.
Appropriate correction is required.
Claim Rejections - 35 USC § 112(b)
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.
Claim 150 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 pre-AIA the applicant regards as the invention.
In claim 150, lines 1-2, the recitation of “further comprising a 1 Gly, 2 Gly, or 3Gly junction amino acid adjacent to…” is indefinite because 2Gly and 3Gly are linkers of two or three amino acids, respectively, but the claim refers to “amino acid” in the singular.
Claim Rejections - 35 USC § 112(a), written description
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.
Claims 139-152 and 154-158 are 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 pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention.
In making a determination of whether the application complies with the written description requirement of 35 U.S.C. 112(a), it is necessary to understand what Applicants are claiming and what Applicants have possession of.
The claims include products and a related method. Independent claim 139, and dependent claims 140-152, are directed to a product that is an “activity-inducible” fusion protein comprising at least two parts: (1) “an hsp90 binding domain” (HBD) or (2) “an intracellular signaling domain” (ISD) of a co-stimulatory immune molecule or an inhibitory immune molecule. The term “activity-inducible” is not provided with a limiting definition in the instant specification, and is therefore interpreted broadly as encompassing any activity that is induced or caused by, or by using, the fusion protein. The elected species of “fusion partner (co-stimulatory immune molecule or inhibitory immune molecule” is the protein 4-1BB. The fusion protein may be part of a chimeric antigen receptor (CAR), as required by dependent claim 147, but the broadest claims do not require this. The specification teaches that in the case where the fusion protein is part of a CAR, hsp90 binds to the hsp90 binding domain and keeps the CAR in the “off’ state (¶ 13). Independent claim 154 is directed to a related product; specifically, a nucleic acid encoding an activity-inducible fusion protein having the same limitations. Independent claim 157 is directed to a method of treating a subject in need thereof comprising administering a nucleic acid encoding an activity-inducible fusion protein having the same limitations.
The claims are directed to a genus of proteins (or nucleic acids encoding such) having different amino acid sequences but having the requisite functional activity. The broadest claims, i.e., independent claim 139, encompass any fusion protein that can perform the required functions: (1) inducing an activity; and (2) binding to hsp90 (heat shock protein 90). However, a protein otherwise defined only by its function(s) is not alone sufficient to define the genus because it is only an indication of what the polypeptide does, rather than what it is (i.e., its amino acid sequence). It is only a definition of a useful result rather than a definition of what achieves that result. Instead, what is necessary is a description of the genus of specific amino acid sequences that can perform the required function.
The specification teaches that the “hsp90 binding domain” can be a “hormone binding domain” (HBD) (¶ 12) or “modified form thereof” (¶ 64). The specification further teaches the HBD can “be an estrogen binding domain (EBD)” that “can be derived from the natural estrogen receptor but include at least one mutation such that the EBD no longer binds estrogen, but instead binds a drug molecule with a higher affinity than hsp90” (¶ 12). However, the specification does not provide any other examples of hsp90 binding domains that are not HBDs, and does not provide any other examples of HBDs other than the EBD that bind to hsp90. Thus, the limited examples of hsp90 binding domains provided by the specification fail to correspond to the scope of the genus encompassed by the claims. The specification fails to describe a scope of protein domains having the required functionality, i.e., binding to hsp90 and being activity-inducible. As such, the specification fails to disclose relevant identifying characteristics sufficient to describe the claimed invention in such full, clear, concise, and exact terms that a skilled artisan would recognize applicant was in possession of the claimed invention with respect to an “activity-inducible fusion protein” or a “hsp90 binding domain” (as recited in independent claim 139) or an hsp90 binding domain that binds hsp90 with a lower affinity than a drug molecule (as recited in dependent claim 140).
Furthermore, while dependent claims 141-143 are limited to a fusion protein comprising engineered (i.e., mutated) estrogen receptor binding domain (EBD), the specification also does not provide a sufficient description of such a mutated EBD that retains the required functionality, i.e., binding to hsp90 and also binding to a drug molecule with higher affinity than hsp90. The specification teaches a wild type EBD having an amino acid sequence of SEQ ID NO: 2 (¶ 51), which is 314 amino acid in length. The specification further expressly teaches that variants of protein sequences of the invention include those with 70% sequence identity, or 30% of the sequence changed, which in the case of SEQ ID NO: 2 includes variants with up to 93 amino acids changed anywhere in the sequence in combination.
Furthermore, the language used in claims 143, 154, and 155, (“…a sequence as set forth in…” encompasses fusion proteins comprising fragments of the recited reference sequences. Specifically, the phrases "a sequence as set forth in SEQ ID NO: X" or "the sequence as set forth in SEQ ID NO: X" result in claims of very different scope, because while the latter encompasses only sequences that comprise the full length of SEQ ID NO: X, with or without additional amino acids at either or both ends, the latter encompasses sequences that comprise the full-length sequence of SEQ ID NO: X or any portion of SEQ ID NO: X; i.e., fragments of SEQ ID NO: X of as small as two consecutive amino acids. As such, the instant claims encompass fusion proteins comprising fragments of SEQ ID NO: 13 (the elected species under consideration), as well nucleic acid comprising fragments of SEQ ID NO: 14 (the sequence encoding SEQ ID NO: 13) and fragments of SEQ ID NO: 125 (which comprises SEQ ID NO: 13). Thus, the engineered EBDs of the claims encompass a large genus of variants of the elected species of SEQ ID NO: 13.
As taught by the prior art, "[m]utations … are generally destabilizing, and can reduce protein … fitness" and "In general, more comprehensive understanding of how mutations affect protein fitness within living cells is needed, including their combined effects on function, thermodynamic and kinetic stability, and clearance through aggregation and degradation" (pg 602 of Tokuriki et al, 2009, Current Opinion in Structural Biology. 19: 596-604). The prior art also appreciates that "the range of possible SNV [single nucleotide variation] effects at the protein level are significantly greater than currently assumed by existing software prediction methods, and that correct prediction of consequences remains a significant challenge" (pg 18 of Bhattacharya et al, 2017. Plos One. 12(3): e0171355, pages 1-22 as printed). Thus, the knowledge that a particular defined amino acid sequence binds hsp90 and another drug (e.g., tamoxifen) was not sufficient in and of itself for the skilled artisan at the time of the effective filing date to predict which mutations (substitutions, additions and deletions) will result in a mutated sequence that retains said functionality.
In the instant case, in support of the claimed genus the specification provides only limited description of which EBD variants actually have the required activity; i.e., hsp90 binding and rendering the overall fusion protein activity-inducible. Specifically, the specification provides SEQ ID NO: 4, 6, 9, 11 and 13, each of which comprise one to three mutations with respect to the wild type sequence of SEQ ID NO: 2. These limited examples fail to correspond to the scope of the genus of protein variants encompassed by the claims. The specification fails to describe the scope of amino acid changes can be made to the wild type EBD and still retain the required functionality. As such, the specification fails to disclose relevant identifying characteristics sufficient to describe the claimed invention in such full, clear, concise, and exact terms that a skilled artisan would recognize applicant was in possession of the claimed invention.
MPEP 2163 provides guidance for complying with the written description requirement of 35 U.S.C. 112(a) that the “specification shall contain a written description of the invention…”; this requirement is separate and distinct from the enablement requirement (Ariad Pharm., Inc. v. Eli Lilly & Co., 598 F.3d 1336, 1355 (Fed. Cir. 2010)). Written description for a claimed genus may be satisfied through sufficient description of a relevant number of species. This is dependent on whether one of skill in the art would recognize necessary common attributes or features possessed by the members of the genus. Generally, in an unpredictable art, adequate written description of a genus which embraces widely variant species cannot be achieved by disclosing only one species within the genus. Written description for a claimed genus can also be satisfied when relevant identifying characteristics are disclosed. Per MPEP 2163, “[d]etermine whether the specification discloses other relevant identifying characteristics sufficient to describe the claimed invention in such full, clear, concise, and exact terms that a skilled artisan would recognize applicant was in possession of the claimed invention. For example, if the art has established a strong correlation between structure and function, one skilled in the art would be able to predict with a reasonable degree of confidence the structure of the claimed invention from a recitation of its function. Thus, the written description requirement may be satisfied through disclosure of function and minimal structure when there is a well-established correlation between structure and function.” However, claiming by function does not necessarily satisfy the written description requirement. “[A] generic statement such as "vertebrate insulin cDNA" or "mammalian insulin cDNA," without more, is not an adequate written description of the genus because it does not distinguish the claimed genus from others, except by function. It does not specifically define any of the genes that fall within its definition. It does not define any structural features commonly possessed by members of the genus that distinguish them from others … A definition by function, as we have previously indicated, does not suffice to define the genus because it is only an indication of what the gene does, rather than what it is. It is only a definition of a useful result rather than a definition of what achieves that result” (Regents of the University of California v. Eli Lilly Co., 119 F.3d 1559 (Fed. Cir. 1997)). Also, “[w]hen a patent claims a genus using functional language to define a desired result, the specification must demonstrate that the applicant has made a generic invention that achieves the claimed result and do so by showing that the applicant has invented species sufficient to support a claim to the functionally-defined genus" (Capon v. Eshhar, 418 F.3d 1349 (Fed. Cir. 2005)), and “[A] sufficient description of a genus . . . requires the disclosure of either a representative number of species falling within the scope of the genus or structural features common to the members of the genus so that one of skill in the art can 'visualize or recognize' the members of the genus” (AbbVie, 759 F.3d at 1297, reiterating Eli Lilly, 119 F.3d at 1568-69).
Vas-Cath Inc. v. Mahurkar, 19USPQ2d 1111 (Fed. Cir. 1991), clearly states “applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the ‘written description’ inquiry, whatever is now claimed” (pg 1117). The specification does not “clearly allow persons of ordinary skill in the art to recognize that [he or she] invented what is claimed” (pg 1116). As discussed above, the skilled artisan cannot envision the detailed chemical structure of the encompassed genus of fusion proteins and therefore conception is not achieved until reduction to practice has occurred, regardless of the complexity or simplicity of the method of isolation. Adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method of isolating it. The compound itself is required. See Fiers v. Revel, 25 USPQ2d 1601 at 1606 (CAFC 1993) and Amgen Inc. v. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016 (Fed. Cir. 1991). One cannot describe what one has not conceived. See Fiddes v. Baird, 30 USPQ2d 1481 at 1483 (BPAI 1993). In Fiddes, claims directed to mammalian FGFs were found unpatentable due to lack of written description for that broad class.
Therefore, only an activity-inducible fusion protein comprising an engineered estrogen receptor binding domain (EBD) comprising the amino acid sequence set forth in SEQ ID NO: 4, 6, 9, 11 or 13, but not the full breadth of the claim meets the written description provision of 35 U.S.C. §112, first paragraph. Applicants are reminded that Vas-Cath makes clear that the written description provision of 35 U.S.C. §112 is severable from its enablement provision (pg 1115).
Note on Prior Art Rejection(s)
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.
Claim Rejections - 35 USC § 102
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.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 139-152 and 154-158 are rejected under 35 U.S.C. 102(a)(1) and 102(a)(2) as being anticipated by Taunton, U.S. Patent Application Publication 2017/0306303, published 10/26/17, filed 1/21/17 and claiming priority to 1/8/16. The earliest date to which the instant application claims priority is 2/12/21.
Claim 139 encompasses an activity-inducible fusion protein comprising an hsp90 binding domain (HBD) and an intracellular signaling domain (ISD) of 4-1BB, which is the elected species of ISD under consideration. The term “activity-inducible” is not provided with a limiting definition in the instant specification, and is therefore interpreted broadly as encompassing any activity that is induced, or caused, by or by using the fusion protein. The “hsp90 binding domain” encompasses an estrogen receptor binding domain (EBD), as taught by the instant specification at ¶ 12: “Certain embodiments disclosed herein utilize a hormone binding domain as the hsp90 binding domain. The hormone binding domain can be an estrogen receptor binding domain (EBD)”. Thus, claim 139 encompasses a fusion protein comprising an EBD and the intracellular signaling domain of 41BB, and wherein the fusion protein can induce an activity.
Taunton teaches “conditionally active, heterodimeric polypeptides” (see Abstract). Taunton further teaches:
“a heterodimeric, conditionally active polypeptide comprising: a) a first chimeric polypeptide comprising a first member of a dimerization pair and a first heterologous polypeptide; and b) a second chimeric polypeptide comprising a second member of a dimerization pair and a second heterologous polypeptide, wherein the first member of the dimerization pair comprises a ligand-binding domain (LBD) of a nuclear hormone receptor, and the second member of the dimerization pair comprises a co-regulator of the nuclear hormone receptor, or wherein the first member of the dimerization pair is a co-regulator of a nuclear hormone receptor, and the second member of the dimerization pair comprises an LBD of the nuclear hormone receptor; and wherein the first chimeric polypeptide and the second chimeric polypeptide are dimerized in the presence of a dimerization agent that induces binding of the LBD to the co-regulator” (¶ 6).
Taunton further teaches that “[i]n some cases, an LBD suitable for or inclusion as a member of a dimerization pair of a conditionally active, heterodimeric polypeptide of the present disclosure is an LBD of estrogen receptor-alpha (ERα)” (¶ 519). Taunton further provides an example of such a dimerization pair in Figure 15, where one member of the pair is a fusion protein comprising the “LBD of human estrogen receptor alpha” and the “co-stim motif” is “4-1BB”, and dimerization is induced by 4-hydroxytamoxifen (4-OH-tamoxifen or 4OHT). Taunton further teaches that “a suitable dimerization agent” such as 4-OH-tamoxifen, conditionally activates the heterodimeric polypeptide (¶ 392). As such, Taunton teaches an activity-inducible fusion protein comprising an hsp90 binding domain (i.e., LBD of EBD) and a co-stimulatory molecule (i.e., 4-1BB). As such, the teachings of Taunton anticipate claim 139.
Claims 140 and 141 each encompass a fusion protein of claim 139 wherein the HSD is an engineered EBD that binds hsp90 with a lower affinity than it binds a drug molecule. Such an engineered EBD encompasses an EBD with a G521R mutation, as evidenced by claim 142 depending from claim 141. Taunton further teaches that the LBD of ERα comprises a G521R mutation, e.g., at ¶ 877, 888, 890. As such, the teachings of Taunton also anticipate claims 140 and 141.
Claims 142 and 143 each encompass a fusion protein of claim 141 wherein the engineered EBD comprises a binding domain portion of the estrogen receptor and a G521R mutation (claim 142), the sequence of which is presented as SEQ ID NO: 4 (claim 143). Furthermore, the language used in claim 143 (“…a sequence as set forth in”) encompasses “a” sequence (i.e., any two or more amino acids) that is “in” a reference sequence; e.g., any portion of SEQ ID NO: 4 of two or more consecutive amino acids. As set forth above for claims 140-141, Taunton further teaches that the EBD comprises a G521R mutation. As such, the teachings of Taunton also anticipate claims 142 and 143.
Claims 144-146 each encompass a fusion protein of claim 140 wherein the drug molecule comprises a small molecule estrogen analog (claim 144) that is 4-OHT [4-hydroxytamoxifen] (encompassed by claim 145 and expressly recited in claim 146). As described above, Taunton teaches a drug molecule that binds the EBD that is 4-OHT as shown in Figure 15. As such, the teachings of Taunton also anticipate claims 144-146.
Claim 147 encompasses a fusion protein of claim 139, wherein the protein is a chimeric antigen receptor (CAR) that when expressed by a cell comprises: (i) extracellular and intracellular components linked by a transmembrane domain; (ii) an extracellular component comprising a ligand binding domain; and (iii) an intracellular component comprising the intracellular signaling domain of the co-stimulatory immune molecule and the hsp90 binding domain. As set forth above for claim 139, the teachings of Taunton in ¶ 6 include a heterodimeric pair wherein the first chimeric polypeptide comprises a first member of a dimerization pair and a first heterologous polypeptide, wherein the first member of the dimerization pair comprises a ligand-binding domain of a nuclear hormone receptor (NHR). Taunton further describes this embodiment in ¶ 779 as including “a first chimeric polypeptide comprising: i) a first member of a specific binding pair; ii) a first modulatory domain; iii) a first member of a dimerization pair; and iv) a transmembrane domain interposed between the first member of a specific binding pair and the first modulatory domain” and “wherein the first member of the dimerization pair comprises a ligand-binding domain (LBD) of a nuclear hormone receptor”. Thus, in this embodiment of the invention, the first chimeric polypeptide comprising an extracellular component (“the first member of a specific binding pair”, an intracellular component (“a first modulatory domain” and “first member of a dimerization pair”, and a transmembrane domain between the two. Taunton further teaches that in the intracellular component said modulatory domain can be from 4-1BB (¶ 783), and the first member of the dimerization pair that is the LBD of a NHR can be from the estrogen receptor (¶ 786). As such, this embodiment of Taunton anticipates claim 147.
Claim 148 encompasses a fusion protein of claim 147 wherein the ligand binding domain binds a cancer antigen. Taunton further teaches that the specific binding pair can be an antigen-binding domain (¶ 122-125) and further that can be one that is specific for an epitope in an antigen expressed by a cancer cell (¶ 126). As such, the teachings of Taunton also anticipate claim 148.
Claim 149 encompasses a fusion protein of claim 147 wherein the transmembrane domain is from CD28, the ISD is from 4-1BB and wherein the intracellular component further comprises a CD3-zeta intracellular signalling domain. Taunton teaches an ISD that is from 4-1BB as described above. Taunton further teaches that the transmembrane domain can be from CD28 (¶ 191) and that the intracellular component can comprise a CD3-zeta intracellular signaling domain (¶ 337-355). As such, the teachings of Taunton also anticipate claim 149.
Claim 150 encompasses a fusion protein of claim 147 that comprises no linker adjacent to the hsp90 binding domain. The fusion protein taught by Taunton described above for claim 147 does not expressly require a linker. As such, the teachings of Taunton also anticipate claim 150.
Claim 151 encompasses a fusion protein of claim 139 that does not comprises a degron sequence. The fusion protein taught by Taunton in Figure 15 does not include a degron sequence. As such, the teachings of Taunton also anticipate claim 151.
Claim 152 encompasses a fusion protein of claim 139 wherein the co-stimulatory immune molecule is 4-1BB. The teachings of Taunton that anticipate claim 139 are directed to a co-stimulatory immune molecule that is 4-1BB. As such, the teachings of Taunton also anticipate claim 152.
Claim 154 is an independent claim that encompasses a nucleic acid sequence encoding a fusion protein having the same limitations as claim 139. Taunton further teaches nucleic acids encoding the heterodimeric conditionally active polypeptides of the invention (¶ 13). As such, the teachings of Taunton also anticipate claim 154.
Claims 155 and 156 encompass a nucleic acid sequence of claim 154 wherein the hsp90 binding domain “is encoded by a sequence as set forth in” SEQ ID NO: 7, 14 or 15 (claim 155) or having “a sequence as set forth in SEQ ID NO: 125”. The language used in the claim (“…a sequence as set forth in”) encompasses any portion of two or more nucleic acids of any of the recited reference sequences, e.g., SEQ ID NO: 7, 14, 15, or 125. The specification ¶ 51 teaches that SEQ ID NO: 14 encodes the mutated EBD known as ERT2, and that SEQ ID NO: 125 also includes the ERT2 sequence. The specification elsewhere teaches that ERT2 differs from a wild type EBD by including three point mutations, G400V, M543A and L544A. Thus, the ERT2 sequence includes numerous portions that are identical to the wild type EBD sequence. As such, “a sequence selected from” SEQ ID NO: 14 or 125 encompasses the EBD sequence taught by Taunton that includes the G521R mutation (see above for claims 142 and 143). As described above for claim 154, Taunton in ¶ 13 teaches that the invention includes nucleic acids encoded the polypeptides of the invention. Thus, the nucleic acids of Taunton include those encompassed by claims 155 and 156. As such, the teachings of Taunton also anticipate claims 155 and 156.
Claims 157 and 158 encompass a method of treating a subject in need thereof comprising administering a nucleic acid sequence encoding a fusion protein having the same limitations as that of claim 139 (claim 157) and further wherein the subject is in need of treatment for cancer (claim 158). Taunton further teaches that the heterodimeric constructs of the invention can be expressed in a T-cell using an nucleic acid, for the purpose of administration for treatment of cancer (e.g., at ¶ 17). As such, the teachings of Taunton also anticipate claims 157 and 158.
Conclusion
No claims are allowable.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ZACHARY C HOWARD whose telephone number is (571)272-2877. The examiner can normally be reached on Monday to Friday from 9 AM to 5 PM. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Vanessa Ford, can be reached at telephone number (571) 272-0857. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/ZACHARY C HOWARD/Primary Examiner, Art Unit 1674
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