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 .
DETAILED ACTION
Amendments
In the reply filed 03/20/2026, Applicant has amended claims 1, 7 and 25, canceled claims 5-6, and added new claims 44-45.
Claim Status
Claims 1, 7-11, 15, 16, 19-21, 24-27, 31, 32, 35, 37, 38, 40-42 and 44-45 are pending. Claims 1, 7 and 25 have been amended, claims 5-6 have been canceled, and claims 44-45 have been added by Applicants’ amendment filed on 03/20/2026.
Claims 16, 20, 37, 38, 40-42 have been withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to non-elected inventions, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 08/13/2025.
Claims 1, 7-11, 15, 19, 21, 24-27, 31, 32, 35 and 44-45 are considered on the merits.
Withdrawn Specification Objections
The prior objection to the disclosure because of an embedded hyperlink is withdrawn in light of Applicant’s amendment to the specification.
Withdrawn Claim Objections
The objection to claim 6 is rendered moot in view of Applicants’ cancelation of claim 6.
New 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 44-45 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.
Claims 44 and 45 recite the limitation that the mutation or truncation of the CD2 extracellular domain or a portion thereof comprises a “D111H mutation”. Since a CD2 gene occurs in multiple isoforms across multiple species with distinct amino acid sequences, it is unclear which reference sequence Applicant intends to refer to in order to arrive at the claimed “D111H”. A claim may be rendered indefinite by reference to term of an object that is variable (see MPEP 2173.05(b), II). The reference sequence required to determine the claimed mutation 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.
Withdrawn Claim Rejections - 35 USC § 103
The prior rejection of claims 1, 5, 8-11, 15, 19, 21, 25-27, 31-32 and 35 under 35 U.S.C. 103 as being unpatentable over Feldhaus et al., (Gene Therapy. 1997; 4: 833-838), as evidenced by Seed et al., (Proc. Natl. Acad. Sci. USA. 1987; 84: 3365-3369) and in view of Abel et al., (WO 2020/030979 A2, published February 13, 2020. Cited in IDS 04/11/2024) has been withdrawn in light of Applicant’s amendment to claim 1 to recite limitations from previous claim 6.
The prior rejection of claims 6-7 and 24 under 35 U.S.C. 103 as being unpatentable over Feldhaus et al., (Gene Therapy. 1997; 4: 833-838), as evidenced by Seed et al., (Proc. Natl. Acad. Sci. USA. 1987; 84: 3365-3369) and in view of Abel et al., (WO 2020/030979 A2, published February 13, 2020. Cited in IDS 04/11/2024), and further in view of Peterson et al., (Nature. 1987; 329: 842-846) has been withdrawn in light of Applicant’s amendment to claim 1 to recite limitations from previous claim 6.
Response to Trversal:
Applicant’s arguments filed on 03/20/2026 are acknowledged.
Applicant argues that Feldhaus teaches away from the claimed CSR by disclosing a chimeric receptor comprising a CD2 extracellular domain and a CD28 intracellular domain (see Fig. 1) which was designed as an adoptive immunotherapy strategy for activating the CD28 pathway via the binding of CD58 to the CD2 extracellular domain (see, e.g., Abstract). In particular, Feldhaus discloses that in its cells "CD58 will trigger both the CD2 pathway via endogenous CD2 and the CD28 pathway through the CD2/CD28 chimeric receptor”. See page 836, left col., lines 22-24. Feldhaus further discloses that the CD2 and CD28 pathways synergize, but only when the ligands for both CD2 and CD28 are present. See, page 836, left col., lines 24-31. Feldhaus continues that CD58 was chosen because it is expressed on all cell types and was found to be expressed on all primary tumors and tumor derived cells. See, page 836, left col., lines 32-49. As demonstrated above, the explicitly stated purpose of Feldhaus is to use the ubiquitously present CD58 ligand to stimulate synergistic levels of T cell activation and proliferation. See, page 836, left col., lines 24-49. To do so, the Feldhaus’ CSR must necessarily be bound and activated by CD58 (Remarks, p. 10-11). Furthermore, Applicants’ arguments at pages 11-12 of the remarks filed on 3/20/2026 that the “ Peterson identified an epitope ("region 2") that was involved in adhesion but not CD2 activation, it did not attribute any benefit or detriment to that region. It also did not teach or suggest that any adhesion-blocking mutations in this region were useful for any purpose …. The mere disclosure of a CD2 amino acid variant, without any suggestion that it has a particular utility, is insufficient to establish prima facie obviousness” have been considered and found persuasive.
In response, it is noted that independent claims 1 and 25 (and dependent claims) have been amended to recite subject matters from previous claim 6, thus the prior rejections have been withdrawn.
A response to Applicant’s arguments with regard to a withdrawn rejection is moot. A response to any argument pertaining to a new or maintained rejection can be found below.
New Claim Rejections - 35 USC § 112(a)
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 1, 7-11, 15, 19, 21, 24-27, 31, 32, 35 and 44-45 are newly 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. This is a new rejection necessitated by amendment of the claims in the response filed 3/20/2026.
Under the written description guidelines (see MPEP 2163) the Examiner is directed to determine whether one skilled in the art would recognize that the Applicant was in possession of the claimed invention as a whole at the time of filing. The following considerations are critical to this determination.
To satisfy the written description requirement, a patent specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. See, e.g., Moba, B.V. v. Diamond Automation, Inc., 325 F.3d 1306, 1319, 66 USPQ2d 1429, 1438 (Fed. Cir. 2003); Vas-Cath, Inc. v. Mahurkar, 935 F.2d at 1563, 19 USPQ2d at 1116. An original claim may lack written description support when (1) the claim defines the invention in functional language specifying a desired result but the disclosure fails to sufficiently identify how the function is performed or the result is achieved or (2) a broad genus claim is presented but the disclosure only describes a narrow species with no evidence that the genus is contemplated. See Ariad Pharms., Inc. v. Eli Lilly & Co., 598 F.3d 1336, 1349-50 (Fed. Cir. 2010) (en banc). The written description requirement is not necessarily met when the claim language appears in ipsis verbis in the specification. "Even if a claim is supported by the specification, the language of the specification, to the extent possible, must describe the claimed invention so that one skilled in the art can recognize what is claimed. The appearance of mere indistinct words in a specification or a claim, even an original claim, does not necessarily satisfy that requirement." Enzo Biochem, Inc. v. Gen-Probe, Inc., 323 F.3d 956, 968, 63 USPQ2d 1609, 1616 (Fed. Cir. 2002).
Accordingly, to satisfy the written description requirement, the specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. Vas-Cath, Inc. v. Mahurkar, 935 F.2d 1555, 1562-63, 19 USPQ2d 1111 (Fed. Cir. 1991). See also MPEP 2163.
SCOPE OF THE INVENTION
Independent claims 1 and 25 encompass a genus of chimeric stimulatory receptors (CSR) comprising a genus of CD2 extracellular domain or a portion thereof that comprises a genus of mutations or truncations that do not bind CD58 while simultaneously binding an agonist of CD2. However, the specification only discloses one single species of the mutation of the CD2 extracellular domain comprising the amino acid sequence of SEQ ID NO: 4 that has an amino acid mutation (referred to as “D111H” mutation, see e.g., [0308]-[0315]) and does not bind CD58.
Dependent claims 7-11, 15, 19, 21, 24, 26-27, 31, 32, 35 and 44-45 encompass the CD2 extracellular domain comprising the mutation or truncation comprising SEQ ID NO: 4, the intracellular domain further comprising a CD3ζ, the sequences of CD3ζ and TNFR2 intracellular domains, the signal peptide, the transmembrane domain, the amino acid sequences of the CSR, a nucleic acid sequence encoding the CSR, a cell comprising the CSR, the cell being a T cell, a regulatory T cell, a composition comprising a population of modified T cells comprising the CSR, and the mutation or truncation of the CD2 extracellular domain or a portion thereof comprising a D111H mutation. However, the specification only discloses one single species of the mutation of the CD2 extracellular domain comprising the amino acid sequence of SEQ ID NO: 4 that has an amino acid mutation and does not bind CD58.
ACTUAL REDUCTION TO PRACTICE
Accordingly, Applicant did not demonstrate a reduction to practice a genus of CSRs comprising a genus of CD2 extracellular domain or a portion thereof that comprises a genus of mutations or truncations that do not bind CD58, nor did Applicant adequately set forth in terms of distinguishing identifying characteristics as evidenced by other descriptions of the invention that are sufficiently detailed to show that Applicant was in possession of the claimed genus of CSRs.
DISCLOSURE OF STRUCTURE
The Applicant has provided only one single species of the mutation of the CD2 extracellular domain comprising the amino acid sequence of SEQ ID NO: 4 that has an amino acid mutation and does not bind CD58.
Applicants disclose in Figure 1 four different constructs identified as 11, 12, 33 and 34 all of them containing the amino acid sequence of SEQ ID NO: 4, the TNFR2 transmembrane or the CD2 transmembrane domain wherein the intracellular domain comprises a TNFR2 intracellular domain or a portion thereof and a CD3ζ protein or a portion thereof.
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These constructs were used to transfect Pan-T cells (Example 2) and Treg cells (Example 3) to track expression and cell viability as well as activation of pSTAT5 expression in Treg (Table 5).
The Specification is silent about any other constructs comprising a genus of CD2 extracellular domains or portions thereof where a mutated or truncated CD2 extracellular domain binds anti-CD2 activating agonists but does not bind naturally occurring CD58, the TNFR2 transmembrane or the CD2 transmembrane domain wherein the intracellular domain comprises a TNFR2 intracellular domain or a portion thereof and a CD3ζ protein that are able to enhance Treg cellular expansion relative to a control (para [0747] of the published application) and activate pSTAT5 expression (Table 5).
Although gene mutation or truncation techniques are known in the field of molecular biology, the prior art is silent on how to make mutations or truncations of CD2 extracellular domain or a portion thereof so that it does not bind CD58, nor indicate a relationship between the structure of the claimed CD2 extracellular domain or a portion thereof and the ability to not bind CD58.
SUFFICIENT RELEVANT IDENTIFYING CHARACTERISTICS
As mentioned in above, gene editing tools are available in the art, and the skilled artisan could make mutations or truncations on a CD2 extracellular domain or a portion thereof.
The breadth of the claims encompasses a genus of CSRs comprising a genus of CD2 extracellular domain or a portion thereof that comprises a genus of mutations or truncations that do not bind CD58, yet the present specification provides no guidance nor description on how to make mutations or truncations on CD2 extracellular domain or a portion thereof so that it does not bind CD58, therefore the skilled artisan would not know what rational approach to take to make the claimed CSRs comprising the claimed mutations or truncations of CD2 extracellular domain or a portion thereof to obtain any predictable outcome of not binding CD58. Therefore, it is incumbent on the applicant to provide this nexus between structure and function, in order to be given credit for possession of the claimed genus of CSRs comprising a genus of CD2 extracellular domain or a portion thereof that comprises a genus of mutations or truncations that do not bind CD58.
An applicant may show that an invention is complete by disclosure of sufficiently detailed, relevant identifying characteristics which provide evidence that applicant was in possession of the claimed invention, i.e., complete or partial structure, other physical and/or chemical properties, functional characteristics when coupled with a known or disclosed correlation between function and structure, or some combination of such characteristics. Enzo Biochem, 323 F.3d at 964, 63 USPQ2d at 1613.
STATE OF THE ART & QUANTITY OF EXPERIMENTATION
The method of making the claimed invention is not well established. Although gene editing tools were known in the state of the art and the skilled artisan could make mutations or truncations on a CD2 extracellular domain or a portion thereof, one of skill in the art would neither expect nor predict the outcome of the mutations or truncations that results in not binding CD58.
As Applicant has argued, prior art Peterson et al., (Nature. 1987; 329: 842-846, prior art of record) generates 47 different amino acid variants of CD2 extracellular domain and evaluates the ability of the variants to adhere to human erythrocytes via binding to CD58. Peterson teaches that even within a discrete region (e.g., amino acids 42-57 in Fig 2a or amino acids 87-101 in Fig 2b), the mutations result in different erythrocyte adhesion abilities (see rosette formation columns in Fig 2a and Fig 2b), indicating different binding capabilities to CD58 (also see Applicant’s argument, Remarks, p. 11, last para – p. 12, para 1). Consequently, there is ample reason to conclude that there would be a high degree of unpredictability in the characteristic of not binding CD58 among a genus of any mutations or truncations of the CD2 extracellular domain or a portion thereof. Thus, the claimed genus of mutations or truncations of CD2 extracellular domain or a portion thereof that does not bind CD58 is highly unpredictable, and is not well established.
Applicant has claimed a genus of CSRs comprising a genus of CD2 extracellular domain or a portion thereof that comprises a genus of mutations or truncations that do not bind CD58, yet the specification has only disclosed one single species of one specific mutation of the CD2 extracellular domain that does not bind CD58, has not set forth in terms of distinguishing identifying characteristics as evidenced by other descriptions of the invention that are sufficiently detailed to show that Applicant was in possession of the claimed genus of CSRs. Furthermore, the state of the art indicated that any mutations or truncations of the CD2 extracellular domain or a portion thereof that do not bind CD58 is not well established and would require undue experimentation, and one of skill in the art would neither expect nor predict the claimed outcome of not binding CD58 according to the claimed genus of any mutations or truncations of the CD2 extracellular domain or a portion thereof.
CONCLUSION
Therefore, the Examiner concludes that there is insufficient written description of the instantly claimed genus of CSRs comprising a genus of CD2 extracellular domain or a portion thereof that comprises a genus of mutations or truncations that do not bind CD58. Specifically, there is limited disclosure, i.e., only a single species of mutation of the CD2 extracellular domain (i.e., SEQ ID NO: 4) having the claimed outcome of not binding CD58, thus does not provide sufficient number of species to represent the entire scope of the claimed extremely broad genus of any mutation or truncation of the CD2 extracellular domain or a portion thereof that does not bind CD58.
Therefore, the Examiner concludes that there is insufficient written description to show that Applicant was in possession of the entire scope of the claimed genus of CSRs comprising a genus of CD2 extracellular domain or a portion thereof that comprises a genus of mutations or truncations that do not bind CD58.
Response to Trversal:
Applicant’s arguments filed on 03/20/2026 are acknowledged.
Applicant is reminded that as necessitated by amendment to claims 1 and 25, a new ground of rejection under 35 USC § 112(a) Written Description has been made as discussed above. Applicant is also reminded that the single species of a mutation of the CD2 extracellular domain comprising the amino acid sequence of SEQ ID NO: 4, although being taught by prior art Peterson, has not been taught or suggested in the context of constructing a chimeric stimulatory receptor together with a TNFR2 intracellular domain.
Maintained Provisional Double Patenting Rejections
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 USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The 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/process/file/efs/guidance/eTD-info-I.jsp.
Claims 1, 7-11, 15, 19, 21, 24-27, 31, 32, 35 and 44-45 stand provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over copending claims of Application Nos: 17/640176 as per claims filed on 2/19/2026 and 17/273030 as per claims filed on 3/24/2026 in view of Abel et al., (WO 2020/030979 A2, published February 13, 2020. Cited in IDS 04/11/2024). Although the claims at issue are not identical, they are not patentably distinct from each other.
Copending claims of the Applications recite a non-naturally occurring chimeric stimulatory receptor (CSR) comprising (a) an ectodomain comprising a CD2 signal peptide and an activation component comprising a CD2 extracellular domain, (b) a CD2 transmembrane domain, (c) an endodomain comprising a cytoplasmic domain selected from a list of genes and a signal transduction domain comprising a CD3ζ protein. The activation component comprises a modification, the modification comprises a mutation or a truncation as compared to the wildtype sequence of the CD2 extracellular domain, the mutation or truncation of the CD2 extracellular domain does not bind CD58. The CD2 signal peptide, the CD2 extracellular domain, the CD2 transmembrane domain and the CD3ζ intracellular domain comprise the same sequences as instantly claimed.
However, copending claims of the Applications are silent on a TNFR2 intracellular domain, nor recite its sequence.
Abel teaches a chimeric antigen receptor (CAR) comprising a human TNFR2 costimulatory intracellular signaling domain (see e.g., abstract and reference claim 1). Abel teaches engineered T cells and engineered Treg cells expressing said CAR constructs present a strong decrease of tonic signaling as compared to said cells expressing a conventional CAR. Following CAR engagement, the engineered Treg cells showed highly efficient suppressive activity on T effector cell proliferation, thereby demonstrating the advantage of these Treg cells for cell therapy ([0009]). Abel teaches the TNFR2 intracellular domain comprises the amino acid sequence of Abel SEQ ID NO: 34 (e.g., [0268] and Abel claim 17), which is 100% identical to the instant SEQ ID NO: 6 (see SCORE search 06/05/2025, -6.rapm file, Result #1 “US-17-267-410-34”. It is noted that Abel WO2020/030979 is the WIPO publication of US application 17/267,410).
Therefore, it would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the chimeric stimulatory receptor comprising a CD3ζ intracellular domain and another intracellular domain recited in the copending claims of the Applications, by combining a TNFR2 intracellular signaling domain with the recited sequence as suggested by Abel with a reasonable expectation of success. Since Abel teaches including a TNFR2 intracellular domain in a chimeric antigen receptor reduces tonic signaling and the engineered Treg cells show highly efficient suppressive activity on T effector cells, thereby demonstrating the advantage of these Treg cells for cell therapy ([0009]) and Abel further reduces to practice a combination of at least two intracellular domains of TNFR2 and CD3ζ (see e.g., [0303]), one of ordinary skill in the art would have had a reason to combine a TNFR2 intracellular domain in the chimeric receptor as suggested by Abel in order to take advantage of the reduced tonic signaling and the efficient suppressive activity in engineered Treg cells to improve adoptive cell therapy. One of ordinary skill in the art would have chosen the sequence taught by Abel since Abel reduces to practice the sequence. It would have also been obvious for one of ordinary skill in the art to have used this chimeric receptor in T cells, especially in Treg cells as suggested by Abel for cell therapy.
Since the instant application claims are obvious over cited application claims, in view of Abel, said claims are not patentably distinct.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims in the copending applications have not in fact been patented.
Response to Traversal:
Applicant’s arguments filed on 03/20/2026 are acknowledged.
Applicant argues the pending claims and the reference claims are both directed to chimeric stimulatory receptors (CSRs) while Abel discloses chimeric antigen receptors (CARs). These are different molecules that have different purposes (killing versus survival). (Remarks, p. 12).
Applicant’s arguments have been fully considered but they are not persuasive. Although CSRs and CARs have different names, they have similar structures comprising an extracellular domain, a transmembrane domain and a intracellular domain. Abel specifically teaches “engineered T cells and engineered Treg cells expressing said CAR constructs present a strong decrease of tonic signaling” (e.g., [0009]). Thus, one of ordinary skill in the art would have immediately acknowledged that the strong decrease of tonic signaling by the CAR having TNFR2 intracellular domain would reduce CAR-T cell exhaustion and enhance CAR T cell survival, i.e., the same function as that of a CSR as argued by Applicant.
Applicant further argues that the reference applications recite co-stimulatory intracellular domains involved in the activation, survival, proliferation, and differentiation of effector T cells and memory T cells, or a CD2 cytoplasmic domain in ‘030, and Abel would not have motivated a POSA to replace the recited intracellular domains of the claims the '176 and ‘030 applications with a TNFR2 intracellular domain because Abel only proposes to solve tonic signaling caused by scFv in a CAR, while the CSRs of the reference applications have a CD2 extracellular domain but does not have a scFv thus does not suffer from tonic signaling (Remarks, p. 13-14 and reference Long et al).
Applicant’s arguments have been fully considered but they are not persuasive. As stated supra, Abel teaches including a TNFR2 intracellular domain in a chimeric antigen receptor reduces tonic signaling, and furthermore, the engineered Treg cells show highly efficient suppressive activity on T effector cells, thereby demonstrating the advantage of these Treg cells for cell therapy ([0009]). Accordingly, Abel does not only propose to solve tonic signaling caused by scFv in a CAR, but rather, also suggests that the TNFR2 intracellular domain enhances the activity of the Treg cells. Since the reference applications recite a CSR with a CD3ζ intracellular domain, and Abel further reduces to practice a combination of intracellular domains of TNFR2 and CD3ζ (see e.g., [0303]), one of ordinary skill in the art would have had a reason to combine a TNFR2 intracellular domain together with CD3ζ in the CSRs as suggested by Abel to engineer the CSRs in regulatory T cells in order to take advantage of the efficient suppressive activity in engineered Treg cells to improve adoptive cell therapy.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any extension fee pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the date of this final action.
No claims are allowed.
Examiner Contact Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Jianjian Zhu whose telephone number is (571)272-0956. The examiner can normally be reached M - F 8:30AM - 4PM (EST).
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/JIANJIAN ZHU/Examiner, Art Unit 1631
/MARIA G LEAVITT/Supervisory Patent Examiner, Art Unit 1634
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