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 .
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
This action is in response to the papers filed March 11, 2026.
Claims 1, 2, 7, 8, 10, 12, 26, 30-31 and 34 are currently pending. Claims 15 and 16 are canceled, claims 1, 7 and 12 are amended, and no new claims are added as set forth in the claim set filed 03/11/2026.
Therefore, claims 1-2, 7-8, 10, 12, 26, 30, 31, and 34 are pending in the application and examined on the merits.
Priority
The present application is a 35 U.S.C. 371 national stage filing of International Application No. PCT/EP2019/057469, filed March 25, 2019.
Applicant’s claim for the benefit of a prior-filed UNITED KINGDOM patent 1804701.9 filed March 23, 2018 under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) is acknowledged.
Thus, the earliest possible priority for the instant application is March 23, 2018.
Response to arguments
Withdrawn objections/ Rejections in response to Applicants’ arguments or amendments
Claim Rejections - 35 USC § 112(b)
The rejection of claims 1-2, 7-8, 10, 12, 15, 16, 26, 30, 31, and 34 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second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter is withdrawn.
Applicant’s arguments and amendments filed 03/11/2026 have been considered and are persuasive. In particular, Applicant’s amendment to remove “capable” limitations.
Maintained objections/ Rejections in response to Applicants’ arguments or amendments
Claim Rejections - 35 USC § 112(a)
Claims 1-2, 7-8, 10, 12, 26, 30, 31, and 34 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
This rejection has been modified as necessitated by amendment of the claims in the response filed 3/11/2026
In analyzing whether the written description requirement is met for genus claims, it is first determined whether a representative number of species have been described by their complete structure. To provide adequate written description and evidence of possession of a claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of complete or partial structure, physical and/or chemical properties, functional characteristics, structure/function correlation, methods of making the claimed product, or any combination thereof. The disclosure of a single species is rarely, if ever, sufficient to describe a broad genus, particularly when the specification fails to describe the features of that genus, even in passing. (see In re Shokal 113USPQ283(CCPA1957); Purdue Pharma L.P. vs Faulding Inc. 56 USPQ2nd 1481 (CAFC 2000).
The court explained that “reading a claim in light of the specification, to thereby interpret limitations explicitly recited in the claim, is a quite different thing from ‘reading limitations of the specification into a claim,’ to thereby narrow the scope of the claim by implicitly adding disclosed limitations which have no express basis in the claim.” The court found that applicant was advocating the latter, i.e., the impermissible importation of subject matter from the specification into the claim.). See also In re Morris, 127 F.3d 1048, 1054-55, 44 USPQ2d 1023, 1027-28 (Fed. Cir. 1997).
Claim 1 recites an engineered gamma-delta T cell comprising a heterologous targeting construct, wherein the heterologous targeting construct comprises an extracellular antigen binding domain and a terminal transmembrane domain operatively linked to the antigen binding domain, wherein the antigen-binding domain binds to CD19. Based upon the structure of heterologous targeting construct , the y8 T cells are activated and yields certain functional properties as claimed. Claim 1 has been amended to recite a plurality of terminal transmembrane domain that participate in an intracellular signaling pathway
Written Description for Transmembrane Domain
Previously recited reference Leek (WO2016166544A1; IDS Reference filed 03/16/2021) taught an engineered delta gamma T cell comprising a heterologous construct comprising an extracellular antigen recognition domain, a hinge domain (stalk domain), and a transmembrane domain. Furthermore, Leek teaches that it also comprises a non-functioning CD3 zeta domain wherein the signaling is not sufficiently provided to cause activation (p. 4, 2nd paragraph; p. 3, 3rd paragraph). Leek teaches that the engineered gamma T cell’s non-functioning CD3 zeta domain is facilitated by the absence of the domain (claim 3, p. 6, last paragraph). Furthermore, Leek teaches that the signaling is not sufficiently provided to cause activation and that the CAR is incapable of providing signal 1 activation via the absence of CD3 zeta (p. 4, 2nd paragraph; p. 3, 3rd paragraph; p. 7, 2nd-3rd paragraphs).
It does not speak directly to the structure/function relationship of the terminal transmembrane domain itself.
As defined by Applicant’s specification, “terminal transmembrane domain” refers to a transmembrane domain having an unlinked terminal end. Thus it is not linked to an intracellular domain and in some embodiments, a terminal transmembrane domain does not participate in intracellular signaling pathways (p. 14, lines 23-27).
The ordinary artisan is dependent upon Applicant’s disclosure to make up for the deficiencies of the prior art, especially as it pertains to the instantly claimed invention.
Applicant’s specification does not disclose the particular modification to the terminal transmembrane domain which occurs and merely states that an artisan can be modified or substituted to minimize interactions with the binding domains without description of what the present invention has reduced to practice. (p. 23). Applicant’s specification only includes a broad genus of possible transmembrane regions as well as that it could be derived from a transmembrane portion of NKG2D (p. 23, line 4). The only Example shown is where the terminal transmembrane domain does not participate in an intracellular signaling pathway is an NKG2D transmembrane domain with endogenous DAP10 or DAP12 (See Figure 3 of the present application). There is also support in Figure 3B for the NCR (natural cytotoxicity receptors) NKp30 (left-hand column), NKp44 (middle column), on Vδ1 cells that are untransduced (UTD; top row).
Furthermore, Sallman (Haematologica, 2018, 103(9):e424-e426) teaches that a broad range of primary tumors express NKG2D ligands and can be targeted by NKG2D based immunotherapy (Introduction). The present application does not provide support for each and every tumor expressing NKG2D.
According to Watson (2001. Transmembrane domain length determines intracellular membrane compartment localization of syntaxins 3, 4, and 5, Am J Physiol Cell Physio 281: C215–C223), the short transmembrane domains (which are around 17 amino acids) direct the cis-Golgi localizations syntaxins whereas long transmembrane domains which are 23 amino acids or greater (25, in certain cases) direct plasma membrane localization (Abstract).
Therefore, the transmembrane domain of the present invention encompasses as many as 17-25 amino acids and within those 20 possible amino acid substitutions, insertions or deletions.
Transmembrane domains with 17 AA = (20)17 = about 1x1022 possible amino acid combinations for any transmembrane domain.
Transmembrane domains with 25 AA = (20)25 = about 3x1032 possible amino acid combinations for any transmembrane domain.
Thus the claims encompass up to 3 x 1032 variants of the transmembrane domain. (www.calculator.net/exponent-calculator.html; last visited August 29, 2024)
Thus, it is immediately apparent to the ordinary artisan that the instant claims are vastly broader in scope to Applicant’s actual invention. Those of ordinary skill in the art would immediately recognize that Applicant simply does not possess the enormously vast genus of 1x1022 to 3x1032 terminal transmembrane domains that will necessarily and predictably confer the recited functional properties of: not participating in an intracellular signaling pathway and not activating the engineered T cell (Claim 1).
A “representative number of species” means that the species which are adequately described are representative of the entire genus. Thus, when there is substantial variation within the genus, one must describe a sufficient variety of species to reflect the variation within the genus. See AbbVie Deutschland GmbH & Co., KG v. Janssen Biotech, Inc., 759 F.3d 1285, 1300, 111 USPQ2d 1780, 1790 (Fed. Cir. 2014) (Claims directed to a functionally defined genus of antibodies were not supported by a disclosure that “only describe[d] one type of structurally similar antibodies” that “are not representative of the full variety or scope of the genus.”).
Noelle v. Lederman, 355 F.3d 1343, 1350, 69 USPQ2d 1508, 1514 (Fed. Cir. 2004) (Fed. Cir. 2004) (“[A] patentee of a biotechnological invention cannot necessarily claim a genus after only describing a limited number of species because there may be unpredictability in the results obtained from species other than those specifically enumerated.”). “A patentee will not be deemed to have invented species sufficient to constitute the genus by virtue of having disclosed a single species when … the evidence indicates ordinary artisans could not predict the operability in the invention of any species other than the one disclosed.” In re Curtis, 354 F.3d 1347, 1358, 69 USPQ2d 1274, 1282 (Fed. Cir. 2004)
The Federal Circuit has explained that a specification cannot always support expansive claim language and satisfy the requirements of 35 U.S.C. 112 “merely by clearly describing one embodiment of the thing claimed.” LizardTech v. Earth Resource Mapping, Inc., 424 F.3d 1336, 1346, 76 USPQ2d 1731, 1733 (Fed. Cir. 2005).
For inventions 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. See, e.g., Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406. Instead, the disclosure must adequately reflect the structural diversity of the claimed genus, either through the disclosure of sufficient species that are “representative of the full variety or scope of the genus,” or by the establishment of “a reasonable structure-function correlation.” Such correlations may be established “by the inventor as described in the specification,” or they may be “known in the art at the time of the filing date.” See AbbVie, 759 F.3d at 1300-01, 111 USPQ2d 1780, 1790-91 (Fed. Cir. 2014)
The gap between the enormously vast genus of about 1x1022 to 3x1032 amino acids structurally and functionally undisclosed, yet to be discovered, claimed variants of the terminal transmembrane domain is considered to be tremendous, notoriously difficult, slow, very laborious and time-consuming for the ordinary artisans to determine for themselves that which Applicant has failed to disclose.
Therefore, based on the art's recognition that one cannot rely upon structural similarity alone to determine functionality, the specification fails to reasonably inform the ordinary artisan how to make and use the claimed enormously vast genus of structurally undisclosed terminal transmembrane domains having the disclosed and recited biological and functional properties. Without a correlation between structure and function, the claim does little more than define the claimed invention by function. That is not sufficient to satisfy the written description requirement. See Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406 (“definition by function … does not suffice to define the genus because it is only an indication of what the gene does, rather than what it is”).
Thus, for the reasons outlined above, it is concluded that the claims do not meet the requirements for written description under 35 U.S.C. 112, first paragraph.
MPEP 2163 - 35 U.S.C. 112(a) and the first paragraph of pre-AIA 35 U.S.C. 112 require 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, 1340, 94 USPQ2d 1161, 1167 (Fed. Cir. 2010) (en banc)
Dependent claims are included in the basis of the rejection because they do not correct the primary deficiencies of the independent claim(s).
In response to Applicant’s arguments regarding the 112a rejection of the written description in claims 1-2, 7-8, 10, 12, 26, 30, 31, and 34.
Applicant’s arguments have been considered, however they are not persuasive. The antigen binding domain written description has been remedied by the amendment to CD19, however the transmembrane domain still stands.
Applicant once again states that the amendments made to claim 1 to specify a long list of intracellular domains is sufficient enough to provide adequate written description.
Examiner reiterates that the specification defines a terminal transmembrane domain as “a transmembrane domain having an unlinked terminal end, e.g., a C-terminus that is not linked to a peptide or protein (p. 2 of the instant specification) and merely discloses one example of a heterologous targeting construct lacking a functional intracellular domain capable of “activating” the T cell on which it is expressed where its transmembrane domain propagates co-stimulation, e.g., upon association of an NKG2D transmembrane domain with endogenous DAP10 or DAP12 (p. 7 of the instant specification). Figure 4 shows results from a 16-hour killing assay at 1:1 effector to target ratio (FIGS. 4B and 4C). FIG. 4B shows killing of CD19+Nalm-6 cells, and FIG. 4C shows killing of primary B-ALL cells. These are only accomplished with a NKG2D transmembrane domain. Furthermore, Sallman (Haematologica, 2018, 103(9):e424-e426) teaches that a broad range of primary tumors express NKG2D ligands and can be targeted by NKG2D based immunotherapy (Introduction). The present application does not provide support for each and every tumor expressing NKG2D. Therefore, a representative number of species which have the same structure and function relationship is not present.
While Applicant points to a list within the specification of the transmembrane domains, this does not establish the structure and function relationship needed to adequately detail written description. Applicant points to Examples 2 and 3 for support and Examiner agrees that written description is shown through these. The only Example shown is where the terminal transmembrane domain does not participate in an intracellular signaling pathway is an NKG2D transmembrane domain with endogenous DAP10 or DAP12 (See Figure 3 of the present application). There is also support in Figure 3B for the NCR (natural cytotoxicity receptors) NKp30 (left-hand column), NKp44 (middle column), on Vδ1 cells that are untransduced (UTD; top row). Example 3 details a potential treatment to be carried out with a CD8 transmembrane domain. This does not adequately provide written description for the entire genus and list of transmembrane domains in that these structures do not all show a demonstration of the same function.
Claim Rejections - 35 USC § 103
Claims 1-2, 7, 10, 12, 26, 30, 31, and 34 remain rejected under 35 U.S.C. 103 as being unpatentable over Zhao (J Immunol (2009) 183 (9): 5563–5574) in view of Legut (Cellular & Molecular Immunology (2015) 12, 656–668)
This rejection has been modified as necessitated by Applicant’s remarks and amendment filed 03/11/2026.
Regarding claim 1, Zhao teaches an engineered T CAR cell wherein the construct transduced into the T cell comprises scFV, a hinge region, and a terminal transmembrane region wherein the CD28 and CD3 zeta intracellular domains have been deleted (Fig 3A: 4D5-28D, see below). The extracellular antigen binding domain and the terminal transmembrane domain are operatively linked to the antigen binding domain (scFv) (See 4D5-28D of figure 3A). Moreover, Zhao teaches that the antigen binding domain comprises scFv and that the terminal transmembrane domain is a CD28 transmembrane domain (See 4D5-28D).
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This construct resulted in no transgene decrease and the transgene expression was sustained. Based on the structure of the construct of Zhao (e.g., a 4D5 CAR with both CD28 and CD3 signaling domains being truncated (4D5-28D)), it would be an inherent property of the construct in the T cell to not participate in an intracellular signaling pathway, to trigger at last 5% less cytolysis by the T cell relative to the reference cell comprising an intracellular domain when binding to a healthy cell, and to trigger cytolysis when binding to the tumor cell. Zhao also teaches Ag-specific activities against ErbB2tumors.
However, Zhao does not teach that the engineered cells are gamma delta (γδ) T cells. Zhao does not teach Ag-specific activities against CD19 tumors.
Legut teaches utilizing γδ T cells for cancer immunotherapy (Abstract). While to the publication date, most CAR transduction experiments have been conducted on alpha beta T cells, gamma delta T cells are also an appealing target due to their broad anti-tumor cytotoxicity (‘they may be used as a potent anticancer vaccine in addition to their broad antineoplastic cytotoxicity”) and numerous effector functions, where transduction of γδ T cells with a TCR circumvents mispairing problems (p. 663, 1st column; Figure 6). Legut also teaches that γδ T cells “recognize their targets irrespective of HLA haplotype and therefore offer exciting possibilities for off-the-shelf, pan-population cancer immunotherapies” (Abstract)
Based on Legut’s teachings on the benefits of using γδ T cells for cancer immunotherapy, it would have been obvious to one of ordinary skill in the art at the time of the effective filing date to utilize γδ T cells in place of other T cells as described by Zhao with a reasonable expectation of success. An artisan would be motivated to substitute one T cell type for another as Legut teaches that γδ T cells are an appealing target due to their broad anti-tumor cytotoxicity and numerous effector functions (p. 663, 1st column; Figure 6).
However, while Zhao and Legut teach an engineered delta gamma T cell comprising a construct which comprises an antigen binding domain which is a scFV, a terminal transmembrane domain and a stalk domain, these references do not teach that the construct targets CD19 cells with an CD19 antigen binding domain.
Miller teaches that CD19 targeting CAR T cells have shown clinical utility in various leukemias (Abstract). CD19 directed CARs have been generated from scFV regions with hinge and transmembrane domains derived from CD8 or CD28 (p. 684).
Based on such teachings it would have been obvious to one of ordinary skill in the art to direct the Her2 tumor cell antigen targeting delta gamma cells of Legut and Zhao to CD19 by replacing the scFv region in the construct 4D5-28D to one which targets CD19 with an appropriate antigen binding domain with a reasonable expectation of success. An artisan would be motivated to replace one tumor cell antigen targeting scFv region for another as CD19 targeting CAR Ts have shown clinical utility in various leukemias (Abstract).
Regarding claim 2, Zhao teaches that the construct comprises a hinge domain (i.e. stalk domain) operatively linking the antigen binding domain to the terminal transmembrane domain (See 4D5-28D of figure 3).
Regarding claim 7, Zhao teaches that antigen binding domain is scFv (See 4D5-28D of figure 3A).
Regarding claim 10, Zhao teaches that the hinge domain is a CD28 hinge domain. Therefore, the hinge domain of 4D5-28D is not of the group recited in claim 10. However, Zhao teaches that in other constructs, the hinge domain and transmembrane domain is utilized from CD8 in order to create the construct (See 4D5-CD8HTZ in Figure 3). Therefore it would have been obvious to one of ordinary skill in the art to substitute equivalent hinge domains (CD8 for CD28) for the same purpose of creating a CAR for tumor recognition.
Regarding claims 12, Zhao teaches that the construct 4D5-28D is made without the intracellular domain of the transmembrane domain of CD28 (Figure 3A), therefore, less than 50% of the amino acid residues would reside intracellularly with a reasonable expectation of success.
Regarding claim 26, as Legut and Zhao make obvious claim 1, teaching each and every structural limitation of the TCR and cell comprising said TCR and there are no further structural limitations recited in these claims, the cytolysis characterizations are taught by the combination of Zhao and Legut.
Regarding claim 30 and 31, Zhao teaches that over 10 transduced PBLs (peripheral blood leukocytes) were incubated with target cells overnight or injected into tumor models (p. 5565). Therefore the population of engineered T cells is greater than 2% of the cells.
Regarding claim 34, Zhao teaches that the constructs are derived via sequences utilizing web-based codon optimization algorithms (polynucleotides) (p. 5564).
Therefore the invention would have been prima facie obvious at the time of the effective filing date.
In response to Applicant’s arguments regarding the 103 rejections over the combination of Zhao, Legut and Sallman, over claims 1-2, 6, 7, 10, 12, 23, 26, 30, 31, and 34
Applicant’s arguments filed 03/11/2026 have been considered, however they are not persuasive.
Applicant reiterates their previous arguments that Examiner has not pointed to any part of Zhao that teaches or suggests that a construct lacking an intracellular signaling domain is functional, let alone that such a construct would effectively trigger cytolysis of a tumor cell. At most, Zhao demonstrates that CAR constructs lacking an intracellular signaling domain “resulted in sustained transgene expression, similar to TCR- or control CAR-engineered cells." Zhao, page 7. Zhao does not teach or suggest that "sustained transgene expression" means that the CAR construct will be effective, or even functional.” Moreover, Applicant argues again that Zhao found constructs with 4- 1BB sequences demonstrated increased cytokine secretion and lytic activity in 4D5 CAR-transduced T cells, therefore needing the intracellular domain.
The examiner reiterates that “functional” and “effective” is relative to what function or effect is desired. As Zhao teaches CAR constructs lacking an intracellular signaling domain "resulted in sustained transgene expression, similar to TCR- or control CAR-engineered cells." The claims don't require any astounding levels of efficacy: all that is required under 103 is what KSR has told us. As the structure of Zhao’s construct 4D5-28D is identical to the claimed heterologous targeting construct of claim 1, the properties of imparted by the construct would be expected to be the same. Otherwise, the claim is not enabled. Therefore, it is showing an equivalent function or effect to that of the TCR or CAR engineered cells which express a transgene. Regarding the argument that Zhao teaches the need for the intracellular domain for cytolytic activity and increased cytokine secretion, Zhao does not teach away or disparage the usage of 4D5-28Z which lacks intracellular signaling domains as Zhao says that its function in transgene expression is that of TCR or CAR engineered cells, demonstrating it as a known alternate construct to those with intracellular signaling domains, though adding 4-1BB signaling domains maintains transgene expression and enhances effector function of 4D5 CAR-transduced PBLs (Zhao et al p.5569; col.1) . While intracellular domains of 4-1BB enhance different characteristics, this does not teach away from the utilization of a construct lacking intracellular domains. It is not the position of the Office to test other inventions for their enablement or other characteristics where the author of the cited reference has not detailed specific results. Moreover, such a characteristic could be found with a reasonable expectation of success due to the structural limitations being met.
Applicant once again reiterates that a person of ordinary skill in the art would not have been motivated to combine Zhao's 4D5-28D CAR construct with Legut's y8 T cells with a reasonable expectation of success.. Applicant additionally reiterates, “Examiner has not demonstrated that there would have been a reasonable expectation of success in modifying T cells with Zhao's CAR construct. The Examiner has not demonstrated that a skilled artisan would have had a reasonable expectation of success in modifying gamma delta T cells as they “require co-stimulatory stress molecules.”
The examiner reiterates their position. As stated in the rejection above, Legut teaches “most CAR transduction experiments have been conducted on alpha beta T cells – nevertheless, gamma delta T cells are also an appealing target, due to their broad antitumor cytotoxicity and numerous effector functions” (p. 663, 1st column; Figure 6). This provides teaching, suggestion and/or motivation to combine a CAR with a gamma delta T cell in an alternative to the other type of T cell described by Zhao. Moreover, Applicant has taken the “requirement” out of context, the Abstract states that “TCR often requires accessory/co-stimulatory stress molecules on both T cells.” This indicates that the co-stimulatory stress molecules are not aways required for function. Additionally, as evidenced by the present application, that co-stimulatory region is not required.
Applicant reiterates arguments that the specification demonstrates that engineered T cells of the amended claims unexpectedly (1) have target cell cytotoxicity comparable to cells with full-length constructs containing an intracellular domain capable of activating the cell, and (2) spare the killing of healthy cells compared to untransduced cells. These results would not have been expected in view of the cited references.
Examiner disagrees. And once again points to the reference of Boyd. At the time of the effective filing date, Boyd (WO2017088012A1) had been filed which describes non-signaling CARs. Specifically, Boyd states “while this receptor could also bind to normal cells which express lower levels of CD47, there would be no signal transduction and hence no damage to the normal cells” (para. 0071). Therefore the results of Applicant’s experiments were known at the time of the effective filing date. The comparison for unexpected results is of that of the art such as 4D5-28Z of Zhao and showing that the construct has unexpected results distinguishable from the art, not from untransduced cells as argued. Furthermore, even if the results were unexpected the construct of the claims is much broader than that of the construct utilized to obtain said unexpected results and therefore the scope of the claims would not be in commensurate with the unexpected results demonstrated.
Claim 8 remains rejected under 35 U.S.C. 103 as being unpatentable over Zhao (supra) in view of Legut (supra) and Miller (supra) as applied to claims 1 and 7 above, and in further view of Kabelitz (OncoImmunology 2:3, e23304; March 2013; previously cited).
This rejection has been modified as necessitated by Applicant’s remarks and amendment filed 03/11/2026.
Zhao, Legut and Miller teach an engineered delta gamma T cell comprising a construct which comprises an antigen binding domain, a terminal transmembrane domain and a stalk domain described in the 103 rejection above and incorporated here in its entirety.
Regarding claim 8, these references do not teach that the delta gamma t cells are Vδ2 negative and Vδ1 positive.
Kabelitz teaches that Vδ2 negative, Vδ1 positive cells positive cells have a redundancy with the antitumor activity of Vδ2 positive cells (p. 4). Vδ1 positive cells exert potent cytotoxic effects against blasts from patients with acute lymphoblastic leukemia as well as chronic leukemia cells (p. 2, last paragraph). Kabelitz further teaches that there is a “super stimulation” of Vδ1 positive cells via NKG2D (p. 3, 1st paragraph).
It would have been obvious to one of ordinary skill in the art to transduce Vδ2 negative, Vδ1 positive cells as taught by Kabelitz in place of the delta gamma cells of Legut and Zhao with a reasonable expectation of success. As Zhao and Legut are directed towards a method of targeting cancer cells via TCRs in delta gamma cells, an artisan would be motivated to transduce the Vδ2 negative, Vδ1 positive cells as Kabelitz teaches that Vδ1 positive cells exert potent cytotoxic effects against blasts from patients with acute lymphoblastic leukemia as well as chronic leukemia cells (p. 2).
Therefore the invention would have been prima facie obvious at the time of the effective filing date.
Conclusion
No claims are allowed.
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 nonprovisional extension fee (37 CFR 1.17(a)) 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 mailing date of this final action.
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/ALEXANDRA F CONNORS/ Examiner, Art Unit 1634
/MARIA G LEAVITT/Supervisory Patent Examiner, Art Unit 1634