DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 11/24/2025 has been entered.
Claims status
Claims 10, 15-18 is/are currently pending with claims 17, 18 is/are withdrawn. Claims 10, 15, 16 is/are under examination.
Incorporation by Reference – Reiterated from previous Office Action
The incorporation of essential material in the specification by reference to an unpublished U.S. application, foreign application or patent, or to a publication is improper. Applicant is required to amend the disclosure to include the material incorporated by reference, if the material is relied upon to overcome any objection, rejection, or other requirement imposed by the Office. The amendment must be accompanied by a statement executed by the applicant, or a practitioner representing the applicant, stating that the material being inserted is the material previously incorporated by reference and that the amendment contains no new matter. 37 CFR 1.57(g).
Claim Rejections - 35 USC § 112(b) – Withdrawn
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.
Rejection of Claim 16 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or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention is withdrawn in light of claim amendment.
Claim Rejections - 35 USC § 112(a) -Maintained in part
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.
Written Description
Claims 10, 15, 16 remain rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
In making a determination of whether the application complies with the written description requirement under 35 U.S.C. 112(a) or 35 U.S.C. 112, first paragraph, it is necessary to understand what Applicant is claiming and what Applicant has possession of.
Claim 10 is directed an immune cell comprising a system for the treatment of glioblastoma comprising a nucleotide sequence encoding a “binding-triggered transcriptional switch (BTTS)” that binds a myelin oligodendrocyte glycoprotein (MOG) and directly induces the expression of a nucleotide sequence encoding a tandem CAR via a transcriptional activator.
A structure for BTTS recited comprises: (i) a MOG-binding extracellular domain that has the structure of the antigen binding region of any MOG-specific antibody, (ii) a proteolytic cleavage sequence comprising one more proteolytic cleavage sites, and (iii) an intracellular domain comprising a transcription activator.
The claim embraces the antigen binding region of a MOG-binding extracellular domain that has the structure of the antigen binding region of any MOG-specific antibody.
Claims 15 and 16 embrace the same BTTS structure as claim 10 and thus do not limit it.
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. Possession may be shown in a variety of ways including description of an actual reduction to practice, or by showing that the invention was “ready for patenting” such as by the disclosure of drawings or structural chemical formulas that show that the invention was complete, or by describing distinguishing identifying characteristics sufficient to show that the applicant was in possession of the claimed invention. See, e.g., Pfaff v. Wells Eiees., Inc., 525 U.S. 55, 68, 119 S.Ct. 304, 312, 48 USPQ2d 1641,1647 (1998); Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406; Amgen, Inc. v. Chugai Pharm., 927 F. 2d 1200, 1206, 18 USPQ2d 1016, 1021 (Fed. Cir. 1991) (one must define a compound by “whatever characteristics sufficiently distinguish if). An adequate written description of a chemical invention also requires a precise definition, such as by structure, formula, chemical name, or physical properties, and not merely a wish or plan for obtaining the chemical invention claimed. See, e.g., Univ. of Rochester v. G. D. Searie & Co., 358 F.3d 916, 927, 69 USPQ2d 1886, 1894-95 (Fed. Cir. 2004). See MPEP § 2163.
Regarding MOG-binding domain, the specification only provides the structure of MOG protein in [0175] but does not provide the structure of the any MOG-binding domain. In [0360], the specification states that the “MOG M26 scFv (von Budingen et al, 2002)” is the MOG-binding domain however no structure is provided.
According to the MPEP § 2163, “The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice (see i)(A) above), reduction to drawings (see i)(B) above), or by disclosure of relevant, identifying characteristics, i.e., structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the applicant was in possession of the claimed genus (see i)(C) above). See Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406. 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.").”
Reference to “von Budingen et al, 2002” could not be considered sufficient disclosure for the structure of MOG-binding domain since, as was noted in the previous OA dated, incorporation of essential material in the specification by reference to a publication is improper. Furthermore, “von Budingen et al, 2002” could not considered proper citation. Thus, the specification fails to disclose even a single structure for the genus of structures embraced by MOG-binding domain.
The claim requires that the claimed MOG-binding domain when present in a BTTS in an immune cell allow the immune cell to function for treating glioblastoma. Even the structure of at least the epitome of MOG protein that is present in glioblastoma is not disclosed such that an appropriate antibody fragment could be envisioned.
A skilled artisan cannot readily envision the various structures of the BTTS comprised in the immune cell wherein the BTTS could comprise any MOG-binding domain.
Therefore, the claimed invention, as a whole, is not adequately described. The claims require essential or critical elements which are not adequately described in the specification, and are not conventional in the art before the effective filing date.
Scope of Enablement
Rejection of Claims 10, 15, 16 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification failed to comply with the scope of enablement requirement is withdrawn in light of amendment to claim 10 that specifically recites an intracellular domain comprising a transcription activator.
Claim Rejections - 35 USC § 103 - Maintained
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claim(s) 10, 15, 16 is/are rejected under 35 U.S.C. 103 as being unpatentable over Lim et al (WO 2017 /193059 A1, Publication date 11/9/2017; ref of record), and further in view of Hegde et al (J Clin Invest. 2016;126(8):3036–3052; ref of record).
Regarding claims 10, Lim discloses immune cells modified to produce antigen-triggered polypeptides recognizing a cell surface antigen (=BTTS) for use in a method of killing a target cancer cells such as glioblastoma (Abstract, 0046). In some embodiments, the immune cell comprises nucleic acids encoding a synNotch receptor (=BTTS) and a TCR or CAR-based antigen-specific therapeutic (= element (b) in part).
Lim discloses synNotch receptors comprise an antigen-binding extracellular domain and discloses MOG as an antigen (=BTTS, element (a)(i)) [0061, 00434-437]. Lim further discloses synNotch receptors comprise proteolytic cleavage sites and an intracellular domain comprising a transcriptional activator (BTTS, element (a)(ii, iii))[0061]. Lim discloses that synNotch receptors undergo proteolytic cleavage upon antigen binding that releases the gene expression regulator from the intracellular domain that activates the regulatory sequence ([0060-0069], ([0044], Figure 3A, Figure 5).
Regarding claim 15 and 16, Lim discloses T-cells, B- cells and NK-cells, including cytotoxic T-cells as immune cells [0024-0025].
Therefore, Lim teaches an immune cell which comprises sequences encoding a BTTS and CAR such that BTTS-induces CAR expression.
Although, Lim discloses EphA2 and IL13RA2 as a target antigens for cancer (Table 3, Figure 4, [339]), Lim does not teach a CAR that binds these two target antigens simultaneously.
Hedge teaches a tandem CAR that binds two cancer-specific antigens simultaneously (Figure 2A). Hegde exemplify their tandem CAR design and evaluate its efficacy by generating a tandem CAR that targets two glioblastoma antigens HER2/IL13Ra2 (Figure 2, Figure 9; as required by claim 24). Although Hegde use the HER2/IL13Ra2 combination for their tandem CAR, Hedge teach that “A mathematical model of the expression hierarchy of 3 validated glioma antigens (21, 25–28), HER2, IL13Rα2, and EphA2, predicted enhanced odds of tumor elimination on targeting of any 2 of these 3 antigens” (emphasis added; Introduction, para 2).
Therefore, it would be obvious to a person of ordinary skill in the art to modify the immune cell of Lim to comprise a tandem CAR that targets two tumor-specific antigens simultaneously such as EphA2 and IL13Ra2 as taught by Hegde. An ordinary artisan would be motivated to include a tandem CAR as taught by Hegde in Lim’s immune cell because Hegde teaches that a tandem CAR has much higher potency than a single-target CAR (see increased cytokine released in Figure 3B C, increased detection range for tumor antigens in Figure 4, reduced T-cell exhaustion in Figure 5 and improved in vivo efficacy in Figure 9). An ordinary artisan would reasonably produce an immune cell comprising a tandem CAR because Hegde teaches the method to produce a tandem CAR (Construction, delivery, and expression of the TanCAR-encoding transgene).
Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in
the art at the effective time of filing of the invention, especially in the absence of evidence to the
contrary.
Claim(s) 10, 15, 16 is/are rejected under 35 U.S.C. 103 as being unpatentable over Roybal et al (Cell, Vol. 164, 2016; ref of record) in view of Peschl et al (Front. Immunol. 8:529, 2017; ref of record) and Hegde et al (J Clin Invest. 2016;126(8):3036–3052; ref of record).
Regarding claims 10, Roybal teaches an immune cell comprising a nucleic acid sequence encoding a synNotch receptor (=BTTS) and a nucleic acid sequence encoding a CAR, wherein antigen binding to the synNotch receptor induces expression of CAR (= element (b) in part; Figure 1D, Experimental procedures: SynNotch Receptor and Response Element Construct Design, Generation of SynNotch AND-Gate Jurkat T Cells).
Roybal teaches the structure of synNotch receptor to comprise an antigen-binding extracellular domain, a proteolytic cleavage domain and intracellular transcription activator wherein antigen binding releases the transcription activator that induces the expression of CAR (=BTTS; elements (a) (i in part, ii-iii completely); Introduction, para 3; Figure 1C; SynNotch Receptor and Response Element Construct Design).
Regarding claims 15 and 16, Roybal teaches T cells as immune cells that are CD8+ are result in lysis of tumor cells i.e. are cytotoxic (Generation of SynNotch AND-Gate Jurkat T Cells, In Vitro Stimulation of SynNotch T cells).
Roybal exemplifies the use of their synNotch and CAR-based circuits using a GFP or CD19 antigen for the synNotch receptor and CD19 or mesothelin cancer “killing” antigens for the CAR (Figure 2, 4).
Roybal does not teach MOG as a synNotch antigen or a tandem-CAR that recognizes EphA2 and IL13RA2.
Peschl teaches MOG as a highly conserved protein that is exclusively present in the brain (page 2, para 1, line 8).
Hedge teaches a tandem CAR that binds two tumor-specific antigens simultaneously (Figure 2A). Hegde exemplify their tandem CAR design and evaluate its efficacy by generating a tandem CAR that targets two glioblastoma antigens HER2/IL13Ra2 (Figure 2, Figure 9; as required by claims 21 and 24). Although Hegde use the HER2/IL13Ra2 combination for their tandem CAR, Hedge teach that “A mathematical model of the expression hierarchy of 3 validated glioma antigens (21, 25–28), HER2, IL13Rα2, and EphA2, predicted enhanced odds of tumor elimination on targeting of any 2 of these 3 antigens” (emphasis added; Introduction, para 2).
Therefore, it would be obvious to a person of ordinary skill in the art to combine the teachings of Roybal, Peschl and Hegde to generate an immune cell that comprise a SynNotch (as taught by Roybal) that is triggered by a CNS specific MOG protein (as taught by Peschl) to induce the expression of a tandem CAR targeting EphA2 and IL13RA2 (as taught by Hegde).
An ordinary artisan would be motivated to make such modifications because it would allow for more precise targeting of brain cancers such as glioblastoma by CAR-T cells that comprise the MOG-activated SynNotch receptor. Roybal teaches that their system that comprises dual antigen sensing is more sensitive to target cancer cells since it requires recognition of two antigens and can be used to target particular tissues using tissue-specific normal antigens (Section: The Discriminatory Power of Dual Antigen Sensing SynNotch/CAR Circuits in Therapeutic T Cells, Section: SynNotch Receptors Increase the Landscape of Targetable Antigens for T Cell Therapies, Figure 6). Furthermore, an ordinary artisan would be motivated to include a tandem CAR as taught by Hegde to target glioblastomas because Hegde teaches that a tandem CAR has much higher potency than a single-target CAR and teach that IL13Rα2, and EphA2 are two out of 3 antigens that are predicted to have enhanced odds of tumor elimination (see increased cytokine released in Figure 3B C, increased detection range for tumor antigens in Figure 4, reduced T-cell exhaustion in Figure 5 and improved in vivo efficacy in Figure 9).
An ordinary artisan would reasonably expect to generate such a modification because Roybal teaches the method to generate SynNotch receptors that comprise an antigen-specific antibody fragment fused to Notch1 and transcription factor (Methods: SynNotch Receptor and Response Element Construct Design), Peschl teaches MOG antibodies (page 2, right column, para 2; Table 1) and Hegde teaches the method to produce a tandem CAR (Construction, delivery, and expression of the TanCAR-encoding transgene) which can be combined using routine methods.
Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in
the art at the effective time of filing of the invention, especially in the absence of evidence to the
contrary.
Response to Arguments
Applicant's arguments filed 11/24/2025 regarding the U.S.C.112a – Written Description rejection of claims 10, 15, 16 have been fully considered. Claim 10 is amended to resolve one of the Written Description issues raised, specifically pertaining to the breadth of structure of intracellular domain and lack of support. However, issue regarding the continued lack of support for “the MOG-binding extracellular domain that has the structure of the antigen binding domain of any MOG-specific antibody” remains.
Applicant argue that “the claims are not limited to the domain described by van Budingen. Instead, the claims are directed to an immune cell for the treatment of glioblastoma that makes use of a MOG antigen. In other words, the invention of the present claims can be performed using binding domains that bind to MOG other than the van Budingen binding domain and thus there is no reason to limit the present claims to a single sequence. Applicant respectfully notes that there are thousands of granted U.S. claims in this field that refer to antigens generically, without specifying a sequence. For consistency of examination, this rejection may be withdrawn.” (page 4-5, bridging para; page 5, para 1).
In response, the discussion pertaining to van Budingen is not assert that the claims are limited to a domain described in that reference but that the only structure that specification provides for “the MOG-binding extracellular domain that has the structure of the antigen binding domain of any MOG-specific antibody” is by improperly referencing van Budingen. Even the citation for this reference is incomplete. A skilled artisan cannot envision the structure of the claimed MOG-binding domain that was used in the specification and examples disclosed therein. Thus, the specification lacks written description support for this claim element.
MPEP 2163 (I) guides that “The written description requirement has several policy objectives. "[T]he ‘essential goal’ of the description of the invention requirement is to clearly convey the information that an applicant [inventor] has invented the subject matter which is claimed." In re Barker, 559 F.2d 588, 592 n.4, 194 USPQ 470, 473 n.4 (CCPA 1977). Another objective is to convey to the public what the applicant claims as the invention. See Regents of the Univ. of Cal. v. Eli Lilly, 119 F.3d 1559, 1566, 43 USPQ2d 1398, 1404 (Fed. Cir. 1997), cert. denied, 523 U.S. 1089 (1998). "The ‘written description’ requirement implements the principle that a patent must describe the technology that is sought to be patented; the requirement serves both to satisfy the inventor’s obligation to disclose the technologic knowledge upon which the patent is based, and to demonstrate that the patentee [inventor] was in possession of the invention that is claimed." Capon v. Eshhar, 418 F.3d 1349, 1357, 76 USPQ2d 1078, 1084 (Fed. Cir. 2005). Further, the written description requirement promotes the progress of the useful arts by ensuring that patentees adequately describe their inventions in their patent specifications in exchange for the right to exclude others from practicing the invention for the duration of the patent’s term”. (emphasis added)
Regarding claim language in other patents in the field, the rejection is a written description issue and it is unclear how this argument is pertinent to the rejection of record.
Applicant's arguments filed 11/24/2025 regarding the U.S.C.103 rejection of claims 10, 15, 16 as unpatentable over Lim in view of Hegde have been fully considered but they are not persuasive.
Applicant argue that “the claimed method is contrary to accepted wisdom in the field and is thus non-obvious.” (page 5, para 6). Applicant allege that “the prevailing wisdom at that time was that: (a) glioblastoma (GBM) is extremely difficult to treat, and (b) the path to a successful chimeric antigen receptor (CAR) based treatment for GBM was through better tumor antigens” (page 6, para 1). In support, Applicant point to Jarboe as allegedly showing that GBM is extremely difficult to treat (page 6-7, bridging para), and point to Razpotnik, Johnson, Choi, Watanabe, Mao, Akhavan, Nehama, and Nakagawa as allegedly suggesting that researchers in the field were only focused on finding cancer antigens (pages 7-8). Applicant state that “The
present invention (to the extent that it is claimed here), on the other hand, went fully against the grain of the conventional wisdom because the immune cell recited in the claims targets an antigen (i.e., MOG) that is tissue-specifically expressed in the brain. These markers are not associated with GBM. Rather, they are expressed in non-malignant cells, even in the brains of subjects that do not have GBM. As such, they cannot be thought of as tumor antigens. This is unconventional thinking (particularly against others that thought that better tumor antigens were required)”.
In response, at first it must be noted that the claims are not directed to a method but a product.
Further, Lim teaches this “unconventional thinking” (see the image of text from Lim below; [434-436]). Lim describe an immune cell that is modified to target not only a cancer but also non-target cell such as from normal brain tissue. Next para [437] identifies MOG as a normal brain tissue antigen. Thus, Lim taught an artisan to focus on non-cancer cells for targeting the immune cells.
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Regarding Hegde, applicant argue that “Hegde, as cited in this rejection, echoes this same conventional wisdom of targeting GBM-specific antigens. Specifically, Hegde's treatment is focused on identifying better tumor antigens” (page 9, para 3).
In response, Hegde teaches the tandem CAR recited in the claim. The limitations pertaining to MOG-targeting BTTS in an immune cell were provided by Lim. Of note, identification of better tumor antigens remains a requirement for even the claimed invention despite use of a different gating strategy (i.e. targeting normal cells, such as taught by Lim). This is because even the claimed invention still continues to require a means to target the malignant cells.
Applicant point to discussion pertaining to Choe and Hegde in the response to arguments presented in OA dated 9/29/2025 and allege that “Therefore, contrary to the Office's assertion that enhanced tumor elimination was expected based on the gating schemes of Hegde, Hegde is completely focused on targeting two tumor associated antigens (TAAs). Accordingly, there is no teaching or suggestion in Hegde of using an antigen universally present in a tissue, e.g., a tissue-specific antigen expressed by cells throughout the central nervous system” (page 10, para 3).
In response, first, the discussion in the OA dated 9/29/2025 regarding comparison of Choe and Hegde did note that “enhanced tumor elimination was expected based on teachings of Hegde regarding tandem CARs and specifically regarding the 3 specific antigens taught by them (Introduction, para 2 and 3; Figure 3, 9).” No evidence against this expectation is presented.
Second, as noted above, Hegde teaches the tandem CAR recited in the claim and is not relied upon for targeting MOG.
Applicant's arguments filed 11/24/2025 regarding the U.S.C.103 rejection of claims 10, 15, 16 as unpatentable over Roybal in view of Peschl and Hegde have been fully considered but they are not persuasive.
Applicant reiterate the argument from before that “the claimed method is contrary to accepted wisdom in the field and is thus non-obvious.”
This argument was unpersuasive (see detailed response above).
Regarding Roybal, Applicant argue that “Moreover, and to the extent that any further discussion is necessary, one of ordinary skill in the art when attempting to modify Roybal's disclosure in a way that would comport with the present claims would have also realized that the present MOG antigen must be expressed by 'normal' (i.e., non-malignant) cells in the brain and, as such, in some cases the therapeutic cells may prime on one cell (a normal cell) and kill another (a malignant cell). This is what is referred to as killing 'in trans'. However, Roybal tested the ability of therapeutic cells to do just that in a bilateral tumor model and concluded that "Thus, there appears to be no evidence for priming of the AND gate T cells and subsequent killing of bystander ... cells elsewhere" (Roybal, page 6, second paragraph; wherein the term "CD19" has been replaced by the Applicant by" ... " to remove unnecessary details). Given Roybal's comment, which essentially says that, based on the data, there is "no evidence" that an AND gated therapeutic cell can prime on one cell and kill another, one would be led directly away from the present method.” (page 11, para 3).
In response, it is unclear how this data teaches away from instantly claimed immune cell (not method!). Roybal state the following as a rationale for their experiment “An important concern was whether the AND-gate T cells could engage a tumor expressing the synNotch ligand (GFP), become primed by expressing the a-CD19 CAR, and then migrate elsewhere to then kill single antigen (CD19+ only) bystander tissues” (page 774, para 2). Roybal confirm that indeed AND-gate T cells do not kill cells in bystander tissue and remain restricted to their cancer microenvironment. This is promising result to an ordinary artisan because it suggests that MOG-primed GBM targeting immune cell would remain active only in the MOG-expressing microenvironment and would be unable to target non-GBM bystander cells that happen to express the cancer antigen in other tissue since those would not express MOG. As noted in the rejection, Peschl teaches that MOG is highly brain specific.
Conclusion
No claim is allowed.
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/MATASHA DHAR/Examiner, Art Unit 1632
Prosecution Insights