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 .
Election/Restrictions
Applicant’s election without traverse of Group I (claims 1, 3, 9-18, and 20-22) in the reply filed on April 27, 2026 is acknowledged. Claims 3-8 and 19 are cancelled.
Applicant’s election without traverse of Species Group A: ADA2B genetic subunit of the SAGA gene regulation complex, and Species Group B: an inhibitor comprising a CRISPR-Cas system and guide RNA in the reply filed on April 27, 2026 is acknowledged. However, following a search of the prior art, the Species Group A election requirement is withdrawn.
Claims 12-13 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected species, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on April 27, 2026.
Accordingly, claims 1, 9-11, 14-18, and 20-22 are examined herein.
Priority
Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged. Applicant has not complied with one or more conditions for receiving the benefit of an earlier filing date under 35 U.S.C. 119(e) as follows:
The later-filed application must be an application for a patent for an invention which is also disclosed in the prior application (the parent or original nonprovisional application or provisional application). The disclosure of the invention in the parent application and in the later-filed application must be sufficient to comply with the requirements of 35 U.S.C. 112(a) or the first paragraph of pre-AIA 35 U.S.C. 112, except for the best mode requirement. See Transco Products, Inc. v. Performance Contracting, Inc., 38 F.3d 551, 32 USPQ2d 1077 (Fed. Cir. 1994).
The disclosure of the prior-filed application, Application No. 63/006,455 (filed on April 07, 2020), provides adequate support or enablement in the manner provided by 35 U.S.C. 112(a) or pre-AIA 35 U.S.C. 112, first paragraph for one or more claims of this application: instant claim 1 (claim 8), instant claim 9 (claim 3), instant claim 10 (claim 4), instant claim 14 (claim 7). However, this Application fails to disclose T cells comprising a Chimeric Antigen Receptor recited in instant claims 11, 15, 16, 18, and 20-22.
Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55. Adequate support for claims 11, 15, 16, 18, and 20-22 are found in International Patent Application PCT/ CA2021/050464, filed on April 07, 2021.
Accordingly, claims 1, 9, 10, and 14 have an effective filling date of April 07, 2020. Claims 11, 15, 16, 18, and 20-22 have an effective filling date of April 07, 2021.
Specification
The disclosure is objected to because it contains an embedded hyperlink (pg. 10, line 18) and/or other form of browser-executable code. Applicant is required to delete the embedded hyperlink and/or other form of browser-executable code; references to websites should be limited to the top-level domain name without any prefix such as http:// or other browser-executable code. See MPEP § 608.01.
Drawings
The drawings are objected to because 37 CFR 1.84 (u)(1) states “Partial views intended to form one complete view, on one or several sheets, must be identified by the same number followed by a capital letter.” In the current case, the view numbers for the partial views for Figure 6F that appear on several sheets are followed by "Cont." instead of a capital letter such as FIG. 1A, FIG. 1B, etc.
Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. 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). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Claim Objections
Claims 15, 18, and 22 are objected to because of the following informalities:
In claim 15, line 2, the acronym “CAR” is defined as being “Chimeric Antigen Receptor”. However, the acronym has previously been defined in claim 11. An acronym should only be defined the first time it appears in an independent claim or in the group of claims under an independent claim;
Appropriate correction is required.
Applicant is advised that should claim 18 be found allowable, claim 22 will be objected to under 37 CFR 1.75 as being a substantial duplicate thereof. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m). The scope of claim 18 is directed to activated CD8+ T cells that express a chimeric antigen receptor, wherein the expression or function of one or more subunits of a SAGA gene regulation complex is inhibited, and wherein the genetic subunits are selected from the group… The scope of claim 22 is also directed to activated CD8+ T cells that comprises the recited limitations of claim 15, which are the same recited limitations in claim 18. Therefore, claims 18 and 22 recite the same scope.
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.
Claim 1, 9-11, 14-18, and 20-22 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.
The following claims have insufficient antecedent basis for the recited limitation in the claim:
Claim 1: "the SAGA gene regulation complex" in line 2
Claim 10: "the activity" in line 1
Claim 15: "the SAGA gene regulation complex" in line 2
Claim 20: "the activity" in line 1
Claim 21: "the inhibitor" in line 1
Those claims included in the statement of rejection but not otherwise discussed are rejected for depending from a rejected claim but failing to remedy the indefiniteness therein.
Claim Rejections - 35 USC § 112
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, 9-11, 15-18, 20, and 22 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 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.
MPEP 2163.II.A.3.(a).i) states, “Whether the specification shows that applicant was in possession of the claimed invention is not a single, simple determination, but rather is a factual determination reached by considering a number of factors. Factors to be considered in determining whether there is sufficient evidence of possession include the level of skill and knowledge in the art, partial structure, physical and/or chemical properties, functional characteristics alone or coupled with a known or disclosed correlation between structure and function, and the method of making the claimed invention”.
In making a determination of whether the application complies with the written description requirement of 35 U.S.C. 112, first paragraph, it is necessary to understand what Applicant has possession of and what Applicant is claiming. Claims 1 and 15 are directed to modified T cells wherein i) the expression or function of the SAGA (spt-Ada-Gcn5-acetyltransferase) gene regulation complex is inhibited, or ii) wherein the one or more genetic subunits of the SAGA complex is inhibited. The breadth of the claims is drawn to possession of a genus of inhibitor that i) directly inhibit the expression of the whole SAGA complex of one of its subunits, ii) has upstream or downstream effects on the expression of whole SAGA complex of one of its subunits, iii) directly or indirectly inhibit the function of the whole SAGA complex of one of its subunits.
The specification discloses actual reduction to practice of CRISPR-Cas9 system wherein the guide RNA is designed to directly target one or more genetic subunits of the SAGA complex including ADA2B, CCDC101, TADA1, TAFSL, TAF6L, TAFl0, SUPT7L, and TRAAP (Example 1 and 3). The specification further discloses a few species of small molecule inhibitors including: GSK4027 and L-Moses inhibitor (inhibitors of KAT2A), trichostatin A, pirarubicin have been reported to affect USP22 expression in cancer cells (pg. 13, lines 5-8). The specification fails to disclose additional species that are representative to the claimed genus. Disclosing species that directly inhibit one of 19 subunits of the SAGA complex and species that directly inhibit transcription of SAGA’s subunits via CRISPR-Cas system do not represent the entire claimed genus that encompass much broader species (see statement above regarding the breath of the claims). The specification fails to disclose identifying characteristics of additional inhibitors that indirectly inhibit the expression or function of the whole SAGA complex or SAGA subunits. MPEP 2163 states “describing a composition by its function alone typically will not suffice to sufficiently describe the composition”. See Eli Lilly, 119 F.3 at 1568, 43 USPQ2d at 1406.
Further, the specification discloses “methods of confirming the activity of small molecule inhibitors will be known to persons of skill in the art…in particular, the methodology shown in Figures 6 and 7…may be followed” (pg. 13, lines 8-11). Figures 6 and 7 do not provide precise definition of the small inhibitors, instead the figures show an illustrative workflow of CRISPR screen and sorting for T cells post gene knockout. “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. Searle & Co., 358 F.3d 916, 927, 69 USPQ2d 1886, 1894-95 (Fed. Cir. 2004)(see MPEP 2163 (II)(A)(3)(a)).
It is unknown in the art and not discussed in the disclosure regarding small molecule inhibitors that target any of the recited genetic subunits, or any inhibitors that have upstream or downstream effect on the function of the SAGA complex. Kassem et al (Not5-dependent co-translational assembly of Ada2 and Spt20 is essential for functional integrity of SAGA; NAR, 2016, 45(3): 1186-1199) teaches the SAGA complex participates in various transcriptional programs including binding to transcriptional activators, facilitating the assembly of the pre-initiation complex, interacting with the TATA binding protein TBP, and sharing a subunit with mRNA export complex TREX2 (pg. 1186, paragraph bridging col. 1 and 2). Kassem et al further demonstrates that Not2 of the Ccr4-Not complex associates with Ada2 subunit of the SAGA complex (pg. 1187, col. 1, para. 2), “GCN5, SPT20 and ADA2 mRNAs are tethered together and Not5 is important to retain Ada2 at this site of Spt20 production…allow[ing] correct SAGA assembly” (pg. 1187, col. 2, para. 2), and Not1 and Tdh3 are also needed for SAGA assembly (pg. 1195, col. 1-2). Therefore, prior art teaches the SAGA complex is connected to a vast number of transcriptional and translational complexes, and accordingly, the recited genus of inhibitors comprises a significant large number of undisclosed species including those that target complexes involved in SAGA assembly.
On the other hand, dependent claims 14 and 21 narrow the scope of the genus to CRISPR-Cas9 system which is well-known in the art to inhibit expression of proteins via silencing transcription of known genetic sequences. Therefore, dependent claims 14 and 21 remedy the lack of written description therein.
Based on the preponderance of the evidence, including the relevant teachings of the specification, the absence of working examples, and the state of prior art including the knowledge of the SAGA complex, one skilled in the art would conclude that Applicant was not in possession of the claimed genus of inhibitors encompassed by the breath of the claims.
Claims 1, 9, 10, 14, and 17 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for a method of using CRISPR-Cas9 system to inhibit expression of one or more genetic subunits (ADA2B, CCDC101, TADA1, TAFSL, TAF6L, TAFl0, SUPT7L, and TRAAP) of the SAGA complex, does not reasonably provide enablement for a method for increasing T cell effector function in a T cell population wherein the expression or function of i) the SAGA complex, or ii) one or more genetic subunits of the SAGA complex. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the invention commensurate in scope with these claims.
The test of enablement is whether one skilled in the art could make and use the claimed invention from the disclosures in the specification coupled with information known in the art without undue experimentation (United States v. Telectronics., 8 USPQ2d 1217 (Fed. Cir. 1988)). Whether undue experimentation is needed is not based upon a single factor but rather is a conclusion reached by weighing many factors. These factors were outlined in Ex parte Forman, 230 USPQ 546 (Bd. Pat. App. & Inter. 1986) and again in In re Wands, 8 USPQ2d 1400 (Fed. Cir. 1988), and the most relevant factors are indicated below:
Nature of the Invention and Breadth of the Claims
Claims 1, 9, 10, 14, and 17 are directed to a method for increasing T cell effector function in a T cell population by inhibiting the expression or function of i) the SAGA complex, or ii) one or more genetic subunits (ADA2B, CCDC101, TADA1, TAFSL, TAF6L, TAFl0, SUPT7L, and TRAAP) of the SAGA complex. The specification refers “increasing” to enhancing the ability of a T cell population to recognize and/or have increased cytotoxic effect against a target cell, which may include increasing the proliferation of a T cell population, increasing the expression and/or excretion of cytotoxic molecules” (pg. 10, lines 26-30). Accordingly, the breadth of the claims covers a method to engineer T cell populations that recognize and/or have increased cytotoxic effect against a target cell through inhibition of the expression or function of i) the entire SAGA complex or ii) one or more genetic subunits including ADA2B, CCDC101, TADA1, TAFSL, TAF6L, TAFl0, SUPT7L, and TRAAP.
Guidance of the Specification
The specification teaches that activated CD8+ T cells kill target cells through degranulation-mediated delivery granzyme B and perforin at the immunological synapses between the T cell and target cell, and that actively degranulating CD8+ T cells can be identified through staining of a cell surface marker CD107a (pg. 18; Example 3). The specification further teaches CRISPR-Cas9-based screening in activated CD8+ T cells identified genes that regulate CD8+ T cells’ degranulation activity, and these genes include including “TADA2B and CCDC101 (HAT module) and TADA1, TAF5L, TAF6L, TAF10, and SUPT7L (core structure module), and TRRAP (TF binding module) among the negative regulators of CD8+ T cell degranulation” (pg. 18-19; Example 3). In addition, the specification teaches NY-ESO-1-specific CD8+ T cells with USP22 gene knockout was effective at killing target NY-ESO-1+ melanoma cell line A375 (pg. 19; Example 4).
Although Example 3 teaches that CRISPR-mediated disruption of recited genetic subunits of the SAGA complex correlates with increased CD107a degranulation in screened CD8+ T cells and Example 4 demonstrates gene knockout of USP22 was effective at killing target cell, the specification does not reasonably enable a broad method of increasing T cell effector function through inhibition of SAGA subunits other than USP22, which is not recited in claims. Further, the specification fails to support the breadth of the claims: i) whether inhibition of the entire SAGA complex, or ii) whether inhibition of any one of the genetic subunits identified ((TADA2B, CCDC101, TADA1, TAF5L, TAF6L, TAF10, SUPT7L, and TRRAP) will successfully increases T cell effector function as required in claims. In addition, CD107a staining represents one marker associated with degranulation and does not establish that all aspects of effector function are “increased”, including proliferation, cytotoxicity against a target cell, and cytokine excretion which are guidance to determine whether a T cell population has “increased” effector function (pg. 10, lines 26-30).
State of the Art
At the time of the filling, the state of the art teaches the SAGA is a transcription coactivator complex involved in histone acetylation of chromatin and inducible gene expression. Wang et al (Structure of the transcription coactivator SAGA; Nature, 2020, 577: 717-720) teach SAGA complex contains 19 subunits, distributed over four modules as matching to genetic subunits recited in claims: i) HAT module (TADA2B, CCDC101), ii) DUB module, iii) Core module (TAF5L, TAF6L, TAF10, SUPT7L), and iv) Tra1 module (TRRAP) (Extended Data Table 3). Wang et al further teach each module of the SAGA complex perform mechanistically distinct roles including i) histone acetylation, ii) histone deubiquitination, iii) recruitment of TATA box-binding protein, and iv) activator binding (abstract; pg. 717, col. 1, para. 1). Gao et al further teach each of the recited genetic subunit plays crucial role in maintaining each module’s architecture, for instance, the core module contains a histone octamer-like fold that comprises TAF6L-TAF9, and TAF10L-SUPT7L pairs, the TAF5L connects this octamer-like fold to the core module, incorporation of TADA2B into the octamer-like fold may trigger assembly of the SAGA complex, and the core module tethers the TRRAP subunit (pg. 717, col. 2, para. 1-3; pg. 719, col.1, para. 1-2). In addition, Setiaputra et al (Conformational Flexibility and Subunit Arrangement of the Modular Yeast Spt-Ada-Gcn5 Acetyltransferase Complex; J. Biol. Chem., 2015, 290(16): 10057–10070) positively teach that all genetic subunits of the SAGA complex are interconnected (Figure 5 shown below). Setiaputra et al “identified 78 unique intersubunit and 185 unique intrasubunit cross-links” within the subunits (pg. 10065, col. 1, para. 2). Setiaputra et al further teach ADA2B is essential for structural integrity of the SAGA complex, especially in attaching the HAT module, and TRRAP as the largest subunit is responsible for recruit of the SAGA complex to its target genes (pg. 10061, col. 2, para. 2; pg. 10063, col. 2, para. 2).
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At the time of the filling, no prior art teaches or suggests inhibition of one or more genetic subunits (ADA2B, CCDC101, TADA1, TAFSL, TAF6L, TAFl0, SUPT7L, and TRAAP) could increase T cell effector function. On the other hand, the state of the art demonstrates deletion of GCN5, the catalytic core of the SAGA complex, impairs T cell activation rather than increase T cell effector function. Gao et al (The Histone Acetyltransferase Gcn5 Positively Regulates T Cell Activation; The Journal of Immunology, 2017, 198(10):3927–3938) demonstrate that deletion of GCN5, the catalytic subunit of the SAGA complex, in T lymphocytes impairs T cell activation, T cell differentiation, T cell proliferation and cytokine production (pg. 3929, col. 1, para. 2; pg. 3932, col. 1, para. 1; Fig. 1L and 1N; Fig. 4E and 4F). Gao et al further teach that disruption of GCN5 resulted in “a dramatic reduction in the expression of the lineage-specific transcription factor for Th1, T-bet, and Th17, ROR-γT” (pg. 3937, col. 2, para. 2). In addition, Gao et al teach that “although Gcn5 gene deletion did not affect CD4 T cell homeostasis proliferation, Gcn5 is indispensable for CD8 T cell homeostasis and/or survival” (pg. 3929, col. 2, para. 1), which positively suggests that inhibition of one or more genetic subunits of the SAGA complex in T cell is unpredictable because the consequences vary depending on T cell genotype and phenotype.
Considering teachings of the structure and interconnectivity between the subunits of the SAGA complex, it is highly unpredictable that deleting GCN5 impairs T cell function while inhibiting other subunits would offer the complete opposite as recited in claims.
It is after the filling date that Long et al (CRISPR screens unveil signal hubs for nutrient licensing of T cell immunity; Nature, 2021, 600: 308-313) demonstrates specific deletion of CCDC101 in regulatory T cells “increased TCR-induced mTORC1 activity…indicating that the SAGA complex has an inhibitory role in TCR-and nutrient-induced activation of mTORC1” (pg. 311, col. 1, para. 2). Long et al further teach deletion of CCDC101 reduced CD8+ T cells in the spleen, but not CD4+ T cells (pg. 312, col. 1, para. 3), which positively support teachings of Gao et al that inhibition of SAGA subunits in T cells is unpredictable, evidenced by deletion of GCN5 affected CD8+ T cells survival but not CD4+ T cells (pg. 3929, col. 2, para. 1). Further, Long et al teach deletion of CCDC101 increased effector-memory populations and IL-2+ and IFNγ+ cells (Fig. 5a; pg. 312, col. 2, para. 4), as opposed to Gao et al wherein deletion of GCN5 impaired production of IL-2, and T cell proliferation in GCN5-null T cells is independent of IL-2 (pg. 3929, col. 1, para. 3). These findings positively support that inhibition of SAGA subunits in T cells is unpredictable because inhibition of each subunit yields different outcomes.
Experimentation Required
In order to practice the claimed invention, a person ordinary skill in the art would need to conduct substantial and unpredictable experimentation to determine inhibition of which exact genetic subunit(s) can result in T cells with increased effector function, to determine which exact function was “increased”, and to determine whether the result is consistent across T cell types.
Taking into consideration the factors outlined above, including the nature of the invention, the breadth of the claims, the state of the art, the guidance provided by the applicant and the specific examples, it is the conclusion that an unreasonable amount experimentation would be required to make and use the invention as claimed. Therefore, claims 1, 9, 10, 14, and 17 are not considered to be enabled by the instant disclosure.
Claims 11, 15-16, 18, and 20-22 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 enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
The test of enablement is whether one skilled in the art could make and use the claimed invention from the disclosures in the specification coupled with information known in the art without undue experimentation (United States v. Telectronics., 8 USPQ2d 1217 (Fed. Cir. 1988)). Whether undue experimentation is needed is not based upon a single factor but rather is a conclusion reached by weighing many factors. These factors were outlined in Ex parte Forman, 230 USPQ 546 (Bd. Pat. App. & Inter. 1986) and again in In re Wands, 8 USPQ2d 1400 (Fed. Cir. 1988), and the most relevant factors are indicated below:
Nature of the Invention and Breadth of the Claims
Claims 11, 15-16, 18, and 20-22 are directed to modified T cells that express chimeric antigen receptor (CAR-T cells) wherein the expression or function of one or more subunits (ADA2B, CCDC101, TADA1, TAFSL, TAF6L, TAFl0, SUPT7L, and TRAAP) of the SAGA gene regulation complex is inhibited.
Guidance of the Specification
The specification discloses “this invention may be used in combination with other cell therapy…CAR-T cells” (pg. 15, lines 21-23). However, this general statement does not provide specific guidance for one ordinary skill in the art to make and/or use the invention. The specification does not teach working examples of CAR-T cells, does not evaluate activity, exhaustion, expansion, or manufacturing of modified CAR-T cells while the expression of function of one or more genetic subunits of the SAGA complex is inhibited.
State of the Art
As discussed above and applied to claims 1, 9, 10, 14, and 17, Wang et al teach the SAGA complex contains 19 subunits divided into four modules, each performing mechanistically distinct and noninterchangeable roles. Setiaputra et al further teach all genetic subunits of the SAGA complex are highly interconnected. Gao et al and Long et al further demonstrate that deletion of one of the genetic subunits in T cells produce divergent and opposite outcomes, including decreased IL-2 production, impaired proliferation, lineage-specific survival differences between CD4+ and CD8+ T cells. Accordingly, the state of the art does not support a reasonable expectation that inhibition of one genetic subunit would predictably result in similar outcomes from inhibition of another subunit. This unpredictability further amplifies in CAR-T cells. At the time of the filling, the state of the art lacked successful examples of modified CAR-T cells engineered through inhibition of SAGA subunits, or modified CAR-T cells with expression or function of SAGA subunits inhibited.
Experimentation Required
In order to practice the claimed invention, a person ordinary skill in the art would need to conduct substantial and unpredictable experimentation to determine inhibition of which exact genetic subunits of the SAGA complex would result in functional CAR-T cells, and to determine any type of T cells can be modified to be a CAR-T cells with the recited inhibition.
Taking into consideration the factors outlined above, including the nature of the invention, the breadth of the claims, the state of the art, the guidance provided by the applicant and the specific examples, it is the conclusion that an unreasonable amount experimentation would be required to make and use the invention as claimed. Therefore, claims 11, 15-16, 18, and 20-22 are not considered to be enabled by the instant disclosure.
Double Patenting
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 filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual 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/apply/applying-online/eterminal-disclaimer.
Claims 1, 9, 11, and 15-17 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 5, and 6 of copending Application No. 18/699,121 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the method of ‘121 is directed to administering the product of the instant application.
Regarding instant claims 1 and 17, ‘121 teaches a population of modified immune cells having decreased expression (i.e., wherein the expression or function is inhibited) of one or more components of the SAGA (Spt-Ada-Gcn5-acetyltransferase) complex (claim 1).
Regarding instant claim 9, ‘121 teaches wherein the T cells are activated CD8+ T cells (claim 5)
Regarding instant claims 11, 15, and 16, ‘121 teaches wherein the modified immune cells expresses a chimeric antigen receptor and have decreased expression of one or more components of the SAGA complex (claim 6).
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
No claims are allowable.
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Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
QIWEN SU-TOBON
Examiner
Art Unit 1636
/NEIL P HAMMELL/Supervisory Patent Examiner, Art Unit 1636
Prosecution Insights