DETAILED ACTION
1. The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
2. Applicant’s election of claims 1-32 and 37 (group I), drawn to compositions and kits comprising a cell expressing an antigen-recognizing receptor and further election of a single species from the genus of antigen-recognizing receptor in the reply filed on 07/21/2025 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)). Upon further consideration, claim 36, drawn to a method for producing a cell comprising an antigen-recognizing receptor of claim 1, is included in compositions and kits comprising a cell expressing an antigen-recognizing receptor. Therefore, claim 36 is hereby included in the elected invention (group I).
Claims 1-37 are pending.
Claims 33-35 are withdrawn from consideration under 37 CFR 1.142(b) as being drawn to nonelected invention and species.
Claims 1-32 and 36-37 are currently under examination.
3. 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. This application is a continuation of PCT/US2020/050386 filed 09/11/2020, which claims benefit of US provisional application 62/936,951 filed 11/18/2019 and US provisional application 62/900,141 filed 09/13/2019. Claims 1-32 and 37 have an effective filing date of 09/13/2019.
4. The information disclosure statements (IDSs) submitted on 03/17/2023, 04/11/2023, 09/14/2023, 09/25/2023, 12/05/2023, 02/13/2024, 03/07/2025 and 06/12/2025 are in compliance with the provisions of 37 CFR 1.97. Accordingly, these information disclosure statements are being considered by the examiner in their entireties.
Claim Objections
5. Claim 4 is objected to because of the following informalities: claim 4 recites a heavy chain variable region CDR 1 comprising the amino acid sequence set forth in SEQ ID NO: 40, a CDR2 comprising the amino acid sequence set forth in SEQ ID NO: 42 and a CDR3 comprising the amino acid sequence set forth in SEQ ID NO: 43 (claim 4c). The VH CDR2 and CDR3 sequence SEQ ID NOs recited here appear to be a typographical errors because the rest of the disclosure, such as table 3 of the specification (pg. 39) recites VHCDR2 as SEQ ID NO: 41 and VHCDR3 as SEQ ID NO: 42. Appropriate correction is required.
Claim Rejections - 35 USC § 112
6. 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.
7. Claims 1-5, 8, 11-32 and 36-37 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.
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. Claim 1 recites “antigen-recognizing receptor comprising an extracellular antigen-binding domain, a transmembrane domain, and an intracellular signaling domain” that is capable of specifically binding to CD371, which encompasses a genus of agents. Claims 2-3, 11-32 and 36-37 are dependent from Claim 1, do not materially limit the genus of agents, and are therefore included in the rejection. Claims 4-5 and 8 recite structural limitations to the antigen binding domains (e.g., as amino acid sequences for the CDRs or amino acid sequences for the full VH and VL domains), but also include conservative modifications thereof, including the amino acid sequences for the CDRs. Similarly, claim 8 recites heavy and light chain variable regions comprising 80% to 99% homology to specific amino acid sequences. However, there is no teaching identifying what amino acids can be varied within the VH-CDRs and/or VL-CDRs of the antigen binding regions and still retain the claimed functionality of specifically binding to CD371. Brown et al. (J. Immuno. 1996 May, 3285-91 at 3290 and Tables 1 and 2) describes how a one amino acid change in the VH CDR2 of a particular antibody was tolerated whereas, the antibody lost binding upon introduction of two amino changes in the same region. Vajdos et al. (J. Mol. Biol. 2002, Jul 5, 320(2):415-28 at 416) teach that amino acid sequence and conformation of each of the heavy and light chain CDRs are critical in maintaining the antigen binding specificity and affinity. Aside from the CDRs, the Fv also contains more highly conserved framework segments which connect the CDRs and are mainly involved in supporting the CDR loop conformations, although in some cases, framework residues also contact antigen. The scope of the claims encompasses antigen binding domains with VH or VL that encompass variation (addition, deletion, substitution) in their CDRs. Therefore, taken on the whole, these claims do not require that the genus of the claims possess any particular structure or other distinguishing feature that is characteristic of the genus in its entirety. Therefore the claims are drawn to a genus of “antigen-recognizing receptors” for which there is inadequate written description.
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 MPEP 2163(II)(3)(a)(i)(A), reduction to drawings MPEP 2163(II)(3)(a)(i)(B), 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 MPEP 2163(II)(3)(a)(i)(C).
In the instant case, the only identifying characteristic present in the claim is a recitation of requisite activity (------------------e.g., capable of binding CD371). There is not even identification of any particular portion of a structure that must be conserved for said activity. Regarding the genus of the claims the specification describes 6 specific species within the genus claimed (e.g., pg. 106, lines 21-25; see also figure 1). From the specification, it is clear that Applicant is in possession of a limited number of species, including the “B10”-based constructs (pg. 106, lines 26-32). The claims, however are not limited to those species but also includes an expansive number of other antigen binding domain containing constructs, and the specification fails to provide a representative number of species within the recited genus. Accordingly, in the absence of sufficient recitation of distinguishing identifying characteristics, or representative number of species, the specification does not provide adequate written description of the claimed genus.
Claim Rejections - 35 USC § 102
8. The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
9. Claims 1-3 and 11-32 and 36-37 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by BROGDON et al (US 20160051651 A1; published 02/25/2016) as evidenced by the instant specification as-filed on page 26.
Regarding claim 1, BROGDON discloses compositions and methods for treating diseases associated with expression of C-type lectin-like-1 (CLL-1) (e.g., abstract; ¶0004). While BROGDON refers to the target antigen as CLL-1, it is also known in the art as CD371, CLEC12A, DCAL-2, MICL or CLL-1 (see instant specification pg. 26, lines 7-8). BROGDON discloses isolated nucleic acid molecules encoding a chimeric antigen receptor (CAR), wherein the CAR comprises an antibody or antibody fragment which includes a human anti-CLL-1 (anti-CD371) binding domain, a transmembrane domain, and an intracellular signaling domain (¶0005). Therefore, BROGDON anticipates instant claim 1.
Regarding claims 2 and 3, BROGDON discloses the anti-CD371 antigen recognizing receptor of claim 1 (discussed above); BROGDON also teaches that the CD371 binding domain comprises single-chain variable fragments (ScFv) connected via a glycine-serine linker, wherein the light chain variable region and heavy chain variable region of the scFv can be constructed in a number of orientations, including light chain variable region-linker-heavy chain variable region (VL-liner-VH) or VH-linker-VL (e.g., ¶0013). Therefore, the antigen binding domain of BROGDON comprise fusion proteins comprising operably linked, heterologous polypeptides, thereby anticipating instant claims 2 and 3.
Regarding claims 11 and 12, BROGDON discloses the anti-CD371 antigen recognizing receptor of claim 1 (see above). Also previously discussed, BROGDON teaches the CD371 binding domain comprises single-chain variable fragments (ScFv) connected via a glycine-serine linker (¶0013; ¶0033; ¶0039). BROGDON specifies that the linker is comprised of (G4S)n repeats, wherein n=1-6 (e.g., ¶0013). Therefore, BROGDON teaches linkers recited in instant claim 12, such as GGGS (SEQ ID NO: 93) and GGGSGGGS (SEQ ID NO: 94). Therefore, BROGDON anticipates instant claims 11-12.
As previously discussed, BROGDON discloses that the CD371 binding domain single-chain variable fragments (ScFv) connected via a glycine-serine linker can be oriented in either direction VL-linker-VH or VH-linker-VL (¶0013; ¶0033; see also constructs detailed in table 2). Therefore, the anti-CD371 binding domain variable region may be positioned from the N-to the C-terminus in a VH to VL direction, thus anticipating instant claim 13.
Regarding claims 15-17, BROGDON teaches the anti-CD371 receptor of claim 1 (discussed above), wherein the transmembrane domain is selected from the group including CD28, CD3 epsilon, CD4, CD8, CD33 and CD37 (e.g., ¶0014). BROGDON also discloses that the intracellular signaling domain comprises a costimulatory domain and a primary signaling domain (¶0016), wherein the costimulatory domain is selected from a group of polypeptides including those of CD28, 4-1BB, OX40 and ICOS (CD278) (¶0017). Therefore, BROGDON anticipates instant claims 15-17.
Regarding claims 18-22, BROGDON teaches the anti-CD371 receptor of claim 1 (discussed above), wherein said receptor is a chimeric antigen receptor (CAR) (previously discussed; see also ¶0005). BROGDON also discloses, vectors encoding the CD371 CAR under constitutive promotors (e.g., EF-1) (¶0055-0057), as well as recombinant cells comprising the constitutively expressed CD371 CAR (¶0058). Therefore, BROGDON anticipates claims 18-22.
Regarding claim 26, BROGDON teaches the cell comprising the CD371 CAR of claim 21 (see above). BROGDON specifies that said cell is an immunoresponsive cell, such as an immune effector cell e.g., a human T cell or a human NK cell (¶0058). Since claim 26 recites 5 alternative limitations (i-v) reciting the compound conjunction “and/or”, BROGDON anticipates instant claim 26.
Regarding claim 28-32, BROGDON teaches the anti-CD371 receptor of claim 1 (discussed above), wherein a vector comprising a nucleic acid molecule encoding said CD371 receptor is expressed in a host cell (e.g., an immune effector cell, human T cell or human NK cell). BROGDON also teaches pharmaceutical compositions of the present invention may comprise a CAR-expressing cell, e.g., a plurality of CAR-expressing cells, as described herein, in combination with one or more pharmaceutically or physiologically acceptable carriers, diluents or excipients (e.g., ¶0996). Therefore, BROGDON anticipates instant claims 28-32.
Regarding claim 36, BROGDON teaches the anti-CD371 receptor of claim 1 (discussed above). BROGDON further discloses a vector (such as a lentiviral vector) comprising a nucleic acid encoding said CD371 receptor, wherein said vector comprises an EF-1 promoter (¶0055-0057). BROGDON also discloses a cell, such as an immune effector cell (e.g., a human T cell) comprising the previously discussed vector encoding the anti-CD371 receptor (¶0058). Further, BROGDON discloses method of making an immune effector cell (e.g., a T cell or a NK cell) comprising the vector comprising a nucleic acid encoding the anti-CD371 CAR (¶0060). Therefore, BROGDON anticipates instant claim 36.
Regarding claim 37, BROGDON teaches the cell comprising the CD371 CAR of claim 21 (see above). BROGDON discloses methods for providing an anti-tumor immunity in a mammal comprising administering to the mammal an effective amount of a cell expressing said CD371 CAR molecule (¶0062) and BROGDON also teaches the use of the CD371 CAR expressing T cell can be used in combination with a chemotherapeutic agent (e.g., ¶0787). BROGDON also discloses kits that include one or more combination treatment and pharmaceutically acceptable excipient (e.g., ¶0887); as an example of a pharmaceutically acceptable excipient taught by BROGDON in a working embodiment, CD371 CAR expressing T cells were administered with PBS in a murine tumor model experiments (¶1054). Therefore, BROGDON anticipates instant claim 37.
Claim Rejections - 35 USC § 103
10. 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.
11. 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.
12. Claims 1, 21 and 23-25 are rejected under 35 U.S.C. 103 as being unpatentable over BROGDON et al., (US 20160051651 A1; published 02/25/2016) in view of MA et al., (WO2019075395 A1; published 04/18/2019; listed on the IDS filed 03/17/2023 as ICell Gene Therapeutics, LLC).
Regarding claims 1 and 21, BROGDON teaches the cell comprising a CD371 antigen recognizing receptor (discussed above). Regarding claims 23-25, BROGDON explains how in response to target expressing cells, the intracellular signaling domain generates a signal that promotes an immune effector function of the CAR containing cell, such as immune effector functions including the secretion of cytokines (¶0234), indeed suggesting that potency can be determined by various T cell functions, e.g. proliferation, target cell killing, cytokine production, activation, migration, or combinations thereof (¶0698). BROGDON discloses that the CD371 CAR T cells are capable of cytokine expression and secretion upon exposure to CD371 expressing cells in vitro (e.g., Figs 5A-5C). BROGDON also discloses that the cytokine level or activity (e.g., quality of cytokine repertoire) in a CAR-expressing cell is one metric for determining the value of effectiveness to the CAR therapy (¶0941).
BROGDON differs from instant claims 23-25 by not disclosing that the CD371 CAR T cells were engineered to express an exogenous cytokine, such as IL-18, IL-33 or IL-36 (or combinations thereof).
MA et al., in the field of compound chimeric antigen receptors (cCARs) (e.g., title; abstract), discloses engineered cells comprising chimeric antigen receptor polypeptides with antigen recognition domains targeted to multiple antigens including CLL-1 (or CD371) (e.g., pg.3 lines 10-22). MA also teaches cCAR constructs engineered to include an enhancer (pg. 3), which includes IL-18 (pg.5, ¶2). In one embodiment (see fig. 53A), MA discloses a CAR with an antigen recognition domain comprising ScFv domains joined by linkers, a CD28 transmembrane domain, CD3zeta signaling domain and 4-1BB costimulatory signaling domain all of which are operably linked to an IL-15/IL-15 sushi domain enhancer construct (Fig. 53A; see pg.61 lines 27). MA explicitly states that the secreting enhancer(s) of the construct may also include, but are not limited to, IL-21, IL-18, IL-7 and IL-12 (pg. 61, lines 25-27). MA discloses an example construct in figure 26 where the CAR is linked to IL-18 with a self-cleavable linker (see fig. 26). MA explains that CAR T or NK cells are engineered to co-express a secretory IL-18 are targeted to the tumor microenvironment and bind to the CAR antigen, thus triggering lysis of tumor cells and massive secretion of soluble IL-18 from the expansion of CART or NK cells (pg. 95, lines 4-9).
BROGDON et al. and MA et al. are both directed to engineered cells comprising antigen receptors capable of binding to CD371 (CLL-1). Based on these teachings, it would have been prima facie obvious to one of ordinary skill in the art, at the time the invention was filed, to modify the CD371 CAR expressing cell of BROGDON to also express secreted IL-18, as taught by MA to achieve the predictable result of obtaining a CAR T or NK cell composition suitable for the targeted delivery of IL-18 to the tumor microenvironment. One of ordinary skill in the art would have been motivated to do so because MA teaches that the targeted expression of IL-18 is advantageous for the longer persistence and enhanced activity of the T cells and NK cells targeting tumor cells (pg. 94, line 31 through pg. 95 line 3).
Double Patenting
13. 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.
14. Claims 1-32 and 36-37 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-16 of copending Application No. 17/692,979 in view of BROGDON et al (US 20160051651 A1; published 02/25/2016).
Reference application claims 1-16 recite anti-CD371 antibodies or antigen binding fragments comprising a heavy chain variable region and a light chain variable region defined by specific SEQ ID NOs (reference claim 1). As shown in the sequence alignments below, reference SEQ ID NOs 1 and 2 (Db) are identical to the heavy chain and light chain variable regions of the elected species of antigen-recognizing receptor of the instant invention (Qy).
RESULT 1
US-17-692-979-1
Query Match 100.0%; Score 650; Length 122;
Best Local Similarity 100.0%;
Matches 122; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVQLLESGGGLVQPGGSLRLSCAASGFTFSDYQMSWVRQAPGKGLEWVSGIQGGGGSTYY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVQLLESGGGLVQPGGSLRLSCAASGFTFSDYQMSWVRQAPGKGLEWVSGIQGGGGSTYY 60
Qy 61 ADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAREMWRGDYYSGMDVWGQGTTVTV 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 ADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAREMWRGDYYSGMDVWGQGTTVTV 120
Qy 121 SS 122
||
Db 121 SS 122
RESULT 1
US-17-692-979-2
Query Match 100.0%; Score 589; Length 113;
Best Local Similarity 100.0%;
Matches 113; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIVMTQSPDSLAVSLGERATINCKSSQSVLDSYNNENNLAWYQQKPGQPPKLLIYWASTR 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIVMTQSPDSLAVSLGERATINCKSSQSVLDSYNNENNLAWYQQKPGQPPKLLIYWASTR 60
Qy 61 ESGVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQYTSEPITFGQGTKVEIK 113
|||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 ESGVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQYTSEPITFGQGTKVEIK 113
The reference claims differ from the instant claims by not reciting that the anti-CD371 antigen binding fragment is comprised by an antigen-recognizing receptor construct.
BROGDON, in teaches compositions and methods for treating diseases associated with expression of C-type lectin-like-1 (CLL-1) (e.g., abstract; ¶0004). While BROGDON refers to the target antigen as CLL-1, it is also known in the art as CD371, CLEC12A, DCAL-2, MICL or CLL-1 (see instant specification pg. 26, lines 7-8). BROGDON discloses isolated nucleic acid molecules encoding a chimeric antigen receptor (CAR), wherein the CAR comprises an antibody or antibody fragment which includes a human anti-CLL-1 (anti-CD371) binding domain, a transmembrane domain, and an intracellular signaling domain (¶0005). BROGDON also teaches that the CD371 binding domain comprises single-chain variable fragments (ScFv) connected via a glycine-serine linker, wherein the light chain variable region and heavy chain variable region of the scFv can be constructed in a number of orientations, including light chain variable region-linker-heavy chain variable region (VL-liner-VH) or VH-linker-VL (e.g., ¶0013). BROGDON teaches the CD371 binding domain comprises single-chain variable fragments (ScFv) connected via a glycine-serine linker (¶0013; ¶0033; ¶0039). BROGDON specifies that the linker is comprised of (G4S)n repeats, wherein n=1-6 (e.g., ¶0013). Therefore, BROGDON teaches linkers recited in instant claim 12, such as GGGS (SEQ ID NO: 93) and GGGSGGGS (SEQ ID NO: 94).
In the CD371 receptor of BROGDON, the binding domain single-chain variable fragments (ScFv) are connected via a glycine-serine linker can be oriented in either direction VL-linker-VH or VH-linker-VL (¶0013; ¶0033; see also constructs detailed in table 2). Therefore, the anti-CD371 binding domain variable region may be positioned from the N-to the C-terminus in a VH to VL direction. The anti-CD371 receptor of BROGDON includes a transmembrane domain selected from the group including CD28, CD3 epsilon, CD4, CD8, CD33 and CD37 (e.g., ¶0014). BROGDON also discloses that the intracellular signaling domain comprises a costimulatory domain and a primary signaling domain (¶0016), wherein the costimulatory domain is selected from a group of polypeptides including those of CD28, 4-1BB, OX40 and ICOS (CD278) (¶0017).
BROGDON discloses vectors encoding the CD371 CAR under constitutive promotors (e.g., EF-1) (¶0055-0057), and recombinant cells comprising the constitutively expressed CD371 CAR (¶0058). BROGDON teaches the anti-CD371 receptor of claim 1 (discussed above), wherein a vector comprising a nucleic acid molecule encoding said CD371 receptor is expressed in a host cell (e.g., an immune effector cell, human T cell or human NK cell). BROGDON also teaches pharmaceutical compositions of the present invention may comprise a CAR-expressing cell, e.g., a plurality of CAR-expressing cells, as described herein, in combination with one or more pharmaceutically or physiologically acceptable carriers, diluents or excipients (e.g., ¶0996). BROGDON also discloses methods of making an immune effector cell (e.g., a T cell or a NK cell) comprising the vector comprising a nucleic acid encoding the anti-CD371 CAR (¶0060). BROGDON also discloses methods for providing an anti-tumor immunity in a mammal comprising administering to the mammal an effective amount of a cell expressing said CD371 CAR molecule (¶0062) and BROGDON also teaches the use of the CD371 CAR expressing T cell can be used in combination with a chemotherapeutic agent (e.g., ¶0787). BROGDON also discloses kits that include one or more combination treatment and pharmaceutically acceptable excipient (e.g., ¶0887); as an example of a pharmaceutically acceptable excipient taught by BROGDON in a working embodiment, CD371 CAR expressing T cells were administered with PBS in a murine tumor model experiments (¶1054).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the anti-CD371 antigen-binding fragment recited in reference claim 1 to be included in the CD371 (CLL-1) antigen-recognizing receptor taught by BROGDON et al, to achieve the predictable result of obtaining a CD371 targeted CAR T cell. One of ordinary skill in the art would have been motivated to do so because BROGDON teaches it is advantageous for treating diseases associated with the expression of CD371 (CLL-1) such as acute myeloid leukemia (¶0003-0004).
This is a provisional nonstatutory double patenting rejection.
Conclusion
15. No claims are allowed.
16. Any inquiry concerning this communication or earlier communications from the examiner should be directed to JAMES L MCLELLAN whose telephone number is (703)756-1906. The examiner can normally be reached Monday - Thursday 7:30 am - 5:30 pm. *Compressed day off on first Friday of each Bi-week.
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/JAMES LYLE MCLELLAN/Examiner, Art Unit 1641
/CHUN W DAHLE/Primary Examiner, Art Unit 1641