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 .
Claim Status
Claims 1-15 have been cancelled.
Claims 16-35 are currently pending.
Claims 25-31 and 35 have been withdrawn.
Claims 16-24 and 32-34 are being examined in this application.
Election/Restrictions
Applicant’s election without traverse of Group I invention (Claims 16-24 and 32-34) as well species of “SIRPa” as the intracellular domain, SIRPa TM, scFv as the binding domain, CD8 hinge as the spacer, and T or NK cell in the reply filed on 7/18/25 is acknowledged.
Claim 25-31 and 35 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 7/18/25.
Priority
This application is a CON of PCT/US2021/018847 (filed on 02/19/2021), which claims priority to US provisional applications 63/127,843 (filed on 12/18/2020) and 62/979,310 (filed on 02/20/2020).
Specification
The specification has not been checked to the extent necessary to determine the presence of all possible minor errors. Applicant's cooperation is requested in correcting any errors of which applicant may become aware in the specification. MPEP 608.01.
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 16-24 and 32-34 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.
The instant claims recite a chimeric inhibitory receptor or CAR comprising various extracellular binding domain, TMs, intracellular domain “derived” from various proteins.
To satisfy the written description requirement, applicants may convey reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention.
Applicants may show possession of an invention by disclosure of drawings or structural chemical formulas that are sufficiently detailed to show that applicant was in possession of the claimed invention as a whole. See, e.g., Vas-Cath, 935 F.2d at 1565, 19 USPQ2d at 1118.
The written description requirement of 35 U.SC. 112 exists independently of enablement requirement, and the requirement applies whether or not the case involves questions of priority. The requirement applies to all inventions and includes chemical inventions. The fact that the patent is directed to method entailing use of compounds, rather than to compounds per se, does not remove patentee’s obligation to provide a description of the compound sufficient to distinguish infringing methods from non-infringing methods. See Univ. of Rochester v. G.D. Searle & Co., 358 F.3d 916, 920-23, 69 USPQ 2d 1886, 1890-93 (Fed. Cir. 2004).
With regard to the description requirement, applicants’ attention is invited to consider the decision of the Court of Appeals for the Federal Circuit, which holds that a “written description of an invention involving a chemical genus, like a description of a chemical species, ‘requires a precise definition, such as by structure, formula [or] chemical name,’ of the claimed subject matter sufficient to distinguish it form other materials.” University of California v. Eli Lilly and Co., 43 USPQ2d 1398, 1405 (1997), quoting Fiers v. Revel, 25 USPQ2d 1601, 1606 (Fed. Cir. 1993) (bracketed material in original) [The claims at issue in University of California v. Eli Lilly defined the invention by function of the claimed DNA (encoding insulin)].
The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species or by actual reduction to practice, reduction to drawings, 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 Eli Lilly, 119 F. 3d at 1568, 43 USPQ2d at 1406.
Claims 16-24 and 32-34 are drawn to a genus of CAR comprising various extracellular binding domain, TMs, intracellular domain. Neither the instant specification nor the claims have demonstrated common structure and/or function for the claimed genus of CARs. In addition, no representative numbers of species for each claimed genus are provided to show possession of the claimed genus of CAR and/or “domains” that can be used in CAR.
To provide evidence of possession of a claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of complete or partial structure, physical and/or chemical properties, functional characteristics, structure/function correlation, methods of making the claimed product, or any combination thereof. (see MPEP 2163 II).
In this case, the claimed domains are “derived” from various proteins, which given the broadest and reasonable interpretation can include any truncated fragments and mutations. Claim 18 recites various percent identities to the naturally occurring sequences of various domains, which encompasses a large number of possible sequences. However, the instant specification does not provide representative number of species and/or common core structure that would have the functionalities/properties of the claimed genus of chimeric inhibitory receptors.
Therefore, applicants are not in possession of the claimed genus of chimeric inhibitory receptor.
Claim Rejections - 35 USC § 102
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.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Pule et al
Claim(s) 16-19 and 21-24 is/are rejected under 35 U.S.C. 102 (a)(1)/(a)(2) as being anticipated by Pule et al (US10172886; 1/8/2019; filed on 11/21/2014 or earlier; cited in 892).
The instant claims are drawn to compositions comprising Chimeric antigen receptor (CAR) of various sequences.
Pule et al, throughout the reference, teach CAR comprising various sequences. (e.g. Abstract).
For claim 16: A chimeric inhibitory receptor comprising:
an extracellular protein binding domain;
Pule et al teach CAR comprising “an antigen binding domain” (extracellular), a spacer, a transmembrane domain, and an extracellular protein binding domain. (e.g. Claims 1-16; col.17, lines 1+). The reference teaches the extracellular domain can be a scFv (e.g. col.3, lines 20+; col.4, lines 6+; col.16, lines 19+).
(b) a transmembrane domain, wherein the transmembrane domain is operably linked to the extracellular protein binding domain; and
Pule et al teach Transmembrane domain for CAR such as CD28, CD45, or CD148 transmembrane domains (e.g. Figure 15; col.4, lines 1+).
(c) one or more intracellular signaling domains, wherein the one or more intracellular signaling domains are operably linked to the transmembrane domain, and wherein each of the one or more intracellular signaling domains is derived from a protein selected from the group consisting of: SLAP1, SLAP2, Dok-1, Dok-2, GRiB-2, CD200R, SIRPa, HAVR, GITR, PD-Li, KIR2DL2, KIR2DL3, KIR3DL2, CD94, KLRG-1, CEACAM1, LIR2, LIR3, LIR5, SIGLEC-2, and SIGLEC-1 0, and wherein at least one of the one or more intracellular signaling domains is capable of preventing, attenuating, or inhibiting activation of an immunomodulatory cell.
Pule et al teach using endodomain of CD22 (which is also known as SIGLEC-2) in CAR (e.g. col.31-32; col.32, lines 49+), which the endodomain reads on the intracellular signal domain of the instant claim.
The reference also teaches the antigen binding domain is linked to the Transmembrane (e.g. Figure 5; Claims 1-16).
The reference also teaches the endodomain can be an “immunoreceptor Tyrosine-based inhibition motify” (e.g. col.31-32; col.32, lines 49+), which reads on the claimed property recited in the last lines of the claim.
For claim 17: The reference teaches the TM and the intracellular domain can be from the same protein or different proteins (such as CD28, CD22) (e.g. Claims 1-16; cols. 10-12; Figures 4-5).
For claim 18: The reference teaches using endodomain of CD22 (which is also known as SIGLEC-2) in CAR (e.g. col.31-32; col.32, lines 49+), which the endodomain reads on the intracellular signal domain of the instant claim.
For Claim 19: Pule et al teach Transmembrane domain for CAR such as CD28, CD45, or CD148 transmembrane domains (e.g. Figure 15; col.4, lines 1+).
For Claim 21: Pule et al teach the extracellular domain can be a scFv (e.g. col.3, lines 20+; col.4, lines 6+; col.16, lines 19+).
For Claim 22: Pule et al teach a “spacer” region between the antigen binding domain and the TM region (e.g. Claim 1; Figures 18 and 31; col.11, lines 25+).
For Claim 23: Pule et al teach CAR comprising “an antigen binding domain” (extracellular), a spacer, a transmembrane domain, and an intracellular domain. (e.g. Claims 1-16; col.17, lines 1+).
For Claim 24: Pule et al teach T and NK cells with CAR (e.g. col.12, line 1+; claims 1-3).
Oda et al
Claim(s) 16-19, 21-24 and 33 is/are rejected under 35 U.S.C. 102 (a)(1)/(a)(2) as being anticipated by Oda et al (WO2016141357; 9/9/2016; filed on 3/4/2016 or earlier; cited in 892).
The instant claims are drawn to compositions comprising Chimeric antigen receptor (CAR) of various sequences.
Oda et al, throughout the reference, teach CAR comprising various sequences. (e.g. Abstract; p.2, lines 5+; p.35, lines 14+).
For claim 16: A chimeric inhibitory receptor comprising:
an extracellular protein binding domain;
Oda et al., teach CAR comprising an extracellular domain, intracellular signal domain, a transmembrane domain. (e.g. p.35, lines 20+; Claims 6+). The reference teaches the binding domain (or the extracellular domain) can be a scFv (e.g. p.22, lines 4+; p.48, ll6+).
(b) a transmembrane domain, wherein the transmembrane domain is operably linked to the extracellular protein binding domain; and
Oda et al teach Transmembrane domain for CAR can be from various proteins such as “SIRPa” transmembrane domains (e.g. p.54, lines 22+).
(c) one or more intracellular signaling domains, wherein the one or more intracellular signaling domains are operably linked to the transmembrane domain, and wherein each of the one or more intracellular signaling domains is derived from a protein selected from the group consisting of: SLAP1, SLAP2, Dok-1, Dok-2, GRiB-2, CD200R, SIRPat, HAVR, GITR, PD-Li, KIR2DL2, KIR2DL3, KIR3DL2, CD94, KLRG-1, CEACAM1, LIR2, LIR3, LIR5, SIGLEC-2, and SIGLEC-1 0, and wherein at least one of the one or more intracellular signaling domains is capable of preventing, attenuating, or inhibiting activation of an immunomodulatory cell.
Oda et al teach using intracellular domain of various proteins such as GITR in CAR (or CD357) (e.g. p.24, ll 20+).
The reference also teaches the extracellular domain is linked to the Transmembrane via a spacer region (e.g. p.5, ll 25+; Claim 17; Figure 1A).
The reference also teaches engineering T cells with CAR for immunomodulation (e.g. pp.77+), which reads on the claimed property recited in the last lines of the claim.
For claim 17: The reference teaches the TM and the intracellular domain can be from the same protein or different proteins (such as CD28, GITR, SIRPa) (e.g. p.24, ll 20+; p.54, lines 22+).
For claim 18: Oda et al teach using intracellular domain of various proteins such as GITR in CAR (or CD357) (e.g. p.24, ll 20+).
For Claim 19: Oda et al teach Transmembrane domain for CAR can be from various proteins such as “SIRPa” transmembrane domains (e.g. p.54, lines 22+).
For Claim 21: The reference teaches the binding domain (or the extracellular domain) can be a scFv (e.g. p.22, lines 4+; p.48, ll6+).
For Claim 22: The reference also teaches the extracellular domain is linked to the Transmembrane via a spacer region (e.g. p.5, ll 25+; Claim 17; Figure 1A).
For Claim 23: Oda et al teach CAR comprising extracellular binding domain, a spacer, a transmembrane domain, and an intracellular domain. (e.g. p.35, lines 20+; Claims 6+).
For Claim 24: Oda et al teach T and NK cells with CAR (e.g. p.20, ll 9+; claims 1+).
For Claim 33: Oda et al teach Transmembrane domain for CAR can be from various proteins such as “SIRPa” transmembrane domains (e.g. p.54, lines 22+).
Arvind et al
Claim(s) 16-19, 21-24 and 33 is/are rejected under 35 U.S.C. 102 (a)(1)/(a)(2) as being anticipated by Arvind et al (WO2016075612; 5/19/2016; filed on 11/9/2015 or earlier; cited in IDS).
The instant claims are drawn to compositions comprising Chimeric antigen receptor (CAR) of various sequences.
Arvind et al, throughout the reference, teach CAR comprising various sequences. (e.g. Abstract).
For claim 16: A chimeric inhibitory receptor comprising:
an extracellular protein binding domain;
Arvind et al., teach CAR comprising an extracellular domain, intracellular signal domain, a transmembrane domain. (e.g. Abstract; Claims 1+). The reference teaches the binding domain (or the extracellular domain) can be a scFv (e.g. p.20, lines 8+; Claim 11).
(b) a transmembrane domain, wherein the transmembrane domain is operably linked to the extracellular protein binding domain; and
Arvind et al teach Transmembrane domain for CAR can be from various proteins such as “SIRPa” transmembrane domains (e.g. Claim 10).
(c) one or more intracellular signaling domains, wherein the one or more intracellular signaling domains are operably linked to the transmembrane domain, and wherein each of the one or more intracellular signaling domains is derived from a protein selected from the group consisting of: SLAP1, SLAP2, Dok-1, Dok-2, GRiB-2, CD200R, SIRPat, HAVR, GITR, PD-Li, KIR2DL2, KIR2DL3, KIR3DL2, CD94, KLRG-1, CEACAM1, LIR2, LIR3, LIR5, SIGLEC-2, and SIGLEC-1 0, and wherein at least one of the one or more intracellular signaling domains is capable of preventing, attenuating, or inhibiting activation of an immunomodulatory cell.
Arvind et al teach using intracellular domain of various proteins such as KIR2DL2 in CAR (e.g. p.22, ll 20+; p.136, lines 2+).
The reference also teaches the extracellular domain is linked to the Transmembrane via a spacer region (e.g. claims 1+).
The reference also teaches engineering T cells with CAR for immunomodulation (e.g. p.2), which reads on the claimed property recited in the last lines of the claim.
For claim 17: The reference teaches the TM and the intracellular domain can be from the same protein or different proteins (such as CD22, SIRPa, KIR2DL2) (e.g. p.112, lines 1+; p.22, ll 20+; p.136, lines 2+; Claim 10).
For claim 18: Arvind et al teach using intracellular domain of various proteins such as KIR2DL2 in CAR (e.g. p.22, ll 20+; p.136, lines 2+).
For Claim 19: Arvind et al teach Transmembrane domain for CAR can be from various proteins such as “SIRPa” transmembrane domains (e.g. Claim 10).
For Claim 21: The reference teaches the binding domain (or the extracellular domain) can be a scFv (e.g. p.20, lines 8+; Claim 11).
For Claim 22: The reference also teaches the extracellular domain is linked to the Transmembrane via a spacer region (e.g. claims 1+). The reference also teaches the alpha chain of CD8 and/or CD8alpha hinge used in CAR (e.g. p.117, lines 1+; claim 91), which the CD8 alpha chain contains the hinge region.
For Claim 23: Arvind et al teach CAR comprising extracellular binding domain, a spacer, a transmembrane domain, and an intracellular domain. (e.g. Claims 1+).
For Claim 24: Arvind et al teach T cells with CAR (e.g. p.2).
For Claim 33: Arvind et al teach Transmembrane domain for CAR can be from various proteins such as “SIRPa” transmembrane domains (e.g. Claim 10).
Claim Rejections - 35 USC § 103
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.
Pule, Arvind & Zen
Claim(s) 16-19, 20, 21-24, 32, 33, and 34 is/are rejected under 35 U.S.C. 103 as being unpatentable over Pule et al (US10172886; 1/8/2019; filed on 11/21/2014 or earlier; cited in 892) in view of Arvind et al (WO2016075612; 5/19/2016; filed on 11/9/2015 or earlier; cited in IDS, and Zen et al (Inflammation-induced proteolytic processing of the SIRPα cytoplasmic ITIM in neutrophils propagates a proinflammatory state. Nature Communications. Vol.4:2436; pp.1-23; 2013).
Pule et al, throughout the reference, teach CAR comprising various sequences. (e.g. Abstract) as discussed supra.
Pule et al, teach including Immunoreceptor Tyrosine-based Inhibition motif (ITIM) domain from various proteins as the intracellular signaling domain in CAR for the specific function of “ligation-on” signaling pathway as desired.
Pule et al., does not explicit teach CAR with a first intracellular domain from KIR2DL1 and a second intracellular domain from LIR2, Or that the intracellular domain and the TM are from SIRPa as recited in claims 20, 32-34. The reference also does not teach the spacer region is from CD8a as recited in claim 34.
However, Arvind et al, throughout the reference, teach CAR comprising various sequences. (e.g. Abstract). The Arvind reference also teaches using ITIM domain of various proteins as the intracellular signaling domain (e.g. pp.8+; claims 6-7). Arvind et al teach Transmembrane domain for CAR can be from various proteins such as “SIRPa” transmembrane domains (e.g. Claim 10). The reference also teaches the alpha chain of CD8 and/or CD8alpha hinge used in CAR (e.g. p.117, lines 1+; claims 91, 96), which the CD8 alpha chain contains the hinge region.
Zen et al., throughout the reference, teach SIRPa protein and its cytoplasmic ITIM functionalities (e.g. Abstract). Zen teaches SIRPa comprises an ITIM that is an “essential negative regulator of leukocyte inflammatory responses (i.e. immune responses) (e.g. pp.1-2). The reference also teaches the various domains for SIRPa are known (e.g. top of p 2).
Therefore, it would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to using the ITIM from SIRPa as the intracellular signaling domain in CAR. Generating CAR using various combinations of TM, Intracellular domain and extracellular binding domain are known and routine in the art as taught by Pule and Arvind. In addition, Both Pule and Arvind teach the need and advantage of using ITIMs (from various proteins) as the intracellular domain for CAR. Arvind also teaches using SIRPa as the TM for CAR, and the various domains/structures (with functionalities) of SIRPa are known in the art as taught by Zen et al. Thus, one of skilled in the art would be motivated to substitute one ITIM (ones taught in Pule and Arvind) with another (the one from SIRPa) for the to achieve the specific ligation-on signaling pathway. Alternatively, it would have been obvious for one of skilled in the art to swap out the extracellular binding domain of SIRPa with another antigen binding domain, as these binding domains are well known in the art as taught by Pule and Arvind.
Therefore, it would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to using CD8alpha chain hinge region as the spacer in CAR. Various hinge region have been known and routinely used in generating CAR as taught by Arvind. In addition, Both Pule and Arvind teach the need and advantage of using spacer regions for CAR
A person of ordinary skill in the art would have reasonable expectation of success of achieving such modifications since Pule and Arvind have demonstrated it is routine and known in the art to generate various CAR with different known TM, intracellular, extracellular domains and spacers for the purpose of achieve desired immunoresponse modulations.
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.
‘081
Claims 16, 17, 18 and 21-24 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-28 of U.S. Patent No.12,005,081 (hereinafter referred to as ‘081 patent). Although the claims at issue are not identical, they are not patentably distinct from each other because the claimed invention in ‘081 reads on the instant claims.
‘081 Patent claims CAR and usage in treatment, where the CAR comprise various intracellular, TM and extracellular binding domain. (Claims 1-28).
‘525
Claims 16, 17, 18 and 21-24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 16, 19, 21, 22-26, 31-34 and 36-39 of copending Application No. 17/820525 (reference application; hereinafter referred to as ‘525 application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claimed invention in ‘525 reads on the instant claims.
‘525 application claims CAR or cells containing CAR, where the CAR comprise various intracellular, TM and extracellular binding domain. (Claims 16, 19, 21, 22-26, 31-34 and 36-39).
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
‘301
Claims 16, 17, 18 and 21-24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 3-20 of copending Application No. 17636301 (reference application; hereinafter referred to as ‘301 application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claimed invention in ‘301 reads on the instant claims.
‘301 application claims CAR or cells containing CAR, where the CAR comprise various intracellular, TM and extracellular binding domain. (Claims 1 and 3-20).
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
‘925
Claims 16, 17, 18 and 21-24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of copending Application No. 18501925 (reference application; hereinafter referred to as ‘925 application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claimed invention in ‘925 reads on the instant claims.
‘925 application claims CAR or cells containing CAR, where the CAR comprise various intracellular, TM and extracellular binding domain. (Claims 1-20).
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
‘596
Claims 16, 17, 18 and 21-24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of copending Application No. 18201596 (reference application; hereinafter referred to as ‘596 application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claimed invention in ‘596 reads on the instant claims.
‘596 application claims CAR or cells containing CAR, where the CAR comprise various intracellular, TM and extracellular binding domain. (Claims 1-20).
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
‘037
Claims 16, 17, 18 and 21-24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-9 and 11-19 of copending Application No. 18504037 (reference application; hereinafter referred to as ‘037 application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claimed invention in ‘037 reads on the instant claims.
‘037 application claims CAR or cells containing CAR, where the CAR comprise various intracellular, TM and extracellular binding domain. (Claims 1-9 and 11-19).
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
‘956
Claims 16, 17, 18 and 21-24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-21 of copending Application No. 19036956 (reference application; hereinafter referred to as ‘956 application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claimed invention in ‘956 reads on the instant claims.
‘956 application claims CAR or cells containing CAR, where the CAR comprise various intracellular, TM and extracellular binding domain. (Claims 1-21).
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
‘943
Claims 16, 17, 18 and 21-24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of copending Application No. 19471943 (reference application; hereinafter referred to as ‘943 application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claimed invention in ‘943 reads on the instant claims.
‘943 application claims CAR or cells containing CAR, where the CAR comprise various intracellular, TM and extracellular binding domain. (Claims 1-20).
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion and Correspondence
No claims are allowed.
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