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 .
Status of Claims
Claims 9 and 18 are amended. Claims 1-23 are currently pending and under examination.
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. Claims 1-23 have an earliest effective filing date of 06/02/2020, corresponding to provisional application 63/033,385.
Response to Remarks filed 11/24/2025
Applicant’s arguments and amendments regarding the objection of claim 9 have been fully considered and are persuasive. Specifically, amending “and” to “an” remedied the objection. Therefore, the objection is withdrawn.
Applicant’s arguments and amendments regarding the 35 USC 112 rejection of claim 18 have been fully considered and are persuasive. Specifically, amending the claim to recite “claim 15” remedied the rejection. Therefore the rejection is withdrawn.
Applicant’s arguments and amendments regarding the 35 USC 102 and 103 rejections have been fully considered and are not persuasive. Applicant claims the Mule is a coinventor on the instant application, and filed a declaration on 11/24/2025. However, Mule is not listed as an inventor on instant application 18/000,425. Therefore the 35 USC 102 and 35 USC 103 rejections are maintained.
Previous Rejections Maintained- Nonfinal 07/29/2025
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
(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.
Claim(s) 1-2, 8-21, and 23 are rejected under 35 U.S.C. 102a1 as being anticipated by Mule et al (WO2019241334, published 12/19/2019).
Regarding claims 1, 2, and 9, Mule et al teach an SSTR CAR wherein the binding domain is a scFv of an antibody that specifically binds SSTR (Mule et al, pg. 5, paragraphs 1-3). Mule et al further teach that the CAR can include SP, SSTR, HG, TM, CSR, ISD, and bivalent linkers (Mule et al, pg. 7 paragraph 4- pg. 9 paragraph 3).
Regarding claim 8, claim 1 is discussed above. Mule et al further teach costimulatory signaling regions including CD27, CD28, 4-1BB, OX40, CD30, CD40, PD-1, ICOS, LFA-1, CD2, CD7, LIGHT, NKG2C, B7-H3, and a ligand that specifically binds CD83.
Regarding claim 10, claim 1 is discussed above. Mule et al further teach the intracellular signaling domain comprising CD3 zeta (Mule et al, pg. 7, paragraph 3).
Regarding claims 11 and 13, claim 1 is discussed above. Mule et al teach an isolated nucleic acid sequence encoding the CAR and immune effector cell comprising the vector (Mule et al, pg. 10, paragraph 4).
Regarding claim 12, Mule et al teach a vector comprising the isolated nucleic acid sequence (Mule et al, pg. 11, paragraph 1-2).
Regarding claim 14, claim 1 is discussed above. Mule et al teach the immune effector cell comprising the vector can be CD8+ T-cells (includes CTLs) (Mule et al, pg. 10, paragraph 3-4).
Regarding claim 15, claim 13 is discussed above. Mule et al teach the effector functions of the immune effector cell are activated upon antigen recognition (i.e. inherently known in the art to kill cancerous cells; Mule et al, pg. 6, paragraph 3).
Regarding claim 16, Mule et al teach the CAR can be constructed to secrete cytokines (Mule et al, pg. 3, paragraph 6).
Regarding claim 17, Mule et al teach the CARs are intended to combine a second CAR, the CARs can have incomplete ectodomains requiring the second CAR for activation (Mule et al, pg. 3, paragraph 2). Mule et al further teach the SSTR-binding domain and CD56-binding domain (Mule et al, pg. 5, paragraph 3). Mule et al additionally teach a dual CART in which two separate CARs are expressed, one with the CD3z (intracellular domain) and the other with the costimulatory domains (Mule et al, pg. 4, paragraph 9).
Regarding claims 18 and 23, Mule et al teach providing an immunologically effective amount of the immune effector cell to a patient with cancer (Mule et al, pg. 14, paragraph 4). Mule et al further teach the patient can have neuroblastoma, which is an SSTR-expressing neuroendocrine tumor (Mule et al, pg. 16, paragraph 2).
Regarding claims 19 and 20, Mule et al teach the method of claim 18 can be administered in combination with immune checkpoint inhibitors including anti-PD1, anti-PDL1, and anti-CTLA4 (Mule et al, pg. 16, paragraph 4).
Regarding claim 21, Mule et al teach administering chemotherapy to the subject (Mule et al, pg. 15, paragraph 3). It is noted that chemotherapy is known to upregulate SSTR.
Therefore, claims 1-2, 8-21, and 23 are rejected as being anticipated by Mule et al.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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.
Claims 3 and 22 are rejected under 35 U.S.C. 103 as being unpatentable over Mule et al (WO2019241334, published 12/19/2019) in view of Moore et al (US20180118827, published 05/03/2018).
The teachings of Mule et al. are discussed in detail above and are incorporated by reference herein.
Mule et al. teach an SSTR CAR wherein the binding domain is a scFv of an antibody that specifically binds SSTR (Mule et al, pg. 5, paragraphs 1-3). Mule et al. further teach that the CAR can include SP, SSTR, HG, TM, CSR, ISD, and bivalent linkers (Mule et al, pg. 7 paragraph 4- pg. 9 paragraph 3). Mule et al. do not teach VH or VL of the CAR polypeptide comprising HCDR1-3 comprising SEQ ID NO:12-14 and LCDR1-3 comprising SEQ ID NO:15-17, respectively. This deficiency is remedied by Moore et al.
Moore et al. teach an SSTR2 antibody comprising a VH with reference SEQ ID NO:958 (100% identity instant SEQ ID NO:12-14) and a VL with reference SEQ ID NO: 962 (100% identity instant SEQ ID NO:15-17) (Moore et al., pg. 25, Figure 11A).
One of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to combine the teachings of Mule et al. and Moore at al. to arrive at a CAR capable of binding SSTR comprising instant SEQ ID NO:12-17. One of ordinary skill in the art would be motivated to do so, because Mule et al teach an SSTR CAR wherein the binding domain is a scFv of an antibody that specifically binds SSTR (Mule et al., pg. 5, paragraphs 1-3). Mule et al further teach that the CAR can include SP, SSTR, HG, TM, CSR, ISD, and bivalent linkers (Mule et al, pg. 7 paragraph 4- pg. 9 paragraph 3). Furthermore based on the teachings of Moore et al., one of ordinary skill in the art would be motivated to use the sequences of Moore et al. that are capable of binding SSTR in a CAR capable of binding SSTR. As such one of ordinary skill in the art would be motivated to modify the invention of Mule et al. which teaches a CAR capable of binding SSTR to further include the VH and VL sequences of Moore et al. to create a CAR capable of binding SSTR. The teachings or Mule et al. and Moore et al. meet the limitation of claim 3.
Regarding claim 22 Moore et al. disclose that the antibody can be a bispecific antibody capable of binding SSTR2 and CD3. One skilled in the art would be motivated to combine the teachings to better treat cancer by directing effector T-cells to SSTR2+ cancer (Moore et al., pg. 7, paragraph 0072-0073).
The teachings of Mule et al. and Moore et al. meet the limitations of claims 3 and 22. Therefore, claims 3 and 22 were prima facie obvious at the time of effective filing.
Claims 4 5, and 7 are rejected under 35 U.S.C. 103 as being unpatentable over Mule et al. (WO2019241334, published 12/19/2019) in view of Bonnet et al. (US20190328887, published 10/31/2019).
The teachings of Mule et al. are discussed in detail above and are incorporated by reference herein.
Mule et al. teach an SSTR CAR wherein the binding domain is a scFv of an antibody that specifically binds SSTR (Mule et al, pg. 5, paragraphs 1-3). Mule et al. further teach that the CAR can include SP, SSTR, HG, TM, CSR, ISD, and bivalent linkers (Mule et al, pg. 7 paragraph 4- pg. 9 paragraph 3). Mule et al. do not teach the CAR polypeptide wherein the SSTR antigen binding domain is octreotide derived or comprises 1, 2, 3, or 4 copies of the amino acid sequence FCFWKTCT optionally separated by a linker. This is remedied by Bonnet et al.
Bonnet et al. teach the octreotide derived polypeptide of reference SEQ ID NO: 49 (Bonnet et al, FCFWKTCT, 100% instant SEQ ID NO: 1, pg. 6, paragraph 0066) and the peptide lanreotide (Bonnet et al., pg. 8, paragraph 0070).
One of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to combine the teachings of Mule et al. and Bonnet et al. to arrive at a CAR capable of binding SSTR comprising instant SEQ ID NO: 1. One of ordinary skill in the art would be motivated to do so, because Mule et al. teach an SSTR CAR wherein the binding domain is a scFv of an antibody that specifically binds SSTR (Mule et al., pg. 5, paragraphs 1-3). Mule et al. further teach that the CAR can include SP, SSTR, HG, TM, CSR, ISD, and bivalent linkers (Mule et al, pg. 7 paragraph 4- pg. 9 paragraph 3). Furthermore based on the teachings of Bonnet et al., one of ordinary skill in the art would be motivated to use the sequences of Bonnet et al. that are capable of binding SSTR in a CAR capable of binding SSTR. As such one of ordinary skill in the art would be motivated to modify the invention of Mule et al. which teaches a CAR capable of binding SSTR to further include the octreotide sequence of lanreotide peptide of Bonnet et al. to further improve the binding of the SSTR CAR.
Mule et al. and Bonnet et al. meet the limitations of claims 4, 5, and 7. Therefore, claims 4, 5, and 7 were prima facie obvious at the time of effective filing.
Allowable Subject Matter
Claim 6 is objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims.
Conclusion
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/J.K.D./Examiner, Art Unit 1642
/NELSON B MOSELEY II/Primary Examiner, Art Unit 1642