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 .
Response to Amendment
The rejections of claims 41-46, 48 and 51-54 are moot in view of the cancellation of the claims.
The rejection of claims 17, 24, 31-34, 38, 40-46 and 51-54 under 35 USC 112(a), for lacking written description, is withdrawn in view of the amendment to claim 17 introducing CDR sequences the antibody is required to contain and cancellation of claims. Also, because claims 32 and 34 limit treatment after a parameter related to Treg% is met, such that if it is not met, then there is no administration, they were determined upon further consideration not to have an issue of written description. Note claim 39 remains rejected.
The rejection of claims 17, 24 and 31-54 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, for lacking enablement, is withdrawn in view of the amendment to claim 17 introducing CDR sequences the antibody is required to contain and cancellation of claims.
The rejection of claims 17, 24, 31, 33, 38, 40, 42, 43, 45, 48, 51 and 53 on the ground of nonstatutory double patenting as being unpatentable over claims 16, 18, 31, 32 and 38-40 of copending Application No. 18/666,545 (‘545) in view of US 2021/0277129 A1 (McGrath) in light of Campbell et al. (Canc. Res. 81(11):2983-2994, 01 June 2021) is withdrawn in view of cancellation of claims and because the instant claims have been amended to recite specific antibody CDR sequences comprised by the antibody administered in the instantly claimed method, which sequences the claims of ‘545 do not recite and which are not obvious over the prior art.
The rejection of claim(s) 17, 24, 31-34, 38, 40, 42-45, 48, 51 and 53 is/are rejected under 35 U.S.C. 102(a)(2) as being anticipated by US 2021/0277129 A1 (McGrath, cited in the IDS filed 5/16/20204) in light of CN 118852430 A (Google English translation also attached) is withdrawn in view of the amendment to claim 17 introducing CDR sequences the antibody is required to contain, which the prior art did not teach, and in view of the cancellation of claims.
The rejection of claim(s) 17, 24, 31, 33 and 34 under 35 U.S.C. 103 as being unpatentable over WO 2018/181425 A1 (WO’425, cited in the IDS filed 5/16/2024) in view of Liu et al. (J. Haematol. Oncol. 11:104, 15 pages, 2018) is withdrawn in view of the amendment to claim 17 introducing CDR sequences the antibody is required to contain. The prior art does not teach or suggest an antibody comprising those CDRs.
Claim Rejections - 35 USC § 112(b)
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 40 is 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.
Claim 40 as it now depends from amended claim 17 is indefinite because it recites preparing the antibody … that specifically binds to CCR8 using a sulfated polypeptide…” The antibody now must comprise specific CDRs. In accordance with MPEP 2173.05(q), a process that does not set forth any steps involved in the process is indefinite if it has no active, positive steps delimiting how this use is actually practiced (Ex parte Erlich, 3 USPQ2d 1011 (Bd. Pat. App. & Inter. 1986).
Claim Rejections - 35 USC § 112(a)
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.
Claim 39 remains 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 for the reasons set forth in the previous Office action and as recast here to remove references to the now cancelled claims and address the amendment to independent claim 17 introducing specific antibody CDR sequences.
Claim 39 limits the antibody or antigen-binding fragment thereof to one that binds human CCR8 and also binds CCR8 from one or both of mouse and cynomolgus. Table 10.1.1.6 lists isolated antibodies that bound both human and cynomolgus CCR8. These antibodies meet the written description for claim 39. Antibodies binding murine sulfated CCR8 TRD were isolated through selection by panning (e.g., Table 10.1.1.5 and Example 8), but they do not necessarily bind human or cynomolgus CCR8 (p. 227, lines 22-24 and Table 10.1.2.1). The specification discusses (Example 2) that human and cynomolgus CCR8 protein share 94.37% identity, with the TRD thereof sharing 68% identity, but only 71% identity is shared between mouse and human CCR8 and 52% over the TRD. This supports the lack of reasonable expectation that an anti-CCR8 antibody binding human or cynomolgus CCR8, particularly the TRD, would also bind murine CCR8, including in the TRD. As stated on p. 9, lines 1-3, “According to the current invention, cross reactive antibodies for CCR8 can be generated in particular by using small sulfated tyrosine comprising motifs which have a higher conservation between species,…” This again, points to the difficulty of producing anti-CCR8 antibodies that are cross-reactive between animal species other than for those animals with significant CCR8 sequence identity, especially of the TRD domain, e.g., human and cynomolgus monkey. The need for surrogate antibodies, e.g., anti-murine CCR8 antibodies TPP-15285 and TPP-14099, to use in syngeneic mouse tumor models also supports the lack of expectation of cross-reactivity between antibodies binding human and/or cynomolgus sulfated CCR8 and those binding murine sulfated CCR8 (see, e.g., Example 12 and Table 12.1.1.2).
The specification discloses data primarily for antibody TPP15285, a surrogate anti-mouse CCR8 antibody that stands in for an anti-human CCR8 antibody. TPP15285 comprises a mouse IgG2a Lambda Fc region, while anti-human CCR8 antibody TPP-23411 comprises a human IgG1 Lambda Fc region (Table on pp. 26 and 34, respectively, and, e.g., p. 239, lines 4-5 and 13). These particular anti-mouse and anti-human antibodies share only about 87% identity in their variable heavy chain regions (VH), with most of that being in the framework regions. The HCDR3 of the human antibody is missing in the mouse surrogate antibody and the HCDR2s of the antibodies share only 60% identity. (See Sequence Comparison at the end of the rejection.) Therefore, there is insufficient written description for the antibodies of claim 39 which cross-react and bind CCR8 from mouse. One skilled in the art could not readily envision the structure of a representative number of species of the genus of CCR8-binding antibodies of claim 17 that bind mouse or bind mouse and cynomolgus CCR8.
Vas-Cath Inc. v. Mahurkar, 19USPQ2d 1111 (Fed. Cir. 1991), clearly states that “applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the ‘written description' inquiry, whatever is now claimed.” (See page 1117.) The specification does not “clearly allow persons of ordinary skill in the art to recognize that [they] invented what is claimed.” (See Vas-Cath at page 1116).
Adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method of isolating it. See Fiers v. Revel, 25 USPQ2d 1601 at 1606 (CAFC 1993) and Amgen Inc. v. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016 (Fed. Cir. 1991).
Therefore, only the method of claim 17 wherein the anti-CCR8 antibody or antigen-binding fragment thereof is cross-reactive and binds with CCR8 from cynomolgus, but not the full breadth of the claim, i.e., including wherein it binds mouse CCR8, meets the written description provision of 35 U.S.C. § 112(a). Applicant is reminded that Vas-Cath makes clear that the written description provision of 35 U.S.C. § 112 is severable from its enablement provision (see page 1115).
Applicant argues (p. 10 of REMARKS) that claim 17 has been amended to recite CDR sequences for the CCR8 antibodies and so the remaining claims are in compliance with the written description requirements. The argument has been fully considered but is not persuasive. Claim 30 remains rejected for the reasons set forth in the previous rejection and as recast above. The amendment to claim 17 defining the antibody CDRs further removes the antibodies from those which would reasonably be expected to bind mouse CCR8 as discussed above.
Sequence Comparison
anti-murine CCR8 TPP-15285 (Qy) v. anti-human CCR8 TPP-23411 (Db)
Variable Heavy Chain region (SEQ ID NO:229 v. 617)
Query Match 86.6%;Score 515;DB 1;Length 122;Best Local Similarity 82.1%;
Matches 101; Conservative 3; Mismatches 7; Indels 12; Gaps 2;
Qy 1 EVQLLESGGGLVQPGGSLRLSCAASGFTFSDYGVHWVRQAPGKGLEWVSGVSWNGSRTHY 60
|||||||||||||||||||||||||||||| ||:||||||||||||||| ::||| | |
Db 1 EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYGMHWVRQAPGKGLEWVSAINWNGGSTGY 60
Qy 61 ADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCVTRG-----------AWGQGTLVT 109
|||||||||||||||||||||||||||||||||||| || ||||||||
Db 61 ADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYC-ARGHHSGYDGRFFDYWGQGTLVT 119
Qy 110 VSS 112
|||
Db 120 VSS 122
Variable Light Chain Region (SEQ ID NO:233 v. 621)
Query Match 85.3%;Score 496.5;DB 1;Length 111; Best Local Similarity 87.4%;
Matches 97; Conservative 6; Mismatches 7; Indels 1; Gaps 1;
Qy 1 QSVLTQPPSASGTPGQRVTISCSGSSFNIGSHF-VYWYQQLPGTAPKLLIYKNNQRPSGV 59
||||||||| || |||||||||:||| |||: : |:||||||||||||||| ||:|||||
Db 1 QSVLTQPPSVSGAPGQRVTISCTGSSSNIGAGYNVHWYQQLPGTAPKLLIYTNNRRPSGV 60
Qy 60 PDRFSGSKSGTSASLAISGLRSEDEADYYCAAWDDSLNGPVFGGGTKLTVL 110
|||||||||||||||||||||||||||||||||| ||:| |||||||||||
Db 61 PDRFSGSKSGTSASLAISGLRSEDEADYYCAAWDASLSGWVFGGGTKLTVL 1112
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 17, 24, 31, 33, 38, 39 remain and claims 32, 34 and 40 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 8-16 of U.S. Patent No. 12,065,497 (‘497) in view of US 2021/0277129 A1 (McGrath) for the reasons set forth in the previous Office action and as recast here to reflect the amendment to independent claim 17 introducing the CDR sequences of the antibody used in the method.
Both instant claim 17 and patented claims 1 and 12 are drawn to a method of treating a tumor in a subject by administering an antibody or antigen-binding-fragment thereof that specifically binds CCR8 and comprises a specific set of CDR sequences of the variable heavy and light chain region, which CDRs are the same between the instant application and patent. These CDR sequences are also comprised by the variable heavy and light chain regions of patented claims 7 and 8. Both recite that the antibody can induce depletion of activated CCR8-expressing Treg cells or tumor cells (instant claims 17, 32 and 34 and claim 2 and 12 of ‘497), and require a further therapeutically active compound or therapy; although claim 2 of ‘497 specifies this is a checkpoint protein inhibitor and instant claim 17 specifies it is not. Note that claims 1 and 12 of ‘497 are silent with respect to an additional therapeutic or therapy. The properties of ADCC and/or ADCP are inherent to the structure of the antibodies, as is the fact that they bind sulfated human CCR8 (e.g., Examples 6 and 7 of both the instant application and patent). The patent does not claim administration of the antibody or antigen-binding fragment thereof with a second therapeutic compound or therapy which is not a target of a checkpoint protein.
McGrath teaches treatment of a tumor with tumor infiltrating Tregs that express CCR8 by administering to a subject with the tumor an effective amount of anti-CCR8 antibody 1-K17 or 7-B16 ([0299]). The anti-CCR8 antibodies possess ADCC activity by human IgG1 chimeric anti-CCR8 antibodies 1-K17 and 7-B16 (Fig. 6). Antibodies having a mIgG2a Fc domain led to tumor infiltrating Treg depletion and reduced tumor growth in an in vivo MC38 syngeneic mouse model ([0054]-[0055] and Example 11). The paratope of 7-B16 was identified and “represented amino acids 1-35 of the CCR8 protein, and within this sequence, all the tyrosine residues… could be sulfated “([0703]). The antibody may be administered in conjunction with another anti-cancer treatment, including radiation therapy or chemotherapy ([0316]) e.g., gemcitabine, docetaxel, doxorubicin, cisplatin, paclitaxel or oxaliplatin ([0322]). Administration may be sequential, including wherein the antibody is administered sequentially with a second therapeutic agent ([0317]).
It would have been obvious wherein treatment of a tumor with an anti-CCR8 antibody as set forth in the patent claims additionally comprised administration with a further therapeutic agent or therapy that was a chemotherapeutic agent or radiation as taught by McGrath and which second therapies were well known and routinely used for the treatment of tumors. Because the antibodies of the patent inherently bind sulfated CCR8 and because McGarth teaches optional sulfation of tyrosines within a CCR8-binding paratope, which comprises the N-terminus of CCR8, it would have been obvious wherein the antibodies of the method were prepared by identification and isolation using a sulfated CCR8 tyrosine rich domain to screen antibody display systems (see instant Fig. 2B for a schematic definition of the location of the tyrosine rich domain).
Applicant argues (p. 12 of REMARKS, third to last paragraph) that the instant application is a divisional application from a common restricted (grandparent) application and, therefore, should not be subject to double patenting with another divisional application from the same restricted application. The patent claims are drawn to a method of treating a tumor characterized by CCR8-expressing cells by administering a CCR8 antibody or antigen-binding fragment thereof, wherein as the instant claims are amended they recite the same CDRs of the antibodies of the patented claims. As stated in the non-final Office action mailed 1/22/2026 in the instant application, the claims were amended (9/5/2025) so they are drawn to a method of treating a tumor, which “is most similar to Group IX, a method of treating a tumor or disease characterized by the involvement of cells expressing CCR8 by administering an antibody or antigen-binding fragment according to claim 17 as set forth in the restriction mailed 6/18/2025,…” Therefore, both the instant application and patent are drawn to the same elected invention. The rejection is maintained as recast to better address the instantly amended claims. It is noted there was no restriction in the parent application but only a species election.
Claims 17, 24, 31-34, 38-40 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 14-15 of U.S. Patent No. 11,427,640 B1 (‘640) in view of US 2021/0277129 A1 (McGrath).
Both the instant claims 17 and patented claims 14 and 15 are drawn to a method of treating a tumor in a subject by administering an antibody or antigen-binding-fragment thereof that specifically binds CCR8, wherein the antibody induces antibody-dependent cellular phagocytosis (ADCP). In the instant claims the antibody induces at least one of ADCP and antibody-dependent cellular cytotoxicity (ADCC), however, this includes antibodies inducing ADCP. Both the patent and application limit the antibody to having specific sets of variable heavy and light chain region CDR sequences. Instant claim 17 recites the same antibody CDR sequences as in claim 1 of the patent. ADCC and/or ADCP is inherent to the structure (sequence) of the antibody. The patent does not claim administration of the antibody or antigen-binding fragment thereof with a second therapeutic compound or therapy which is not a target of a checkpoint protein.
McGrath teaches treatment of a tumor with tumor infiltrating Tregs that express CCR8 by administering to a subject with the tumor an effective amount of anti-CCR8 antibody 1-K17 or 7-B16 ([0299]). The anti-CCR8 antibodies possess ADCC activity by human IgG1 chimeric anti-CCR8 antibodies 1-K17 and 7-B16 (Fig. 6). Antibodies having a mIgG2a Fc domain led to tumor infiltrating Treg depletion and reduced tumor growth in an in vivo MC38 syngeneic mouse model ([0054]-[0055] and Example 11). The paratope of 7-B16 was identified and “represented amino acids 1-35 of the CCR8 protein, and within this sequence, all the tyrosine residues… could be sulfated “([0703]). The antibody may be administered in conjunction with another anti-cancer treatment, including radiation therapy or chemotherapy ([0316]) e.g., gemcitabine, docetaxel, doxorubicin, cisplatin, paclitaxel or oxaliplatin ([0322]). Administration may be sequential, including wherein the antibody is administered sequentially with a second therapeutic agent ([0317]).
It would have been obvious wherein treatment of a tumor with an anti-CCR8 antibody as set forth in the patent claims additionally comprised administration with a further therapeutic agent or therapy that was a chemotherapeutic agent or radiation as taught by McGrath and which second therapies were well known and routinely used for the treatment of tumors. Because the antibodies of the patent inherently bind sulfated CCR8 and because McGarth teaches optional sulfation of tyrosines within a CCR8-binding paratope, which comprises the N-terminus of CCR8, it would have been obvious wherein the antibodies of the method were prepared by identification and isolation using a sulfated CCR8 tyrosine rich domain to screen antibody display systems (see instant Fig. 2B for a schematic definition of the location of the tyrosine rich domain).
Note the restriction in 17/358,841, from which Patent ‘640 issued, was withdrawn between the antibody (group I) and method (group VIII, restriction mailed 11/9/2021), which was rejoined after indication of allowability of a product claim from which the new method claims depended and which required all the limitations of the allowable claim (see Office Action mailed 4/20/2022 in Application No. 17/358,841).
Claims 17, 24, 31, 33, 38 and 39 remain and claims 32, 34 and 40 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, 17, 18, 13 and 25 of copending Application No. 19/110,032 (‘032) in view of US 2021/0277129 A1 (McGrath) in light of Campbell et al. (Canc. Res. 81(11):2983-2994, 01 June 2021) for the reasons set forth in the previous Office action and as recast here to reflect the amendment to independent claim 17 introducing the CDR sequences of the antibody used in the method.
Both the instant claim 17 and claims 1 and 2 of ’032 are drawn to a method of treating a subject by administering an antibody or antigen-binding-fragment thereof that binds CCR8. Claim 17 of ‘032 further defines the antibody as comprising respectively HCDR1-3 and LCDR1-3 of SEQ ID NO:2-4 and 6-8, VH and VL of SEQ ID NO:1 and 5 and HC and LC of SEQ ID NO:17 and 18. These HC and LC of ‘032 comprise instant SEQ ID NO: 618-620 and 622-624, respectively (instant claim 17). The instant method is for treatment of a tumor and with an anti-CCR8 antibody that induces ADCC and/or ADCP and is selected from one of (a) to (r). The antibody of ‘032 with the sequences of claim 17 is TPP23411 as defined in the table on p. 12 of that specification and which inherently induces ADCC and ADCP (Examples 5 and 6 of ‘032) and binds human and cynomolgus CCR8 (p. 70, middle). This antibody has the same CDRs as instant SEQ ID NO:618-620 and 622-624, respectively (see table on instant p. 34). The claims of ‘032 do not recite administration of a further therapeutic agent or therapy that does not target a checkpoint protein and that consists of at least one of a) docetaxel, paclitaxel, doxorubicin, oxaliplatin or gemcitabine, b) radiation therapy, and c) depletion of intra-tumoral B cells.
McGrath teaches treatment of a tumor with tumor infiltrating Tregs that express CCR8 by administering to a subject with the tumor an effective amount of anti-CCR8 antibody 1-K17 or 7-B16 ([0299]). The anti-CCR8 antibodies possess ADCC activity by human IgG1 chimeric anti-CCR8 antibodies 1-K17 and 7-B16 (Fig. 6). Antibodies having a mIgG2a Fc domain led to tumor infiltrating Treg depletion and reduced tumor growth in an in vivo MC38 syngeneic mouse model ([0054]-[0055] and Example 11). The paratope of 7-B16 was identified and “represented amino acids 1-35 of the CCR8 protein, and within this sequence, all the tyrosine residues… could be sulfated “([0703]). The antibody may be administered in conjunction with another anti-cancer treatment, including radiation therapy or chemotherapy ([0316]) e.g., gemcitabine, docetaxel, doxorubicin, cisplatin, paclitaxel or oxaliplatin ([0322]). Administration may be sequential, including wherein the antibody is administered sequentially with a second therapeutic agent ([0317]).
It would have been obvious wherein treatment was of a tumor with an anti-CCR8 antibody as set forth in the copending claims additionally comprised administration with a further therapeutic agent or therapy that was a chemotherapeutic agent or radiation as taught by McGrath and which second therapies were well known and routinely used for the treatment of tumors. Because the antibodies of the patent inherently bind sulfated CCR8 and because McGarth teaches optional sulfation of tyrosines within a CCR8-binding paratope, which comprises the N-terminus of CCR8, it would have been obvious wherein the antibodies of the method were prepared by identification and isolation using a sulfated CCR8 tyrosine rich domain to screen antibody display systems (see instant Fig. 2B for a schematic definition of the location of the tyrosine rich domain).
This is a provisional nonstatutory double patenting rejection.
Applicant argues (p. 12 of Remarks, second to last paragraph), the instantly amended claims “are patentable distinct from those of the ‘032 application.” The argument has been fully considered but is not persuasive. For the reasons set forth in the recast rejection above addressing the amendment to the instant claims, they remain not patentable on the grounds of nonstatutory double patenting.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Claire Kaufman, whose telephone number is (571) 272-0873. Examiner Kaufman can generally be reached Monday through Friday 7am-3:30pm, Eastern Time.
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Claire Kaufman
/Claire Kaufman/
Primary Examiner, Art Unit 1674
June 25, 2026
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