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 the Claims
Claims 304 – 337 were pending. Claims 304 – 309, 311 – 312, 314, and 330 – 335 have been amended, and claims 313 and 315 – 329 have been canceled. Claims 304 – 312, 314, 330 – 337 are currently pending and are the subject of this Office Action.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 07/23/2026 follows the provisions of 37 CFR 1.97 and has been considered.
WITHDRAWN
Claim Rejections - 35 USC § 112
Claims 305 – 308, 312 – 313, 317 – 319, 325, 327 – 329 and 331 – 335 were 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.
In view of the claim amendments in the reply of 07/22/2026, this rejection is withdrawn.
Double Patenting
Claims 304 – 329 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 32, 76 – 77 and 90 – 93 of copending Application No. 17/767,682 in view of VOLKERS (WO 2021/068074 A1, filed 10/08/2020, published 04/15/2021; see PTO-892: Notice of References Cited of 04/22/2026).
In view of the claim amendments in the reply of 07/22/2026, this rejection is withdrawn.
Allowable Subject Matter Withdrawn
Claims 330, 334 and 336 – 337 were allowed.
In view of the correction to independent claim 330, the allowable claim and its dependent claims 334 and 336 – 337 no longer consist of allowable subject matter. See rejection under 102 and 103 below.
REJECTIONS MAINTAINED IN MODIFIED FORM
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.
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.
Claims 304 – 312 and 314 are rejected under 35 U.S.C. 102(a)((2)as being anticipated by VOLKERS (WO 2021/068074 A1, filed 10/08/2020, published 04/15/2021; see PTO-892 of 04/22/2026).
Present independent claim 304 is directed to a variant Granulocyte Colony-Stimulating Factor (G-CSF), wherein the variant G-CSF comprises: (i) E46R, L108K, D1 12R, and E122K mutations; (ii) E46R, L108K, D1 12R, and E123K mutations;(iii) E46R, L108K, D1 12R, and E122R mutations; (iv) E46R, L108K, D112R, and E123R mutations; or (v) E46R, L108K, D1 12R, E122K, and E123K mutations, wherein amino acid numbering is according to the sequence of SEQ ID NO. 1, and wherein the variant G-CSF binds selectively to a receptor comprising a variant extracellular domain (ECD) of Granulocyte Colony-Stimulating Factor Receptor (G-CSFR).
VOLKERS is directed to a variant Granulocyte Colony-Stimulating Factor (G-CSF), wherein the variant G-CSF comprises at least one mutation in a site II interface region, at least one mutation in a site III interface region, or combinations thereof (see VOLKERS’ independent claim 16). VOLKERS teaches that the variant G-CSF comprises the E46R, L108K, D112R, E122R, and E123R mutations corresponding to an amino acid position of SEQ ID NO.1 (see VOLKERS at claim 39), and VOLKERS’ SEQ ID NO. 1 is identical to present SEQ ID NO. 1 of the present claims. See Appendix.
VOLKERS also teaches a receptor, comprising: a variant extracellular domain (ECD) of Granulocyte Colony-Stimulating Factor Receptor (G-CSFR) (see VOLKERS at claim 1) and that the variant G-CSF binds selectively to the receptor (see VOLKERS at claim 23).
Thus, VOLKERS anticipates alternative (iii) or (iv) of variant G-CSF of present claim 304.
Regarding claims 305 – 308, VOLKERS teaches that the receptor comprises the R41E, R141E, and R167D mutations corresponding to an amino acid position of SEQ ID NO. 2. See VOLKERS at claim 41. VOLKERS’ SEQ ID NO. 2 is identical to present SEQ ID NO. 2 of the present claims. See Appendix. VOLKERS also teaches a system for selective activation of a receptor expressed on a cell surface, the system comprising the receptor and the variant G-CSF of present claim 306 (see VOLKERS’ claim 32); VOLKERS teaches a method of administering the variant G-CSF of present claim 307 (see VOLKERS at claim 58); and VOLKERS teaches a kit for producing a chimeric receptor expressed on a cell, comprising: cells comprising an expression vector encoding the variant receptor and instructions for use of present claim 308 (see VOLKERS at claim 71).
Regarding claim 309, VOLKERS teaches a nucleic acid encoding the variant G-CSF (see VOLKERS’ claim 28).
Regarding claim 310, VOLKERS teaches an expression vector comprising the nucleic acid encoding the variant G-CSF (see VOLKERS’ claim 29).
Regarding claim 311, VOLKERS teaches that the receptor is a chimeric receptor. See VOLKERS at claim 8.
Regarding claim 312, VOLKERS teaches the activated chimeric receptor forms a homodimer and that the activation of the chimeric receptor causes a cellular response selected from the group consisting of proliferation, viability and enhanced activity of a cell expressing the chimeric receptor. See paragraph 0019.
Regarding claim 314, VOLKERS teaches the sequence of SEQ ID NO: 90. VOLKERS’ SEQ ID NO: 30 is identical to present SEQ ID NO: 90, and VOLKERS’ SEQ ID NO: 31 is identical to present SEQ ID NO: 91. See Appendix.
NEW REJECTIONS NECESSITATED BY CLAIM AMENDMENTS
Claim Rejections - 35 USC § 102
Claims 330 – 331 and 336 – 337 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by PULÉ (WO 2019/102207-A1, published 05/31/2019; see PTO-892: Notice of References Cited submitted with this Office Action).
PULÉ is directed to a chimeric polypeptide comprising: an antigen-binding domain which constitutively binds to an ectodomain of a first chain of a cytokine receptor; a transmembrane domain; and an endodomain from a second chain of the cytokine receptor which chimeric polypeptide. PULÉ teaches that the type I cytokine receptor α-chain or β-chain is IL-7 receptor α-chain. See PULÉ at claim 5. PULÉ teaches the sequence of present SEQ ID NO: 189 of present claim 330 with 100% identity. PULÉ’s SEQ ID NO: 3 is identical to present SEQ ID NO: 189. See Appendix.
Thus, PULÉ anticipates present claim 330.
Regarding claim 331, PULÉ teaches an ectodomain of a first chain of a cytokine receptor; a transmembrane domain; and an endodomain from a second chain of the cytokine receptor (see at claim 1), which is assumed to be arranged N-terminus to C-terminus, as is the universal convention to list the domains of multi-domain proteins.
Regarding claim 336, PULÉ teaches a nucleic acid sequence encoding the disclosed chimeric polypeptide. See PULÉ at claim 10.
Regarding claim 337, PULÉ teaches a vector comprising the nucleic acid sequence encoding a chimeric polypeptide. See PULÉ at claims 11 – 12.
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
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.
Claim 332 – 335 are rejected under 35 U.S.C. 103 as being unpatentable over PULÉ as applied to claims 330 – 331 and 336 – 337 above, and further in view of VOLKERS.
The teachings of PULÉ and VOLKERS are discussed above and fully incorporated here. Although PULÉ teaches the chimeric receptor of claim 330, from which claims 332 – 335 depend, PULÉ does not expressly teach the limitations of present claims 332 – 335. Nonetheless, PULÉ in view of VOLKERS render claims 332 – 335 obvious for the reasons discussed below.
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Regarding claim 332, PULÉ teaches the receptor of claim 330 and VOLKERS teaches the structure of IL-2Rβ native receptor having the structure:
(see VOLKERS at Figure 20), which teaches the limitations of part (i) of present claim 332. Thus, because PULÉ teaches a cytokine receptor that helps with the persistence and survival of CAR T cells in the treatment of cancer (see PULÉ at p. 2, first and second paragraphs) and VOLKERS also teaches cytokine receptors with specific domains useful for exclusive activation of cells for adoptive cell transfer therapy (see VOLKERS at the abstract), it would have been obvious to one having ordinary skill to modify PULÉ’s structure with VOLKERS’ domains to arrive to the chimeric receptor of present claim 332.
Regarding claims 333 – 335, VOLKERS teaches elective activation of cells using variant cytokine receptor and cytokine pairs (see VOLKERS at the abstract), and thus it would have been obvious to pair a IL-7R with its ligand, the IL-7 cytokine.
At the effective filing date of the present claims, it would have been prima facie obvious to the person of ordinary skill in the art to arrive at the claimed invention from the disclosures of PULÉ and VOLKERS. The artisan would have been motivated to make and use the chimeric receptors of claims 332 - 335 because PULÉ and VOLKERS teach the state of the art of chimeric cytokine receptors and their effectiveness in adoptive cell therapy, such as CAR-T cell therapy. Thus, the artisan would have a reasonable expectation of success from the combined teachings of PULÉ and VOLKERS.
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 304 – 312, 314, and 330 – 337 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 32, 76 – 77 and 90 – 93 of copending Application No. 17/767,682 in view of VOLKERS and PULÉ.
Copending claim 32 recites a system for selective activation of a receptor, the system comprising:(a) a receptor comprising a variant extracellular domain (ECD) of Granulocyte Colony- Stimulating Factor Receptor (G-CSFR) comprising a sequence having at least 85% identity to the sequence of SEQ ID NO: 2,except wherein the variant ECD of G-CSFR comprises (i) at least one mutation in a site II interface region selected from the group consisting of R141E, R167D, K168D, K168E, L171E, L172E, Y173K, Q174E, D197K, D197R, M199D, D200K, D200R, V202D, R288D, and R288E,(i) at least one mutation in a site III interface region selected from the group consisting of S30D, R41E, Q73W, F75K, S79D, L86D, Q87D, 188E, L89A, Q91D, Q91K, and E93K, or (iii) a combination of (i) and (ii), wherein amino acid numbering is according to the sequence of SEQ ID NO: 2 as numbered from 2-308; and(b) a variant G-CSF comprising a sequence having at least 85% identity to SEQ ID NO: 1, except wherein the variant G-CSF comprises (i) at least one mutation in a site II interface region selected from the group consisting of S12E, S 12K, S12R, K16D, L18F, E19K, Q20E, D104K, D104R, L108K, L108R, D109R, D112R, D112K, T115E, T115K, T116D, 0119E, Q1 19R, E122K, E122R, and E123R,(i) at least one mutation in a site III interface region selected from the group consisting of T38R, Y39E, K40D, K40F, L41D, L41E, L41K, E46R, L47D, V48K, V48R, L49K, and R147E, or (iii) a combination
Copending SEQ ID NO: 1 and/or 2 of copending claims 32, 76 – 77 and 90 – 93 teaches present SEQ ID NOs. 1 and 2, respectively, of the present claims with 100% identity. See Appendix.
The main difference between the present claims and the copending claims is that the present claims 307 recites a method of increasing an immune response and present claims 330 – 337 recite an IL-7Rα chimeric receptor and methods of using the IL-7Rα chimeric receptor. However, VOLKERS and PULÉ teach these differences. The teachings of VOLKERS and PULÉ, and how they relate to the claims, are set forth in the rejections under 35 U.S.C. 102 and 103 above.
Because the copending claims recite a receptor comprising a variant ECD of G-CSFR; VOLKERS teaches that the receptor may be used in the method of present claim 307; and PULÉ teaches the IL-7Rα chimeric receptor of present claims 330 – 337, it would have been obvious to one having ordinary skill in the art to use the copending claims’ receptor and variant G-CSF in the present claims as recited.
It would have been prima facie obvious to the person of ordinary skill in the art to arrive at the claimed invention from the disclosures of the copending claims, VOLKERS, and PULÉ. The artisan would have been motivated to make and use the receptor comprising a variant ECD of G-CSFR and variant G-CSFR of the copending claims because the cited references teach their usefulness in adoptive therapy.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
Claims 304 – 312, 314, and 330 – 337 are rejected.
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 Estella Gustilo whose telephone number is (703)756-1706. The examiner can normally be reached Monday - Friday 9:30 AM - 5:30 PM.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Gregory Emch can be reached at 571-272-8149. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/ESTELLA M. GUSTILO/Examiner, Art Unit 1646
/GREGORY S EMCH/Supervisory Patent Examiner, Art Unit 1678
APPENDIX
Alignment with SEQ ID NO. 1
BJF75414
ID BJF75414 standard; protein; 174 AA.
XX
AC BJF75414;
XX
DT 10-JUN-2021 (first entry)
XX
DE Granulocyte Colony-Stimulating Factor (G-CSF) protein, SEQ ID 1.
XX
KW G-CSF; Granulocyte Colony-Stimulating Factor; antiinflammatory;
KW antimicrobial-gen.; cancer; cytostatic; immunosuppressive;
KW infectious disease; inflammatory disease; therapeutic;
KW transplant rejection.
XX
OS Homo sapiens.
XX
CC PN WO2021068074-A1.
XX
CC PD 15-APR-2021.
XX
CC PF 08-OCT-2020; 2020WO-CA051352.
XX
PR 08-OCT-2019; 2019US-0912318P.
XX
CC PA (ZYME ) ZYMEWORKS INC.
CC PA (PROV-) PROVINCIAL HEALTH SERVICES AUTHORITY.
CC PA (UVIC-) UVIC IND PARTNERSHIPS INC.
XX
CC PI Volkers G, Fuller M, Boulanger MJ, Dixit SB, Nelson B, Sanches M;
CC PI Loveless B;
XX
DR WPI; 2021-39265L/033.
DR UNIPROT; A0A0B4U5E3.
XX
CC PT Receptor for treating a subject, preferably for treating cancer,
CC PT comprises variant extracellular domain of Granulocyte Colony-Stimulating
CC PT Factor Receptor, where variant ECD of G-CSFR comprises mutation in site
CC PT II interface region.
XX
CC PS Claim 17; SEQ ID NO 1; 201pp; English.
XX
CC The invention relates to a novel receptor useful for treating diseases.
CC The receptor, comprises a variant extracellular domain (ECD) of
CC Granulocyte Colony-Stimulating Factor Receptor (G-CSFR). The invention
CC further claims: 1) a nucleic acid, which encodes the receptor; 2) an
CC expression vector, which comprises the nucleic acid; 3) a cell, which is
CC engineered to express the receptor; 4) a system for selective activation
CC of a receptor expressed on a cell surface; 5) a method for selective
CC activation of a receptor expressed on the surface of a cell, which
CC involves contacting a receptor with a variant G-CSFR; 6) a method for
CC producing an immune cell expressing a receptor, which comprises
CC introducing to the cells the nucleic acid or the expression vector; 7) a
CC method for treating a subject in need, which involves infusing into the
CC subject the cell; and 8) a kit for treating a subject in need. The
CC receptor is useful for treating cancer, inflammatory condition, graft
CC rejection and infectious disease. Note: The present sequence is used as
CC the parent sequence for the creation of variants (see BJF75505-BJF75569)
CC based on the information given in claim 22, 33, 34 and 6 of the
CC specification.
XX
SQ Sequence 174 AA;
ALIGNMENT:
Query Match 100.0%; Score 896; Length 174;
Best Local Similarity 100.0%;
Matches 174; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 TPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAP 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 TPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAP 60
Qy 61 LSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQ 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 LSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQ 120
Qy 121 MEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP 174
||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 MEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP 174
US-17-767-682-1
Filing date in PALM: 2022-04-08
Sequence 1, US/17767682
Publication No. US20240115603A1
GENERAL INFORMATION
APPLICANT: ZYMEWORKS INC.
APPLICANT: PROVINCIAL HEALTH SERVICES AUTHORITY
APPLICANT: UVIC INDUSTRY PARTNERSHIPS INC.
TITLE OF INVENTION: MODIFIED EXTRACELLULAR DOMAIN OF GRANULOCYTE COLONY-STIMULATING
TITLE OF INVENTION: FACTOR RECEPTOR (G-CSFR) AND CYTOKINES BINDING SAME
FILE REFERENCE: IKE-068WO
CURRENT APPLICATION NUMBER: US/17/767,682
CURRENT FILING DATE: 2022-04-08
PRIOR APPLICATION NUMBER: 62/912,318
PRIOR FILING DATE: 2019-10-08
NUMBER OF SEQ ID NOS: 90
SEQ ID NO 1
LENGTH: 174
TYPE: PRT
ORGANISM: Homo sapiens
ALIGNMENT:
Query Match 100.0%; Score 896; DB 1; Length 174;
Best Local Similarity 100.0%;
Matches 174; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 TPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAP 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 TPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAP 60
Qy 61 LSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQ 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 LSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQ 120
Qy 121 MEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP 174
||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 MEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP 174
Alignment with SEQ ID NO. 2
BJF75415
(NOTE: this sequence has 2 duplicates in the database searched.
See complete list at the end of this report)
ID BJF75415 standard; protein; 307 AA.
XX
AC BJF75415;
XX
DT 10-JUN-2021 (first entry)
XX
DE Ig-CRH (G-CSFR) protein, SEQ ID 2.
XX
KW G-CSF; Granulocyte Colony-Stimulating Factor; antiinflammatory;
KW antimicrobial-gen.; cancer; cytostatic; immunosuppressive;
KW infectious disease; inflammatory disease; therapeutic;
KW transplant rejection.
XX
OS Homo sapiens.
XX
FH Key Location/Qualifiers
FT Protein 2..97
FT /note= "Ig"
FT Domain 98..307
FT /note= "Cytokine Receptor Homologous (CRH) domain"
XX
CC PN WO2021068074-A1.
XX
CC PD 15-APR-2021.
XX
CC PF 08-OCT-2020; 2020WO-CA051352.
XX
PR 08-OCT-2019; 2019US-0912318P.
XX
CC PA (ZYME ) ZYMEWORKS INC.
CC PA (PROV-) PROVINCIAL HEALTH SERVICES AUTHORITY.
CC PA (UVIC-) UVIC IND PARTNERSHIPS INC.
XX
CC PI Volkers G, Fuller M, Boulanger MJ, Dixit SB, Nelson B, Sanches M;
CC PI Loveless B;
XX
DR WPI; 2021-39265L/033.
DR UNIPROT; Q99062.
XX
CC PT Receptor for treating a subject, preferably for treating cancer,
CC PT comprises variant extracellular domain of Granulocyte Colony-Stimulating
CC PT Factor Receptor, where variant ECD of G-CSFR comprises mutation in site
CC PT II interface region.
XX
CC PS Example 1; SEQ ID NO 2; 201pp; English.
XX
CC The invention relates to a novel receptor useful for treating diseases.
CC The receptor, comprises a variant extracellular domain (ECD) of
CC Granulocyte Colony-Stimulating Factor Receptor (G-CSFR). The invention
CC further claims: 1) a nucleic acid, which encodes the receptor; 2) an
CC expression vector, which comprises the nucleic acid; 3) a cell, which is
CC engineered to express the receptor; 4) a system for selective activation
CC of a receptor expressed on a cell surface; 5) a method for selective
CC activation of a receptor expressed on the surface of a cell, which
CC involves contacting a receptor with a variant G-CSFR; 6) a method for
CC producing an immune cell expressing a receptor, which comprises
CC introducing to the cells the nucleic acid or the expression vector; 7) a
CC method for treating a subject in need, which involves infusing into the
CC subject the cell; and 8) a kit for treating a subject in need. The
CC receptor is useful for treating cancer, inflammatory condition, graft
CC rejection and infectious disease.
XX
SQ Sequence 307 AA;
Query Match 99.7%; Score 1691; Length 307;
Best Local Similarity 100.0%;
Matches 307; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 2 ECGHISVSAPIVHLGDPITASCIIKQNCSHLDPEPQILWRLGAELQPGGRQQRLSDGTQE 61
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 ECGHISVSAPIVHLGDPITASCIIKQNCSHLDPEPQILWRLGAELQPGGRQQRLSDGTQE 60
Qy 62 SIITLPHLNHTQAFLSCSLNWGNSLQILDQVELRAGYPPAIPHNLSCLMNLTTSSLICQW 121
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 SIITLPHLNHTQAFLSCSLNWGNSLQILDQVELRAGYPPAIPHNLSCLMNLTTSSLICQW 120
Qy 122 EPGPETHLPTSFTLKSFKSRGNCQTQGDSILDCVPKDGQSHCSIPRKHLLLYQNMGIWVQ 181
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 EPGPETHLPTSFTLKSFKSRGNCQTQGDSILDCVPKDGQSHCSIPRKHLLLYQNMGIWVQ 180
Qy 182 AENALGTSMSPQLCLDPMDVVKLEPPMLRTMDPSPEAAPPQAGCLQLSWEPWQPGLHINQ 241
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 AENALGTSMSPQLCLDPMDVVKLEPPMLRTMDPSPEAAPPQAGCLQLSWEPWQPGLHINQ 240
Qy 242 KCELRHKPQRGEASWALVGPLPLEALQYELCGLLPATAYTLQIRCIRWPLPGHWSDWSPS 301
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 KCELRHKPQRGEASWALVGPLPLEALQYELCGLLPATAYTLQIRCIRWPLPGHWSDWSPS 300
Qy 302 LELRTTE 308
|||||||
Db 301 LELRTTE 307
US-17-767-682-2
Sequence 2, US/17767682
Publication No. US20240115603A1
GENERAL INFORMATION
APPLICANT: ZYMEWORKS INC.
APPLICANT: PROVINCIAL HEALTH SERVICES AUTHORITY
APPLICANT: UVIC INDUSTRY PARTNERSHIPS INC.
TITLE OF INVENTION: MODIFIED EXTRACELLULAR DOMAIN OF GRANULOCYTE COLONY-STIMULATING
TITLE OF INVENTION: FACTOR RECEPTOR (G-CSFR) AND CYTOKINES BINDING SAME
FILE REFERENCE: IKE-068WO
CURRENT APPLICATION NUMBER: US/17/767,682
CURRENT FILING DATE: 2022-04-08
PRIOR APPLICATION NUMBER: 62/912,318
PRIOR FILING DATE: 2019-10-08
NUMBER OF SEQ ID NOS: 90
SEQ ID NO 2
LENGTH: 307
TYPE: PRT
ORGANISM: Homo sapiens
Query Match 99.7%; Score 1691; Length 307;
Best Local Similarity 100.0%;
Matches 307; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 2 ECGHISVSAPIVHLGDPITASCIIKQNCSHLDPEPQILWRLGAELQPGGRQQRLSDGTQE 61
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 ECGHISVSAPIVHLGDPITASCIIKQNCSHLDPEPQILWRLGAELQPGGRQQRLSDGTQE 60
Qy 62 SIITLPHLNHTQAFLSCSLNWGNSLQILDQVELRAGYPPAIPHNLSCLMNLTTSSLICQW 121
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 SIITLPHLNHTQAFLSCSLNWGNSLQILDQVELRAGYPPAIPHNLSCLMNLTTSSLICQW 120
Qy 122 EPGPETHLPTSFTLKSFKSRGNCQTQGDSILDCVPKDGQSHCSIPRKHLLLYQNMGIWVQ 181
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 EPGPETHLPTSFTLKSFKSRGNCQTQGDSILDCVPKDGQSHCSIPRKHLLLYQNMGIWVQ 180
Qy 182 AENALGTSMSPQLCLDPMDVVKLEPPMLRTMDPSPEAAPPQAGCLQLSWEPWQPGLHINQ 241
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 AENALGTSMSPQLCLDPMDVVKLEPPMLRTMDPSPEAAPPQAGCLQLSWEPWQPGLHINQ 240
Qy 242 KCELRHKPQRGEASWALVGPLPLEALQYELCGLLPATAYTLQIRCIRWPLPGHWSDWSPS 301
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 KCELRHKPQRGEASWALVGPLPLEALQYELCGLLPATAYTLQIRCIRWPLPGHWSDWSPS 300
Qy 302 LELRTTE 308
|||||||
Db 301 LELRTTE 307
Alignment with SEQ ID NO: 90
BJF75442
ID BJF75442 standard; protein; 62 AA.
XX
AC BJF75442;
XX
DT 10-JUN-2021 (first entry)
XX
DE G-CSFR (G2R-3) intracellular domain protein, SEQ ID 30.
XX
KW Granulocyte Colony-Stimulating Factor receptor; antiinflammatory;
KW antimicrobial-gen.; c -G-CSFR; cancer; cytostatic; immunosuppressive;
KW infectious disease; inflammatory disease; therapeutic;
KW transplant rejection.
XX
OS Homo sapiens.
XX
CC PN WO2021068074-A1.
XX
CC PD 15-APR-2021.
XX
CC PF 08-OCT-2020; 2020WO-CA051352.
XX
PR 08-OCT-2019; 2019US-0912318P.
XX
CC PA (ZYME ) ZYMEWORKS INC.
CC PA (PROV-) PROVINCIAL HEALTH SERVICES AUTHORITY.
CC PA (UVIC-) UVIC IND PARTNERSHIPS INC.
XX
CC PI Volkers G, Fuller M, Boulanger MJ, Dixit SB, Nelson B, Sanches M;
CC PI Loveless B;
XX
DR WPI; 2021-39265L/033.
DR N-PSDB; BJF75470.
DR UNIPROT; Q99062.
XX
CC PT Receptor for treating a subject, preferably for treating cancer,
CC PT comprises variant extracellular domain of Granulocyte Colony-Stimulating
CC PT Factor Receptor, where variant ECD of G-CSFR comprises mutation in site
CC PT II interface region.
XX
CC PS Disclosure; SEQ ID NO 30; 201pp; English.
XX
CC The invention relates to a novel receptor useful for treating diseases.
CC The receptor, comprises a variant extracellular domain (ECD) of
CC Granulocyte Colony-Stimulating Factor Receptor (G-CSFR). The invention
CC further claims: 1) a nucleic acid, which encodes the receptor; 2) an
CC expression vector, which comprises the nucleic acid; 3) a cell, which is
CC engineered to express the receptor; 4) a system for selective activation
CC of a receptor expressed on a cell surface; 5) a method for selective
CC activation of a receptor expressed on the surface of a cell, which
CC involves contacting a receptor with a variant G-CSFR; 6) a method for
CC producing an immune cell expressing a receptor, which comprises
CC introducing to the cells the nucleic acid or the expression vector; 7) a
CC method for treating a subject in need, which involves infusing into the
CC subject the cell; and 8) a kit for treating a subject in need. The
CC receptor is useful for treating cancer, inflammatory condition, graft
CC rejection and infectious disease.
XX
SQ Sequence 62 AA;
ALIGNMENT:
Query Match 100.0%; Score 345; Length 62;
Best Local Similarity 100.0%;
Matches 62; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 SPNRKNPLWPSVPDPAHSSLGSWVPTIMEEDAFQLPGLGTPPITKLTVLEEDEKKPVPWE 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 SPNRKNPLWPSVPDPAHSSLGSWVPTIMEEDAFQLPGLGTPPITKLTVLEEDEKKPVPWE 60
Qy 61 SH 62
||
Db 61 SH 62
Alignment with SEQ ID NO: 91
BJF75443
ID BJF75443 standard; peptide; 202 AA.
XX
AC BJF75443;
XX
DT 10-JUN-2021 (first entry)
XX
DE IL-2R beta (G2R-3) intracellular domain peptide, SEQ ID 31.
XX
KW CD122 antigen; IL-2R beta; Interleukin-2 receptor beta; antiinflammatory;
KW antimicrobial-gen.; cancer; cytostatic; immunosuppressive;
KW infectious disease; inflammatory disease; therapeutic;
KW transplant rejection.
XX
OS Homo sapiens.
XX
CC PN WO2021068074-A1.
XX
CC PD 15-APR-2021.
XX
CC PF 08-OCT-2020; 2020WO-CA051352.
XX
PR 08-OCT-2019; 2019US-0912318P.
XX
CC PA (ZYME ) ZYMEWORKS INC.
CC PA (PROV-) PROVINCIAL HEALTH SERVICES AUTHORITY.
CC PA (UVIC-) UVIC IND PARTNERSHIPS INC.
XX
CC PI Volkers G, Fuller M, Boulanger MJ, Dixit SB, Nelson B, Sanches M;
CC PI Loveless B;
XX
DR WPI; 2021-39265L/033.
DR N-PSDB; BJF75471.
DR UNIPROT; P14784.
XX
CC PT Receptor for treating a subject, preferably for treating cancer,
CC PT comprises variant extracellular domain of Granulocyte Colony-Stimulating
CC PT Factor Receptor, where variant ECD of G-CSFR comprises mutation in site
CC PT II interface region.
XX
CC PS Disclosure; SEQ ID NO 31; 201pp; English.
XX
CC The invention relates to a novel receptor useful for treating diseases.
CC The receptor, comprises a variant extracellular domain (ECD) of
CC Granulocyte Colony-Stimulating Factor Receptor (G-CSFR). The invention
CC further claims: 1) a nucleic acid, which encodes the receptor; 2) an
CC expression vector, which comprises the nucleic acid; 3) a cell, which is
CC engineered to express the receptor; 4) a system for selective activation
CC of a receptor expressed on a cell surface; 5) a method for selective
CC activation of a receptor expressed on the surface of a cell, which
CC involves contacting a receptor with a variant G-CSFR; 6) a method for
CC producing an immune cell expressing a receptor, which comprises
CC introducing to the cells the nucleic acid or the expression vector; 7) a
CC method for treating a subject in need, which involves infusing into the
CC subject the cell; and 8) a kit for treating a subject in need. The
CC receptor is useful for treating cancer, inflammatory condition, graft
CC rejection and infectious disease.
XX
SQ Sequence 202 AA;
ALIGNMENT:
Query Match 100.0%; Score 1105; Length 202;
Best Local Similarity 100.0%;
Matches 202; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 SSNHSLTSCFTNQGYFFFHLPDALEIEACQVYFTYDPYSEEDPDEGVAGAPTGSSPQPLQ 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 SSNHSLTSCFTNQGYFFFHLPDALEIEACQVYFTYDPYSEEDPDEGVAGAPTGSSPQPLQ 60
Qy 61 PLSGEDDAYCTFPSRDDLLLFSPSLLGGPSPPSTAPGGSGAGEERMPPSLQERVPRDWDP 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 PLSGEDDAYCTFPSRDDLLLFSPSLLGGPSPPSTAPGGSGAGEERMPPSLQERVPRDWDP 120
Qy 121 QPLGPPTPGVPDLVDFQPPPELVLREAGEEVPDAGPREGVSFPWSRPPGQGEFRALNARL 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 QPLGPPTPGVPDLVDFQPPPELVLREAGEEVPDAGPREGVSFPWSRPPGQGEFRALNARL 180
Qy 181 PLNTDAYLSLQELQGQDPTHLV 202
||||||||||||||||||||||
Db 181 PLNTDAYLSLQELQGQDPTHLV 202
Alignment with SEQ ID NO: 189
BGJ69963
ID BGJ69963 standard; protein; 195 AA.
XX
AC BGJ69963;
XX
DT 11-JUL-2019 (first entry)
XX
DE Human IL7Ralpha derived endodomain, SEQ:3.
XX
KW IL7RA protein; bladder cancer; breast tumor; cancer; cell culture;
KW colon tumor; cytokine signaling; cytostatic; endometrioid carcinoma;
KW interleukin-7 receptor alpha; leukemia; lung tumor; melanoma;
KW non-hodgkin lymphoma; pancreas tumor; prophylactic to disease;
KW prostate tumor; recombinant protein; renal tumor; therapeutic;
KW thyroid tumor.
XX
OS Homo sapiens.
XX
CC PN WO2019102207-A1.
XX
CC PD 31-MAY-2019.
XX
CC PF 23-NOV-2018; 2018WO-GB053390.
XX
PR 24-NOV-2017; 2017GB-00019557.
XX
CC PA (AUTO-) AUTOLUS LTD.
XX
CC PI Pule M, Righi M, Thomas S, Onuoha S, Cordoba S;
XX
DR WPI; 2019-484249/45.
XX
CC PT New chimeric polypeptide useful in pharmaceutical composition for
CC PT treating or preventing disease, preferably cancer e.g. bladder cancer,
CC PT breast cancer, colon cancer, kidney cancer, and leukemia in human,
CC PT comprises antigen-binding domain.
XX
CC PS Example 1; SEQ ID NO 3; 41pp; English.
XX
CC The present invention relates to a novel chimeric polypeptide, which when
CC expressed in a cell causes constitutive cytokine signaling. The chimeric
CC polypeptide comprises an antigen-binding domain which constitutively
CC binds to an ectodomain of a first chain of a cytokine receptor, a
CC transmembrane domain and an endodomain from a second chain of the
CC cytokine receptor, which when expressed in a cell, binds to an endogenous
CC first chain of the cytokine receptor causing constitutive cytokine
CC signaling. The invention further discloses: (1) a constitutively-active
CC cytokine receptor comprising the chimeric polypeptide in association with
CC the first chain of the cytokine receptor; (2) a cell comprising the
CC constitutively-active cytokine receptor; (3) a nucleic acid sequence
CC encoding the chimeric polypeptide; (4) a nucleic acid construct
CC comprising a first nucleic acid sequence encoding the chimeric
CC polypeptide and a second nucleic acid encoding a chimeric antigen
CC receptor or an engineered T-cell receptor; (5) a vector comprising the
CC nucleic acid sequence or the nucleic acid construct; (6) a method for
CC making a cell, which involves: (a) introducing the nucleic acid sequence,
CC the nucleic acid construct or the vector into a cell; (7) a method for
CC inducing constitutive cytokine signaling in a cell, which involves
CC expressing the chimeric polypeptide in the cell; (8) a method for
CC blocking deleterious cytokine signaling in a cell, which involves
CC expressing the chimeric polypeptide in the cell, where the antigen
CC binding domain constitutively binds to common gamma chain and one or more
CC deleterious cytokine signal through a cytokine receptor which comprises
CC common gamma chain; (9) a pharmaceutical composition comprising a
CC plurality of the cells; and (10) a method for treating or preventing a
CC disease, which involves administering a pharmaceutical composition to a
CC subject. The novel chimeric polypeptide of the invention is useful for
CC manufacturing a medicament to treat or prevent cancer, where the cancer
CC is selected from bladder cancer, breast cancer, colon cancer, endometrial
CC cancer, kidney cancer (renal cell), leukemia, lung cancer, melanoma, non-
CC Hodgkin lymphoma, pancreatic cancer, prostate cancer and thyroid cancer.
XX
SQ Sequence 195 AA;
ALIGNMENT:
Query Match 100.0%; Score 1025; Length 195;
Best Local Similarity 100.0%;
Matches 195; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 KKRIKPIVWPSLPDHKKTLEHLCKKPRKNLNVSFNPESFLDCQIHRVDDIQARDEVEGFL 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 KKRIKPIVWPSLPDHKKTLEHLCKKPRKNLNVSFNPESFLDCQIHRVDDIQARDEVEGFL 60
Qy 61 QDTFPQQLEESEKQRLGGDVQSPNCPSEDVVITPESFGRDSSLTCLAGNVSACDAPILSS 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 QDTFPQQLEESEKQRLGGDVQSPNCPSEDVVITPESFGRDSSLTCLAGNVSACDAPILSS 120
Qy 121 SRSLDCRESGKNGPHVYQDLLLSLGTTNSTLPPPFSLQSGILTLNPVAQGQPILTSLGSN 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 SRSLDCRESGKNGPHVYQDLLLSLGTTNSTLPPPFSLQSGILTLNPVAQGQPILTSLGSN 180
Qy 181 QEEAYVTMSSFYQNQ 195
|||||||||||||||
Db 181 QEEAYVTMSSFYQNQ 195
Prosecution Insights