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 .
DETAILED ACTION
Status of Application/Election/Restrictions
2. Claims 1-52 and 55-56 are canceled. Claims 53-54 and 57-66 are pending in this application and under examination in this office action.
Priority
3. Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) is acknowledged. Applicant has not complied with one or more conditions for receiving the benefit of an earlier filing date under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) as follows:
The later-filed application must be an application for a patent for an invention which is also disclosed in the prior application (the parent or original nonprovisional application or provisional application). The disclosure of the invention in the parent application and in the later-filed application must be sufficient to comply with the requirements of the first paragraph of 35 U.S.C. 112. See Transco Products, Inc. v. Performance Contracting, Inc., 38 F.3d 551, 32 USPQ2d 1077 (Fed. Cir. 1994).
The disclosure of the prior-filed application, provisional Application No. 62/542944, fails to provide adequate support or enablement in the manner provided by the first paragraph of 35 U.S.C. 112 for one or more claims of this application. The instant application claims a Clec9A binding agent comprising a recombinant VHH comprising CDR1-3 of SEQ ID NOs: 53, 138 and 256 respectively or at least 98% identity to SEQ ID NO:330 or 331 and wherein CDR1-3 of SEQ ID NOs:53, 138 and 256 respectively, and a chimeric protein comprising the claimed Clec9A binding agent and a mutated human IFN-a2 comprising one or more mutations at recited positions relative to SEQ ID NO:337 or 338, or a mutated human IFN-b comprising one or more mutations at recited positions relative to SEQ ID NO:339, a recombinant nucleic acid thereof and a host cell thereof, which are not presented in the provisional Application No. 62/542944, filed on August 09, 2017. The claimed Clec9A binding agent, chimeric protein, recombinant nucleic acid thereof and host cell thereof were only disclosed in PCT/US18/14742 filed on August 08, 2018 (see p.15 of the specification of PCT/US18/14742).
Therefore, the priority for the claimed subject matter in the instant application is August 08, 2018.
Claim Objections
4. Claims 53 and 57-58 are objected to because of the following informalities:
i. Regarding claim 53, the limitation “CDR1 is the amino acid sequence…..CDR2 is the amino acid sequence…; and CDR3 is the amino acid sequence…” is objected to because “CDR1” is CDR1, not the amino acid sequence. The limitation should be “wherein the sequence of CDR1 is the amino acid sequence of SEQ ID NO:53; the sequence of CDR2 is the amino acid sequence of SEQ ID NO:138 and the sequence of CDR3 is the amino acid sequence of SEQ ID NO:256”, or “wherein the CDR1 consists of the amino acid sequence of SEQ ID NO;53, the CDR2 consists of the amino acid sequence of SEQ ID NO;138; and the CDR3 consists of the amino acid sequence of SEQ ID NO: 256”. Appropriate correction is required.
ii. Regarding claim 57-58, the limitation “comprising an amino acid sequence having at least 98% identity with one of SEQ ID NOs:330 and 331” is objected to because the recitation “SEQ ID NOs:330 and 331” is only a text, not the sequence. The limitation should be “comprising an amino acid sequence having at least 98% identity with the amino acid sequence of SEQ ID NO:330 or SEQ ID NO:331”. Appropriate correction is required.
Claim Rejections - 35 USC § 112
5. 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.
Claims 58, 60, 62-63 and 65-66 are 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 pre-AIA the applicant regards as the invention.
Claims 58, 60, 62-63 and 65-66 are indefinite because:
i. Claim 62 recites “a polynucleotide encoding the Clec9A the chimeric protein of claim 61” and claim 65 recites “a polynucleotide encoding the Clec9A the chimeric protein of claim 64”. It is unclear whether the recited polynucleotide encodes the Clec9A in the chimeric protein of claim 61/65 or encodes the whole chimeric protein of claim 61/65, which renders the claims indefinite. For examination purposes, the limitation “a polynucleotide encoding the Clec9A the chimeric protein of claim 61/64” is interpretated as “a polynucleotide encoding the chimeric protein of claim 61/64”.
ii. Claim 58 recites the limitation “….wherein the amino acid sequence”. It is unclear which sequence in claim 57 the limitation “the amino acid sequence” is referred to. Thus, the claim is indefinite. For examination purposes, claim 58 is interpreted as “the Clec9A binding agent of claim 53, comprising the amino acid sequence of SEQ ID NO:330 or SEQ ID NO:331”.
iii. Claim 60 recites the limitation “a nucleic acid of claim 59”, claim 63 recites the limitation “a nucleic acid of claim 62”, and claim 66 recites the limitation a nucleic acid of claim 65”. The article “A” connotes that there is more than a single molecule encompassed within the base claim and since only a single “recombinant nucleic acid comprising a polynucleotide….” was set forth therein, it is unclear what, if any, additional molecules/nucleic acid molecules are encompassed. Thus, claims 60, 63 and 66 are indefinite. For examination purposes, the limitation “a nucleic acid of claim 59/62/65” is interpretated as “the recombinant nucleic acid composition of claim 59/62/65”.
Claim Rejections - 35 USC § 112
6. The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 61-66 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 pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention.
To provide adequate written description and 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.
Claims 61-63 encompass a genus of chimeric protein comprising (a) the claimed Cle9A binding agent of claim 53 and a genus of mutated human IFN-a2 comprising one or more mutations at positions R120, M148, R146 and L153 relative to SEQ ID NO:337 or 338, a genus of nucleic acid composition comprising a genus of polynucleotides encoding the claimed genus of chimeric protein and a genus of isolated host cells comprising the claimed genus of nucleic acid composition or the claimed genus of polynucleotides.
Claims 64-66 encompass a genus of chimeric protein comprising (a) the claimed Cle9A binding agent of claim 53 and a genus of mutated human IFN-b comprising one or more mutations at positions W22, R27, L32, R35, V148, L151, R152 and Y155 relative to SEQ ID NO:339, a genus of nucleic acid composition comprising a genus of polynucleotides encoding the claimed genus of chimeric protein and a genus of isolated host cells comprising the claimed genus of nucleic acid composition or the claimed genus of polynucleotides.
Applicant has not disclosed sufficient species for the broad genus of chimeric protein, the broad genus of mutated human IFN-a2, the broad genus of one or more mutations at positions R120, M148, R146 and L153 relative to SEQ ID NO:337 or 338, the broad genus of mutated human IFN-b, the broad genus of one or more mutations at positions W22, R27, L32, R35, V148, L151, R152 and Y155 relative to SEQ ID NO:339, the broad genus of recombinant nucleic acid composition, the broad genus of polynucleotides encoding the claimed chimeric protein, and the broad genus of isolated host cells comprising the broad genus of recombinant nucleic acid compositions.
The specification only describes the anti-human Clec9A VHH comprising the amino acid sequence selected from R1CHCL50: SEQ ID NOs: 327-331; or an anti-human Clec9A VHH chimera, wherein the anti-human Clec9A VHH chimera is a fusion protein of the anti-human Clec9A VHH fused to a human IFN2-R149A (see p. 131-134, examples 2-4, figures 4-7A). The specification teaches that 2LEC16-hIFNa2_R149A, 3LEC22-hIFNa2_R149A, 1LEC28-hIFNa2_R149A, 3LEC30-hIFNa2_R149A and 3LEC89-hIFNa2_R149A have anti-tumor activity in human RL follicular lymphoma cell line tumor model in mice (example 6, Figure 8).
However, the claims are not limited to the anti-human Clec9A chimera comprising the anti-human Clec9A VHH fused to a human IFN2-R149A set forth above but also encompass a genus of structurally and functionally undefined chimeric proteins comprising the claimed Clec9A binding agent and a structurally and functionally undefined mutated human IFN-a2 comprising a genus of structurally and functionally undefined one or more mutations at positions R120, M148, R146 and L153 relative to SEQ ID NO:337 or 338 or a genus of structurally and functionally undefined chimeric proteins comprising the claimed Clec9A binding agent and a structurally and functionally undefined mutated human IFN-b comprising a genus of structurally and functionally undefined one or more mutations at positions W22, R27, L32, R35, V148, L151, R152 and Y155 relative to SEQ ID NO:339.
In making a determination of whether the application complies with the written description requirement of 35 U.S.C. 112, first paragraph, it is necessary to understand what Applicant is in possession of and what Applicant is claiming.
M.P.E.P. § 2163 instructs:
An invention described solely in terms of a method of making and/or its function may lack written descriptive support where there is no described or art-recognized correlation between the disclosed function and the structure(s) responsible for the function. . . .
An applicant 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. . . .
An applicant may also show that an invention is complete by disclosure of sufficiently detailed, relevant identifying characteristics which provide evidence that applicant was in possession of the claimed invention, i.e., complete or partial structure, other physical and/or chemical properties, functional characteristics when coupled with a known or disclosed correlation between function and structure, or some combination of such characteristics.”
This standard has not been met in this case. From the specification, it is clear that Applicant is in possession of R1CHCL50: SEQ ID NOs: 327-331; or an anti-human Clec9A VHH chimera, wherein the anti-human Clec9A VHH chimera is a fusion protein of the anti-human Clec9A VHH fused to a human IFN2-R149A (see p. 131-134, examples 2-4, figures 4-7A); and 2LEC16-hIFNa2_R149A, 3LEC22-hIFNa2_R149A, 1LEC28-hIFNa2_R149A, 3LEC30-hIFNa2_R149A and 3LEC89-hIFNa2_R149A which have anti-tumor activity in human RL follicular lymphoma cell line tumor model in mice (example 6, Figure 8).
However, Applicant is not in possession of other chimeric proteins comprising the claimed Clec9A binding agent and a genus of structurally and functionally undefined mutated human IFN-a2 comprising a genus of structurally and functionally undefined one or more mutations at positions R120, M148, R146 and L153 relative to SEQ ID NO:337 or 338 or other chimeric proteins comprising the claimed Clec9A binding agent and a genus of structurally and functionally undefined mutated human IFN-b comprising a genus of structurally and functionally undefined one or more mutations at positions W22, R27, L32, R35, V148, L151, R152 and Y155 relative to SEQ ID NO:339.
It is well established a single amino acid change on a molecule or protein can abolish the binding ability or the activity of the molecule or protein. For example, a substitution of lysine residue by glutamic acid at position 118 of acidic fibroblast growth factor results in a substantial loss of its biological activity including the binding ability to heparin and its receptor (Burgess et al. J of Cell Bio. 1990, 111:2129-2138). Although many amino acid substitutions are possible in any given protein, the position of where such amino acid substitutions can be made is critical for maintaining the function of a protein; i.e. only certain positions can tolerate conservative substitutions without changing the relationship of three dimensional structure and function of the protein (col 2, p. 1306, Bowie et al. Science, 1990, 247:1306-1310). Even if an active or binding site were identified in the specification, they may not be sufficient, as the ordinary artisan would not immediately recognize that an active or binding site must assume the proper three-dimensional configuration to be active because conformation is dependent upon surrounding residues; i.e. substitution of non-essential residues can often destroy activity. In addition to a core determinant sequence, the protein-protein interaction also relies on the flanking or noncontiguous residues (see p. 445 the second column, first paragraph, Pawson et al. 2003, Science 300:445-452). The optimal binding motif for a domain is not necessarily suitable for physiological or in vivo interaction. The predictive data always need to be validated by actual analyses in cells (see p. 445, the third column, second paragraph, Pawson et al. 2003, Science 300:445-452). Alaoui-lsmaili teaches that designing a mutein having predictable activities is difficult because of the complexity of the interactions between ligands and receptors (Alaoui-lsmaili et al., Cytokine Growth Factor Rev. 2009; 20:501-507). For example, given the complexity of BMP-BMP receptor interactions, it is difficult to design BMPs with improved affinity and/or specificity for one specific receptor. More importantly, predicting the in vivo biological activity of such altered BMPs remains a challenging undertaking (see p. 502, right col., 2th paragraph). Further, when multiple mutations are introduced, there is even less predictability because Guo et al. teaches that the effects of mutations on protein function are largely additive (see p. 9207, left col., 2th paragraph, Guo et al., PNAS 2004; 101:9205-9210). Moreover, even minor changes in the amino acid sequences of the heavy and light variable regions, particularly in the CDRs, may dramatically affect antigen-binding function as evidenced by Rudikoff et al. (Proc. Natl. Acad. Sci. USA 1982 Vol. 79: page 1979). Rudikoff et al teach that the alteration of a single amino acid in the CDR of a phosphocholine-binding myeloma protein resulted in the loss of antigen-binding function. Applicant fails to teach what other structures/amino acid sequences are for the claimed chimeric proteins, nucleic acids encoding thereof and host cells thereof.
The specification provides no identification of any particular portion of the structure that must be conserved. The instant specification fails to provide sufficient descriptive information, such as definitive structural or functional features of the claimed genus of chimeric proteins, nucleic acids encoding thereof and host cells thereof, the claimed genus of mutated human IFN-a2 comprising one or more mutations at recited positions relative to SEQ ID NO:337 or 338 and the claimed genus of mutated human IFN-b comprising one or more mutations at recited positions relative to SEQ ID NO:339. There is no description of the conserved regions which are critical to the function of the genus claimed. There is no description of the sites at which variability may be tolerated and there is no information regarding the relation of structure of other chimeric proteins, nucleic acids encoding thereof and host cells thereof to the function of the anti-human Clec9A VHH comprising the amino acid sequence of SEQ ID NO: 330 or 331 or the function of the chimeric protein of 2LEC16-hIFNa2_R149A, 3LEC22-hIFNa2_R149A, 1LEC28-hIFNa2_R149A, 3LEC30-hIFNa2_R149A and 3LEC89-hIFNa2_R149A shown in Examples 2-6 and figures 4-8 of the instant specification. Furthermore, the prior art does not provide compensatory structural or correlative teachings sufficient to enable one of skill to identify what other chimeric proteins, nucleic acids encoding thereof and host cells thereof might be.
Since the common characteristics/features of other chimeric protein, nucleic acids thereof and host cells are unknown, a skilled artisan cannot envision the functional correlations of the genus with the claimed invention. Accordingly, in the absence of sufficient recitation of distinguishing identifying characteristics, the specification does not provide adequate written description of the genus of chimeric proteins, nucleic acids encoding thereof and host cells thereof.
Based on MPEP § 2161.01 and §2163, “to satisfy the written description requirement, a patent specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. See, e.g., Moba, B.V. v. Diamond Automation, Inc., 325 F.3d 1306, 1319, 66 USPQ2d 1429, 1438 (Fed. Cir. 2003); Vas-Cath, Inc. v. Mahurkar, 935 F.2d at 1563, 19 USPQ2d at 1116”.
Vas-Cath Inc. v. Mahurkar, 19USPQ2d 1111, clearly states “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 [he or she] invented what is claimed.” (See Vas-Cath at page 1116).
As discussed above, the skilled artisan cannot envision the detailed chemical structure of the encompassed genus of chimeric proteins, nucleic acid composition thereof or polynucleotides encoding thereof, or isolated host cells thereof, and therefore conception is not achieved until reduction to practice has occurred, regardless of the complexity or simplicity of the method of isolation. 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. The compound itself is required. See Fiers v. Revel, 25 USPQ2d 1601 at 1606 (CAFC 1993) and Amgen Inc. v. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016. One cannot describe what one has not conceived. See Fiddes v. Baird, 30 USPQ2d 1481 at 1483.
Therefore, the claimed chimeric proteins have not met the written description provision of 35 U.S.C. §112, first paragraph. 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 is directed to the Guidelines for the Examination of Patent Applications Under the 35 U.S.C. 112, ¶ 1 "Written Description" Requirement. See MPEP § 2161.01 and 2163.
Double Patenting
7. 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 53-54 and 57-66 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 198, 200-202, 206-213, 215-220, 222, 226-233 and 235-237 of copending Application No. 17042512, or claims1, 15, 19, 22, 64-65, 86-87, 89 and 91 of copending Application No. 17763342. Although the claims at issue are not identical, they are not patentably distinct from each other because the chimeric protein comprising a targeting moiety binding to Clec9A, a modified human IFN2 and an Fc domain, a nucleic acid encoding thereof and a host cell comprising the nucleic acid thereof recited in the claims of Application Nos. 17042512 and 17763342 anticipate the claimed chimeric protein, a nucleic acid encoding thereof and a host cell thereof recited in instant claims.
Claims 198, 200-202, 206-213, 215-220, 222, 226-233 and 235-237 of Application No. 17042512 (the ‘512 Application) claim a chimeric protein comprising a targeting moiety binding to Clec9A (i.e. Clec9A binding agent), a modified human IFN2 and an Fc domain, wherein the Clec9A binding agent comprises the sequence that is 99.1% identical to instant SEQ ID NO:330, and the modified human IFNa2 comprises a mutation at position R149 relative to SEQ ID NO:337, which anticipates instant claims (see the sequence alignment below)..
Claims1, 15, 19, 22, 64-65, 86-87, 89 and 91 of Application No. 17763342 (the ‘342 Application) claim a chimeric protein comprising the claimed Clec9A binding agent and a mutated human IFN2 comprising one of more mutations at recited positions relative to SEQ ID NO:337, which anticipates instant claims (see the sequence alignment below).
Therefore, claims 53-54 and 57-66 of instant Application are not patentably distinct from claims 198, 200-202, 206-213, 215-220, 222, 226-233 and 235-237 of the ‘512 Application, or claims1, 15, 19, 22, 64-65, 86-87, 89 and 91 of the ‘342 Application because claims 53-54 and 57-66 of instant Application are anticipated by claims 198, 200-202, 206-213, 215-220, 222, 226-233 and 235-237 of the ‘512 Application, or claims1, 15, 19, 22, 64-65, 86-87, 89 and 91 of the ‘342 Application.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
SEQ ID NO:330
US-17-763-342-288
Sequence 288, US/17763342
Publication No. US20220378925A1
GENERAL INFORMATION
APPLICANT: Orionis Biosciences Inc.
TITLE OF INVENTION: CONJUGATED CHIMERIC PROTEINS
FILE REFERENCE: ORN-058/114384-5058
CURRENT APPLICATION NUMBER: US/17/763,342
CURRENT FILING DATE: 2022-03-24
PRIOR APPLICATION NUMBER: PCT/US20/52761
PRIOR FILING DATE: 2020-09-25
PRIOR APPLICATION NUMBER: US 62/906,433
PRIOR FILING DATE: 2019-09-26
NUMBER OF SEQ ID NOS: 295
SEQ ID NO 288
LENGTH: 310
TYPE: PRT
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: Synthetic Sequence
Query Match 98.7%; Score 589; Length 310;
Best Local Similarity 99.1%;
Matches 114; Conservative 0; Mismatches 1; Indels 0; Gaps 0;
Qy 1 DVQLVESGGGLVHPGGSLRLSCAASGSFSSINVMGWYRQAPGKERELVARITNLGLPNYA 60
|||||||||||| |||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DVQLVESGGGLVQPGGSLRLSCAASGSFSSINVMGWYRQAPGKERELVARITNLGLPNYA 60
Qy 61 DSVKGRFTISRDNSKNTVYLQMNSLRPEDTAVYYCYLVALKAEYWGQGTLVTVSS 115
|||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 DSVKGRFTISRDNSKNTVYLQMNSLRPEDTAVYYCYLVALKAEYWGQGTLVTVSS 115
SEQ ID NO:337
US-17-763-342-289
Sequence 289, US/17763342
Publication No. US20220378925A1
GENERAL INFORMATION
APPLICANT: Orionis Biosciences Inc.
TITLE OF INVENTION: CONJUGATED CHIMERIC PROTEINS
FILE REFERENCE: ORN-058/114384-5058
CURRENT APPLICATION NUMBER: US/17/763,342
CURRENT FILING DATE: 2022-03-24
PRIOR APPLICATION NUMBER: PCT/US20/52761
PRIOR FILING DATE: 2020-09-25
PRIOR APPLICATION NUMBER: US 62/906,433
PRIOR FILING DATE: 2019-09-26
NUMBER OF SEQ ID NOS: 295
SEQ ID NO 289
LENGTH: 310
TYPE: PRT
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: Synthetic Sequence
Query Match 99.3%; Score 845; Length 310;
Best Local Similarity 99.4%;
Matches 164; Conservative 0; Mismatches 1; Indels 0; Gaps 0;
Qy 1 CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMI 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 146 CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMI 205
Qy 61 QQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVR 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 206 QQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVR 265
Qy 121 KYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE 165
|||||||||||||||||||||||||||| ||||||||||||||||
Db 266 KYFQRITLYLKEKKYSPCAWEVVRAEIMASFSLSTNLQESLRSKE 310
SEQ ID NO:330
US-17-042-512-1443
(NOTE: this sequence has 1 duplicate in the database searched)
Sequence 1443, US/17042512
Publication No. US20210024631A1
GENERAL INFORMATION
APPLICANT: Orionis Biosciences, Inc.
APPLICANT: Orionis Biosciences BV
TITLE OF INVENTION: BI-FUNCTIONAL PROTEINS AND CONSTRUCTION THEREOF
FILE REFERENCE: ORN-042/114384-5042
CURRENT APPLICATION NUMBER: US/17/042,512
CURRENT FILING DATE: 2020-09-28
PRIOR APPLICATION NUMBER: PCT/US19/24714
PRIOR FILING DATE: 2019-03-28
PRIOR APPLICATION NUMBER: 62/649,238
PRIOR FILING DATE: 2018-03-28
PRIOR APPLICATION NUMBER: 62/649,264
PRIOR FILING DATE: 2018-03-28
PRIOR APPLICATION NUMBER: 62/649,248
PRIOR FILING DATE: 2018-03-28
NUMBER OF SEQ ID NOS: 1570
SEQ ID NO 1443
LENGTH: 351
TYPE: PRT
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: Synthetic Sequence
Query Match 98.7%; Score 589; Length 351;
Best Local Similarity 99.1%;
Matches 114; Conservative 0; Mismatches 1; Indels 0; Gaps 0;
Qy 1 DVQLVESGGGLVHPGGSLRLSCAASGSFSSINVMGWYRQAPGKERELVARITNLGLPNYA 60
|||||||||||| |||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DVQLVESGGGLVQPGGSLRLSCAASGSFSSINVMGWYRQAPGKERELVARITNLGLPNYA 60
Qy 61 DSVKGRFTISRDNSKNTVYLQMNSLRPEDTAVYYCYLVALKAEYWGQGTLVTVSS 115
|||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 DSVKGRFTISRDNSKNTVYLQMNSLRPEDTAVYYCYLVALKAEYWGQGTLVTVSS 115
SEQ ID NO:337
US-17-042-512-1448
(NOTE: this sequence has 1 duplicate in the database searched)
Sequence 1448, US/17042512
Publication No. US20210024631A1
GENERAL INFORMATION
APPLICANT: Orionis Biosciences, Inc.
APPLICANT: Orionis Biosciences BV
TITLE OF INVENTION: BI-FUNCTIONAL PROTEINS AND CONSTRUCTION THEREOF
FILE REFERENCE: ORN-042/114384-5042
CURRENT APPLICATION NUMBER: US/17/042,512
CURRENT FILING DATE: 2020-09-28
PRIOR APPLICATION NUMBER: PCT/US19/24714
PRIOR FILING DATE: 2019-03-28
PRIOR APPLICATION NUMBER: 62/649,238
PRIOR FILING DATE: 2018-03-28
PRIOR APPLICATION NUMBER: 62/649,264
PRIOR FILING DATE: 2018-03-28
PRIOR APPLICATION NUMBER: 62/649,248
PRIOR FILING DATE: 2018-03-28
NUMBER OF SEQ ID NOS: 1570
SEQ ID NO 1448
LENGTH: 402
TYPE: PRT
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: Synthetic Sequence
Query Match 99.3%; Score 845; Length 402;
Best Local Similarity 99.4%;
Matches 164; Conservative 0; Mismatches 1; Indels 0; Gaps 0;
Qy 1 CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMI 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 238 CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMI 297
Qy 61 QQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVR 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 298 QQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVR 357
Qy 121 KYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE 165
|||||||||||||||||||||||||||| ||||||||||||||||
Db 358 KYFQRITLYLKEKKYSPCAWEVVRAEIMASFSLSTNLQESLRSKE 402
Conclusion
7. NO CLAIM IS ALLOWED.
8. The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
WO2020033646 teaches an anti-Clec9A mutant single-domain antibody VHH comprising the amino acid sequence of SEQ ID 330, which is 100% identical to instant SEQ ID NO:330 and comprises SEQ ID NOs: 53, 138 and 256 for CDRs1-3 respectively (see the sequence alignments below).
SEQ ID NO:330
ID BHI37692 standard; protein; 115 AA.
XX
AC BHI37692;
XX
DT 02-APR-2020 (first entry)
XX
DE Anti-Clec9A single domain antibody VHH region mutant, SEQ ID 1155.
XX
KW C-type lectin domain protein 9A; CLEC9A protein; autoimmune disease;
KW cancer; cytostatic; heavy chain variable region; immunosuppressive;
KW immunotherapy; mutein; neurodegenerative disease; neuroprotective;
KW prophylactic to disease; recombinant protein; single domain antibody;
KW therapeutic.
XX
OS Synthetic.
OS Unidentified.
XX
CC PN WO2020033646-A1.
XX
CC PD 13-FEB-2020.
XX
CC PF 08-AUG-2019; 2019WO-US045654.
XX
PR 08-AUG-2018; 2018US-0715903P.
XX
CC PA (ORIO-) ORIONIS BIOSCIENCES INC.
CC PA (ORIO-) ORIONIS BIOSCI NV.
XX
CC PI Kley N, Tavernier J;
XX
DR WPI; 2020-13953L/021.
XX
CC PT SIRPIa targeting moiety used for manufacturing a medicament for treating
CC PT or preventing cancer, autoimmune or neurodegenerative disease, comprises
CC PT three complementarity determining regions CDR1 , CDR2, and CDR3.
XX
CC PS Disclosure; SEQ ID NO 1155; 276pp; English.
XX
CC The present invention relates to a novel signal regulatory protein alpha-
CC 1 (SIRP1 alpha) targeting moiety, useful for manufacturing a medicament
CC for treating or preventing cancer, autoimmune or neurodegenerative
CC disease. The SIRP1 alpha targeting moiety comprises three complementarity
CC determining regions CDR1 , CDR2, and CDR3. The invention further
CC provides: (1) a recombinant nucleic acid composition encoding the SIRP1
CC alpha targeting moiety; (2) a host cell comprising the nucleic acid; (3)
CC a method for treating or preventing cancer, which involves administering
CC a chimera comprising the targeting moiety comprising an antigen or
CC receptor recognition domain targeting SIRP1 alpha, where the SIRP1 alpha
CC targeting moiety is a SIRP1 alpha targeting moiety and a signaling agent
CC selected from one or more of an interferon, an interleukin, and a tumor
CC necrosis factor; (4) a method for treating or preventing autoimmune or
CC neurodegenerative disease; (5) a chimeric protein, which comprises the
CC SIRP1 alpha targeting moiety, and a modified human IFN-alpha 2, modified
CC human IFN-alpha 2 having one or more mutations that confer improved
CC safety as compared to a wild type IFN-alpha 2, and where the SIRP1 alpha
CC targeting moiety and the modified human IFN-alpha 2 are optionally
CC connected with one or more linkers; and (6) a Fc-based chimeric protein
CC complex, which comprises the targeting moiety comprising a recognition
CC domain that recognizes and/or binds to SIRP1 alpha, a signaling agent,
CC where the signaling agent is a wild type signaling agent or a modified
CC signaling agent that has one or more mutations that confer improved
CC safety relative to the wild type signaling agent, and a Fc domain, where
CC the Fc domain optionally having one or more mutations that reduces or
CC eliminates one or more effector functions of the Fc domain, promotes Fc
CC chain pairing in the Fc domain, or stabilizes a hinge region in the Fc
CC domain.
XX
SQ Sequence 115 AA;
Query Match 100.0%; Score 597; Length 115;
Best Local Similarity 100.0%;
Matches 115; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DVQLVESGGGLVHPGGSLRLSCAASGSFSSINVMGWYRQAPGKERELVARITNLGLPNYA 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DVQLVESGGGLVHPGGSLRLSCAASGSFSSINVMGWYRQAPGKERELVARITNLGLPNYA 60
Qy 61 DSVKGRFTISRDNSKNTVYLQMNSLRPEDTAVYYCYLVALKAEYWGQGTLVTVSS 115
|||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 DSVKGRFTISRDNSKNTVYLQMNSLRPEDTAVYYCYLVALKAEYWGQGTLVTVSS 115
SEQ ID NO:53-SEQ ID NO:138-SEQ ID NO:256
BHI37693
ID BHI37693 standard; protein; 112 AA.
XX
AC BHI37693;
XX
DT 02-APR-2020 (first entry)
XX
DE Anti-Clec9A single domain antibody VHH region mutant, SEQ ID 1156.
XX
KW C-type lectin domain protein 9A; CLEC9A protein; autoimmune disease;
KW cancer; cytostatic; heavy chain variable region; immunosuppressive;
KW immunotherapy; mutein; neurodegenerative disease; neuroprotective;
KW prophylactic to disease; recombinant protein; single domain antibody;
KW therapeutic.
XX
OS Synthetic.
OS Unidentified.
XX
CC PN WO2020033646-A1.
XX
CC PD 13-FEB-2020.
XX
CC PF 08-AUG-2019; 2019WO-US045654.
XX
PR 08-AUG-2018; 2018US-0715903P.
XX
CC PA (ORIO-) ORIONIS BIOSCIENCES INC.
CC PA (ORIO-) ORIONIS BIOSCI NV.
XX
CC PI Kley N, Tavernier J;
XX
DR WPI; 2020-13953L/021.
XX
CC PT SIRPIa targeting moiety used for manufacturing a medicament for treating
CC PT or preventing cancer, autoimmune or neurodegenerative disease, comprises
CC PT three complementarity determining regions CDR1 , CDR2, and CDR3.
XX
CC PS Disclosure; SEQ ID NO 1156; 276pp; English.
XX
CC The present invention relates to a novel signal regulatory protein alpha-
CC 1 (SIRP1 alpha) targeting moiety, useful for manufacturing a medicament
CC for treating or preventing cancer, autoimmune or neurodegenerative
CC disease. The SIRP1 alpha targeting moiety comprises three complementarity
CC determining regions CDR1 , CDR2, and CDR3. The invention further
CC provides: (1) a recombinant nucleic acid composition encoding the SIRP1
CC alpha targeting moiety; (2) a host cell comprising the nucleic acid; (3)
CC a method for treating or preventing cancer, which involves administering
CC a chimera comprising the targeting moiety comprising an antigen or
CC receptor recognition domain targeting SIRP1 alpha, where the SIRP1 alpha
CC targeting moiety is a SIRP1 alpha targeting moiety and a signaling agent
CC selected from one or more of an interferon, an interleukin, and a tumor
CC necrosis factor; (4) a method for treating or preventing autoimmune or
CC neurodegenerative disease; (5) a chimeric protein, which comprises the
CC SIRP1 alpha targeting moiety, and a modified human IFN-alpha 2, modified
CC human IFN-alpha 2 having one or more mutations that confer improved
CC safety as compared to a wild type IFN-alpha 2, and where the SIRP1 alpha
CC targeting moiety and the modified human IFN-alpha 2 are optionally
CC connected with one or more linkers; and (6) a Fc-based chimeric protein
CC complex, which comprises the targeting moiety comprising a recognition
CC domain that recognizes and/or binds to SIRP1 alpha, a signaling agent,
CC where the signaling agent is a wild type signaling agent or a modified
CC signaling agent that has one or more mutations that confer improved
CC safety relative to the wild type signaling agent, and a Fc domain, where
CC the Fc domain optionally having one or more mutations that reduces or
CC eliminates one or more effector functions of the Fc domain, promotes Fc
CC chain pairing in the Fc domain, or stabilizes a hinge region in the Fc
CC domain.
XX
SQ Sequence 112 AA;
Query Match 85.1%; Score 140.4; Length 112;
Best Local Similarity 41.8%;
Matches 33; Conservative 0; Mismatches 0; Indels 46; Gaps 2;
Qy 1 GSFSSINVMG--------------RITNLGLPNYADSVKG-------------------- 26
|||||||||| ||||||||||||||||
Db 26 GSFSSINVMGWYRQAPGKERELVARITNLGLPNYADSVKGRFTISRDNSKNTVYLQMNSL 85
Qy 27 ------------VALKAEY 33
|||||||
Db 86 RPEDTAVYYCYLVALKAEY 104
WO2019032662 teaches an anti-Clec9A mutant single-domain antibody VHH comprising the amino acid sequence of SEQ ID 330, which is 100% identical to instant SEQ ID NO:330 and comprises SEQ ID NOs: 53, 138 and 256 for CDRs1-3 respectively (see the sequence alignments below).
SEQ ID NO:330
BGB94234
(NOTE: this sequence has 2 duplicates in the database searched)
ID BGB94234 standard; protein; 115 AA.
XX
AC BGB94234;
XX
DT 04-APR-2019 (first entry)
XX
DE Anti-clec9A nanobody VHH region mutant E1D-A74S-K83R-Q108L-T64K, SEQ 330.
XX
KW C-type lectin domain protein 9A; antibody therapy; antimicrobial-gen.;
KW autoimmune disease; cancer; clec9A protein; cytostatic;
KW heavy chain variable region; immune disorder; immunomodulator;
KW immunosuppressive; infectious disease; monoclonal antibody; mutein;
KW nanobody; neurodegenerative disease; neuroprotective;
KW prophylactic to disease; recombinant protein; therapeutic.
XX
OS Lama sp.
OS Synthetic.
XX
CC PN WO2019032662-A1.
XX
CC PD 14-FEB-2019.
XX
CC PF 08-AUG-2018; 2018WO-US045742.
XX
PR 09-AUG-2017; 2017US-0542944P.
XX
CC PA (ORIO-) ORIONIS BIOSCIENCES INC.
CC PA (ORIO-) ORIONIS BIOSCI NV.
XX
CC PI Kley N, Tavernier J, Zabeau L, Depla E;
XX
DR WPI; 2019-154379/16.
XX
CC PT C-type lectin domain family 9 member A (Clec9A) binding agent comprises
CC PT targeting moiety comprising complementarity determining regions (CDR1,
CC PT CDR2, and CDR3), for treating cancer, infections, immune disorders,
CC PT and/or autoimmune diseases.
XX
CC PS Claim 22; SEQ ID NO 330; 166pp; English.
XX
CC The present invention relates to a novel clec9A binding agent, useful in
CC treating or preventing cancer in a subject. The clec9A binding agent
CC comprises an amino acid sequence of SEQ ID NO: 332 (see BGB94236). The
CC invention also provides: a recombinant nucleic acid composition encoding
CC the clec9A binding agent; a host cell comprising the nucleic acid; a
CC method for treating or preventing cancer, autoimmune disease and/or
CC neurodegenerative disease; a chimeric protein comprising the clec9A
CC binding agent and a modified human IFN-alpha 2 comprising one or more
CC mutations conferring improved safety. The clec9A binding agent is also
CC useful in preparing a medicament for treating infections and immune
CC disorders. The present sequence represents an anti-clec9A nanobody heavy
CC chain variable region mutant E1D-A74S-K83R-Q108L-T64K derived from the
CC wild-type sequence of SEQ ID NO: 332 (see BGB94236), which is used in
CC preparing the clec9A binding agent involved in preparing a medicament for
CC treating or preventing the above mentioned diseases in a subject.
XX
SQ Sequence 115 AA;
Query Match 100.0%; Score 597; Length 115;
Best Local Similarity 100.0%;
Matches 115; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DVQLVESGGGLVHPGGSLRLSCAASGSFSSINVMGWYRQAPGKERELVARITNLGLPNYA 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DVQLVESGGGLVHPGGSLRLSCAASGSFSSINVMGWYRQAPGKERELVARITNLGLPNYA 60
Qy 61 DSVKGRFTISRDNSKNTVYLQMNSLRPEDTAVYYCYLVALKAEYWGQGTLVTVSS 115
|||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 DSVKGRFTISRDNSKNTVYLQMNSLRPEDTAVYYCYLVALKAEYWGQGTLVTVSS 115
SEQ ID NO:53-SEQ ID NO:138-SEQ ID NO:256
BGB94235
(NOTE: this sequence has 5 duplicates in the database searched)
ID BGB94235 standard; protein; 115 AA.
XX
AC BGB94235;
XX
DT 04-APR-2019 (first entry)
XX
DE Anti-clec9A nanobody VHH mutant E1D-A74S-K83R-Q108L-H13Q-T64K, SEQ 331.
XX
KW C-type lectin domain protein 9A; antibody therapy; antimicrobial-gen.;
KW autoimmune disease; cancer; clec9A protein; cytostatic;
KW heavy chain variable region; immune disorder; immunomodulator;
KW immunosuppressive; infectious disease; monoclonal antibody; mutein;
KW nanobody; neurodegenerative disease; neuroprotective;
KW prophylactic to disease; recombinant protein; therapeutic.
XX
OS Lama sp.
OS Synthetic.
XX
CC PN WO2019032662-A1.
XX
CC PD 14-FEB-2019.
XX
CC PF 08-AUG-2018; 2018WO-US045742.
XX
PR 09-AUG-2017; 2017US-0542944P.
XX
CC PA (ORIO-) ORIONIS BIOSCIENCES INC.
CC PA (ORIO-) ORIONIS BIOSCI NV.
XX
CC PI Kley N, Tavernier J, Zabeau L, Depla E;
XX
DR WPI; 2019-154379/16.
XX
CC PT C-type lectin domain family 9 member A (Clec9A) binding agent comprises
CC PT targeting moiety comprising complementarity determining regions (CDR1,
CC PT CDR2, and CDR3), for treating cancer, infections, immune disorders,
CC PT and/or autoimmune diseases.
XX
CC PS Claim 22; SEQ ID NO 331; 166pp; English.
XX
CC The present invention relates to a novel clec9A binding agent, useful in
CC treating or preventing cancer in a subject. The clec9A binding agent
CC comprises an amino acid sequence of SEQ ID NO: 332 (see BGB94236). The
CC invention also provides: a recombinant nucleic acid composition encoding
CC the clec9A binding agent; a host cell comprising the nucleic acid; a
CC method for treating or preventing cancer, autoimmune disease and/or
CC neurodegenerative disease; a chimeric protein comprising the clec9A
CC binding agent and a modified human IFN-alpha 2 comprising one or more
CC mutations conferring improved safety. The clec9A binding agent is also
CC useful in preparing a medicament for treating infections and immune
CC disorders. The present sequence represents an anti-clec9A nanobody heavy
CC chain variable region mutant E1D-A74S-K83R-Q108L-H13Q-T64K derived from
CC the wild-type sequence of SEQ ID NO: 332 (see BGB94236), which is used in
CC preparing the clec9A binding agent involved in preparing a medicament for
CC treating or preventing the above mentioned diseases in a subject.
XX
SQ Sequence 115 AA;
Query Match 85.1%; Score 140.4; Length 115;
Best Local Similarity 41.8%;
Matches 33; Conservative 0; Mismatches 0; Indels 46; Gaps 2;
Qy 1 GSFSSINVMG--------------RITNLGLPNYADSVKG-------------------- 26
|||||||||| ||||||||||||||||
Db 26 GSFSSINVMGWYRQAPGKERELVARITNLGLPNYADSVKGRFTISRDNSKNTVYLQMNSL 85
Qy 27 ------------VALKAEY 33
|||||||
Db 86 RPEDTAVYYCYLVALKAEY 104
WO2019191519 teaches an anti-Clec9A mutant single-domain antibody VHH comprising the amino acid sequence of SEQ ID 1569, which is 99.1% identical to instant SEQ ID NO:330 and comprises SEQ ID NOs: 53, 138 and 256 for CDRs1-3 respectively (see the sequence alignments below).
SEQ ID NO:330
ID BGU40166 standard; protein; 115 AA.
XX
AC BGU40166;
XX
DT 14-NOV-2019 (first entry)
XX
DE Anti-Clec9A mutant single-domain antibody VHH, SEQ ID 1569.
XX
KW C-type lectin domain containing 9A; C-type lectin domain protein 9A;
KW Clec9A protein; autoimmune disease; cancer; cardiovascular disease;
KW cardiovascular-gen.; chimeric antigen receptor; chimeric protein;
KW cytostatic; heavy chain variable region; immunosuppressive;
KW immunotherapy; metabolic disorder; metabolic-gen.; mutein;
KW neurodegenerative disease; neuroprotective; recombinant protein;
KW single-domain antibody; therapeutic.
XX
OS Synthetic.
OS Unidentified.
XX
CC PN WO2019191519-A1.
XX
CC PD 03-OCT-2019.
XX
CC PF 28-MAR-2019; 2019WO-US024714.
XX
PR 28-MAR-2018; 2018US-0649238P.
PR 28-MAR-2018; 2018US-0649248P.
PR 28-MAR-2018; 2018US-0649264P.
XX
CC PA (ORIO-) ORIONIS BIOSCIENCES INC.
CC PA (ORIO-) ORIONIS BIOSCI NV.
XX
CC PI Kley N, Depla E, Zabeau L, Tavernier J;
XX
DR WPI; 2019-83275N/81.
XX
CC PT New chimeric protein complex useful for treating or preventing cancer,
CC PT autoimmune disease, neurodegenerative disease, metabolic disease, and/or
CC PT cardiovascular disease.
XX
CC PS Example; SEQ ID NO 1569; 329pp; English.
XX
CC The present invention relates to a novel Fc-based chimeric protein
CC complex (e.g., a chimeric antigen receptor (CAR) T-cell), useful for
CC preparing a medicament capable of treating or preventing cancer,
CC autoimmune disease, neurodegenerative disease, metabolic disease, and/or
CC cardiovascular disease. The Fc-based chimeric protein complex comprises:
CC (a) a targeting moiety (e.g., an antibody which comprises a heavy chain
CC variable region (VH), a light chain variable region (VL), a heavy chain
CC constant region (CH), a light chain constant region (CL), complementarity
CC determining regions (CDRs), and framework regions (FRs)) comprising a
CC recognition domain which recognizes and/or binds to a target; (b) a
CC signaling agent, where the signaling agent is a wild type signaling
CC agent, or a modified signaling agent that has one or more mutations which
CC confer improved safety relative to the wild type signaling agent; and (c)
CC an Fc domain, where the Fc domain comprising an Fc chain and optionally
CC having one or more mutations which reduce or eliminate one or more
CC effector functions of the Fc domain, promotes Fc chain pairing of the Fc
CC domain, and/or stabilizes a hinge region in the Fc domain. The invention
CC further relates to a nucleic acid encoding the Fc-based chimeric protein
CC complex. The novel Fc-based chimeric protein complex of the invention can
CC be used for treating or preventing cancer such as basal cell carcinoma,
CC biliary tract cancer, bladder cancer, bone cancer, brain and central
CC nervous system cancer, breast cancer, cancer of peritoneum, cervical
CC cancer, choriocarcinoma, colon and rectum cancer, connective tissue
CC cancer, cancer of digestive system, endometrial cancer, esophageal
CC cancer, eye cancer, cancer of head and neck, gastric cancer (e.g.,
CC gastrointestinal cancer), glioblastoma, hepatic carcinoma, hepatoma,
CC intra-epithelial neoplasm, kidney or renal cancer, larynx cancer,
CC leukemia, liver cancer, lung cancer (e.g. small-cell lung cancer, non-
CC small cell lung cancer, adenocarcinoma of lung, and squamous carcinoma of
CC lung), melanoma, myeloma, neuroblastoma, oral cavity cancer (e.g., lip,
CC tongue, mouth, and pharynx), ovarian cancer, pancreatic cancer, prostate
CC cancer, retinoblastoma, rhabdomyosarcoma, rectal cancer, cancer of the
CC respiratory system, salivary gland carcinoma, sarcoma, skin cancer,
CC squamous cell cancer, stomach cancer, testicular cancer, thyroid cancer,
CC uterine or endometrial cancer, cancer of urinary system, vulval cancer,
CC lymphoma such as Hodgkin's and non-Hodgkin's lymphoma, and B-cell
CC lymphoma such as low grade/follicular non-Hodgkin's lymphoma (NHL), small
CC lymphocytic (SL) NHL, intermediate grade/follicular NHL, intermediate
CC grade diffuse NHL, high grade immunoblastic NHL, high grade lymphoblastic
CC NHL, high grade small non-cleaved cell NHL, bulky disease NHL, mantle
CC cell lymphoma, AIDS-related lymphoma, and Waldenstrom's
CC macroglobulinemia, chronic lymphocytic leukemia (CLL), acute
CC lymphoblastic leukemia (ALL), hairy cell leukemia, chronic myeloblastic
CC leukemia, and other carcinoma and sarcoma, and post-transplant
CC lymphoproliferative disorder (PTLD), and abnormal vascular proliferation
CC associated with phakomatoses, edema (e.g. associated with brain tumors),
CC and Meigs' syndrome, autoimmune disease, neurodegenerative disease,
CC metabolic disease, and/or cardiovascular disease such as multiple
CC sclerosis, diabetes mellitus, lupus, celiac disease, Crohn's disease,
CC ulcerative colitis, Guillain-Barre syndrome, scleroderma, Goodpasture's
CC syndrome, Wegener's granulomatosis, autoimmune epilepsy, Rasmussen's
CC encephalitis, primary biliary sclerosis, sclerosing cholangitis,
CC autoimmune hepatitis, Addison's disease, Hashimoto's thyroiditis,
CC fibromyalgia, Meniere's syndrome, transplantation rejection (e.g.
CC preventing allograft rejection) pernicious anemia, rheumatoid arthritis,
CC systemic lupus erythematosus, dermatomyositis, Sjogren's syndrome, lupus
CC erythematosus, myasthenia gravis, Reiter's syndrome, and Grave's disease.
XX
SQ Sequence 115 AA;
Query Match 98.7%; Score 589; Length 115;
Best Local Similarity 99.1%;
Matches 114; Conservative 0; Mismatches 1; Indels 0; Gaps 0;
Qy 1 DVQLVESGGGLVHPGGSLRLSCAASGSFSSINVMGWYRQAPGKERELVARITNLGLPNYA 60
|||||||||||| |||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DVQLVESGGGLVQPGGSLRLSCAASGSFSSINVMGWYRQAPGKERELVARITNLGLPNYA 60
Qy 61 DSVKGRFTISRDNSKNTVYLQMNSLRPEDTAVYYCYLVALKAEYWGQGTLVTVSS 115
|||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 DSVKGRFTISRDNSKNTVYLQMNSLRPEDTAVYYCYLVALKAEYWGQGTLVTVSS 115
SEQ ID NO:53-SEQ ID NO:138-SEQ ID NO:256
ID BGU40135 standard; protein; 402 AA.
XX
AC BGU40135;
XX
DT 14-NOV-2019 (first entry)
XX
DE Fc1-20*GGS-R1CHCL50 construct, SEQ ID 1538.
XX
KW autoimmune disease; cancer; cardiovascular disease; cardiovascular-gen.;
KW chimeric antigen receptor; chimeric protein; cytostatic;
KW immunosuppressive; immunotherapy; metabolic disorder; metabolic-gen.;
KW neurodegenerative disease; neuroprotective; recombinant protein;
KW therapeutic.
XX
OS Synthetic.
OS Unidentified.
XX
CC PN WO2019191519-A1.
XX
CC PD 03-OCT-2019.
XX
CC PF 28-MAR-2019; 2019WO-US024714.
XX
PR 28-MAR-2018; 2018US-0649238P.
PR 28-MAR-2018; 2018US-0649248P.
PR 28-MAR-2018; 2018US-0649264P.
XX
CC PA (ORIO-) ORIONIS BIOSCIENCES INC.
CC PA (ORIO-) ORIONIS BIOSCI NV.
XX
CC PI Kley N, Depla E, Zabeau L, Tavernier J;
XX
DR WPI; 2019-83275N/81.
XX
CC PT New chimeric protein complex useful for treating or preventing cancer,
CC PT autoimmune disease, neurodegenerative disease, metabolic disease, and/or
CC PT cardiovascular disease.
XX
CC PS Example 34; SEQ ID NO 1538; 329pp; English.
XX
CC The present invention relates to a novel Fc-based chimeric protein
CC complex (e.g., a chimeric antigen receptor (CAR) T-cell), useful for
CC preparing a medicament capable of treating or preventing cancer,
CC autoimmune disease, neurodegenerative disease, metabolic disease, and/or
CC cardiovascular disease. The Fc-based chimeric protein complex comprises:
CC (a) a targeting moiety (e.g., an antibody which comprises a heavy chain
CC variable region (VH), a light chain variable region (VL), a heavy chain
CC constant region (CH), a light chain constant region (CL), complementarity
CC determining regions (CDRs), and framework regions (FRs)) comprising a
CC recognition domain which recognizes and/or binds to a target; (b) a
CC signaling agent, where the signaling agent is a wild type signaling
CC agent, or a modified signaling agent that has one or more mutations which
CC confer improved safety relative to the wild type signaling agent; and (c)
CC an Fc domain, where the Fc domain comprising an Fc chain and optionally
CC having one or more mutations which reduce or eliminate one or more
CC effector functions of the Fc domain, promotes Fc chain pairing of the Fc
CC domain, and/or stabilizes a hinge region in the Fc domain. The invention
CC further relates to a nucleic acid encoding the Fc-based chimeric protein
CC complex. The novel Fc-based chimeric protein complex of the invention can
CC be used for treating or preventing cancer such as basal cell carcinoma,
CC biliary tract cancer, bladder cancer, bone cancer, brain and central
CC nervous system cancer, breast cancer, cancer of peritoneum, cervical
CC cancer, choriocarcinoma, colon and rectum cancer, connective tissue
CC cancer, cancer of digestive system, endometrial cancer, esophageal
CC cancer, eye cancer, cancer of head and neck, gastric cancer (e.g.,
CC gastrointestinal cancer), glioblastoma, hepatic carcinoma, hepatoma,
CC intra-epithelial neoplasm, kidney or renal cancer, larynx cancer,
CC leukemia, liver cancer, lung cancer (e.g. small-cell lung cancer, non-
CC small cell lung cancer, adenocarcinoma of lung, and squamous carcinoma of
CC lung), melanoma, myeloma, neuroblastoma, oral cavity cancer (e.g., lip,
CC tongue, mouth, and pharynx), ovarian cancer, pancreatic cancer, prostate
CC cancer, retinoblastoma, rhabdomyosarcoma, rectal cancer, cancer of the
CC respiratory system, salivary gland carcinoma, sarcoma, skin cancer,
CC squamous cell cancer, stomach cancer, testicular cancer, thyroid cancer,
CC uterine or endometrial cancer, cancer of urinary system, vulval cancer,
CC lymphoma such as Hodgkin's and non-Hodgkin's lymphoma, and B-cell
CC lymphoma such as low grade/follicular non-Hodgkin's lymphoma (NHL), small
CC lymphocytic (SL) NHL, intermediate grade/follicular NHL, intermediate
CC grade diffuse NHL, high grade immunoblastic NHL, high grade lymphoblastic
CC NHL, high grade small non-cleaved cell NHL, bulky disease NHL, mantle
CC cell lymphoma, AIDS-related lymphoma, and Waldenstrom's
CC macroglobulinemia, chronic lymphocytic leukemia (CLL), acute
CC lymphoblastic leukemia (ALL), hairy cell leukemia, chronic myeloblastic
CC leukemia, and other carcinoma and sarcoma, and post-transplant
CC lymphoproliferative disorder (PTLD), and abnormal vascular proliferation
CC associated with phakomatoses, edema (e.g. associated with brain tumors),
CC and Meigs' syndrome, autoimmune disease, neurodegenerative disease,
CC metabolic disease, and/or cardiovascular disease such as multiple
CC sclerosis, diabetes mellitus, lupus, celiac disease, Crohn's disease,
CC ulcerative colitis, Guillain-Barre syndrome, scleroderma, Goodpasture's
CC syndrome, Wegener's granulomatosis, autoimmune epilepsy, Rasmussen's
CC encephalitis, primary biliary sclerosis, sclerosing cholangitis,
CC autoimmune hepatitis, Addison's disease, Hashimoto's thyroiditis,
CC fibromyalgia, Meniere's syndrome, transplantation rejection (e.g.
CC preventing allograft rejection) pernicious anemia, rheumatoid arthritis,
CC systemic lupus erythematosus, dermatomyositis, Sjogren's syndrome, lupus
CC erythematosus, myasthenia gravis, Reiter's syndrome, and Grave's disease.
XX
SQ Sequence 402 AA;
Query Match 85.1%; Score 140.4; Length 402;
Best Local Similarity 41.8%;
Matches 33; Conservative 0; Mismatches 0; Indels 46; Gaps 2;
Qy 1 GSFSSINVMG--------------RITNLGLPNYADSVKG-------------------- 26
|||||||||| ||||||||||||||||
Db 313 GSFSSINVMGWYRQAPGKERELVARITNLGLPNYADSVKGRFTISRDNSKNTVYLQMNSL 372
Qy 27 ------------VALKAEY 33
|||||||
Db 373 RPEDTAVYYCYLVALKAEY 391
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Chang-Yu Wang
September 15, 2026
/CHANG-YU WANG/Primary Examiner, Art Unit 1649
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