DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Status of Application, Amendments and/or Claims
The amendment, filed 21 February 2023, has been entered in full. The amendment, filed 30 August 2023, has been entered in full. Claims 1-125 are canceled. New claims 126-154 are added.
Applicant's election with traverse of Group I (claims 126-140, drawn to an engineered receptor comprising a ligand binding domain derived from human a7 nicotinic acetylcholine receptor (a7-nAChr)) and the species election of an amino acid substitution at an amino acid residue corresponding to R101 of SEQ ID NO:4 in addition to at least one amino acid substitution at a residue corresponding to W77, Y115, L131, S172 or Y210 of SEQ ID NO:4 and for claims 126, 127-127(b) R101 and L131, claim 129(g) R101M, L131A and claim 136, SEQ ID NO:71, in the reply filed on 11 December 2025 is acknowledged.
The traversal is on the ground(s) that Seal et al. (US 202/0131537; published April 30, 2020) does not disclose engineered receptors having an amino acid substitution at an amino acid residue corresponding to R101 of SEQ ID NO: 4. Therefore, the claims of each group share a special technical feature over the cited prior art and should all be examined in the present application.
Applicant’s arguments have been fully considered but are not found persuasive for the following reasons.
The previous claims were drawn to an engineered receptor, comprising a ligand binding domain derived from human a7 nicotinic acetylcholine receptor (a7-nAChR), wherein the ligand binding domain comprises: (a) mutations at amino acid residues corresponding to (i) R101 and (ii) L131, Y210, or W77 and L131, of SEQ ID NO: 4; (b) mutations at amino acid residues corresponding to (i) Y115 and (ii) Y210, S170 or L131, of SEQ ID NO: 4; (c) mutations at amino acid residues corresponding to (i) S172 and (ii) L131, Q139 or Y210, of SEQ ID NO: 4; or (d) a mutation at an amino acid residue corresponding to Y140 of SEQ ID NO: 4.
As was stated in the previous Office Action, Seal et al. (US 2020/0131537; published April 30, 2020) teach an engineered receptor comprising a ligand binding domain derived from human a7 nicotinic acetylcholine receptor (Figure 2 and Figure 3, paras 0010-0011, 0044, 0047, 0049 and 0051). Seal et al. teach mutations at amino acid residues corresponding to Y115 and Y131 or Y210 of SEQ ID NO:4 (para 0056). The requirement is still deemed proper and is therefore made FINAL.
The Examiner will, however, withdraw the species election requirement.
Claims 141-154 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected Group, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on 11 December 2025.
The amendment, filed 11 December 2025, has been entered in full. Claims 128 and 131 are canceled. Claims 126, 127, 129, 132 and 133 are amended. Claims 126, 127,129, 130, 132-140 are under examination.
Information Disclosure Statement
The information disclosure statement(s) (IDS) (filed 2/6/26; 11/19/25; 7/31/25; 6/23/25; 5/14/25; 3/17/25; 11/14/24; 9/16/24; 8/7/24; 6/18/24; 10/13/23; 8/31/23 and 4/26/23) were received and comply with the provisions of 37 CFR §§1.97, 1.98 and MPEP § 609. They have been placed in the application file and the information referred to therein has been considered as to the merits.
Claim Objections
Claim 133 is objected to because of the following informalities: Claim 133 has a typo. The recitation, “..260-452..” should be “..amino acids 260-452..” (see line 2 of claim 133).
Appropriate correction is required.
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 126, 127, 129, 130, 132-140 are rejected under 35 U.S.C. 102(a1) and 35 U.S.C. 102(a2) as being anticipated by Greenberg et al. (Reference submitted by Applicant; US 2019/0161529; published May 30, 2019).
Greenberg et al. teach an engineered receptor comprising a ligand binding domain derived from human a7 nicotinic acetylcholine receptor (a7-nAChR), wherein the ligand binding domain comprises an amino acid substitution at an amino acid residue corresponding to R101 of SEQ ID NO:4 and at least one amino acid substitution at a residue corresponding to a residue of α7-nAChR selected from the group consisting of W77, Y94, W108, Y115, T128, N129, V130, L131, Q139, L141, Y151, S170, W171, S172, S188, Y190, Y210, C212, C213 and Y217 of SEQ ID NO:4 and an ion pore domain (IPD) derived from human glycine receptor (GlyR)(paras 0021, 0022, 0123, 0124, 0126-0128)(applies to claims 126 and 127). Chemical compounds and their properties are inseparable (In re Papesch, 315 F.2d 381, 137 USPQ 43 (CCPA1963)), as are their processes and yields (In re Von Schickh, 362 F.2d 821, 150 USPQ 300 (CCPA 1966)). Therefore, the engineered receptor taught by Greenberg et al., would have the associated biological properties (applies to claims 137-140).
In addition to teaching an amino acid substitution at an amino acid residue corresponding to R101 of SEQ ID NO:4, Greenberg et al. teach an amino acid substitution at an amino acid residue corresponding to Y115D and S170T (paras 022 and 0124-0125)(applies to claim 129m); Y115D and L131Q (paras 0124 and 0126)(applies to claim 129n); L131S and S172D (paras 0018, 0124)(applies to claims 129p); L131T and S172D (paras 0018, 0124, 0255)(applies to claim 129q); L131D and S172D (paras 0022 and 0124)(applies to claim 129r).
Greenberg et al. teach wherein the human glycine receptor is a human GlyRa1 (para 0102)(applies to claim 132). Greenberg et al. teach wherein the ligand binding domain of the engineered receptor comprises a Cys-loop domain derived from the human glycine receptor (paras 0021, 0024)(applies to claim 134).
Greenberg et al. teach wherein the ligand binding domain comprises amino acid residues 23-220 of SEQ ID NO:4. See below, Sequence Search Result A (applies to claim 130). Greenberg et al. teach wherein the ion pore domains comprises amino acid residues 255-457 of SEQ ID NO:2. See below, Sequence Search Result B (applies to claims 133 and 135).
Greenberg et al. teach an engineered receptor comprising a sequence that is 99.3% identical to instant SEQ ID NO:58. Instant SEQ ID NO:58 comprises an aspartic acid (D) at residue 131 and an aspartic acid (D) at residue 172. See below, Sequence Search Result C. As was stated above, Greenberg et al. teach an amino acid substitution at amino acid residue corresponding to R101 and wherein leucine (L) at residue 131 can be an aspartic acid (L131D) and wherein serine (S) at residue 172 can be an aspartic acid (S172D)(applies to claim 136, instant SEQ ID NO:58).
Greenberg et al. teach an engineered receptor comprising a sequence that is 99.5% identical to instant SEQ ID NO:59. Instant SEQ ID NO:59 comprises a serine (S) at residue 131 and an aspartic acid (D) at residue 172. See below, Sequence Search Result D. As was stated above, Greenberg et al. teach an amino acid substitution at amino acid residue corresponding to R101 and wherein leucine (L) at residue 131 can be a serine (L131S) and wherein serine (S) at residue 172 can be an aspartic acid (S172D)(applies to claim 136, instant SEQ ID NO:59).
Greenberg et al. teach an engineered receptor comprising a sequence that is 99.5% identical to instant SEQ ID NO:60. Instant SEQ ID NO:60 comprises a threonine (T) at residue 131 and an aspartic acid (D) at residue 172. See below, Sequence Search Result E. As was stated above, Greenberg et al. teach an amino acid substitution at amino acid residue corresponding to R101 and wherein leucine (L) at residue 131 can be a threonine (L131T) and wherein serine (S) at residue 172 can be an aspartic acid (S172D)(applies to claim 136, instant SEQ ID NO:60).
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.
1. Claims 126, 127, 129, 130, 132-140 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-10 of U.S. Patent No. 10,538,571.
The instant claims are drawn to an engineered receptor, comprising a ligand binding domain derived from human a7 nicotinic acetylcholine receptor (a7- nAChR), wherein the ligand binding domain comprises an amino acid substitution at an amino acid residue corresponding to R101 of SEQ ID NO: 4 and at least one amino acid substitution at a residue corresponding to W77, Y115, L131, S172 or Y210 of SEQ ID NO: 4, and an ion pore domain (IPD) derived from human glycine receptor (GlyR). The claims are further drawn to wherein the ligand binding domain comprising amino acid substitutions at R101 and Y115; R101 and L131; R101 and S172 or R101 and Y210 of SEQ ID NO: 4. The claims are further drawn to wherein the ligand binding domain comprises an amino acid sequence having at least 85% identity to amino acid residues 23-220 of SEQ ID NO: 4; wherein the human Glycine receptor is human Glycine receptor a1, human Glycine receptor a2, or human Glycine receptor a3. The claims are further drawn to wherein the ion pore domain comprises an amino acid sequence having at least 85% identity to amino acids 255- 457 of SEQ ID NO: 2, amino acids 260-452 of SEQ ID NO:83, amino acids 259-464 of SEQ ID NO:85 or amino acid s 259-449 of SEQ ID NO;87. The claims are further drawn to wherein the ligand binding domain of the engineered receptor comprises a Cys-loop domain derived from the human Glycine receptor. The claims are further drawn to amino acid substitution mutations such as R101, L131S and S127D; R101, L131T and S172D; R101, L131D and S172D.
The claims of US Patent No. 10,538,571 teach an engineered receptor comprising a ligand binding domain derived from the human α7 nicotinic acetylcholine receptor (α7-nAChR) and comprising a Cys-loop domain from the human Glycine receptor α1 subunit; and an ion pore domain derived from the human Glycine receptor α1 subunit. The claims of US Patent No. 10,538,571 further teach wherein the Cys-loop domain comprises amino acids 166-172 of SEQ ID NO:2 and wherein the receptor has a sequence identity of 85% or more to SEQ ID NO:33. The claims of US Patent No. 10,538,571 further teach wherein the ligand binding domain comprises one or more amino acid substitutions at a residue corresponding to a residue of α7-nAChR selected from the group consisting of W77, Y94, R101, W108, Y115, T128, N129, V130, L131, Q139, L141, Y151, S170, W171, S172, S188, Y190, Y210, C212, C213 and Y217. The claims further teach wherein the substitution is selected from a substitution corresponding to L131S, L131T, L131D, or S172D of α7-nAChR. The claims of US Patent No. 10,538,571 further teach wherein the ligand binding domain further comprises a β1-2 loop domain from the human Glycine receptor α1 subunit, wherein the β1-2 loop domain comprises amino acids 81-84 of SEQ ID NO:2 and wherein the receptor has a sequence identity of 85% or more to SEQ ID NO:41. The claims of US Patent No. 10,538,571 further teach wherein the ligand binding domain comprises one or more amino acid substitutions at a residue corresponding to a residue of α7-nAChR selected from the group consisting of W77, Y94, R101, W108, Y115, T128, N129, V130, L131, Q139, L141, Y151, S170, W171, S172, S188, Y190, Y210, C212, C213 and Y217 and wherein the substitution is selected from a substitution corresponding to L131S, L131T, L131D, or S172D of α7-nAChR.
Although the claims at issue are not identical, they are not patentably distinct from each other. It would have been obvious for one of ordinary skill in the art before the effective filling date to modify the engineered receptor taught in the claims of US Patent No. 10,538,571 to make the instant invention. One of ordinary skill in the art before the effective filing date, would have been motivated to make such modifications and expect success because both sets of claims are drawn to a chimeric engineered receptor comprising a ligand binding domain derived from human alpha7 nicotinic acetylcholine receptor and an ion pore domain derived from human glycine receptor. Both sets of claims overlap in amino acid substitution mutations corresponding to amino acid residues in human alpha7 nicotinic acetylcholine receptor, in particular at amino acid residues R101, L131 and/or S172; and further L131S, L131T, L131D and S172D, which would apply to instant SEQ ID Nos: 58, 59 and 60.
2. Claims 126, 127, 129, 130, 132-140 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 30-35 and 39 of copending Application No. 16/925,174 (reference application).
The instant claims are described above.
The claims of copending Application 16/925,174 teach an engineered receptor comprising a ligand binding domain derived from human a7 nicotinic acetylcholine receptor (a7-nAChR) and comprising a heterologous Cys-loop domain derived from a ligand binding domain of a human glycine receptor a (GlyRa) subunit, wherein the Cys-loop domain of human a7-nAChR corresponds to amino acids 150-164 of SEQ ID NO: 4, and wherein the Cys-loop domain of human a7-nAChR is replaced by the heterologous Cys-loop domain; and an ion pore domain derived from the human GlyRa subunit, wherein the human GyRa subunit is GlyRa1, GlyRa2, or GyRa3. The claims further teach wherein the Cys-loop domain of human GlyRa1, human GlyRa2, and human GlyRa3 corresponds to amino acids 166-180 of SEQ ID NO: 2, and wherein the engineered receptor comprises at least 90% sequence identity with SEQ ID NO:33. The claims copending Application No. 16/925,174 further teach wherein the ligand binding domain comprises one or more amino acid substitutions at a residue corresponding to one or more of a residue of human a7-nAChR selected from the group consisting of W77, Y94, R101, W108, Y115, T128, N129, V130, L131, Q139, L141, Y151, S170, W171, S172, S188, Y190, Y210, C212, C213 or Y217 and wherein the one or more amino acid substitutions is selected from a substitution corresponding to comprise one or more of Y115D, L131S, L131T, L131D, S170T, or S172D and wherein the ligand binding domain further comprises a beta1-2 loop domain derived from the human GlyRa subunit.
Although the claims at issue are not identical, they are not patentably distinct from each other. It would have been obvious for one of ordinary skill in the art before the effective filling date to modify the engineered receptor taught in the claims of copending Application No. 16/925,174 to make the instant invention. One of ordinary skill in the art before the effective filing date, would have been motivated to make such modifications and expect success because both sets of claims are drawn to a chimeric engineered receptor comprising a ligand binding domain derived from human alpha7 nicotinic acetylcholine receptor and an ion pore domain derived from human glycine receptor. Both sets of claims overlap in amino acid substitution mutations corresponding to amino acid residues in human alpha7 nicotinic acetylcholine receptor, in particular at amino acid residues R101, L131 and/or S172; and further L131S, L131T, L131D and S172D, which would apply to instant SEQ ID Nos: 58, 59 and 60.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
3. Claims 126, 127, 130, 132-135, 137-140 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 17, 18, 20-22, 25, 28 and 31 of copending Application No. 18/839,199 (reference application).
The instant claims are described above.
The claims of copending Application No. 18/839,199 teach an engineered receptor, comprising a ligand binding domain derived from human a7 nicotinic acetylcholine receptor (a7-nAChR), and an ion pore domain derived from human glycine receptor (GlyR); wherein the ligand binding domain comprises a Cys-loop domain derived from GlyR, and an amino acid mutation at an amino acid residue corresponding to R101, Y115, L131, Q139, Y140, S172, Y210 or Y217 of SEQ ID NO:4. The claims further teach wherein the ligand binding domain amino acid mutation(s) correspond to position(s) comprises a mutation at the amino acid residue(s) corresponding to the indicated position(s) Y140; Y115 and L131; Q139 and S172; Q139 and Y210; Q139, S172 and Y217; Y115, Q139 and S172; R101, L131, Q139 and Y217; Y115 and S172; L141, S172, and Y210; or R101, L131 and Y217 of SEQ ID NO: 4. The claims are further drawn to wherein the receptor comprises polypeptide sequence having at least 85% sequence identity to SEQ ID NO: 33. The claims of copending Application No. 18/839,199 further teach wherein the ligand binding domain comprises amino acid substitution(s) corresponding to the indicated position Y140R; Y115E and L131M; Q139W and S172D; Q139W and Y210W; Q139W, S172D and Y2171; Y115E, Q139E, and S172D; R101F, L131G, Q139L, and Y217F; Y115Q and S172D; L141M, S172D and Y210W; R101F, L131N and Y217F; L131G; L131M; Q139E; Q139L; Q139W; or L141M of SEQ ID NO: 4.
Although the claims at issue are not identical, they are not patentably distinct from each other. It would have been obvious for one of ordinary skill in the art before the effective filling date to modify the engineered receptor taught in the claims of copending Application No. 18/839,199 to make the instant invention. One of ordinary skill in the art before the effective filing date, would have been motivated to make such modifications and expect success because the species of amino acid substitution mutations in SEQ ID NO:4, as taught in the claims of copending Application No. 18/839,199, renders obvious the genus amino acid substitution mutations in SEQ ID NO:4 (i.e., R101, Y115, L131, S172 and/or Y201 of SEQ ID NO:4), recited in the instant claims. In addition, both sets of claims are drawn to a chimeric engineered receptor comprising a ligand binding domain derived from human alpha7 nicotinic acetylcholine receptor and an ion pore domain derived from human glycine receptor.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
4. Claims 126, 127, 129, 130, 132-135, 137-140 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 6, 18, 32, 51, 52, 58, 61, 64, 67 of copending Application No. 18/839,624 (reference application).
The instant claims are taught above.
The claims of copending Application No.18/839,624 teach an engineered receptor comprising a ligand binding domain derived from human a7 nicotinic acetylcholine receptor (a7- nAChR) and an ion pore domain derived from a human glycine receptor (GlyR), wherein the ligand binding domain comprises a Cys-loop domain derived from the GlyR. The claims further teach wherein the human glycine receptor is glycine receptor a1, glycine receptor a2 or glycine receptor a3. The claims further teach wherein the ion pore domain comprises an amino acid sequence having at least 85% sequence identity to amino acid residues 248-457 of SEQ ID NO:2 and the Cys-loop domain of the ligand binding domain comprises an amino acid sequence having at least 80% identity to amino acid residues 166-180 of SEQ ID NO:2. The claims further teach wherein the ion pore domain comprises an amino acid sequence having at least 85% identity according to amino acids 253-464 of SEQ ID NO:61 or amino acids 253-449 of SEQ ID NO:69 and the Cys-loop domain of the ligand binding domain comprises an amino acid sequence having at least 80% identity according to amino acids 171-185 of SEQ ID NO: 61 or 69. The claims of copending Application No.18/839,624 further teach wherein the ligand binding domain comprises an amino acid substitution at one or more residues comprising W77, Y94, RI01, W108, Y115, T128, N129, V130, L131, Q139, Y140, L141, Y151, S170, W171, S172, Y173, S188, Y190, Y210, C212, C213, E215, Y217, or any combination thereof, of humana7-nAChR and wherein the ligand binding domain comprises two amino acid substitutions at a pair of residues comprising RI01 and L131, Y115 and Y210, or RI01 and Y210, of human a7-nAChR.
Although the claims at issue are not identical, they are not patentably distinct from each other. It would have been obvious for one of ordinary skill in the art before the effective filling date to modify the engineered receptor taught in the claims of copending Application No. 18/839,624 to make the instant invention. One of ordinary skill in the art before the effective filing date, would have been motivated to make such modifications and expect success because the species of ion pore domains derived from human glycine receptor a1, human glycine receptor a2 or human glycine receptor a3, as taught in the claims of copending Application No. 18/839,624, renders obvious the genus of the ion pore domain derived from human glycine receptor, as recited in the instant claims. In addition, both sets of claims are drawn to a chimeric engineered receptor comprising a ligand binding domain derived from human alpha7 nicotinic acetylcholine receptor and an ion pore domain derived from human glycine receptor and both set of claims overlap in amino acid substitution mutations corresponding to amino acid residues in human alpha7 nicotinic acetylcholine receptor, in particular at amino acid residues W77, R101, Y115, L131, S172 and/or Y210.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
No claims are allowed.
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/R.M.D/Examiner, Art Unit 1647
2/12/2026
/BRIDGET E BUNNER/Primary Examiner, Art Unit 1647
SEQUENCE SEARCH RESULT A
This page gives you Search Results detail for the Application 18022358 and Search Result 20260209_075231_us-18-022-358-4_copy_23_220.minpct84.rapbm
Title: US-18-022-358-4_COPY_23_220
Perfect score: 1106
Sequence: 1 GEFQRKLYKELVKNYNPLER..........IPGKRSERFYECCKEPYPDV 198
SUMMARIES
%
Result Query Filing
No. Score Match Length ID Date Dups Description
-------------------------------------------------------------------------------------------------------------
9 1106 100.0 439 US-16-201-142-17 2018-11-27 5 COMPOSITIONS AND METHODS FOR NEUROLOGICAL DISEASES
RESULT 9
US-16-201-142-17
Sequence 17, US/16201142
Publication No. US20190161529A1
GENERAL INFORMATION
APPLICANT: Coda Biotherapeutics, Inc.
APPLICANT: Greenberg, Kenneth P.
APPLICANT: Keifer, Orion Jr.
APPLICANT: Makinson, Stefanie
APPLICANT: Lau, Anthony
TITLE OF INVENTION: COMPOSITIONS AND METHODS FOR NEUROLOGICAL DISEASES
FILE REFERENCE: SWCH-012/04US 322917-2121
CURRENT APPLICATION NUMBER: US/16/201,142
CURRENT FILING DATE: 2018-11-27
PRIOR APPLICATION NUMBER: 62/590,911
PRIOR FILING DATE: 2017-11-27
PRIOR APPLICATION NUMBER: 62/659,911
PRIOR FILING DATE: 2018-04-19
NUMBER OF SEQ ID NOS: 57
SEQ ID NO 17
LENGTH: 439
TYPE: PRT
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: synthetic sequence of chimeric LGIC
Query Match 100.0%; Score 1106; Length 439;
Best Local Similarity 100.0%;
Matches 198; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 GEFQRKLYKELVKNYNPLERPVANDSQPLTVYFSLSLLQIMDVDEKNQVLTTNIWLQMSW 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 23 GEFQRKLYKELVKNYNPLERPVANDSQPLTVYFSLSLLQIMDVDEKNQVLTTNIWLQMSW 82
Qy 61 TDHYLQWNVSEYPGVKTVRFPDGQIWKPDILLYNSADERFDATFHTNVLVNSSGHCQYLP 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 83 TDHYLQWNVSEYPGVKTVRFPDGQIWKPDILLYNSADERFDATFHTNVLVNSSGHCQYLP 142
Qy 121 PGIFKSSCYIDVRWFPFDVQHCKLKFGSWSYGGWSLDLQMQEADISGYIPNGEWDLVGIP 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 143 PGIFKSSCYIDVRWFPFDVQHCKLKFGSWSYGGWSLDLQMQEADISGYIPNGEWDLVGIP 202
Qy 181 GKRSERFYECCKEPYPDV 198
||||||||||||||||||
Db 203 GKRSERFYECCKEPYPDV 220
SEQUENCE SEARCH RESULT B
This page gives you Search Results detail for the Application 18022358 and Search Result 20260209_075231_us-18-022-358-2_copy_255_457.minpct84.rapbm
Title: US-18-022-358-2_COPY_255_457
Perfect score: 1052
Sequence: 1 MYIPSLLIVILSWISFWINM..........FNMFYWIIYKIVRREDVHNQ 203
SUMMARIES
%
Result Query Filing
No. Score Match Length ID Date Dups Description
-------------------------------------------------------------------------------------------------------------
2 1052 100.0 439 US-16-201-142-17 2018-11-27 5 COMPOSITIONS AND METHODS FOR NEUROLOGICAL DISEASES
RESULT 2
US-16-201-142-17
Sequence 17, US/16201142
Publication No. US20190161529A1
GENERAL INFORMATION
APPLICANT: Coda Biotherapeutics, Inc.
APPLICANT: Greenberg, Kenneth P.
APPLICANT: Keifer, Orion Jr.
APPLICANT: Makinson, Stefanie
APPLICANT: Lau, Anthony
TITLE OF INVENTION: COMPOSITIONS AND METHODS FOR NEUROLOGICAL DISEASES
FILE REFERENCE: SWCH-012/04US 322917-2121
CURRENT APPLICATION NUMBER: US/16/201,142
CURRENT FILING DATE: 2018-11-27
PRIOR APPLICATION NUMBER: 62/590,911
PRIOR FILING DATE: 2017-11-27
PRIOR APPLICATION NUMBER: 62/659,911
PRIOR FILING DATE: 2018-04-19
NUMBER OF SEQ ID NOS: 57
SEQ ID NO 17
LENGTH: 439
TYPE: PRT
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: synthetic sequence of chimeric LGIC
Query Match 100.0%; Score 1052; Length 439;
Best Local Similarity 100.0%;
Matches 203; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 MYIPSLLIVILSWISFWINMDAAPARVGLGITTVLTMTTQSSGSRASLPKVSYVKAIDIW 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 237 MYIPSLLIVILSWISFWINMDAAPARVGLGITTVLTMTTQSSGSRASLPKVSYVKAIDIW 296
Qy 61 MAVCLLFVFSALLEYAAVNFVSRQHKELLRFRRKRRHHKSPMLNLFQEDEAGEGRFNFSA 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 297 MAVCLLFVFSALLEYAAVNFVSRQHKELLRFRRKRRHHKSPMLNLFQEDEAGEGRFNFSA 356
Qy 121 YGMGPACLQAKDGISVKGANNSNTTNPPPAPSKSPEEMRKLFIQRAKKIDKISRIGFPMA 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 357 YGMGPACLQAKDGISVKGANNSNTTNPPPAPSKSPEEMRKLFIQRAKKIDKISRIGFPMA 416
Qy 181 FLIFNMFYWIIYKIVRREDVHNQ 203
|||||||||||||||||||||||
Db 417 FLIFNMFYWIIYKIVRREDVHNQ 439
SEQUENCE SEARCH RESULT C
This page gives you Search Results detail for the Application 18022358 and Search Result 20260211_102318_us-18-022-358-58.minpct98.rag
Title: US-18-022-358-58
Perfect score: 2351
Sequence: 1 MRCSPGGVWLALAASLLHVS..........FNMFYWIIYKIVRREDVHNQ 439
SUMMARIES
%
Result Query Filing
No. Score Match Length ID Date Dups Description
-------------------------------------------------------------------------------------------------------------
23 2335 99.3 439 BGJ70858 -- 7 Chimeric LGIC receptor protein, SEQ ID 33.
RESULT 23
BGJ70858
ID BGJ70858 standard; protein; 439 AA.
XX
AC BGJ70858;
XX
DT 11-JUL-2019 (first entry)
XX
DE Chimeric LGIC receptor protein, SEQ ID 33.
XX
KW CHRNA7 protein; GlyR alpha1; Nicotinic ACh receptor alpha 7 subunit;
KW alpha 1 glycine receptor; alpha7-nAchR; analgesic; anticonvulsant;
KW antipruritic; chimeric protein; eating disorder; eating-disorders-gen.;
KW movement disorder; muscle hypertonia; muscle relaxant;
KW neurogenic bladder; neurological disease; neuroprotective;
KW nicotinic cholinergic receptor alpha 7 subunit; pain;
KW protein engineering; protein therapy; pruritus; seizure disorder;
KW spinal cord disease; therapeutic; uropathic.
XX
OS Homo sapiens.
OS Synthetic.
XX
FH Key Location/Qualifiers
FT Peptide 1..22
FT /note= "Human alpha7-nAChR signal peptide"
FT Domain 23..229
FT /note= "Human alpha7-nAChR ligand binding domain"
FT Peptide 150..164
FT /note= "Human GlyR alpha1 Cys-loop sequence"
FT Domain 230..439
FT /note= "Human GlyR alpha1 ion pore domain"
XX
CC PN US2019161529-A1.
XX
CC PD 30-MAY-2019.
XX
CC PF 27-NOV-2018; 2018US-00201142.
XX
PR 27-NOV-2017; 2017US-0590911P.
PR 19-APR-2018; 2018US-0659911P.
XX
CC PA (CODA-) CODA BIOTHERAPEUTICS INC.
XX
CC PI Greenberg KP, Keifer O, Makinson S, Lau A;
XX
DR WPI; 2019-46769W/43.
DR N-PSDB; BGJ70857.
XX
CC PT New engineered receptor i.e. chimeric ligand gated ion channel (LGIC)
CC PT receptor comprising e.g. ligand binding domain derived from first wild
CC PT type Cys-loop LGIC receptor used to ameliorate neurological disorder e.g.
CC PT spinal cord injury.
XX
CC PS Claim 4; SEQ ID NO 33; 140pp; English.
XX
CC The invention relates to a novel engineered chimeric ligand gated ion
CC channel (LGIC) receptor, useful for ameliorating neurological disorder.
CC The engineered receptor comprises ligand binding domain derived from
CC first wild type Cys-loop LGIC receptor. The invention also claims: 1) a
CC polynucleotide encoding the engineered receptor; 2) a vector comprising
CC the polynucleotide; and 3) a method for ameliorating a neurological
CC disorder in a subject. The engineered receptor is useful for ameliorating
CC a neurological disorder in a subject suffering from pain, seizure
CC disorder, movement disorder, eating disorder, spinal cord injury,
CC neurogenic bladder, spasticity disorder or pruritus. The engineered
CC receptor is safe, efficient and cost-effective. The present sequence
CC represents a chimeric LGIC receptor (CHRNA7/GLRA1) protein comprising
CC human alpha7-nAChR signal peptide and ligand binding domain comprising
CC GlyR alpha1 Cys-loop sequence, fused to the human GlyR alpha1 ion pore
CC domain, used in the method for ameliorating a neurological disorder in a
CC subject. Note: The present sequence is used as a parent sequence for
CC creating variants (see BGJ70883-BGJ71067) shown in figure 8 of the
CC specification.
XX
SQ Sequence 439 AA;
Query Match 99.3%; Score 2335; Length 439;
Best Local Similarity 99.5%;
Matches 437; Conservative 0; Mismatches 2; Indels 0; Gaps 0;
Qy 1 MRCSPGGVWLALAASLLHVSLQGEFQRKLYKELVKNYNPLERPVANDSQPLTVYFSLSLL 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 MRCSPGGVWLALAASLLHVSLQGEFQRKLYKELVKNYNPLERPVANDSQPLTVYFSLSLL 60
Qy 61 QIMDVDEKNQVLTTNIWLQMSWTDHYLQWNVSEYPGVKTVRFPDGQIWKPDILLYNSADE 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 QIMDVDEKNQVLTTNIWLQMSWTDHYLQWNVSEYPGVKTVRFPDGQIWKPDILLYNSADE 120
Qy 121 RFDATFHTNVDVNSSGHCQYLPPGIFKSSCPMDLKNFPMDVQTCKLKFGSWDYGGWSLDL 180
|||||||||| |||||||||||||||||||||||||||||||||||||||| ||||||||
Db 121 RFDATFHTNVLVNSSGHCQYLPPGIFKSSCPMDLKNFPMDVQTCKLKFGSWSYGGWSLDL 180
Qy 181 QMQEADISGYIPNGEWDLVGIPGKRSERFYECCKEPYPDVTFTVTMRRRMGYYLIQMYIP 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 QMQEADISGYIPNGEWDLVGIPGKRSERFYECCKEPYPDVTFTVTMRRRMGYYLIQMYIP 240
Qy 241 SLLIVILSWISFWINMDAAPARVGLGITTVLTMTTQSSGSRASLPKVSYVKAIDIWMAVC 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 SLLIVILSWISFWINMDAAPARVGLGITTVLTMTTQSSGSRASLPKVSYVKAIDIWMAVC 300
Qy 301 LLFVFSALLEYAAVNFVSRQHKELLRFRRKRRHHKSPMLNLFQEDEAGEGRFNFSAYGMG 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 301 LLFVFSALLEYAAVNFVSRQHKELLRFRRKRRHHKSPMLNLFQEDEAGEGRFNFSAYGMG 360
Qy 361 PACLQAKDGISVKGANNSNTTNPPPAPSKSPEEMRKLFIQRAKKIDKISRIGFPMAFLIF 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 361 PACLQAKDGISVKGANNSNTTNPPPAPSKSPEEMRKLFIQRAKKIDKISRIGFPMAFLIF 420
Qy 421 NMFYWIIYKIVRREDVHNQ 439
|||||||||||||||||||
Db 421 NMFYWIIYKIVRREDVHNQ 439
SEQUENCE SEARCH RESULT D
This page gives you Search Results detail for the Application 18022358 and Search Result 20260211_102318_us-18-022-358-59.minpct98.rag
Title: US-18-022-358-59
Perfect score: 2349
Sequence: 1 MRCSPGGVWLALAASLLHVS..........FNMFYWIIYKIVRREDVHNQ 439
SUMMARIES
%
Result Query Filing
No. Score Match Length ID Date Dups Description
-------------------------------------------------------------------------------------------------------------
22 2337 99.5 439 BGJ70858 -- 7 Chimeric LGIC receptor protein, SEQ ID 33.
RESULT 22
BGJ70858
(NOTE: this sequence has 7 duplicates in the database searched.
See complete list at the end of this report)
ID BGJ70858 standard; protein; 439 AA.
XX
AC BGJ70858;
XX
DT 11-JUL-2019 (first entry)
XX
DE Chimeric LGIC receptor protein, SEQ ID 33.
XX
KW CHRNA7 protein; GlyR alpha1; Nicotinic ACh receptor alpha 7 subunit;
KW alpha 1 glycine receptor; alpha7-nAchR; analgesic; anticonvulsant;
KW antipruritic; chimeric protein; eating disorder; eating-disorders-gen.;
KW movement disorder; muscle hypertonia; muscle relaxant;
KW neurogenic bladder; neurological disease; neuroprotective;
KW nicotinic cholinergic receptor alpha 7 subunit; pain;
KW protein engineering; protein therapy; pruritus; seizure disorder;
KW spinal cord disease; therapeutic; uropathic.
XX
OS Homo sapiens.
OS Synthetic.
XX
FH Key Location/Qualifiers
FT Peptide 1..22
FT /note= "Human alpha7-nAChR signal peptide"
FT Domain 23..229
FT /note= "Human alpha7-nAChR ligand binding domain"
FT Peptide 150..164
FT /note= "Human GlyR alpha1 Cys-loop sequence"
FT Domain 230..439
FT /note= "Human GlyR alpha1 ion pore domain"
XX
CC PN US2019161529-A1.
XX
CC PD 30-MAY-2019.
XX
CC PF 27-NOV-2018; 2018US-00201142.
XX
PR 27-NOV-2017; 2017US-0590911P.
PR 19-APR-2018; 2018US-0659911P.
XX
CC PA (CODA-) CODA BIOTHERAPEUTICS INC.
XX
CC PI Greenberg KP, Keifer O, Makinson S, Lau A;
XX
DR WPI; 2019-46769W/43.
DR N-PSDB; BGJ70857.
XX
CC PT New engineered receptor i.e. chimeric ligand gated ion channel (LGIC)
CC PT receptor comprising e.g. ligand binding domain derived from first wild
CC PT type Cys-loop LGIC receptor used to ameliorate neurological disorder e.g.
CC PT spinal cord injury.
XX
CC PS Claim 4; SEQ ID NO 33; 140pp; English.
XX
CC The invention relates to a novel engineered chimeric ligand gated ion
CC channel (LGIC) receptor, useful for ameliorating neurological disorder.
CC The engineered receptor comprises ligand binding domain derived from
CC first wild type Cys-loop LGIC receptor. The invention also claims: 1) a
CC polynucleotide encoding the engineered receptor; 2) a vector comprising
CC the polynucleotide; and 3) a method for ameliorating a neurological
CC disorder in a subject. The engineered receptor is useful for ameliorating
CC a neurological disorder in a subject suffering from pain, seizure
CC disorder, movement disorder, eating disorder, spinal cord injury,
CC neurogenic bladder, spasticity disorder or pruritus. The engineered
CC receptor is safe, efficient and cost-effective. The present sequence
CC represents a chimeric LGIC receptor (CHRNA7/GLRA1) protein comprising
CC human alpha7-nAChR signal peptide and ligand binding domain comprising
CC GlyR alpha1 Cys-loop sequence, fused to the human GlyR alpha1 ion pore
CC domain, used in the method for ameliorating a neurological disorder in a
CC subject. Note: The present sequence is used as a parent sequence for
CC creating variants (see BGJ70883-BGJ71067) shown in figure 8 of the
CC specification.
XX
SQ Sequence 439 AA;
Query Match 99.5%; Score 2337; Length 439;
Best Local Similarity 99.5%;
Matches 437; Conservative 0; Mismatches 2; Indels 0; Gaps 0;
Qy 1 MRCSPGGVWLALAASLLHVSLQGEFQRKLYKELVKNYNPLERPVANDSQPLTVYFSLSLL 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 MRCSPGGVWLALAASLLHVSLQGEFQRKLYKELVKNYNPLERPVANDSQPLTVYFSLSLL 60
Qy 61 QIMDVDEKNQVLTTNIWLQMSWTDHYLQWNVSEYPGVKTVRFPDGQIWKPDILLYNSADE 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 QIMDVDEKNQVLTTNIWLQMSWTDHYLQWNVSEYPGVKTVRFPDGQIWKPDILLYNSADE 120
Qy 121 RFDATFHTNVSVNSSGHCQYLPPGIFKSSCPMDLKNFPMDVQTCKLKFGSWDYGGWSLDL 180
|||||||||| |||||||||||||||||||||||||||||||||||||||| ||||||||
Db 121 RFDATFHTNVLVNSSGHCQYLPPGIFKSSCPMDLKNFPMDVQTCKLKFGSWSYGGWSLDL 180
Qy 181 QMQEADISGYIPNGEWDLVGIPGKRSERFYECCKEPYPDVTFTVTMRRRMGYYLIQMYIP 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 QMQEADISGYIPNGEWDLVGIPGKRSERFYECCKEPYPDVTFTVTMRRRMGYYLIQMYIP 240
Qy 241 SLLIVILSWISFWINMDAAPARVGLGITTVLTMTTQSSGSRASLPKVSYVKAIDIWMAVC 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 SLLIVILSWISFWINMDAAPARVGLGITTVLTMTTQSSGSRASLPKVSYVKAIDIWMAVC 300
Qy 301 LLFVFSALLEYAAVNFVSRQHKELLRFRRKRRHHKSPMLNLFQEDEAGEGRFNFSAYGMG 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 301 LLFVFSALLEYAAVNFVSRQHKELLRFRRKRRHHKSPMLNLFQEDEAGEGRFNFSAYGMG 360
Qy 361 PACLQAKDGISVKGANNSNTTNPPPAPSKSPEEMRKLFIQRAKKIDKISRIGFPMAFLIF 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 361 PACLQAKDGISVKGANNSNTTNPPPAPSKSPEEMRKLFIQRAKKIDKISRIGFPMAFLIF 420
Qy 421 NMFYWIIYKIVRREDVHNQ 439
|||||||||||||||||||
Db 421 NMFYWIIYKIVRREDVHNQ 439
SEQUENCE SEARCH RESULT E
This page gives you Search Results detail for the Application 18022358 and Search Result 20260211_102318_us-18-022-358-60.minpct98.rag
Title: US-18-022-358-60
Perfect score: 2350
Sequence: 1 MRCSPGGVWLALAASLLHVS..........FNMFYWIIYKIVRREDVHNQ 439
SUMMARIES
%
Result Query Filing
No. Score Match Length ID Date Dups Description
-------------------------------------------------------------------------------------------------------------
18 2338 99.5 439 BGJ70858 -- 7 Chimeric LGIC receptor protein, SEQ ID 33.
RESULT 18
BGJ70858
(NOTE: this sequence has 7 duplicates in the database searched.
See complete list at the end of this report)
ID BGJ70858 standard; protein; 439 AA.
XX
AC BGJ70858;
XX
DT 11-JUL-2019 (first entry)
XX
DE Chimeric LGIC receptor protein, SEQ ID 33.
XX
KW CHRNA7 protein; GlyR alpha1; Nicotinic ACh receptor alpha 7 subunit;
KW alpha 1 glycine receptor; alpha7-nAchR; analgesic; anticonvulsant;
KW antipruritic; chimeric protein; eating disorder; eating-disorders-gen.;
KW movement disorder; muscle hypertonia; muscle relaxant;
KW neurogenic bladder; neurological disease; neuroprotective;
KW nicotinic cholinergic receptor alpha 7 subunit; pain;
KW protein engineering; protein therapy; pruritus; seizure disorder;
KW spinal cord disease; therapeutic; uropathic.
XX
OS Homo sapiens.
OS Synthetic.
XX
FH Key Location/Qualifiers
FT Peptide 1..22
FT /note= "Human alpha7-nAChR signal peptide"
FT Domain 23..229
FT /note= "Human alpha7-nAChR ligand binding domain"
FT Peptide 150..164
FT /note= "Human GlyR alpha1 Cys-loop sequence"
FT Domain 230..439
FT /note= "Human GlyR alpha1 ion pore domain"
XX
CC PN US2019161529-A1.
XX
CC PD 30-MAY-2019.
XX
CC PF 27-NOV-2018; 2018US-00201142.
XX
PR 27-NOV-2017; 2017US-0590911P.
PR 19-APR-2018; 2018US-0659911P.
XX
CC PA (CODA-) CODA BIOTHERAPEUTICS INC.
XX
CC PI Greenberg KP, Keifer O, Makinson S, Lau A;
XX
DR WPI; 2019-46769W/43.
DR N-PSDB; BGJ70857.
XX
CC PT New engineered receptor i.e. chimeric ligand gated ion channel (LGIC)
CC PT receptor comprising e.g. ligand binding domain derived from first wild
CC PT type Cys-loop LGIC receptor used to ameliorate neurological disorder e.g.
CC PT spinal cord injury.
XX
CC PS Claim 4; SEQ ID NO 33; 140pp; English.
XX
CC The invention relates to a novel engineered chimeric ligand gated ion
CC channel (LGIC) receptor, useful for ameliorating neurological disorder.
CC The engineered receptor comprises ligand binding domain derived from
CC first wild type Cys-loop LGIC receptor. The invention also claims: 1) a
CC polynucleotide encoding the engineered receptor; 2) a vector comprising
CC the polynucleotide; and 3) a method for ameliorating a neurological
CC disorder in a subject. The engineered receptor is useful for ameliorating
CC a neurological disorder in a subject suffering from pain, seizure
CC disorder, movement disorder, eating disorder, spinal cord injury,
CC neurogenic bladder, spasticity disorder or pruritus. The engineered
CC receptor is safe, efficient and cost-effective. The present sequence
CC represents a chimeric LGIC receptor (CHRNA7/GLRA1) protein comprising
CC human alpha7-nAChR signal peptide and ligand binding domain comprising
CC GlyR alpha1 Cys-loop sequence, fused to the human GlyR alpha1 ion pore
CC domain, used in the method for ameliorating a neurological disorder in a
CC subject. Note: The present sequence is used as a parent sequence for
CC creating variants (see BGJ70883-BGJ71067) shown in figure 8 of the
CC specification.
XX
SQ Sequence 439 AA;
Query Match 99.5%; Score 2338; Length 439;
Best Local Similarity 99.5%;
Matches 437; Conservative 0; Mismatches 2; Indels 0; Gaps 0;
Qy 1 MRCSPGGVWLALAASLLHVSLQGEFQRKLYKELVKNYNPLERPVANDSQPLTVYFSLSLL 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 MRCSPGGVWLALAASLLHVSLQGEFQRKLYKELVKNYNPLERPVANDSQPLTVYFSLSLL 60
Qy 61 QIMDVDEKNQVLTTNIWLQMSWTDHYLQWNVSEYPGVKTVRFPDGQIWKPDILLYNSADE 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 QIMDVDEKNQVLTTNIWLQMSWTDHYLQWNVSEYPGVKTVRFPDGQIWKPDILLYNSADE 120
Qy 121 RFDATFHTNVTVNSSGHCQYLPPGIFKSSCPMDLKNFPMDVQTCKLKFGSWDYGGWSLDL 180
|||||||||| |||||||||||||||||||||||||||||||||||||||| ||||||||
Db 121 RFDATFHTNVLVNSSGHCQYLPPGIFKSSCPMDLKNFPMDVQTCKLKFGSWSYGGWSLDL 180
Qy 181 QMQEADISGYIPNGEWDLVGIPGKRSERFYECCKEPYPDVTFTVTMRRRMGYYLIQMYIP 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 QMQEADISGYIPNGEWDLVGIPGKRSERFYECCKEPYPDVTFTVTMRRRMGYYLIQMYIP 240
Qy 241 SLLIVILSWISFWINMDAAPARVGLGITTVLTMTTQSSGSRASLPKVSYVKAIDIWMAVC 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 SLLIVILSWISFWINMDAAPARVGLGITTVLTMTTQSSGSRASLPKVSYVKAIDIWMAVC 300
Qy 301 LLFVFSALLEYAAVNFVSRQHKELLRFRRKRRHHKSPMLNLFQEDEAGEGRFNFSAYGMG 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 301 LLFVFSALLEYAAVNFVSRQHKELLRFRRKRRHHKSPMLNLFQEDEAGEGRFNFSAYGMG 360
Qy 361 PACLQAKDGISVKGANNSNTTNPPPAPSKSPEEMRKLFIQRAKKIDKISRIGFPMAFLIF 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 361 PACLQAKDGISVKGANNSNTTNPPPAPSKSPEEMRKLFIQRAKKIDKISRIGFPMAFLIF 420
Qy 421 NMFYWIIYKIVRREDVHNQ 439
|||||||||||||||||||
Db 421 NMFYWIIYKIVRREDVHNQ 439