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
Applicant’s election without traverse of Group I (claims 1-14) in the reply filed on November 3, 2025 is acknowledged.
Claims 1 and 15 are amended. Claims 1-28 are pending in this application. Claims 15-28 are withdrawn without traverse (filed 11/03/2025) from further consideration pursuant to 37 CFR 1.142(b) as being drawn to nonelected inventions, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on November 3, 2025.
Claims 1-14 are under examination in this office action.
Claim Objections
Claims 15-28 are objected to because of the following informalities: the status of the claims 15-28 is incorrect because these claims are withdrawn from consideration. Appropriate correction is required.
See MPEP 714 & 37 CFR 1.121.
“In the claim listing, the status of every claim must be indicated after its claim number by using one of the following identifiers in a parenthetical expression: (Original), (Currently amended), (Canceled), (Withdrawn), (Previously presented), (New), and (Not entered).”
Claim Rejections - 35 USC § 112
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 1-14 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 1-14 are indefinite because:
i. Claim 1 recites the limitation "the treatment" in line 1 of the claim. There is insufficient antecedent basis for this limitation in the claim.
ii. The rest of claims are indefinite as depending from an indefinite claim.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claim 5 is rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
The invention appears to employ novel biological materials, specifically t monoclonal antibodies VX15/2503 and Mab67. Since the biological materials are essential to the claimed invention they must be obtainable by a repeatable method set forth in the specification or otherwise readily available to the public. If the biological materials are not so obtainable or available, the requirements of 35 U.S.C. § 112 may be satisfied by a deposit of the biological materials. The specification does not disclose a repeatable process to obtain the biological materials and it is not apparent if the biological materials are readily available to the public. The specification lacks sufficient deposit information for the monoclonal antibody VX15/2503 and Mab67. Because this undefined monoclonal antibody is unknown, and therefore, publicly not available or can reproducibly isolated from nature without undue experimentation, a suitable deposit for patent purposes is required. See M.P.E.P. 608. 01(p)(C).
If the deposit is made under the Budapest Treaty, then an affidavit or declaration by Applicant, or a statement by an attorney of record over his or her signature and registration number, stating that the specific biological materials have been deposited under the Budapest Treaty and that the biological materials will be irrevocably and without restriction or condition released to the public upon the issuance of a patent, would satisfy the deposit requirement made herein. If the deposit has not been made under the Budapest Treaty, then in order to certify that the deposit meets the criteria set forth in 37 C.F.R. §§ 1.801-1.809, Applicant may provide assurance of compliance by an affidavit or declaration, or by a statement by an attorney of record over his or her signature and registration number, showing that:
(a) during the pendency of this application, access to the invention will be afforded to the Commissioner upon request;
(b) all restrictions upon availability to the public will be irrevocably removed upon granting of the patent;
(c) the deposit will be maintained in a public depository for a period of 30 years or 5 years after the last request or for the effective life of the patent, whichever is longer;
(d) a test of the viability of the biological material at the time of deposit will be made (see 37 C.F.R. § 1.807); and
(e) the deposit will be replaced if it should ever become inviable.
Applicant' s attention is directed to M.P.E.P. §2400 in general, and specifically to §2411.05, as well as to 37 C.F.R. § 1.809(d), wherein it is set forth that “the specification shall contain the accession number for the deposit, the date of the deposit, the name and address of the depository, and a description of the deposited material sufficient to specifically identify it and to permit examination.” The specification should be amended to include this information, however, Applicant is cautioned to avoid the entry of new matter into the specification by adding any other information. Finally, the address for the ATCC should appear in the specification. The address is:
American Type Culture Collection
10801 University Boulevard
Manassas, VA 20110-2209
Claim Rejections - 35 USC § 112
Claims 1-14 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 1-14 are drawn to a combination therapy for treatment of Huntington’s disease (HD) comprising at least one isolated anti-SEMA4D antibody or antigen-binding fragment there of, and a therapeutically effective amount of at least one huntingtin protein (HTT)-lowering agent.
The claims encompass a genus of anti-SEMA4D antibody or antigen binding fragment thereof and a genus of HTT-lowering agent. Claim 5 encompasses a genus of anti-SEMA4D antibodies or antigen-binding fragments there of that competitively inhibit monoclonal antibody VX15/2503 or MAb67 binding to SEMA4D. Claims 8-9 encompass a genus of antisense oligonucleotide (ASO) against HTT (HTT-ASO) including allele-selective and non-selective ASO.
Applicant has not disclosed sufficient species for the broad genus of anti-SEMA4D antibody or antigen binding fragment thereof, the broad genus of HTT-lowering agent agonists, the broad genus of competitive anti-SEMA4D antibody or antigen binding fragment thereof and the genus of HTT-ASO including allele-selective and non-selective ASO.
The specification only describes: i) monoclonal antibodies VX15/2503, MAb67, Mab76, D2517, D2585 as described in US8496938 and BD16 and BB18 described in US806247 or humanized anti-CD100 monoclonal antibodies described in US20080219971 (issued as US7919594) (see para [00091]); ii) an HTT-ASO (non-selective ASO) having the sequence of SEQ ID NO:48 (HH1-ASO) or tominersen (SEQ ID NO:47) ([000103]); iii) administration of a combination of HH1 ASO + MAb67 to HD Hu97/18 mice resulted in improvement in behavior tests for anxiety or hypoactivity as compared to HH1 ASO or MAb67 alone (Examples 1-4, Figure 1-3), preserving striatal, cortical and corpus callosum volume in HD Hu97/18 mice relative to age-matched Hu97/18 control mice (Example 5, Figure 4-6), reducing levels of SEMA4D in Hu97/18 mice (Example 6,Figure 7), or reducing the number of GFAP+ and SERPINA3+ reactive astrocytes in the cortex and hypothalamus of Hu97/18 (Example 8, Figure 9).
However, the claims are not limited to the structurally and functionally defined anti-SEMA4D/anti-CD100 antibodies and HTT-ASO: HH1-ASO (SEQ ID NO:48) and tominersen (SEQ ID NO:47) set forth above but also encompass a genus of structurally and functionally undefined anti-SEMA4D antibody or antigen binding fragment thereof or competitive anti-SEMA4D antibody or antigen binding fragment thereof, a genus of HTT-lowering agent agonists, HTT-ASO including allele-selective and non-selective ASO.
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 a combination of HH1 ASO + MAb67 for improving anxiety or hypoactivity in HD Hu97/18 mice as compared to HH1 ASO or MAb67 alone. However, Applicant is not in possession of a combination of a structurally and functionally undefined anti-SEMA4D/anti-CD100 antibody with a structurally and functionally undefined HTT-ASO including structurally and functionally undefined allele-selective and non-selective ASO.
The specification provides no identification of any particular portion of the structure that must be conserved for the claimed anti-SEMA4D antibody or competitive anti-SEMA4D antibody, or antigen binding fragment thereof. The specification provides no structural and functional relationship or correlation between the claimed genus of anti-SEMA4D antibody and MAb67 or between the antibodies described in paragraph [0091] and MAb67.
The specification also provides no identification of any particular portion of the structure that must be conserved for the claimed HTT-ASO including allele-selective and non-selective ASO. The instant specification fails to provide sufficient descriptive information, such as definitive structural or functional features of the claimed genus of anti-SEMA4D antibody or competitive anti-SEMA4D antibody, or antigen binding fragment thereof or the claimed genus of HTT-ASO including structurally and functionally undefined allele-selective and non-selective ASO.
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 what other anti-SEMA4D/anti-CD100 antibodies or competitive anti-SEMA4D/anti-CD100 antibodies to the function of the MAb67 antibody. There is also no description of the sites at which variability may be tolerated and there is no information regarding the relation of structure of what other HTT-ASO including structurally and functionally undefined allele-selective and non-selective ASO to the function of HH1 ASO (SEQ ID NO:48). Furthermore, the prior art does not provide compensatory structural or correlative teachings sufficient to enable one of skill to identify what other anti-SEMA4D/anti-CD100 antibodies or competitive anti-SEMA4D/anti-CD100 antibodies might be or what other HTT-ASO including structurally and functionally undefined allele-selective and non-selective ASO might be.
Since the common characteristics/features of other anti-SEMA4D/anti-CD100 antibodies or competitive anti-SEMA4D/anti-CD100 antibodies or other HTT-ASO including structurally and functionally undefined allele-selective and non-selective ASO 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 anti-SEMA4D/anti-CD100 antibodies, the genus of competitive anti-SEMA4D/anti-CD100 antibodies and the genus of HTT-ASO including allele-selective and non-selective ASO.
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 anti-SEMA4D/anti-CD100 antibodies, the genus of competitive anti-SEMA4D/anti-CD100 antibodies and the genus of HTT-ASO including allele-selective and non-selective ASO, 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 combination therapy comprising at least one anti-SEMA4D antibody or antigen-binding fragment thereof and at least one HTT-lowering agent has 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.
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 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.
Claim Rejections - 35 USC § 102
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 1-14 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Jamwal et al. (Exp. Rev. Neurothera. 2020; 20:11, 1123-1141. DOI:10.1080/1437175.2020.1801424, published online on 05 Aug 2020). Doi.org/10.1080) as evidenced by Basile et al. (US8790652, issued Jul 29, 2014, priority Dec 15, 2011).
Claims 1-14 are drawn to a combination therapy for treatment of Huntington’s disease (HD) comprising at least one isolated anti-SEMA4D antibody or antigen-binding fragment there of, and a therapeutically effective amount of at least one huntingtin protein (HTT)-lowering agent.
Jamwal et al. teaches a combination therapy comprising immunotherapy with gene therapy (see p. 1135-1136), wherein the immunotherapy includes anti-SEMA4D antibody (see p. 1134-1135; p. 1137, table 5) and the gene therapy includes an antisense oligonucleotide (ASO) against Huntingtin (HTT) (HTT-ASO) (see p. 1127, section: 2.1.2.1 Antisense Oligonucleotide-based RNA targeting to p. 1128), which meet the limitations recited in instant claims 1-14. The anti-SEMA4D antibody disclosed by Jamwal includes Pepinemab (VX15/2503) as recited in claims 5-6 (see p. 1134-1135; p. 1137, table 5) and the HTT-ASO disclosed by Jamwal includes non-selective (p.1128, 1st col., 2nd para) and allele-specific HTT-ASO (p. 1128, 1st col., 2nd para) as recited in claims 8-10 (see p. 1127, section: 2.1.2.1 Antisense Oligonucleotide-based RNA targeting to p. 1128, 2nd col., 1st paragraph).
The anti-SEMA4D antibody including Pepinemab (VX15/2503) disclosed by Jamwal comprises SEQ ID NOs: 6-8 and 14-16 for VHCDRs1-3 and LCDRs1-3 respectively, or SEQ ID NOs: 9 and 17 for VH and VL respectively recited in claims 6-7 as evidenced by Basile et al. (US8790652; col. 3, line 1; col. 15-16), which can inhibit SEMA4D interaction with its receptor including Plexin-B1 or inhibit SEMA4D-mediated Plexin-B1 signal transduction and can compete with VX15/2503 or MAb67 (see the sequence alignment below).
The limitations “wherein administration of the combination….results in enhanced therapeutic efficacy relative to…. either the isolated antibody or antigen-binding fragment thereof or the HTT-lowering agent alone” recited in claim 12, “wherein administration of the combination ….results in improvement of neuropsychiatric….or any combination thereof” in claim 13 and “the improvement of neuropsychiatric symptoms….” recited in claim 14 are inherent features and results of administration of the combination therapy disclosed by Jamwal because the Jamwal’s combination therapy comprising the same anti-SEMA4D antibody and the same HTT-lowering agent including HTT-ASO including non-selective or allele-specific HTT-ASO”. Thus, claims 1-14 are anticipated by Jamwal as evidenced by Basile (US8790652).
The sequence search results disclose as follows:
SEQ ID NO:17
S-13-707-299-17
Filing date in PALM: 2012-12-06
Sequence 17, US/13707299
Patent No. 8790652
GENERAL INFORMATION
APPLICANT: Basile, John R.
APPLICANT: Evans, Elizabeth E.
APPLICANT: Smith, Ernest S.
TITLE OF INVENTION: USE OF THE COMBINATION OF SEMAPHORIN-4D INHIBITORY MOLECULES AND
TITLE OF INVENTION: VEGF INHIBITORY MOLECULES TO INHIBIT ANGIOGENESIS
FILE REFERENCE: 1843.0690002/EJH/BNC
CURRENT APPLICATION NUMBER: US/13/707,299
CURRENT FILING DATE: 2012-12-06
PRIOR APPLICATION NUMBER: US 61/576,188
PRIOR FILING DATE: 2011-12-15
PRIOR APPLICATION NUMBER: US 61/567,531
PRIOR FILING DATE: 2011-12-06
NUMBER OF SEQ ID NOS: 56
SEQ ID NO 17
LENGTH: 111
TYPE: PRT
ORGANISM: Artificial
FEATURE:
OTHER INFORMATION: Polypeptide anti-CD100 VL 2503
ALIGNMENT:
Query Match 100.0%; Score 580; Length 111;
Best Local Similarity 100.0%;
Matches 111; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
Qy 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
|||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
SEQ ID NO:9
US-13-707-299-9
Filing date in PALM: 2012-12-06
Sequence 9, US/13707299
Patent No. 8790652
GENERAL INFORMATION
APPLICANT: Basile, John R.
APPLICANT: Evans, Elizabeth E.
APPLICANT: Smith, Ernest S.
TITLE OF INVENTION: USE OF THE COMBINATION OF SEMAPHORIN-4D INHIBITORY MOLECULES AND
TITLE OF INVENTION: VEGF INHIBITORY MOLECULES TO INHIBIT ANGIOGENESIS
FILE REFERENCE: 1843.0690002/EJH/BNC
CURRENT APPLICATION NUMBER: US/13/707,299
CURRENT FILING DATE: 2012-12-06
PRIOR APPLICATION NUMBER: US 61/576,188
PRIOR FILING DATE: 2011-12-15
PRIOR APPLICATION NUMBER: US 61/567,531
PRIOR FILING DATE: 2011-12-06
NUMBER OF SEQ ID NOS: 56
SEQ ID NO 9
LENGTH: 118
TYPE: PRT
ORGANISM: Artificial
FEATURE:
OTHER INFORMATION: Polypeptide anti-CD100 VH 2503
ALIGNMENT:
Query Match 100.0%; Score 629; Length 118;
Best Local Similarity 100.0%;
Matches 118; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
Qy 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
SEQ ID NO:18
US-13-707-299-18
Filing date in PALM: 2012-12-06
Sequence 18, US/13707299
Patent No. 8790652
GENERAL INFORMATION
APPLICANT: Basile, John R.
APPLICANT: Evans, Elizabeth E.
APPLICANT: Smith, Ernest S.
TITLE OF INVENTION: USE OF THE COMBINATION OF SEMAPHORIN-4D INHIBITORY MOLECULES AND
TITLE OF INVENTION: VEGF INHIBITORY MOLECULES TO INHIBIT ANGIOGENESIS
FILE REFERENCE: 1843.0690002/EJH/BNC
CURRENT APPLICATION NUMBER: US/13/707,299
CURRENT FILING DATE: 2012-12-06
PRIOR APPLICATION NUMBER: US 61/576,188
PRIOR FILING DATE: 2011-12-15
PRIOR APPLICATION NUMBER: US 61/567,531
PRIOR FILING DATE: 2011-12-06
NUMBER OF SEQ ID NOS: 56
SEQ ID NO 18
LENGTH: 111
TYPE: PRT
ORGANISM: Artificial
FEATURE:
OTHER INFORMATION: Polypeptide anti-CD100 VL 67
ALIGNMENT:
Query Match 100.0%; Score 585; Length 111;
Best Local Similarity 100.0%;
Matches 111; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIVMTQSPASLAVSLGQRATISCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIVMTQSPASLAVSLGQRATISCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
Qy 61 GIPARFSGSGSGTDFTLNIHPVEEEDAATYYCQQSNEDPYTFGGGTKLEIK 111
|||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 GIPARFSGSGSGTDFTLNIHPVEEEDAATYYCQQSNEDPYTFGGGTKLEIK 111
SEQ ID NO:10
US-13-707-299-10
Filing date in PALM: 2012-12-06
Sequence 10, US/13707299
Patent No. 8790652
GENERAL INFORMATION
APPLICANT: Basile, John R.
APPLICANT: Evans, Elizabeth E.
APPLICANT: Smith, Ernest S.
TITLE OF INVENTION: USE OF THE COMBINATION OF SEMAPHORIN-4D INHIBITORY MOLECULES AND
TITLE OF INVENTION: VEGF INHIBITORY MOLECULES TO INHIBIT ANGIOGENESIS
FILE REFERENCE: 1843.0690002/EJH/BNC
CURRENT APPLICATION NUMBER: US/13/707,299
CURRENT FILING DATE: 2012-12-06
PRIOR APPLICATION NUMBER: US 61/576,188
PRIOR FILING DATE: 2011-12-15
PRIOR APPLICATION NUMBER: US 61/567,531
PRIOR FILING DATE: 2011-12-06
NUMBER OF SEQ ID NOS: 56
SEQ ID NO 10
LENGTH: 118
TYPE: PRT
ORGANISM: Artificial
FEATURE:
OTHER INFORMATION: Polypeptide anti-CD100 VH 67
ALIGNMENT:
Query Match 100.0%; Score 628; Length 118;
Best Local Similarity 100.0%;
Matches 118; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLQQSGPELVKPGASVKISCKASGYSFSDYYMHWVKQSPENSLEWIGQINPTTGGASY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLQQSGPELVKPGASVKISCKASGYSFSDYYMHWVKQSPENSLEWIGQINPTTGGASY 60
Qy 61 NQKFKGKATLTVDKSSSTAYMQLKSLTSEESAVYYCTRYYYGRHFDVWGQGTTVTVSS 118
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGKATLTVDKSSSTAYMQLKSLTSEESAVYYCTRYYYGRHFDVWGQGTTVTVSS 118
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1-14 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims of U.S. Patent No. 10731160 or claims of U.S. Patent No. 10533172 in view of Jamwal et al. (Exp. Rev. Neurothera. 2020; 20:11, 1123-1141) and Basile et al. (US8790652).
Claims 1-24 of US10731160 (the ‘160 Patent) claim a method of reducing mutant HTTmRNA or mutant HTT protein in a cell or tissue comprising contacting the cell or tissue an oligomer targeting a differentiating polymorphism including rs72239206, rs363107, rs362313, rs2530595, rs113407847 or treating HD in a mammal comprising administering to the mammal an oligomer targeting a differentiating polymorphism including rs72239206, rs363107, rs362313, rs2530595, rs113407847.
Claims 1-34 of US10533172 (the ‘172 Patent) claim an oligomer targeting and reducing mutant mRNA or mutant HTT protein in a cell or tissue, wherein the oligomer is SEQ ID NOs: 6-517.
While the claims of the ‘160 patent or the ‘172 patent do not recite the oligomer is in combination with an anti-SEMA4D antibody for treatment of HD, wherein the anti-SEMA4D antibody includes anti-SEMA4D antibodies having SEQ ID NOs: 6-8 and 14-16 for HCDRs1-3 and LCDRs1-3 or SEQ ID NO:9 and 17 or SEQ ID NO:10 and 18 for VH and VL respectively, Jamwal and Basile (US8790652) teach these limitations and provide motivation and an expectation of success in generating a combination therapy for treatment of HD comprising at least one anti-SEMA4D antibody and at least one HTT protein-lowering agent including HTT-ASO for the reasons set forth above under the 102 rejection. Thus, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to select and apply the known combination therapy for treatment of HD comprising an anti-SEMA4D antibody and a HTT-lowering agent including HTT-ASO including allele-selective or non-selective HTT-ASO and the known technique disclosed by Jamwal and Basile to the oligomer targeting and reducing mutant mRNA or mutant HTT protein in a cell or tissue of the ‘160 and ‘172 patents and yield the predictable result of a combination therapy for treatment of HD, comprising an anti-SEMA4D antibody and a HTT-lowering agent including HTT-ASO including allele-selective or non-selective HTT-ASO.
Claims 1-14 are rejected on the ground of nonstatutory double patenting as being unpatentable over Claims 1-27 of U.S. Patent No.12006364, claims 1-50 of U.S. Patent No. 11427634, Claims 1-15 of U.S. Patent No. 10800853, Claims 1-28 of U.S. Patent No. 9676840, Claims 1-24 of U.S. Patent No. 8816058, Claims 1-19 of US8496938or claims 1-36 of U.S. Patent No. 7919594 in view of Jamwal et al. (Exp. Rev. Neurothera. 2020; 20:11, 1123-1141) and Basile et al. (US8790652)
Claims 1-27 of US12006364 (the ‘364 patent) claim a composition comprising an anti-SEMA4D antibody and a method of treating neurodegenerative diseases wherein the anti-SEMA4D antibody comprises SEQ ID NO:2-4 and 6-8 for HCDRs1-3 and LCDRs1-3 respectively or SEQ ID NOs: 1 and 5 for VH and VL respectively.
Claims 1-50 of US11427634 (the ‘634 patent) claim an anti-SEMA4D antibody and a method of treating neurodegenerative diseases including HD wherein the anti-SEMA4D antibody comprises SEQ ID NO:2-4 and 6-8 for HCDRs1-3 and LCDRs1-3 respectively or SEQ ID NOs: 1 and 5 for VH and VL respectively.
Claims 1-15 of US10800853 (the ‘853 patent) claim a method of treating neurodegenerative diseases including HD using an anti-SEMA4D antibody, wherein the anti-SEMA4D antibody comprises SEQ ID NO:6-8 and 14-16 for HCDRs1-3 and LCDRs1-3 respectively or SEQ ID NOs: 9 and 10 for VH and VL respectively.
Claims 1-28 of US9676840 (the ‘840 patent) claim an anti-CD100/SEMA4D antibody comprising a VH comprising SEQ ID NO:9 and a VL comprising SEQ ID NO: 17.
Claims 1-24 of US8816058 (the ‘058 patent) claim an isolated polynucleotide encoding an anti-CD100/SEMA4D antibody comprising a VH comprising SEQ ID NO:9 and a VL comprising SEQ ID NOs: 14-16 for LCDRs1-3 respectively, or a VL comprising SEQ ID NO:17 and SEQ ID NOs: 6-8 for HCDRs1-3 respectively.
Claims 1-19 of US8496938 (the ‘938 patent) claim an isolated anti-CD100/SEMA4D antibody comprising SEQ ID NOs: 6-8 and SEQ ID NOs: 14-16 for HCDRs1-3 and LCDRs1-3 respectively or SEQ ID NO: 9 or 10 for VH and SEQ ID NO:17 or 18 for VL.
Claims 1-36 of US7919594 (the ‘594 patent) claim a humanized anti-SEMA4D antibody comprising a VH comprising SEQ ID NO:32, 45 or 50 and a VL comprising SEQ ID NO:4 or 5 or SEQ ID NOs: 9, 17 and 11 for HCDRs1-3 and aa 24-40, aa 56-62 and aa 95-103 of SEQ ID NO:4 or 5 for LCDR1-3.
While the claims of the ‘364, the ‘634, the ‘853, the ‘840, the ‘058, the ‘938 and the ‘594 patents do not recite that the anti-SEMA4D antibody including anti-SEMA4D antibodies having SEQ ID NOs: 6-8 and 14-16 for HCDRs1-3 and LCDRs1-3 or SEQ ID NO:9 and 17 or SEQ ID NO:10 and 18 for VH and VL respectively is in combination with a HTT-lowering agent including HTT-ASO for treatment of HD, Jamwal and Basile (US8790652) teach these limitations and provide motivation and an expectation of success in generating a combination therapy for treatment of HD, comprising at least one anti-SEMA4D antibody and at least one HTT protein-lowering agent including HTT-ASO for the reasons set forth above under the 102 rejection. Thus, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to select and apply the known combination therapy for treatment of HD comprising an anti-SEMA4D antibody and a HTT-lowering agent including HTT-ASO including allele-selective or non-selective HTT-ASO and the known technique disclosed by Jamwal and Basile to the anti-SEMA4D antibody of the ‘364, the ‘634, the ‘853, the ‘840, the ‘058, the ‘938 and the ‘594 patents and yield the predictable result of a combination therapy for treatment of HD, comprising an anti-SEMA4D antibody and a HTT-lowering agent including HTT-ASO including allele-selective or non-selective HTT-ASO.
Claims 1-14 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of copending Application No. 18/654538, claims 1-28 of copending Application No. 17/934660 in view of Jamwal et al. (Exp. Rev. Neurothera. 2020; 20:11, 1123-1141) and Basile et al. (US8790652).
Claims 1-20 of Application No. 18/654538 (the ‘538 Application) claim a method of treating a neurodegenerative disease including HD using an anti-SEMA4D antibody wherein the anti-SEMA4D antibody comprises SEQ ID NOs: 2-8 for HCDRs1-3 and LCDRs1-3 or SEQ ID NOs: 1 and 5 for VH and VL respectively
Claims 1-28 of Application No. 17/934660 (the ‘660 Application) claim a method of treating a neurodegenerative disease including HD using an anti-SEMA4D antibody wherein the anti-SEMA4D antibody comprises SEQ ID NOs: 6-8 and 14-16 for HCDRs1-3 and LCDRs1-3 respectively or SEQ ID NOs: 42-48 for HCDRs1-3 and LCDRs1-3 respectively
While the claims of the ‘538 Application or the ‘660 Application do not recite that the anti-SEMA4D antibody including anti-SEMA4D antibodies having SEQ ID NOs: 6-8 and 14-16 for HCDRs1-3 and LCDRs1-3 or SEQ ID NO:9 and 17 or SEQ ID NO:10 and 18 for VH and VL respectively is in combination with a HTT-lowering agent including HTT-ASO for treatment of HD, Jamwal and Basile (US8790652) teach these limitations and provide motivation and an expectation of success in generating a combination therapy for treatment of HD, comprising at least one anti-SEMA4D antibody and at least one HTT protein-lowering agent including HTT-ASO for the reasons set forth above under the 102 rejection. Thus, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to select and apply the known combination therapy for treatment of HD comprising an anti-SEMA4D antibody and a HTT-lowering agent including HTT-ASO including allele-selective or non-selective HTT-ASO and the known technique disclosed by Jamwal and Basile to the anti-SEMA4D antibody of the ‘538 Application or the ‘660 Application and yield the predictable result of a combination therapy for treatment of HD, comprising an anti-SEMA4D antibody and a HTT-lowering agent including HTT-ASO including allele-selective or non-selective HTT-ASO.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
NO CLAIM IS ALLOWED.
The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
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US8496938 teaches an anti-Sema4D/CD100 antibody that comprises a VL having the amino acid sequence of SEQ ID NO:17 or 18 and a VH having the amino acid sequence of SEQ ID NO:9 or 10, and methods of treating inflammatory diseases and autoimmune diseases including multiple sclerosis (see the sequence alignment below).
SEQ ID NO:17
US-12-776-187-17
(NOTE: this sequence has 24 duplicates in the database searched)
Sequence 17, US/12776187
Patent No. 8496938
GENERAL INFORMATION
APPLICANT: Smith, Ernest S.
APPLICANT: Fisher, Terrence Lee
TITLE OF INVENTION: Anti-CD100 Antibodies and Methods for Using the Same
FILE REFERENCE: 1843.0600002/EJH/BNC
CURRENT APPLICATION NUMBER: US/12/776,187
CURRENT FILING DATE: 2010-05-07
PRIOR APPLICATION NUMBER: 61/325,213
PRIOR FILING DATE: 2010-04-16
PRIOR APPLICATION NUMBER: 61/176,826
PRIOR FILING DATE: 2009-05-08
NUMBER OF SEQ ID NOS: 40
SEQ ID NO 17
LENGTH: 111
TYPE: PRT
ORGANISM: Artificial
FEATURE:
OTHER INFORMATION: Polypeptide anti-CD100 VL 2503
Query Match 100.0%; Score 580; Length 111;
Best Local Similarity 100.0%;
Matches 111; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
Qy 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
|||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
SEQ ID NO:9
US-12-776-187-9
(NOTE: this sequence has 24 duplicates in the database searched)
Sequence 9, US/12776187
Patent No. 8496938
GENERAL INFORMATION
APPLICANT: Smith, Ernest S.
APPLICANT: Fisher, Terrence Lee
TITLE OF INVENTION: Anti-CD100 Antibodies and Methods for Using the Same
FILE REFERENCE: 1843.0600002/EJH/BNC
CURRENT APPLICATION NUMBER: US/12/776,187
CURRENT FILING DATE: 2010-05-07
PRIOR APPLICATION NUMBER: 61/325,213
PRIOR FILING DATE: 2010-04-16
PRIOR APPLICATION NUMBER: 61/176,826
PRIOR FILING DATE: 2009-05-08
NUMBER OF SEQ ID NOS: 40
SEQ ID NO 9
LENGTH: 118
TYPE: PRT
ORGANISM: Artificial
FEATURE:
OTHER INFORMATION: Polypeptide anti-CD100 VH 2503
Query Match 100.0%; Score 629; Length 118;
Best Local Similarity 100.0%;
Matches 118; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
Qy 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
SEQ ID NO:10
US-12-776-187-10
(NOTE: this sequence has 24 duplicates in the database searched.
See complete list at the end of this report)
Sequence 10, US/12776187
Patent No. 8496938
GENERAL INFORMATION
APPLICANT: Smith, Ernest S.
APPLICANT: Fisher, Terrence Lee
TITLE OF INVENTION: Anti-CD100 Antibodies and Methods for Using the Same
FILE REFERENCE: 1843.0600002/EJH/BNC
CURRENT APPLICATION NUMBER: US/12/776,187
CURRENT FILING DATE: 2010-05-07
PRIOR APPLICATION NUMBER: 61/325,213
PRIOR FILING DATE: 2010-04-16
PRIOR APPLICATION NUMBER: 61/176,826
PRIOR FILING DATE: 2009-05-08
NUMBER OF SEQ ID NOS: 40
SEQ ID NO 10
LENGTH: 118
TYPE: PRT
ORGANISM: Artificial
FEATURE:
OTHER INFORMATION: Polypeptide anti-CD100 VH 67
Query Match 100.0%; Score 628; Length 118;
Best Local Similarity 100.0%;
Matches 118; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLQQSGPELVKPGASVKISCKASGYSFSDYYMHWVKQSPENSLEWIGQINPTTGGASY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLQQSGPELVKPGASVKISCKASGYSFSDYYMHWVKQSPENSLEWIGQINPTTGGASY 60
Qy 61 NQKFKGKATLTVDKSSSTAYMQLKSLTSEESAVYYCTRYYYGRHFDVWGQGTTVTVSS 118
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGKATLTVDKSSSTAYMQLKSLTSEESAVYYCTRYYYGRHFDVWGQGTTVTVSS 118
SEQ ID NO:18
US-12-776-187-18
(NOTE: this sequence has 24 duplicates in the database searched.
See complete list at the end of this report)
Sequence 18, US/12776187
Patent No. 8496938
GENERAL INFORMATION
APPLICANT: Smith, Ernest S.
APPLICANT: Fisher, Terrence Lee
TITLE OF INVENTION: Anti-CD100 Antibodies and Methods for Using the Same
FILE REFERENCE: 1843.0600002/EJH/BNC
CURRENT APPLICATION NUMBER: US/12/776,187
CURRENT FILING DATE: 2010-05-07
PRIOR APPLICATION NUMBER: 61/325,213
PRIOR FILING DATE: 2010-04-16
PRIOR APPLICATION NUMBER: 61/176,826
PRIOR FILING DATE: 2009-05-08
NUMBER OF SEQ ID NOS: 40
SEQ ID NO 18
LENGTH: 111
TYPE: PRT
ORGANISM: Artificial
FEATURE:
OTHER INFORMATION: Polypeptide anti-CD100 VL 67
Query Match 100.0%; Score 585; Length 111;
Best Local Similarity 100.0%;
Matches 111; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIVMTQSPASLAVSLGQRATISCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIVMTQSPASLAVSLGQRATISCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
Qy 61 GIPARFSGSGSGTDFTLNIHPVEEEDAATYYCQQSNEDPYTFGGGTKLEIK 111
|||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 GIPARFSGSGSGTDFTLNIHPVEEEDAATYYCQQSNEDPYTFGGGTKLEIK 111
US20150110800 teaches a method of treating neurodegenerative disease including Huntington’s disease comprising administering to a subject in need thereof an anti-Sema4D/CD100 antibody that comprises a VL having the amino acid sequence of SEQ ID NO:17 and a VH having the amino acid sequence of SEQ ID NO:9 (see the sequence alignment below).
SEQ ID NO:17
BBY73156
ID BBY73156 standard; protein; 111 AA.
XX
AC BBY73156;
XX
DT 18-JUN-2015 (first entry)
XX
DE Anti-SEMA4D monoclonal antibody light chain variable region, SEQ ID 17.
XX
KW CD100 protein; SEMA4D protein; Semaphorin-4D; alzheimers disease;
KW amnesia; antibody therapy; antiinflammatory; anxiety disorder;
KW astrocyte activation; ataxia; central nervous system disease;
KW cognitive disorder; down syndrome; frontotemporal dementia;
KW hiv associated dementia; huntingtons chorea; light chain variable region;
KW mild cognitive impairment; monoclonal antibody; motor neurone disease;
KW movement disorder; neuritis; neurodegenerative disease; neuroleptic;
KW neuroprotective; neuropsychologic disorder; nootropic;
KW parkinsons disease; prophylactic to disease; protein interaction;
KW therapeutic.
XX
OS Unidentified.
XX
FH Key Location/Qualifiers
FT Region 24..38
FT /note= "CDR1 of SEQ ID NO: 14 (see BBY73153)"
FT Region 54..60
FT /note= "CDR2 of SEQ ID NO: 15 (see BBY73154)"
FT Region 93..101
FT /note= "CDR3 of SEQ ID NO: 16 (see BBY73155)"
XX
CC PN US2015110800-A1.
XX
CC PD 23-APR-2015.
XX
CC PF 21-OCT-2014; 2014US-00519965.
XX
PR 21-OCT-2013; 2013US-0893814P.
PR 14-APR-2014; 2014US-0979384P.
PR 16-JUN-2014; 2014US-0012805P.
XX
CC PA (BOWE/) BOWERS W J.
CC PA (JONA/) JONASON A.
CC PA (SMIT/) SMITH E S.
CC PA (ZAUD/) ZAUDERER M.
XX
CC PI Bowers WJ, Jonason A, Smith ES, Zauderer M;
XX
DR WPI; 2015-261909/31.
DR N-PSDB; BBY73160.
XX
CC PT Alleviating symptoms in human having neurodegenerative disorder e.g.
CC PT Alzheimer's disease, and Huntington's disease, involves administering
CC PT isolated binding molecule which specifically binds to semaphorin-4D to
CC PT human.
XX
CC PS Claim 18; SEQ ID NO 17; 58pp; English.
XX
CC The present invention relates to a novel method for alleviating symptoms
CC in a subject having neurodegenerative disorder. The method comprises:
CC administering an effective amount of an isolated binding molecule
CC (preferably an antibody) which specifically binds to a semaphorin-4D
CC (SEMA4D) protein to the subject, where the binding molecule inhibits
CC SEMA4D interaction with its receptor. Also described are: (1) method for
CC preventing astrocyte activation in the subject having neuroinflammatory
CC disorder or neurodegenerative disorder; and (2) a method for maintaining
CC or restoring astrocyte-mediated trophic support of oligodendrocyte
CC precursor cells (OPCs) in the subject having neuroinflammatory disorder
CC or neurodegenerative disorder. The method of the present invention is
CC useful for preventing and treating neuroinflammatory disorder,
CC neurodegenerative disorder (chosen from Alzheimer's disease, Parkinson's
CC disease, Huntington's disease, down syndrome, ataxia, amyotrophic lateral
CC sclerosis (ALS), frontotemporal dementia (FTD), HIV-related cognitive
CC impairment, CNS lupus and mild cognitive impairment) and its symptoms
CC such as neuropsychiatric symptoms (preferably reducing anxiety-like
CC behavior, improving spatial memory and increasing locomotion), cognitive
CC symptoms and motor dysfunction. The present sequence represents a light
CC chain variable region of an anti-SEMA4D monoclonal antibody (VX15/2503),
CC where the antibody can be used for preventing and treating
CC neuroinflammatory disorder, neurodegenerative disorder and its symptoms.
XX
SQ Sequence 111 AA;
ALIGNMENT:
Query Match 100.0%; Score 580; Length 111;
Best Local Similarity 100.0%;
Matches 111; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
Qy 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
|||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
SEQ ID NO:9
BBY73148
ID BBY73148 standard; protein; 118 AA.
XX
AC BBY73148;
XX
DT 18-JUN-2015 (first entry)
XX
DE Anti-SEMA4D monoclonal antibody heavy chain variable region, SEQ ID 9.
XX
KW CD100 protein; SEMA4D protein; Semaphorin-4D; alzheimers disease;
KW amnesia; antibody therapy; antiinflammatory; anxiety disorder;
KW astrocyte activation; ataxia; central nervous system disease;
KW cognitive disorder; down syndrome; frontotemporal dementia;
KW heavy chain variable region; hiv associated dementia; huntingtons chorea;
KW mild cognitive impairment; monoclonal antibody; motor neurone disease;
KW movement disorder; neuritis; neurodegenerative disease; neuroleptic;
KW neuroprotective; neuropsychologic disorder; nootropic;
KW parkinsons disease; prophylactic to disease; protein interaction;
KW therapeutic.
XX
OS Unidentified.
XX
FH Key Location/Qualifiers
FT Region 26..35
FT /note= "CDR1 of SEQ ID NO: 6 (see BBY73145)"
FT Region 50..66
FT /note= "CDR2 of SEQ ID NO: 7 (see BBY73146)"
FT Region 99..107
FT /note= "CDR3 of SEQ ID NO: 8 (see BBY73147)"
XX
CC PN US2015110800-A1.
XX
CC PD 23-APR-2015.
XX
CC PF 21-OCT-2014; 2014US-00519965.
XX
PR 21-OCT-2013; 2013US-0893814P.
PR 14-APR-2014; 2014US-0979384P.
PR 16-JUN-2014; 2014US-0012805P.
XX
CC PA (BOWE/) BOWERS W J.
CC PA (JONA/) JONASON A.
CC PA (SMIT/) SMITH E S.
CC PA (ZAUD/) ZAUDERER M.
XX
CC PI Bowers WJ, Jonason A, Smith ES, Zauderer M;
XX
DR WPI; 2015-261909/31.
DR N-PSDB; BBY73158.
XX
CC PT Alleviating symptoms in human having neurodegenerative disorder e.g.
CC PT Alzheimer's disease, and Huntington's disease, involves administering
CC PT isolated binding molecule which specifically binds to semaphorin-4D to
CC PT human.
XX
CC PS Claim 18; SEQ ID NO 9; 58pp; English.
XX
CC The present invention relates to a novel method for alleviating symptoms
CC in a subject having neurodegenerative disorder. The method comprises:
CC administering an effective amount of an isolated binding molecule
CC (preferably an antibody) which specifically binds to a semaphorin-4D
CC (SEMA4D) protein to the subject, where the binding molecule inhibits
CC SEMA4D interaction with its receptor. Also described are: (1) method for
CC preventing astrocyte activation in the subject having neuroinflammatory
CC disorder or neurodegenerative disorder; and (2) a method for maintaining
CC or restoring astrocyte-mediated trophic support of oligodendrocyte
CC precursor cells (OPCs) in the subject having neuroinflammatory disorder
CC or neurodegenerative disorder. The method of the present invention is
CC useful for preventing and treating neuroinflammatory disorder,
CC neurodegenerative disorder (chosen from Alzheimer's disease, Parkinson's
CC disease, Huntington's disease, down syndrome, ataxia, amyotrophic lateral
CC sclerosis (ALS), frontotemporal dementia (FTD), HIV-related cognitive
CC impairment, CNS lupus and mild cognitive impairment) and its symptoms
CC such as neuropsychiatric symptoms (preferably reducing anxiety-like
CC behavior, improving spatial memory and increasing locomotion), cognitive
CC symptoms and motor dysfunction. The present sequence represents a heavy
CC chain variable region of an anti-SEMA4D monoclonal antibody (VX15/2503),
CC where the antibody can be used for preventing and treating
CC neuroinflammatory disorder, neurodegenerative disorder and its symptoms.
XX
SQ Sequence 118 AA;
ALIGNMENT:
Query Match 100.0%; Score 629; Length 118;
Best Local Similarity 100.0%;
Matches 118; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
Qy 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
SEQ ID NO:10
ID BBY73149 standard; protein; 118 AA.
XX
AC BBY73149;
XX
DT 18-JUN-2015 (first entry)
XX
DE Anti-SEMA4D monoclonal antibody heavy chain variable region, SEQ ID 10.
XX
KW CD100 protein; SEMA4D protein; Semaphorin-4D; alzheimers disease;
KW amnesia; antibody therapy; antiinflammatory; anxiety disorder;
KW astrocyte activation; ataxia; central nervous system disease;
KW cognitive disorder; down syndrome; frontotemporal dementia;
KW heavy chain variable region; hiv associated dementia; huntingtons chorea;
KW mild cognitive impairment; monoclonal antibody; motor neurone disease;
KW movement disorder; neuritis; neurodegenerative disease; neuroleptic;
KW neuroprotective; neuropsychologic disorder; nootropic;
KW parkinsons disease; prophylactic to disease; protein interaction;
KW therapeutic.
XX
OS Unidentified.
XX
FH Key Location/Qualifiers
FT Region 26..35
FT /note= "CDR1 of SEQ ID NO: 6 (see BBY73145)"
FT Region 50..66
FT /note= "CDR2 of SEQ ID NO: 7 (see BBY73146)"
FT Region 99..107
FT /note= "CDR3 of SEQ ID NO: 8 (see BBY73147)"
XX
CC PN US2015110800-A1.
XX
CC PD 23-APR-2015.
XX
CC PF 21-OCT-2014; 2014US-00519965.
XX
PR 21-OCT-2013; 2013US-0893814P.
PR 14-APR-2014; 2014US-0979384P.
PR 16-JUN-2014; 2014US-0012805P.
XX
CC PA (BOWE/) BOWERS W J.
CC PA (JONA/) JONASON A.
CC PA (SMIT/) SMITH E S.
CC PA (ZAUD/) ZAUDERER M.
XX
CC PI Bowers WJ, Jonason A, Smith ES, Zauderer M;
XX
DR WPI; 2015-261909/31.
DR N-PSDB; BBY73159.
XX
CC PT Alleviating symptoms in human having neurodegenerative disorder e.g.
CC PT Alzheimer's disease, and Huntington's disease, involves administering
CC PT isolated binding molecule which specifically binds to semaphorin-4D to
CC PT human.
XX
CC PS Claim 18; SEQ ID NO 10; 58pp; English.
XX
CC The present invention relates to a novel method for alleviating symptoms
CC in a subject having neurodegenerative disorder. The method comprises:
CC administering an effective amount of an isolated binding molecule
CC (preferably an antibody) which specifically binds to a semaphorin-4D
CC (SEMA4D) protein to the subject, where the binding molecule inhibits
CC SEMA4D interaction with its receptor. Also described are: (1) method for
CC preventing astrocyte activation in the subject having neuroinflammatory
CC disorder or neurodegenerative disorder; and (2) a method for maintaining
CC or restoring astrocyte-mediated trophic support of oligodendrocyte
CC precursor cells (OPCs) in the subject having neuroinflammatory disorder
CC or neurodegenerative disorder. The method of the present invention is
CC useful for preventing and treating neuroinflammatory disorder,
CC neurodegenerative disorder (chosen from Alzheimer's disease, Parkinson's
CC disease, Huntington's disease, down syndrome, ataxia, amyotrophic lateral
CC sclerosis (ALS), frontotemporal dementia (FTD), HIV-related cognitive
CC impairment, CNS lupus and mild cognitive impairment) and its symptoms
CC such as neuropsychiatric symptoms (preferably reducing anxiety-like
CC behavior, improving spatial memory and increasing locomotion), cognitive
CC symptoms and motor dysfunction. The present sequence represents a heavy
CC chain variable region of an anti-SEMA4D monoclonal antibody (MAb 67),
CC where the antibody can be used for preventing and treating
CC neuroinflammatory disorder, neurodegenerative disorder and its symptoms.
XX
SQ Sequence 118 AA;
Query Match 100.0%; Score 628; Length 118;
Best Local Similarity 100.0%;
Matches 118; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLQQSGPELVKPGASVKISCKASGYSFSDYYMHWVKQSPENSLEWIGQINPTTGGASY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLQQSGPELVKPGASVKISCKASGYSFSDYYMHWVKQSPENSLEWIGQINPTTGGASY 60
Qy 61 NQKFKGKATLTVDKSSSTAYMQLKSLTSEESAVYYCTRYYYGRHFDVWGQGTTVTVSS 118
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGKATLTVDKSSSTAYMQLKSLTSEESAVYYCTRYYYGRHFDVWGQGTTVTVSS 118
US20150353641 teaches a method of treating neurodegenerative disease including Huntington’s disease comprising administering to a subject in need thereof an anti-Sema4D/CD100 antibody that comprises a VL having the amino acid sequence of SEQ ID NO:17 and a VH having the amino acid sequence of SEQ ID NO:9 (see the sequence alignment below).
SEQ ID NO:17
BCJ65936
ID BCJ65936 standard; protein; 111 AA.
XX
AC BCJ65936;
XX
DT 28-JAN-2016 (first entry)
XX
DE Anti-CD100 monoclonal antibody 2503 light chain variable region, SEQ 17.
XX
KW CD100; SEMA4D protein; Semaphorin-4D; alzheimers disease;
KW angiogenesis disorder; antibody therapy; antiinflammatory;
KW anxiety disorder; ataxia; autoimmune disease; cancer; cell culture;
KW cerebral edema; cognitive disorder; cytostatic; down syndrome; epilepsy;
KW frontotemporal dementia; genetic-disease-gen.; huntingtons chorea;
KW immunosuppressive; inflammatory disease; light chain variable region;
KW lymphoma; meningitis; mild cognitive impairment; monoclonal antibody;
KW motor neurone disease; multiple sclerosis; nervous system inflammation;
KW neuritis; neurodegenerative disease; neuroleptic; neuroprotective;
KW neuropsychologic disorder; nootropic; parkinsons disease;
KW prophylactic to disease; stroke; systemic lupus erythematosus;
KW therapeutic; transplant rejection; vasotropic.
XX
OS Unidentified.
XX
CC PN US2015353641-A1.
XX
CC PD 10-DEC-2015.
XX
CC PF 29-JUN-2015; 2015US-00753882.
XX
PR 21-OCT-2013; 2013US-0893614P.
PR 21-OCT-2013; 2013US-0893814P.
PR 14-APR-2014; 2014US-0979384P.
PR 16-JUN-2014; 2014US-0012805P.
PR 21-OCT-2014; 2014US-00519965.
PR 21-OCT-2014; 2014WO-US061592.
XX
CC PA (VACC-) VACCINEX INC.
XX
CC PI Bowers WJ, Jonason A, Smith ES, Zauderer M;
XX
DR WPI; 2015-823125/06.
DR N-PSDB; BCJ65940.
XX
CC PT Alleviating symptoms in subject having, or suspected of having
CC PT Huntington's disease (HD) comprises administering isolated binding
CC PT molecule that specifically binds to semaphorin-4D (SEMA4D) to subject.
XX
CC PS Disclosure; SEQ ID NO 17; 58pp; English.
XX
CC The present invention relates to a novel method for alleviating symptoms
CC in a subject having or suspected of having huntington's disease (HD). The
CC method involves administering an isolated binding molecule capable of
CC specifically binding to semaphorin-4D (SEMA4D, CD100). The invention also
CC provides: a method for reducing astrocyte activation in a subject having
CC or suspected of having huntington's disease; and a method for maintaining
CC or restoring astrocyte-mediated trophic support of oligodendrocyte
CC precursor cells (OPCs) in a subject having or suspected of having
CC huntington's disease. The SEMA4D binding molecules is also useful for
CC treating or preventing neuroinflammatory disease (e.g., multiple
CC sclerosis), cancer (e.g., lymphomas), autoimmune disease, inflammatory
CC disease including central nervous system (CNS) and peripheral nervous
CC system (PNS) inflammatory diseases, transplant rejection, invasive
CC angiogenesis and neurodegenerative disorders (e.g., Alzheimer's disease
CC (AD), meningitis, brain edema, epilepsy, stroke, Parkinson's disease
CC (PD), Huntington's disease, Down syndrome, ataxia, amyotrophic lateral
CC sclerosis (ALS), frontotemporal dementia (FTD), HIV-related cognitive
CC impairment, CNS lupus and mild cognitive impairment). The symptoms are
CC neuropsychiatric symptoms (e.g., anxiety-like behavior, reduced spatial
CC memory and impaired locomotion), cognitive symptoms and motor
CC dysfunction. The present sequence represents an anti-CD100 monoclonal
CC antibody (mAb) light chain variable region (VL), which can be used for
CC reducing astrocyte activation and alleviating symptoms in a subject
CC having huntington's disease.
XX
SQ Sequence 111 AA;
ALIGNMENT:
Query Match 100.0%; Score 580; Length 111;
Best Local Similarity 100.0%;
Matches 111; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
Qy 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
|||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
SEQ ID NO:9
BCJ65928
ID BCJ65928 standard; protein; 118 AA.
XX
AC BCJ65928;
XX
DT 28-JAN-2016 (first entry)
XX
DE Anti-CD100 monoclonal antibody 2503 heavy chain variable region, SEQ 9.
XX
KW CD100; SEMA4D protein; Semaphorin-4D; alzheimers disease;
KW angiogenesis disorder; antibody therapy; antiinflammatory;
KW anxiety disorder; ataxia; autoimmune disease; cancer; cell culture;
KW cerebral edema; cognitive disorder; cytostatic; down syndrome; epilepsy;
KW frontotemporal dementia; genetic-disease-gen.;
KW heavy chain variable region; huntingtons chorea; immunosuppressive;
KW inflammatory disease; lymphoma; meningitis; mild cognitive impairment;
KW monoclonal antibody; motor neurone disease; multiple sclerosis;
KW nervous system inflammation; neuritis; neurodegenerative disease;
KW neuroleptic; neuroprotective; neuropsychologic disorder; nootropic;
KW parkinsons disease; prophylactic to disease; stroke;
KW systemic lupus erythematosus; therapeutic; transplant rejection;
KW vasotropic.
XX
OS Unidentified.
XX
CC PN US2015353641-A1.
XX
CC PD 10-DEC-2015.
XX
CC PF 29-JUN-2015; 2015US-00753882.
XX
PR 21-OCT-2013; 2013US-0893614P.
PR 21-OCT-2013; 2013US-0893814P.
PR 14-APR-2014; 2014US-0979384P.
PR 16-JUN-2014; 2014US-0012805P.
PR 21-OCT-2014; 2014US-00519965.
PR 21-OCT-2014; 2014WO-US061592.
XX
CC PA (VACC-) VACCINEX INC.
XX
CC PI Bowers WJ, Jonason A, Smith ES, Zauderer M;
XX
DR WPI; 2015-823125/06.
DR N-PSDB; BCJ65938.
XX
CC PT Alleviating symptoms in subject having, or suspected of having
CC PT Huntington's disease (HD) comprises administering isolated binding
CC PT molecule that specifically binds to semaphorin-4D (SEMA4D) to subject.
XX
CC PS Disclosure; SEQ ID NO 9; 58pp; English.
XX
CC The present invention relates to a novel method for alleviating symptoms
CC in a subject having or suspected of having huntington's disease (HD). The
CC method involves administering an isolated binding molecule capable of
CC specifically binding to semaphorin-4D (SEMA4D, CD100). The invention also
CC provides: a method for reducing astrocyte activation in a subject having
CC or suspected of having huntington's disease; and a method for maintaining
CC or restoring astrocyte-mediated trophic support of oligodendrocyte
CC precursor cells (OPCs) in a subject having or suspected of having
CC huntington's disease. The SEMA4D binding molecules is also useful for
CC treating or preventing neuroinflammatory disease (e.g., multiple
CC sclerosis), cancer (e.g., lymphomas), autoimmune disease, inflammatory
CC disease including central nervous system (CNS) and peripheral nervous
CC system (PNS) inflammatory diseases, transplant rejection, invasive
CC angiogenesis and neurodegenerative disorders (e.g., Alzheimer's disease
CC (AD), meningitis, brain edema, epilepsy, stroke, Parkinson's disease
CC (PD), Huntington's disease, Down syndrome, ataxia, amyotrophic lateral
CC sclerosis (ALS), frontotemporal dementia (FTD), HIV-related cognitive
CC impairment, CNS lupus and mild cognitive impairment). The symptoms are
CC neuropsychiatric symptoms (e.g., anxiety-like behavior, reduced spatial
CC memory and impaired locomotion), cognitive symptoms and motor
CC dysfunction. The present sequence represents an anti-CD100 monoclonal
CC antibody (mAb) heavy chain variable region (VH), which can be used for
CC reducing astrocyte activation and alleviating symptoms in a subject
CC having huntington's disease.
XX
SQ Sequence 118 AA;
ALIGNMENT:
Query Match 100.0%; Score 629; Length 118;
Best Local Similarity 100.0%;
Matches 118; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
Qy 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
SEQ ID NO:10
ID BCJ65929 standard; protein; 118 AA.
XX
AC BCJ65929;
XX
DT 28-JAN-2016 (first entry)
XX
DE Anti-CD100 monoclonal antibody 67 heavy chain variable region, SEQ ID 10.
XX
KW CD100; SEMA4D protein; Semaphorin-4D; alzheimers disease;
KW angiogenesis disorder; antibody therapy; antiinflammatory;
KW anxiety disorder; ataxia; autoimmune disease; cancer; cell culture;
KW cerebral edema; cognitive disorder; cytostatic; down syndrome; epilepsy;
KW frontotemporal dementia; genetic-disease-gen.;
KW heavy chain variable region; huntingtons chorea; immunosuppressive;
KW inflammatory disease; lymphoma; meningitis; mild cognitive impairment;
KW monoclonal antibody; motor neurone disease; multiple sclerosis;
KW nervous system inflammation; neuritis; neurodegenerative disease;
KW neuroleptic; neuroprotective; neuropsychologic disorder; nootropic;
KW parkinsons disease; prophylactic to disease; stroke;
KW systemic lupus erythematosus; therapeutic; transplant rejection;
KW vasotropic.
XX
OS Unidentified.
XX
CC PN US2015353641-A1.
XX
CC PD 10-DEC-2015.
XX
CC PF 29-JUN-2015; 2015US-00753882.
XX
PR 21-OCT-2013; 2013US-0893614P.
PR 21-OCT-2013; 2013US-0893814P.
PR 14-APR-2014; 2014US-0979384P.
PR 16-JUN-2014; 2014US-0012805P.
PR 21-OCT-2014; 2014US-00519965.
PR 21-OCT-2014; 2014WO-US061592.
XX
CC PA (VACC-) VACCINEX INC.
XX
CC PI Bowers WJ, Jonason A, Smith ES, Zauderer M;
XX
DR WPI; 2015-823125/06.
DR N-PSDB; BCJ65939.
XX
CC PT Alleviating symptoms in subject having, or suspected of having
CC PT Huntington's disease (HD) comprises administering isolated binding
CC PT molecule that specifically binds to semaphorin-4D (SEMA4D) to subject.
XX
CC PS Disclosure; SEQ ID NO 10; 58pp; English.
XX
CC The present invention relates to a novel method for alleviating symptoms
CC in a subject having or suspected of having huntington's disease (HD). The
CC method involves administering an isolated binding molecule capable of
CC specifically binding to semaphorin-4D (SEMA4D, CD100). The invention also
CC provides: a method for reducing astrocyte activation in a subject having
CC or suspected of having huntington's disease; and a method for maintaining
CC or restoring astrocyte-mediated trophic support of oligodendrocyte
CC precursor cells (OPCs) in a subject having or suspected of having
CC huntington's disease. The SEMA4D binding molecules is also useful for
CC treating or preventing neuroinflammatory disease (e.g., multiple
CC sclerosis), cancer (e.g., lymphomas), autoimmune disease, inflammatory
CC disease including central nervous system (CNS) and peripheral nervous
CC system (PNS) inflammatory diseases, transplant rejection, invasive
CC angiogenesis and neurodegenerative disorders (e.g., Alzheimer's disease
CC (AD), meningitis, brain edema, epilepsy, stroke, Parkinson's disease
CC (PD), Huntington's disease, Down syndrome, ataxia, amyotrophic lateral
CC sclerosis (ALS), frontotemporal dementia (FTD), HIV-related cognitive
CC impairment, CNS lupus and mild cognitive impairment). The symptoms are
CC neuropsychiatric symptoms (e.g., anxiety-like behavior, reduced spatial
CC memory and impaired locomotion), cognitive symptoms and motor
CC dysfunction. The present sequence represents an anti-CD100 monoclonal
CC antibody (mAb) heavy chain variable region (VH), which can be used for
CC reducing astrocyte activation and alleviating symptoms in a subject
CC having huntington's disease.
XX
SQ Sequence 118 AA;
Query Match 100.0%; Score 628; Length 118;
Best Local Similarity 100.0%;
Matches 118; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLQQSGPELVKPGASVKISCKASGYSFSDYYMHWVKQSPENSLEWIGQINPTTGGASY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLQQSGPELVKPGASVKISCKASGYSFSDYYMHWVKQSPENSLEWIGQINPTTGGASY 60
Qy 61 NQKFKGKATLTVDKSSSTAYMQLKSLTSEESAVYYCTRYYYGRHFDVWGQGTTVTVSS 118
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGKATLTVDKSSSTAYMQLKSLTSEESAVYYCTRYYYGRHFDVWGQGTTVTVSS 118
US20170198053 teaches a method of treating neurodegenerative disease including Huntington’s disease comprising administering to a subject in need thereof an anti-Sema4D/CD100 antibody that comprises a VL having the amino acid sequence of SEQ ID NO:17 and a VH having the amino acid sequence of SEQ ID NO:9 (see the sequence alignment below).
SEQ ID NO:17
BED58116
ID BED58116 standard; protein; 111 AA.
XX
AC BED58116;
XX
DT 07-SEP-2017 (first entry)
XX
DE Anti-SEMA4D mAb light chain variable region (VL) 2503, SEQ ID 17.
XX
KW CD100; SEMA4D protein; Semaphorin-4D; alzheimers disease;
KW antibody therapy; antiinflammatory; ataxia; cognitive disorder;
KW degeneration; down syndrome; frontotemporal dementia; huntingtons chorea;
KW light chain variable region; monoclonal antibody; motor neurone disease;
KW neuritis; neurodegenerative disease; neuroprotective; parkinsons disease;
KW therapeutic.
XX
OS Unidentified.
XX
CC PN US2017198053-A1.
XX
CC PD 13-JUL-2017.
XX
CC PF 21-MAR-2017; 2017US-00465509.
XX
PR 21-OCT-2013; 2013US-0893814P.
PR 14-APR-2014; 2014US-0979384P.
PR 16-JUN-2014; 2014US-0012805P.
PR 21-OCT-2014; 2014US-00519965.
PR 31-JAN-2017; 2017US-00420662.
XX
CC PA (VACC-) VACCINEX INC.
XX
CC PI Smith ES, Zauderer M, Bowers WJ, Jonason A;
XX
DR WPI; 2017-478433/50.
DR N-PSDB; BED58120.
XX
CC PT Treating subject having, or suspected of having neuroinflammatory or
CC PT neurodegenerative disorder involves administering subject with effective
CC PT amount of isolated binding molecule which specifically binds to
CC PT semaphorin-4D.
XX
CC PS Claim 9; SEQ ID NO 17; 59pp; English.
XX
CC The present invention relates to a method for treating a subject having
CC or suspected of having neuroinflammatory or neurodegenerative disorder.
CC The method involves administering an effective amount of an isolated
CC binding molecule which specifically binds to semaphorin-4D (SEMA4D,
CC CD100) to the subject. The invention further relates to: (1) a method for
CC maintaining or restoring astrocyte-mediated trophic support of
CC oligodendrocyte precursor cells (OPCs) in a subject; and (2) a method for
CC protecting inhibitory neurons from degeneration in early Alzheimer's
CC disease in the subject. The neurodegenerative disorder includes
CC Alzheimer's disease, Parkinson's disease, Huntington's disease, down
CC syndrome, ataxia, amyotrophic lateral sclerosis (ALS), frontotemporal
CC dementia (FTD), HIV-related cognitive impairment, CNS lupus, mild
CC cognitive impairment. The present sequence represents a light chain
CC variable region (VL) of anti-SEMA4D monoclonal antibody, useful for
CC treating the above-mentioned diseases.
XX
SQ Sequence 111 AA;
ALIGNMENT:
Query Match 100.0%; Score 580; Length 111;
Best Local Similarity 100.0%;
Matches 111; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
Qy 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
|||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
SEQ ID NO:9
BED58108
ID BED58108 standard; protein; 118 AA.
XX
AC BED58108;
XX
DT 07-SEP-2017 (first entry)
XX
DE Anti-SEMA4D mAb heavy chain variable region (VH) 2503, SEQ ID 9.
XX
KW CD100; SEMA4D protein; Semaphorin-4D; alzheimers disease;
KW antibody therapy; antiinflammatory; ataxia; cognitive disorder;
KW degeneration; down syndrome; frontotemporal dementia;
KW heavy chain variable region; huntingtons chorea; monoclonal antibody;
KW motor neurone disease; neuritis; neurodegenerative disease;
KW neuroprotective; parkinsons disease; therapeutic.
XX
OS Unidentified.
XX
CC PN US2017198053-A1.
XX
CC PD 13-JUL-2017.
XX
CC PF 21-MAR-2017; 2017US-00465509.
XX
PR 21-OCT-2013; 2013US-0893814P.
PR 14-APR-2014; 2014US-0979384P.
PR 16-JUN-2014; 2014US-0012805P.
PR 21-OCT-2014; 2014US-00519965.
PR 31-JAN-2017; 2017US-00420662.
XX
CC PA (VACC-) VACCINEX INC.
XX
CC PI Smith ES, Zauderer M, Bowers WJ, Jonason A;
XX
DR WPI; 2017-478433/50.
DR N-PSDB; BED58118.
XX
CC PT Treating subject having, or suspected of having neuroinflammatory or
CC PT neurodegenerative disorder involves administering subject with effective
CC PT amount of isolated binding molecule which specifically binds to
CC PT semaphorin-4D.
XX
CC PS Claim 5; SEQ ID NO 9; 59pp; English.
XX
CC The present invention relates to a method for treating a subject having
CC or suspected of having neuroinflammatory or neurodegenerative disorder.
CC The method involves administering an effective amount of an isolated
CC binding molecule which specifically binds to semaphorin-4D (SEMA4D,
CC CD100) to the subject. The invention further relates to: (1) a method for
CC maintaining or restoring astrocyte-mediated trophic support of
CC oligodendrocyte precursor cells (OPCs) in a subject; and (2) a method for
CC protecting inhibitory neurons from degeneration in early Alzheimer's
CC disease in the subject. The neurodegenerative disorder includes
CC Alzheimer's disease, Parkinson's disease, Huntington's disease, down
CC syndrome, ataxia, amyotrophic lateral sclerosis (ALS), frontotemporal
CC dementia (FTD), HIV-related cognitive impairment, CNS lupus, mild
CC cognitive impairment. The present sequence represents a heavy chain
CC variable region (VH) of anti-SEMA4D monoclonal antibody, useful for
CC treating the above-mentioned diseases.
XX
SQ Sequence 118 AA;
ALIGNMENT:
Query Match 100.0%; Score 629; Length 118;
Best Local Similarity 100.0%;
Matches 118; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
Qy 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
SEQ ID NO:10
ID BED58109 standard; protein; 118 AA.
XX
AC BED58109;
XX
DT 07-SEP-2017 (first entry)
XX
DE Anti-SEMA4D mAb heavy chain variable region (VH) 67, SEQ ID 10.
XX
KW CD100; SEMA4D protein; Semaphorin-4D; alzheimers disease;
KW antibody therapy; antiinflammatory; ataxia; cognitive disorder;
KW degeneration; down syndrome; frontotemporal dementia;
KW heavy chain variable region; huntingtons chorea; monoclonal antibody;
KW motor neurone disease; neuritis; neurodegenerative disease;
KW neuroprotective; parkinsons disease; therapeutic.
XX
OS Unidentified.
XX
CC PN US2017198053-A1.
XX
CC PD 13-JUL-2017.
XX
CC PF 21-MAR-2017; 2017US-00465509.
XX
PR 21-OCT-2013; 2013US-0893814P.
PR 14-APR-2014; 2014US-0979384P.
PR 16-JUN-2014; 2014US-0012805P.
PR 21-OCT-2014; 2014US-00519965.
PR 31-JAN-2017; 2017US-00420662.
XX
CC PA (VACC-) VACCINEX INC.
XX
CC PI Smith ES, Zauderer M, Bowers WJ, Jonason A;
XX
DR WPI; 2017-478433/50.
DR N-PSDB; BED58119.
XX
CC PT Treating subject having, or suspected of having neuroinflammatory or
CC PT neurodegenerative disorder involves administering subject with effective
CC PT amount of isolated binding molecule which specifically binds to
CC PT semaphorin-4D.
XX
CC PS Claim 5; SEQ ID NO 10; 59pp; English.
XX
CC The present invention relates to a method for treating a subject having
CC or suspected of having neuroinflammatory or neurodegenerative disorder.
CC The method involves administering an effective amount of an isolated
CC binding molecule which specifically binds to semaphorin-4D (SEMA4D,
CC CD100) to the subject. The invention further relates to: (1) a method for
CC maintaining or restoring astrocyte-mediated trophic support of
CC oligodendrocyte precursor cells (OPCs) in a subject; and (2) a method for
CC protecting inhibitory neurons from degeneration in early Alzheimer's
CC disease in the subject. The neurodegenerative disorder includes
CC Alzheimer's disease, Parkinson's disease, Huntington's disease, down
CC syndrome, ataxia, amyotrophic lateral sclerosis (ALS), frontotemporal
CC dementia (FTD), HIV-related cognitive impairment, CNS lupus, mild
CC cognitive impairment. The present sequence represents a heavy chain
CC variable region (VH) of anti-SEMA4D monoclonal antibody, useful for
CC treating the above-mentioned diseases.
XX
SQ Sequence 118 AA;
Query Match 100.0%; Score 628; Length 118;
Best Local Similarity 100.0%;
Matches 118; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLQQSGPELVKPGASVKISCKASGYSFSDYYMHWVKQSPENSLEWIGQINPTTGGASY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLQQSGPELVKPGASVKISCKASGYSFSDYYMHWVKQSPENSLEWIGQINPTTGGASY 60
Qy 61 NQKFKGKATLTVDKSSSTAYMQLKSLTSEESAVYYCTRYYYGRHFDVWGQGTTVTVSS 118
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGKATLTVDKSSSTAYMQLKSLTSEESAVYYCTRYYYGRHFDVWGQGTTVTVSS 118
US20190322757 teaches a method of treating neurodegenerative disease including Huntington’s disease comprising administering to a subject in need thereof an anti-Sema4D/CD100 antibody that comprises a VL having the amino acid sequence of SEQ ID NO:17 and a VH having the amino acid sequence of SEQ ID NO:9 (see the sequence alignment below).
SEQ ID NO:17
BGV86372
ID BGV86372 standard; protein; 111 AA.
XX
AC BGV86372;
XX
DT 28-NOV-2019 (first entry)
XX
DE Anti-SEMA4D mAb (2503) light chain variable region, SEQ ID 17.
XX
KW CD100 protein; SEMA4D protein; Semaphorin 4D; Semaphorin-4D;
KW alzheimers disease; antibody therapy; antiinflammatory; antiparkinsonian;
KW ataxia; cognitive disorder; down syndrome; frontotemporal dementia;
KW genetic-disease-gen.; growth-disorder-gen.; huntingtons chorea;
KW light chain variable region; lupus erythematosus;
KW mild cognitive impairment; monoclonal antibody; motor neurone disease;
KW neuritis; neurodegenerative disease; neuroprotective; nootropic;
KW parkinsons disease; therapeutic.
XX
OS Unidentified.
XX
CC PN US2019322757-A1.
XX
CC PD 24-OCT-2019.
XX
CC PF 02-JUL-2019; 2019US-00460593.
XX
PR 21-OCT-2013; 2013US-0893814P.
PR 14-APR-2014; 2014US-0979384P.
PR 16-JUN-2014; 2014US-0012805P.
PR 21-OCT-2014; 2014US-00519965.
PR 31-JAN-2017; 2017US-00420662.
PR 21-MAR-2017; 2017US-00465509.
XX
CC PA (VACC-) VACCINEX INC.
XX
CC PI Smith ES, Zauderer M, Bowers WJ, Jonason A;
XX
DR WPI; 2019-88094G/84.
DR N-PSDB; BGV86376.
XX
CC PT Treating subject having neuroinflammatory or neurodegenerative disorder
CC PT including e.g. Alzheimer's disease, comprises administering isolated
CC PT binding molecule to subject, in which isolated binding molecule
CC PT specifically binds to semaphorin-4D.
XX
CC PS Claim 9; SEQ ID NO 17; 59pp; English.
XX
CC The present invention relates to a method for treating a subject having a
CC neuroinflammatory or neurodegenerative disorder by administering to the
CC subject an effective amount of an isolated binding molecule which
CC specifically binds to Semaphorin 4D (SEMA4D, CD100). The isolated binding
CC molecule comprises an antibody or antigen-binding fragment which has a
CC heavy chain variable region (VH), a light chain variable region (VL) and
CC their corresponding complementarity determining regions. The invention
CC further refers to: (1) a method for maintaining or restoring astrocyte-
CC mediated trophic support of oligodendrocyte precursor cells (OPCs) in
CC subject having neuroinflammatory or neurodegenerative disorder by
CC administering the isolated binding molecule to subject; and (2) a method
CC for protecting inhibitory neurons from degeneration in early Alzheimer's
CC disease by administering the isolated binding molecule to subject, where
CC the binding molecule restores number of somatostatin positive neurons,
CC NYP-positive neurons or both in the subject. The method of the invention
CC can be used for treating Alzheimer's disease, Parkinson's disease,
CC Huntington's disease, Down syndrome, ataxia, amyotrophic lateral
CC sclerosis (ALS), frontotemporal dementia (FTD), HIV-related cognitive
CC impairment, CNS Lupus, mild cognitive impairment.
XX
SQ Sequence 111 AA;
ALIGNMENT:
Query Match 100.0%; Score 580; Length 111;
Best Local Similarity 100.0%;
Matches 111; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
Qy 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
|||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
SEQ ID NO:9
BGV86364
ID BGV86364 standard; protein; 118 AA.
XX
AC BGV86364;
XX
DT 28-NOV-2019 (first entry)
XX
DE Anti-SEMA4D mAb (2503) heavy chain variable region, SEQ ID 9.
XX
KW CD100 protein; SEMA4D protein; Semaphorin 4D; Semaphorin-4D;
KW alzheimers disease; antibody therapy; antiinflammatory; antiparkinsonian;
KW ataxia; cognitive disorder; down syndrome; frontotemporal dementia;
KW genetic-disease-gen.; growth-disorder-gen.; heavy chain variable region;
KW huntingtons chorea; lupus erythematosus; mild cognitive impairment;
KW monoclonal antibody; motor neurone disease; neuritis;
KW neurodegenerative disease; neuroprotective; nootropic;
KW parkinsons disease; therapeutic.
XX
OS Unidentified.
XX
CC PN US2019322757-A1.
XX
CC PD 24-OCT-2019.
XX
CC PF 02-JUL-2019; 2019US-00460593.
XX
PR 21-OCT-2013; 2013US-0893814P.
PR 14-APR-2014; 2014US-0979384P.
PR 16-JUN-2014; 2014US-0012805P.
PR 21-OCT-2014; 2014US-00519965.
PR 31-JAN-2017; 2017US-00420662.
PR 21-MAR-2017; 2017US-00465509.
XX
CC PA (VACC-) VACCINEX INC.
XX
CC PI Smith ES, Zauderer M, Bowers WJ, Jonason A;
XX
DR WPI; 2019-88094G/84.
DR N-PSDB; BGV86374.
XX
CC PT Treating subject having neuroinflammatory or neurodegenerative disorder
CC PT including e.g. Alzheimer's disease, comprises administering isolated
CC PT binding molecule to subject, in which isolated binding molecule
CC PT specifically binds to semaphorin-4D.
XX
CC PS Claim 5; SEQ ID NO 9; 59pp; English.
XX
CC The present invention relates to a method for treating a subject having a
CC neuroinflammatory or neurodegenerative disorder by administering to the
CC subject an effective amount of an isolated binding molecule which
CC specifically binds to Semaphorin 4D (SEMA4D, CD100). The isolated binding
CC molecule comprises an antibody or antigen-binding fragment which has a
CC heavy chain variable region (VH), a light chain variable region (VL) and
CC their corresponding complementarity determining regions. The invention
CC further refers to: (1) a method for maintaining or restoring astrocyte-
CC mediated trophic support of oligodendrocyte precursor cells (OPCs) in
CC subject having neuroinflammatory or neurodegenerative disorder by
CC administering the isolated binding molecule to subject; and (2) a method
CC for protecting inhibitory neurons from degeneration in early Alzheimer's
CC disease by administering the isolated binding molecule to subject, where
CC the binding molecule restores number of somatostatin positive neurons,
CC NYP-positive neurons or both in the subject. The method of the invention
CC can be used for treating Alzheimer's disease, Parkinson's disease,
CC Huntington's disease, Down syndrome, ataxia, amyotrophic lateral
CC sclerosis (ALS), frontotemporal dementia (FTD), HIV-related cognitive
CC impairment, CNS Lupus, mild cognitive impairment.
XX
SQ Sequence 118 AA;
ALIGNMENT:
Query Match 100.0%; Score 629; Length 118;
Best Local Similarity 100.0%;
Matches 118; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
Qy 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
SEQ ID NO:10
ID BGV86365 standard; protein; 118 AA.
XX
AC BGV86365;
XX
DT 28-NOV-2019 (first entry)
XX
DE Anti-SEMA4D mAb (67) heavy chain variable region, SEQ ID 10.
XX
KW CD100 protein; SEMA4D protein; Semaphorin 4D; Semaphorin-4D;
KW alzheimers disease; antibody therapy; antiinflammatory; antiparkinsonian;
KW ataxia; cognitive disorder; down syndrome; frontotemporal dementia;
KW genetic-disease-gen.; growth-disorder-gen.; heavy chain variable region;
KW huntingtons chorea; lupus erythematosus; mild cognitive impairment;
KW monoclonal antibody; motor neurone disease; neuritis;
KW neurodegenerative disease; neuroprotective; nootropic;
KW parkinsons disease; therapeutic.
XX
OS Unidentified.
XX
CC PN US2019322757-A1.
XX
CC PD 24-OCT-2019.
XX
CC PF 02-JUL-2019; 2019US-00460593.
XX
PR 21-OCT-2013; 2013US-0893814P.
PR 14-APR-2014; 2014US-0979384P.
PR 16-JUN-2014; 2014US-0012805P.
PR 21-OCT-2014; 2014US-00519965.
PR 31-JAN-2017; 2017US-00420662.
PR 21-MAR-2017; 2017US-00465509.
XX
CC PA (VACC-) VACCINEX INC.
XX
CC PI Smith ES, Zauderer M, Bowers WJ, Jonason A;
XX
DR WPI; 2019-88094G/84.
DR N-PSDB; BGV86375.
XX
CC PT Treating subject having neuroinflammatory or neurodegenerative disorder
CC PT including e.g. Alzheimer's disease, comprises administering isolated
CC PT binding molecule to subject, in which isolated binding molecule
CC PT specifically binds to semaphorin-4D.
XX
CC PS Claim 5; SEQ ID NO 10; 59pp; English.
XX
CC The present invention relates to a method for treating a subject having a
CC neuroinflammatory or neurodegenerative disorder by administering to the
CC subject an effective amount of an isolated binding molecule which
CC specifically binds to Semaphorin 4D (SEMA4D, CD100). The isolated binding
CC molecule comprises an antibody or antigen-binding fragment which has a
CC heavy chain variable region (VH), a light chain variable region (VL) and
CC their corresponding complementarity determining regions. The invention
CC further refers to: (1) a method for maintaining or restoring astrocyte-
CC mediated trophic support of oligodendrocyte precursor cells (OPCs) in
CC subject having neuroinflammatory or neurodegenerative disorder by
CC administering the isolated binding molecule to subject; and (2) a method
CC for protecting inhibitory neurons from degeneration in early Alzheimer's
CC disease by administering the isolated binding molecule to subject, where
CC the binding molecule restores number of somatostatin positive neurons,
CC NYP-positive neurons or both in the subject. The method of the invention
CC can be used for treating Alzheimer's disease, Parkinson's disease,
CC Huntington's disease, Down syndrome, ataxia, amyotrophic lateral
CC sclerosis (ALS), frontotemporal dementia (FTD), HIV-related cognitive
CC impairment, CNS Lupus, mild cognitive impairment.
XX
SQ Sequence 118 AA;
Query Match 100.0%; Score 628; Length 118;
Best Local Similarity 100.0%;
Matches 118; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLQQSGPELVKPGASVKISCKASGYSFSDYYMHWVKQSPENSLEWIGQINPTTGGASY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLQQSGPELVKPGASVKISCKASGYSFSDYYMHWVKQSPENSLEWIGQINPTTGGASY 60
Qy 61 NQKFKGKATLTVDKSSSTAYMQLKSLTSEESAVYYCTRYYYGRHFDVWGQGTTVTVSS 118
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGKATLTVDKSSSTAYMQLKSLTSEESAVYYCTRYYYGRHFDVWGQGTTVTVSS 118
WO2020219868 teaches a method of treating neurodegenerative disease including Huntington’s disease comprising administering to a subject in need thereof an anti-Sema4D/CD100 antibody that comprises a VL having the amino acid sequence of SEQ ID NO:14 and a VH having the amino acid sequence of SEQ ID NO:13 (see the sequence alignment below).
SEQ ID NO:17
BIN28552
ID BIN28552 standard; protein; 210 AA.
XX
AC BIN28552;
XX
DT 24-DEC-2020 (first entry)
XX
DE Anti-SEMA4D monoclonal antibody (VX15/2503) light chain region, SEQ 14.
XX
KW SEMA4D protein; antibody therapy; antiinflammatory;
KW cardiovascular disease; cardiovascular-gen.; dermatological;
KW dermatological disease; drug delivery; gastrointestinal disease;
KW gastrointestinal-gen.; gene therapy; growth disorder;
KW growth-disorder-gen.; hematological disease; hematological-gen.;
KW immune disorder; immune inhibition; immunomodulator;
KW inflammatory disease; light chain; metabolic disorder; metabolic-gen.;
KW monoclonal antibody; neurological disease; neuroprotective;
KW ocular disease; ophthalmological; prophylactic to disease;
KW protein kinetics; respiratory disease; respiratory-gen.; screening;
KW therapeutic.
XX
OS Unidentified.
XX
CC PN WO2020219868-A1.
XX
CC PD 29-OCT-2020.
XX
CC PF 24-APR-2020; 2020WO-US029802.
XX
PR 24-APR-2019; 2019US-0838165P.
PR 29-JAN-2020; 2020US-0967472P.
XX
CC PA (REGE-) REGENXBIO INC.
XX
CC PI Danos O, Wu Z, Liu Y, Everen SV, Gerner F, Bruder J, Qiao C;
CC PI Mcdougald D, Wang X, Glenn J;
XX
DR WPI; 2020-A5954K/092.
DR N-PSDB; BIN28622.
XX
CC PT Pharmaceutical composition useful for treating e.g. angioedema, non-
CC PT infectious uveitis, or Alzheimer's disease, comprises adeno-
CC PT associated virus vector comprising viral capsid and artificial genome
CC PT comprising expression cassette.
XX
CC PS Example 7; SEQ ID NO 14; 608pp; English.
XX
CC The present invention relates to a novel pharmaceutical composition,
CC useful for treating angioedema such as hereditary angioedema in a human
CC subject. The pharmaceutical composition comprises an adeno-associated
CC virus (AAV) vector comprising a viral capsid of SEQ ID NOs: 143-145 (see
CC BIN28680-BIN28682) and artificial genome comprising an expression
CC cassette flanked by AAV inverted terminal repeat (ITR)s, where the AAV
CC vector is formulated for administering to the subject. The invention
CC further claims: (1) a pharmaceutical composition for delivering
CC lanadelumab (antibody) to the bloodstream for treating hereditary
CC angioedema, non-infectious uveitis, Alzheimer's disease, frontotemporal
CC dementia (FD), tauopathies, progressive supranuclear palsy, chronic
CC traumatic encephalopathy, Pick's complex, primary age-related tauopathy,
CC Huntington's disease, juvenile Huntington's disease, Parkinson's disease,
CC synucleinopathies, amyotrophic lateral sclerosis (ALS), migraines,
CC cluster headaches, retinal disorders including diabetic retinopathy,
CC myopic choroidal neovascularization (mCNV), macular degeneration
CC (neovascular (wet) or dry age-related macular degeneration (nAMD)),
CC macular edema (macular edema following a retinal vein occlusion (RVO) or
CC diabetic macular edema (DME)), retinal vein occlusion, diabetic
CC retinopathy (DR), glaucoma, abnormal vascularization of the retina,
CC multiple sclerosis, amyloidosis (ATTR), familial amyloid cardiomyopathy
CC (FAC), familial amyloid polyneuropathy (FAP), fibrotic disorders,
CC pulmonary fibrosis, cystic fibrosis (CF), idiopathic pulmonary fibrosis
CC (IPF), liver cirrhosis, atrial fibrosis, endomyocardial fibrosis, old
CC myocardial infarction, arthrofibrosis, Crohn's disease, ulcerative
CC colitis, mediastinal fibrosis, myelofibrosis (MF), nephrogenic systemic
CC fibrosis (NSF), progressive massive fibrosis (PMF), retroperitoneal
CC fibrosis (RPF), neuromyelitis optica (NMO), diabetic macular edema (DME),
CC retinopathy (DR), inflammatory bowel disease (IBD) including ulcerative
CC colitis, Crohn's disease, atopic dermatitis, eosinophilic asthma, asthma,
CC chronic obstructive pulmonary disease (COPD), chronic idiopathic
CC urticaria, and myasthenia gravis in a human subject; (2) a pharmaceutical
CC composition for treating osteoporosis or abnormal bone loss or weakness
CC such as giant cell tumor of bone, treatment-induced bone loss, slowing
CC the loss of (or increasing) bone mass in breast and prostate cancer
CC patients, preventing skeletal-related events due to bone metastasis, or
CC decreasing bone resorption and turnover in a human subject; (3) a
CC pharmaceutical composition for reducing, inhibiting, or ameliorating a
CC detrimental immune response in a human subject; and (4) a method for
CC determining human anti-plasma kallikrein (pKal) antibody activity in a
CC sample. The fully human post-translationally modified antibody is useful
CC for treating and preventing the above-mentioned diseases by delivering
CC the antibody through gene therapy method using recombinant AAV vector to
CC the appropriate tissue. Note: SEQ ID NOs: 226, 252, 234, 235, 410, 402,
CC 404-408, and 410 are describd in the specification, but no corresponding
CC sequences are shown.
XX
SQ Sequence 210 AA;
Query Match 100.0%; Score 580; Length 210;
Best Local Similarity 100.0%;
Matches 111; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
Qy 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
|||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
SEQ ID NO:9
BIN28551
ID BIN28551 standard; protein; 245 AA.
XX
AC BIN28551;
XX
DT 24-DEC-2020 (first entry)
XX
DE Anti-SEMA4D monoclonal antibody (VX15/2503) heavy chain region, SEQ 13.
XX
KW SEMA4D protein; antibody therapy; antiinflammatory;
KW cardiovascular disease; cardiovascular-gen.; dermatological;
KW dermatological disease; drug delivery; gastrointestinal disease;
KW gastrointestinal-gen.; gene therapy; growth disorder;
KW growth-disorder-gen.; heavy chain; hematological disease;
KW hematological-gen.; immune disorder; immune inhibition; immunomodulator;
KW inflammatory disease; metabolic disorder; metabolic-gen.;
KW monoclonal antibody; neurological disease; neuroprotective;
KW ocular disease; ophthalmological; prophylactic to disease;
KW protein kinetics; respiratory disease; respiratory-gen.; screening;
KW therapeutic.
XX
OS Unidentified.
XX
CC PN WO2020219868-A1.
XX
CC PD 29-OCT-2020.
XX
CC PF 24-APR-2020; 2020WO-US029802.
XX
PR 24-APR-2019; 2019US-0838165P.
PR 29-JAN-2020; 2020US-0967472P.
XX
CC PA (REGE-) REGENXBIO INC.
XX
CC PI Danos O, Wu Z, Liu Y, Everen SV, Gerner F, Bruder J, Qiao C;
CC PI Mcdougald D, Wang X, Glenn J;
XX
DR WPI; 2020-A5954K/092.
DR N-PSDB; BIN28621.
XX
CC PT Pharmaceutical composition useful for treating e.g. angioedema, non-
CC PT infectious uveitis, or Alzheimer's disease, comprises adeno-
CC PT associated virus vector comprising viral capsid and artificial genome
CC PT comprising expression cassette.
XX
CC PS Example 7; SEQ ID NO 13; 608pp; English.
XX
CC The present invention relates to a novel pharmaceutical composition,
CC useful for treating angioedema such as hereditary angioedema in a human
CC subject. The pharmaceutical composition comprises an adeno-associated
CC virus (AAV) vector comprising a viral capsid of SEQ ID NOs: 143-145 (see
CC BIN28680-BIN28682) and artificial genome comprising an expression
CC cassette flanked by AAV inverted terminal repeat (ITR)s, where the AAV
CC vector is formulated for administering to the subject. The invention
CC further claims: (1) a pharmaceutical composition for delivering
CC lanadelumab (antibody) to the bloodstream for treating hereditary
CC angioedema, non-infectious uveitis, Alzheimer's disease, frontotemporal
CC dementia (FD), tauopathies, progressive supranuclear palsy, chronic
CC traumatic encephalopathy, Pick's complex, primary age-related tauopathy,
CC Huntington's disease, juvenile Huntington's disease, Parkinson's disease,
CC synucleinopathies, amyotrophic lateral sclerosis (ALS), migraines,
CC cluster headaches, retinal disorders including diabetic retinopathy,
CC myopic choroidal neovascularization (mCNV), macular degeneration
CC (neovascular (wet) or dry age-related macular degeneration (nAMD)),
CC macular edema (macular edema following a retinal vein occlusion (RVO) or
CC diabetic macular edema (DME)), retinal vein occlusion, diabetic
CC retinopathy (DR), glaucoma, abnormal vascularization of the retina,
CC multiple sclerosis, amyloidosis (ATTR), familial amyloid cardiomyopathy
CC (FAC), familial amyloid polyneuropathy (FAP), fibrotic disorders,
CC pulmonary fibrosis, cystic fibrosis (CF), idiopathic pulmonary fibrosis
CC (IPF), liver cirrhosis, atrial fibrosis, endomyocardial fibrosis, old
CC myocardial infarction, arthrofibrosis, Crohn's disease, ulcerative
CC colitis, mediastinal fibrosis, myelofibrosis (MF), nephrogenic systemic
CC fibrosis (NSF), progressive massive fibrosis (PMF), retroperitoneal
CC fibrosis (RPF), neuromyelitis optica (NMO), diabetic macular edema (DME),
CC retinopathy (DR), inflammatory bowel disease (IBD) including ulcerative
CC colitis, Crohn's disease, atopic dermatitis, eosinophilic asthma, asthma,
CC chronic obstructive pulmonary disease (COPD), chronic idiopathic
CC urticaria, and myasthenia gravis in a human subject; (2) a pharmaceutical
CC composition for treating osteoporosis or abnormal bone loss or weakness
CC such as giant cell tumor of bone, treatment-induced bone loss, slowing
CC the loss of (or increasing) bone mass in breast and prostate cancer
CC patients, preventing skeletal-related events due to bone metastasis, or
CC decreasing bone resorption and turnover in a human subject; (3) a
CC pharmaceutical composition for reducing, inhibiting, or ameliorating a
CC detrimental immune response in a human subject; and (4) a method for
CC determining human anti-plasma kallikrein (pKal) antibody activity in a
CC sample. The fully human post-translationally modified antibody is useful
CC for treating and preventing the above-mentioned diseases by delivering
CC the antibody through gene therapy method using recombinant AAV vector to
CC the appropriate tissue. Note: SEQ ID NOs: 226, 252, 234, 235, 410, 402,
CC 404-408, and 410 are describd in the specification, but no corresponding
CC sequences are shown.
XX
SQ Sequence 245 AA;
Query Match 100.0%; Score 629; Length 245;
Best Local Similarity 100.0%;
Matches 118; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
Qy 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
US20130302320 teaches a method of treating neurodegenerative disease including Huntington’s disease comprising administering to a subject in need thereof an anti-Sema4D/CD100 antibody that comprises a VL having the amino acid sequence of SEQ ID NO:4 and a VH having the amino acid sequence of SEQ ID NO:3 (see the sequence alignment below).
SEQ ID NO:17
BAY62909
ID BAY62909 standard; protein; 111 AA.
XX
AC BAY62909;
XX
DT 02-JAN-2014 (first entry)
XX
DE Humanized anti-SEMA4D antibody MAb 2503 L553 variable light chain SEQ:4.
XX
KW CD100; SEMA4D protein; Semaphorin-4D; alzheimers disease;
KW antibody therapy; brain injury; cell differentiation; cell proliferation;
KW central nervous system disease; cerebral infarction; cerebral palsy;
KW cerebroprotective; epilepsy; head injury; humanized antibody;
KW huntingtons chorea; light chain variable region;
KW major depressive disorder; monoclonal antibody; motor neurone disease;
KW multiple sclerosis; nerve injury; neurodegenerative disease;
KW neurogenesis; parkinsons disease; schizophrenia; spinal cord injury;
KW stroke; therapeutic; vasotropic.
XX
OS Synthetic.
OS Unidentified.
XX
FH Key Location/Qualifiers
FT Region 24..38
FT /label= CDR1
FT /note= "Complementarity determining region 1"
FT Region 26..35
FT /label= CDR1
FT /note= "Complementarity determining region 1"
FT Region 50..66
FT /label= CDR2
FT /note= "Complementarity determining region 2"
FT Region 54..60
FT /label= CDR2
FT /note= "Complementarity determining region 2"
FT Region 93..101
FT /label= CDR3
FT /note= "Complementarity determining region 3"
FT Region 99..107
FT /label= CDR3
FT /note= "Complementarity determining region 3"
XX
CC PN US2013302320-A1.
XX
CC PD 14-NOV-2013.
XX
CC PF 15-MAR-2013; 2013US-00842523.
XX
PR 11-MAY-2012; 2012US-0646119P.
XX
CC PA (SMIT/) SMITH E S.
CC PA (ZAUD/) ZAUDERER M.
XX
CC PI Smith ES, Zauderer M;
XX
DR WPI; 2013-U97791/78.
XX
CC PT Promoting neurogenesis in neural tissue of patient with symptom of CNS
CC PT disorder e.g. acute brain injury, and increasing number of progenitor
CC PT cells, comprises administering isolated binding molecule which
CC PT specifically binds semaphorin-4D.
XX
CC PS Claim 22; SEQ ID NO 4; 31pp; English.
XX
CC The invention relates to a novel method for promoting neurogenesis in
CC neural tissue of a patient exhibiting at least one symptom of a central
CC nervous system disorder (CNS). The method comprises administering to a
CC subject an isolated binding molecule which specifically binds semaphorin-
CC 4D (SEMA4D). The method is useful for: promoting neurogenesis in neural
CC tissue of a patient exhibiting at least one symptom of CNS disorder which
CC is neurodegenerative disorder, acute brain injury, and certain CNS
CC dysfunctions, where the neurodegenerative disorder is Alzheimer's
CC disease, Huntington's disease, amyotrophic lateral sclerosis, Parkinson's
CC disease and multiple sclerosis, the CNS dysfunction is depression,
CC epilepsy and schizophrenia, and the acute brain injury is head injury,
CC cerebral palsy, cerebral infarction, spinal cord injury and traumatic
CC injury; increasing the number of progenitor cells in the subject with the
CC CNS disorder; and treating stroke in a patient. The method: reduces the
CC burden of CNS disorder in the subject and increases the number of,
CC enhances differentiation of and/or increases survival of progenitor
CC cells. The present sequence is a light chain variable region of the
CC humanized anti-SEMA4D antibody, which is used in a method of the
CC invention for promoting neurogenesis in neural tissue.
XX
SQ Sequence 111 AA;
ALIGNMENT:
Query Match 100.0%; Score 580; Length 111;
Best Local Similarity 100.0%;
Matches 111; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIVMTQSPDSLAVSLGERATINCKASQSVDYDGDSYMNWYQQKPGQPPKLLIYAASNLES 60
Qy 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
|||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSNEDPYTFGQGTKLEIK 111
SEQ ID NO:9
BAY62908
ID BAY62908 standard; protein; 118 AA.
XX
AC BAY62908;
XX
DT 02-JAN-2014 (first entry)
XX
DE Humanized anti-SEMA4D antibody MAb 2503 H2160 variable heavy chain SEQ:3.
XX
KW CD100; SEMA4D protein; Semaphorin-4D; alzheimers disease;
KW antibody therapy; brain injury; cell differentiation; cell proliferation;
KW central nervous system disease; cerebral infarction; cerebral palsy;
KW cerebroprotective; epilepsy; head injury; heavy chain variable region;
KW humanized antibody; huntingtons chorea; major depressive disorder;
KW monoclonal antibody; motor neurone disease; multiple sclerosis;
KW nerve injury; neurodegenerative disease; neurogenesis;
KW parkinsons disease; schizophrenia; spinal cord injury; stroke;
KW therapeutic; vasotropic.
XX
OS Synthetic.
OS Unidentified.
XX
FH Key Location/Qualifiers
FT Region 26..35
FT /label= CDR1
FT /note= "Complementarity determining region 1"
FT Region 50..66
FT /label= CDR2
FT /note= "Complementarity determining region 2"
FT Region 99..107
FT /label= CDR3
FT /note= "Complementarity determining region 3"
XX
CC PN US2013302320-A1.
XX
CC PD 14-NOV-2013.
XX
CC PF 15-MAR-2013; 2013US-00842523.
XX
PR 11-MAY-2012; 2012US-0646119P.
XX
CC PA (SMIT/) SMITH E S.
CC PA (ZAUD/) ZAUDERER M.
XX
CC PI Smith ES, Zauderer M;
XX
DR WPI; 2013-U97791/78.
XX
CC PT Promoting neurogenesis in neural tissue of patient with symptom of CNS
CC PT disorder e.g. acute brain injury, and increasing number of progenitor
CC PT cells, comprises administering isolated binding molecule which
CC PT specifically binds semaphorin-4D.
XX
CC PS Claim 22; SEQ ID NO 3; 31pp; English.
XX
CC The invention relates to a novel method for promoting neurogenesis in
CC neural tissue of a patient exhibiting at least one symptom of a central
CC nervous system disorder (CNS). The method comprises administering to a
CC subject an isolated binding molecule which specifically binds semaphorin-
CC 4D (SEMA4D). The method is useful for: promoting neurogenesis in neural
CC tissue of a patient exhibiting at least one symptom of CNS disorder which
CC is neurodegenerative disorder, acute brain injury, and certain CNS
CC dysfunctions, where the neurodegenerative disorder is Alzheimer's
CC disease, Huntington's disease, amyotrophic lateral sclerosis, Parkinson's
CC disease and multiple sclerosis, the CNS dysfunction is depression,
CC epilepsy and schizophrenia, and the acute brain injury is head injury,
CC cerebral palsy, cerebral infarction, spinal cord injury and traumatic
CC injury; increasing the number of progenitor cells in the subject with the
CC CNS disorder; and treating stroke in a patient. The method: reduces the
CC burden of CNS disorder in the subject and increases the number of,
CC enhances differentiation of and/or increases survival of progenitor
CC cells. The present sequence is a heavy chain variable region of the
CC humanized anti-SEMA4D antibody, which is used in a method of the
CC invention for promoting neurogenesis in neural tissue.
XX
SQ Sequence 118 AA;
ALIGNMENT:
Query Match 100.0%; Score 629; Length 118;
Best Local Similarity 100.0%;
Matches 118; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLVQSGAEVKKPGSSVKVSCKASGYSFSDYYMHWVRQAPGQGLEWMGQINPTTGGASY 60
Qy 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQKFKGKATITVDKSTSTAYMELSSLRSEDTAVYYCARYYYGRHFDVWGQGTTVTVSS 118
US7951934 teaches an antisense oligonucleotide comprising the sequence of SEQ ID NO:1010, which is 100% identical to instant SEQ ID NO:47 or 48 and method of treating Huntington’s disease (See the sequence alignment below).
SEQ ID NO:47
US-11-627-916-118
(NOTE: this sequence has 27 duplicates in the database searched)
Sequence 118, US/11627916
Patent No. 7951934
GENERAL INFORMATION
APPLICANT: Susan M. Freier
TITLE OF INVENTION: COMPOSITIONS AND THEIR USES DIRECTED TO HUNTINGTIN
FILE REFERENCE: RTS-0838US
CURRENT APPLICATION NUMBER: US/11/627,916
CURRENT FILING DATE: 2007-01-26
PRIOR APPLICATION NUMBER: 60/762,954
PRIOR FILING DATE: 2006-01-26
PRIOR APPLICATION NUMBER: 60/836,290
PRIOR FILING DATE: 2006-08-07
NUMBER OF SEQ ID NOS: 369
SEQ ID NO 118
LENGTH: 20
TYPE: DNA
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: Oligomeric Compound
Query Match 100.0%; Score 20; Length 20;
Best Local Similarity 100.0%;
Matches 20; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 CTCAGTAACATTGACACCAC 20
||||||||||||||||||||
Db 1 CTCAGTAACATTGACACCAC 20
SEQ ID NO:48
US-11-627-916-118
(NOTE: this sequence has 27 duplicates in the database searched.
See complete list at the end of this report)
Sequence 118, US/11627916
Patent No. 7951934
GENERAL INFORMATION
APPLICANT: Susan M. Freier
TITLE OF INVENTION: COMPOSITIONS AND THEIR USES DIRECTED TO HUNTINGTIN
FILE REFERENCE: RTS-0838US
CURRENT APPLICATION NUMBER: US/11/627,916
CURRENT FILING DATE: 2007-01-26
PRIOR APPLICATION NUMBER: 60/762,954
PRIOR FILING DATE: 2006-01-26
PRIOR APPLICATION NUMBER: 60/836,290
PRIOR FILING DATE: 2006-08-07
NUMBER OF SEQ ID NOS: 369
SEQ ID NO 118
LENGTH: 20
TYPE: DNA
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: Oligomeric Compound
Query Match 100.0%; Score 20; Length 20;
Best Local Similarity 100.0%;
Matches 20; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 CTCAGTAACATTGACACCAC 20
||||||||||||||||||||
Db 1 CTCAGTAACATTGACACCAC 20
US10479995 teaches an antisense oligonucleotide comprising the sequence of SEQ ID NO:1010, which is 100% identical to instant SEQ ID NO:47 and method of treating Huntington’s disease (See the sequence alignment below).
Sequence 1010, US/15746220
Patent No. 10479995
GENERAL INFORMATION
APPLICANT: WAVE LIFE SCIENCES LTD.
TITLE OF INVENTION: OLIGONUCLEOTIDE COMPOSITIONS AND METHODS THEREOF
FILE REFERENCE: 2010581-0228
CURRENT APPLICATION NUMBER: US/15/746,220
CURRENT FILING DATE: 2018-01-19
PRIOR APPLICATION NUMBER: PCT/US2016/043542
PRIOR FILING DATE: 2016-07-22
PRIOR APPLICATION NUMBER: 62/331,960
PRIOR FILING DATE: 2016-05-04
PRIOR APPLICATION NUMBER: 62/236,847
PRIOR FILING DATE: 2015-10-02
PRIOR APPLICATION NUMBER: 62/195,779
PRIOR FILING DATE: 2015-07-22
NUMBER OF SEQ ID NOS: 1565
SEQ ID NO 1010
LENGTH: 20
TYPE: DNA
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: Description of Artificial Sequence: Synthetic
oligonucleotide
Query Match 100.0%; Score 20; Length 20;
Best Local Similarity 100.0%;
Matches 20; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 CTCAGTAACATTGACACCAC 20
||||||||||||||||||||
Db 1 CTCAGTAACATTGACACCAC 20
US-15-746-220-1011
(NOTE: this sequence has 7 duplicates in the database searched)
Sequence 1011, US/15746220
Patent No. 10479995
GENERAL INFORMATION
APPLICANT: WAVE LIFE SCIENCES LTD.
TITLE OF INVENTION: OLIGONUCLEOTIDE COMPOSITIONS AND METHODS THEREOF
FILE REFERENCE: 2010581-0228
CURRENT APPLICATION NUMBER: US/15/746,220
CURRENT FILING DATE: 2018-01-19
PRIOR APPLICATION NUMBER: PCT/US2016/043542
PRIOR FILING DATE: 2016-07-22
PRIOR APPLICATION NUMBER: 62/331,960
PRIOR FILING DATE: 2016-05-04
PRIOR APPLICATION NUMBER: 62/236,847
PRIOR FILING DATE: 2015-10-02
PRIOR APPLICATION NUMBER: 62/195,779
PRIOR FILING DATE: 2015-07-22
NUMBER OF SEQ ID NOS: 1565
SEQ ID NO 1011
LENGTH: 20
TYPE: DNA
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: Description of Artificial Sequence: Synthetic
oligonucleotide
FEATURE:
OTHER INFORMATION: Description of Combined DNA/RNA Molecule: Synthetic
oligonucleotide
Query Match 100.0%; Score 20; Length 20;
Best Local Similarity 95.0%;
Matches 19; Conservative 1; Mismatches 0; Indels 0; Gaps 0;
Qy 1 CTCAGTAACATTGACACCAC 20
|:||||||||||||||||||
Db 1 CUCAGTAACATTGACACCAC 20
US9353372 teaches an antisense oligonucleotide comprising the sequence of SEQ ID NO:118, which is 100% identical to SEQ ID NO:47 and method of treating Huntington’s disease (See the sequence alignment below).
SEQ ID NO:47
Sequence 118, US/14589833
Patent No. 9353372
GENERAL INFORMATION
APPLICANT: Isis Pharmaceuticals, Inc.
TITLE OF INVENTION: COMPOSITIONS AND THEIR USES DIRECTED TO HUNTINGTIN
FILE REFERENCE: RTS-0838US.C2
CURRENT APPLICATION NUMBER: US/14/589,833
CURRENT FILING DATE: 2015-01-05
PRIOR APPLICATION NUMBER: 13/789,368
PRIOR FILING DATE: 2013-03-07
PRIOR APPLICATION NUMBER: 13/090,146
PRIOR FILING DATE: 2011-04-19
PRIOR APPLICATION NUMBER: 11/627,916
PRIOR FILING DATE: 2007-01-26
PRIOR APPLICATION NUMBER: 60/836,290
PRIOR FILING DATE: 2006-08-07
PRIOR APPLICATION NUMBER: 60/762,954
PRIOR FILING DATE: 2006-01-26
NUMBER OF SEQ ID NOS: 369
SEQ ID NO 118
LENGTH: 20
TYPE: DNA
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: Oligomeric Compound
Query Match 100.0%; Score 20; Length 20;
Best Local Similarity 100.0%;
Matches 20; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 CTCAGTAACATTGACACCAC 20
||||||||||||||||||||
Db 1 CTCAGTAACATTGACACCAC 20
US11028390 teaches an antisense oligonucleotide comprising the sequence of SEQ ID NO:97, which is 100% identical to instant SEQ ID NO:47 and method of treating Huntington’s disease (See the sequence alignment below).
SEQ ID NO:47
US-16-630-141-97
Sequence 97, US/16630141
Patent No. 11028390
GENERAL INFORMATION
APPLICANT: Osaka University
APPLICANT: KNC Laboratories Co., Ltd.
APPLICANT: National University Corporation Nagoya University
TITLE OF INVENTION: ANTISENSE OLIGONUCLEOTIDE CONTROLLING EXPRESSION AMOUNT
TITLE OF INVENTION: OF TDP-43 AND USE THEREOF
FILE REFERENCE: 747233
CURRENT APPLICATION NUMBER: US/16/630,141
CURRENT FILING DATE: 2020-01-10
PRIOR APPLICATION NUMBER: PCT/JP2018/025792
PRIOR FILING DATE: 2018-07-06
PRIOR APPLICATION NUMBER: JP 2017-134890
PRIOR FILING DATE: 2017-07-10
NUMBER OF SEQ ID NOS: 101
SEQ ID NO 97
LENGTH: 20
TYPE: DNA
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: Synthetic Sequence - control oligonucleotide
FEATURE:
NAME/KEY: modified_base
LOCATION: (1)..(3)
OTHER INFORMATION: 2 '-O,4 '-C-ethylene-linked bicyclic ribonucleotide
FEATURE:
NAME/KEY: modified_base
LOCATION: (2)..(2)
OTHER INFORMATION: t
FEATURE:
NAME/KEY: modified_base
LOCATION: (4)..(4)
OTHER INFORMATION: 2'-O-methyladenosine
FEATURE:
NAME/KEY: modified_base
LOCATION: (5)..(5)
OTHER INFORMATION: gm
FEATURE:
NAME/KEY: modified_base
LOCATION: (6)..(6)
OTHER INFORMATION: 2 '-O,4 '-C-ethylene-linked bicyclic ribonucleotide
FEATURE:
NAME/KEY: modified_base
LOCATION: (6)..(6)
OTHER INFORMATION: t
FEATURE:
NAME/KEY: modified_base
LOCATION: (7)..(8)
OTHER INFORMATION: 2'-O-methyladenosine
FEATURE:
NAME/KEY: modified_base
LOCATION: (9)..(9)
OTHER INFORMATION: 2 '-O,4 '-C-ethylene-linked bicyclic ribonucleotide
FEATURE:
NAME/KEY: modified_base
LOCATION: (10)..(10)
OTHER INFORMATION: 2'-O-methyladenosine
FEATURE:
NAME/KEY: modified_base
LOCATION: (11)..(12)
OTHER INFORMATION: 2 '-O,4 '-C-ethylene-linked bicyclic ribonucleotide
FEATURE:
NAME/KEY: modified_base
LOCATION: (11)..(12)
OTHER INFORMATION: t
FEATURE:
NAME/KEY: modified_base
LOCATION: (13)..(13)
OTHER INFORMATION: gm
FEATURE:
NAME/KEY: modified_base
LOCATION: (14)..(14)
OTHER INFORMATION: 2'-O-methyladenosine
FEATURE:
NAME/KEY: modified_base
LOCATION: (15)..(15)
OTHER INFORMATION: 2 '-O,4 '-C-ethylene-linked bicyclic ribonucleotide
FEATURE:
NAME/KEY: modified_base
LOCATION: (16)..(16)
OTHER INFORMATION: 2'-O-methyladenosine
FEATURE:
NAME/KEY: modified_base
LOCATION: (17)..(18)
OTHER INFORMATION: 2 '-O,4 '-C-ethylene-linked bicyclic ribonucleotide
FEATURE:
NAME/KEY: modified_base
LOCATION: (19)..(19)
OTHER INFORMATION: 2'-O-methyladenosine
FEATURE:
NAME/KEY: modified_base
LOCATION: (20)..(20)
OTHER INFORMATION: 2 '-O,4 '-C-ethylene-linked bicyclic ribonucleotide
Query Match 100.0%; Score 20; Length 20;
Best Local Similarity 80.0%;
Matches 16; Conservative 4; Mismatches 0; Indels 0; Gaps 0;
Qy 1 CTCAGTAACATTGACACCAC 20
|:|||:||||::||||||||
Db 1 CUCAGUAACAUUGACACCAC 20
Any inquiry concerning this communication or earlier communications from the examiner should be directed to CHANG-YU WANG whose telephone number is (571)272-4521. The examiner can normally be reached on Monday-Thursday, 7:00am-5:00pm EST.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Jeffrey Stucker can be reached on 571-272-0911. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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Chang-Yu Wang
November 15, 2025
/CHANG-YU WANG/Primary Examiner, Art Unit 1675