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
1. The Amendment filed December 22, 2025 in response to the Office Action of August 22, 2025 is acknowledged and has been entered. Claims 2, 4-10, 12, 14, 17-19, 24, 26, 31, 32, and 34-36 have been cancelled. Claims 1, 3, 11, 13, 15, 20, 21-23, 25, 30, and 33 have been amended. New claims 39 and 40 have been added.
2. Claims 1, 3, 11, 13, 15-16, 20-23, 25, 27-30, 33, and 37-40 are currently being examined.
Priority
3. Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) is acknowledged. Applicant has not complied with one or more conditions for receiving the benefit of an earlier filing date under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) as follows:
The later-filed application must be an application for a patent for an invention which is also disclosed in the prior application (the parent or original nonprovisional application or provisional application). The disclosure of the invention in the parent application and in the later-filed application must be sufficient to comply with the requirements of the first paragraph of 35 U.S.C. 112. See Transco Products, Inc. v. Performance Contracting, Inc., 38 F.3d 551, 32 USPQ2d 1077 (Fed. Cir. 1994).
The disclosure of the prior-filed Application No. 63/011,819 fails to provide adequate support or enablement in the manner provided by the first paragraph of 35 U.S.C. 112 for one or more claims of this application. Examiner has established a priority date of April 16, 2021 claims 1, 3, 11, 13, 15-16, 20-23, 25, 27-30, 33, and 37-40 because the claims as currently constituted recite 1) A nucleic acid molecule encoding an anti-FMS-like tyrosine kinase 3 (FLT3) chimeric antigen receptor (CAR), wherein the CAR comprises : an FLT3 scFv comprising or consisting of the amino acid sequence of SEQ ID NO: 4;a spacer comprising or consisting of the amino acid sequence of SEQ ID NO: 5;a transmembrane domain comprising or consisting of the amino acid sequence of SEQ ID NO: 6:a costimulatory domain comprising or consisting of the amino acid sequence of SEQ ID NO: 7; and a CD3z domain comprising or consisting of the amino acid sequence of SEQ ID NO: 8, 2) A nucleic acid molecule of claim 1 encoding an anti-FMS- like tyrosine kinase 3 (FLT3) chimeric antigen receptor (CAR), wherein the CAR comprises the amino acid sequence of amino acids 19-259 of SEQ ID NO:2 and 3) treating a human patient with the cancers of claims 30 or 40.
A review of the ‘819 application does not reveal support for the nucleic acids encoding the broadly claimed FLT3 CARs and treating the numerous cancers claimed. The ‘819 application only provides support for the FLT3 CAR of nucleic acid SEQ ID NO: 1 and treating acute myeloid leukemia. Applicant is invited to submit evidence pointing to the serial number, page and line where support can be found establishing an earlier priority date.
New Grounds of Rejection
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.
4. Claims 3, 22, 25, 27, 28, 39 and 40 are rejected under 35 U.S.C. 102(a)(1) and (a)(2) as being anticipated by WO 2019/025484 (Hudecek, M. et al. Feb. 07, 2019, of record), “Hudecek”
Hudecek teaches using FLT3 CAR-T cells and FLT3 inhibitors to treat acute myeloid leukemia. See abstract and p. 1-Field of Invention.
Hudecek teaches the FLT3 CAR-T of SEQ ID NO: 2 which is encoded by a polynucleotide identical to the polynucleotide 55 to 777 of SEQ ID NO: 1 or 12. See p. 4, embodiment 10, claim 10 and Appendix of the Office Acton of 08/22/2025.
SEQ ID NO: 2 of Hudecek comprises aa 19 to aa 259 of SEQ ID NO: 2. See Appendix of the Office Acton of 08/22/2025.
SEQ ID NO: 1 of Hudecek encodes aa 19 to aa 259 of SEQ ID NO: 2. See Appendix of the Office Acton of 08/22/2025.
SEQ ID NO: 2 of Hudecek comprises the heavy chain sequences of SEQ ID NO: 18-21. See Appendix of the Office Acton of 08/22/2025.
SEQ ID NO: 2 of Hudecek comprises the light chain sequences of SEQ ID NO: 15-17 and 22. See Appendix of the Office Acton of 08/22/2025.
Codon optimized SEQ ID NO: 1 of Hudecek has an 81.6% identity to SEQ ID NO: 1. See CAR Construction-p. 50-1st paragraph and Appendix of the Office Acton of 08/22/2025 of the Office Acton of 08/22/2025.
Hudecek teaches a codon optimized targeting domain comprising the VH and VL segments of the FLT3-specific 4G8 mAb was synthesized and fused to a CAR backbone comprising a short IgG4-Fc Hinge spacer, a CD28 transmembrane and costimulatory moiety and CD3z, in-frame with a T2A element and EGFRt transduction marker. The entire transgene was encoded in a lentiviral vector epHIV7 and expressed under control of an EF1/HTLV hybrid promotor. See CAR Construction-p. 50-1st and Fig. 1.
Hudecek teaches that peripheral blood was obtained from human donors and adult AML patients. See p. 49-Human Subjects.
Hudecek teaches lentiviral gene-transfer was performed into CD3/28-bead activated CD4+ and CD8+ T cells and CAR-transduced T cells were enriched using biotinylated anti-EGFR mAb. See EGFR Preparation of CAR-Modified T cells-p. 50.
Hudecek teaches FLT3 CAR transduced T cells were enriched to >90% purity using the EGFRt transduction marker prior to expansion and functional testing. See p. 53-1st paragraph and Fig. 2
Hudecek teaches other T cell (including but not limited to: naïve T cell, memory T cell, memory stem T cell, gamma delta T cell, cytokine-induced killer cell, regulatory T cell), NK cell or B-cell modified with the FLT3 CAR is used in combination with crenolanib to treat FLT3-ITD+AML. See p. 37-6th paragraph.
Hudecek teaches placing the compositions of the invention in a pharmaceutically acceptable carrier. See p. 11-embodiments 85, 86, and 90 and p. 35-1st and 2nd paragraph.
Hudecek teaches treating mutated FLT3-ITD+AML with the FLT3 CAR T cells. See p. 3-3rd paragraph, p. 12-emodiment 103, p. 31-4th paragraph, p. 33-1st paragraph, p. 36-1st to 4th paragraph., p. 37-6th paragraph, and p. 39-4th and 5th paragraph.
Hudecek teaches treating FLT3-ITD+AML with the FLT3 CAR in autologous or allogeneic T cells. See p. 36-5th to 8th paragraphs.
Hudecek teaches treating lymphoma with the FLT3 CAR T cells. See p. 39-3rd paragraph.
Hudecek teaches treating humans. See p. 35-4th paragraph and p. 44-1st paragraph.
Response to Arguments
5. Applicant argues that without conceding to the rejection and in the sole interest of expediting prosecution, claim 3 has been amended to recite limitations that were previously found in claim 11, and claim 1 has been amended to recite the domain sequences of the FLT3 CAR encoded by the sequences listed in claim 11. Specifically, Applicant has amended claim 3 to be directed to a nucleic acid encoding a CAR comprising an amino acid sequence identical to the amino acid sequence of amino acids 19-259 of SEQ ID NO:2. Applicant also amended claim 1 to be directed to a nucleic acid encoding a CAR having the CAR domains that are within the CAR encoded by SEQ ID NO:2 specifically reciting:
...wherein the CAR comprises:
an FLT3 scFv comprising or consisting of the amino acid sequence of SEQ ID
NO: 4;
a spacer comprising or consisting of the amino acid sequence of SEQ ID NO: 5;
a transmembrane domain comprising or consisting of the amino acid sequence of
SEQ ID NO: 6;
a costimulatory domain comprising or consisting of the amino acid sequence of
SEQ ID NO: 7; and a CD3( domain comprising or consisting of the amino acid sequence of SEQ ID NO: 8."
Applicant argues that as discussed below, Applicant's claims cannot be obvious over the cited art at least because the prior art does not disclose or suggest the sequence of amino acids 19-259 of SEQ ID NO:2 as required by claim 3 nor a CAR comprising domains having the sequences of SEQ ID NOs: 4, 5, 6, 7, and 8 as required by claim 1.
Applicant argues that Hudecek, which "relates to adoptive immunotherapy of Acute Myeloid Leukemia (AML) with chimeric antigen receptor (CAR)-modified T cells specific for FMS-like tyrosine kinase (FLT3) in combination with FLT3 inhibitors" does not teach nor suggest the sequence of amino acids 19-259 of SEQ ID NO:2 nor a CAR comprising domains having the sequences of SEQ ID NOs: 4, 5, 6, 7, and 8. See Hudecek at abstract and throughout.
Applicant argues that neither Hudecek nor the previously cited Hanson teach the claims as amended.
Applicant’s arguments have been considered, and have been found partially persuasive. The rejection of claim 1 and its dependent claims under 35 USC 103 over Hudecek in view of Hanson are withdrawn.
However, given that claim 3 and its dependent claims are no longer limited to SEQ ID NO: 1 or SEQ ID NO: 12 encoding the FLT3 CAR, claims 3, 22, 25, 27, 28, 39 and 40 are rejected under 35 U.S.C. 102(a)(1) and (a)(2) as being anticipated by Hudecek because Hudecek teaches the FLT3 CAR-T of SEQ ID NO: 2 which is encoded by a polynucleotide identical to the polynucleotide 55 to 777 of SEQ ID NO: 1 or 12. See p. 4, embodiment 10, claim 10 and Appendix of the Office Acton of 08/22/2025. SEQ ID NO: 2 of Hudecek comprises aa 19 to aa 259 of SEQ ID NO: 2 and is encoded by SEQ ID NO: 1. See Appendix, pp.16-21, of the Office Acton of 08/22/2025. Thus the rejection of claims 3, 22, 25, 27, 28, 39 and 40 is made and maintained for the reasons set forth above.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
6. Claim(s) 13, 15, and 16 are rejected under 35 U.S.C. 103 as being unpatentable over WO 2019/025484 (Hudecek, M. et al. Feb. 07, 2019), “Hudecek” as applied to claims 3, 22, 25, 27, 28, 39 and 40 above, and further in view of US 2010/0233200 A1 (Medin JA Sep. 16, 2020, of record), “Medin”.
Hudecek teaches as set forth above.
Hudecek does not teach a truncated CD19 of SEQ ID NO: 11 encoded by SEQ ID NO: 28.
Medin teaches at paragraph [0008]
Incorporating an effective suicide gene into a therapeutic vector ensures that any malignant clones arising from deleterious insertion of the vector are specifically killed. Likewise, such a control schema is useful as an inserted safety component for a variety of transplants, including stem cell transplants reducing teratomas, for example, should these outgrowth events develop. A suicide gene schema us also useful to control post-transplant complications such as Graft v Host disease. The invention provides vectors with improved safety elements to effectively clear transduced cells to further decrease risk to the patient.
Medin teaches a docking polynucleotide encoding a docking polypeptide that selectively binds a toxic binding agent as a suicide gene. ¶¶ 0010, 0015 and 0016.
Medin teaches that the docking polypeptide can be a truncated CD19. See ¶¶ 0015, 0016, 0035, and 0036 and Examples 2 and 3.
Medin teaches that a truncated CD19 can also be used as a detection marker. See ¶¶ 0092-0095.
Medin teaches SEQ ID NO: 30, which comprises the instant SEQ ID NO: 28, and encodes SEQ ID NO: 29, which comprises the instant SEQ ID NO: 29. See ¶¶ 0092 and 0095 and Appendix of the Office Acton of 08/22/2025.
It would have been prima facie obvious at the time the invention was filed given that the level of skill in the art was high to combine the teachings of Hudecek and Medin and express the truncated CD19/SEQ ID NO: 30 from the vector expressing the FLT3 CAR of Hudecek, linked by a T2A skip sequence as taught by Hudecek, because Medin teaches that the truncated CD19 can be used as docking polypeptide to eliminate unwanted cells or as a detection marker. One would have been motivated to express the truncated CD19 of Medini in the FLT3 CAR T cells to eliminate CAR T cells after treatment is finished or if the FLT3 CAR T cells are causing complications such as Graft v Host disease or to detect the FLT3 CAR T cells.
7. Claim 23 is rejected under 35 U.S.C. 103 as being unpatentable over WO 2019/025484 (Hudecek, M. et al. Feb. 07, 2019), “Hudecek” as applied to claims 3, 22, 25, 27, 28, 39 and 40 above, and further in view of WO 2017/015490 A1 (Brown et al. June 13, 2019, of record), “Brown”
Hudecek teaches as set forth above, but does not teach that the population of human T cells are substantially depleted for CD25+ and CD14+ cells..
Brown teaches methods for preparing T cell populations useful for a variety of purposes requiring a highly active, long-lived T cell population. The T cell populations are enriched for: nave T cells (TN), memory stem cells (TSCM) and central memory T cells (TCM). These cell populations can be derived from peripheral blood mononuclear cells (PBMC) by both: 1) depleting unwanted cell populations such as CD14 expressing myeloid cells and CD25 expressing cells; and 2) enriching for CD62L expressing memory and nave T cells.. See Abstract and ¶ 002.
Brown teaches that the T cells can be engineered to express chimeric antigen receptors. See ¶ 003.
Brown teaches TCM/SCM/N cells produced by this CD14 and CD25 depletion method expressing a CD19 CAR produced enhanced and robust antitumor activity compared to other T cell populations. See Examples 2 and 5, ¶ 0070 and Fig 7A/7B.
It would have been prima facie obvious at the time the invention was filed given that the level of skill in the art was high to combine the teachings of Hudecek and Brown and use the CD14 and CD25 depletion method of Brown to produce CD14 and CD25 depleted TCM/SCM/N cells for FLT3 CAR T cell production because Brown teaches TCM/SCM/N cells produced expressing a CD19 CAR produced enhanced and robust antitumor activity compared to other T cell populations. Thus one would have been motivated to use the CD14 and CD25 depleted TCM/SCM/N cells of Brown for expression of the FLT3 CAR of Hudecek to enhance the anti-tumor activity of the FLT3 CAR T cells of Hudecek.
Response to Arguments
8. Applicant argues that neither Hudecek, Medin nor Brown teach or suggest a nucleic acid encoding a CAR comprising amino acids 19-259 of SEQ ID NO:2 as in amended claim 3.
Applicant’s arguments have been considered, but have not been found persuasive. Hudecek teaches the FLT3 CAR-T of SEQ ID NO: 2 which is encoded by a polynucleotide identical to the polynucleotide 55 to 777 of SEQ ID NO: 1 or 12. See p. 4, embodiment 10, claim 10 and Appendix of the Office Acton of 08/22/2025. SEQ ID NO: 2 of Hudecek comprises aa 19 to aa 259 of SEQ ID NO: 2 and is encoded by SEQ ID NO: 1. See Appendix, pp.16-21, of the Office Acton of 08/22/2025. Thus, Medin and Brown do not need to teach a CAR comprising amino acids 19-259 of SEQ ID NO:2 because it is taught by Hudecek. Thus the 35 USC 103 rejections over Hudecek in view of Medin or over Hudecek in view of Brown are made and maintained for the reasons set forth above.
9. Claim(s) 1, 11, 20, 21, 29, 30, 33, 37, and 38 are rejected under 35 U.S.C. 103 as being unpatentable over WO 2019/025484 (Hudecek, M. et al. Feb. 07, 2019), “Hudecek” as applied to claims 3, 22, 25, 27, 28, 39 and 40 above, and further in view of US 2018/0118838 A1 (Yu et al. May 3, 2018), “Yu” in view of US 2023/0331872 A1 (Zhang L. Oct. 19, 2023, effectively filed Sep. 8, 2020), “Zhang”.
Hudecek teaches as set forth above, but does not teach the combination of a spacer comprising or consisting of the amino acid sequence of SEQ ID NO: 5 (IgG1); a transmembrane domain comprising or consisting of the amino acid sequence of SEQ ID NO: 6 (CD28):a costimulatory domain comprising or consisting of the amino acid sequence of SEQ ID NO: 7 (CD28) ; and a CD3z domain comprising or consisting of the amino acid sequence of SEQ ID NO: 8 or the signal peptide of amino acids 1-18 of SEQ ID NO: 2.
Yu teaches making anti-FLT3 CARs. See abstract.
Yu teaches the FLT3 CARs can comprise (a) an antigen binding domain of a FLT3 antibody; (b) a hinge domain; (c) a transmembrane domain; and (d) an intracellular domain. Further aspects of the disclosure relate to a chimeric antigen receptor (CAR) comprising: (a) an antigen binding domain of a FLT3 antibody; (b) a hinge domain; (c) a CD28 transmembrane domain; (d) one or more costimulatory regions selected from a CD28 costimulatory signaling region, a 4-1BB costimulatory signaling region, an ICOS costimulatory signaling region, and an OX40 costimulatory region; and (e) a CD3 zeta signaling domain.. See ¶¶ 0012.
Yu teaches that the FLT3 antibody can be 4G8. See ¶ 0232.
Yu teaches the FLT3 CARs can comprise the signal peptide of SEQ ID NO: 43: MGWSCIILFLVATATGVHS or an equivalent thereof. See ¶ 0269. SEQ ID NO: 43 comprises residues 1-18 of SEQ ID NO: 2.
Yu teaches IgG1 heavy chain hinge sequence, SEQ. ID NO: 1: CTCGAGCCCAAATCTTGTGACAAAACTCACACATGCCCACCGTGCCCG or optionally an equivalent thereof. See ¶ 0080. SEQ. ID NO: 1: encodes the IgG1 hinge protein LEPKSCDKTHTCPPCP.
Yu teaches nucleic acids encoding CD28 transmembrane domain and CD28 costimulatory signaling region of SEQ ID NO: 15, which comprises the claimed SEQ ID NOs: 6 and 7. See ¶¶ 0081, 0083 and 0100-0101 and Appendix.
Yu teaches nucleic acids encoding the CD3 zeta signaling domain of SEQ ID NO: 16, which comprises the claimed SEQ ID NO: 8. See ¶¶ 0084 and 0102 and Appendix.
Zhang teaches making FLT3 CARs. See ¶¶ 0269-0270 and 0614-0615.
Zhang teaches using the CAR signal peptide of MGWSSIILFLVATATGVH (SEQ ID NO: 21). See ¶¶ 0176, 0293, 0294, and 0305.
Zhang teaches using the IgG1 hinge amino acid sequence comprising, or consisting essentially of, or yet further consisting of LEPKSCDKTHTCPPCP (SEQ ID NO: 83), or LEPKSCDKTHTCPPCPDPKGT (SEQ ID NO: 47) or an equivalent of each thereof. See ¶¶ 0146, 0313 and 0317.
Zhang teaches SEQ ID NO: 196 a conventional BCMA-CAR with the claimed spacer, transmembrane and signaling domains of SEQ ID NOs: 5-8. See Tables 1d and 2c and Appendix.
It would have been prima facie obvious at the time the invention was filed given that the level of skill in the art was high to combine the teachings of Hudecek, Yu and Zhang and use the signal peptide, spacer/hinge, transmembrane and signaling domains of Yu and/or Zhang in the 4G8 FLT3 CAR of Hudecek because Yu and Zhang teach making functional CARs with these domains. One would have been motivated to use the signal peptide, spacer/hinge, transmembrane and signaling domains of Yu and/or Zhang in the 4G8 FLT3 CAR of Hudecek to optimize the activity of the FLT3 CAR and these domains are routinely used in the art as shown by Yu and Zhang to construct CARs, like FLT3 CARs.
Conclusion
10. All other objections and rejections recited in the Office Action of Office Action of August 22, 2025 are withdrawn in view of Applicant’s amendments and/or arguments.
11. No claims allowed.
12. Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any extension fee pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the date of this final action.
13. Any inquiry concerning this communication or earlier communications from the examiner should be directed to PETER J REDDIG whose telephone number is (571)272-9031. The examiner can normally be reached on M-F 8:30-5:30 Eastern Time
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Gregory Emch can be reached on 571-272-8149. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of an application may be obtained from the Patent Application Information Retrieval (PAIR) system. Status information for published applications may be obtained from either Private PAIR or Public PAIR. Status information for unpublished applications is available through Private PAIR only. For more information about the PAIR system, see http://pair-direct.uspto.gov. Should you have questions on access to the Private PAIR system, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative or access to the automated information system, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/Peter J Reddig/
Primary Examiner, Art Unit 1642
APPENDIX
Alignment of SEQ ID NO: 6 with SEQ ID NO: 15 of Yu.
Title: US-17-919-178-6
Perfect score: 141
Sequence: 1 FWVLVVVGGVLACYSLLVTVAFIIFWV 27
Scoring table: BLOSUM62
Gapop 10.0 , Gapext 0.5
Searched: 1 seqs, 220 residues
Total number of hits satisfying chosen parameters: 1
Minimum DB seq length: 0
Maximum DB seq length: inf
Post-processing: Minimum Match 0%
Maximum Match 100%
Listing first 1 summaries
Database : AASEQ2_02172026_152913.pep:*
SUMMARIES
%
Result Query
No. Score Match Length DB ID Description
----------------------------------------------------------------------------
1 141 100.0 220 1 AASEQ2_02172026_152913
ALIGNMENTS
RESULT 1
AASEQ2_02172026_152913
Query Match 100.0%; Score 141; DB 1; Length 220;
Best Local Similarity 100.0%;
Matches 27; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 FWVLVVVGGVLACYSLLVTVAFIIFWV 27
|||||||||||||||||||||||||||
Db 153 FWVLVVVGGVLACYSLLVTVAFIIFWV 179
Alignment of SEQ ID NO:7 with SEQ ID NO: 15 of Yu.
Title: US-17-919-178-7
Perfect score: 227
Sequence: 1 RSKRSRLLHSDYMNMTPRRP..........PTRKHYQPYAPPRDFAAYRS 41
Scoring table: BLOSUM62
Gapop 10.0 , Gapext 0.5
Searched: 1 seqs, 220 residues
Total number of hits satisfying chosen parameters: 1
Minimum DB seq length: 0
Maximum DB seq length: inf
Post-processing: Minimum Match 0%
Maximum Match 100%
Listing first 1 summaries
Database : AASEQ2_02172026_152755.pep:*
SUMMARIES
%
Result Query
No. Score Match Length DB ID Description
----------------------------------------------------------------------------
1 227 100.0 220 1 AASEQ2_02172026_152755
ALIGNMENTS
RESULT 1
AASEQ2_02172026_152755
Query Match 100.0%; Score 227; DB 1; Length 220;
Best Local Similarity 100.0%;
Matches 41; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 RSKRSRLLHSDYMNMTPRRPGPTRKHYQPYAPPRDFAAYRS 41
|||||||||||||||||||||||||||||||||||||||||
Db 180 RSKRSRLLHSDYMNMTPRRPGPTRKHYQPYAPPRDFAAYRS 220
Alignment of SEQ ID NO:8 with SEQ ID NO: 16 of Yu.
Title: US-17-919-178-8
Perfect score: 593
Sequence: 1 RVKFSRSADAPAYQQGQNQL..........LSTATKDTYDALHMQALPPR 112
Scoring table: BLOSUM62
Gapop 10.0 , Gapext 0.5
Searched: 1 seqs, 112 residues
Total number of hits satisfying chosen parameters: 1
Minimum DB seq length: 0
Maximum DB seq length: inf
Post-processing: Minimum Match 0%
Maximum Match 100%
Listing first 1 summaries
Database : AASEQ2_02172026_153152.pep:*
SUMMARIES
%
Result Query
No. Score Match Length DB ID Description
----------------------------------------------------------------------------
1 593 100.0 112 1 AASEQ2_02172026_153152
ALIGNMENTS
RESULT 1
AASEQ2_02172026_153152
Query Match 100.0%; Score 593; DB 1; Length 112;
Best Local Similarity 100.0%;
Matches 112; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 RVKFSRSADAPAYQQGQNQLYNELNLGRREEYDVLDKRRGRDPEMGGKPRRKNPQEGLYN 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 RVKFSRSADAPAYQQGQNQLYNELNLGRREEYDVLDKRRGRDPEMGGKPRRKNPQEGLYN 60
Qy 61 ELQKDKMAEAYSEIGMKGERRRGKGHDGLYQGLSTATKDTYDALHMQALPPR 112
||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 ELQKDKMAEAYSEIGMKGERRRGKGHDGLYQGLSTATKDTYDALHMQALPPR 112
Alignment of SEQ ID NOs:5-8 with SEQ ID NO: 196 of Yu.
US-18-022-741-196
Sequence 196, US/18022741
Publication No. US20230331872A1
GENERAL INFORMATION
APPLICANT: CYTOIMMUNE THERAPEUTICS, INC.
TITLE OF INVENTION: BISPECIFIC ANTIBODY CAR CELL IMMUNOTHERAPY
FILE REFERENCE: 113086-9266
CURRENT APPLICATION NUMBER: US/18/022,741
CURRENT FILING DATE: 2023-02-22
PRIOR APPLICATION NUMBER: PCT/US2021/047375
PRIOR FILING DATE: 2021-08-24
PRIOR APPLICATION NUMBER: 63/193,024
PRIOR FILING DATE: 2021-05-25
PRIOR APPLICATION NUMBER: 63/142,426
PRIOR FILING DATE: 2021-01-27
PRIOR APPLICATION NUMBER: 63/075,750
PRIOR FILING DATE: 2020-09-08
PRIOR APPLICATION NUMBER: 63/070,219
PRIOR FILING DATE: 2020-08-25
NUMBER OF SEQ ID NOS: 252
SEQ ID NO 196
LENGTH: 464
TYPE: PRT
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: Description of Artificial Sequence: Synthetic
polypeptide
Query Match 100.0%; Score 1092; Length 464;
Best Local Similarity 100.0%;
Matches 201; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 LEPKSCDKTHTCPPCPDPKGTFWVLVVVGGVLACYSLLVTVAFIIFWVRSKRSRLLHSDY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 264 LEPKSCDKTHTCPPCPDPKGTFWVLVVVGGVLACYSLLVTVAFIIFWVRSKRSRLLHSDY 323
Qy 61 MNMTPRRPGPTRKHYQPYAPPRDFAAYRSRVKFSRSADAPAYQQGQNQLYNELNLGRREE 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 324 MNMTPRRPGPTRKHYQPYAPPRDFAAYRSRVKFSRSADAPAYQQGQNQLYNELNLGRREE 383
Qy 121 YDVLDKRRGRDPEMGGKPRRKNPQEGLYNELQKDKMAEAYSEIGMKGERRRGKGHDGLYQ 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 384 YDVLDKRRGRDPEMGGKPRRKNPQEGLYNELQKDKMAEAYSEIGMKGERRRGKGHDGLYQ 443
Qy 181 GLSTATKDTYDALHMQALPPR 201
|||||||||||||||||||||
Db 444 GLSTATKDTYDALHMQALPPR 464