DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Response to Amendments and Arguments
2. Claims 1, 2, 6, 7 and 20 are pending.
Claims 3-5, 9, 13-16, 21-23, 28, 31, 38 and 40 have been cancelled.
Claims 1 and 6 have been amended.
Claims 1, 2, 6, 7 and 20 are examined on the merits.
3. The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Withdrawn Objections
Claim Objections
4. Claim 1 is no longer objected to because the verb, administrating is cited in the steps of the claim, see Listing of the Claims submitted June 9, 2026.
Withdrawn Grounds of Rejection
Claim Rejections - 35 USC § 112
5. The rejection of claims 4 and 6 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112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement is withdrawn in light of the amendment to claim 1 reciting the conserved structure provided by the listing of all six CDRs in the context of appropriate VH and VL framework sequences, see Listing of the Claims submitted June 9, 2026. Claims 4, 5 and 13-19 have been cancelled.
Claim Rejections - 35 USC § 102
6. The rejection of claim(s) 22 under 35 U.S.C. 102(a)(1) as being anticipated by Chu et al., (Annals of Oncology 28 (Supplement 5: v539-v542, 2017/ IDS reference 3C submitted April 18, 2024) is withdrawn in light of the cancellation of the claim, see Listing of the Claims submitted June 9, 2026, page 3.
Claim Rejections - 35 USC § 103
7. The rejection of claim(s) 22, 23, 28, 31, 38 and 40 under 35 U.S.C. 103 as being unpatentable over Chu et al., (Annals of Oncology 28 (Supplement 5: v539-v542, 2017/ IDS reference 3C submitted April 18, 2024), and further in view of Vangsted et al. (Cancer Research 51: 2879-2884, June 1, 1991), Cardarelli et al., (WO 2017/181034 A1 published 19 October 2017/ IDS reference 2B submitted April 18, 2024) and Cardarelli, J.M., WO 2016/201425 (published 15 December 2016) further referenced herein, Bristol-Myers Squibb Company is withdrawn in light of the cancellation of the claims, see Listing of the Claims submitted June 9, 2026, page 3.
Maintained Grounds of Rejection
Claim Rejections - 35 USC § 103
8. 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.
9. The rejection of claim(s) 1, 2, 6, 7 and 20 under 35 U.S.C. 103 as being unpatentable over Lopez-Chavez, WO 2019/246557 A1 (published 26 December 2019/ IDS reference 2B submitted February 23, 2026), and further in view of Cardarelli et al., (WO 2017/181034 A1 published 19 October 2017/ IDS reference 2B submitted April 18, 2024) is maintained. Claims 3-5, 9, 13-16 and 21 have been cancelled.
Applicant argues the only antibody dosing Lopez-Chavez teaches “… is 1200 mg of atezolizumab in both the induction and maintenance phases, which is not the same as, and does not suggest, administration of 360 mg of nivolumab in the induction phase and 480 mg of nivolumab in the maintenance phase.”, see Remarks submitted June 9, 2026, page 5, 3rd paragraph (para.).
Applicant also argues primary reference, “…Lopez-Chavez does not disclose maintenance dosing cycle longer than 21 days, let alone precisely 28 days, and instead includes a footnote specifying that Maintenance Phase cycles are "21-day cycles.", see Remarks, page 5, last para.
Applicant further argues secondary reference, “Cardarelli...does not disclose or suggest further administration of an anti-PD-1 antibody, does not disclose co-administration of carboplatin, and does not disclose a method of treatment comprising an induction phase and a maintenance phase, that these phases are Q3W and Q4W respectively, or that the dosing of the anti-FucGM1 antibody is 420 mg and 560 mg in the two phases.”, see page 6 of the Remarks, 1st para.
Applicant concludes arguments stating neither reference “… discloses or suggests the claimed combination therapy with an anti-FucGM1 antibody (BMS-986012) and an anti-PD-1 antibody (nivolumab). Neither reference, nor the combination if one were somehow motivated to combine them, discloses or suggests Q3W/Q4W induction/maintenance cycles, nor do they disclose or suggest dosing the anti-FucGM1 antibody at 420 mg and 560 mg and the anti-PD-1 at 360 mg and 480 mg during such induction and maintenance cycles, respectively.”, see 2nd para. on page 6 of the Remarks.
Applicant’s arguments and points of view have been carefully considered, but fail to persuade.
While Lopez-Chavez does not teach the anti-PD-1 antibody was administered at 360 mg during each round of induction therapy and at 480 mg in the maintenance phase, the publication makes clear “[v]arious modifications of the invention in addition to those shown and described herein will become apparent to those skilled in the art from the foregoing description and fall within the scope of the appended claims.”, see page 94, section 0348.
Moreover, Cardarelli teaches the administration of anti-fucosyl-GM1 that is BMS-986012 may be administered at a dose ranging from 10 to 2000 mg once every 1, 2, 3 or 4 weeks. For example, the antibody is administered at a dose ranging from 20 to 1000 mg once every 3 weeks. Optionally, the method comprises at least one treatment cycle of three weeks. For example, the method comprises at least four treatment cycles of three weeks. To illustrate, the antibody is administered on Days 1, 22, 43, and 64… In one embodiment antibody is administered at a dose between 400 and 1000 mg, inclusive. Whether stated or not, any dose range recited herein is intended to be inclusive, i.e. it the doses recited as the boundaries of the ranges are included within the recited dosing range. Preferably, administration of the antibody induces a durable clinical response in the subject. Optionally, administration of the antibody is continued for as long as clinical benefit is observed or until unmanageable toxicity or disease progression occurs. The efficacy of the treatment methods provided herein can be assessed using any suitable means. In one embodiment, the treatment produces at least one therapeutic effect selected from the group consisting of reduction in size of the cancer, reduction in number of metastatic lesions over time, complete response, partial response, and stable disease.”, see sections 0071 and 0072 spanning pages 19 and 20.
"[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation." In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235(CCPA 1955). Hence, it would not be unreasonable for one of ordinary skill in the art to achieve the dosages at designated time points as cited in the claims. These known therapeutic agents at the achieved dosages and time points would inevitably render and reach Applicant’s desired method endpoint designated amounts would be met given it is art known dosage ranges and their effects would naturally flow from the combination of prior art herein.
The Examiner has provided articulated reasoning with rational underpinning supporting the legal conclusion of obviousness. For the reasons cited herein, the combination of therapeutic agents would expectedly and predictably render synergistic treatment effects to the treated subject. Hence, the rejection is maintained for the reasons of record and cited herein. Thus, the rejection is maintained for the
reasons of record herein.
Lopez-Chavez teaches treating extensive-stage small cell lung cancer (ES-SCLC) administering to the individual a PD-1 axis binding antagonist, carboplatin and etoposide, see abstract. “In particular, the methods and uses are based on data from a randomized Phase III clinical study of atezolizumab…in combination with carboplatin and etoposide in individuals with previously -untreated…(ES-SCLC).”, see page 2, section 0009; section 0014 bridging pages 3 and 4.
“[T]reatment comprises an induction phase and a maintenance phase (or “maintenance therapy”). In some embodiments, the induction phase comprises administering the PD-1 axis binding antagonist (e.g., an anti-PD-Ll antibody such as atezolizumab) at a dose of 1200 mg on Day 1, the platinum agent (e.g., carboplatin or cisplatin) at a dose sufficient to achieve an initial target Area Under the Curve (AUC) of 5 mg/mL/min on Day 1, and the topoisomerase II inhibitor (e.g., etoposide) at a dose of 100 mg/m2 on each of Days 1, 2, and 3 of each 21-day cycle for Cycles 1-4. In some embodiments, the maintenance phase comprises administering the PD-1 axis binding antagonist (e.g., an anti-PD-L1 antibody such as atezolizumab) at a dose of 1200 mg on Day l of each 21-day cycle following Cycle 4.”, see page 75, section 0287.
“During the induction phase, etoposide (100 mg/m2) was also administered intravenously over 60 minutes on Days 2 and 3.”, see page 107, section 0382. And the maintenance phase comprising the PD-1 axis binding antagonist may extend past 21 days, thus reading on one or more 28-day rounds of maintenance therapy, see Table 4 on page 75.
The cycles are equivalent to rounds. Hence, the induction phase for 4 cycles, reads on Applicant’s exactly four rounds for induction therapy. The induction phase last 21 days for each round, see page 30, section 0124; page 75, section 0287; page 99, section 0358.
The PD-1 axis binding antagonist is also an anti-PD-1 antibody including nivolumab, see page 31, sections 0127 and 0128. Lopez-Chavez teaches heavy chain comprising SEQ ID NO: 13 and light chain comprising SEQ ID NO: 14.
Lopez-Chavez does not teach the claimed method, wherein an anti-fucosyl-GM1 antibody comprises a heavy chain variable region (VH) (comprising SEQ ID NO: 1), light chain variable region (VL) (comprising SEQ ID NO: 2), heavy chain (comprising SEQ ID NO: 3) and light chain (comprising SEQ ID NO: 4) is administered with the taught combination at the induction and maintenance phases at the dosages cited in claim 1. Nor, does Lopez-Chavez teach the anti-PD-1 antibody, nivolumab (comprising heavy chain, SEQ ID NO: 13 and light chain, SEQ ID NO: 14) is administered during induction and maintenance phases at the dosages cited in claim 1.
However, Cardarelli teaches treating SCLC with the administration of anti-fucosyl-GM1 BMS-986012 antibody with etoposide, see page 4, section 0016; and Example 3 on page 22.
The anti-fucosyl-GM1 antibody contains a VH comprising the sequence of SEQ ID NO: 1 and VL comprising the sequence of SEQ ID NO: 2, as well as a heavy chain comprising the sequence of SEQ ID NO: 3 and light chain containing a light chain comprising the sequence of SEQ ID NO: 4 and non-fucosylated, see sequence summaries and alignments at close of rejection.
“[T]he anti-fucosyl-GMl mAb competes with BMS- 986012, comprises the same CDRs as BMS-986012, comprises the same heavy and light chain variable domains as BMS-986012”, see page 2, section 0006; page 14, section 0055; and segment V. beginning on page 17.
It would have been obvious to one of ordinary skill in the art at the
effective filing date of the claimed invention to combine the therapeutic agents of Lopez-Chavez and Cardarelli to treat ESLC with the combination of carboplatin, etoposide, anti-fucosyl-GM1 and an immune checkpoint inhibitor, as well as arrive at the specific dosages set forth in the claims.
One of ordinary skill in the art would have been motivated to do so
with a reasonable expectation of success by teachings in all the references treating lung cancer with a combinatorial approach, which extends progression free survival (PFS) and overall survival (OS), see both references in their entirety. Notwithstanding, it is art known one of ordinary skill in the art would have been motivated to do so with a reasonable expectation of success by teachings well known in the art, that dosages of any pharmaceutical composition must be adjusted and optimized to arrive at the desired result.
BHB92903 from 13.rag database.
ID BHB92903 standard; protein; 440 AA.
XX
AC BHB92903;
XX
DT 20-FEB-2020 (first entry)
XX
DE Anti-PD-L1 antibody heavy chain, SEQ ID 11.
XX
KW PD-L1 protein; antibody; antibody therapy; cytostatic; enzyme inhibition;
KW heavy chain; lung tumor; metastasis; metastatic lung cancer;
KW respiratory-gen.; small-cell lung cancer; therapeutic.
XX
OS Unidentified.
XX
CC PN WO2019246557-A1.
XX
CC PD 26-DEC-2019.
XX
CC PF 21-JUN-2019; 2019WO-US038534.
XX
PR 23-JUN-2018; 2018US-0689105P.
PR 17-AUG-2018; 2018US-0719461P.
PR 25-SEP-2018; 2018US-0736326P.
XX
CC PA (GETH ) GENENTECH INC.
XX
CC PI Lopez-Chavez A;
XX
DR WPI; 2019-A8465F/007.
XX
CC PT Treating individual having lung cancer by administering to individual,
CC PT anti-programmed cell death ligand (PD-L)1 antibody, platinum agent (e.g.
CC PT carboplatin), and topoisomerase II inhibitor (e.g. etoposide).
XX
CC PS Disclosure; SEQ ID NO 11; 146pp; English.
XX
CC The present invention relates to a novel method for treating an
CC individual having lung cancer. The method involves administering an anti-
CC PD-L1 antibody, a platinum agent and a topoisomerase II inhibitor,
CC wherein the treatment extends the progression free survival (PFS) of the
CC individual. The invention also provides: a method for treating an
CC individual having extensive-stage small cell lung cancer (ES-SCLC); a kit
CC (k1) comprising the anti-PD-L1 antibody for use in combination with the
CC platinum agent and topoisomerase II inhibitor; and a kit (k2) comprising
CC atezolizumab for use in combination with carboplatin and etoposide for
CC treating an individual having lung cancer. The lung cancer or ES-SCLC can
CC be metastasized to the brain, liver, lymph nodes, or adrenal gland.
XX
SQ Sequence 440 AA;
BHB92904 from 14.rag database.
ID BHB92904 standard; protein; 214 AA.
XX
AC BHB92904;
XX
DT 20-FEB-2020 (first entry)
XX
DE Anti-PD-L1 antibody light chain, SEQ ID 12.
XX
KW PD-L1 protein; antibody; antibody therapy; cytostatic; enzyme inhibition;
KW light chain; lung tumor; metastasis; metastatic lung cancer;
KW respiratory-gen.; small-cell lung cancer; therapeutic.
XX
OS Unidentified.
XX
CC PN WO2019246557-A1.
XX
CC PD 26-DEC-2019.
XX
CC PF 21-JUN-2019; 2019WO-US038534.
XX
PR 23-JUN-2018; 2018US-0689105P.
PR 17-AUG-2018; 2018US-0719461P.
PR 25-SEP-2018; 2018US-0736326P.
XX
CC PA (GETH ) GENENTECH INC.
XX
CC PI Lopez-Chavez A;
XX
DR WPI; 2019-A8465F/007.
XX
CC PT Treating individual having lung cancer by administering to individual,
CC PT anti-programmed cell death ligand (PD-L)1 antibody, platinum agent (e.g.
CC PT carboplatin), and topoisomerase II inhibitor (e.g. etoposide).
XX
CC PS Disclosure; SEQ ID NO 12; 146pp; English.
XX
CC The present invention relates to a novel method for treating an
CC individual having lung cancer. The method involves administering an anti-
CC PD-L1 antibody, a platinum agent and a topoisomerase II inhibitor,
CC wherein the treatment extends the progression free survival (PFS) of the
CC individual. The invention also provides: a method for treating an
CC individual having extensive-stage small cell lung cancer (ES-SCLC); a kit
CC (k1) comprising the anti-PD-L1 antibody for use in combination with the
CC platinum agent and topoisomerase II inhibitor; and a kit (k2) comprising
CC atezolizumab for use in combination with carboplatin and etoposide for
CC treating an individual having lung cancer. The lung cancer or ES-SCLC can
CC be metastasized to the brain, liver, lymph nodes, or adrenal gland.
RESULT 15 from 1.rag database including underlined CDRHs 5-7.
BEM82341
(NOTE: this sequence has 1 duplicate in the database searched.
See complete list at the end of this report)
ID BEM82341 standard; protein; 451 AA.
XX
AC BEM82341;
XX
DT 14-DEC-2017 (first entry)
XX
DE Anti-FucGM1 antibody heavy chain, SEQ ID 3.
XX
KW FucGM1 protein; antibody; antibody therapy; cancer; cytostatic;
KW heavy chain; therapeutic.
XX
OS Homo sapiens.
XX
CC PN WO2017181034-A1.
XX
CC PD 19-OCT-2017.
XX
CC PF 14-APR-2017; 2017WO-US027663.
XX
PR 14-APR-2016; 2016US-0322407P.
XX
CC PA (BRIM ) BRISTOL-MYERS SQUIBB CO.
XX
CC PI Cardarelli JM, Chen B, Lopes De Menezes DE, Pan C, Ponath PD;
XX
DR WPI; 2017-71604F/74.
XX
CC PT Treating subject afflicted with cancer involves administering to subject
CC PT therapeutically effective combination of anti-fucosyl GMl antibody, or
CC PT their antigen-binding portion and anti-CD 137 antibody, or their antigen-
CC PT binding portion.
XX
CC PS Claim 5; SEQ ID NO 3; 33pp; English.
XX
CC The present invention relates to a novel method for treating a subject
CC afflicted with cancer. The method involves: administering to the subject
CC a therapeutically effective combination of: (a) an anti-fucosyl GM1
CC antibody, or an antigen-binding portion thereof; and (b) an anti-CD137
CC antibody, or its antigen-binding portion. The method enables to treat
CC subject afflicted with cancer provides fucosyl-GMl as highly specific
CC tumor antigen, which may be targeted by an immunotherapeutic in effective
CC manner. The present sequence is an anti-FucGM1 antibody heavy chain,
CC where the antibody is used in the invention for treating a subject
CC afflicted with cancer.
XX
SQ Sequence 451 AA;
Query Match 100.0%; Score 645; Length 451;
Best Local Similarity 100.0%;
Matches 122; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVQLVESGGGSVQPGESLRLSCVASGFTFSRYKMNWVRQAPGKGLEWVSYISRSGRDIYY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVQLVESGGGSVQPGESLRLSCVASGFTFSRYKMNWVRQAPGKGLEWVSYISRSGRDIYY 60
Qy 61 ADSVKGRFTISRDNAKNSLYLQMNSLRDEDTAVYYCAGTVTTYYYDFGMDVWGQGTTVTV 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 ADSVKGRFTISRDNAKNSLYLQMNSLRDEDTAVYYCAGTVTTYYYDFGMDVWGQGTTVTV 120
Qy 121 SS 122
||
Db 121 SS 122
BEM82340 from 2.rag database include CDRLs, SEQ ID Nos. 8-10.
ID BEM82340 standard; protein; 107 AA.
XX
AC BEM82340;
XX
DT 14-DEC-2017 (first entry)
XX
DE Anti-FucGM1 antibody VL region, SEQ ID 2.
XX
KW FucGM1 protein; antibody; antibody therapy; cancer; cytostatic;
KW light chain variable region; therapeutic.
XX
OS Homo sapiens.
XX
CC PN WO2017181034-A1.
XX
CC PD 19-OCT-2017.
XX
CC PF 14-APR-2017; 2017WO-US027663.
XX
PR 14-APR-2016; 2016US-0322407P.
XX
CC PA (BRIM ) BRISTOL-MYERS SQUIBB CO.
XX
CC PI Cardarelli JM, Chen B, Lopes De Menezes DE, Pan C, Ponath PD;
XX
DR WPI; 2017-71604F/74.
XX
CC PT Treating subject afflicted with cancer involves administering to subject
CC PT therapeutically effective combination of anti-fucosyl GMl antibody, or
CC PT their antigen-binding portion and anti-CD 137 antibody, or their antigen-
CC PT binding portion.
XX
CC PS Claim 7; SEQ ID NO 2; 33pp; English.
XX
CC The present invention relates to a novel method for treating a subject
CC afflicted with cancer. The method involves: administering to the subject
CC a therapeutically effective combination of: (a) an anti-fucosyl GM1
CC antibody, or an antigen-binding portion thereof; and (b) an anti-CD137
CC antibody, or its antigen-binding portion. The method enables to treat
CC subject afflicted with cancer provides fucosyl-GMl as highly specific
CC tumor antigen, which may be targeted by an immunotherapeutic in effective
CC manner. The present sequence is an anti-FucGM1 antibody light chain
CC variable region, where the antibody is used in the invention for treating
CC a subject afflicted with cancer.
XX
SQ Sequence 107 AA;
Title: US-18-271-579-2
Perfect score: 557
Sequence: 1 DIQMTQSPSSLSASVGDRVT..........CQQYNSYPPTFGGGTKVEIK 107
Scoring table: BLOSUM62
Gapop 10.0 , Gapext 0.5
Searched: 1 seqs, 107 residues
Post-processing: Minimum Match 0%
Maximum Match 100%
Listing first 50 summaries
Database : PCT-US17-27663-2.fasta:*
%
Result Query
No. Score Match Length DB ID Description
----------------------------------------------------------------------------
1 557 100.0 107 1 PCT-US17-27663-2 COMBINATION THERAP
RESULT 1 sequence-to-sequence alignment SEQ ID NO: 2 vs seqid#2
PCT-US17-27663-2
Query Match 100.0%; Score 557; DB 1; Length 107;
Best Local Similarity 100.0%;
Matches 107; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIQMTQSPSSLSASVGDRVTITCRASQGISSWLAWYQQKPEKAPKSLIYAASSLQSGVPS 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIQMTQSPSSLSASVGDRVTITCRASQGISSWLAWYQQKPEKAPKSLIYAASSLQSGVPS 60
Qy 61 RFSGSGSGTDFTLTISSLQPEDFATYYCQQYNSYPPTFGGGTKVEIK 107
|||||||||||||||||||||||||||||||||||||||||||||||
Db 61 RFSGSGSGTDFTLTISSLQPEDFATYYCQQYNSYPPTFGGGTKVEIK 107
RESULT 1 from 3.rag database.
BEM82341
(NOTE: this sequence has 1 duplicate in the database searched.
See complete list at the end of this report)
ID BEM82341 standard; protein; 451 AA.
XX
AC BEM82341;
XX
DT 14-DEC-2017 (first entry)
XX
DE Anti-FucGM1 antibody heavy chain, SEQ ID 3.
XX
KW FucGM1 protein; antibody; antibody therapy; cancer; cytostatic;
KW heavy chain; therapeutic.
XX
OS Homo sapiens.
XX
CC PN WO2017181034-A1.
XX
CC PD 19-OCT-2017.
XX
CC PF 14-APR-2017; 2017WO-US027663.
XX
PR 14-APR-2016; 2016US-0322407P.
XX
CC PA (BRIM ) BRISTOL-MYERS SQUIBB CO.
XX
CC PI Cardarelli JM, Chen B, Lopes De Menezes DE, Pan C, Ponath PD;
XX
DR WPI; 2017-71604F/74.
XX
CC PT Treating subject afflicted with cancer involves administering to subject
CC PT therapeutically effective combination of anti-fucosyl GMl antibody, or
CC PT their antigen-binding portion and anti-CD 137 antibody, or their antigen-
CC PT binding portion.
XX
CC PS Claim 5; SEQ ID NO 3; 33pp; English.
XX
CC The present invention relates to a novel method for treating a subject
CC afflicted with cancer. The method involves: administering to the subject
CC a therapeutically effective combination of: (a) an anti-fucosyl GM1
CC antibody, or an antigen-binding portion thereof; and (b) an anti-CD137
CC antibody, or its antigen-binding portion. The method enables to treat
CC subject afflicted with cancer provides fucosyl-GMl as highly specific
CC tumor antigen, which may be targeted by an immunotherapeutic in effective
CC manner. The present sequence is an anti-FucGM1 antibody heavy chain,
CC where the antibody is used in the invention for treating a subject
CC afflicted with cancer.
XX
SQ Sequence 451 AA;
Query Match 100.0%; Score 2407; Length 451;
Best Local Similarity 100.0%;
Matches 451; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVQLVESGGGSVQPGESLRLSCVASGFTFSRYKMNWVRQAPGKGLEWVSYISRSGRDIYY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVQLVESGGGSVQPGESLRLSCVASGFTFSRYKMNWVRQAPGKGLEWVSYISRSGRDIYY 60
Qy 61 ADSVKGRFTISRDNAKNSLYLQMNSLRDEDTAVYYCAGTVTTYYYDFGMDVWGQGTTVTV 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 ADSVKGRFTISRDNAKNSLYLQMNSLRDEDTAVYYCAGTVTTYYYDFGMDVWGQGTTVTV 120
Qy 121 SSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQ 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 SSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQ 180
Qy 181 SSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELL 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 SSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELL 240
Qy 241 GGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQ 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 GGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQ 300
Qy 301 YNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSR 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 301 YNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSR 360
Qy 361 EEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKS 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 361 EEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKS 420
Qy 421 RWQQGNVFSCSVMHEALHNHYTQKSLSLSPG 451
|||||||||||||||||||||||||||||||
Db 421 RWQQGNVFSCSVMHEALHNHYTQKSLSLSPG 451
BEM82342 from 4.rag database.
ID BEM82342 standard; protein; 214 AA.
XX
AC BEM82342;
XX
DT 14-DEC-2017 (first entry)
XX
DE Anti-FucGM1 antibody light chain, SEQ ID 4.
XX
KW FucGM1 protein; antibody; antibody therapy; cancer; cytostatic;
KW light chain; therapeutic.
XX
OS Homo sapiens.
XX
CC PN WO2017181034-A1.
XX
CC PD 19-OCT-2017.
XX
CC PF 14-APR-2017; 2017WO-US027663.
XX
PR 14-APR-2016; 2016US-0322407P.
XX
CC PA (BRIM ) BRISTOL-MYERS SQUIBB CO.
XX
CC PI Cardarelli JM, Chen B, Lopes De Menezes DE, Pan C, Ponath PD;
XX
DR WPI; 2017-71604F/74.
XX
CC PT Treating subject afflicted with cancer involves administering to subject
CC PT therapeutically effective combination of anti-fucosyl GMl antibody, or
CC PT their antigen-binding portion and anti-CD 137 antibody, or their antigen-
CC PT binding portion.
XX
CC PS Claim 5; SEQ ID NO 4; 33pp; English.
XX
CC The present invention relates to a novel method for treating a subject
CC afflicted with cancer. The method involves: administering to the subject
CC a therapeutically effective combination of: (a) an anti-fucosyl GM1
CC antibody, or an antigen-binding portion thereof; and (b) an anti-CD137
CC antibody, or its antigen-binding portion. The method enables to treat
CC subject afflicted with cancer provides fucosyl-GMl as highly specific
CC tumor antigen, which may be targeted by an immunotherapeutic in effective
CC manner. The present sequence is an anti-FucGM1 antibody light chain,
CC where the antibody is used in the invention for treating a subject
CC afflicted with cancer.
XX
SQ Sequence 214 AA;
Title: US-18-271-579-4
Perfect score: 1110
Sequence: 1 DIQMTQSPSSLSASVGDRVT..........EVTHQGLSSPVTKSFNRGEC 214
Scoring table: BLOSUM62
Gapop 10.0 , Gapext 0.5
Searched: 1 seqs, 214 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 50 summaries
Database : PCT-US17-27663-4.fasta:*
SUMMARIES
%
Result Query
No. Score Match Length DB ID Description
----------------------------------------------------------------------------
1 1110 100.0 214 1 PCT-US17-27663-4 COMBINATION THERAP
RESULT 1 sequence-to-sequence alignment SEQ ID NO: 4 vs seqid#4
PCT-US17-27663-4
Query Match 100.0%; Score 1110; DB 1; Length 214;
Best Local Similarity 100.0%;
Matches 214; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIQMTQSPSSLSASVGDRVTITCRASQGISSWLAWYQQKPEKAPKSLIYAASSLQSGVPS 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIQMTQSPSSLSASVGDRVTITCRASQGISSWLAWYQQKPEKAPKSLIYAASSLQSGVPS 60
Qy 61 RFSGSGSGTDFTLTISSLQPEDFATYYCQQYNSYPPTFGGGTKVEIKRTVAAPSVFIFPP 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 RFSGSGSGTDFTLTISSLQPEDFATYYCQQYNSYPPTFGGGTKVEIKRTVAAPSVFIFPP 120
Qy 121 SDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLT 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 SDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLT 180
Qy 181 LSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC 214
||||||||||||||||||||||||||||||||||
Db 181 LSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC 214
Conclusion
10. Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
11. Any inquiry concerning this communication or earlier communications from the Examiner should be directed to ALANA HARRIS DENT whose telephone number is (571)272-0831. The Examiner works a flexible schedule, however she can generally be reached 8AM-8PM, Monday through Friday.
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, Julie Wu can be reached at 571-272-5205. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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ALANA HARRIS DENT
Primary Examiner
Art Unit 1643
26 August 2026
/Alana Harris Dent/Primary Examiner, Art Unit 1643
Prosecution Insights