DETAILED ACTION
Notice of Pre-AIA or AIA Status
1. The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
2. Claims 1-13, 16, 20 and 22-26 are pending.
Claims 11, 12 and 26 have been amended.
Claims 14, 15, 17-19, 21 and 27-29 have been cancelled.
Claims 1-13, 16, 20 and 22-26 are examined on the merits.
3. Applicant is put on notice that claims should note proper status identifiers. For instance, claim 12 should cite (currently amended) instead of (original), see page 5 of the claim set submitted July 20, 2023. Most of the text within the claim has been underlined indicative of claim amendments.
Applicant should carefully review all claims and ensure the corresponding status identifier properly reflects the listing of the claim. Improper status identifiers or no status identifiers may result in the receipt of a Notice of Non-Compliant Amendment (37 CFR 1.121), see MPEP 714 for
further explanation of the amendment format.
Claim Rejections - 35 USC § 102
4. 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.
5. Claim(s) 1, 7, 9-13, 16, 20, 22 and 23 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Grogan et al., WO 2015/009856 A2 (published 22 January 2015). Grogan discloses “…a method for treating or delaying progression of cancer…comprising administering…an effective amount of PD-1 axis binding antagonist and an agent that decreases or inhibits [T-cell immunoreceptor with Ig and ITIM domains] TIGIT expression and/or activity.”, see page 3, sections 0010-0014; and page 13, section 0077. The PD-1 axis antagonist is an anti-PD-1 antibody, see page 12, section 0075. The method may further comprise administering additional therapy including bevacizumab, as well as chemotherapy, radiotherapy and a combination of the foregoing, see page 74, last 4 lines; and page 83, section 0264.
The agent that is able to modulate “…TIGIT expression and/or activity is an anti-TIGIT antibody or antigen-binding fragment thereof”, including Fab, Fv and F(ab’)2 fragments, see page 5, sections 0025 and 0026; page 7, section 0046; page 56, section 0167; page 59, section 0174; and page 103, section 0336.
The PD-1 axis antagonist is an anti-PD-1 antibody, see page 12, section 0075.
The disclosed combination treatment is ablet to treat breast cancer, colorectal cancer, pancreatic cancer, head and neck cancer, gastric carcinoma, renal (kidney) cell cancer, liver cancer (hepatocellular cancer), small cell lung cancer, non-small cell lung cancer, esophageal cancer, ovarian cancer, uterine carcinoma, cervical cancer, melanoma, mesothelioma, lymphomas, leukemia, myelomas, sarcoma and other hematologic malignancies, see section 209 spanning pages 69 and 70; and section 257 spanning pages 81 and 82. The disclosed method also provides “…for reducing or inhibiting cancer relapse or cancer progression in an individual comprising administering to the individual an effect amount of a PD-1 axis binding antagonist in combination with an agent that that decreases or inhibits TIGIT expression and/or activity. As disclosed herein, cancer relapse and/or cancer progression include, without limitation, cancer metastasis.”, see section 0231 bridging pages 76 and 77.
Claim Rejections - 35 USC § 103
6. 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.
7. Claim(s) 1, 7-13, 16, 20 and 22-26 is/are rejected under 35 U.S.C. 103 as being unpatentable over Grogan et al., WO 2015/009856 A2 (published 22 January 2015), and further in view of Meng et al., WO 2019/165434 A1 (published 29 August 2019). Grogan teaches “…a method for treating or delaying progression of cancer…comprising administering…an effective amount of PD-1 axis binding antagonist and an agent that decreases or inhibits [T-cell immunoreceptor with Ig and ITIM domains] TIGIT expression and/or activity.”, see page 3, sections 0010-0014; and page 13, section 0077. The PD-1 axis antagonist is an anti-PD-1 antibody, see page 12, section 0075.
The method may further comprise administering additional therapy including bevacizumab, as well as chemotherapy, radiotherapy and a combination of the foregoing, see page 74, last 4 lines; and page 83, section 0264.
The agent that is able to modulate “…TIGIT expression and/or activity is an anti-TIGIT antibody or antigen-binding fragment thereof”, including Fab, Fv and F(ab’)2 fragments, see page 5, sections 0025 and 0026; page 7, section 0046; page 56, section 0167; page 59, section 0174; and page 103, section 0336.
The taught combination treatment is ablet to treat breast cancer, colorectal cancer, pancreatic cancer, head and neck cancer, gastric carcinoma, renal (kidney) cell cancer, liver cancer (hepatocellular cancer), small cell lung cancer, non-small cell lung cancer, esophageal cancer, ovarian cancer, uterine carcinoma, cervical cancer, melanoma, mesothelioma, lymphomas, leukemia, myelomas, sarcoma and other hematologic malignancies, see section 209 spanning pages 69 and 70; and section 257 spanning pages 81 and 82. The disclosed method also provides “…for reducing or inhibiting cancer relapse or cancer progression in an individual comprising administering to the individual an effect amount of a PD-1 axis binding antagonist in combination with an agent that that decreases or inhibits TIGIT expression and/or activity. As disclosed herein, cancer relapse and/or cancer progression include, without limitation, cancer metastasis.”, see section 0231 bridging pages 76 and 77.
Grogan does not teach the method, the administered dosages of anti-PD-1 and anti-TIGIT antibody set forth in claims 24-26. Grogan does not teach other PD-1 axis binding antibodies that are administered as antibody fragments, see sections 0268-0272 spanning pages 84 and 85.
However, Meng teaches anti-TIGIT antagonist antibody can be administered at a fixed dose range between 30 mg to about 1200 mg every three weeks and an anti-PD-L1 antibody at a fixed dose range between about 80 mg to 1600 mg every three weeks to treat a cancer, a lung cancer, as well as other solid cancers, see page 2, lines 1-14; and page 25, lines 23-36. Meng also teaches additional immunomodulatory agents, such as a PD-1 antagonist antibody can be administered, see page 25, lines 23-36.
“The term “antibody” includes monoclonal antibodies (including full-length antibodies which have an immunoglobulin Fc region), antibody compositions with polyepitopic specificity, multispecific antibodies (e.g., bispecific antibodies), diabodies, and single-chain molecules, as well as antibody fragments, including antigen-binding fragments, such as Fab, F(ab’)2, and Fv.”, see page 34, lines 36-39; and segment 2, spanning pages 89 and 90.
It would have been obvious to one of ordinary skill in the art at the
effective filing date of the claimed invention to administer both, the anti-TIGIT antibody and anti-PD1 antibody, as well as antigen-binding fragments, thereof at the dosages set forth in claims 24-26 because the range of dosages for the TIGIT antibody and other immune checkpoint antibodies have been successfully administered for treatment, see entire Meng.
One of ordinary skill in the art would have been motivated to
conclude with a reasonable expectation of success by teachings in both
references, these antibodies in combination are able to treat a number of solid cancers with the requisite dosages, see both references in their entirety.
8. Claim(s) 1-13, 16, 20 and 22-26 is/are rejected under 35 U.S.C. 103 as being unpatentable over Grogan et al., WO 2015/009856 A2 (published 22 January 2015), and further in view of Xue et al., WO 2019/129261 (published 04 July 2019/ IDS reference #B1 submitted January 15, 2025), Li et al., US 8,735,553 B1 (issued May 27, 2014/ IDS reference #11 on sheet 2 submitted November 22, 2023) and Meng et al., WO 2019/165434 A1 (published 29 August 2019). Grogan teaches “…a method for treating or delaying progression of cancer…comprising administering…an effective amount of PD-1 axis binding antagonist and an agent that decreases or inhibits [T-cell immunoreceptor with Ig and ITIM domains] TIGIT expression and/or activity.”, see page 3, sections 0010-0014; and page 13, section 0077. The PD-1 axis antagonist is an anti-PD-1 antibody, see page 12, section 0075.
The method may further comprise administering additional therapy including bevacizumab, as well as chemotherapy, radiotherapy and a combination of the foregoing, see page 74, last 4 lines; and page 83, section 0264.
The agent that is able to modulate “…TIGIT expression and/or activity is an anti-TIGIT antibody or antigen-binding fragment thereof”, including Fab, Fv and F(ab’)2 fragments, see page 5, sections 0025 and 0026; page 7, section 0046; page 56, section 0167; page 59, section 0174; and page 103, section 0336.
The taught combination treatment is ablet to treat breast cancer, colorectal cancer, pancreatic cancer, head and neck cancer, gastric carcinoma, renal (kidney) cell cancer, liver cancer (hepatocellular cancer), small cell lung cancer, non-small cell lung cancer, esophageal cancer, ovarian cancer, uterine carcinoma, cervical cancer, melanoma, mesothelioma, lymphomas, leukemia, myelomas, sarcoma and other hematologic malignancies, see section 209 spanning pages 69 and 70; and section 257 spanning pages 81 and 82. The disclosed method also provides “…for reducing or inhibiting cancer relapse or cancer progression in an individual comprising administering to the individual an effect amount of a PD-1 axis binding antagonist in combination with an agent that that decreases or inhibits TIGIT expression and/or activity. As disclosed herein, cancer relapse and/or cancer progression include, without limitation, cancer metastasis.”, see section 0231 bridging pages 76 and 77.
Grogan does not teach the method, wherein the TIGIT antibody contains the heavy chain variable region (VH) that comprises SEQ ID NO: 19 and a light chain variable region (VL) that comprises SEQ ID NO: 21 with the noted complementarity determining regions cited in claim 2 (i) and the PD-1 antibody contains the VH region comprising SEQ ID NO: 32 and VL region comprising SEQ ID NO: 34 with the noted CDRs cited in claim 4.
Grogan does not the method, wherein the TIGIT antibody contains the VH region comprises SEQ ID NO: 14 and a VL region comprises SEQ ID NO: 16 with the noted complementarity determining regions cited in claim 2 (ii); or the VH region comprises SEQ ID NO: 9 and a VL region comprises SEQ ID NO: 11 with the noted complementarity determining regions cited in claim 2 (ii).
Grogan does not the method, wherein the administered dosages of anti-PD-1 and anti-TIGIT antibody set forth in claims 24-26. Grogan does teach other PD-1 axis binding antibodies that are administered as antibody fragments, see sections 0268-0272 spanning pages 84 and 85.
However, Xue teaches the TIGIT antibody that is the same as Applicant’s comprising VH region comprising SEQ ID NO: 19 and VL region comprising SEQ ID NO: 21 with (a) a HCDR (Heavy Chain Complementarity Determining Region) 1 of SEQ ID NO: 3, (b) a HCDR2 of SEQ ID NO: 13, and (c) a HCDR3 of SEQ ID NO:5; and a light chain variable region that comprises (d) a LCDR (Light Chain Complementarity Determining Region) 1 of SEQ ID NO:6, (e) a LCDR2 of SEQ ID NO:7, and (f) a LCDR3 of SEQ ID NO:8, see sequence listing at close of instant rejection.
Xue teaches the TIGIT antibody that is the same as Applicant’s comprising VH region comprising SEQ ID NO: 19 and VL region comprising SEQ ID NO: 21 with (a) a HCDR 1 of SEQ ID NO: 3, (b) a HCDR2 of SEQ ID NO: 4, and (c) a HCDR3 of SEQ ID NO:5; and a light chain variable region that comprises (d) a LCDR 1 of SEQ ID NO:6, (e) a LCDR2 of SEQ ID NO:7, and (f) a LCDR3 of SEQ ID NO:8, see sequence listing at close of instant rejection.
Li teaches wherein the anti-PD1 antibody comprises an antibody or an antigen binding fragment thereof which specifically binds human PD1, and comprises:
(a) heavy chain variable region that comprises (a) a HCDR1 of SEQ ID NO: 25, (b) HCDR2 of SEQ ID NO: 26, and (c) HCDR3 of SEQ ID NO: 27; and a light chain variable region that comprises (d) LCDR1 of SEQ ID NO: 28, (e) LCDR2 of SEQ ID NO: 29, and (f) LCDR3 of SEQ ID NO: 30;
the anti-PD1 antibody or antigen binding fragment thereof which specifically binds human PD1 and comprises a VH region comprising an amino acid sequence of SEQ ID NO:32 and a VL region comprising an amino acid sequence of SEQ ID NO: 34 and the anti-PD1 antibody comprises an IgG4 constant domain comprising SEQ ID NO: 35.
Meng teaches anti-TIGIT antagonist antibody can be administered at a fixed dose range between 30 mg to about 1200 mg every three weeks and an anti-PD-L1 antibody at a fixed dose range between about 80 mg to 1600 mg every three weeks to treat a cancer, a lung cancer, as well as other solid cancers, see page 2, lines 1-14; and page 25, lines 23-36. Meng also teaches additional immunomodulatory agents, such as a PD-1 antagonist antibody can be administered, see page 25, lines 23-36.
“The term “antibody” includes monoclonal antibodies (including full-length antibodies which have an immunoglobulin Fc region), antibody compositions with polyepitopic specificity, multispecific antibodies (e.g., bispecific antibodies), diabodies, and single-chain molecules, as well as antibody fragments, including antigen-binding fragments, such as Fab, F(ab’)2, and Fv.”, see page 34, lines 36-39; and segment 2, spanning pages 89 and 90.
It would have been obvious to one of ordinary skill in the art at the effective filing date of the claimed invention to substitute the TIGIT antibody of Grogan with the anti-TIGIT antibody of Xue with known structure given it has successfully targeted the TIGIT antigen, as well as substitute the PD1 antibody of Grogan with the known PD-1 antibody of Li because it too has successfully targeted its receptor and administer both antibodies at the designated 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 the secondary
references that the targets of the antibodies with known CDRs are art recognized as a plausible alternative.
It would have been obvious to one of ordinary skill in the art at the
effective filing date of the claimed invention to administer both, the anti-TIGIT antibody and anti-PD1 antibody, as well as antigen-binding fragments, thereof at the dosages set forth in claims 24-26 because the range of dosages for the TIGIT antibody and other immune checkpoint antibodies have been successfully administered for treatment, see entire Meng. 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.
One of ordinary skill in the art would have been motivated to
conclude with a reasonable expectation of success by teachings in both
references, these antibodies in combination are able to treat a number of solid cancers with the requisite dosages, see both references in their entirety.
RESULT 1 from 19.rag database including underlined CDRs 3, 13 and 5, respectively.
BGM43640
(NOTE: this sequence has 9 duplicates in the database searched.
See complete list at the end of this report)
ID BGM43640 standard; protein; 119 AA.
XX
AC BGM43640;
XX
DT 08-AUG-2019 (first entry)
XX
DE Anti-TIGIT humanized monoclonal antibody VH domain, SEQ ID 19.
XX
KW Heavy chain variable region; T cell immunoreceptor Ig ITIM protein;
KW TIGIT protein; antibody therapy; antimicrobial-gen.; cancer; cytostatic;
KW diagnostic test; humanized antibody; immune stimulation;
KW immuno-diagnosis; infectious disease; monoclonal antibody; therapeutic;
KW viral infection; virucide.
XX
OS Mus musculus.
OS Homo sapiens.
OS Chimeric.
XX
FH Key Location/Qualifiers
FT Region 31..35
FT /note= "CDR1"
FT Region 50..66
FT /note= "CDR2"
FT Region 99..108
FT /note= "CDR3"
XX
CC PN WO2019129261-A1.
XX
CC PD 04-JUL-2019.
XX
CC PF 29-DEC-2018; 2018WO-CN125375.
XX
PR 30-DEC-2017; 2017WO-CN120392.
XX
CC PA (BEIG-) BEIGENE LTD.
CC PA (ZHAN/) ZHANG T.
XX
CC PI Xue L, Liu Q, Wei M, Li K;
XX
DR WPI; 2019-58574C/55.
DR N-PSDB; BGM43641.
XX
CC PT New antibody or its antigen-binding fragment, which is capable of binding
CC PT to human T cell immunoglobulin and ITIM domain (Tigit), comprises heavy
CC PT and light chain variable regions, for treating cancer, tumor or
CC PT infectious disease.
XX
CC PS Claim 4; SEQ ID NO 19; 43pp; English.
XX
CC The present invention relates to a novel antibody or its antigen-binding
CC fragment, useful in a pharmaceutical composition for treating cancer. The
CC antibody or its antigen-binding fragment specifically binds to a T cell
CC immunoglobulin and ITIM domain (TIGIT) protein and comprises: (a) a heavy
CC chain variable region (VH) of SEQ ID NO: 9, 14 or 19 (see BGM43630,
CC BGM43635 or BGM43640) containing complementarity determining regions
CC (CDRs) of SEQ ID NO: 3-5 (see BGM43624-BGM43626) or SEQ ID NO: 13 (see
CC BGM43634); and (b) a light chain variable region (VL) of SEQ ID NO: 11,
CC 16 or 21 (see BGM43632, BGM43637 or BGM43642) containing CDRs of SEQ ID
CC NO: 6-8 (see BGM43627-BGM43629). The invention further claims: (1) a
CC pharmaceutical composition comprising the antibody or its antigen-binding
CC fragment and a pharmaceutical acceptable excipient; (2) a method for
CC stimulating an immune response in a subject; (3) a method for treating
CC cancer or tumor in the subject; and (4) a method for treating infectious
CC diseases in the subject. The anti-TIGIT antibody or its antigen-binding
CC fragment is useful for: diagnosing or treating cancer, tumor and
CC infectious disease (viral infection); and stimulating an immune response
CC in a subject.
XX
SQ Sequence 119 AA;
Query Match 100.0%; Score 638; Length 119;
Best Local Similarity 100.0%;
Matches 119; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVQLVESGGGLVQPGGSLRLSCAASGFTFSDYYMYWVRQAPGKGLEWVAYITKGGGSTYY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVQLVESGGGLVQPGGSLRLSCAASGFTFSDYYMYWVRQAPGKGLEWVAYITKGGGSTYY 60
Qy 61 PDSVKGRFTISRDNAKNTLYLQMNSLRAEDTAVYYCARQTNYDFTMDYWGQGTLVTVSS 119
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 PDSVKGRFTISRDNAKNTLYLQMNSLRAEDTAVYYCARQTNYDFTMDYWGQGTLVTVSS 119
RESULT 1 from 21.rag database including CRS 6, 7 and 8, respectively.
BGM43642
(NOTE: this sequence has 11 duplicates in the database searched.
See complete list at the end of this report)
ID BGM43642 standard; protein; 107 AA.
XX
DT 08-AUG-2019 (first entry)
XX
DE Anti-TIGIT humanized monoclonal antibody VL domain, SEQ ID 21.
XX
KW Light chain variable region; T cell immunoreceptor Ig ITIM protein;
KW TIGIT protein; antibody therapy; antimicrobial-gen.; cancer; cytostatic;
KW diagnostic test; humanized antibody; immune stimulation;
KW immuno-diagnosis; infectious disease; monoclonal antibody; therapeutic;
KW viral infection; virucide.
XX
FH Key Location/Qualifiers
FT Region 24..34
FT /note= "CDR1"
FT Region 50..56
FT /note= "CDR2"
FT Region 89..97
FT /note= "CDR3"
XX
CC PN WO2019129261-A1.
XX
CC PD 04-JUL-2019.
XX
CC PF 29-DEC-2018; 2018WO-CN125375.
XX
PR 30-DEC-2017; 2017WO-CN120392.
XX
CC PA (BEIG-) BEIGENE LTD.
CC PA (ZHAN/) ZHANG T.
XX
CC PI Xue L, Liu Q, Wei M, Li K;
XX
DR WPI; 2019-58574C/55.
DR N-PSDB; BGM43643.
XX
CC PT New antibody or its antigen-binding fragment, which is capable of binding
CC PT to human T cell immunoglobulin and ITIM domain (Tigit), comprises heavy
CC PT and light chain variable regions, for treating cancer, tumor or
CC PT infectious disease.
XX
CC PS Claim 5; SEQ ID NO 21; 43pp; English.
XX
CC The present invention relates to a novel antibody or its antigen-binding
CC fragment, useful in a pharmaceutical composition for treating cancer. The
CC antibody or its antigen-binding fragment specifically binds to a T cell
CC immunoglobulin and ITIM domain (TIGIT) protein and comprises: (a) a heavy
CC chain variable region (VH) of SEQ ID NO: 9, 14 or 19 (see BGM43630,
CC BGM43635 or BGM43640) containing complementarity determining regions
CC (CDRs) of SEQ ID NO: 3-5 (see BGM43624-BGM43626) or SEQ ID NO: 13 (see
CC BGM43634); and (b) a light chain variable region (VL) of SEQ ID NO: 11,
CC 16 or 21 (see BGM43632, BGM43637 or BGM43642) containing CDRs of SEQ ID
CC NO: 6-8 (see BGM43627-BGM43629). The invention further claims: (1) a
CC pharmaceutical composition comprising the antibody or its antigen-binding
CC fragment and a pharmaceutical acceptable excipient; (2) a method for
CC stimulating an immune response in a subject; (3) a method for treating
CC cancer or tumor in the subject; and (4) a method for treating infectious
CC diseases in the subject. The anti-TIGIT antibody or its antigen-binding
CC fragment is useful for: diagnosing or treating cancer, tumor and
CC infectious disease (viral infection); and stimulating an immune response
CC in a subject. Note: The present sequence is also described as a heavy
CC chain variable region on Page 5 of the specification.
XX
SQ Sequence 107 AA;
Query Match 100.0%; Score 556; Length 107;
Best Local Similarity 100.0%;
Matches 107; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EIVMTQSPATLSVSPGERATLSCKASQDVGTSVAWYQQKPGQAPRLLIYWASARHTGIPA 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EIVMTQSPATLSVSPGERATLSCKASQDVGTSVAWYQQKPGQAPRLLIYWASARHTGIPA 60
Qy 61 RFSGSGSGTEFTLTISSLQSEDFAVYYCQQYSSYPLTFGGGTKVEIK 107
|||||||||||||||||||||||||||||||||||||||||||||||
Db 61 RFSGSGSGTEFTLTISSLQSEDFAVYYCQQYSSYPLTFGGGTKVEIK 107
RESULT 1 from 14.rag database including CDRs 6, 7 and 8, respectively.
BGM43635
(NOTE: this sequence has 1 duplicate in the database searched.
See complete list at the end of this report)
ID BGM43635 standard; protein; 119 AA.
XX
AC BGM43635;
XX
DT 08-AUG-2019 (first entry)
XX
DE Anti-TIGIT humanized antibody heavy chain variable region, SEQ ID 14.
XX
KW Heavy chain variable region; T cell immunoreceptor Ig ITIM protein;
KW TIGIT protein; antibody therapy; antimicrobial-gen.; cancer; cytostatic;
KW diagnostic test; humanized antibody; immune stimulation;
KW immuno-diagnosis; infectious disease; therapeutic; viral infection;
KW virucide.
XX
OS Mus musculus.
OS Synthetic.
XX
FH Key Location/Qualifiers
FT Misc-difference 24
FT /note= "Wild-type Thr is optionally substituted by Ala"
FT Region 31..35
FT /note= "CDR1"
FT Misc-difference 37
FT /note= "Wild-type Ile is optionally substituted by Val"
FT Region 50..66
FT /note= "CDR2"
FT Region 99..108
FT /note= "CDR3"
XX
CC PN WO2019129261-A1.
XX
CC PD 04-JUL-2019.
XX
CC PF 29-DEC-2018; 2018WO-CN125375.
XX
PR 30-DEC-2017; 2017WO-CN120392.
XX
CC PA (BEIG-) BEIGENE LTD.
CC PA (ZHAN/) ZHANG T.
XX
CC PI Xue L, Liu Q, Wei M, Li K;
XX
DR WPI; 2019-58574C/55.
DR N-PSDB; BGM43636.
XX
CC PT New antibody or its antigen-binding fragment, which is capable of binding
CC PT to human T cell immunoglobulin and ITIM domain (Tigit), comprises heavy
CC PT and light chain variable regions, for treating cancer, tumor or
CC PT infectious disease.
XX
CC PS Claim 4; SEQ ID NO 14; 43pp; English.
XX
CC The present invention relates to a novel antibody or its antigen-binding
CC fragment, useful in a pharmaceutical composition for treating cancer. The
CC antibody or its antigen-binding fragment specifically binds to a T cell
CC immunoglobulin and ITIM domain (TIGIT) protein and comprises: (a) a heavy
CC chain variable region (VH) of SEQ ID NO: 9, 14 or 19 (see BGM43630,
CC BGM43635 or BGM43640) containing complementarity determining regions
CC (CDRs) of SEQ ID NO: 3-5 (see BGM43624-BGM43626) or SEQ ID NO: 13 (see
CC BGM43634); and (b) a light chain variable region (VL) of SEQ ID NO: 11,
CC 16 or 21 (see BGM43632, BGM43637 or BGM43642) containing CDRs of SEQ ID
CC NO: 6-8 (see BGM43627-BGM43629). The invention further claims: (1) a
CC pharmaceutical composition comprising the antibody or its antigen-binding
CC fragment and a pharmaceutical acceptable excipient; (2) a method for
CC stimulating an immune response in a subject; (3) a method for treating
CC cancer or tumor in the subject; and (4) a method for treating infectious
CC diseases in the subject. The anti-TIGIT antibody or its antigen-binding
CC fragment is useful for: diagnosing or treating cancer, tumor and
CC infectious disease (viral infection); and stimulating an immune response
CC in a subject. Note: Claim 9 of the specification lists possible optional
CC alterations at various positions in the present sequence which are
CC further detailed in the Features Table.
XX
SQ Sequence 119 AA;
Query Match 100.0%; Score 639; Length 119;
Best Local Similarity 100.0%;
Matches 119; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVQLVESGGGLVQPGGSLRLSCATSGFTFSDYYMYWIRQAPGKGLEWVAYITKGGGSTYY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVQLVESGGGLVQPGGSLRLSCATSGFTFSDYYMYWIRQAPGKGLEWVAYITKGGGSTYY 60
Qy 61 PDSVKGRFTISRDNAKNTLYLQMNSLRAEDTAVYYCARQTNYDFTMDYWGQGTLVTVSS 119
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 PDSVKGRFTISRDNAKNTLYLQMNSLRAEDTAVYYCARQTNYDFTMDYWGQGTLVTVSS 119
RESULT 1 from 16.rag database including CDRs 6, 7 and 8, respectively.
BGM43637
(NOTE: this sequence has 1 duplicate in the database searched.
See complete list at the end of this report)
ID BGM43637 standard; protein; 107 AA.
XX
AC BGM43637;
XX
DT 08-AUG-2019 (first entry)
XX
DE Anti-TIGIT humanized antibody light chain variable region, SEQ ID 16.
XX
KW T cell immunoreceptor Ig ITIM protein; TIGIT protein; antibody therapy;
KW antimicrobial-gen.; cancer; cytostatic; diagnostic test;
KW humanized antibody; immune stimulation; immuno-diagnosis;
KW infectious disease; light chain variable region; therapeutic;
KW viral infection; virucide.
XX
OS Mus musculus.
OS Synthetic.
XX
FH Key Location/Qualifiers
FT Region 24..34
FT /note= "CDR1"
FT Region 50..56
FT /note= "CDR2"
FT Misc-difference 58
FT /note= "Wild-type Val is optionally substituted by Ile"
FT Region 89..97
FT /note= "CDR3"
XX
CC PN WO2019129261-A1.
XX
CC PD 04-JUL-2019.
XX
CC PF 29-DEC-2018; 2018WO-CN125375.
XX
PR 30-DEC-2017; 2017WO-CN120392.
XX
CC PA (BEIG-) BEIGENE LTD.
CC PA (ZHAN/) ZHANG T.
XX
CC PI Xue L, Liu Q, Wei M, Li K;
XX
DR WPI; 2019-58574C/55.
DR N-PSDB; BGM43638.
XX
CC PT New antibody or its antigen-binding fragment, which is capable of binding
CC PT to human T cell immunoglobulin and ITIM domain (Tigit), comprises heavy
CC PT and light chain variable regions, for treating cancer, tumor or
CC PT infectious disease.
XX
CC PS Claim 5; SEQ ID NO 16; 43pp; English.
XX
CC The present invention relates to a novel antibody or its antigen-binding
CC fragment, useful in a pharmaceutical composition for treating cancer. The
CC antibody or its antigen-binding fragment specifically binds to a T cell
CC immunoglobulin and ITIM domain (TIGIT) protein and comprises: (a) a heavy
CC chain variable region (VH) of SEQ ID NO: 9, 14 or 19 (see BGM43630,
CC BGM43635 or BGM43640) containing complementarity determining regions
CC (CDRs) of SEQ ID NO: 3-5 (see BGM43624-BGM43626) or SEQ ID NO: 13 (see
CC BGM43634); and (b) a light chain variable region (VL) of SEQ ID NO: 11,
CC 16 or 21 (see BGM43632, BGM43637 or BGM43642) containing CDRs of SEQ ID
CC NO: 6-8 (see BGM43627-BGM43629). The invention further claims: (1) a
CC pharmaceutical composition comprising the antibody or its antigen-binding
CC fragment and a pharmaceutical acceptable excipient; (2) a method for
CC stimulating an immune response in a subject; (3) a method for treating
CC cancer or tumor in the subject; and (4) a method for treating infectious
CC diseases in the subject. The anti-TIGIT antibody or its antigen-binding
CC fragment is useful for: diagnosing or treating cancer, tumor and
CC infectious disease (viral infection); and stimulating an immune response
CC in a subject. Note: Claim 9 of the specification lists possible optional
CC alterations at various positions in the present sequence which are
CC further detailed in the Features Table.
XX
SQ Sequence 107 AA;
Query Match 100.0%; Score 556; Length 107;
Best Local Similarity 100.0%;
Matches 107; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EIVMTQSPATLSVSPGERATLSCKASQDVGTSVAWYQQKPGQAPRLLIYWASARHTGVPA 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EIVMTQSPATLSVSPGERATLSCKASQDVGTSVAWYQQKPGQAPRLLIYWASARHTGVPA 60
Qy 61 RFSGSGSGTEFTLTISSLQSEDFAVYYCQQYSSYPLTFGGGTKVEIK 107
|||||||||||||||||||||||||||||||||||||||||||||||
Db 61 RFSGSGSGTEFTLTISSLQSEDFAVYYCQQYSSYPLTFGGGTKVEIK 107
RESULT 1 from 9.rag database including CDRs 3, 4 and 5, respectively.
BGM43630
(NOTE: this sequence has 2 duplicates in the database searched.
See complete list at the end of this report)
ID BGM43630 standard; protein; 119 AA.
XX
AC BGM43630;
XX
DT 08-AUG-2019 (first entry)
XX
DE Anti-TIGIT monoclonal antibody heavy chain variable region, SEQ ID 9.
XX
KW Heavy chain variable region; T cell immunoreceptor Ig ITIM protein;
KW TIGIT protein; antibody therapy; antimicrobial-gen.; cancer; cytostatic;
KW diagnostic test; immune stimulation; immuno-diagnosis;
KW infectious disease; monoclonal antibody; therapeutic; viral infection;
KW virucide.
XX
OS Mus musculus.
XX
FH Key Location/Qualifiers
FT Region 31..35
FT /note= "CDR1"
FT Region 50..66
FT /note= "CDR2"
FT Region 99..108
FT /note= "CDR3"
XX
CC PN WO2019129261-A1.
XX
CC PD 04-JUL-2019.
XX
CC PF 29-DEC-2018; 2018WO-CN125375.
XX
PR 30-DEC-2017; 2017WO-CN120392.
XX
CC PA (BEIG-) BEIGENE LTD.
CC PA (ZHAN/) ZHANG T.
XX
CC PI Xue L, Liu Q, Wei M, Li K;
XX
DR WPI; 2019-58574C/55.
DR N-PSDB; BGM43631.
XX
CC PT New antibody or its antigen-binding fragment, which is capable of binding
CC PT to human T cell immunoglobulin and ITIM domain (Tigit), comprises heavy
CC PT and light chain variable regions, for treating cancer, tumor or
CC PT infectious disease.
XX
CC PS Claim 4; SEQ ID NO 9; 43pp; English.
XX
CC The present invention relates to a novel antibody or its antigen-binding
CC fragment, useful in a pharmaceutical composition for treating cancer. The
CC antibody or its antigen-binding fragment specifically binds to a T cell
CC immunoglobulin and ITIM domain (TIGIT) protein and comprises: (a) a heavy
CC chain variable region (VH) of SEQ ID NO: 9, 14 or 19 (see BGM43630,
CC BGM43635 or BGM43640) containing complementarity determining regions
CC (CDRs) of SEQ ID NO: 3-5 (see BGM43624-BGM43626) or SEQ ID NO: 13 (see
CC BGM43634); and (b) a light chain variable region (VL) of SEQ ID NO: 11,
CC 16 or 21 (see BGM43632, BGM43637 or BGM43642) containing CDRs of SEQ ID
CC NO: 6-8 (see BGM43627-BGM43629). The invention further claims: (1) a
CC pharmaceutical composition comprising the antibody or its antigen-binding
CC fragment and a pharmaceutical acceptable excipient; (2) a method for
CC stimulating an immune response in a subject; (3) a method for treating
CC cancer or tumor in the subject; and (4) a method for treating infectious
CC diseases in the subject. The anti-TIGIT antibody or its antigen-binding
CC fragment is useful for: diagnosing or treating cancer, tumor and
CC infectious disease (viral infection); and stimulating an immune response
CC in a subject.
XX
SQ Sequence 119 AA;
Query Match 100.0%; Score 637; Length 119;
Best Local Similarity 100.0%;
Matches 119; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVKLVESGGGLVQPGGSLKLSCATSGFTFSDYYMYWIRQTPEKRLEWVAYITKGGGSTYY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVKLVESGGGLVQPGGSLKLSCATSGFTFSDYYMYWIRQTPEKRLEWVAYITKGGGSTYY 60
Qy 61 PDTVKGRFTISRDNAKNTLYLQVSRLKSEDTAIYYCARQTNYDFTMDYWGQGTSVTVSS 119
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 PDTVKGRFTISRDNAKNTLYLQVSRLKSEDTAIYYCARQTNYDFTMDYWGQGTSVTVSS 119
RESULT 1 from 11.rag database including CDRs 6, 7 and 8, respectively.
BGM43632
(NOTE: this sequence has 2 duplicates in the database searched.
See complete list at the end of this report)
ID BGM43632 standard; protein; 107 AA.
XX
AC BGM43632;
XX
DT 08-AUG-2019 (first entry)
XX
DE Anti-TIGIT monoclonal antibody light chain variable region, SEQ ID 11.
XX
KW Light chain variable region; T cell immunoreceptor Ig ITIM protein;
KW TIGIT protein; antibody therapy; antimicrobial-gen.; cancer; cytostatic;
KW diagnostic test; immune stimulation; immuno-diagnosis;
KW infectious disease; monoclonal antibody; therapeutic; viral infection;
KW virucide.
XX
OS Mus musculus.
XX
FH Key Location/Qualifiers
FT Region 24..34
FT /note= "CDR1"
FT Region 50..56
FT /note= "CDR2"
FT Region 89..97
FT /note= "CDR3"
XX
CC PN WO2019129261-A1.
XX
CC PD 04-JUL-2019.
XX
CC PF 29-DEC-2018; 2018WO-CN125375.
XX
PR 30-DEC-2017; 2017WO-CN120392.
XX
CC PA (BEIG-) BEIGENE LTD.
CC PA (ZHAN/) ZHANG T.
XX
CC PI Xue L, Liu Q, Wei M, Li K;
XX
DR WPI; 2019-58574C/55.
DR N-PSDB; BGM43633.
XX
CC PT New antibody or its antigen-binding fragment, which is capable of binding
CC PT to human T cell immunoglobulin and ITIM domain (Tigit), comprises heavy
CC PT and light chain variable regions, for treating cancer, tumor or
CC PT infectious disease.
XX
CC PS Claim 5; SEQ ID NO 11; 43pp; English.
XX
CC The present invention relates to a novel antibody or its antigen-binding
CC fragment, useful in a pharmaceutical composition for treating cancer. The
CC antibody or its antigen-binding fragment specifically binds to a T cell
CC immunoglobulin and ITIM domain (TIGIT) protein and comprises: (a) a heavy
CC chain variable region (VH) of SEQ ID NO: 9, 14 or 19 (see BGM43630,
CC BGM43635 or BGM43640) containing complementarity determining regions
CC (CDRs) of SEQ ID NO: 3-5 (see BGM43624-BGM43626) or SEQ ID NO: 13 (see
CC BGM43634); and (b) a light chain variable region (VL) of SEQ ID NO: 11,
CC 16 or 21 (see BGM43632, BGM43637 or BGM43642) containing CDRs of SEQ ID
CC NO: 6-8 (see BGM43627-BGM43629). The invention further claims: (1) a
CC pharmaceutical composition comprising the antibody or its antigen-binding
CC fragment and a pharmaceutical acceptable excipient; (2) a method for
CC stimulating an immune response in a subject; (3) a method for treating
CC cancer or tumor in the subject; and (4) a method for treating infectious
CC diseases in the subject. The anti-TIGIT antibody or its antigen-binding
CC fragment is useful for: diagnosing or treating cancer, tumor and
CC infectious disease (viral infection); and stimulating an immune response
CC in a subject. Note: The present sequence is also described as a heavy
CC chain variable region on Page 5 of the specification.
XX
SQ Sequence 107 AA;
Query Match 100.0%; Score 563; Length 107;
Best Local Similarity 100.0%;
Matches 107; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIVMTQSHKFMSTSVGDRVSIICKASQDVGTSVAWYQQKPGQSPNLLIYWASARHTGVPD 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIVMTQSHKFMSTSVGDRVSIICKASQDVGTSVAWYQQKPGQSPNLLIYWASARHTGVPD 60
Qy 61 RFTGSGSGTDFTLTISNVQSEDLADYFCQQYSSYPLTFGAGTKLELK 107
|||||||||||||||||||||||||||||||||||||||||||||||
Db 61 RFTGSGSGTDFTLTISNVQSEDLADYFCQQYSSYPLTFGAGTKLELK 107
Double Patenting
9. 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.
10. Claims 1-3, 7-13, 16, 20 and 22-26 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-4 and 6-20 of U.S. Patent No. 12,234,286 B2 (issued February 25, 2025) and in further view of Grogan et al., WO 2015/009856 A2 (published 22 January 2015) and Meng et al., WO 2019/165434 A1 (published 29 August 2019). Both sets of claims read on a method of treating cancer comprising an antibody that binds TIGIT or antigen binding fragment, thereof with the same CDRs comprising in combination with additional therapeutic agents, chemotherapy, a targeted therapy, an oncolytic drug, a cytotoxic agent, an immune-based therapy, a cytokine, a surgical procedure, a radiation procedure, an activator of a costimulatory molecule, an inhibitor of an inhibitory molecule, a vaccine, or a cellular immunotherapy.
Patent No. 12,234,286 does not teach the administration of TIGIT in combination with the additional therapeutic agent that is anti PD-1 antibody.
However, Grogan teaches “…a method for treating or delaying progression of cancer…comprising administering…an effective amount of PD-1 axis binding antagonist and an agent that decreases or inhibits [T-cell immunoreceptor with Ig and ITIM domains] TIGIT expression and/or activity.”, see page 3, sections 0010-0014; and page 13, section 0077. The PD-1 axis antagonist is an anti-PD-1 antibody, see page 12, section 0075.
The method may further comprise administering additional therapy including bevacizumab, as well as chemotherapy, radiotherapy and a combination of the foregoing, see page 74, last 4 lines; and page 83, section 0264.
The agent that is able to modulate “…TIGIT expression and/or activity is an anti-TIGIT antibody or antigen-binding fragment thereof”, including Fab, Fv and F(ab’)2 fragments, see page 5, sections 0025 and 0026; page 7, section 0046; page 56, section 0167; page 59, section 0174; and page 103, section 0336.
The taught combination treatment is ablet to treat breast cancer, colorectal cancer, pancreatic cancer, head and neck cancer, gastric carcinoma, renal (kidney) cell cancer, liver cancer (hepatocellular cancer), small cell lung cancer, non-small cell lung cancer, esophageal cancer, ovarian cancer, uterine carcinoma, cervical cancer, melanoma, mesothelioma, lymphomas, leukemia, myelomas, sarcoma and other hematologic malignancies, see section 209 spanning pages 69 and 70; and section 257 spanning pages 81 and 82. The disclosed method also provides “…for reducing or inhibiting cancer relapse or cancer progression in an individual comprising administering to the individual an effect amount of a PD-1 axis binding antagonist in combination with an agent that that decreases or inhibits TIGIT expression and/or activity. As disclosed herein, cancer relapse and/or cancer progression include, without limitation, cancer metastasis.”, see section 0231 bridging pages 76 and 77.
However, Meng teaches anti-TIGIT antagonist antibody can be administered at a fixed dose range between 30 mg to about 1200 mg every three weeks and an anti-PD-L1 antibody at a fixed dose range between about 80 mg to 1600 mg every three weeks to treat a cancer, a lung cancer, as well as other solid cancers, see page 2, lines 1-14; and page 25, lines 23-36. Meng also teaches additional immunomodulatory agents, such as a PD-1 antagonist antibody can be administered, see page 25, lines 23-36.
“The term “antibody” includes monoclonal antibodies (including full-length antibodies which have an immunoglobulin Fc region), antibody compositions with polyepitopic specificity, multispecific antibodies (e.g., bispecific antibodies), diabodies, and single-chain molecules, as well as antibody fragments, including antigen-binding fragments, such as Fab, F(ab’)2, and Fv.”, see page 34, lines 36-39; and segment 2, spanning pages 89 and 90.
It would have been obvious to one of ordinary skill in the art at the
effective filing date of the claimed invention to administer both, the anti-TIGIT antibody and anti-PD1 antibody, as well as antigen-binding fragments, thereof at the dosages set forth in claims 24-26 because the range of dosages for the TIGIT antibody and other immune checkpoint antibodies have been successfully administered for treatment, see entire Meng.
One of ordinary skill in the art would have been motivated to
conclude with a reasonable expectation of success by teachings in both
references, these antibodies in combination are able to treat a number of solid cancers with the requisite dosages, see both references in their entirety.
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11. Claims 1-3, 7, 9-13, 16, 20 and 22-26 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-8, 10 and 11 of U.S. Patent No. 11,214,616 B2 (issued January 4, 2022) in view of Grogan et al., WO 2015/009856 A2 (published 22 January 2015) and Meng et al., WO 2019/165434 A1 (published 29 August 2019). Both sets of claims read on treating disorders comprising administering an antibody that binds TIGIT or antigen binding fragment, thereof with the same CDRS.
Patent No. 11,214,616 does not teach administering the TIGIT antibody in combination with additional therapeutic agents, anti PD-1 antibody, chemotherapy, chemoradiotherapy and bevacizumab at requisite dosages.
However, Grogan teaches “…a method for treating or delaying progression of cancer…comprising administering…an effective amount of PD-1 axis binding antagonist and an agent that decreases or inhibits [T-cell immunoreceptor with Ig and ITIM domains] TIGIT expression and/or activity.”, see page 3, sections 0010-0014; and page 13, section 0077. The PD-1 axis antagonist is an anti-PD-1 antibody, see page 12, section 0075.
The method may further comprise administering additional therapy including bevacizumab, as well as chemotherapy, radiotherapy and a combination of the foregoing, see page 74, last 4 lines; and page 83, section 0264.
The agent that is able to modulate “…TIGIT expression and/or activity is an anti-TIGIT antibody or antigen-binding fragment thereof”, including Fab, Fv and F(ab’)2 fragments, see page 5, sections 0025 and 0026; page 7, section 0046; page 56, section 0167; page 59, section 0174; and page 103, section 0336.
The taught combination treatment is ablet to treat breast cancer, colorectal cancer, pancreatic cancer, head and neck cancer, gastric carcinoma, renal (kidney) cell cancer, liver cancer (hepatocellular cancer), small cell lung cancer, non-small cell lung cancer, esophageal cancer, ovarian cancer, uterine carcinoma, cervical cancer, melanoma, mesothelioma, lymphomas, leukemia, myelomas, sarcoma and other hematologic malignancies, see section 209 spanning pages 69 and 70; and section 257 spanning pages 81 and 82. The disclosed method also provides “…for reducing or inhibiting cancer relapse or cancer progression in an individual comprising administering to the individual an effect amount of a PD-1 axis binding antagonist in combination with an agent that that decreases or inhibits TIGIT expression and/or activity. As disclosed herein, cancer relapse and/or cancer progression include, without limitation, cancer metastasis.”, see section 0231 bridging pages 76 and 77.
However, Meng teaches anti-TIGIT antagonist antibody can be administered at a fixed dose range between 30 mg to about 1200 mg every three weeks and an anti-PD-L1 antibody at a fixed dose range between about 80 mg to 1600 mg every three weeks to treat a cancer, a lung cancer, as well as other solid cancers, see page 2, lines 1-14; and page 25, lines 23-36. Meng also teaches additional immunomodulatory agents, such as a PD-1 antagonist antibody can be administered, see page 25, lines 23-36.
“The term “antibody” includes monoclonal antibodies (including full-length antibodies which have an immunoglobulin Fc region), antibody compositions with polyepitopic specificity, multispecific antibodies (e.g., bispecific antibodies), diabodies, and single-chain molecules, as well as antibody fragments, including antigen-binding fragments, such as Fab, F(ab’)2, and Fv.”, see page 34, lines 36-39; and segment 2, spanning pages 89 and 90.
It would have been obvious to one of ordinary skill in the art at the
effective filing date of the claimed invention to administer both, the anti-TIGIT antibody and anti-PD1 antibody, as well as antigen-binding fragments, thereof at the dosages set forth in claims 24-26 because the range of dosages for the TIGIT antibody and other immune checkpoint antibodies have been successfully administered for treatment, see entire Meng.
One of ordinary skill in the art would have been motivated to
conclude with a reasonable expectation of success by teachings in both
references, these antibodies in combination are able to treat a number of solid cancers with the requisite dosages, see both references in their entirety.
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RESULT 1 from 3fus4fus5.align.rapbm database.
US-16-958-262-9
(NOTE: this sequence has 4 duplicates in the database searched.
See complete list at the end of this report)
Sequence 9, US/16958262
Publication No. US20200331999A1
GENERAL INFORMATION
APPLICANT: BeiGene, Ltd.
APPLICANT: Zhang, Tong
APPLICANT: Xue, Liu
APPLICANT: Liu, Qi
APPLICANT: Wei, Min
APPLICANT: Li, Kang
TITLE OF INVENTION: Anti-TIGIT antibodies and their use as therapeutics and
TITLE OF INVENTION: diagnostics
FILE REFERENCE: BEIG-033/01US
CURRENT APPLICATION NUMBER: US/16/958,262
CURRENT FILING DATE: 2020-06-26
PRIOR APPLICATION NUMBER: PCT/CN2018/125375
PRIOR FILING DATE: 2018-12-29
PRIOR APPLICATION NUMBER: PCT/CN2017/120392
PRIOR FILING DATE: 2017-12-30
NUMBER OF SEQ ID NOS: 24
SEQ ID NO 9
LENGTH: 119
TYPE: PRT
ORGANISM: Mus musculus
Query Match 86.7%; Score 160.4; Length 119;
Best Local Similarity 41.0%;
Matches 32; Conservative 0; Mismatches 0; Indels 46; Gaps 2;
Qy 1 DYYMY--------------YITKGGGSTYYPDTVKG------------------------ 22
||||| |||||||||||||||||
Db 31 DYYMYWIRQTPEKRLEWVAYITKGGGSTYYPDTVKGRFTISRDNAKNTLYLQVSRLKSED 90
Qy 23 --------QTNYDFTMDY 32
||||||||||
Db 91 TAIYYCARQTNYDFTMDY 108
Conclusion
14. 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.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
ALANA HARRIS DENT
Primary Examiner
Art Unit 1643
06 February 2026
/Alana Harris Dent/ Primary Examiner, Art Unit 1643