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 .
Response to Arguments and Amendments
2. Claims 1, 13-28, 33-35 and 40-56 are pending.
Claims 41 and 43, drawn to non-elected inventions and non-elected species are withdrawn from consideration.
Claims 17, 19, 20 and 27 have been amended.
Claims 1, 13-28, 33-35, 40, 42 and 44-56 are examined on the merits with the species (solid tumor): melanoma.
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Withdrawn Objections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. The objection of claims 17, 19 and 20 is withdrawn in light of the amendment (addition of the punctuation mark, a period at the end of the claim text) to the said claims, see Amendments to the Claims submitted April 15, 2026, page 2.
Withdrawn Grounds of Rejection
Claim Rejections - 35 USC § 103
5. The rejection of claim(s) 1, 13-28, 33-35, 40, 42 and 44-56 under 35 U.S.C. 103 as being unpatentable over Brennan et al., WO 2017/079117 A1 (published 11 May 2017/ IDS reference C1 submitted May 2, 2022), and further in view of Inamdar et al., WO 2020/047087 A1 (effective priority date 29 August 2018/ IDS reference C3 submitted May 2, 2022) is withdrawn in light of Applicant’s signed statement on the record that the common ownership existed “not later than the effective filing date of the claimed invention” pursuant to the First-Inventor-to-File (FITF) provisions of the America Invents Act (AIA ) invoking exception under 35 U.S.C. 102(b)(2)(C), see Remarks submitted April 15, 2026, page 6, 4th and 5th paragraphs (paras.).
Double Patenting
6. The nonstatutory double patenting rejection of claims 1, 13-28, 33-35, 40, 42 and 44-56 over claims 1-4, 10-14, 24, 25 and 35 of U.S. Patent No. 10,273,281 B2 (issued April 30, 2019) in view of Inamdar et al., WO 2020/047087 A1 (effective priority date 29 August 2018/ IDS reference C3 submitted May 2, 2022) is withdrawn in light of Applicant’s signed statement on the record that the common ownership existed “not later than the effective filing date of the claimed invention” pursuant to the First-Inventor-to-File (FITF) provisions of the America Invents Act (AIA ) invoking exception under 35 U.S.C. 102(b)(2)(C), see Remarks submitted April 15, 2026, page 6, 4th and 5th paras.
7. The provisional nonstatutory double patenting rejection of claims 1, 13-28, 33-35, 40, 42 and 44-56 provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3-50, 52, 53, 55 and 58-69 of copending Application No. 17/904,928 (filed August 24, 2022) is withdrawn in light of the abandonment of the said copending application.
New 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. Claim(s) 1, 13-28, 33-35, 40, 42 and 44-56 is/are rejected under 35 U.S.C. 103 as being unpatentable over Brennan et al., WO 2017/079117 A1 (published 11 May 2017/ IDS reference C1 submitted May 2, 2022), and further in view of Brennan, Bellovin et al., US 2017/0145071 A1 (published May 25, 2017) referenced herein as Bellovin and Koya et al. (Cancer Res. 72(16):3928-3937, August 15, 2012). Brennan teaches the fusion protein (sequence 20) comprising the amino acid sequence set forth in SEQ ID NO: 5, see sequence alignment at close of rejection; and page 67, sequence 20. Brennan teaches the extracellular domain (ECD) of human cluster of differentiation 80 (CD80) comprises the amino acid sequence (sequence 5) set forth in SEQ ID NO: 1, see sequence alignment; and page 65, sequence 5. Brennan also teaches the fragment crystallizable (Fc) domain of human immunoglobulin G1 (IgGI) comprising the amino acid sequence (sequence 9) set forth in SEQ ID NO: 3, see sequence alignment at close of rejection; and page 66, sequence 9; and page 67, underlined amino acid residues within sequence 20. All three of Applicant’s sequences share 100% sequence similarity with Brennan’s sequences, see sequence alignments.
“[T]he fusion molecule comprises an Fc domain, such as an Fc domain comprising a sequence selected from SEQ ID NOs: 9…[which is the same as Applicant’s SEQ ID NO 3]. .. In some embodiments, the CD80 ECD fusion molecule comprises an amino acid sequence … SEQ ID NO: 20 [which is the same as Applicant’s SEQ ID NO: 5] ..., see section 006 spanning pages 2 and 3. “In some embodiments, the CD80 ECD fusion molecule and the fusion partner… are directly linked such that the…C-terminal amino acid of the Fc immediately precedes or follows the N- or C-terminal amino acid of the CD80 ECD amino acid sequence, see page 31, section 00101. “In some embodiments, the CD80 ECD fusion molecule may be attached to the CD80 ECD through a linker peptide, such as a GS linker.”, see section 006 spanning pages 2 and 3.
“In some embodiments, the CD80 ECD fusion molecule has a sialic acid content of 10-60 mol sialic acid (SA)/mol protein, such as 15-60 mol SA/mol protein.”, see page 3, 1st sentence in section 007; and section 00110 spanning pages 34 and 35.
These fusion molecules are implemented in “…methods of treating cancer in a subject comprising administering to the subject an effective amount of a CD80 ECD or CD80 ECD fusion protein or a composition from among the embodiments described above. In some embodiments, the cancer is a solid tumor.”, see section 0015 on page 5. “In some embodiments, the cancer is recurrent or progressive after a therapy selected from surgery, chemotherapy, radiation therapy, or a combination thereof.”, see page 6, lines 1 and 2; and page 10, last 3 lines.
Brennan used the murine melanoma cell line B16-F10, art known to be a highly metastatic cell and implemented in experiments for studying tumor growth and metastasis, see B16 tumor model segment beginning on page 63. “[T]reatment with murine CD80 ECD-Fc at 20 mol/mol SA…”, see page 64, section 00205. Hence, administration of taught disclosed therapeutic agents is recognized as within an advanced or metastatic stetting.
The “…fusion molecules may be administered in vivo by various routes, including…intravenous,”, see page 43, section 00150. “[A]n effective dose is administered more than once a month, such as, for example, every three weeks, every two weeks or every week. In some embodiments, an effective dose is administered once per 1, 2, 3, 4, or 5 weeks.”, see page 45, section 00155.
“Also provided herein are compositions comprising a CD80 ECD or CD80 ECD fusion molecule of any of the embodiments described above, and further comprising at least one pharmaceutically acceptable carrier. Some such compositions further comprise at least one additional therapeutic agent.”, see page 5, section 011. The said fusion protein can be administered “…in combination with other therapeutic agents, such as immune stimulating agents such as PD-1/PD-L1 inhibitors”… comprising nivolumab and pembrolizumab, see abstract; and pages 5-9. “In some cases, one or more doses of the PD-l/PD-L1 inhibitor are administered prior to administering the CD 80 ECD or CD 80 ECD fusion molecule. In some cases, the subject has received a complete course of immune stimulating agent, e.g., PD-l/PD-L1 inhibitor therapy prior to administration of the CD80 ECD or CD80 ECD fusion molecule.”, see page 6, section 0019. Given Brennan notes “[i]n some cases”, conversely, in other cases there are no doses or prior therapy of PD-1/PD-L1 antagonists. Likewise, Brennan states “CD80 ECDs or CD80 ECD fusion molecules may be administered alone, with PD-1 /PD-L1 inhibitors, and/ or with other modes of treatment. CD80 ECDs or CD80 ECD fusion molecules may be provided before, substantially contemporaneous with, or after other modes of treatment, for example, surgery, chemotherapy, radiation therapy, or the administration of another biologic.“, see page 46, lines 1-3. Hence, conversely, the patient may also receive prior therapy with at least one anti-angiogenic agent.
Additional therapeutic agents that can be administered in combination with the said fusion protein includes anti-angiogenesis agents, “…antibodies to VEGF-A (e.g., bevacizumab (Avastin®),… Sutent®/SU11248 (sunitinib malate),… Anti-angiogenesis agents also include native angiogenesis inhibitors, e.g., angiostatin, endostatin,…”, page 49, section 00162.
Brennan does not teach the taught ECD CD80 IgG1 is administered to the subject in the dosage of about 140 mg to about 1,260 mg. Nor does Brennan teach the malignant melanoma taught has a BRAF mutation and the subject has received prior therapy with a BRAF inhibitor, vemurafenib or dabrafenib.
Bellovin teaches CD80 (B7-1) extracellular domain (ECD) polypeptides and CD80-ECD fusion molecules and their use in treatment of cancer including melanoma in a range of 0.3mg/kg to 3mg/kg, alone and in combination with other therapeutic agents, such as immune stimulating agents such as PD-1/PD-L1 inhibitors, as well as anti-angiogenesis agents., see page 1, section 0002; page 2, sections 0009 and 0015; page 3, section 0022; page 4; Therapeutic…segment beginning on page 11-13.
Koya teaches combinatorial anti-cancer therapy includes immunotherapy with targeted therapy blocking oncogenic BRAFV600 -driven murine model of melanoma, SM1, see Abstract on page 3928.
BRAF inhibitors are vemurafenib (formerly PLX4032 or RG7204) or dabrafenib (formerly GSK2118436), which are two highly active agents for the treatment of BRAFV600 mutant melanoma.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to administer the therapeutic ECD CD80 fusion protein at the dosages ranging from about 140 mg to about 1,260 mg and administer a BRAF inhibitor in manner cited in claims 53-55 because both, Brennan and Bellovin teach an “effective amount” or “therapeutically effective amount”, see Brennan, page 25, section 0081; and Bellovin, page 9, section 0081. These said amounts refer “…to an amount of a drug effective to treat a disease or disorder in a subject. In certain embodiments, an effective amount refers to an amount effective, at dosages and for periods of time necessary, to achieve the desired therapeutic or prophylactic result.”, see Brennan, page 25, section 0081; and Bellovin, page 9, section 0081.
One of ordinary skill in the art would have been motivated to administer BRAF inhibitor in the manner cited in claims 53-55 because Brennan teaches administering additional therapeutics in the same manner.
One of ordinary skill in the art would have been motivated to arrive at the designated dosages in claims 1 and 13-20 given teachings well known in the art and noted herein that dosages of any pharmaceutical composition may be adjusted and optimized.
It also would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to substitute the melanoma model of Brennan with the BRAFV600 -driven murine model of melanoma of Bellovin and include a BRAF inhibitor to implement another anti-angiogenesis, thereby allowing assessment of a single agent or a combination of agents. One of ordinary skill in the art would have been motivated to because it is obvious to those skilled in the art to substitute one known equivalent for another. See In re Omeprazole Patent Litigation, 483 F.3d 1364, 1374 (Fed. Cir. 2007) (“[T]his court finds no . . . error in [the] conclusion that it would have been obvious to one skilled in the art to substitute one ARC [alkaline reactive compound] for another.”).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to treat the melanoma with a BRAF inhibitor given it is art known a high percentage of skin melanomas have a BRAF mutation and Koya plainly states this particular model is able “…to test the potential beneficial effects of adding an immunotherapy strategy to the treatment with vemurafenib.”, see page 3931, last sentence in column 2. One of ordinary skill in the art would have been motivated to treat this mutation with a BRAF inhibitor given the experiments within Koya have an overlapping treatment regimen, as well as it is known “combined therapy with the BRAFV600-specific inhibitor vemurafenib and TCR-engineered ACT resulted in superior antitumor effects against a fully [syngeneic] BRAFV600E mutant melanoma., see page 3936, 1st column; and entire Koya document.
RESULT 1 from 5.rag database. The human IgG1 Fc region, SEQ ID NO:9 is underlined herein.
BDW52843
(NOTE: this sequence has 10 duplicates in the database searched)
ID BDW52843 standard; protein; 440 AA.
DT 29-JUN-2017 (first entry)
XX
DE CD80-IgG1 Fc fusion protein, SEQ:20.
XX
KW CD80; Immunoglobulin G1; bladder cancer; breast tumor; cancer;
KW colorectal tumor; cytostatic; endometrioid carcinoma; fusion protein;
KW head and neck tumor; hepatocellular carcinoma; immunoglobulin gamma 1;
KW melanoma; non-small-cell lung cancer; ovary tumor; pancreas tumor;
KW protein therapy; recombinant protein; renal cell carcinoma;
KW squamous cell carcinoma; stomach tumor; therapeutic.
XX
OS Homo sapiens.
OS Synthetic.
XX
FH Key Location/Qualifiers
FT Region 1..208
FT /note= "CD80 protein"
FT Region 209..440
FT /note= "IgG1 protein"
XX
CC PN WO2017079117-A1.
XX
CC PD 11-MAY-2017.
XX
CC PF 01-NOV-2016; 2016WO-US059838.
XX
PR 02-NOV-2015; 2015US-0249836P.
PR 11-AUG-2016; 2016US-0373654P.
XX
CC PA (FIVE-) FIVE PRIME THERAPEUTICS INC.
XX
CC PI Brennan T, Bellovin D, Busha D, Sennino B;
XX
DR WPI; 2017-301449/39.
XX
CC PT New cluster of differentiation (CD)-80 extracellular domain (ECD) fusion
CC PT molecule comprising human CD80 ECD polypeptide and immunoglobulin-G1
CC PT fragment crystallizable domain and having specified amount of sialic
CC PT acid, used to treat cancer.
XX
CC PS Claim 45; SEQ ID NO 20; 94pp; English.
XX
CC The present invention relates to a novel cluster of differentiation (CD)-
CC 80 extracellular domain (ECD) fusion molecule useful for treating cancer
CC in a subject. The invention further claims: (1) a method for enhancing
CC the efficacy of CD80 ECD fusion protein in treating cancer in a subject;
CC (2) a method for treating cancer in a subject; (3) a CD80 ECD fusion
CC molecule comprising a human CD80 ECD polypeptide and a human IgG1 Fc
CC domain with L234F, L235E, and P331S amino acid substitutions; and (4) a
CC composition comprising the CD80 ECD fusion molecule. Cancer can be
CC colorectal cancer, breast cancer, gastric cancer, non-small cell lung
CC cancer, melanoma, squamous cell carcinoma of head and neck, ovarian
CC cancer, pancreatic cancer, renal cell carcinoma, hepatocellular
CC carcinoma, bladder cancer or endometrial cancer. The present sequence is
CC a CD80-IgG1 Fc fusion protein comprising human CD80 ECD fused with human
CC IgG1 Fc region, which is useful in preparing a pharmaceutical composition
CC for treating cancer in a subject.
XX
SQ Sequence 440 AA;
Query Match 100.0%; Score 2360; Length 440;
Best Local Similarity 100.0%;
Matches 440; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 VIHVTKEVKEVATLSCGHNVSVEELAQTRIYWQKEKKMVLTMMSGDMNIWPEYKNRTIFD 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 VIHVTKEVKEVATLSCGHNVSVEELAQTRIYWQKEKKMVLTMMSGDMNIWPEYKNRTIFD 60
Qy 61 ITNNLSIVILALRPSDEGTYECVVLKYEKDAFKREHLAEVTLSVKADFPTPSISDFEIPT 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 ITNNLSIVILALRPSDEGTYECVVLKYEKDAFKREHLAEVTLSVKADFPTPSISDFEIPT 120
Qy 121 SNIRRIICSTSGGFPEPHLSWLENGEELNAINTTVSQDPETELYAVSSKLDFNMTTNHSF 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 SNIRRIICSTSGGFPEPHLSWLENGEELNAINTTVSQDPETELYAVSSKLDFNMTTNHSF 180
Qy 181 MCLIKYGHLRVNQTFNWNTTKQEHFPDNEPKSSDKTHTCPPCPAPELLGGPSVFLFPPKP 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 MCLIKYGHLRVNQTFNWNTTKQEHFPDNEPKSSDKTHTCPPCPAPELLGGPSVFLFPPKP 240
Qy 241 KDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLT 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 KDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLT 300
Qy 301 VLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTC 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 301 VLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTC 360
Qy 361 LVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSV 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 361 LVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSV 420
Qy 421 MHEALHNHYTQKSLSLSPGK 440
||||||||||||||||||||
Db 421 MHEALHNHYTQKSLSLSPGK 440
BDW52828 from 1.rag database.
ID BDW52828 standard; protein; 208 AA.
DT 29-JUN-2017 (first entry)
XX
DE Human CD80 ECD protein, SEQ:5.
XX
KW CD80; bladder cancer; breast tumor; cancer; colorectal tumor; cytostatic;
KW endometrioid carcinoma; head and neck tumor; hepatocellular carcinoma;
KW melanoma; non-small-cell lung cancer; ovary tumor; pancreas tumor;
KW protein therapy; recombinant protein; renal cell carcinoma;
KW squamous cell carcinoma; stomach tumor; therapeutic.
XX
OS Homo sapiens.
XX
FH Key Location/Qualifiers
FT Misc-difference 1..208
XX
CC PN WO2017079117-A1.
XX
CC PD 11-MAY-2017.
XX
CC PF 01-NOV-2016; 2016WO-US059838.
XX
PR 02-NOV-2015; 2015US-0249836P.
PR 11-AUG-2016; 2016US-0373654P.
XX
CC PA (FIVE-) FIVE PRIME THERAPEUTICS INC.
XX
CC PI Brennan T, Bellovin D, Busha D, Sennino B;
XX
DR WPI; 2017-301449/39.
XX
CC PT New cluster of differentiation (CD)-80 extracellular domain (ECD) fusion
CC PT molecule comprising human CD80 ECD polypeptide and immunoglobulin-G1
CC PT fragment crystallizable domain and having specified amount of sialic
CC PT acid, used to treat cancer.
XX
CC PS Claim 45; SEQ ID NO 5; 94pp; English.
XX
CC The present invention relates to a novel cluster of differentiation (CD)-
CC 80 extracellular domain (ECD) fusion molecule useful for treating cancer
CC in a subject. The invention further claims: (1) a method for enhancing
CC the efficacy of CD80 ECD fusion protein in treating cancer in a subject;
CC (2) a method for treating cancer in a subject; (3) a CD80 ECD fusion
CC molecule comprising a human CD80 ECD polypeptide and a human IgG1 Fc
CC domain with L234F, L235E, and P331S amino acid substitutions; and (4) a
CC composition comprising the CD80 ECD fusion molecule. Cancer can be
CC colorectal cancer, breast cancer, gastric cancer, non-small cell lung
CC cancer, melanoma, squamous cell carcinoma of head and neck, ovarian
CC cancer, pancreatic cancer, renal cell carcinoma, hepatocellular
CC carcinoma, bladder cancer or endometrial cancer. The present sequence is
CC a human CD80 ECD protein, which is useful in preparing a pharmaceutical
CC composition for treating cancer in a subject.
XX
SQ Sequence 208 AA;
BDW52832 from 3.rag database.
ID BDW52832 standard; protein; 232 AA.
DT 29-JUN-2017 (first entry)
XX
DE Human IgG1 Fc region, SEQ:9.
XX
KW Immunoglobulin G1; Immunoglobulin gamma 1; bladder cancer; breast tumor;
KW cancer; colorectal tumor; cytostatic; endometrioid carcinoma;
KW head and neck tumor; heavy chain constant region;
KW hepatocellular carcinoma; melanoma; non-small-cell lung cancer;
KW ovary tumor; pancreas tumor; protein therapy; recombinant protein;
KW renal cell carcinoma; squamous cell carcinoma; stomach tumor;
KW therapeutic.
XX
OS Homo sapiens.
XX
CC PN WO2017079117-A1.
XX
CC PD 11-MAY-2017.
XX
CC PF 01-NOV-2016; 2016WO-US059838.
XX
PR 02-NOV-2015; 2015US-0249836P.
PR 11-AUG-2016; 2016US-0373654P.
XX
CC PA (FIVE-) FIVE PRIME THERAPEUTICS INC.
XX
CC PI Brennan T, Bellovin D, Busha D, Sennino B;
XX
DR WPI; 2017-301449/39.
XX
CC PT New cluster of differentiation (CD)-80 extracellular domain (ECD) fusion
CC PT molecule comprising human CD80 ECD polypeptide and immunoglobulin-G1
CC PT fragment crystallizable domain and having specified amount of sialic
CC PT acid, used to treat cancer.
XX
CC PS Claim 44; SEQ ID NO 9; 94pp; English.
XX
CC The present invention relates to a novel cluster of differentiation (CD)-
CC 80 extracellular domain (ECD) fusion molecule useful for treating cancer
CC in a subject. The invention further claims: (1) a method for enhancing
CC the efficacy of CD80 ECD fusion protein in treating cancer in a subject;
CC (2) a method for treating cancer in a subject; (3) a CD80 ECD fusion
CC molecule comprising a human CD80 ECD polypeptide and a human IgG1 Fc
CC domain with L234F, L235E, and P331S amino acid substitutions; and (4) a
CC composition comprising the CD80 ECD fusion molecule. Cancer can be
CC colorectal cancer, breast cancer, gastric cancer, non-small cell lung
CC cancer, melanoma, squamous cell carcinoma of head and neck, ovarian
CC cancer, pancreatic cancer, renal cell carcinoma, hepatocellular
CC carcinoma, bladder cancer or endometrial cancer. The present sequence is
CC a human IgG1 Fc region, which is useful in preparing a pharmaceutical
CC composition for treating cancer in a subject.
XX
SQ Sequence 232 AA;
Query Match 100.0%; Score 1258; Length 232;
Best Local Similarity 100.0%;
Matches 232; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EPKSSDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKF 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EPKSSDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKF 60
Qy 61 NWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKT 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKT 120
Qy 121 ISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTP 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 ISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTP 180
Qy 181 PVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK 232
||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 PVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK 232
Conclusion
10. 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 normally 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 on 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
17 June 2026
/Alana Harris Dent/Primary Examiner, Art Unit 1643
Prosecution Insights