Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
DETAILED ACTION
Status of the Claims
1. Claims 1-17 are the original claims filed 3/14/2024. IN the preliminary amendment of 7/22/2024, Claims 16-17 are canceled and new claims 18-19 are added.
Claims 1-15 and 18-19 are the claims under examination.
Priority
2. USAN 18/605,139, filed 03/14/2024, is a Continuation of 16/449,154, filed 06/21/2019, now abandoned and having 1 RCE-type filing therein,
16/449,154 is a Continuation of 15/379,058, filed 12/14/2016, now U.S. Patent # 10/358,500, 15/379,058 is a Divisional of 14/677,815, filed 04/02/2015, now U.S. Patent # 9546214, 14/677,815 Claims Priority from Provisional Application 62/081,497, filed 11/18/2014, 14/677,815 Claims Priority from Provisional Application 61/975,589, filed 04/04/2014.
Applicants effective date of filing for a human or humanized antibody binding human LRG5 and having anti-neoplastic activity along with cancer stem cell reducing activity for colon cancer is 4/4/2014 for Provisional Application No. 61/975,589.
Information Disclosure Statement
3. As of 9/10/2026, one (1) IDS is filed: 7/22/2024. The corresponding initialed and dated 1449 form is considered and of record.
Objections
Specification
4. The disclosure is objected to because of the following informalities:
a) The use of the term RNeasy, NCBI, SpectraMax, ATCC, and TGEN, which is a trade name or a mark used in commerce, has been noted in this application. The term should be accompanied by the generic terminology; furthermore the term should be capitalized wherever it appears or, where appropriate, include a proper symbol indicating use in commerce such as ™, SM , or ® following the term.
Although the use of trade names and marks used in commerce (i.e., trademarks, service marks, certification marks, and collective marks) are permissible in patent applications, the proprietary nature of the marks should be respected and every effort made to prevent their use in any manner which might adversely affect their validity as commercial marks.
Claim Objections
5. Claims 1-15 and 18-19 are objected to because of the following informalities:
a) Claims 1-15 and 18-19 are objected to for improper punctuation throughout. Amend the claims to recite: “LGR5-expressing”; “in vivo,”; “claim 1,”; and “claim 14,”.
b) Amend claim 13 to recite “...of claim 1, comprised in a lyophilized form.”
c) Amend claim 15 to recite “...of claim 14, wherein the composition is for intravenous administration.”
Appropriate correction is required.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
6. Claims 1-15 and 18-19 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
a) Claims 1-15 and 18-19 are indefinite for reciting “SEQ ID NO: 31” that is otherwise shown in the XML file of 7/22/2026 as a skipped sequence. The specification shows the sequence for SEQ ID NO 31 in “LTS” at [0066]. The phrase “SEQ ID NO:31” is required to be replaced with the actual sequence throughout the claim set. MPEP 2412.05(a).
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Scope of Enablement
7. Claims 8-11 and 18-19 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for:
a) for inhibiting growth of an LGR5-expressing lung, breast, colon, colorectal or pancreatic cancer or neoplastic cell, in vivo, using the anti-LGR5 antibody, 18G7H6A3 (BNC101), in standard of care (SOC) therapy (i.e., Gemzar® and Abraxane® in JH109 and Gemzar® alone in PANCl and ASPC1; and
b) for inhibiting metastatic colorectal cancer growth in vivo, by prophylactic treatment with FOLFIRI in combination with 18G7H6A3 (BNC101),
does not reasonably provide enablement for inhibiting growth of any humanLGR5-expressing tumor, in vivo, with just any variant to the VHCDR1 for the 18G7H6A3 (BNC101) clone and absent the SOC or chemotherapy combination. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
Factors to be considered in determining whether undue experimentation is required, are summarized in In re Wands, 8 USPQ2d 1400 (Fed. Cir. 1988). They include the nature of the invention, the state of the prior art, the relative skill of those in the art, the amount of direction or guidance disclosed in the specification, the presence or absence of working examples, the predictability of the art, the breadth of the claims, the quantity of experimentation which would be required in order to practice the invention as claimed.
Disclosure in the Specification
The working examples demonstrate the results from the in vitro experiments and importantly the in vivo animal model correlates for human cancer models (colorectal, lung, breast, colon or pancreatic cancer) in Examples 8-10 (colorectal); 11, 17-18, 51 (pancreatic); 12 (triple negative breast); 50 (lung). Example 23 exemplifies 18G7H6A3 in combination with FOLFIRI showed significant prophylactic anti-tumor activity compared to FOLFIRI alone (FIG. 10).
The scope of the claims must bear a reasonable correlation with the scope of enablement. See In re Fisher, 166 USPQ 19, 24 (CCPA 1970). "[T]o be enabling, the specification of a patent must teach those skilled in the art how to make and use the full scope of the claimed invention without undue experimentation.'" Genentech, Inc. v. Novo Nordisk, A/S, 108 F.3d 1361, 1365 (Fed. Cir. 1997) (quoting In re Wright, 999 F.2d 1557, 1561 (Fed. Cir. 1993)).
Prior Art Status: Immunotherapeutics in cancer therapy is unpredictable
The use of antibody immunotherapy for the treatment of tumors has been shown to have limitations. Five (5) art references spanning over 25 years in the field of immunotherapeutics and recognizing the complexity of antibody delivery to tumors in vivo are Fujimori et al. (J. Nuc. Med. 31:1191-1198 (1990) IDS 7/22/2024); Beckman et al. (Can. 109:170-179 (2007) IDS 7/22/2024); Thurber et al. (Adv. Drug Deliv. Rev. 60:1421-1434 (2008) IDS 7/22/2024); Rudnick et al. (Can. Biotherp. & Radiopharm. 24: 155-162 (2009) IDS 7/22/2024); and Huang et al. (Appl Microbiol Biotechnol (2010) 87:401–410) IDS 7/22/2024).
Fujimori teaches for further understanding of Mab distribution in the tumor, one must consider the microscopic pharmacology as well: transport across the capillary wall, transport in tumor interstitium, cellular binding and metabolism. Fujimori discusses predictive models for accessing tumor antigen availability by Mab to examine the relationship between affinity and distribution. Fujimori teaches on p. 1196, Col. 2, ¶1:
“One strategy to overcome the binding-site barrier would be to increase the initial Mab dose. Even though Mab concentration in tumors does not always increase linearly as initial Mab concentration increases, a high initial plasma concentration leads to better percolation and results in more uniform distribution in tumor. Increasing Mab dose, however, decreases the specificity ratio and may cause toxicity or other side effects. For each Mab species and set of circumstances, there is an inherent balance of factors. Other causes of heterogeneous distribution include the functional and anatomical heterogeneity of tumors and their vessels..., and the elevated interstitial tissues…”
Beckman teaches on p. 175, Col. 2, ¶2-4:
“Optimizing biodistribution properties of Ab constructs depends on many host and tumor variables. These include: the density and distribution of target Ag in tumors and normal tissues: the degree of target occupancy and residence time required for tumor cell kill; possible toxicities from normal tissue distribution; tumor size and vascularity; tumor interstitial pressure, convection and diffusion; and metabolism and internalization rates for Ab-Ag constructs. An equally large number of Ab construct and therapy variables are available for optimization, including size, charge, and valence; constant region type and glycosylation pattern; presence or absence of a radioisotope or a toxic moiety; dose, route, and schedule of administration; and use of a traditional or a pretargeting strategy. Given the complexity of the problem, systematic preclinical programs may enhance the likelihood of success in subsequent clinical studies. Such preclinical investigations should integrate both experimental and theoretical approaches.
Preclinical studies of a putative Ab-based therapeutic agent can encompass a variety of constructs, differing in molecular weight, affinity, valence, and/or other features of interest, which bind to the same epitope as demonstrated by competition experiments. The Ag density and target affinities should be known for both tumor cells and cross-reacting normal tissues, and the percent target occupancy and required residence time for tumor cell kill should ideally be investigated in vitro. Similarly, rate constants for Ab-Ag internalization should be determined, if applicable. Dose and schedule should be varied and antitumor efficacy, pharmacokinetics, overall biodistribution, homogeneity of intratumoral distribution, and tumor microvessel density and distribution ideally should be measured in tumor-bearing animals with a variety of tumor sizes.”
Studies in tumor-bearing rodents are often confounded by lack of normal tissue reactivity with Ab constructs directed toward human Ags, but studies in transgenic animal can be performed in some instances to alleviate this issue.”
Thurber teaches on p. 1431, Col 2, ¶3:
“Analyzing the fundamental rates that determine antibody uptake and distribution provides a theoretical framework for understanding and interpreting targeting experiments and improving on the limitations of uptake. It also provides a background for a more rational design of in vitro experiments, animal studies, and clinical trials. The insight gained from this type of modeling has multiple implications for imaging and therapy. For example, not all cells are exposed to the “average” concentration obtained in a tumor. A significant portion of cells can survive even if the tumor-averaged concentration is well above the LD50 in vitro. Also, the concentration that cells in a solid tumor are exposed to ([Ab]surf) is well below the plasma concentration. This means that the bulk antibody concentration in an in vitro spheroid experiment is not analogous to the plasma concentration but is actually well below it; large doses are required to overcome this poor extravasation. Knowing the rate of uptake in a tumor and clearance from the plasma and normal tissues also provides estimates of ratios between tumor and normal tissue concentrations, and these ratios are important in both imaging and therapy. These examples illustrate the utility of combining theoretical analysis also suggest ways to rationally improve uptake, and determining the limiting rates is the first step in overcoming these problems.”
Rudnick teaches on p. 155, Col. 2:
“Not strictly limited to tumor cells, target antigen is commonly expressed on normal tissue, found in circulation, and shed into the tumor interstitial space. These nontarget pools of antigens can reduce treatment effectiveness, increase systemic clearance, and increase side-effects (especially for radioimmunoconjugates) by impairing mAb specificity for the tumor.”
and on p. 158, Col. 2, last ¶ - p. 159, Col. 1:
“…antigen selection will be a critical factor for internalization and catabolism of mAbs. The relative rates of antigen recycling and dissociation are important in mAb penetration into tumors. Therefore, in applications dependent on targeting every cell of a tumor, the mAb needs to dissociate before it is internalized and degraded. In the case of ADCC, a slow internalizing antigen would be the best target. However, if one is trying to deliver a cytotoxic agent to the cytoplasm of cells in a limited region of a tumor, such as the vasculature, a mAb with slow dissociation targeting a rapidly recycling antigen would be appropriate. These are just simple examples of the interplay of affinity, avidity, and efficacy in tumor targeting.”
Huang supports and substantiates the challenges for recombinant antibodies as immunotherapeutic agents (p. 403 and 408):
“Genetic engineering has long been employed to increase the affinity of mAb to its target by altering the amino acid sequence in complementary determining region (CDR; Maynard and Georgiou 2000; Reff et al. 2002). However, high specificity must be maintained while increasing antibody affinity as it might augment cross reactivity with other nonspecific antigens, causing unwanted side effects (Hu et al. 2009). High-affinity CDR also can be suboptimal for targeting solid tumors; thus, a suitable affinity may need to be determined (Chames et al. 2009).”
“Many hurdles remain, however, due to the complexity of human immunology as demonstrated by our limited success in chronic infectious diseases and cancer. The approach to combine both active and passive immunotherapies to have synergic effects to maximize desired immune responses may lead a way for treatments of these diseases in the near future.”
One skilled in the art would reasonably conclude that the broadly claimed invention was not fully enabled in the specification, thereby removing applicants from full possession of the invention.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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.
8. Claim(s) 1, 5-11, 14-15 and 18-19 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Chu et al. (Molecular Cancer Therapeutics, (November 2013) Vol. 12, No. 11, Supp. SUPPL. 1. Abstract Number: A48; Meeting Info: 19 Oct 2013‐23 Oct 2013; IDS 7/22/2024) and as evidenced by the specification.
Claim 1 of VHCDR1-3 SEQ ID NOs: 23-25-27 and VLCDR1-3 SEQ ID NOs: 29-(LTS)-33 correspond to the VH/VL CDRs for the anti-LGR5 antibody clone, BNC101.
Claim 5 corresponds to VHCDR1 of SEQ ID NO:23.
Claim 6 corresponds to the VH/VL humanized domains of BNC101.
Claim 7 corresponds to the HC and LC of BNC101.
Claims 8-9 correspond to the CRC as evidenced in the specification at [0030] FIG. 7 is a point plot showing that antibody 18G7H6A3 reduces the number of live events in a CT1 cancer stem cell population; and at [0074-0076].
Claims 10-11 correspond to the colorectal cancer.
Claims 18-19 correspond to the genus of cancers where Chu teaches CRC.
Chu teaches the BNC101 antibody in combination with chemotherapy in the application to treat colorectal cancer in animal models as follows:
PNG
media_image1.png
715
643
media_image1.png
Greyscale
PNG
media_image2.png
518
676
media_image2.png
Greyscale
PNG
media_image3.png
362
693
media_image3.png
Greyscale
As evidenced by the specification at [0041; 0108] the clone BNC101 and 18G7H6A3 are identical structures.
As evidenced by the specification at BNC101 is a humanized antibody.
Claims 14-15 correspond to Chu teaching the application of the mab BNC101 in a pharmaceutical composition for in vivo use in the inhibition colon cancer growth, subcloning of the colorectal tumors to obtain cancer stem cells (CSC) with evaluation of the BNC101 antibody on subsequent growth inhibition, in vivo.
Claims 1, 5-11, 14-15 and 18-19 are anticipated by Chu as proper reference art.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
9. Claims 1-12, 14-15 and 18-19 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3, 10, 12, 13-19 of U.S. Patent No. 9546214 (IDS 7/22/2024). Although the claims at issue are not identical, they are not patentably distinct from each other because the claimed human or humanized anti-LGR5 antibody comprising the VHCDR1-3 and VLCDR1-3 of the 18G7H6A3 (BNC101) clone is a common shared technical feature between the generic claims for the instant claimed invention and the reference patent:
PNG
media_image4.png
110
1180
media_image4.png
Greyscale
PNG
media_image5.png
105
1180
media_image5.png
Greyscale
PNG
media_image6.png
60
1161
media_image6.png
Greyscale
PNG
media_image7.png
46
896
media_image7.png
Greyscale
PNG
media_image8.png
30
1050
media_image8.png
Greyscale
PNG
media_image9.png
55
1166
media_image9.png
Greyscale
PNG
media_image10.png
42
1062
media_image10.png
Greyscale
PNG
media_image11.png
313
975
media_image11.png
Greyscale
10. Claims 1-12, 14-15 and 18-19 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3 and 11-13 of U.S. Patent No. 10745487 (IDS 7/22/2024). The patent reference is not afforded safe harbor protection under 35 USC 121 as the reference does not share any continuity with the instant application.
Although the claims at issue are not identical, they are not patentably distinct from each other because the claimed human or humanized anti-LGR5 antibody comprising the VHCDR1-3 and VLCDR1-3 of the 18G7H6A3 (BNC101) clone is a common shared technical feature between the generic claims for the instant claimed invention and the reference patent as follows:
PNG
media_image12.png
231
942
media_image12.png
Greyscale
PNG
media_image13.png
143
954
media_image13.png
Greyscale
The claims are not patentably distinct from each other because instant claims are drawn to antibodies, compositions and implied methods of using the same antibodies as those covered by the patent. It is noted that the instant application is not a DIV of US 10,745,487 and, therefore, does not receive safe-harbor protection. See MPEP 804.01 and Pfizer, Inc. v. Teva Pharmaceuticals USA, Inc., 518 F.3d 1353, 1362 (Fed. Cir. 2008).
PNG
media_image14.png
212
572
media_image14.png
Greyscale
11. Claims 1-12, 14-15 and 18-19 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-15 of U.S. Patent No. 10358500 (IDS 7/22/2024). The patent reference is not afforded safe harbor protection under 35 USC 121 as the instant application is a continuation of the reference patent. See the filing receipt of the instant application.
PNG
media_image15.png
266
573
media_image15.png
Greyscale
Although the claims at issue are not identical, they are not patentably distinct from each other because the claimed human or humanized anti-LGR5 antibody comprising the VHCDR1-3 and VLCDR1-3 of the 18G7H6A3 (BNC101) clone is a common shared technical feature between the generic claims for the instant claimed invention and the reference patent as follows:
Ref 1. A method of treating a subject having an LGR5-expressing cancer selected from a lung cancer, a breast cancer, a colon cancer, a colorectal cancer, and a pancreatic cancer, the method comprising administering an effective amount of a human or humanized antibody or epitope-binding fragment thereof that specifically binds human leucine-rich repeat containing G-protein-coupled receptor 5 (LGR5) to a subject in need thereof, wherein the human or humanized antibody or epitope-binding fragment thereof comprises: a heavy chain complementary determining region 1 (CDR1) comprising an amino acid sequence as shown in SEQ ID NO:23, or conservative variations thereof; a heavy chain complementary determining region 2 (CDR2) comprising an amino acid sequence as shown in SEQ ID NO:25; a heavy chain complementary determining region 3 (CDR3) comprising an amino acid sequence as shown in SEQ ID NO:27; a light chain CDR1 comprising an amino acid sequence as shown in SEQ ID NO:29; a light chain CDR2 comprising an amino acid sequence as shown in SEQ ID NO:31; and a light chain CDR3 comprising an amino acid sequence as shown in SEQ ID NO:33.
Ref 2. The method of claim 1 comprising administering an additional therapy in combination with the administration of the human or humanized antibody or epitope-binding fragment thereof, wherein the additional therapy is selected from the group consisting of: radiotherapy and a chemotherapeutic agent.
Ref 3. The method of claim 2, wherein administration of the human or humanized antibody or epitope-binding fragment thereof is concurrent with administration of the additional therapy.
Ref 4. The method of claim 2, wherein the chemotherapeutic agent is selected from the group consisting of: folinic acid, fluorouracil, irinotecan, gemcitabine, paclitaxel, nab-paclitaxel, cetuximab, PI3K/mTOR dual inhibitor (NVP), and SN38.
Ref 5. The method of claim 2, wherein the chemotherapeutic agent comprises folinic acid, fluorouracil, and irinotecan.
Ref 6. The method of claim 2, wherein the chemotherapeutic agent comprises gemcitabine.
Ref 7. The method of claim 1, wherein the administration is via injection.
Ref 8. The method of claim 1, wherein the subject is administered a dose of the human or humanized antibody or epitope-binding fragment thereof of at least 10 mg/kg.
Ref 9. The method of claim 1, wherein the human or humanized antibody or epitope-binding fragment thereof is administered weekly.
Ref 10. The method of claim 1, wherein the subject is administered at least 2 doses of the human or humanized antibody or epitope-binding fragment thereof.
Ref 11. The method of claim 1, wherein the cancer comprises a solid tumor.
Ref 12. The method of claim 1, wherein the cancer comprises a cancer stem cell.
Ref 13. The method of claim 1, wherein the cancer comprises a cell selected from the group consisting of: a triple negative breast cancer cell, a colon cancer cell having a mutation in a gene selected from the group consisting of K-Ras, H-Ras, APC, PI3K, PTEN, STK11, RB1, TP53, FGFR2, VANGL2, and ISCO, and a small cell lung cancer cell.
Ref 14. The method of claim 1, wherein the subject is human.
Ref 15. The method of claim 1, wherein the heavy chain CDR1 comprises an amino acid sequence as shown in SEQ ID NO:23.
The claims are not patentably distinct from each other because instant claims are drawn to antibodies, compositions and implied methods of using the same antibodies as those covered by the patent.
Conclusion
12. No claims are allowed.
13. Any inquiry concerning this communication or earlier communications from the examiner should be directed to LYNN A. BRISTOL whose telephone number is (571)272-6883. The examiner can normally be reached Mon-Fri 9 AM-5 PM.
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, Wu Julie 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.
/LYNN A BRISTOL/Primary Examiner, Art Unit 1643
Prosecution Insights