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 .
Sequence Noncompliance
As stated in the restriction requirement, Applicant is required to state the size of the sequence file in bytes. Furthermore, under ST.26 amino acid sequences with at least four specifically defined amino acids are required to be listed in the sequence listing and with a corresponding SEQ ID NO. in the specification. For example, on page 184, paragraph [0894], the sequence of the cleavage site requires a SEQ ID NO. There are other instances throughout the specification that need correction as well. This application is examined solely for the purposes of compact prosecution. Applicant is required to resolve these issues. Otherwise, the response will be considered “non-responsive”.
Election/Restrictions
Applicant's election with traverse of Group II in the reply filed on 04/09/2026 is acknowledged. The traversal is on the ground(s) that Groups I and II are not independent or distinct because the recited antibodies of Group I and II both bind to IL-33 and block IL-33 signaling. This is not found persuasive because two antibodies comprised of different complementary determining regions (CDRs) may be regarded as distinct due to effects on functionality that even a single amino acid change within the CDR can have. Furthermore, the two antibodies would require different searches.
The requirement is still deemed proper and is therefore made FINAL.
Claims 1-6, 10-17 are herein examined. Claims 7-9 are withdrawn.
Priority
The application filing receipt currently only claims priority to application U.S. Patent No. 11,738, 081 filed on 04/10/2020 which is a divisional of U.S. Patent No. 10,668,150 filed on 09/27/2017. If applicant wishes for the instant application to receive the benefit of PCT/EP2016/056973 or provisional application 62/140,913, the application filing receipt must be corrected.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 12/13/2023 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure is being considered by the examiner.
Drawings
The drawings are objected to because Figure 58A depicts pre-treatment with IL-33 (on the x-axis) whereas Figure 58B depicts pre-treatment with DSB IL-33; however, in the specification, in the last sentence of paragraphs [1090, 1091] it states that both experiments were pre-treated with DSB IL-33. Furthermore, Figures 43A and B measure DSB IL-33 according to the specification, but the y-axis is labeled IL-33. For increased clarity, please appropriately label IL-33 as the oxidized form where necessary. Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Claim Objections
Claim 16 is objected to because of the following informality: Claim 16 recites an antibody or antigen-binding sequence selected from of group including both a single chain antibody and an scFv fragment, which are the same thing. Appropriate correction is required.
Claim Rejections - 35 USC § 112(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.
Claims 1 and 3 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Scope of the claimed genus:
Claim 3 recite a method of treating a subject with an inflammatory condition by administering an antibody that binds to IL-33 wherein the antibody inhibits RAGE mediated effects. Accordingly, the claims encompass all IL-33 antibodies, including those directed to both the reduced and oxidized forms of IL-33, as well as those directed to the full-length and mutated versions of IL-33.
State of the relevant prior art:
At the time of filing, it was known that IL-33 had two distinct binding sites for the ST2 receptor (Lingel et al., 2009, see instant PTO-892) and antibodies for IL-33 which prevented the binding of IL-33 to ST2 were known in the art (Liu et al. 2009, see instant PTO-892). In 2015, the Applicant discovered that IL-33 existed in both a reduced and oxidized state (Cohen et al., 2015, see instant PTO-892). Furthermore, Applicant discovered that the oxidized form binds to Receptor for Advanced Glycation End-products (RAGE) (Cohen et al. 2015). However, at the time of filing, there were no known antibodies for the oxidized form and the precise epitope(s) necessary to bind to oxidized form (i.e. DSB IL-33) were not elucidated. Furthermore, it was unknown whether DSB IL-33 inhibition would result in inhibition of RAGE mediated effects sufficient to treat an inflammatory condition.
While antibodies directed to what would later be realized as the reduced for of IL-33 were known in the art, the relationship between reduced IL-33 inhibition and inhibition of RAGE mediated effects was not sufficiently established in the art such that one of ordinary skill in the art would envisage which, if any, known IL-33 antibodies have the recited effect.
Altogether, the state of the art does not provide any possession of DSB IL-33 antibodies, and although antibodies directed to the reduced form were known, the state of the art does not indicate that these antibodies necessarily possessed the recited function of inhibition of RAGE mediated effects. One of ordinary skill in the art would not be able to envisage an IL-33 antibody that inhibits RAGE based on the state of the art.
Description of representative species in the specification:
Because the relationship between IL-33 antibody inhibition and RAGE mediated effects was not well known in the art, a representative number of species must be described in the specification in order to demonstrate possession of the genus of IL-33 antibodies which have this effect.
MPEP § 2163 states that a “representative number of species” means that the species which are adequately described are representative of the entire genus. Thus, when there is substantial variation within the genus, one must describe a sufficient variety of species to reflect the variation within the genus.
First, the specification does not provide examples of antibodies for DSB IL-33 (i.e. the oxidized IL-33 version) or demonstrate that those antibodies would perform the recited RAGE mediated effects.
Furthermore, of the antibodies in the instant specification directed to reduced IL-33, there are not a representative number of species demonstrated to inhibit RAGE mediated effects. Applicant asserts in the specification [1092] that inhibiting the reduced IL-33 version inhibits RAGE mediated effects indirectly by preventing conversion to the oxidized form. Three antibodies (IL330004, 33v20064, and 33_640050) were indeed able to slow or prevent conversion of IL-33 from the reduced to the oxidized form (Fig. 43 A). However, the IL330004 antibody was unable to treat an airway inflammation model in vivo (Fig. 47), which teaches that even if an antibody can slow IL-33 oxidation, this does not necessarily demonstrate possession of treating an inflammatory condition with an antil-IL-33 antibody. Only one antibody directed to the reduced version (i.e. 33_640087-7B ) was tested for its ability to inhibit RAGE mediated effects (Fig. 58A) and was able to treat an airway inflammation model in mice (Fig. 52).
Altogether the species described in the specification are not representative of the entire genus of IL-33 antibodies that would inhibit RAGE mediated effects.
Description of structure/function relationship:
In the absence of a representative number of species, the written description requirement for a claimed genus may be satisfied by disclosure of relevant, identifying characteristics; i.e., structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the applicant was in possession of the claimed genus. To meet this requirement in the instant case, the specification must describe structural features that the skilled artisan as of the effective filing date would have expected to convey the claimed inhibition of RAGE mediated effects.
The specification discloses mutation hotspots associated with increased affinity in the design of IL-33 antibodies ([1013], [1017]). The specification also teaches some epitope mapping (Tables 12, 23; Fig. 12). However, these structural features while pertinent to binding to IL-33, do not necessarily lead to functional inhibition of RAGE mediated effects. The specification identifies cystine residues (i.e. C208) that facilitate transformation to the oxidized form; however, H338L293, a monoclonal antibody directed to an epitope near this region actually accelerated oxidation (Fig. 30c), demonstrating that targeting these cysteine locations is highly sensitive and does not necessarily result in a functional outcome of inhibition of RAGE mediated effects. In other words, there is no disclosure in the specification regarding the structure of IL-33 antibodies such that one of ordinary skill in the art would envisage inhibition of RAGE mediated effects from such antibodies sufficient to treat an inflammatory condition.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claim(s) 1-6 and 15-17 is/are rejected under 35 U.S.C. 102(a)(2) as being anticipated by Horlick et al. US 10,836,820 B2 (hereafter Horlick et al.), which has an earliest effective filing date of 01/10/2014, as evidenced by Liu et al. Anti-IL-33 antibody treatment inhibits airway inflammation in a murine model of allergic asthma, 2009, Biochemical and Biophysical Research Communications, pgs. 181-185 (see instant PTO-892).
Regarding claims 1,4, and 5, Horlick et al. teaches administering an effective amount (Column 2, lines 50-54) of a humanized (Column 10, lines 22- 25) monoclonal antibody that binds to IL-33 (Column 231, Claim 1) to treat allergic asthma (Column 15, lines 35-60). Regarding claim 6, as evidenced by Lui et al., allergic asthma is an inflammatory condition in the airway (pg. 181, left side, first paragraph). Regarding Claim 2, Horlick et al. teaches that IL-33 drives production of cytokines such as IL-4, IL-5 (Column 1, lines 32-37) and the anti-IL-33 antibody inhibits production (Column 19, Example 1, last line) of IL-5 (Fig. 1A). Regarding claim 16, Horlick et al. teaches that the IL-33 binding agent can be a whole antibody (Column 8, last paragraph), a Fab fragment, F(ab')2 fragment, (Column 9, first paragraph) and an scFv (Column 9, fourth paragraph, lines 35-40).
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.
Claims 1- 6, 10, 11, 15 -17 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1,2, 4-6, 14, 15, 17-18, 21, 23-26,28, 29-30, 32-35 copending Application No. 18/850,285 (hereafter reference A). Although the claims at issue are not identical, they are not patentably distinct from each other.
Regarding instant claims 1 and 10, claims 1,2, 4-6, 14, 15, 17-18, 21, 23-26,28, 29-30, 32-35 of the reference A recite administering a specific IL-33 antibody, with the same CDRs as instant claim 10 (as defined by Table 1 of the reference A) to reduce or prevent a respiratory tract infection. Furthermore, the species of respiratory disorder recited in claims 4 and 5 of the reference A, namely a viral infection caused by influenza virus and a bacterial infection caused by Chlamydia pneumoniae, anticipate the genus of inflammatory condition recited in instant claim 1. Regarding instant claim 2, the antibody recited by claim 1 of the reference A would inherently inhibit IL-33 driven cytokine production because instant Fig. 51 shows the 33_640087-7B antibody with the same CDRs inhibiting IL-33 production of IL-8. Regarding instant claim 3, the antibody recited by claim 1 of the reference A would inherently inhibit RAGE mediated effects, as shown by instant Fig. 58A where the 33_640087-7B antibody with the same CDRs of reference A claim 1 inhibited RAGE mediated effects. Regarding claims 4 and 6, the antibody recited by claim 1 of the reference A would inherently treat an allergic condition of the airway because instant Fig. 52 demonstrates the 33_640087-7B antibody with the same CDRs successfully treating an airway inflammation model of Alternaria alternata (ALT) [1048]. As evidenced by Daines et al., 2020 (see instant PTO- 892) ALT is fungal allergen that can cause allergic and asthma responses (abstract). Regarding instant claim 5, claims 2 and 26 of the reference A recite reducing the annualized exacerbation rate of COPD. Regarding instant claim 6, as evidenced by Mair, COPD is a condition in the airway (abstract; pg. 1689, left side, first paragraph) and therefore claim 2 of the reference A also reads on instant claim 6. Regarding instant claims 11, claim 32 recites an IL-33 antibody with an identical VH domain to instant claim 11 and a VL domain with a single amino acid difference (~99% identity of instant claim 11 VL domain). Regarding instant claims 15 -17, claim 32 recites VH and VL domains as SEQ ID NOs 4 and 8, respectively, which are defined in the reference specification (pg. 39) as tozorakimab, which as evidenced by Reid et al., 2023 (see instant PTO-892) is a human monoclonal antibody.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 1-6, 10, 11 and 15-17 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim 37-40, 44, 46, 56, 57, 60, 61, and 62 of copending Application No. 17/755604 (reference B) as evidenced by Daines et al., and Reference A. Although the claims at issue are not identical, they are not patentably distinct from each other.
Regarding instant claims 1, 3, and 10, claims 37-40, 60-62 of the reference B recite a method of treating chronic kidney disease by administering an anti-IL-33 therapeutic antibody to inhibit ST2 signaling and IL-33-mediated RAGE effects, wherein the agent comprises CDR sequences identical to those recited in instant claim 10. Regarding instant claim 2, the antibody recited by claim 1 of the reference B would inherently inhibit IL-33 driven cytokine production because instant Fig. 51 shows the 33_640087-7B antibody with the same CDRs inhibiting IL-33 production of IL-8. Regarding claims 4-6, the antibody recited by claim 1 of the reference B would inherently treat an allergic disorder, asthma and a condition of the airway because instant Fig. 52 demonstrates the 33_640087-7B antibody with the same CDRs successfully treating an airway inflammation model of Alternaria alternata (ALT) [1048]. As evidenced by Daines et al., ALT is fungal allergen that can cause allergic and asthma responses (abstract). Claim 44 of the reference application further recites that the chronic kidney disease is diabetic kidney disease, which anticipates the genus of inflammatory condition recited instant claim 1. Claim 46 of the reference B teaches that the therapeutic agent can be an antibody. Regarding instant claim 11, claims 46, 56, and 57 of the reference B further limit that the therapeutic agent is an antibody with an identical VH domain to instant claim 11 and a VL domain with a single amino acid difference (~99% identity of instant claim 11 VL domain). Regarding instant claims 15-16, the antibody recited by claim 57 of the reference B is identical to the antibody recited in claim 32 of reference A, which is a human monoclonal antibody. Therefore, as evidenced by reference A, claim 57 reads on instant claims 15-16. Regarding instant claim 17, claim 60 of the reference application further limits that the antibody is monoclonal.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 1-6, 10,11, and 16-17 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 60, 69, 71, 89, and 90 of copending Application No. 17/755605 (reference C), as evidenced by Mair et al., Airway Dimensions in COPD: Relationships with Clinical Variables, 2010, Respiratory Medicine, pgs. 1683-1690 and Ramos et al. Clinical issues of mucus accumulation in COPD, 2014, International Journal of COPD, abstract, Daines et al., and Reference A (see instant PTO-892). Although the claims at issue are not identical, they are not patentably distinct from each other.
Regarding instant claims 1 and 10, claims 60 and 89 of reference C recite administering an IL-33 antagonist, wherein the antagonist is an IL-33 antibody, to treat a respiratory disease, wherein the disease is COPD, wherein the antagonist is a binding molecule that comprises CDR sequences identical to those recited in instant claim 10. Regarding instant claim 2, the IL-33 antagonist recited by claim 1 of reference C would inherently inhibit IL-33 driven cytokine production because instant Fig. 51 shows the 33_640087-7B antibody with the same CDRs inhibiting IL-33 production of IL-8. Regarding claims 4 and 6, the antibody recited by claim 1 of the reference C would inherently treat an allergic disorder, asthma and an inflammatory condition of the airway because instant Fig. 52 demonstrates the 33_640087-7B antibody with the same CDRs successfully treating an airway inflammation model of Alternaria alternata (ALT) [1048]. As evidenced by Daines et al., ALT is fungal allergen that can cause allergic and asthma responses (abstract). Regarding instant claim 5, claim 69 of reference C recites that the respiratory disease is COPD. As evidenced by Mair, COPD is a condition in the airway (abstract; pg. 1689, left side, first paragraph) and therefore there claim 1 of the reference C also reads on instant claim 6. Claim 71 of reference C further recites reducing abnormal mucus production. As evidenced by Ramos et al., abnormal mucus production is a symptom of COPD. As defined in the instant specification [560], “treating” of an inflammatory disorder includes reducing a symptom; therefore, claim 71 of the reference C reads on instant claim 1. Regarding instant claim 11, claim 89 of the reference C recites that the antagonist is an IL-33 antibody or antigen binding fragment thereof with an identical VH domain and VL domain with a single amino acid difference (~99% identity of instant VL domain). Reference claim 90 limits that the respiratory disease is bronchitis COPD, which anticipates the genus of inflammatory condition in instant claim 1. Regarding instant claims 15-17, the antibody recited by claim 89 of the reference C is identical to the antibody recited in claim 32 of reference A, which is a human monoclonal antibody. Therefore, as evidenced by reference A, claim 57 reads on instant claims 15-17.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 1-6 and 10, 15-17 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-4, 8, 16-19, 25 and 28 of copending Application No. 17/995507 (reference D), in view of Kim et al. ,Antibody Engineering for the Development of Therapeutic Antibodies, 2005, Molecules and Cells, pgs. 17-29, as evidenced by Han et al., Daines et al., and Reference A (see instant PTO-892). Although the claims at issue are not identical, they are not patentably distinct from each other.
Regarding instant claims 1 and 10, claims 1, 2, 3, 6, 8, 16, 17, 19, and 25 of the reference D recite treating acute respiratory distress syndrome (ARDS) by administering an IL-33 axis binding antagonist, wherein the antagonist is an antibody and comprises CDR sequences identical to those recited in instant claim 10. As evidenced by Han et al. 2015(abstract), ARDS is an inflammatory condition and therefore anticipates the genus of inflammatory condition recited instant claim 1. As evidenced by reference D claim 8, ARDS is a condition in the airway of the subject, which reads on instant claim 6. Regarding instant claim 2, the IL-33 antagonist recited by claim 1 of reference D would inherently inhibit IL-33 driven cytokine production because instant Fig. 51 shows the 33_640087-7B antibody with the same CDRs inhibiting IL-33 production of IL-8. Regarding claims 4 -6, the antibody recited by claim 1 of the reference D would inherently treat an allergic disorder, asthma and an inflammatory condition of the airway because instant Fig. 52 demonstrates the 33_640087-7B antibody with the same CDRs successfully treating an airway inflammation model of Alternaria alternata (ALT) [1048]. As evidenced by Daines et al., ALT is fungal allergen that can cause allergic and asthma responses (abstract).
Regarding instant claims 1 and 10, Claims 4 and 28 of the reference D recite treating hypoxemia caused by severe acute respiratory coronavirus 2 by administering an IL-33 axis binding antagonist, wherein the antagonist comprises CDR sequences identical to those recited in instant claim 10. As defined in the instant specification [560], “treating” of an inflammatory disorder includes reducing a symptom; because hypoxemia is a symptom of severe acute respiratory coronavirus 2, Claims 4 and 28 read on “treating” of an inflammatory condition, as recited by instant claim 1.
Regarding instant claims 15-17, the CDRs recited by claims 1 and 25 of reference D are human CDRs, because they are the same as those defined by claim 32 of Reference A, which recites a human monoclonal antibody.
Kim et al. teaches that making human monoclonal antibodies is routine in the art (pg. 19, right side, last paragraph). Kim et al. teaches that human Mabs are more developed than chimeric or humanized antibodies (pg. 20, left side, second paragraph).
It would be obvious to modify the antibodies recited in claims 1 and 25 of reference D to arrive at a human, monoclonal anti-IL-33 antibody in a naturally occurring antibody using routine methods in the art. One of ordinary skill would have been motivated to combine the teachings of Kim et al. and reference D because they are both in the field of antibody engineering. There would be a reasonable expectation of success implementing a conventional method of producing human monoclonal antibodies using human CDRs.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
No claims allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to MICHELLE C BUCCINI whose telephone number is (571)272-1352. The examiner can normally be reached M-F 7:30-5 EST.
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, Jeffrey Stucker can be reached at 5712720911. 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.
/MICHELLE CALLAHAN BUCCINI/Examiner, Art Unit 1675
/JULIE WU/Supervisory Patent Examiner, Art Unit 1643
Prosecution Insights