DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Election/Restrictions
Applicant’s election, with no comment, of Group I (claims 1-5, 9-10, 15, 21, and 26) and the below listed species in the reply filed on 12/11/2025 is acknowledged.
Elected Species:
CDRs of mAb 20-10 comprising heavy chain CDRs of SEQ ID NOs: 16, 18, and 20, and light chain CDRs of SEQ ID NOs: 4, 7, and the sequence GIS;
Full heavy chain sequence of SEQ ID NO: 14 and full light chain sequence of SEQ ID NO: 2.
Because Applicant did not distinctly and specifically point out any errors in the restriction requirement, the election has been treated as an election without traverse (MPEP 818.03(a)).
Claim Status
Claims 6-8, 16-20, and 25 have been cancelled, as requested in the amendment filed on 12/11/2025. Following the amendment, claims 1-5, 9-15, 21-24, and 26 are pending in the instant application.
Claims 11-14 and 22-24 stand as withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to nonelected inventions in the Response filed 12/11/2025, there being no allowable generic or linking claim.
Claims 1-5, 9-10, 15, 21, and 26 are under examination in the instant office action.
Priority
Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged.
Claims 1-5, 9-10, 15, 21, and 26 have an effective filing date of July 09, 2020 corresponding to PRO 63/049,819.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 10/03/2024 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Drawings
The drawings are objected to because Figure 6C is blurry and very difficult to read. 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.
Specification
Applicant is reminded of the proper content of an abstract of the disclosure.
A patent abstract is a concise statement of the technical disclosure of the patent and should include that which is new in the art to which the invention pertains. The abstract should not refer to purported merits or speculative applications of the invention and should not compare the invention with the prior art.
If the patent is of a basic nature, the entire technical disclosure may be new in the art, and the abstract should be directed to the entire disclosure. If the patent is in the nature of an improvement in an old apparatus, process, product, or composition, the abstract should include the technical disclosure of the improvement. The abstract should also mention by way of example any preferred modifications or alternatives.
Where applicable, the abstract should include the following: (1) if a machine or apparatus, its organization and operation; (2) if an article, its method of making; (3) if a chemical compound, its identity and use; (4) if a mixture, its ingredients; (5) if a process, the steps.
Extensive mechanical and design details of an apparatus should not be included in the abstract. The abstract should be in narrative form and generally limited to a single paragraph within the range of 50 to 150 words in length.
See MPEP § 608.01(b) for guidelines for the preparation of patent abstracts.
The abstract of the disclosure is objected to because it is less than 50 words in length. A corrected abstract of the disclosure is required and must be presented on a separate sheet, apart from any other text. See MPEP § 608.01(b).
The use of the terms, for example, DVD-Ig, nanobody, affibody, affilin, affimer, alphabody, anticalin, avimer, DARPin, and Fynomer, which are trade names or marks used in commerce, have been noted in this application. The terms should be accompanied by the generic terminology; furthermore the terms should be capitalized wherever it appears or, where appropriate, include a proper symbol indicating use in commerce such as ™, SM , or ® following the terms.
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 Rejections - 35 USC § 112
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 1-5, 9-10, 15, 21, and 26 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. This is a WRITTEN DESCRIPTION rejection.
The claims are drawn a recombinant, synthetic, or monoclonal human antibody or antibody construct that binds to an epitope or a fragment of said antibody that specifically or preferentially binds human IDO2, wherein said antibody or construct comprises at least one heavy chain variable region CDR selected from SEQ ID NO: 16, 18, or 20.
Thus, the claims identify the antibody by the function of binding human IDO2, and a partial sequence structure that comprises at least one heavy chain variable region CDR with an amino acid sequence of SEQ ID NO: 16, 18, or 20. The claims also fail to require the light chain CDR 1-3 sequences critical to IDO2 binding function. Thus, the claims encompass a vast genus of antibody variants comprising as few as one of the recited heavy chain CDRs, and lacking light chain CDRs 1-3 critical to antigen binding function.
The instant specification discloses three structurally similar anti-IDO2 antibodies at Pages 29-31 of the instant specification; said antibodies are identified as mAb 13-3, mAb 18-1, and mAb 20-10. It is specifically noted that these antibodies are defined by their full-length heavy and light chain sequences, which comprise HCDRs 1-3 and LCDRs 1-3, respectively. Notably, said HCDRs 1-3 correspond to SEQ ID NOs: 16, 18, and 20, respectively, and the LCDRs correspond to SEQ ID NOs: 4, 7, and the sequence GIS wherein the order of the LCDRs differs between the antibody species.
Thus, the instant specification discloses making three structurally similar antibodies and describes the complete HCDR 1-3, LCDR 1-3, full heavy chain, and full light chain sequences that all function to bind human IDO-2. The specification fails to disclose any other antibodies, antibody constructs, or antibody fragments thereof that comprise as few as one HCDR or comprise different CDR sequences than those recited above that possess the function of binding to human IDO2.
To provide adequate written description and evidence of possession of the claimed antibody genus, the instant specification can structurally describe representative antibody variants that function to bind human IDO2, or describe structural features common to the members of the genus, which features constitute a substantial portion of the genus. Alternatively, the specification can show that the claimed invention is complete by disclosure of sufficiently detailed, relevant identifying characteristics, functional characteristics when coupled with a known or disclosed correlation between function and structure, or some combination of such characteristics (see University of California v. Eli Lilly and Co., 119 F.3d 1559, 43 USPQ2d 1398 (Fed. Cir. 1997) and Enzo Biochem, Inc. V. Gen-Probe Inc.).
In this case, the only factor present in the claims is a recitation of the antibody function, “specifically or preferentially binds human IDO2”, and partial sequence structure as stated above. The instant specification fails to describe structural features common to the members of the antibody genus, which features constitute a substantial portion of the genus because the instant specification fails to disclose representative antibody variant sequences that function as claimed. A definition by function does not suffice to define the genus because it is only an indication of what the antibody does, rather than what it is. Other than for the antibodies identified as mAb 13-3, mAb 18-1, and mAb 20-10 disclosed at Pages 29-31 of the instant specification, the specification fails to provide any single heavy chain CDR structural features coupled to the claimed functional characteristics. The instant specification fails to describe a representative number of antibody sequence variants for the genus of antibodies that function as claimed. Accordingly, in the absence of sufficient recitation of distinguishing identifying characteristics, the specification does not provide adequate written description of the claimed genus required to make the claimed antibodies.
The claims broadly encompass any antibody that comprises a single HCDR corresponding to SEQ ID NOs: 16, 18, or 20 that functions to bind human IDO2. Applicants have not established any reasonable structure-function correlation with regards to the sequences of a single heavy chain CDR that, regardless of the other CDR sequences, will maintain human IDO2 binding function. Given the well-known high level of polymorphism of antibody CDR sequences and structure, the skilled artisan would not have been in possession of the vast repertoire of antibodies encompassed by the claimed invention. One could not reasonably or predictably extrapolate the structure of a single human IDO2-binding antibody comprising at least one of the recited heavy chain CDR structures to the structure of any variants required to bind human IDO2 as broadly claimed. Therefore, one could not readily envision members of the broadly claimed genus.
Although Applicants may argue that it is possible to screen for antibodies that bind human IDO2 and function as claimed, the court found in (Rochester v. Searle, 358 F.3d 916, Fed Cir., 2004) that screening assays are not sufficient to provide adequate written description for an invention because they are merely a wish or plan for obtaining the claimed chemical invention. “As we held in Lilly, “[a]n adequate written description of a DNA … ‘requires a precise definition, such as by structure, formula, chemical name, or physical properties,’ not a mere wish or plan for obtaining the claimed chemical invention.” 119 F.3d at 1566 (quoting Fiers, 984 F.2d at 1171). For reasons stated above, that requirement applies just as well to non-DNA (or RNA) chemical inventions.” Knowledge of screening methods provides no information about the structure of any future antibodies yet to be discovered that may function as claimed. The IDO2 antigen provides no information about the structure of an antibody that binds to it.
Given the lack of representative examples to support the full scope of the claimed variant antibodies, and lack of reasonable structure-function correlation with regards to the unknown variable sequences in the CDRs that provide human IDO2-binding function, the present claims lack adequate written description. Thus, the specification does not provide an adequate written description of antibody variants that comprise as few as one of the recited heavy chain CDRs that retain the ability to bind human IDO2 that is required to practice the claimed invention.
Examiner Suggestion: Amend the claims to recite and require the antibody or antigen binding fragments to comprise, at minimum, all three CDR SEQ ID NOs from the heavy chain and all three CDR SEQ ID NOs from the light chain, which are the shared, critical sequence structures for IDO2 binding function of the claimed genus.
Claims 1-5, 9-10, 15, 21, and 26 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 recombinant or synthetic monoclonal antibodies that specifically or preferentially bind human IDO2, wherein said antibody or construct comprises at least one heavy chain variable region CDR selected from SEQ ID NO: 16, 18, or 20, does not reasonably provide enablement for fully human monoclonal antibodies. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make the invention commensurate in scope with these claims. This is a SCOPE OF ENABLEMENT rejection.
The Breadth of the Claims
The independent claims (claims 1 and 15) are drawn to a recombinant, synthetic, or monoclonal human antibody or antibody construct that binds to an epitope or a fragment of said antibody that specifically or preferentially binds human IDO2, wherein said antibody or construct comprises at least one heavy chain variable region CDR selected from SEQ ID NO: 16, 18, or 20 (see claim 1). However, based on the instant disclosure (see for example, instant specification Example 1), it appears that the recited heavy chain CDR sequences of instant claim 1 are not human CDRs, but rather murine, and therefore the antibodies of the instant disclosure cannot be fully human antibodies. Specifically, Example 1 of the specification discloses the three hybridomas were generated against human IDO2 amino acids, and the IDO2-binding antibodies were detected with an anti-mouse IgG Fc labeled antibody. As such, the full scope of the instant claims as pertain to human antibodies is not enabled.
The State of the Prior Art/Level of Predictability in the Art
As disclosed by Bernett et. al. (J. Mol. Biol., 2010, 396, 1474-1490; herein after referred to as “Bernett”), deriving fully human antibodies from transgenic mice or full human antibody libraries was well known and understood in the prior art, and Bernett further disclosed a novel method of generating fully human mAbs from nonhuman variable regions using information from the human germline repertoire comprising the rational engineering of residues within and proximal to CDRs and the VH/VL interface by iteratively exploring substitutions to the closest human germline sequences using semi-automated computational methods to generate fully human antibodies comprising over 40 substitutions relative to the parental murine variable regions with a large number of substitutions occurring in the CDRs (Abstract; Figure 2; see entire document). Thus, Bernett establishes known methods of producing fully human antibodies, including transgenic animals and fully human antibody libraries, or generating fully human antibodies from murine sequences; however the production of fully human antibodies from non-human sequences requires extensive sequence modifications (e.g., over 40 substitutions total) wherein many substitutions occur within the CDRs themselves. Thus, while fully human antibodies may be generated from non-human parental antibodies, significant modification and more specifically CDR modification is required.
The Amount of Direction Provided by the Inventor/Existence of Working Examples
Example 1 of the instant specification discloses the production of mAbs 13-3, 18-1, and 20-10, wherein three cloned hybridomas were generated against the human IDO2 amino acids #331-351 from which the three anti-human IDO2 monoclonal antibodies 13-3, 18-1 and 20-10 were isolated from. Page 6 of the instant specification specifically indicates that the hybridoma cell lines utilized to generate antibodies of the invention (mAbs 13-3, 18-1, and 20-10) were generated and secrete monoclonal antibodies that recognize human IDO2, wherein in certain embodiments these antibodies may be “humanized” for use as therapeutic biomolecules. Taken together, the instant specification demonstrates that the only working example for producing antibodies of the invention yields non-human antibodies. No working examples of the production of fully-human antibodies are provided.
In view of the state of the prior art, lack of the predictability of the art to which the invention pertains as evidenced by Bernett above, the lack of guidance and direction provided by Applicant, and the absence of working examples, undue experimentation would be required to make functional, fully human monoclonal antibodies comprising antibody construct that binds to an epitope or a fragment of said antibody that specifically or preferentially binds human IDO2, wherein said antibody or construct comprises at least one heavy chain variable region CDR selected from SEQ ID NO: 16, 18, or 20, with a reasonable expectation of success, absent a specific and detailed description in Applicant’s specification of how to effectively practice this and absent working examples providing evidence which is reasonably predictive that the claimed antibodies are (1) fully human and (2) functional, commensurate in scope with the claimed invention. Claims 2-5, 9-10, 20, and 26 are included in this rejection as they depend from and/or incorporate claim 1.
Examiner Suggestion: Delete the word “human” from the claims. It is noted that all subsequently dependent claims must also be appropriately amended.
Claim 26 is 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 the treatment of an autoimmune disease, does not reasonably provide enablement for preventing an autoimmune diseases. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make the invention commensurate in scope with these claims. This is a SCOPE OF ENABLEMENT rejection.
The Breadth of the Claims
Claim 26 is drawn to a pharmaceutical composition for the prevention or treatment of an autoimmune disease comprising at least one antibody or epitope-binding fragment of claim 1. Thus, the claim scope includes the intended use/function of preventing autoimmune disease, the full scope of which is not enabled.
The State of the Prior Art
It is specifically noted that with regard to the current state of the art, and the state of the art as of the effective filing date of the instant application, there are no methods, pharmaceutically relevant compositions, or specific treatments that can “prevent” autoimmune diseases as instantly claimed. More specifically, there is no indication that anti-IDO2 antibodies would be capable of preventing autoimmune diseases.
The Level of Unpredictability in the Art
There is a high level of unpredictability associated with the prevention autoimmune diseases as pertains to targeting IDO2. Merlo and Mandik-Nayak (Clinical Medicine Insights: Pathology, 2016, 9(S1), 21-28; herein after referred to as “Merlo”) disclose that several studies have demonstrated an immunosuppressive role for IDO in inducible models of autoimmunity, including models of colitis, collagen-induced arthritis, and experimental autoimmune encephalomyelitis while other models, including allergy, contact hypersensitivity (CHS), and inflammatory airway disease, have provided evidence that IDO positively influences inflammatory responses; even within a single model, the contribution of IDO can be controversial and dependent on whether small molecule inhibitors or genetic knockouts are used to study its effects (Page 22, Column 2, Last Paragraph). Human populations have two common IDO2-inactivating polymorphisms, wherein both polymorphisms are relatively common in human populations, with at least 25% of the population estimated to have a functionally inactive IDO2; other non-synonymous variants have been identified from HapMap and other databases (Page 26, Column 2, First Paragraph). Generally, the contribution of the different isoforms and polymorphisms to immunity, both in the context of cancer and autoimmune disorders, remain undiscovered; genetic evidence indicates that inactivating IDO2
polymorphisms may be less prevalent in the African-American population, which may be of relevance to health disparities associated with this ethnic group including disproportionate
rates of SLE onset and disease severity and the Y359STOP mutation is slightly associated with a reduced risk of Crohn’s disease, supporting the idea of IDO2 as a pro-inflammatory mediator in an autoimmune environment (Id.). Current evidence reveals IDO2 to be an immunomodulatory
enzyme that acts in B cells to modulate autoimmune disease; although its enzymatic function is poorly characterized, it is clear that the mechanism of immune modulation by IDO2 is distinct from its better-studied homolog, IDO1 (Page 27, Column 1, Third Paragraph). IDO2 acts as a pro-inflammatory mediator in multiple models of autoimmune inflammatory disorders, including RA, CHS, and SLE; because IDO2 is acting to promote inflammation, it is an obvious candidate for therapeutic targeting for treatment of these diseases, particularly in a co-therapeutic setting (Id.). Thus, Merlo indicates that there are aspect of IDO2 and its functionality that remain unclear and are even controversial in the context of autoimmunity, thought various models and studies indicate it may be a viable target for therapeutic intervention in autoimmune diseases. However, there is no indication that it could reliably prevent autoimmune diseases.
The Amount of Direction Provided by the Inventor/Existence of Working Examples
It is noted that Applicant has not provided any working examples to demonstrate that the anti-IDO2 antibodies of the instant invention are capable of preventing autoimmune diseases as claimed.
In view of the state of the prior art, lack of the predictability of the art to which the invention pertains as evidenced by Merlo above, the lack of guidance and direction provided by Applicant, and the absence of working examples, undue experimentation would be required to make a pharmaceutical composition comprising an antibody or antibody construct that binds to an epitope or a fragment of said antibody that specifically or preferentially binds human IDO2, wherein said antibody or construct comprises at least one heavy chain variable region CDR selected from SEQ ID NO: 16, 18, or 20, that would be expected to function as claimed with a reasonable expectation of success, absent a specific and detailed description in Applicant’s specification of how to effectively practice this and absent working examples providing evidence which is reasonably predictive that the claimed antibodies are functional in the context of preventing autoimmune diseases, commensurate in scope with the claimed invention.
Examiner Suggestion: The Examiner suggests amending claim 26 as follows: A pharmaceutical composition for the .
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.
Claims 5, 15, and 21 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.
Claim 5 contains the trademark/trade names DVD-Ig, nanobody, affibody, affilin, affimer, alphabody, anticalin, avimer, DARPin, and Fynomer. Where a trademark or trade name is used in a claim as a limitation to identify or describe a particular material or product, the claim does not comply with the requirements of 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph. See Ex parte Simpson, 218 USPQ 1020 (Bd. App. 1982). The claim scope is uncertain since the trademark or trade name cannot be used properly to identify any particular material or product. A trademark or trade name is used to identify a source of goods, and not the goods themselves. Thus, a trademark or trade name does not identify or describe the goods associated with the trademark or trade name. In the present case, the trademark/trade name is used to identify/describe various antibody constructs/structures and, accordingly, the identification/description is indefinite.
Claim 15 recites “[a]n antigen binding fragment thereof comprising one or more heavy chain CDR selected from the amino acid sequences SEQ ID NOs: 16, 18 or 20 and optionally one of more light chain CDR selected from SEQ ID NO: 4 or 7 or the sequence GIS”; the recitation of “[a]n antigen binding fragment thereof” renders that claim indefinite as it is unclear as to what the “antigen binding fragment thereof” is in reference to as the claim, as currently presented, is an independent claim. For the purposes of examination, the claim is being interpreted as depending on claim 1, such the “antigen binding fragment thereof” is in reference to the antibody of claim 1.
Claim 21 recites: The antibody or epitope binding fragment according to claim 1, wherein said antibody has the FR1/CDR1/FR2/CDR2/FR3CDR3/FR4 sequence combination of the heavy and light chain of mAb 20-10. Claim 21 is unclear with regard to whether the antibody or epitope binding fragment of claim 1 comprises: (1) the order of sequence combinations of FR1/CDR1/FR2/CDR2/FR3CDR3/FR4 like that found in Mab 20-10; or (2) the actual framework 1-4 and CDR 1-3 SEQ ID NOs found in Mab 20-10 heavy and light chain SEQ ID NOs: 14 and 2.
Art-Free Subject Matter
It is noted that full-length HCDRs 1-3 corresponding to SEQ ID NOs: 16, 18, and 20, respectively, full-length LCDRs 1-3 corresponding to SEQ ID NOs: 4, 7, and the sequence GIS, full-length heavy chain variable region corresponding to SEQ ID NO: 14, and full-length light chain variable region corresponding to SEQ ID NO: 2 have been thoroughly searched and are free of the prior art. However, it is noted that the claims suffer from deficiencies under 35 U.S.C. 112(a) and 112(b) as described above.
The closest prior art made of record but not relied upon is US 2019/0062452 A1 (herein after referred to as “Kleintop”). Kleintop teaches compositions and methods for the treatment of an autoantibody disease or disorder (Abstract). More specifically, Kleintop teaches that the methods (and compositions) of the instant invention comprise administering at least one antibody or antibody fragment which is immunologically specific for IDO2 (indoleamine 2,3-dioxygenase 2; anti-IDO2 antibody) to a subject wherein, in particular embodiments, the anti-IDO2 antibody may be (1) immunologically specific for human IDO2 and/or (2) the anti-IDO2 antibody is immunologically specific for human IDO2 to the exclusion of IDO 1. However, Kleintop does not teach or render obvious antibodies, antibody constructs, or antibody fragments that specifically or preferentially bind human IDO2 which comprise full-length HCDRs 1-3 corresponding to SEQ ID NOs: 16, 18, and 20, respectively, full-length LCDRs 1-3 corresponding to SEQ ID NOs: 4, 7, and the sequence GIS, a full-length heavy chain variable region corresponding to SEQ ID NO: 14, and/or a full-length light chain variable region corresponding to SEQ ID NO: 2.
Conclusion
Claims 1-5, 9-15, 21-24, and 26 are pending. Claims 11-14 and 22-24 are withdrawn. Claims 1-5, 9-10, 15, 21, and 26 are rejected. No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ALYSSA RAE STONEBRAKER whose telephone number is (571)270-0863. The examiner can normally be reached Monday-Thursday 7:00 am - 5:00 pm.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Samira Jean-Louis can be reached at (571)270-3503. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/ALYSSA RAE STONEBRAKER/Examiner, Art Unit 1642
/Laura B Goddard/Primary Examiner, Art Unit 1642