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 of Group (II) in the reply filed on 12/31/2024 is acknowledged with Applicant’s election of ALT-306 as the elected compound of the formula (I)
PNG
media_image1.png
216
338
media_image1.png
Greyscale
and ALS (amyotrophic lateral sclerosis as the elected disease in the reply filed on 12/31/2024 is acknowledged and maintained.
Expansion of Election of Species Requirement
A reasonable and comprehensive search conducted by the Examiner determined that the prior art at the time of the present invention was such that it did render obvious the elected ALT-306 compound species
PNG
media_image1.png
216
338
media_image1.png
Greyscale
. In light of this discovery, the search is expanded to compound ALT-201 as depicted below
PNG
media_image2.png
228
336
media_image2.png
Greyscale
. However, the scope of the search and examination have not been extended to the full scope of the compound of the formulae (I).
Priority
This application is a continuation of U.S. Patent Application No. 17/811,021, filed July 6, 2022, which is a National Phase Application of PCT International Application Number PCT/US2020/022972, filed March 16, 2020, and claims the benefit of U.S. Provisional Application No. 62/820,158, filed March 18, 2019.
Claim Status
Acknowledgement is made of the receipt and entry of the amendment to the claims filed on June 11, 2026. Claims 29-34, 39-41, 43-47, and 49-52 are pending. Claims 1-28, 35-38, 42, and 48 are canceled. Claims 43, 44, and 49-50 are withdrawn. Claims 29-34, 39-41, 45-47, and 51-52 are examined in accordance to the elected species and the expanded species.
Action Summary
Claims 29-34, 39-41, 45-47, and 51-52 rejected under 35 U.S.C. 103 as being unpatentable over Cerione et al (US2012/0220610 A1) in view of Wang et al (Brain Behav Immun. 2017 Jun 15; 66:135–145) and Blasco et al (Current Medicinal Chemistry, 2014, 21, 3551-3575), are maintained.
Claims 29-34, 39-41, 45-46, and 52 rejected under 35 U.S.C. 103 as being unpatentable over Cerione et al (US2012/0220610 A1) in view of Wang et al (Brain Behav Immun. 2017 Jun 15;66:135–145) and Blasco et al (Current Medicinal Chemistry, 2014, 21, 3551-3575), are maintained.
Claims 29-34, 39-41, 45-47, and 51-52 rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-14 of U.S. Patent No. 10,532,034 B2 in view of Wang et al (Brain Behav Immun. 2017 Jun 15;66:135–145) and Blasco et al (Current Medicinal Chemistry, 2014, 21, 3551-3575), are withdrawn because Applicant’s argument that U.S. Patent No. 10,532,034 (reference patent) is not commonly owned, assigned, or subject to a joint research agreement with the instant application, is persuasive.
Claim Rejections - 35 USC § 103
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 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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or non-obviousness.
Claims 29-34, 39-41, 45-47, and 51-52 remain rejected under 35 U.S.C. 103 as being unpatentable over Cerione et al (US2012/0220610 A1) in view of Wang et al (Brain Behav Immun. 2017 Jun 15; 66:135–145) and Blasco et al (Current Medicinal Chemistry, 2014, 21, 3551-3575).
Cerione teaches a method of treating a subject with a condition mediated by production of glutamate from glutamine by glutaminase C, said method comprising: selecting a subject with a condition mediated by production of glutamate from glutamine by glutaminase C and
administering to said selected subject an inhibitor of glutaminase C activity under conditions effective to treat the condition mediated by production of glutamate from glutamine. Moreover, Cerione teaches the inhibitor of glutaminase C activity is preferably compound 968
PNG
media_image3.png
266
348
media_image3.png
Greyscale
, wherein the condition is selected from the group consisting of breast cancer, lung cancer, brain cancer, pancreatic cancer, and colon cancer, and wherein said administering is performed parenterally, orally, subcutaneously, intravenously, intramuscularly, extraperitoneally, by intranasal instillation, or by application to mucous membranes. (See claims 14, 20-21, and Figure 1.) This compound is the same as ALT-59. Cerione teaches the method comprising an effective amount of the compound. (See paragraph [0133].) Cerione teaches a compound of the formula (I)
PNG
media_image4.png
549
811
media_image4.png
Greyscale
, wherein R2a, R3a, R4a, R5a, and R6a are each independently H, halogen, NO2, OH, OR14a, —SR14a, NH2, NHR14a, NR14aR15a, R14aC(O)—, R14aOC(O)—, R14aC(O)O—, C1-C6 alkyl, C2-C6 alkenyl, C2-C6 alkynyl, C3-C6 cycloalkyl, C4-C7 cycloalkylalkyl, aryl C1-C6 alkyl and wherein R11a, R12a, R13a, R14a, R15a, R16a, and R17a are each independently H, halogen, OH, NO2, C1-C6 alkyl, C2-C6 alkenyl, C2-C6 alkynyl, C3-C6 cycloalkyl, C4-C7 cycloalkylalkyl, aryl C1-C6 alkyl, mono or polycyclic aryl. (See claim 14.) Cerione teaches the term alkyl includes methyl, ethyl, n-propyl among others and the term halogen means fluoro, chloro, bromo, and iodo. (See paragraphs [0049] & [0055].) In other words, dimethyl amino and methyl are interchangeable and hydrogen and halogen are also interchangeable.
Cerione does not teach the claimed compound.
PNG
media_image1.png
216
338
media_image1.png
Greyscale
. In addition, Cerione does not teach ALS (amyotrophic lateral sclerosis).
Wang teaches the identification of the pathogenic role of GAC in synaptic and neuronal injury in vivo may have an important clinical implication. Glutaminase dysregulation has been implicated in various neurodegenerative and neuroinflammatory diseases such as HIV-1 associated dementia, multiple sclerosis, amyotrophic lateral sclerosis, and Alzheimer's disease, as well as neuropsychiatric diseases such as schizophrenia. Our model is useful in that it provides a novel tool to assess the consequences of excess production of glutamate on brain function and the model may be used to test novel therapeutic strategies to alleviate excitotoxicity. (See second paragraph of page 10.)
Wang does not teach the claimed compound.
Blasco teaches this article provides an overview of excitotoxicity in ALS, focusing on the events that contribute to excess glutamate, how the excess might damage nerve cells, and how this information is being harnessed in the development of potential new neuroprotective agents. (See Abstract.) Moreover, Blasco teaches between 40% and 75% of patients with sporadic ALS (SALS) are estimated to have defects in glutamate transport leading to excessive extracellular glutamate levels. (See last paragraph of the right column of fifth paragraph.)
The differences between Cerione’s compound 968 and the elected compound are depicted in the shaded areas below:
Compound 968 elected claimed compound
PNG
media_image5.png
266
348
media_image5.png
Greyscale
PNG
media_image6.png
232
324
media_image6.png
Greyscale
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to substitute the dimethyl alkyl with a methyl and further substitute the bromine group adjacent to carbon atom that is attached to the dimethyl amino group with hydrogen to give Applicant’s claimed elected compound. One would have been motivated to do so, because Cerione teaches dimethyl amino and methyl are interchangeable at the R4a position and hydrogen and halogen are also interchangeable at R3a position.
It would have further been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to modify the modified method taught by Cerione by including patient with ALS to give the claimed method. One would have been motivated to do so, because Cerione teaches compound 968 which is an inhibitor of glutaminase C can treat cancer, because, Wang teaches Glutaminase dysregulation has been implicated in various neurodegenerative and neuroinflammatory diseases such as amyotrophic lateral sclerosis (ALS) and the excess production of glutamate on brain function may be used to test novel therapeutic strategies to alleviate excitotoxicity, and also because Blasco teaches the events that contribute to the glutamate excess as a biomarker might contribute to damage nerve cells, and how this information is being harnessed in the development of potential new neuroprotective agents. One would reasonably expect the method of Cerione with the modified compound to effectively treat ALS in addition to cancer by inhibiting glutaminase C activity which synthesizes glutamate.
With respect to the identification of a subject in need of a compound that reduces, inhibits, delays, ameliorates, or prevents TDP-43 toxicity. The combination of Cerione, Wang, and Blasco do not teach a subject in need of a compound that reduces, inhibits, delays, ameliorates, or prevents TDP-43 toxicity. However, the subject with ALS would be considered a subject in need of the modified compound 968. The fact that the modified compound 968 taught by Cerione is the same compound claimed and the fact that the obvious subject taught by Cerione, Wang, and Blasco collectively, the identification step claimed would flow naturally from the collective teaching of Cerione, Wang, and Blasco.
Claims 29-34, 39-41, 45-46, and 52 required rejected under 35 U.S.C. 103 as being unpatentable over Cerione et al (US2012/0220610 A1) in view of Wang et al (Brain Behav Immun. 2017 Jun 15;66:135–145) and Blasco et al (Current Medicinal Chemistry, 2014, 21, 3551-3575).
Cerione teaches a method of treating a subject with a condition mediated by production of glutamate from glutamine by glutaminase C, said method comprising: selecting a subject with a condition mediated by production of glutamate from glutamine by glutaminase C and
administering to said selected subject an inhibitor of glutaminase C activity under conditions effective to treat the condition mediated by production of glutamate from glutamine. Moreover, Cerione teaches the inhibitor of glutaminase C activity is preferably this compound of page 10
PNG
media_image2.png
228
336
media_image2.png
Greyscale
, wherein the condition is selected from the group consisting of breast cancer, lung cancer, brain cancer, pancreatic cancer, and colon cancer, and wherein said administering is performed parenterally, orally, subcutaneously, intravenously, intramuscularly, extraperitoneally, by intranasal instillation, or by application to mucous membranes. (See page 10, claims 14, 20-21, and Figure 1.) Cerione teaches the method comprising an effective amount of the compound. (See paragraph [0133].)
Cerione does not teach ALS (amyotrophic lateral sclerosis). Moreover, Cerione does not teach the expanded compound 201
PNG
media_image2.png
228
336
media_image2.png
Greyscale
Wang teaches the identification of the pathogenic role of GAC in synaptic and neuronal injury in vivo may have an important clinical implication. Glutaminase dysregulation has been implicated in various neurodegenerative and neuroinflammatory diseases such as HIV-1 associated dementia, multiple sclerosis, amyotrophic lateral sclerosis, and Alzheimer's disease, as well as neuropsychiatric diseases such as schizophrenia. Our model is useful in that it provides a novel tool to assess the consequences of excess production of glutamate on brain function and the model may be used to test novel therapeutic strategies to alleviate excitotoxicity. (See second paragraph of page 10.)
Wang does not teach the expanded compound 201.
Blasco teaches this article provides an overview of excitotoxicity in ALS, focusing on the events that contribute to excess glutamate, how the excess might damage nerve cells, and how this information is being harnessed in the development of potential new neuroprotective agents. (See Abstract.) Moreover, Blasco teaches between 40% and 75% of patients with sporadic ALS (SALS) are estimated to have defects in glutamate transport leading to excessive extracellular glutamate levels. (See last paragraph of the right column of fifth paragraph.)
Blasco does not teach the expanded compound 201.
Furthermore, in the absence of showing unobvious results, it would have been obvious to one of ordinary skill in the art at the time of the invention when faced with Cerione to make the instantly claimed derivatives of a known product. The instantly claimed compounds and prior art compounds are common derivatives known as isomers. Compounds which are position isomers (compounds having the same radicals in physically different positions on the same nucleus) are generally of sufficiently close structural similarity that there is a presumed expectation that such compounds possess similar properties. In re Wilder, 563 F.2d 457, 195 USPQ 426 (CCPA 1977). See MPEP 2144.09(11).
Prior art structures do not have to be true homologs or isomers to render structurally similar compounds prima facie obvious. In re Payne, 606 F.2d 303, 203 USPQ 245 (CCPA 1979).
The only structural difference between the claimed and prior art compounds and the claimed compounds is that the claimed compound has
PNG
media_image7.png
124
150
media_image7.png
Greyscale
, whereas the prior art compound has
PNG
media_image8.png
120
180
media_image8.png
Greyscale
The court held that although the prior art compounds were not true homologs or isomers of the claimed compounds, the similarity between the chemical structures and properties is sufficiently close that one of ordinary skill in the art would have been motivated to make the claimed compounds in searching for new pesticides.). See MPEP 2144.09 (111).
Guided by the teaching of Wynne et al, one skilled in the art would be able to make similar compounds by making isomers of the known compound. The motivation would be to prepare similar compounds that are pharmacologically active compounds that treat tuberculosis. The instant obviousness rejection is based on the close structural similarity of the instantly claimed compounds to the prior art compounds and the common utility shared among the compounds. There is an expectation among those of ordinary skill in the art that similar structural compounds will have similar properties and that modification of a known structure is mere experimentation within the means of a skilled artisan. See MPEP 2144.09(I).
It would have further been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to modify the method taught by Cerione to include patient with ALS to give the claimed method. One would have been motivated to do so, because Cerione teaches the modified compound which is an inhibitor of glutaminase C can treat cancer, because, Wang teaches Glutaminase dysregulation has been implicated in various neurodegenerative and neuroinflammatory diseases such as amyotrophic lateral sclerosis (ALS) and the excess production of glutamate on brain function may be used to test novel therapeutic strategies to alleviate excitotoxicity, and also because Blasco teaches the events that contribute to the glutamate excess as a biomarker might contribute to damage nerve cells, and how this information is being harnessed in the development of potential new neuroprotective agents. One would reasonably expect the modified method of Cerione to effectively treat ALS in addition to cancer by inhibiting glutaminase C activity which synthesizes glutamate.
With respect to the identification of a subject in need of a compound that reduces, inhibits, delays, ameliorates, or prevents TDP-43 toxicity. The combination of Cerione, Wang, and Blasco do not teach a subject in need of a compound that reduces, inhibits, delays, ameliorates, or prevents TDP-43 toxicity. However, the subject with ALS would be considered a subject in need of compound 968, which is the same compound as ALT-59. The fact that compound 968 taught by Cerione is the same compound claimed and the fact that the obvious subject taught by Cerione, Wang, and Blasco collectively, the identification step claimed would flow naturally from the collective teaching of Cerione, Wang, and Blasco.
Acknowledgement is made of the receipt and entry of Applicant’s arguments/responses filed on June 11, 2026.
I. Applicant’s argument that Cerione does not teach a glutaminase inhibitor is not persuasive.
Applicant argues that compound 968 disclosed by Cerione allegedly does not function as a glutaminase inhibitor based upon the Declaration submitted under 37 CFR 1.132 on 12/05/2025 and therefore cannot provide motivation for the presently claimed invention.
This argument is not persuasive. The rejection does not rely solely upon Applicant’s characterization of the precise biochemical mechanism ultimately responsible for the activity of Compound 9689. Rather, Cerione teaches administration of Compound 968 for treating diseases mediated through glumaminase C (GAC), thereby identifying Compound 968 as a therapeutically useful compound within the disclosed genus. A person of ordinary skill in the art is entitled to rely upon the express teachings of the prior art reference itself. Even assuming, arguendo, that Compound 968 exhibits additional mechanisms of action or that Applicant’s Declaration raises questions regarding its precise biochemical mechanism, such evidence does not negate Cerione’s disclosure or eliminate its teaching that Compound 968 is an appropriate starting point for medicinal chemistry optimization. Furthermore, the claims do not require any particular mechanism by which the administered compound achieves the claimed therapeutic effect. The claims are directed to administration of the claimed compound for treating the recited disease and do not require demonstrating glutaminase inhibition as a claim limitation. Applicant’s argument improperly imports mechanistic limitations from the Specification into the claims. Accordingly, Applicant’s Declaration does not overcome the teachings relied upon in the rejection.
II. Applicant’s argument the excess glutamate is merely a biomarker rather than a therapeutic target is not persuasive.
Applicant argues that Wang and Blasco allegedly demonstrate only that glutamate is a downstream marker for ALS rather than a causative factor and therefore fail to provide motivation to combine with Cerione.
This argument is not persuasive. Neither the rejection nor the cited references require proof that glutamate dysregulation constitutes the sole or primary cause of ALS. Rather, Wang expressly teaches that glutaminase dysregulation has been implicated in multiple neurodegenerative and neuroinflammatory disorders, including amyotrophic lateral sclerosis (ALS), and further teaches that the disclosed transgenic model provides a useful platform for testing therapeutic strategies designed to alleviate glutamate-mediated excitotoxicity. Accordingly, Wang identifies glutaminase-mediated glutamate production as a biologically relevant therapeutic pathway worthy of investigation. Similarly, Blasco teaches that glutamate-mediated excitotoxicity contributes to neuronal injury in ALS and discusses ongoing efforts to develop neuroprotective agents directed toward glutamate-associated pathways. Although Blasco acknowledges that ASL possesses a multifactorial etiology, the reference nevertheless recognizes glutamate-mediated excitotoxicity as an important pathological component of the disease and discuss therapeutic approaches directed toward reducing glutamate activity. A reference needs not establish a proposed therapeutic target is the exclusive cause of a disease in order to provide motivation to investigate or modify known therapeutic agents. Under KSR int’l Co. v. Teleflex Inc. 550 U.S. 398 (2007), obviousness requires only an articulated reason that would have prompted a person of ordinary skill in the art to pursue the claimed modification with a reasonable expectation of success, not absolute certainty regarding disease mechanism. Applicant therefore improperly elevates the legal standard by requiring proof of clinical efficacy or complete understanding of ALS pathogenesis before a motivation to combine can exist.
III. Applicant’s argument that Wang merely provides an experimental model is not persuasive. Applicant further argues that Wang merely establishes a research model and therefore fails to suggest treatment of ALS using glutaminase inhibitors.
This argument is not persuasive. Wang expressly states that the disclosed model may be used to treat novel therapeutic strategies to alleviate excitotoxicity. Such disclosure would reasonably suggest to one of ordinary skill in the art that compounds known to modulate glutaminase-mediated glutamate production represents suitable candidates for investigation in disease involving glutamate dysregulation, including ALS. The obviousness rejection does not rely upon Wang as demonstrating clinical efficacy as demonstrating clinical efficacy. Instead, Wang provides additional evidence that glutaminase dysregulation is biologically relevant in ALS and therefore provides further motivation to evaluate therapeutical active glutaminate-related compounds disclosed in Cerione in the context of ALS.
IV. Applicant’s lead compound arguments are not persuasive. Applicant argues that Cerione fails to identify Compound 968 as a lead compound and therefore the rejection allegedly fails under Takeda Chemical Industries, LTD. V. Alphapharm Pty. Ltd. And Eisai Co. Ltd. V. Dr. Reddy’s Laboratories Ltd.
This argument is not persuasive. Unlike the circumstances presented in Takeda and Eisai, the present rejection is not based upon selecting an arbitrary compound from and expansive disclosure without guidance. Rather, Cerione specifically discloses Compound 968 as an active species compound suitable for therapeutic use and further teaches the interchangeability of the substituents modified by the presently claimed compound. Cerione expressly discloses the relevant substituent variations and identifies those positions as appropriate sites for medicinal chemistry optimization. Moreover, the rejection is independently supported by the close structural similarity between the claimed compound and the prior art compound. As recognized in the in re Wilder, 563 F.2d 457 (CCPA 1977), structurally similar compounds create an expectation that similar compound will possess similar biological properties. Likewise, in re Payne, 606 F.2d 303 (CCPA 1979), explains prior art compounds need not be identical homologs or isomers in order to render structurally similar compounds prima facie obvious. Applicant has not presented persuasive evidence that the structural modifications relied upon in the rejection produce unexpected properties sufficient to rebut the prima facie case.
V. Applicant’s argument that Cerione teaches away is not persuasive.
Applicant argues that Cerione allegedly teaches away because certain analogs exhibit reduced biological activity following modification of substituents.
This argument is not persuasive. A reference teaches away only when it criticizes, discredits, or otherwise discourages the claimed modification. Merely demonstration that some structural modifications produce reduced activity does not amount to teach away. Medical chemistry routinely involves optimization of known scaffolds through systemic modification of substituents with the expectation that some analogs will improve while other may diminish. Indeed, Cerione broadly teaches variation of substituents throughout the disclosed genus expressly contemplates modification at the position relied upon in the rejection. Consequently, Cerione encourages, rather than discourages, medicinal chemistry optimization of the disclosed compound.
VI. Applicant’s argument that there was not reasonable expectation of success is not persuasive. Applicant further argues that the unpredictability of drug discovery preludes any reasonable expectation of success.
The Examiner disagrees. Reasonable expectation of success does not require absolute predictability or certainty of achieving the desired result. Rather, the proper inquiry is whether a person of ordinary skill in the art would have reasonably expected the proposed modification to produce a compound possessing similar biological properties. Here, Cerione teaches therapeutically active compounds, expressly teaches interchangeable substituents relevant to the claimed modification, and provides the medicinal chemistry framework for producing structurally related analogs. Wang and Blasso further identify glutaminase-associated glutamate dysregulation as a biologically relevant pathway implicated in ALS and discuss therapeutic intervention directed toward glutamate-mediated excitotoxicity. Collectively, these teaching would have provided one of ordinary skill in the art with a reasonable expectation that structurally similar glutaminase-related compound could be evaluated for the treatment of ALS. Applicant has not provided objective evidence demonstrating that the presently claimed compound exhibits unexpected results relative to the closest prior art sufficient to outweigh the strong prima facie case established by the structural similarity and collective teachings of the cited references.
VII. Applicant’s arguments directed to the expanded species (ATL-201) are likewise not persuasive. Applicant presents substantially the same arguments with respect to the expanded compound ALT-201.
These arguments are not persuasive for substantially the reasons discussed above. The rejection is based upon the close structurally similarity between the claimed compound and the prior art compound together with Cerione’s express teachings regarding permissible structural modifications and the additional motivation supplied by Wang and Blasco. Applicant has not demonstrated that the modifications relied upon in the rejection produce unexpected results or otherwise rebut the prima facie case of obviousness.
VIII. For the foregoing reasons, Applicant’s arguments have been fully considered and are not persuasive. The combination of Cerione, Wang, and Blasco continues to establish that it would have been obvious to a person of ordinary skill in the art at the time the invention was filed to modify the prior art compounds as set forth in the rejection and to employ the resulting compounds in the treatment of ALS with a reasonable expectation of success.
Conclusion
Claims 29-34, 39-41, 45-47, and 51-52 are not allowed.
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to JEAN P CORNET whose telephone number is (571)270-7669. The examiner can normally be reached Monday-Thursday from 7.00am-5.30pm.
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, Amy L Clark can be reached on 571-272-1310. 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.
/JEAN P CORNET/Primary Examiner, Art Unit 1628
Prosecution Insights