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 .
Priority
The instant application, filed 01/17/2023, is a Continuation-in-Part of PCT/US2021/042044, filed 07/16/2021, which claims domestic priority to provisional U.S. application number 63/052,750, filed 07/16/2020.
Amendments and Claim Status
The following amendment filed on 04/01/2026 is acknowledged and entered.
Claims 1, 3, and 4 are amended;
Claims 2 and 5 are cancelled;
Claims 6, 10, and 13-23 remain withdrawn according to 37 CFR § 1.142(b), as being drawn to a non-elected invention and species;
Claims 1, 3, 4, and 6-23 are pending and are under prosecution.
Information Disclosure Statement
The Information Disclosure Statement filed on 04/01/2026 is acknowledged and found to be in compliance with the provisions of 37 CFR § 1.97. Accordingly, the information disclosure statement is considered.
Response to arguments
Applicant’s arguments filed 04/01/2026 with respect to the objection to the specification and the claim rejections under 35 U.S.C. §§ 112(b), 102 (a) (1/2), and 103 have been fully considered.
With respect to the objection to the specification, the objection was included in error on the part of the examiner. As such, rejection is hereby withdrawn.
With respect to the rejection of claims under 35 U.S.C. § 112(b) as being indefinite, the claim amendments made by Applicant are insufficient to overcome the rejection. The rejection clearly delineates that the “the language of consumption of alcohol associated with a kappa opioid receptor” is the language which creates the indefiniteness. The striking of “optionally,” although appropriate, does not define the association to the kappa opioid receptor any further. Neither the claim nor the specification defines what the association requires, or how to measure it. There is no standard for ascertaining the required association, which continues to render the claim indefinite. As such, the rejection is hereby maintained.
With respect to the rejection of claims 1-3, 7-9, and 11 rejected under 35 U.S.C. § 102(a)(1) as being anticipated by Berkel et al. (International Journal of Neuropsychopharmacology, Volume 22, Issue 4, pages 292-302, published December 24, 2018), hereinafter Berkel, the amendment to claim 1, specifying a human subject is sufficient to overcome the rejection on the grounds of anticipation. Accordingly, said rejection is withdrawn. However, the teachings of Berkel are sufficient for the application in a new rejection under 35 USC § 103, centered on obviousness. The arguments made by Applicant are herein addressed as follows.
Applicant argues that Berkel’s disclosure is centered on anxiety, not alcohol consumption—and that the model relies on injections of alcohol introduced by experimentalists. That is, Applicant argues that Berkel measures alcohol-induced changes in anxiety, not anxiety as the causative factor as in the instant claims.
Applicant’s argument is found unpersuasive because the “anxiety effect” and the reduction in voluntary drinking are two intertwined readouts of the rendered obvious method as taught by Berkel. It is well-established in the art that stress and anxiety drive alcohol intake in humans. This is the well-recognized “self-medication” model of drinking, according to Turner et al. (Depress Anxiety, Volume 35, Issue 9, pages 851–860, published July 12, 2018), hereinafter Turner (Abstract, Table 1, pages 851-853). An agent shown to be anxiolytic is therefore reasonably expected to reduce the motivation to drink, especially in people who drink as a coping mechanism for their anxiety. That is precisely what the art models using alcohol-naïve animals, i.e. subjects which do not voluntarily drink alcohol. Rats do not consume alcohol for the psychosocial reasons that humans do. Voluntary intake paradigms are constructed to quantify, in an animal, the stress driven drive to drink. The drive is the same construct Berkel modulates through its anxiety endpoint.
Applicant further notes that UNC0642, at best, “restored” anti-anxiety-like behavior, and that it reduces anxiety even in rats never given alcohol. On this basis, Applicant concludes that the result is “only an anxiety effect” that has “nothing to do with alcohol.” Finally, applicant argues that the model of the prior art in the disclosed model are completely different, and that the prior art cannot show reduced voluntary drinking.
Applicant’s argument is unconvincing because, a conclusion that UNC6042 is anxiolytic, even in alcohol-naïve animals does not sever the link between the use of alcohol in subjects experiencing anxiety. Rather, it confirms the mechanism by which UNC6042 would reduce self-medicating alcohol consumption in a human model, rendering obvious the instant claims. To the extent that claim 1 recites reduced voluntary drinking as a result, the result is the inherent consequence of the same administration method which is disclosed by Berkel. Finally, under 35 U.S.C. § 102, the question is what teachings the prior art discloses, and not whether the model used in the prior art is identical to that disclosed by Applicant.
Finally, Applicant has amended the claims to recite human subjects in an effort to distinguish the instant claims from the teachings of the prior art.
Applicant’s amendment is unconvincing because, Berkel explains that alcohol use disorder is a human psychiatric condition, and describes rapid ethanol tolerance as a reliable index of chronic tolerance relevant to AUD (page 293). Berkel further concludes that the findings “highly the therapeutic potential of targeting G9a and epigenetic pathways in AUD,” (page 293) establishing “heritable, epigenetic mechanisms that may be targeted for the treatment of AUD and anxiety like chromatin remodeling in the brain” (page 298). In view of these explicit statements of therapeutic potential for the treatment of AUD and anxiety, it would have been obvious to a person of ordinary skill in the art prior to the filing of the instant claims to apply the same G9a-inhibition methods to human subjects suffering from AUD and/or anxiety related disorders, with routine adjustment of dose and regimen as needed. Animal models such as those used by Berkel are standard preclinical predictors for human psychiatric and addiction therapies, and a person of ordinary skill would have had a reasonable expectation of targeting the same G9a-associated epigenetic mechanisms in humans would provide similar therapeutic benefit. Accordingly, the recitation in claim 5 that “the subject is a human” represents only the obvious choice of human patients as the intended beneficiaries of the therapeutic method taught, and does not render the claim patentable over the teachings of Berkel.
Therefore, despite amendment, the prior art still continues to renders obvious the limitations of the instant claims. Accordingly, the rejection under 35 USC § 102 is hereby converted to a rejection under 35 USC § 103, and included herein.
With respect to the rejection of claim 5 under 35 U.S.C. § 103 as being unpatentable over Berkel, the cancellation of said claim 5 is sufficient to render the rejection against said claim moot. Accordingly, the rejection is hereby withdrawn.
With respect to the rejection of claim 4 under 35 U.S.C. § 103 as being unpatentable over Berkel and further in view of Walker et al. (Alcohol, Volume 46, Issue 4, pages 359-370, published March 27, 2012), hereinafter Walker.
No unique arguments to rebut rejection made on the grounds of obviousness are presented. Applicant simply states that the deficiencies of Berkel are not remedied by Walker.
Applicants argument is found unconvincing because, Berkel teaches that targeting G9a mechanisms and amygdala circuits has therapeutic potential for AUD and anxiety related phenotypes. Walker teaches that the same escalated and stress-related drinking behaviors are linked with Kappa opioid receptor biological activity, and are reduced by KOR antagonism. A person of ordinary skill in the art seeking to understand and treat AUD would therefore have been motivated to view Berkel’s ethanol-tolerance and anxiety models as occurring in the KOR-dependent stress circuitry described by Walker. Furthermore, the skilled artisan would recognize that the alcohol consumption treated by Berkel is associated with KOR biological activity, as reflected in the instant claims. This combination merely reflects the routine practice of integrating complementary mechanistic frameworks that address the same clinical endpoint, with a reasonable expectation that the underlying KOR involvement identified by Walker, is present in the AUD phenotypes targeted by Berkel.
The combination of the prior art teachings still continue to render the limitations of the instant claims obvious. Accordingly, the rejection is hereby maintained.
With respect to the rejection of claim 12 under 35 U.S.C. § 103 as being unpatentable over Berkel and further in view of McHugh et al. (Psychiatric Clinics of North America, Volume 33, Issue 3, pages 511–525, published July 3, 2010), hereinafter McHugh, no unique arguments to rebut rejection made on the grounds of obviousness are presented. Applicant simply states that the deficiencies of Berkel are not remedied by McHugh.
Applicant’s arguments are unconvincing because McHugh teaches that cognitive behavioral therapy (CBT) for substance use disorders has demonstrated efficacy as both a monotherapy and as part of combination treatment strategies (Abstract). As such, both CBT and treatment with UNC0642 are considered to be used for a common purpose, i.e., the treatment of alcohol use disorder. According to MPEP 2144.06 (I), combining equivalents known for the same purpose is rendered obvious. Therefore, a person of ordinary skill in the art, prior to the effective filing date of the instant claims would have found it obvious to combine Berkel’s pharmacologic G9a-inhibition method with cognitive behavioral therapy, following the teachings of McHugh, because cognitive behavioral therapy is a standard, evidence-based treatment for substance use disorders. Because both Berkel and McHugh’s therapies are directed to the common purpose, treating alcohol use disorder and reducing problematic alcohol consumption, their combination would have been obvious to a person of ordinary skill in the art, with a reasonable expectation of achieving at least additive, if not synergistic benefit. As such, it would have been routine clinical practice to pair a pharmacologic AUD intervention with standard CBT, known to be effective in combination with drug therapy, to address motivational and cognitive barriers, provide skills for relapse prevention, and enhance and maintain reductions in alcohol use.
The combination of the prior art teachings still continue to render the limitations of the instant claims obvious. Accordingly, the rejection is hereby maintained.
Status of Claims
Claims 1, 3, 4, and 6-23 are pending in the instant application. Claims 6, 10, and 13-23 remain withdrawn from further consideration pursuant to 37 CFR § 1.142(b), as being drawn to a non-elected invention and species. Therefore, claims 1, 3, 4, 7-9, 11 and 12 read on an elected invention and species and are therefore under consideration in the instant application.
Claim Interpretation
The instant claims are subject to the following interpretation:
According to the instant specification (page 2, lines 11 -16) the recitation of EHMT2/G9a is centered on the protein euchromatic histone-lysine N-methyltransferase 2, the instant specification. That is, EHMT2 and G9a are different names used to refer to the same protein. As such, any recitation of either EHMT2 or G9a refers to the same protein.
Claim Rejections - 35 U.S.C. § 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.
Claim 4 is 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 4 of the instant application claims that the consumption of alcohol is associated with a kappa opioid receptor (KOR) biological activity in the subject, optionally wherein the KOR biological activity is associated with stress in the subject.
It is unclear what “associated with a kappa opioid receptor biological activity” refers to and how to determine if the alcohol consumption is associated with KOR biological activity. The term “associated with a kappa opioid receptor biological activity” in claim 4 is a relative term which renders the claim indefinite. The term “associated with a kappa opioid receptor biological activity” is not defined by the claims, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention. The specification does not define how to determine if the alcohol consumption is associated with KOR biological activity. Thus it is unclear what would be considered associated with KOR biological activity by a person of ordinary skill in the art. There are a large number of diseases that could be considered associated with KOR biological activity. These diseases can range from Kidney disease to cancer. Moreover, there are diseases that could result from KOR dysfunction that do not directly have KOR at the center of the disease morphology. The claims, as written, do not distinctly claim the disease to which KOR is associated, or how the relation is made—whether it be a disease, condition, or disorder directly implicating KOR dysfunction or a disease which develop as a result of diseases, conditions, or disorders that implicate KOR dysfunction. Thus an ordinary skilled artisan cannot ascertain the metes and bounds of the claimed invention, and thus the claims are properly rejected as being indefinite.
Claim Rejections - 35 U.S.C. § 103
The following is a quotation of pre-AIA 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.
Claims 1, 3, 7-9, and 11 are rejected under 35 U.S.C. § 103 as being unpatentable over Berkel et al. (International Journal of Neuropsychopharmacology, Volume 22, Issue 4, pages 292-302, published December 24, 2018), hereinafter Berkel.
The instant claims are drawn to methods of reducing substance consumption in a human subject with substance use disorder, elected to be alcohol use disorder, by administering an inhibitor of the stone methyl transferase EHMT2/G9a, elected to be the small molecule inhibitor UNC0642. The claims are further drawn to reducing stress or dependence induced alcohol consumption.
Berkel renders obvious the instant claims with the disclosure of the following teachings within the prior art. Within the disclosure, Berkel investigates the role of G9a and G9a-linked H3K9 dimethylation (H3K9me2) in a rapid ethanol tolerance—an established and “reliable index” of chronic tolerance characteristics of alcohol use disorder (AUD) (Abstract). Within the disclosure, adult male rats received saline or ethanol injections, and anxiety like behavior and G9a/HEK9me2 levels in the amygdala are measured (pages 292-294). The paper explains that tolerance to ethanol induced anxiolysis promotes alcohol intake and contributes to AUD development (page 298). Berkel shows that acute ethanol decreases G9a and H3K9me2 in the central amygdala. The G9a inhibitor UNC0642 treatment (2 doses of 2.5 mg/kg at 6 and 23 hours after ethanol exposure) is administered systemically to saline and tolerance groups (page 295). Berkel reports that UNC0642 produces anxiolytic-like effects, and reverses rapid ethanol tolerance without altering general activity (pages 294-296). The treatment using UNC0642 decreases G9a-associated H3K9 in the central amygdala, concluding that this activity within amygdala circuits is a key epigenetic mechanism in AUD and anxiety, and that G9a inhibition (via UNC0642) has the potential to treat AUD as well as anxiety-related disorders (page 298).
Regarding claim 1, Berkel discloses systemic administration of a selective G9a inhibitor (UNC 0642) to adult rats in alcohol relevant rapid ethanol tolerance (RET) model, in order to modulate epigenetic mechanisms that underlie alcohol tolerance and alcohol use disorder (AUD) (Abstract). The treatment produces anxiolytic-like therapeutic effects in subjects exhibiting alcohol-related anxiety and alcohol dependence (pages 294-296).
Further regarding claim 1, Berkel fails to teach the use of human subjects within the disclosure.
However, Berkel explains that alcohol use disorder is a human psychiatric condition, and describes rapid ethanol tolerance as a reliable index of chronic tolerance relevant to AUD (page 293). Berkel further concludes that the findings “highly the therapeutic potential of targeting G9a and epigenetic pathways in AUD,” (page 293) establishing “heritable, epigenetic mechanisms that may be targeted for the treatment of AUD and anxiety like chromatin remodeling in the brain” (page 298).
Although Berkel performs experiments in rats, in view of these explicit statements of therapeutic potential for the treatment of AUD and anxiety, it would have been obvious to a person of ordinary skill in the art prior to the filing of the instant claims to apply the same G9a-inhibition methods to human subjects suffering from AUD and/or anxiety related disorders, with routine adjustment of dose and regimen as needed. Animal models such as those used by Berkel are standard preclinical predictors for human psychiatric and addiction therapies, and a person of ordinary skill would have had a reasonable expectation of targeting the same G9a-associated epigenetic mechanisms in humans would provide similar therapeutic benefit. Accordingly, the recitation in claim 1 that “the subject is a human” represents only the obvious choice of human patients as the intended beneficiaries of the therapeutic method taught, and does not render the claim patentable over the teachings of Berkel.
Regarding claim 2, Berkel teaches that the relevant substance is alcohol, specifically ethanol. All behavioral and molecular studies are conducted in rats exposed to ethanol injections (1g/kg) to induce rapid ethanol tolerance, described as a key component of AUD (Abstract).
Regarding claim 3, Berkel teaches that the alcohol exposure and resulting behavioral changes are dependence- and stress/anxiety-related. In fact, rapid ethanol tolerance is explicitly described as a “reliable index” of chronic tolerance characteristics of AUD. The disclosure explains that tolerance to ethanol’s anxiolytic effects promotes increased alcohol intake, and contributes to AUD development via anxiety/stress-related mechanisms (Abstract, pages 293-295, and 298-300).
Regarding claim 7, Berkel specifically recites levels of H3K9me2 as measured in the nucleus accumbens, related to anxiety, and specifically recites wherein G9a inhibition reduces H3K9me2 in the brain and produce anxiolytic-like effects (page 300).
Regarding claim 8, Berkel teaches repeated administration of UNC0642 over at least one day, wherein rats received two, 2.5 mg/kg doses of UNC0642 at approximately 6 and 23 hours after the first ethanol or saline injection, and before the second ethanol exposure (page 295).
Regarding claim 9, Berkel specifically teaches the use of UNC0642 and inhibiting G9a rapid tolerance to the anxiolytic effects of ethanol (Abstract, page 295).
Regarding claim 11, Berkel teaches that the subjects are in an anxiety-related state and that G9a inhibition with UNC0642 exert significant anxiolytic-like effects. The paper quantifies all anxiety-like behavior, describing ethanol injected subjects as exhibiting anxiety-like phenotypes and concludes that G9a-associated H3K9me2 in amygdala circuits is an epigenetic mechanism of anxiety and AUD (page 299 and 300).
Claim 4 is rejected under 35 U.S.C. § 103 as being unpatentable over Berkel (see earlier citation), as applied to claims 1, 3, 7-9, and 11, above, and further in view of Walker et al. (Alcohol, Volume 46, Issue 4, pages 359-370, published March 27, 2012), hereinafter Walker.
The instant claims are drawn to methods of reducing substance consumption in a human subject with substance use disorder, elected to be alcohol use disorder, by administering an inhibitor of the histone methyl transferase EHMT2/G9a, elected to be the small molecule inhibitor UNC0642. The claims are further drawn to reducing stress or dependence induced alcohol consumption. The instant claims are further drawn to consumption of alcohol associated with an opioid receptor biological activity, associated with stress in the subject (see instant claim 4).
The teachings of Berkel are as set forth above.
Berkel fails to teach wherein the consumption of alcohol is linked to kappa opioid receptor (KOR) biological activity in the subject (see instant claim 4).
The deficiencies of Berkel are remedied by Walker, who teaches wherein the kappa opioid receptor mediates effects of chronic stress on alcohol reward and seeking behaviors, especially in alcohol withdrawal (Abstract). Walker further teaches that the effects of repeated stress can be a precipitating factor for excessive alcohol consumption, and haste in the transition to dependence, or reflective of the repeated cycles of withdrawal that are linked with dependence (page 360). Within the disclosure, Walker indicates that kappa opioid mechanisms play a role in the regulation of stress-related behavior due to withdrawal from alcohol (Abstract, page 360).
Therefore, a person of ordinary skill in the art would be motivated to combine the teachings of Berkel and Walker, because both disclosures are squarely aimed at understanding and treating the same disease—alcohol use disorder, and dependence-related, stressed-linked alcohol consumption. Furthermore, both disclosures act in the same brain and stress/negative affect circuitry. Berkel teaches that targeting G9a mechanisms and amygdala circuits has therapeutic potential for AUD and anxiety related phenotypes. Walker teaches that the same escalated and stress-related drinking behaviors are linked to KOR biological activity, and are reduced by KOR antagonism. A person of ordinary skill in the art seeking to understand and treat AUD would therefore have been motivated to view Berkel’s ethanol-tolerance and anxiety models as occurring in the KOR-dependent stress circuitry described by Walker. Furthermore, the skilled artisan would recognize that the alcohol consumption treated by Berkel is associated with KOR biological activity, as reflected in the instant claims. This combination merely reflects the routine practice of integrating complementary mechanistic frameworks that address the same clinical endpoint, with a reasonable expectation that the underlying KOR involvement identified by Walker, is present in the AUD phenotypes targeted by Berkel.
Claims 12 is rejected under 35 U.S.C. § 103 as being unpatentable over Berkel (see earlier citation), as applied to claims 1, 3, 7-9, and 11, above, and further in view of McHugh et al. (Psychiatric Clinics of North America, Volume 33, Issue 3, pages 511–525, published July 3, 2010), hereinafter McHugh.
The instant claims are drawn to methods of reducing substance consumption in a human subject with substance use disorder, elected to be alcohol use disorder, by administering an inhibitor of the stone methyl transferase EHMT2/G9a, elected to be the small molecule inhibitor UNC0642. The claims are further drawn to reducing stress or dependence induced alcohol consumption.
The teachings of Berkel are as set forth above.
Berkel fails to teach the combination of G9a inhibitor UNC0642 with cognitive behavioral therapy (see instant claim 12).
The deficiencies of Berkel are remedied by McHugh, who teaches that cognitive behavioral therapy (CBT) for substance use disorders has demonstrated efficacy as both a monotherapy and as part of combination treatment strategies (Abstract). McHugh teaches that a number of large-scale trials and quantitative studies support the efficacy of CBT for alcohol use disorders (page 2).
As such, both CBT and treatment with UNC0642 are considered to be used for a common purpose, i.e., the treatment of alcohol use disorder. According to MPEP 2144.06 (I), combining equivalents known for the same purpose is rendered obvious. The courts have said,
It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art." In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) (Claims to a process of preparing a spray-dried detergent by mixing together two conventional spray-dried detergents were held to be prima facie obvious.).
Therefore, it would have been obvious to a person of ordinary skill in the art, prior to the effective filing date of the instant claims to combine Berkel’s pharmacologic G9a-inhibition method with cognitive behavioral therapy, following the teachings of McHugh, because cognitive behavioral therapy is a standard, evidence-based treatment for substance use disorders. As such, it would have been routine clinical practice to pair a pharmacologic AUD intervention with standard CBT, known to be effective in combination with drug therapy, to address motivational and cognitive barriers, provide skills for relapse prevention, and enhance and maintain reductions in alcohol use. Because both Berkel and McHugh’s therapies are directed to the common purpose, treating alcohol use disorder and reducing problematic alcohol consumption, their combination would have been obvious to a person of ordinary skill in the art, with a reasonable expectation of achieving at least additive, if not synergistic benefit.
Conclusion
No claims are allowed.
THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). 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.
Correspondence
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Sophia P. Hirakis whose telephone number is +1 (571) 272-0118. The examiner can normally be reached within the hours of 5:00 am to 5:00pm EST, Monday through Friday.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Adam C. Milligan can be reached on +1 (571) 270-7674. The fax phone number for the organization where this application or proceeding is assigned is +1 (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 +1 (800) 786-9199 (IN USA OR CANADA) or +1 (571) 272-1000.
/SOPHIA P HIRAKIS/Examiner, Art Unit 1623
/KARA R. MCMILLIAN/Primary Examiner, Art Unit 1623
Prosecution Insights