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
Claims 11-30 are pending.
Applicant’s election without traverse of Group I, claims 11-16, in the reply filed on 05/18/2026 is acknowledged. Applicant’s election of species of fatty liver as the disease type and nucleic acid drugs in the reply filed on 05/18/2026 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)).
Thus, claims 11-16 are examined here, along with species of fatty liver disease and nucleic acid drugs.
Priority
Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55.
The application claims priority to Chinese application 202010847559.3, filed on 08/21/2020, via its PCT/CN2021/113811, filed on 08/20/2021. Both applications are in foreign language.
Thus, for rejection purposes, the date used for search purposes will be 08/20/2021.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 02/23/2023, 05/18/2026, 05/19/2026 was filed before the mailing date of the instant Office Action. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Only the English abstracts of foreign patent documents are considered.
Nucleotide and/or Amino Acid Sequence Disclosures
Summary of Requirements for Patent Applications Filed On Or After July 1, 2022, That Have Sequence Disclosures
37 CFR 1.831(a) requires that patent applications which contain disclosures of nucleotide and/or amino acid sequences that fall within the definitions of 37 CFR 1.831(b) must contain a “Sequence Listing XML”, as a separate part of the disclosure, which presents the nucleotide and/or amino acid sequences and associated information using the symbols and format in accordance with the requirements of 37 CFR 1.831-1.835. This “Sequence Listing XML” part of the disclosure may be submitted:
1. In accordance with 37 CFR 1.831(a) using the symbols and format requirements of 37 CFR 1.832 through 1.834 via the USPTO patent electronic filing system (see Section I.1 of the Legal Framework for Patent Electronic System (https://www.uspto.gov/PatentLegalFramework), hereinafter “Legal Framework”) in XML format, together with an incorporation by reference statement of the material in the XML file in a separate paragraph of the specification (an incorporation by reference paragraph) as required by 37 CFR 1.835(a)(2) or 1.835(b)(2) identifying:
a. the name of the XML file
b. the date of creation; and
c. the size of the XML file in bytes; or
2. In accordance with 37 CFR 1.831(a) using the symbols and format requirements of 37 CFR 1.832 through 1.834 on read-only optical disc(s) as permitted by 37 CFR 1.52(e)(1)(ii), labeled according to 37 CFR 1.52(e)(5), with an incorporation by reference statement of the material in the XML format according to 37 CFR 1.52(e)(8) and 37 CFR 1.835(a)(2) or 1.835(b)(2) in a separate paragraph of the specification identifying:
a. the name of the XML file;
b. the date of creation; and
c. the size of the XML file in bytes.
SPECIFIC DEFICIENCIES AND THE REQUIRED RESPONSE TO THIS NOTICE ARE AS FOLLOWS:
Specific deficiency - Sequences appearing in the drawings are not identified by sequence identifiers in accordance with 37 CFR 1.831(c). Sequence identifiers for sequences (i.e., “SEQ ID NO:X” or the like) must appear either in the drawings or in the Brief Description of the Drawings.
Fig. 1D, comprises what appears to be amino acid (a.a.) sequences of at least 4 a.a. residues and no sequence identifiers are provided in figure or in brief description of the drawings.
Required response – Applicant must provide:
Amended drawings in accordance with 37 CFR 1.121(d) inserting the required sequence identifiers;
AND/OR
A substitute specification in compliance with 37 CFR 1.52, 1.121(b)(3), and 1.125 inserting the required sequence identifiers (i.e., “SEQ ID NO:X” or the like) into the Brief Description of the Drawings, consisting of:
• A copy of the previously-submitted specification, with deletions shown with strikethrough or brackets and insertions shown with underlining (marked-up version);
• A copy of the amended specification without markings (clean version); and
• A statement that the substitute specification contains no new matter.
Claim Rejections - 35 USC § 112
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.
Claims 11-16 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.
The claim recites “a substance for improving the gene expression of MCM8, the protein expression of MCM8 or the protein activity of MCM8.”
In light of the specification, the claimed invention encompasses 1) any substance for improving the gene expression of MCM8, 2) any substance for improving the protein expression of MCM8, or 3) any substance for improving the protein activity of MCM8.
“A substance” is not defined.
In analyzing whether the written description requirement is met for genus claims, it is first determined whether a representative number of species have been described by their complete structure. In the instant case, the full-length sequence of MCM8 mRNA (and its truncated form) and its expressed protein (or the expressed truncated form) are the only species whose complete structure is disclosed. The genus any substance for improving the gene expression of MCM8, the protein expression of MCM8 or the protein activity of MCM8 encompasses a large number of variants and molecules that have a different structure, the specification does not describe the complete structure of a representative number of species of the large genus of any substance for improving the gene expression of MCM8, the protein expression of MCM8 or the protein activity of MCM8 or functional equivalents thereof. Additionally, the specification does not describe the complete structure of a representative number of species of the large genus of any substance for improving the gene expression of MCM8, the protein expression of MCM8 or the protein activity of MCM8.
Here, the broad genus of any substance encompasses indirect regulators or direct regulators of MCM8 expression, or its protein expression, or its activity.
Next, then, it is determined whether a representative number of species have been sufficiently described by other relevant identifying characteristics (i.e. other than nucleotide sequence), specific features and functional attributes that would distinguish different members of the claimed genus. In the instant case, the only other identifying characteristic are the functional limitations recited in cl. 1. Such a functional limitation cannot be an identifying characteristic for the claimed diverse genus of molecules since by Applicant’s definition of any substance for improving the gene expression of MCM8, the protein expression of MCM8 or the protein activity of MCM8 or functional equivalent thereof all members of the claimed genus will have that characteristic.
The inventions of dependent claims 12-16 require the use of the inventions of Claim 11 and therefore are likewise rejected under 35 U.S.C. 112, first paragraph, as failing to comply with the written description requirement.
Applicant’s attention is directed to the Guidelines for the Examination of Patent Applications Under the 35 U.S.C. 112(a) or Pre-AIA 35 U.S.C. 112, first paragraph, "Written Description" Requirement (MPEP2163).
In conclusion, Applicant’s disclosure of one species of gene mRNA that expressed its protein of the claimed broad genus is not deemed sufficient to reasonably convey to one skilled in the art that Applicant was in possession of the claimed broad genus at the time the application was filed. Thus, it is concluded that the written description requirement is not satisfied for the claimed genus.
35 USC 112(b)
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.
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 11-16 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.
Regarding claims 15, 16, the phrase "preferably" renders the claim indefinite because it is unclear whether the limitations following the phrase are part of the claimed invention. See MPEP § 2173.05(d).
Claim 11 recites “dysfunctional mitophagy” and “abnormal activation of cGAS-STING-IFN-I signaling pathway” and are indefinite since the “metes and bounds” of the phrases are not clear. Mitophagy is a complex process, a form of macroautophagy that involves selectively targeting and engulfing mitochondria for removal through lysosomal degradation (pg. 1, Killackey et al, J. Cell Biol., 2020, 219, e202004029, pg. 1-15). Since mitophagy is a crucial cellular process, “cells have evolved numerous and often overlapping pathways to ensure that mitophagy can occur in a balanced way in response to wide array of stimuli and triggers” (pg. 1): the redundancy “may actually be a good thing” so “when one protein is absent, the whole pathway can still operate” (pg. 2). The process involves multiple molecules (proteins, nucleic acids, lipid, etc. . . ), multiple organelles (endoplasmic reticulum, the Golgi apparatus, the plasma membrane, and mitochondria), thus dysfunction along any one of these entities can result in mitophagy; thus it is uncertain the meaning of “dysfunction.” Thus the phrase “dysfunctional mitophagy” lacks definiteness. Similarly, “abnormal activation of cGAS-STING-IFN-I” is also not clear since the “metes and bounds” of the phrase is not definite. First, “abnormal” is a relative term depending on the status of the cell and the organ. The “cGAS-STING-IFN-1 signaling pathway” is also not clear, does it require abnormal activation of one of the molecules, cGAS, STING or IFN-1, or all three of them.
Further, for claim 11 it should be made clear that, the enabling specification must teach those skilled in the art to make and use the full scope of the claimed invention without undue experimentation. “Although not explicitly stated in section 112, to be enabling, the specification of a patent must teach those skilled in the art how to make and use the full scope of the claimed invention without "undue experimentation." Vaeck, 947 F.2d at 495, 20 USPQ2d at 1444; Wands, 858 F.2d at 736-37, 8 USPQ2d at 1404; In re Fisher, 427 F.2d 833, 839, 166 USPQ 18, 24 (CCPA 1970) (the first paragraph of section 112 requires that the scope of protection sought in a claim bear a reasonable correlation to the scope of enablement provided by the specification).” In re Wright (CAFC) 27 USPQ2d 1510 at 1513. Although a working example is not required to enable an invention, the skilled artisan must be able to practice the claimed invention without undue experimentation. See also, MPEP §2164.02, which states in part: The specification need not contain an example if the invention is otherwise disclosed in such manner that one skilled in the art will be able to practice it without an undue amount of experimentation. In re Borkowski, 422 F.2d 904, 908, 164 USPQ 642, 645 (CCPA 1970). Lack of a working example, however, is a factor to be considered, especially in a case involving an unpredictable and undeveloped art.
Claim 11 recites “a substance for improving the gene expression of MCM8, the protein expression of MCM8 or the protein activity of MCM8.” The claim lacks definiteness since the lack of structural definition or sufficient description of the structure of a substance in the specification along with lack of definition or clarity regarding each of the functional limitation (improving the gene expression of MCM8, improving the protein expression of MCM8, improving the protein activity of MCM8). Thus, a skilled artisan is not sure what is within the “metes and bounds” of the claim since the claim encompasses both an indirect regulation of each of the function or direct regulation of the function. Here, “a substance,” as further limited in claim 15, encompasses micromolecular drug, a polysaccharide drug, a nucleic acid drug, polypeptide or protein drug, lacks any structural definition or is not clearly defined by its structure/chemical/physical features since. E.g., a nucleic acid drug can be an antisense oligomer or a gene, each works in a distinct and completely opposite manner; here, an antisense oligomer can be targeted to any gene whose product regulates MCM8 in a negative feedback manner, or alternatively, an expressed protein product by a gene can regulate MCM8 in a positive feedback manner and thus, a skilled artisan is not sure what is within scope and what is outside scope.
Claim 15 rejected on the basis that it contains an improper Markush grouping of alternatives. See In re Harnisch, 631 F.2d 716, 721-22 (CCPA 1980) and Ex parte Hozumi, 3 USPQ2d 1059, 1060 (Bd. Pat. App. & Int. 1984). A Markush grouping is proper if the alternatives defined by the Markush group (i.e., alternatives from which a selection is to be made in the context of a combination or process, or alternative chemical compounds as a whole) share a “single structural similarity” and a common use. A Markush grouping meets these requirements in two situations. First, a Markush grouping is proper if the alternatives are all members of the same recognized physical or chemical class or the same art-recognized class, and are disclosed in the specification or known in the art to be functionally equivalent and have a common use. Second, where a Markush grouping describes alternative chemical compounds, whether by words or chemical formulas, and the alternatives do not belong to a recognized class as set forth above, the members of the Markush grouping may be considered to share a “single structural similarity” and common use where the alternatives share both a substantial structural feature and a common use that flows from the substantial structural feature. See MPEP § 2117.
The Markush grouping of substance is improper because the alternatives defined by the Markush grouping do not share both a single structural similarity and a common use for the following reasons: here each of the broad species claimed do not share structural similarity or share same recognized physical or chemical class or the same art recognized class (e.g., lipids, carbohydrates and nucleic acid do not share physical or chemical class), since the mechanisms of how each species carries out their functional activity also vary, they cannot be used for common use since they do not share structural features.
To overcome this rejection, Applicant may set forth each alternative (or grouping of patentably indistinct alternatives) within an improper Markush grouping in a series of independent or dependent claims and/or present convincing arguments that the group members recited in the alternative within a single claim in fact share a single structural similarity as well as a common use.
Claims 11-16 explicitly encompass prevention of any disease in a subject. Looking to the prior art for guidance, a search of the prior art did not identify any methods which effectively prevent any disease in a subject. The specification also does not provide any working example demonstrating prevention of any disease in a subject. Therefore, given the lack of knowledge present in the prior art and the lack of guidance provided in the specification with respect to preventing any disease, further experimentation would be required. Considering that the additional experimentation would require de novo experimentation without a guarantee of success, and further considering that any positive results (i.e., successful prevention of any disease in a subject) would amount to a significant advancement in the state of the art, the additional experimentation required is considered undue.
Furthermore, in In re Vaeck, 947 F.2d 488,495, 20 USPQ2d 1438, 1444 (Fed. Cir. 1991), the Court ruled that a rejection under 35 U.S.C. 112, first paragraph for lack of enablement was appropriate given the relatively incomplete understanding in the biotechnological field involved, and the lack of a reasonable correlation between the narrow disclosure in the specification and the broad scope of protection sought in the claims. Such is the case here, where there is a relatively incomplete understanding in the biotechnological field involved, as described above, and the lack of a reasonable correlation between the narrow disclosure in the specification and the broad scope of protection sought in the claims.
Therefore, it is appropriate to reject the claims under 35 USC 112(a) for not being enabled to their full scope. It is noted that amending the claims to, for example, a method of prevention any disease in a subject in need thereof (i.e., remove “prevention” from the claims), would obviate this rejection.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(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.
Claims 11, 15 and 16 are rejected under 35 U.S.C. 102(a)(1) and 102(a)(2) as being anticipated by Mechali et al. (US20090208938, pub. 08/20/2009, “Mechali”, in IDS), as evidenced by Kerr et al. (Trends in Neurosciences, 2017, 40, 151-166) for cl. 11.
Regarding instant cl. 11, 15 and 16, Mechali discloses “use of MCM8 gene for the preparation of a pharmaceutical composition for the treatment of a human and animal pathology linked to a dysfunction of the expression of the MCM8 gene, or of human or animal cancer (abstract, relevant to instant cl. 11, 16). Mechali demonstrates the role of human MCM8 gene coding for a DNA helicase that is involved at the replication forks during the elongation step of DNA synthesis, replication and/or duplication (par. 11-13). Mechali discloses the human MCM8 nucleotide sequence represented by SEQ ID NO: 3 for gene therapy to express the MCM8 protein (par. 34, cl. 33, relevant to instant cl. 11, 15). One of the dysfunction that the drug is contemplated to treat is Alzheimer’s disease (par. 28, relevant to instant cl. 11). Mechali demonstrates expression of MCM8 via plasmid transfection or transduction in various types of cells, including Xenopus and Sf9 insect cells, or in a test-tube of Xenopus egg and its expression was used to study DNA replication (par. 239-241, 249, see generally various examples, e.g., 261-262).
As evidenced by Kerr et al., emerging findings suggest that the autophagy/lysosome pathway that removes damaged mitochondria (mitophagy) is also compromised in AD, resulting in the accumulation of dysfunctional mitochondria (abstract). Kerr also discloses that animal studies of AD and patients with AD suggest that impaired mitophagy contributes to synaptic dysfunction and cognitive deficits by triggering Amyloid-β and Tau accumulation through increases in oxidative damage and cellular energy deficits, these, in turn, impair mitophagy (abstract, relevant to instant cl. 11).
Thus, cl. 11, 15-16 are anticipated.
Claim 14 is rejected under 35 U.S.C. 102(a)(1) as being anticipated by Mechali et al. (US20090208938, pub. 08/20/2009, “Mechali”, in IDS), as evidenced by Kerr et al. (Trends in Neurosciences, 2017, 40, 151-166) for cl. 11 and McEwan et al., (pg. 575; 2017, PNAS, 114, 574-579) for cl. 14.
As evidenced by McEwan et al., (pg. 575; 2017, PNAS, 114, 574-579), TRIM21 is expressed in neural cells, thus it would naturally follow that they either endogenously or exogenously expressed proteins MCM8 and TRIM21 would bind to each other as it is their inherent properties.
Thus, cl. 14 is rejected.
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 nonobviousness.
Claims 11-13, 15-16 are rejected under 35 U.S.C. 103 as being unpatentable over Mechali et al. (US20090208938, pub. 08/20/2009, “Mechali”, in IDS) and Ke (2020, Cells, 9, pg. 1-65).
Mechali discloses “use of MCM8 gene for the preparation of a pharmaceutical composition for the treatment of a human and animal pathology linked to a dysfunction of the expression of the MCM8 gene, or of human or animal cancer (abstract, relevant to instant cl. 11, 16). Mechali demonstrates the role of human MCM8 gene coding for a DNA helicase that is involved at the replication forks during the elongation step of DNA synthesis, replication and/or duplication (par. 11-13). Mechali discloses the human MCM8 nucleotide sequence represented by SEQ ID NO: 3 for gene therapy to express the MCM8 protein (par. 34, cl. 33, relevant to instant cl. 11, 15). Mechali demonstrates expression of MCM8 via plasmid transfection or transduction in various types of cells, including Xenopus and Sf9 insect cells, or in a test-tube of Xenopus egg and its expression was used to study DNA replication (par. 239-241, 249, see generally various examples, e.g., 261-262). Mechali discloses “inactivation of MCM8 gene by the human hepatitis virus, which has been observed in patients with liver cancer. . . may be a direct consequence of the inactivation of the DNA helicase function of MCM8” and generally “[i]nactivation of the MCM8 protein can lead in general to the establishment of a cancerous state” (par. 139-140).
Mechali does not disclose fatty liver disease (cl. 12) or non-alcoholic/alcoholic fatty liver (cl. 13).
Ke discloses that mitophagy is an important event in the regulation of liver physiology and deregulation of mitophagy is implicated in the development of liver-associated diseases, including liver injury, liver steatosis/fatty liver disease, viral hepatitis, and liver cancer (abstract, pg. 1, relevant to instant cl. 12). Ke discloses the alteration of mitochondrial homeostasis in liver cancer and similarly discloses that induction of mitochondrial damage in alcoholic liver disease is known and that mitophagy plays a protective role in combating alcohol-induced mitochondrial dysfunction, hepatic steatosis (pg. 22, Table 3 illustrates roles of mitophagy in steatosis and fatty liver disease, relevant to instant cl. 13).
One of the KSR’s rationale for supporting conclusion of obviousness is “obvious to try,” requiring the following three findings: (1) a finding that at the relevant time, there had been a recognized problem or need in the art, which may include a design need or market pressure to solve a problem; (2) a finding that there had been a finite number of identified, predictable potential solutions to the recognized need or problem; (3) a finding that one of ordinary skill in the art could have pursued the known potential solutions with a reasonable expectation of success.
As Ke discloses that mitophagy is associated with various types of liver disease, including hepatitis, liver cancer and alcoholic liver diseases, thus providing a underlying commonality between various liver diseases.
Therefore, it would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to have tried substituted the treatment of liver cancer and hepatitis with administration of MCM8 gene of Mechali in view of Ke. Since Mechali indicates inactivation of MCM8 gene by the human hepatitis virus, which has been observed in patients with liver cancer may be a direct consequence of the inactivation of the DNA helicase function of MCM8 thus leading to administration of MCM8 gene, thus it would be obvious to substitute administration of MCM8 gene to treat alcoholic fatty liver disease in view of Ke, since Ke identifies that dysregulated mitophagy phenomenon is an underlying link between the liver diseases and mitophagy is critical for functional liver. Thus, cl. 11-13 are obvious.
Claim 14 is rejected under 35 U.S.C. 103 as being unpatentable over Mechali et al. (US20090208938, pub. 08/20/2009, “Mechali”, in IDS) as applied to claim 11-13 above, and further in view of Ding et al. (2015, Tumor Biol., 36, 8761-8772).
Disclosure of Mechali is noted above.
Mechali does not disclose TRIM21.
Ding et al. indicates that TRIM21 is downregulated in liver cancer samples but is expressed at low level (see Table 1 with expression of TRIM21, Fig. 2 in both cancer and normal liver). Thus, it would necessarily follow that the exogenous expression of MCM8 and TRIM21 in liver cancer cells/extract would bind to each other as it is their inherent properties. Thus, cl. 14 would be prima facie obvious.
Allowable Subject Matter
No claim allowed.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to KEYUR A. VYAS whose telephone number is (571)272-0924. The examiner can normally be reached M-F 9am - 4 pm (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, Jennifer Dunston can be reached at 571-272-2916. 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.
/KEYUR A VYAS/Examiner, Art Unit 1637
/Soren Harward/Primary Examiner, TC 1600
Prosecution Insights