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 .
Application Status
This action is written in response to applicant’s correspondence received 06/15/2026. Claims 2, 4-7, 9-10, 23, 25-27, 41-42, 44-46, 48, 50-51 and 54 are currently pending. Claims 2, 4-7, 9-10, 23, 45,48, 50 and 54 are withdrawn from prosecution as being drawn to non-elected subject matter. Accordingly, claims 25-27, 41-42, 44, 46, and 51 are examined herein.
Specification
The disclosure is objected to because of the following informalities:
Tables 3 and 5 are not clearly labeled/titled (see Tables 1, 2 and/or 4 for comparison). This impacts the clarity of the disclosure.
Appropriate correction is required.
Nucleotide and/or Amino Acid Sequence Disclosures
REQUIREMENTS FOR PATENT APPLICATIONS CONTAINING NUCLEOTIDE AND/OR AMINO ACID SEQUENCE DISCLOSURES
Items 1) and 2) provide general guidance related to requirements for sequence disclosures.
37 CFR 1.821(c) requires that patent applications which contain disclosures of nucleotide and/or amino acid sequences that fall within the definitions of 37 CFR 1.821(a) must contain a "Sequence Listing," 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 1.821 - 1.825. This "Sequence Listing" part of the disclosure may be submitted:
In accordance with 37 CFR 1.821(c)(1) 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") as an ASCII text file, together with an incorporation-by-reference of the material in the ASCII text file in a separate paragraph of the specification as required by 37 CFR 1.823(b)(1) identifying:
the name of the ASCII text file;
ii) the date of creation; and
iii) the size of the ASCII text file in bytes;
In accordance with 37 CFR 1.821(c)(1) 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 of the material in the ASCII text file according to 37 CFR 1.52(e)(8) and 37 CFR 1.823(b)(1) in a separate paragraph of the specification identifying:
the name of the ASCII text file;
the date of creation; and
the size of the ASCII text file in bytes;
In accordance with 37 CFR 1.821(c)(2) via the USPTO patent electronic filing system as a PDF file (not recommended); or
In accordance with 37 CFR 1.821(c)(3) on physical sheets of paper (not recommended).
When a “Sequence Listing” has been submitted as a PDF file as in 1(c) above (37 CFR 1.821(c)(2)) or on physical sheets of paper as in 1(d) above (37 CFR 1.821(c)(3)), 37 CFR 1.821(e)(1) requires a computer readable form (CRF) of the “Sequence Listing” in accordance with the requirements of 37 CFR 1.824.
If the "Sequence Listing" required by 37 CFR 1.821(c) is filed via the USPTO patent electronic filing system as a PDF, then 37 CFR 1.821(e)(1)(ii) or 1.821(e)(2)(ii) requires submission of a statement that the "Sequence Listing" content of the PDF copy and the CRF copy (the ASCII text file copy) are identical.
If the "Sequence Listing" required by 37 CFR 1.821(c) is filed on paper or read-only optical disc, then 37 CFR 1.821(e)(1)(ii) or 1.821(e)(2)(ii) requires submission of a statement that the "Sequence Listing" content of the paper or read-only optical disc copy and the CRF are identical.
Specific deficiencies and the required response to this Office Action are as follows:
Specific deficiency – Nucleotide and/or amino acid sequences appearing in the drawings are not identified by sequence identifiers in accordance with 37 CFR 1.821(d). Sequence identifiers for nucleotide and/or amino acid sequences must appear either in the drawings or in the Brief Description of the Drawings. Please see FIGs. 2D and 2E, which contain nucleotide sequences of 10 or more nucleotides and unbranched sequences of 4 or more amino acids. See MPEP 2412.03, which states, “Generally, nucleotide sequences that are an unbranched sequence or constitute a linear portion of a branched sequence of 10 or more specifically defined nucleotides are required to be listed in a "Sequence Listing XML." and “Similarly, amino acid sequences that are an unbranched sequence or constitute a linear portion of a branched sequence of 4 or more specifically defined amino acids are required to be listed in a "Sequence Listing XML.".
Required response – Applicant must provide:
Replacement and annotated 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 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.
Specific deficiency - This application fails to comply with the requirements of 37 CFR 1.821 - 1.825 because it does not contain a "Sequence Listing" as a separate part of the disclosure or a CRF of the “Sequence Listing.”. As noted above, the drawings contain nucleotide and amino acid sequences that are required to be listed in a sequence listing, but no sequence listing is present in the application.
Required response - Applicant must provide:
A "Sequence Listing" part of the disclosure; together with
An amendment specifically directing its entry into the application in accordance with 37 CFR 1.825(a)(2);
A statement that the "Sequence Listing" includes no new matter as required by 37 CFR 1.821(a)(4); and
A statement that indicates support for the amendment in the application, as filed, as required by 37 CFR 1.825(a)(3).
If the "Sequence Listing" part of the disclosure is submitted according to item 1) a) or b) above, Applicant must also provide:
A substitute specification in compliance with 37 CFR 1.52, 1.121(b)(3) and 1.125 inserting the required incorporation-by-reference paragraph, 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.
If the "Sequence Listing" part of the disclosure is submitted according to item 1) c) or d) above, applicant must also provide:
A CRF in accordance with 37 CFR 1.821(e)(1) or 1.821(e)(2) as required by 1.825(a)(5); and
A statement according to item 2) a) or b) above.
Election/Restrictions
Applicant's election without traverse of the method of claim 25 from Species Group A and the disease breast cancer and gene BRCA2 from Species Group B, in the reply filed on 06/15/2026, is acknowledged.
Claims 2, 4-7, 9-10, 23, 45, 48, 50 and 54 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected species, there being no allowable generic or linking claim.
Please note: in the remarks of 06/15/2026, Applicant stated that the disease breast cancer and gene BRCA2 are drawn to claims 25-27, 41, 42, 44-46 and 51. However, on review of the claims, the BRCA2 gene is not recited in claim 45, and claim 44, from which it depends, generically recites cancer, not the elected species of breast cancer. Therefore, claim 45 is withdrawn because it is not considered drawn to the elected species.
Claim Rejections - 35 USC § 112(b)
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 51 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 51 refers to tables 3-5. MPEP 2173.05(s) states "Where possible, claims are to be complete in themselves. Incorporation by reference to a specific figure or table "is permitted only in exceptional circumstances where there is no practical way to define the invention in words and where it is more concise to incorporate by reference than duplicating a drawing or table into the claim. Incorporation by reference is a necessity doctrine, not for applicant’s convenience." Ex parte Fressola, 27 USPQ2d 1608, 1609 (Bd. Pat. App. & Inter. 1993) (citations omitted)." In the instant case, the genes and diseases could be recited similarly to the way they are recited in claims 50 and 54.
Additionally, the formatting of tables renders the metes and bounds of the claim unclear. The headers and columns in Tables 3 and 5 are misaligned such that in many cases it is not clear which gene IDS are associated with which metadata (position, type of mutation, disease, etc.), and the genes and diseases are not clearly marked.
Claim Rejections - 35 USC § 112(a) – Enablement
Claims 25-27, 41-42, 44, 46, and 51 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification does not reasonably provide enablement for methods of treating patients . The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
The test of enablement is whether one skilled in the art could make and use the claimed invention from the disclosures in the specification coupled with information known in the art without undue experimentation (United States v. Telectronics., 8 USPQ2d 1217 (Fed. Cir. 1988)). Whether undue experimentation is needed is not based upon a single factor but rather is a conclusion reached by weighing many factors. These factors were outlined in Ex parte Forman, 230 USPQ 546 (Bd. Pat. App. & Inter. 1986) and again in In re Wands, 8 USPQ2d 1400 (Fed. Cir. 1988), and the most relevant factors are indicated below:
Nature of the Invention
The invention is the class of invention that the CAFC has characterized as “the unpredictable arts such as chemistry and biology.” Mycogen Plant Sci., Inc. v. Monsanto Co., 243 F.3d 1316, 1330 (Fed. Cir. 2001).
Breadth of the Claims
Claim interpretation: Applicant regards “nORF” or “non-canonical open reading frame” to mean, “an open reading frame that is transcribed in a cell and consists of a sequence that is present in a gene but is distinct from a canonical open reading frame transcribed from the gene. The nORF may be present in (i) an overlapping region of the cORF in an alternate reading frame, (ii) a 5' untranslated region (UTR) of the cORF, (iii) a 3' UTR of the cORF, (iv) an intronic region of the cORF. or (v) an intergenic region of the cORF.” (p. 6). Applicant regards, “cORF” or “canonical open reading frame” to mean, “an open reading frame that is transcribed in a cell and its associated genetic elements, including the 5’ UTR, the 3’ UTR, the intronic regions, the exonic regions, and the intergenic regions flanking the gene that includes the cORF. A cORF includes either the primary open reading frame that is expressed from a gene, the most abundantly expressed open reading frame expressed from a gene, or an ORF that is annotated in a publicly available database as the primary and/or most abundantly expressed open reading frame from a gene.”. (p. 6-7). The term “the stop codon” as recited in claim 25 is considered to have antecedent basis because an open reading frame, by definition, inherently comprises a stop codon.
Claim 25 encompasses methods of treating any disease in a subject comprising providing a protein encoded by a WT nORF, wherein the subject has a sequence variant in a gene comprising a cORF associated with the disease, and the subject has a sequence of the nORF that is distinct from the cORF, wherein the sequence variant encodes the stop codon in the nORF. In other words, the subject has a mutation in the cORF sequence which encodes a stop codon in the nORF sequence, and this mutation is not present in the WT cORF or WT nORF.
The claim encompasses any disease, from the common cold to cancer. The claim also encompasses any nORF present in a gene associated with the disease, as long as the nORF results from a sequence variant in the cORF and that variant sequence encodes the nORF’s stop codon. The nORF itself may be any kind of nORF encoded anywhere in the gene.
The dependent claims limit the vehicle in which the encoded protein is delivered, the size of the product, additional method steps, and limit the disease to cancer (claim 44) or breast cancer (claim 46), or to any disease/gene combinations in Tables 3-5 (claim 51). Claim 46 also limits the gene to BRCA2. The dependent claims do not limit the nORF itself to any particular nORF sequence, and, with the exception of claims 44, 46 and 51, do not limit the disease and/or gene.
Guidance of the Specification
The specification does not reduce to practice any methods of treatment for any disease in a subject. The specification more broadly discloses a process of curating a nORF dataset. The inventors “investigated potential disease-causing variants that could be due to” stop lost and stop gained variants in nORFs (p. 20 ln 10-20). They further, “annotated the 6.2 million coding and 19.7 million non-coding somatic [cancer] variants” and “highlight 109k potential frameshift, stop gained, or stop lost variants in nORFs that have a less severe consequence in canonical genes” (Table 1) (Id.). The inventors further annotated human disease variants present in the Human Gene Mutation Database and ClinVar databases and identified further nORF variants, using a similar approach to that used previously (p. 21 ln 1-5). This list was curated to “create a short list of disease mutations most likely to have a nORF related cause”, identifying “top 20 cancer-associated genes with mutations with benign consequences in CDS but with deleterious consequences in the nORFs” and “show an example where a theoretical synonymous disease variant has a stop gained effect on a nORF…which would normally be missed as a potential mechanism of pathogenicity” (p. 21 ln 10-20). Table 4 lists several of those mutations. However, it is clear from the specification that these are all potential disease-associated variants which were identified on the basis that the gain of a stop codon might lead to a functional change in the nORF, and that this functional change might be pathogenic in the context of a particular disease. It is important to note that the specification does not describe experimental validation, either in the specification or prior art, for these potential associations, so it is not clear whether the nORF mutations are indeed pathogenic, and if so, how. If they are not, then restoration of WT nORF would not predictably yield an effective treatment.
State of the Art
The genus of diseases encompassed by the claims is vast, and even when limited to cancer, it remains a vast and varied genus with significant differences among the genetic causes, symptoms and treatments of various cancers. The genus of genes associated with any disease is correspondingly large, particularly given the genetic diversity of cancers. The genus of nORFs is also vast, varied, and poorly understood.
As described above, the genus of all disease is vast, ranging from the common cold to cancer. Even if the claims are limited to the genus of “cancer”, Krzyszczyk writes:
…cancer is a complex, extremely heterogeneous condition. There are over 100 types of cancers, located in different organs and subtissues and originating from different cell types…Some cancer types (e.g., colon, breast, and non-Hodgkin’s lymphoma) contain even more specific classifications based on their molecular subtypes…Additionally, expression of markers within the same tumor can change depending on the specific location or stage of cancer. (Krzyszczyk et al. The growing role of precision and personalized medicine for cancer treatment. Technology (Singap World Sci). 2018 ; 6(3-4): 79–100.)
Given the genetic heterogeneity of cancer and the vast number of genetic causes, which may vary from individual to individual and are not fully understood, it would have been difficult to practice the method for the full scope of all cancers. This becomes even more complicated when considering nORFs which may be associated with cancer. As discussed by Orr (of record, cited on an IDS), alternative or non-canonical ORFs and the proteins they encode make up the “dark proteome” (Title) of largely unannotated and undiscovered sequences, with several challenges facing further detection and annotation. For example, regarding bioinformatics approaches to nORF detection, Orr states (p. 1030):
Given that little is known about nested, internal ORFs, to date there also are no algorithms aimed at detecting this type of gene in any species. Overall, despite significant efforts to improve bioinfomatic prediction, the computational methods are usually subjected to a high rates of false positives. Many of these new ORF annotation programs also rely on previously identified alt-ORFs for training and validation. Thus, their ability to identify alt-ORFs is limited to genes similar to the ones that have already been found. Experimental validation of many of the predictions also is missing.
Orr further summarizes the state of the field, stating (p. 1031):
The results of these studies underscore the extent to which genome annotation has underestimated the translated proteome. However, given the caveats of each detection method, we stress the importance of additional validation of protein production. Furthermore, given the observation that alt-ORF translation can change based on media type and stress conditions…proteomic and transcriptomic-based studies are limited by the growth condition in which the cells were sampled
The functions of nORFs are also variable and not well-understood. Orr notes that while, “ uORFs were hypothesized to primarily suppress the translation of main-ORFs.”, “A few eukaryotic uORFs stimulate the translation of mRNAs encoding stress responsive proteins.” (p. 1032).
Orr goes on to state (Id.):
It is perplexing to find that uORFs play both stimulatory and inhibitory roles in the translation of main-ORFs. Molecular mechanisms controlling leaky scanning (start codon skipping) versus reinitiation remain incompletely understood. uORF number, length, position and other features might be critical for the overall regulatory effects, and the study of uORFs is an important area for future work given how much remains to be learned.
Orr further discloses that some nORFs encode translational products, i.e., proteins which may have cellular functions, but that these functions are not well-understood, and that many alt-ORFs may be translated spuriously, and it remains difficult to differentiate between the two (p. 1033):
In addition to regulatory roles of uORF and alt-ORF translation mentioned above, the translational products of some these ORFs have cellular functions…Other alt-ORFs, in contrast, may just be translated spuriously. Detailed mutational studies are needed to differentiate between eukaryotic uORFs and altORFs that produce functional proteins and uORFs that simply provide upstream initiation and termination sites or alt-ORFs corresponding to spurious translation.
Overall, Orr describes a nascent field in which a great deal remains to be understood, and insofar as the identity and function of nORFs is understood, it is variable and unpredictable. MPEP 2164.03 states: “The amount of guidance or direction needed to enable the invention is inversely related to the amount of knowledge in the state of the art as well as the predictability in the art…if little is known in the prior art about the nature of the invention and the art is unpredictable, the specification would need more detail as to how to make and use the invention in order to be enabling…The law requires an enabling disclosure for nascent technology because a person of ordinary skill in the art has little or no knowledge independent from the patentee’s instruction.”.
Experimentation Required
To practice the method as claimed, the ordinary artisan would have to devise methods effective to treat at least all types of cancer, and more broadly any disease, by delivering a WT nORF in subjects with a nORF with a variant stop codon. Given the breadth of the diseases, genes, and the variability and unpredictability of nORF function and association with disease, and the fact that the study of nORFs is a nascent technology and the ordinary artisan would have little guidance beyond applicant’s disclosure, it is the conclusion that an undue amount experimentation would be required to make and use the invention as claimed.
Claim Rejections - 35 USC § 103
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:
Determining the scope and contents of the prior art.
Ascertaining the differences between the prior art and the claims at issue.
Resolving the level of ordinary skill in the pertinent art.
Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
In comparing the claims to the prior art, it is noted that while the claims were previously rejected in this Office Action for lack of enablement, the claims are rejected here insofar as the prior art teaches at least some embodiments encompassed by the claims. However, the application as filed is not particularly enabling for, nor does it specifically describe, the methods taught by the prior art where the application does not principally contemplate or describe those elements as provided in the prior art. Additionally, it is noted that the particular embodiments of the prior art are not enabling for the generic breadth of the methods as claimed.
Claims 25-27, 41-42, 44 and 51 are rejected under 35 U.S.C. 103 as being unpatentable over Occhi (Occhi et al. A Novel Mutation in the Upstream Open Reading Frame of the CDKN1B Gene Causes a MEN4 Phenotype. PLOS Genetics 9(3): e1003350.).
Occhi teaches a subject identified with a sequence variant in a gene comprising a cORF, wherein the sequence variant encodes the stop codon in a nORF present in the 5’ UTR of the cORF (Abstract):
a 4-bp deletion in a highly conserved regulatory upstream ORF (uORF) in the 5’UTR of the CDKN1B gene in a patient with a pituitary adenoma and a well-differentiated pancreatic neoplasm. This deletion causes the shift of the uORF termination codon…
Please see also Figure 2, which shows the wild-type nORF (uORF, part A) and the nORF with the sequence variant c.-456_-453delCCTT (part B) with a mutation that eliminates the original stop codon and shifts it further downstream.
Occhi teaches that the sequence variant of the cORF (i.e., the mutant nORF) is associated with disease:
The CDKN1B gene encodes the cyclin-dependent kinase inhibitor p27KIP1, an atypical tumor suppressor playing a key role in cell cycle regulation, cell proliferation, and differentiation. Impaired p27KIP1 expression and/or localization are often observed in tumor cells, further confirming its central role in regulating the cell cycle. (Abstract)
The 4-bp deletion in CDKN1B gene we describe here led to the reduced production of CDKN1B-encoded protein p27KIP1, probably due to a decreased translation reinitiation rate, which then results in predisposition to tumor development. (p. 6)
The phrase, “wherein the absence of the sequence variant in the WT nORF does not encode the stop codon in the nORF” is somewhat unclear due to the inclusion of double negatives, but is interpreted as meaning that the WT nORF does not comprise the sequence variant which results in the variant stop codon. This is considered an inherent characteristic of the WT sequence, because by definition the WT sequence is the canonical sequence, not a variant. Nonetheless, that limitation is taught by Occhi as described above.
Occhi does not teach treating a subject with the WT nORF. However, Occhi does teach that reintroducing a stop codon and thus restoring uORF length and intercistronic distance almost completely rescued the uORF regulatory properties (p. 4, right, last para; Figure 5c). This would have given the ordinary artisan the expectation that expression of the WT nORF would restore the uORF’s regulatory properties, leading to restored expression of the p27KIP1 tumor suppressor cORF.
It would have been prima facie obvious to a person having ordinary skill in the art before the effective filing date of the claimed invention to have tried providing a protein encoded by a WT CDKN1B nORF, capable of facilitating expression of the p27KIP1 tumor suppressor, to a subject identified with having the variant nORF which represses p27KIP1 and a disease associated with the variant. Based on Occhi’s teachings, the ordinary artisan would have understood that the variant uORF was associated with disease in that subject by repression of a key tumor suppressor, and would have had had a reasonable expectation, based on Occhi’s results in vitro, that administration of a protein encoded by the non-variant nORF would have restored the nORF’s regulatory properties and permitted expression of the tumor suppressor, thereby potentially treating the disease. In identifying one specific disease, mutation, and a way to correct the mutation, Occhi suggests a potential therapeutic approach and presents a finite number of options. One of ordinary skill in the art would have had good reason to pursue the known options within his or her technical grasp. If this leads to the anticipated success, it is likely that the product was not of innovation but of ordinary skill and common sense.
Regarding claim 26, Occhi teaches restoring the encoded protein product of the WT nORF without the sequence variant (see above).
Regarding claim 27, Occhi teaches expressing the protein from a plasmid vector, i.e., a polynucleotide encoding the protein product of the WT nORF (see above, Figure 5).
Regarding claim 41, Occhi teaches wherein the encoded protein product of the WT nORF is fewer than 100 amino acids long (“the 4-bp deletion shifts the uORF termination codon, thus lengthening the uORF encoded peptide from 29 to 158 amino”; p. 2).
Regarding claim 42, Occhi teaches performing a statistical analysis between the variant in the nORF and the disease (i.e., a cohort of patients was screened for mutations in the CDKN1B gene, and a second cohort with similar phenotype was analyzed for the uORF sequence; p. 6, Materials and Methods).
Regarding claim 44, Occhi teaches wherein the disease is cancer (see above).
Regarding claim 51, Occhi teaches wherein the gene is CDKN1B and causes a MEN4 phenotype (Title)(the disease “Multiple endocrine neoplasia type 4” and gene CDKN1B are listed in Table 5 of the instant specification, p. 722).
Conclusion
No claim is allowed at this time.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to AMANDA M ZAHORIK whose telephone number is (703)756-1433. The examiner can normally be reached M-F 8:00-16:00 EST.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Neil Hammell can be reached on (571) 270-5919. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/AMANDA M ZAHORIK/Examiner, Art Unit 1636
Prosecution Insights