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
The action is written in response to applicant’s correspondence received on 12/19/2023. Claims 1-18, and 34-35 are currently pending in the instant application.
Priority
The instant application claims foreign priority to CN202110665266.8 with an effective filing date of 6/16/2021. The Certified Copy of Foreign Priority was filed on 12/15/2023 and has been acknowledged.
Specification
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:
In page 7, line 10 of the instant specification, applicant recites a non-limiting example of a N-terminal basic domain NLS as PKKKRKV, exceeding the 4-amino acid limit without an accompanying SEQ ID NO.
Claim Interpretation
Regarding claim 12, applicant recites wherein the vector comprising the nucleic acid molecule comprises a lentiviral vector and an AAV vector. It is unclear if applicant intends to claim a vector that is both a lentiviral vector AND an AAV vector. To one skilled in the art, a viral vector cannot be both an AAV and lentivirus as they are fundamentally different virus families with distinct mechanisms and structures. Looking to the instant specification for guidance, applicant recites “in the present invention, the vector may comprise a viral vector. In the present application, the viral vector may comprise lentiviral vectors, retroviral vectors, adenoviral vectors, AAV vectors, and/or herpes simplex virus vectors” (see page 15, line 24). Applicant does not make mention of a dual vector system comprising of both a lentiviral vector and AAV vector. Therefore, claim 12 will be interpreted as the vector can be a lentiviral vector or an AAV vector.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1-18 and 34-35 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.
Breadth of the Claims
With regards to the breadth of the claims, the instant claim 1 broadly recites a PRPF31 variant comprising an exogenous NLS domain, wherein the PRPF31 variant can be any variant. The applicant does provide limitations regarding the NLS limiting an amino acid sequence comprising SEQ ID NO: 3 to 4. The term “variant” is described as a polypeptide or protein that differs from polypeptide or proteins derived therefrom by one or more lengths of sequence changes. A variant may comprise fragments, or derivatives of the parent polypeptide or protein (see page 6 of the instant specification).
Species Described by Complete Structure or Reduction to Practice
With regards to the species described by complete structure or reduction to practice, the instant specification describes SEQ ID NO: 20 to 21 as amino acid sequence for the PRPF31 variant. In working examples, example 1 proposes a Mcherry-PRPF31 set forth in SEQ ID NO: 34 and the nucleotide sequence of the human PRPF31 variant set forth in SEQ ID NO: 25. Furthermore, Fig. 7-9 of the instant application discloses testing of the different PRPF31 variants describes 9 different variants.
Taken together, given the broadness of the general term “variant” which can refer to a PRPF31 protein or polypeptide with at least one differing sequence change, or a fragment thereof, the instant specification only provides guidance on nine variants. Therefore, it is clear the instant specification adequately describes the claimed invention in such a way to reasonably convey to one skilled in the relevant art that the instant co-inventors had possession of all the claimed inventions (i.e. any PRPF31 variant with an exogenous NLS) at the time the application was filed.
Scope of Enablement
Claims 15-18 and 34-35 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for a method of treating autosomal dominant retinitis pigmentosa (ADRP), does not reasonably provide enablement for a method of treating any disease. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and 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 vs 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 Wands factors are indicated below:
As stated in MPEP §2164.01(a), “there are many factors to consider when determining whether there is sufficient evidence to support a determination that a disclosure does not satisfy the enablement requirement and whether any experimentation is ‘undue’.” These factors include, but are not limited to:
A. The nature of the invention;
B. The breadth of the claims;
C. The state of the prior art;
D. The level of skill in the art;
E. The level of predictability in the art;
F. The amount of direction provided by the inventor;
G. The presence or absence of working examples;
H. The quantity of experimentation necessarily needed to make or use the invention based on the disclosure.
See In re Wands USPQ 2d 1400 (CAFC 1988).
Nature of the Invention
Claim 15 recites a method for treating a disease, comprising the step of administering the PRPF31 variant according to claim 1, a nucleic acid molecule encoding the PRPF31 variant, and/or a vector comprising the nucleic acid molecule to a subject in need thereof. As this is directed to a method of treatment, applicant intends to administer the composition to a subject, wherein the subject can be human, in order to see a therapeutic effect on a disease.
The Breadth of the Claims
Claim 15 is broad. Though applicant claims wherein the vector or nucleic acid molecule comprises of the PRPF31 variant, the method is directed to the treatment of any disease.
The State of the Prior Art and Level of Predictability
The state of the art supports a modified transgene, such as PRPF31, with an exogenous NLS, for the treatment of ocular diseases, specifically retinitis pigmentosa, as evidenced by Lewis et al. (US 2017/0218379 A1, published 8/3/2017) and Yin et al. (Mutant Prpf31 causes pre-mRNA splicing defects and rod photoreceptor cell degeneration in zebrafish model for Retinitis pigmentosa, Molecular Degeneration, Volume 6, Article 56, all pages, published 7/30/2011).
Lewis specifically teaches where the transgenes in the present invention encodes a human gene expression in an ocular cell (see paragraph 0097). Yin teaches where mutations in housekeeping genes are associated with retinitis pigmentosa (RP) etiology, such as PRPF31, which are involved in pre-mRNA splicing and represent the second-largest contribution to RP after mutations in rhodopsin (rho) (see background section).
Clearly, the state of the art discloses PRPF31 is a gene that is associated with ocular diseases, such as retinitis pigmentosa. Therefore, as a method for administering a composition encoding a PRPF31 variant, it is uncertain and unlikely where the administration of such a composition could be applied to any other disease such as cancer, DMD, cardiac diseases, etc.
The Presence or Absence of Working Examples
For working examples, the applicant provides Figs 7-9 which examines the effects on different NLS sequence on mRNA splicing of the RHO report gene. These experiments were done in-vitro, in retinal pigment epithelium (RPE) cells. Applicant does not provide examples of testing the PRPF31 variant in other cell types associated with a plethora of diseases.
The Quantity of Undue Experimentation
The quantity of undue experimentation is very high. One skilled in the art would need to test the claimed PRPF31 variant in all cell types associated with any disease and conclude that the variant results in a therapeutic effective or treatment.
Conclusion of 35 U.S.C. 112(a) Scope of Enablement Analysis
After applying the Wands factors analysis to claims 15-18 and 34-35, taking into the consideration the factors outlined above, it is concluded that the specification is not fully enabled for a method of treatment of a diseases, wherein the disease can be any diseases, through the administration of a PRPF31 variant. Absent evidence to the contrary, applicant only provides evidence of mRNA splicing of the RHO gene with a PRPF31 variant, which is recognized in the art to be associated with a specific ocular disease, better known as retinitis pigmentosa.
Therefore, claims 15-18 and 34-35 are rejected under 35 U.S.C. 112(a) for failing to disclose sufficient information to enable a person of skill in the art to use the invention commensurate in scope with these claims.
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.
Claims 1-9 are rejected under 35 U.S.C. 103 as being unpatentable over Lewis et al. (US 2017/0218379 A1, published 8/3/2017) in view of Anguela et al. (WO 2019/210267 A2, published 10/31/2019), Nelles et al. (WO 2021007529 A1, published 1/14/2021) and Yin et al. (Mutant Prpf31 causes pre-mRNA splicing defects and rod photoreceptor cell degeneration in zebrafish model for Retinitis pigmentosa, Molecular Degeneration, Volume 6, Article 56, all pages, published 7/30/2011).
Regarding claim 1, Lewis teaches a self-regulating gene expression construct which comprises a single promoter with a repressor sequence, operator sequence responsive to the expressed repressor protein, and a transgene (see abstract). The transgene can be PRPF31, wherein Lewis states the transgene encodes a human gene expression in an ocular cell (see paragraph 0097). Lewis further teaches where in other embodiments, the cassette further comprises a nuclear localization sequence (NLS) (see paragraph 0117) and where each component of the cassette is codon optimized for expression in human cells (see paragraph 0117).
Regarding claim 6, Lewis teaches where the transgenes useful in these cassettes are not limited to human transgenes (see paragraph 0112). One skilled in the art would recognize that if the transgenes of this invention are not limited to human transgenes, then the transgenes described in the preferred embodiment corresponds to human transgenes. Therefore a codon optimized variant of PRPF31 would be derived from the human PRPF31 gene.
Regarding claim 8, Lewis teaches the heterologous self-regulating gene expression cassette comprises in operative association, the nucleic acid sequences providing or encoding…(E) a selected transgene sequence (see paragraph 0123).
Regarding claim 1 and 2, Lewis does not teach where the exogenous NLS domain comprises an amino acid sequence set forth in any of SEQ ID NOs: 3-4 (claim 1) or where the NLS domain is NOT wild-type PRPF31 (claim 2).
Regarding claim 3 and 4, Lewis does not specifically teach where the PRPF31 variant comprises an NOSIC domain or NOP domain.
Regarding claim 5, Lewis does not teach where the PRPF31 variant is capable of splicing the mRNA of a gene, wherein the gene comprises a RHO gene.
Regarding claim 7, Lewis does not teach a where the PRPF31 variant according to claim 1 comprises an amino acid sequence set forth in any of SEQ ID NOs 20 to 21. However, shown below are SEQ ID NO: 20 and 21 aligned with the WT human PRPF31 amino acid sequence.
SEQ ID NO: 20
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SEQ ID NO: 21
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One skilled in the art would recognize that through routine optimization for the expression of the PRPF31 variant in human cells as taught by Lewis (paragraph 0117), one would eventually arrive at either SEQ ID NO: 20 or 21, absent evidence to the contrary.
Regarding claim 9, Lewis does not teach where the nucleic acid molecule of claim 8 comprise a nucleotide sequence set forth in any of SEQ ID NOs 28 to 29.
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Regarding claim 1, Anguela teaches modified AAV capsid proteins, wherein proteins have been modified to have a peptide insertion comprising a nuclear localization signal (NLS) (see abstract). Anguela further teaches SEQ ID NO: 88 which has 100% identity and length to SEQ ID NO: 4 of the instant application, as shown below.
Regarding claim 2, Anguela teaches SEQ ID NO: 88 is a NLS domain derived from the hnRNP_D gene, which is not a domain from WT PRPF31 (see paragraph 0226, Table 2).
Regarding claim 3 and 4, Yin teaches the human PRPF31 gene contains 14 exons and encodes a protein of 499 amino acids (aa), which has a predicated NOSIC domain found in the RNA-binding proteins located at aa 93-144, a conserved RNA-binding NOP domain at aa 190-334, and a predicted nuclear localization signal (NLS) at aa 351-364 (see section titled ‘Generation of zebrafish Prpf31 variants mimicking human AD5 and SP117 mutation).
Regarding claim 5, Yin teaches mutations in housekeeping genes are associated with retinitis pigmentosa (RP) etiology, such as PRPF31, which are involved in pre-mRNA splicing and represent the second-largest contribution to RP after mutations in rhodopsin (rho) (see background section). Yin further teaches Fig. 7 which shows a subject (fish) with a control and mutated version of PRPF31 and how the mutation affects Rho splicing (see Fig. 7). It is evidenced by Yin that the PRPF31 gene is responsible for pre-mRNA splicing activity that can be directed at genes associated with RP, including Rho.
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Regarding claim 8 and 9, Nelles teaches a composition comprising a nucleic acid sequence encoding a target RNA knockdown and replacement therapeutic comprising (a) an RNA-binding polypeptide or portion thereof, and (b) a therapeutic protein) (see claim 1) and SEQ ID NO: 489 which has a best local similarity of 98.1% local similarity to SEQ ID NO: 28 (shown below). Nelles teaches where the therapeutic protein is selected from the group consisting…PRPF31 (see claim 3).
It would have been obvious to one with ordinary skill in the art, before the effective filing date of the claimed invention, to have combined the teachings of Lewis, Anguela, Nelles, and Yin to arrive at a PRPF31 variant comprising an exogenous NLS domain or truncated version thereof, wherein the exogenous NLS domain comprises an amino acid sequence set forth in any of SEQ ID NO: 3-4.
One would expect a reasonable chance of success as Lewis teaches a construct wherein the transgene PRPF31 can be expressed on a vector with self-regulating gene expression switches used to regulate transgene expression (see paragraph 0010), wherein the cassette could further comprise of a NLS (see paragraph 0117). Furthermore, Anguela teaches wherein the NLS of SEQ ID NO: 4 can be used to mediate or facilitate nuclear import (passage into the cellular nuclease) of molecules such as proteins by binding to NLS receptors (see paragraph 0083). Though SEQ ID NO: 20 or 21 and SEQ ID NO: 28 to 29 are not taught in the art to 100% identity, Lewis recites that any component of the cassette, including
through routine optimization, one with skill in the art would eventually arrive at SEQ ID NO: 20 or 21 and SEQ ID NO: 28 and 29, absent evidence to the contrary. This is further evidenced by Fougerolles et al. (US 20130115272A1) which teaches modified nucleotides and nucleic acids and SEQ ID NO: 60400 which is only 1 amino acid longer than SEQ ID NO: 20 and has 97.9% identity as well as Nelles, wherein a nucleic acid sequence SEQ ID NO: 489 (see claim 3 and paragraph 0037), would result in a sequence that has 98.1% local similarity to SEQ ID NO: 28.
Furthermore, Yin teaches where human PRPF31 contains a NOSIC and NOP domain, and where PRPF31 is involved in splicing of a variety of genes, including RHO, as described above.
One would be motivated to combine said arts in order to arrive at a nucleic acid sequence encoding a PRPF31 variant that is optimized for expression in human cells. As noted by Yin, mutations in PRPF31 is a large part of RP etiology. Therefore, by using the compositions taught above, one skilled in the art would arrive at a nucleic acid sequence encoding an optimized therapeutic protein, such as PRPF31, which can further be used therapeutically to target ocular diseases (see Lewis paragraph 0097 and 0098).
In view of the foregoing, claims 1-9 is rejected under 35 U.S.C. 103 as being prima facie obvious before the effective filing date.
Claims 10-14 are rejected under 35 U.S.C. 103 as being unpatentable over Lewis et al. (US 2017/0218379 A1, published 8/3/2017) in view of Anguela et al. (WO 2019/210267 A2, published 10/31/2019).
Regarding claim 10, Lewis and Anguela teach the composition of claim 1 and 8 which recites a nucleic acid molecule encoding a PRPF31 variant, achieved through codon optimization, with a NLS of SEQ ID NO: 4, as described above.
Regarding claims 10-12, Lewis teaches where another aspect of this invention is a recombinant vector containing the heterologous gene expression construct or cassette (see paragraph 0127). Lew further teaches where in one embodiment, the vector may be a retroviral vector, such as a lentivector. In another embodiment, a suitable vector is an adeno-associated viral vector (see paragraph 0128).
Regarding claim 13, Lewis teaches where the lentiviral vectors can be the equine infectious anemia virus, feline and bovine immunodeficiency virus, and HIV-based vectors (see paragraph 0135).
Regarding claim 14, Lewis teaches the AAV may have one of the multiple AAV serotypes (i.e., any one of the known AAV1-10 as well as engineered AAV variants) (see paragraph 0131).
It would have been obvious to one with ordinary skill in the art, before the effective filing date of the claimed invention, to combine the teachings of Lewis and Anguela to arrive at a vector comprising a PRPF31 variant comprising an exogenous NLS, as recited in claim 10-14.
One would expect a reasonable chance of success as Lewis teaches wherein the composition expressing the transgene can be in a non-replicating viral vector (paragraph 0128). Lewis further teaches wherein the vector is a lentiviral vector or an adeno-associated viral vector (see paragraph 0128).
One would be motivated to do so as it is known to one skilled in the art that AAV vectors are used as delivery vehicles in modern gene therapy in order to safely transport genetic material, such as therapeutic polypeptide, into cells of interest. Therefore, one would use a vector to therapeutically deliver a variant PRPF31 to a subject. Furthermore, Lewis teaches recombinant AAVs vectors have been developed for gene replacement therapy as they are non-pathogenic and exhibit a broad range of tissue specificity (see paragraph 0129).
In view of the foregoing, claims 10-14 are rejected under 35 U.S.C. 103 as being prima facie obvious before the effective filing date.
Claims 15-18 and 34-35 are rejected under 35 U.S.C. 103 as being unpatentable over Lewis et al. (US 2017/0218379 A1, published 8/3/2017) in view of Anguela et al. (WO 2019/210267 A2, published 10/31/2019) and Yin et al. (Mutant Prpf31 causes pre-mRNA splicing defects and rod photoreceptor cell degeneration in zebrafish model for Retinitis pigmentosa, Molecular Degeneration, Volume 6, Article 56, all pages, published 7/30/2011).
Regarding the PRPF31 variant recited in the method of claim 15, the combined teachings of Lewis and Anguela teach a PRPF31 variant comprising of an exogenous NLS of SEQ ID NO: 4, as described above.
Regarding claim 15-17, Lewis teaches ocular diseases which are suitably treated by this method include, without limitations, ocular neovascular disease, glaucoma, age-related macular degeneration, retinitis pigmentosa…etc. (see paragraph 0155). Furthermore, Lewis teaches a variety of transgenes are useful and would generally depend on the particular use of the virus and where suitable transgenes are RHO, LCA5, PRPF31, etc. (see paragraph 0097).
Though Lewis does not directly teach the diseases is caused by a PRPF31 gene mutation, Lewis does disclose the disease can be retinitis pigmentosa, as recited in claim 17. Furthermore, it is known to one skilled in the art, and evidenced by Yin et al., that mutations of PRP31 is associated with RP etiology (see background of Yin).
Regarding claim 18, Lewis does not teach wherein the disease comprises autosomal dominant retinitis pigmentosa (ADRP).
Regarding claim 34 and 35, Lewis does not teach wherein the PRPF31 variant comprises an amino acid sequence set forth in any of SEQ ID NOs: 20 to 21 or where the PRPF31 variant comprises a nucleotide sequence set forth in any of SEQ ID NOs: 28 to 29. However, Lewis does teach that each component of the construct or cassette (such as the transgene or nucleotide sequence) can be codon optimized for improved expression in human cells (see paragraph 0117).
Furthermore, sequences with near 100% identity to SEQ ID NOs: 20 to 21 or SEQ ID NOs: 28 to 29 are shown to exist in the art, as evidenced above in the arts of Fougerolles and Nelles, wherein routine optimization of amino acid or nucleotide sequences would allow one with ordinary skill to arrive at SEQ ID NOs: 20 to 21 and SEQ ID NOs: 28 to 29.
Regarding claim 18, Yin teaches the investigation of two pathogenic mutations in PRPF31, causing the autosomal dominant form of RP (see results of Yin), therefore implicating the retinitis pigmentosa derived from mutations of PRPF31 as autosomal dominant.
It would have been obvious to one with ordinary skill in the art, before the effective filing date of the claimed invention, to combine the arts of Lewis, Anguela, and Yin, to arrive at a method for treating a disease in a subject, wherein the disease is autosomal dominant retinitis pigmentosa.
One would have expected a reasonable chance of success as Lewis teaches the administration of a gene construct in a vector to treat ocular diseases.
One would be motivated to combine said arts in order to arrive at a codon optimized gene construct expressing a PRPF31 variant with a NLS in order to treat an ocular diseases, wherein the ocular diseases is autosomal dominant retinitis pigmentosa (ADRP).
In view of the foregoing, claims 15-18 and 34-35 are rejected under 35 U.S.C. 103 as being prima facie obvious, before the effective filing date.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to DAVID YU whose telephone number is (571)272-1118. The examiner can normally be reached Monday-Friday 7:30 am -5 pm.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Ram Shukla can be reached at 571-272-0735. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/D.T.Y./Examiner, Art Unit 1635
/RAM R SHUKLA/Supervisory Patent Examiner, Art Unit 1635
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