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 .
DETAILED ACTION
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 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.
Election/Restrictions
Applicant’s election without traverse of Invention II, claims 15-24, and the species election of the parameter of (i) chromatin accessibility of the enhancer, in the reply filed on Nov. 13, 2025 is acknowledged.
Based on the results of the search, the species election requirement between the species of Group 1 or the particular parameter has been withdrawn.
Claims 1-24 remain pending in the current application, claims 1-14 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention.
The requirement for the restriction of Inventions I and II is still deemed proper and is therefore made FINAL.
Claims 15-24 have been considered on the merits.
Status of the Claims
Claims 1-24 currently pending.
Claims 1-14 have been withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected Invention, there being no allowable generic or linking claim.
Claims 15-24 have been considered on the merits.
Specification
The disclosure is objected to because of the following informalities: the use of trademarks.
The use of the terms: Vevo® 3100 High Resolution Imaging System in pg. 37 line 26; Tween®-20 in pg. 39 line 13; QIAzol® in pg. 39 line 23; miRNeasy® kit pg. 39 lines 23, 26; NanoDrop™ in pg. 39 line 27; Agilent® 2100 in pg. 39 line 28, pg. 54 line 17; NuGEN® in pg. 39 line 30; Chromium™ i7 Multiplex Kit in pg. 40 line 11, pg. 42 line 1; Chromium™ Single cell 3’Regent Kit v.2 in pg. 40 line 13-16, 20; NextSeq® 500 in pg. 40 line 16, pg. 42 line 2, in pg. 52 line 24, pg. 54 line 18; NovaSeq® in pg. 40 line 18, pg. 42 lines 3 and 5; 10x Genomics Chromium™ controller in pg. 41 line 33; Chromium™ Chip E Single cell ATAC Kit v.2 in pg. 41 line 34, pg. 42 line 6; TRIzol™ in pg. 46 line 23 pg. 47 lines 25 and 32, pg. 48 line 3; Direct-Zol® RNA kit in pg. 46 line 24; TaqMan® in pg. 46 line 27-30; SsoAdvanced™ Universal SYBR® green supermix in pg. 46 line 31; SYBR® primers in pg. 46 line 32; Superase-In™ in pg. 47 lines 7, 14m, and 30; MyOne Streptavidin C1 Dynabead™ in pg. 47 line 20; Triton™ x-100 in pg. 47 lines 23-25, pg. 53 line 33, pg. 55 line 9; Thermopol® Buffer in pg. 47 line 29; Qubit™ in pg. 48 line 8, pg. 54 line 16; HiSeq® 4000 platform in pg. 48 line 8; FuGENE® HD transfection reagent in pg. 49 line 14; P2 Primary Cell 4D-Nuclofector® x Kit in pg. 50 line 12; Lonze 4D Nucleofector® in pg. 50 line 15; PrimeStar® polymerase in pg. 50 line 24; QX100™ Droplet Generator in pg. 50 line 32; QX200™ Droplet Reader in pg. 51 line 4; Covaris® S2 sonicator in pg. 52 line 5; AMPure® XP beads in pg. 52 line 20; NEBNext® Ultra on pg. 52 line 23; Lipofectamine® RNAiMAX transfection reagent in pg. 54 line 32, pg. 55 line 29, pg. 56 line 7; Zeiss® Axio Observer Z1 in pg. 55 line 14; PurCol® EZ Gel solution on pg. 56 lines 23-24; which are a trade names or a marks used in commerce, have been noted in this application. The terms should be accompanied by the generic terminology; furthermore the terms should be capitalized wherever they appear or, where appropriate, include a proper symbol indicating use in commerce such as ™, SM , or ® following the terms.
Please note that this list may not be exhaustive.
Although the use of trade names and marks used in commerce (i.e., trademarks, service marks, certification marks, and collective marks) are permissible in patent applications, the proprietary nature of the marks should be respected and every effort made to prevent their use in any manner which might adversely affect their validity as commercial marks.
Appropriate correction is required.
Claim Objections
The disclosure is objected to because of the following informalities:
Claim 21 is objected to in the recitation of “which further comprises”, and in the interest of improving claim form, it is suggested that the recited phrase be amended to recite “comprising”.
Claim 22 is objected to for missing a comma after the phrase “claim 20” in line 1.
Appropriate correction is appreciated.
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 15-18 and 20-24 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 claims 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 inventors, at the time the application was filed, had possession of the claimed invention.
The instant claims are drawn to an agent that inhibits Meox1 RNA transcription, Meox1 chromatin accessibility, Meox1 RNA processing and Meox1 translation. Thus, the claims are broadly drawn to any compound or molecule which inhibits the transcription, the chromatin accessibility, the RNA processing or translation of the Meox1 gene. Therefore, the claims are considered genus claims that encompass a wide array of compounds. The claims encompass any inhibitor of the transcription, the chromatin accessibility, the RNA processing or translation of the Meox1 gene which are not described by their function, structure or relation thereto. The genus for the inhibitory factor is highly variant, inclusive to numerous structural variants because a significant number of structural differences between genus members is permitted.
For agents that inhibit Meox1 RNA transcription, Meox1 chromatin accessibility, Meox1 RNA processing and Meox1 translation, the specification only discloses a limited number of potential agents. The specification describes a small molecule inhibitor, JQ1, that is a thienotriazolodiazepine which inhibits Meox1 expression through the inhibition of the BET (Bromodomain and Extra Terminal) family of bromodomain proteins (0028-0029 of the published application). The specification provides evidence that JQ1 inhibits Meox1 expression, CRISPR targeting of the Meox1 enhancer and siRNA inhibition of Brd4 inhibits Meox1 induction (0015, 0153 and 0157). In addition, the specification provides evidence of a siRNA which inhibits Meox1 expression (0158).
The specification does not disclose the diverse genus. The specification does not place any structure, chemical or functional limitations on the embraced by genus “agents that inhibit Meox1 RNA transcription, Meox1 chromatin accessibility, Meox1 RNA processing and Meox1 translation”. The specification instead describes a method of identifying agents that modulate Meox1 (0007, 0031-0037). In addition, specification contemplates different agents that may modulate Meox1 including guide RNAs, and inhibitory nucleic acids, and the CRISPR modification of the Meox1 regulatory element (0007, 0038-0039, 0042, 0045, and 0057). However, there is no description of which particular sequences would inhibit Meox1 expression or what structures are necessary for molecular inhibitors. The recitation of “agents that inhibit Meox1 RNA transcription, Meox1 chromatin accessibility, Meox1 RNA processing and Meox1 translation” does not convey a common structure or function and is not so defined in the specification. In sum, specification and the claim do not provide any guidance on the structure of the agents that inhibit Meox1 RNA transcription, Meox1 chromatin accessibility, Meox1 RNA processing and Meox1 translation.
The MPEP states that written description for a genus can be achieved by a representative number of species within a broad generic. It is unquestionable that the claims are broad generics, with respect to all of the potential species of antagonists that may exhibit one, all, of or any of the claimed activity. The possible variations of compounds are limitless with potentially thousands of compounds that may exhibit the claimed activities. The purpose of the written description requirement is to ensure that the inventor had possession, as of the filing date of the application, of the specific subject matter claimed by them. A patent specification must describe an invention and do so in sufficient detail that one skilled in the art can clearly conclude that the inventor invented the claimed invention. Thus, an applicant complies with the written description requirement "by describing the invention, with all its claimed limitations," and by using "such descriptive means as words, structures, figures, diagrams, formulas, etc., that set forth the claimed invention."
The specification lacks sufficient variety of species of compounds to reflect this variance in the genus since the specification does not provide any examples of such a genus of compounds. Accordingly, the specification fails to provide adequate written description for the genus of “an agent that inhibits Meox1 RNA transcription, Meox1 chromatin accessibility, Meox1 RNA processing and Meox1 translation” and does not reasonably convey to one skilled in the relevant art that the inventors, at the time the application was filed had possession of the entire scope of the claimed invention. Moreover, the specification neither describes the complete structure of a representative number of species, nor describes a representative number of species in terms of partial structure and relevant identifying characteristics. Absent of such teachings and guidance as to the structure and function of these compounds, the specification does not describe the claimed antagonist in such full, clear, concise and exact terms so as to indicate that Applicant had possession of these inhibitors at the time of filing of the present application. Thus, the written description requirement has not been satisfied.
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 21 and 22 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.
In claim 21, line 1, the phrase "modified cells" lacks sufficient antecedent basis and renders the claim and its dependents indefinite. There are no modified cells in claim 15 and it is unclear whether or not modified cells are being produced by contacting the cells with an agent that inhibits Meox1 RNA transcription, Meox1 chromatin accessibility, Meox1 RNA processing and Meox1 translation.
In claim 22, line 1, the phrase "the subject later administered the modified cells" lacks sufficient antecedent basis and renders the claim and its dependents indefinite. There is no subject in claims 20 or 15 from which the claim depends from. For the sake of compact prosecution the claim will be interpreted to depend from claim 21.
Appropriate correction is required.
Claim Rejections - 35 USC § 102
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.
Claims 15, 18-20, 23 and 24 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Lu et al. (Cardiovascular Research, 2018) (ref. of record).
With respect to claim 15, Lu teaches a method of contacting cells with siRNAs targeted against the Meox1 gene, an agent that inhibits Meox1 RNA transcription, Meox1 RNA processing and Meox1 translation (pg. 301 Col. 2 para. 2). Specifically, Lu teaches the siRNAs effectively knock down the target gene in 293T cells (pg. 301 Col. 2 para. 2). With respect to claims 15 and 18, Lu teaches the agent is siRNA which inhibits Meox1 transcription which also inhibit Meox1 RNA processing and Meox1 translation (pg. 301 Col. 2 para. 2 and Supplement). With respect to claim 19, Lu teaches the agent is siRNA, an inhibitory nucleic acid (pg. 301 Col. 2 para. 2). With respect to claim 20, Lu teaches the method where the contacting of the cells occurs in vitro (pg. 301 Col. 2 para. 2). With respect to claim 23, Lu teaches generating a cardiac-specific Meox1 knockout mouse by microinjecting an expression vector containing cloning loops for two siRNAs under the alpha-MHC promoter (pg. 301 Col. 2 para. 2). With respect to claim 24, Lu teaches the method where the cardiac-specific Meox1 knockout mouse have TAC (transverse aortic constriction)-induced cardiac hypertrophy or heart failure (pg. 301 Col. 2 para. 4).
Therefore, the reference anticipates the claimed subject matter.
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:
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.
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.
Claims 15-20, 23 and 24 are rejected under 35 U.S.C. 103 as being unpatentable over Lu et al. (Cardiovascular Research, 2018) (ref. of record) in view of Higo et al. (Circulation Research, 2014).
With respect to claim 15, Lu teaches a method of contacting cells with siRNAs targeted against the Meox1 gene, an agent that inhibits Meox1 RNA transcription, Meox1 RNA processing and Meox1 translation (pg. 301 Col. 2 para. 2). Specifically, Lu teaches the siRNAs effectively knock down the target gene in 293T cells (pg. 301 Col. 2 para. 2). With respect to claims 15 and 18, Lu teaches the agent is siRNA which inhibits Meox1 transcription which also inhibit Meox1 RNA processing and Meox1 translation (pg. 301 Col. 2 para. 2 and Supplement). With respect to claim 19, Lu teaches the agent is siRNA, an inhibitory nucleic acid (pg. 301 Col. 2 para. 2). With respect to claim 20, Lu teaches the method where the contacting of the cells occurs in vitro (pg. 301 Col. 2 para. 2). With respect to claim 23, Lu teaches generating a cardiac-specific Meox1 knockout mouse by microinjecting an expression vector containing cloning loops for two siRNAs under the alpha-MHC promoter (pg. 301 Col. 2 para. 2). With respect to claim 24, Lu teaches the method where the cardiac-specific Meox1 knockout mouse have TAC (transverse aortic constriction)-induced cardiac hypertrophy or heart failure (pg. 301 Col. 2 para. 4).
Lu does not teach the cells are fibroblasts, myofibroblasts, activated fibroblasts, activated myofibroblasts or combinations thereof as recited in claim 16. Likewise, Lu does not teach the cells are fibroblasts are cardiac fibroblasts, lung fibroblasts, liver fibroblasts, kidney fibroblasts, or a combination thereof as recited in claim 17.
However, Higo teaches that Meox1-positive fibroblasts increase in response to a paracrine signal from cardiomyocytes and that the knockdown of Meox1 inhibits the reactive proliferation of cardiac fibroblasts stimulated by conditioned medium from cardiomyocytes (para. 2). Higo reports that Meox1 is heterogeneously expressed in the interstitial fibrotic area of the human ventricular heart tissues from patients with end-stage heart failure and that Meox1 expression is significantly correlated with the fibrosis-related genes in disease ventricular heart tissues (para. 2). Additionally, Higo proposes that Meox1 is a potential target for therapies aimed at preventing tissue fibrosis (para. 3).
Accordingly, at the effective time of filing of the claimed invention, one of ordinary skill in the art would have been motivated to modify the method of Lu so that the cells contacted with an agent that inhibits Meox1 RNA transcription, Meox1 chromatin accessibility, Meox1 RNA processing and Meox1 translation are fibroblasts or cardiac fibroblasts for the benefit of targeting the fibroblast cells and preventing fibrosis as taught by Higo. It would have been obvious to one of ordinary skill in the art to contact additional cell types known to benefit from having the expression of Meox1 inhibited as taught by Higo with an agent that inhibits the expression of Meox1 in the method of Lu. Additionally, one of ordinary skill in the art would have had a reasonable expectation of success in making such a modification, since Lu teaches Meox1 expression is increased in heart tissue form hypertrophic cardiomyopathy patients and animal models (pg. 301 Col. 1 para. 2) and that Meox1 expression was significantly correlated with the fibrosis-related genes in diseased ventricular heart tissues and that Meox1 is expressed in cardiac fibroblasts.
Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective time of filing of the invention, especially in the absence of evidence to the contrary.
Claims 15-24 are rejected under 35 U.S.C. 103 as being unpatentable over Lu et al. (Cardiovascular Research, 2018) (ref. of record) in view of Higo et al. (Circulation Research, 2014) and Zhao et al. (US 2018/0298340 A1) (ref. of record).
With respect to claim 15, Lu teaches a method of contacting cells with siRNAs targeted against the Meox1 gene, an agent that inhibits Meox1 RNA transcription, Meox1 RNA processing and Meox1 translation (pg. 301 Col. 2 para. 2). Specifically, Lu teaches the siRNAs effectively knock down the target gene in 293T cells (pg. 301 Col. 2 para. 2). With respect to claims 15 and 18, Lu teaches the agent is siRNA which inhibits Meox1 transcription which also inhibit Meox1 RNA processing and Meox1 translation (pg. 301 Col. 2 para. 2 and Supplement). With respect to claim 19, Lu teaches the agent is siRNA, an inhibitory nucleic acid (pg. 301 Col. 2 para. 2). With respect to claim 20, Lu teaches the method where the contacting of the cells occurs in vitro (pg. 301 Col. 2 para. 2). With respect to claim 23, Lu teaches generating a cardiac-specific Meox1 knockout mouse by microinjecting an expression vector containing cloning loops for two siRNAs under the alpha-MHC promoter (pg. 301 Col. 2 para. 2). With respect to claim 24, Lu teaches the method where the cardiac-specific Meox1 knockout mouse have TAC (transverse aortic constriction)-induced cardiac hypertrophy or heart failure (pg. 301 Col. 2 para. 4).
Lu does not teach the cells are fibroblasts, myofibroblasts, activated fibroblasts, activated myofibroblasts or combinations thereof as recited in claim 16. Likewise, Lu does not teach the cells are fibroblasts are cardiac fibroblasts, lung fibroblasts, liver fibroblasts, kidney fibroblasts, or a combination thereof as recited in claim 17.
However, Higo teaches that Meox1-positive fibroblasts increased in response to a paracrine signal from cardiomyocytes and that the knockdown of Meox1 inhibited the reactive proliferation of cardiac fibroblasts stimulated by conditioned medium from cardiomyocytes (para. 2). Higo reports that Meox1 is heterogeneously expressed in the interstitial fibrotic area of the human ventricular heart tissues from patients with end-stage heart failure and that Meox1 expression was significantly correlated with the fibrosis-related genes in disease ventricular heart tissues (para. 2). Additionally, Higo proposes that Meox1 is a potential target for therapies aimed at preventing tissue fibrosis (para. 3).
Accordingly, at the effective time of filing of the claimed invention, one of ordinary skill in the art would have been motivated to modify the method of Lu so that the cells contacted with an agent that inhibits Meox1 RNA transcription, Meox1 chromatin accessibility, Meox1 RNA processing and Meox1 translation are fibroblasts or cardiac fibroblasts for the benefit of targeting the fibroblast cells and preventing fibrosis as taught by Higo. It would have been obvious to one of ordinary skill in the art to contact additional cell types known to benefit from having the expression of Meox1 inhibited as taught by Higo with an agent that inhibits the expression of Meox1 in the method of Lu. Additionally, one of ordinary skill in the art would have had a reasonable expectation of success in making such a modification, since Lu teaches Meox1 expression is increased in heart tissue form hypertrophic cardiomyopathy patients and animal models (pg. 301 Col. 1 para. 2) and that Meox1 expression was significantly correlated with the fibrosis-related genes in diseased ventricular heart tissues and that Meox1 is expressed in cardiac fibroblasts.
Lu does not teach the method further comprising isolating modified cells and administrating them to a subject with a cardiac condition or cardiac disease as recited in claim 21. Likewise, Lu does not teach the method where the cells contacted in vitro were from the subject later administered the modified cells as recited in claim 22.
However, Zhao teaches administering isolated modified cells to a subject to treat tissue fibrosis including heart fibrosis (0075-0077, 0288-0290 and 0298). Zhao teaches the engineered or recombinant cells is a fibroblast (0071). Zhao teaches providing an engineered or recombinant cells that directly or indirectly aids in treating or ameliorating a tissue fibrosis (0055, 0058). In further support, Higo reports that Meox1-positive fibroblasts increased in response to a paracrine signal from cardiomyocytes and knockdown of Meox1 inhibited the reactive proliferation of cardiac fibroblasts stimulated by conditioned medium from cardiomyocytes (para. 2). Higo proposes that Meox1 is a potential target for therapies aimed at preventing tissue fibrosis (para. 3).
Accordingly, at the effective time of filing of the claimed invention, one of ordinary skill in the art would have been motivated to modify the method of Lu to further include the steps of isolating cells which have been modified by the agent that inhibits Meox1 expression and the administering of the isolated cells to a subject for the benefit of treating fibrosis as taught by Zhao and Higo. It would have been obvious to one of ordinary skill in the art to include the isolation and administration of fibroblasts that have been modified to have inhibited Meox1 expression, since Higo teaches that Meox1 is expressed in fibroblasts and a potential target for fibrosis and Zhao teaches treating fibrosis by administering modified cells. Additionally, one of ordinary skill in the art would have had a reasonable expectation of success in making such a modification, since Lu teaches Meox1 expression is increased in heart tissue from hypertrophic cardiomyopathy patients and animal models (pg. 301 Col. 1 para. 2), Higo teaches that Meox1 expression was significantly correlated with the fibrosis-related genes in diseased ventricular heart tissues and that Meox1 is expressed in cardiac fibroblasts, and Zhao teaches that cell therapy with genetically modified cells can treat fibrosis in the heart. Although, Zhao is silent with respect to whether the cells are allogeneic or autologous and does not explicitly teach the cells being from a patient as recited in claim 22, a skilled artisan would recognize that autologous cells are preferable to allogeneic cells for use in cell therapy, since there is less chance of an immune reaction to the therapy.
Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective time of filing of the invention, especially in the absence of evidence to the contrary.
Conclusion
No claims are allowed.
Examiner Contact Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to EMILY ANN CORDAS whose telephone number is (571)272-2905. The examiner can normally be reached on M-F 9:00-5:30 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, Peter Paras can be reached on 571-272-4517. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of an application may be obtained from the Patent Application Information Retrieval (PAIR) system. Status information for published applications may be obtained from either Private PAIR or Public PAIR. Status information for unpublished applications is available through Private PAIR only. For more information about the PAIR system, see http://pair-direct.uspto.gov. Should you have questions on access to the Private PAIR system, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative or access to the automated information system, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/EMILY A CORDAS/Primary Examiner, Art Unit 1632