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 .
Applicant is advised that the prior non-final Office Action mailed on June 22, 2026, is vacated in favor of a Final Office Action. Upon further consideration, the examiner has reviewed the grounds of rejection stated in the non-final Office Action and has modified the pending grounds of rejection as necessitated by Applicants’ amendment filed on June 8, 2026. The previous non-final Office Action was improperly issued in place of a proper Final Office Action, as presented below.
Moreover, Applicants’ representative, Tate Tischer, contacted the examiner’s supervisor, Maria Leavitt, on June 18, 2026, to indicate that the claims filed on June 8, 2026, were granted a petition to make the application special under 37 CFR 1.102( c)(1), MPEP § 708.02, Section II. Applicants’ representative argued that an interview should be granted by the special status of the application pursuant to 37 CFR 1.102( c)(1) and MPEP § 708.02. Supervisor Maria Leavitt offered to hold an interview before the issuance of the Final Office Action, but Tate Tischer indicated that he preferred to postpone the interview until after the Final Office Action was issued.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Claims 48-59 are currently pending. Claims 48, 49 and 51-53 have been amended by Applicants amendment filed on 6/8/2026. No claims were canceled or newly added.
The examiner acknowledges receiving the second Declaration under 37 C.F.R. § 1.132 executed by Dr. Robert J. Schneider (“Schneider Decl. 2”).
Therefore, claims 48-59 are currently under examination to which the following grounds of rejection are applicable.
Response to arguments
Priority
Applicant’s claim for the benefit of a prior-filed application PRO 62/962,712 and PRO 63/128,047 filed on 1/17/2020 and 12/19/2020, respectively, under 35 U.S.C 119(e) or under 35 U.S.C 120, 121 or 365(c) is acknowledged.
Accordingly, the effective priority date of the instant application is granted as 1/17/2020.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 6/8/2026 was received. The submissions were in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements were considered by the examiner.
Schneider Decl. 2
The declaration submitted by Dr. Robert J. Schneider on 6/8/2026 was received and fully considered. Briefly, Dr. Schneider described his laboratory’s research into the role AUF1 plays in muscle regeneration and myogenesis. Dr. Schneider describes the unexpected results of continuous strong expression of AUF1 in differentiated mammalian muscle cells of injured or diseased muscle cells yielded an increased generation of slow twitch muscle and muscle fiber diameter. Dr. Schneider describes the examples provided in the specification and previous declarations/applications showing that the promoters selected provided continuous expression (Exhibit I, J, K and L, ect.). Dr. Schneider describes why MyoD and MyoG promoters were not selected for the rAAV.AUF1 vectors, claiming that they are transiently expressed during myogenesis and provides a detailed explanation of each. The Schneider Decl. 2 explains in paragraph 9 that constitutive promoters are “promoters that provide continuous expression of structural proteins and crucial enzymes required for mammalian muscle structure and function-i.e., constitutive promoters” and that “A constitutive promoter is considered to be a strong promoter if it drives expression of a transgene at a level comparable to that of the cytomegalovirus promoter (CMV)”. The Schneider Decl. 2 explains at paragraph 10 that inventors have chosen “the following constitutive promoters that drive continuous expression of proteins critical to adult mammalian muscle structure and function and their derivatives for use in our AAV.AUFI vectors: MCK (muscle creatine kinase), SM22 (Smooth muscle 22a), Desmin, Skeletal a-actin; muscle-specific synthetic promoters including MCK promoter derivatives: CK5-12, CK8e, CK6-CK9, dMCK, tMCK, and MHCK7, and other muscle-specific synthetic promoters Spc512, and Sp301 that all drive constitutive expression in differentiated mammalian muscle cells; Pitx3, a muscle-specific promoter for a transcription factor constitutively expressed in all mammalian skeletal muscle; and U6 and HI, constitutive strong promoters for a small nuclear RNA expressed in mammalian muscle and in most tissues. The foregoing constitutive promoters are compact and suitable for use in rAAV vectors.”. The Schneider Decl. 2 discloses at pages 14-15 that “the MyoG and MyoD promoters are transiently expressed during myogenesis and at minimal undetectable levels in differentiated muscle cells.” and “These promoters have been used for research studies of myogenesis. But they do not efficiently drive expression in differentiated muscle cells and are prone to silencing by recipient host cell factors; thus, they were not candidates for our rAAV.AUFl compositions.”. Furthermore, the Schneider Decl. 2 discloses at paragraph 22-31 that “the MyoD 6 kb enhancer/promoter itself too large to be packaged in an rAAV vector, but it also would not activate transgene expression in differentiated muscle cells” and the “four enhancers comprise about 18 kb of the 40 kb region 5' of the MyoG gene and clearly exceed the 4.7 kb packaging limit of our rAAVAUFl vectors”
Withdrawn objections/ Rejections in response to Applicants’ arguments or amendments
Claim Interpretation
Claim 48 has been amended to recite a composition comprising a means for constitutively expressing exogenous AUF1 in differentiated mammalian muscle cells. The broadest reasonable interpretation of claim 48 does not invoke 112(f) since the structure for performing a given function is now defined in the claims as constitutive expression. The Specification provides a definition of constitutive promoter in paragraph [0057] as “The term “promoter” refers to a minimal sequence of a transgene that is sufficient to initiate transcription of a coding sequence of the transgene. Promoters may be constitutive or inducible. A constitutive promoter is considered to be a strong promoter if it drives expression of a transgene at a level comparable to that of the cytomegalovirus promoter (CMV) (Boshart et al., “A Very Strong Enhancer is Located Upstream of an Immediate Early Gene of Human Cytomegalovirus,” Cell 41:521 (1985), which is hereby incorporated by reference in its entirety).” Constitutive promoters are known in the art be transcriptionally active in a wide range of tissues and drives high-level constitutive expression. Moreover, transcriptional activity of promoters is specific to the type of promoter used and transformed host cells with specific transcription factors (Qin et al., PLos ONE, 5(5):el0611 (2010). The instant claims have been amended to require that the “means” for expression in claim 48 is a constitutive promoter that drives expression in differentiated mammalian muscle cells, operatively coupled to an AUF1 transgene in a recombinant rAAV vector. The Schneider Decl. 2 provides evidence that the MyoD* and *MyoG* promoter/enhancer regions are too large (6–40 kb) to fit in rAAV vectors and these promoters are downregulated in mature muscle (the Schneider Decl. paragraph 22-31).
The examiner is interpreting the constitutive promoter encompassed by claim 48 having a strong promoter if it drives expression of a transgene at a level comparable to that of the cytomegalovirus promoter (CMV) as the muscle creatine kinase (tMCK and MCK) promoters recited in claim 51.
It is noted that AUF1 consists of four related protein isoforms identified by their molecular weight (p37, p40, p42 and p45) derived by differential splicing of a single pre-mRNA. SEQ IDs 10, 14, 18 and 22 relate to specific splice variants.
Claim Rejections -35 USC § 102
In view of Applicants’ amendment of claim 48 and the Declaratory evidence, the rejection of claims 48-50 under 35 U.S.C. 102(a)(1) and 102(a)(2) as being anticipated by Schneider et al. (US 2018/0163178, published 6/14/2018; hereinafter Schneider, reference of record) as evidenced by Ohkawa et al. Journal of Biological Chemistry 282.9 (2007): 6564-6570 (hereinafter Ohkawa), Chargé et al.( BMC Developmental Biology 8.1 (2008): 5 (hereinafter Charge) and Weeratna et al. "(Gene therapy 8.24 (2001): 1872-1878; hereinafter Weeratna, reference of record) has been withdrawn
As applicants affirm at page 7 of the Remarks filed on 6/8/2026 which is further supported by the Schneider Decl. 2 “ the Pax7, MyoD and MyoG promoters drive expression in muscle stem cells (satellite cells) and progenitor cells (myoblasts), and only minimal expression in differentiated muscle cells, in most cases undetectable; they cannot substitute for the claimed promoters that function robustly in mature muscle. (Olwin Deel. ,i 10, and ,i,i 17- 20).” Furthermore, the applicant is on record as stating that these prior art efforts of Schneider et al. (US 2018/0163178)” comprising MyoD and myogenin promoters (e.g, Fax7, MyoD and MyoG ) required to “achieve expression (albeit only transient) in differentiated muscle cells are too large (6 kb and 20 kb) to be packaged by an rAAV vector which has a 4.7 kb limit.”
A response to Applicant’s arguments with regard to a withdrawn rejection is moot. A response to any argument pertaining to a new or maintained rejection can be found below.
Maintained objections/ Rejections in response to Applicants’ arguments or amendments
New Claim Rejections - 35 USC § 103
Claims 48-59 remain rejected under 35 U.S.C. 103 as being unpatentable over Childers et al. (US 2017/0112905, published 4/27/2017 ; hereinafter Childers, reference of record) in view of Weeratna et al. "( Gene therapy 8.24 (2001): 1872-1878; hereinafter Weeratna, reference of record) and Schneider et al. (US 2018/0163178, published 6/14/2018; hereinafter Schneider, reference of record).. This rejection has been modified as necessitated by amendment of the claims in the response filed 06/08/2026.
Claims 48-49 and 51: Childers describes gene therapy approaches for treating X-linked myotubular myopathy (XLMTM) comprising administering AAV vectors that increase the expression of myotubularin in muscle cells (Childers, para 3, 7 and 87). Childers describes the use of expression constructs comprising muscle creatine kinase (tMCK and MCK) promoters with high specificity and efficiency towards driving gene expression in muscle cells (Childers, para 110, 111).
Childers does not specifically describe expressing exogenous AUF1.
Claims 52-53: Childers describes the use of expression constructs comprising muscle creatine kinase (tMCK and MCK) promoters with high specificity and efficiency towards driving gene expression in muscle cells (Childers, para 110, 111).
Claims 54-59: Childers describes the systematic delivery of AAV vectors comprising the MTM1 gene which drastically improved regional and global muscle function (Childers, para 87). Childers describes preferred embodiments toward the use of AAV8 serotype capsids given their preferential expression in muscle cells (Childers, para 99, 101, 186).
Claims 48-49: Schneider describes compositions and methods for the skeletal muscle-specific gene transfer of AU-rich mRNA binding factor 1 (AUF1) to restore muscle mass, increase exercise endurance and provide a therapeutic strategy for treating age-related muscle loss (Schneider, para 4-8, 19, 37 and claims 1, 14 and 32). Schneider states that AUF1 plays a critical role in the control of muscle satellite cell fate and muscle regeneration, through programmed rapid degradation of muscle-differentiation checkpoint mRNAs (Schneider, para 4, 6). Schneider describes gene transfer approaches using recombinant adeno-associated viruses (rAAV) viruses for delivering an AUF1 expression vector to the site of muscle injury (Schneider, para 57, 58, 62, 63 and examples 2-3). Schneider describes the use of additional expression construct elements including enhancers, leader sequences, 3’ regulatory elements and reporter genes which can be cloned into the expression vector (Schneider, para 54).
Claim 50: It is emphasized that the “OR” conjugation used when listing the AUF1 polypeptides in claim 50. Schneider states that the AUF1 protein may include one or more of the AUF1 isoforms including p37, p40, p42 and p45 (Schneider, para 43). Schneider provides the GenBank accession numbers for all related isoforms in Table 1. Schneider discloses SEQ ID NO: 26 which shares a 100% match to instant SEQ ID NO: 22 (sequence search results shown below.
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It would have been prima facie obvious to one of ordinary skill in the art to substitute Schneider’ gene encoding AUF1 expression for Childers’ gene encoding myotubularin in Childers’ AAV8 expression construct with a reasonable expectation of success, particularly because Schneider identifies AUF1 as a key regulator of muscle regeneration and describes a skeletal muscle-specific gene transfer therapy to drive AUF1 expression (Schneider, para 57, 58, 62, 63) and Childers describes a similar gene therapy approach using AAV8 and tMCK promoters which showed high specificity and efficiency towards driving gene expression in muscle cells. Furthermore, the tMCK promoter is only active in skeletal muscle cells and is unlikely to cause unwanted side effects in other tissues. One would have a reasonable expectation of success given that the exchange of one known expression vector element for another is considered routine in the art. Accordingly, in the absence of evidence to the contrary, one of ordinary skill in the art would have considered the claimed invention to have been prima facie obvious to at the time the invention was made.
Response to Traversal
Although the rejection is newly applied, some of applicant’s arguments are relevant and are addressed below.
Applicant traverses the rejection by arguing that Childers is focused on monogenetic gene therapy and unlike AUF1 is normally expressed in mature muscle cells which is why tMCK was selected to supply mature muscle cells with a correct version of the defective gene in those cells. Applicant argues that there would have been no motivation to make the substitution of promoters since AUF1 had no functional effect in mature muscle cells.
These arguments have been fully considered, but are not found persuasive since the tMCK promoter and AAV8 serotype show high specificity and efficiency towards driving gene expression in skeletal muscle cells as shown by Childers. Schneider identifies AUF1 as a key regulator of muscle regeneration and describes a skeletal muscle-specific gene transfer therapy to drive AUF1 expression (Schneider, para 57, 58, 62, 63). Thus, it would have been prima facie obvious to one of ordinary skill in the art to use the AAV8 expression construct employing a tMCK promoter as described by Childers to express AUF1 in muscle cells as described by Schneider as a therapeutic strategy for muscle regeneration. One cannot show non-obviousness by attacking references individually where the rejections are based on combinations of references, see MPEP 2145.
Applicant cites the declaration submitted by Dr. Robert J. Schneider on 6/8/2026 for support. Briefly, Dr. Schneider described his laboratory’s research into the role AUF1 plays in muscle regeneration and myogenesis. Dr. Schneider describes the unexpected results of continuous strong expression of AUF1 in differentiated mammalian muscle cells of injured or diseased muscle cells yielded an increased generation of slow twitch muscle and muscle fiber diameter. Dr. Schneider describes the examples provided in the specification and previous declarations/applications showing that the promoters selected provided continuous expression (Exhibit I, J, K and L, ect.). Dr. Schneider describes why MyoD and MyoG promoters were not selected for the rAAV.AUF1 vectors, claiming that they are transiently expressed during myogenesis and provides a detailed explanation of each.
These arguments have been fully considered, but are not found persuasive since Applicants’ description of a promoter that drives constitutive expression in differentiated mammalian muscle cells in claims 48-49 is interpreted broadly as including,for example, a muscle creatine kinase (MCK) promoter as one that drives expression in differentiated muscle cells (i.e. claim 51). Note, however, that MCK promoters drive strong expression in both myoblasts (undifferentiated cells) and myotubes (differentiated cell) as evidenced by Weeratna (Weeratna, Results para 1). Also note that the Specification provides a definition of constitutive promoter in paragraph [0057] as “The term “promoter” refers to a minimal sequence of a transgene that is sufficient to initiate transcription of a coding sequence of the transgene. Promoters may be constitutive or inducible. A constitutive promoter is considered to be a strong promoter if it drives expression of a transgene at a level comparable to that of the cytomegalovirus promoter (CMV) (Boshart et al., “A Very Strong Enhancer is Located Upstream of an Immediate Early Gene of Human Cytomegalovirus,” Cell 41:521 (1985), which is hereby incorporated by reference in its entirety).” Constitutive promoters are known in the art be transcriptionally active in a wide range of tissues and drives high-level constitutive expression. Thus, the examiner is interpreting the constitutive promoter encompassed by claim 48 having a strong promoter if it drives expression of a transgene at a level comparable to that of the cytomegalovirus promoter (CMV) as the muscle creatine kinase (tMCK and MCK) promoters recited in claim 51.
New Grounds of Rejections in response to Applicants’ arguments or amendments
Claim Rejections - 35 USC § 112(a), Written Description – New Matter
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 48-59 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 for introducing new matter. This is a new rejection necessitated by amendment of the claims in the responses filed 6/8/2026 This is a New Matter rejection.
MPEP § 2163.II.A.3.(b) states, “when filing an amendment an applicant should show support in the original disclosure for new or amended claims” and “[i]f the originally filed disclosure does not provide support for each claim limitation, or if an element which applicant describes as essential or critical is not claimed, a new or amended claim must be rejected under 35 U.S.C. 112, para. 1, as lacking adequate written description”. According to MPEP § 2163.I.B, “While there is no in haec verba requirement, newly added claim limitations must be supported in the specification through express, implicit, or inherent disclosure” and “The fundamental factual inquiry is whether the specification conveys with reasonable clarity to those skilled in the art that, as of the filing date sought, applicant was in possession of the invention as now claimed. See, e.g., Vas-Cath, Inc., 935 F.2d at 1563-64, 19 USPQ2d at 1117”.
Claim 48 has been amended to recite a composition comprising a means for constitutively expressing exogenous AUF1 in differentiated mammalian muscle cells wherein recombinant adeno-associated viruses (rAAV) includes said constitutive promoter expressing exogenous AUF1.
Claim 48 is broadly interpreted as comprising a genus of constitutive promoters that achieve expression of the AUF1 gene in differentiated muscle cells and have to be packaged by an rAAV vector which has a 4.7 kb limit (Applicants remarks page 5).
The Specification as filed only provide a definition of constitutive promotes in paragraph [0057] by stating
“The term “promoter” refers to a minimal sequence of a transgene that is sufficient to initiate transcription of a coding sequence of the transgene. Promoters may be constitutive or inducible. A constitutive promoter is considered to be a strong promoter if it drives expression of a transgene at a level comparable to that of the cytomegalovirus promoter (CMV) (Boshart et al., “A Very Strong Enhancer is Located Upstream of an Immediate Early Gene of Human Cytomegalovirus,” Cell 41:521 (1985), which is hereby incorporated by reference in its entirety).”
Moreover, the applicant is on record as stating that prior art efforts of Schneider et al. (US 2018/0163178)” comprising MyoD and myogenin promoters (e.g, Fax7, MyoD and MyoG ) required to “achieve expression (albeit only transient) in differentiated muscle cells are too large (6 kb and 20 kb) to be packaged by an rAAV vector which has a 4.7 kb limit.”
Moreover, the applicant is on record as stating that “for driving constitutive expression of AUF I in differentiated muscle cells for uses such as gene therapy, viral promoters such as CMV have several limitations that we took into account, e.g., lack of muscle specificity and a short duration of expression as they are silenced by host cell factors over time. For example, we used the CMV promoter in lentivirus vectors to drive expression of AUF I in short term (7 days) gene therapy experiments reported in the' 463 Application in Example 8, FIGs. 25-27. “ (para 9 of the Schneider Decl. 2).
The subgenus of “constitutive promoter” refers to a specific subgenus that is not supported by the generic disclosure and specific examples of the instant specification. Constitutive promoter refers to a promoter that continuously drives expression in all cell types.
For each claim drawn to a genus, the written description requirement may be satisfied through sufficient description of a representative number of species by actual reduction to practice, reduction to drawings, or by disclosure of relevant identifying characteristics, i.e. structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the applicant was in procession of the claimed genius. If a representative number of adequately descried species are not disclosed for a genus, the claim to that genus must be rejected as lacking adequate written description under 35 U.S.C. 112, para. 1.
The instant specification provides no examples to support amending claims 48-59 to specify the promoters in claims 48-59 as constitutive promoters a means for constitutively expressing exogenous AUF1 in differentiated mammalian muscle cells wherein recombinant adeno-associated viruses (rAAV) includes said constitutive promoter expressing exogenous AUF1. For example, the specification describes how promoters like tMCK provide selective activity in skeletal muscle cells and improved muscle repair (Spec, para 54). However, the specification is silent with respect to tMCK being constitutively active in all tissue types when delivered via an rAAV vector.
In fact the prior art of (Qin et al., PLos ONE, 5(5):el0611 (2010) discloses well known constitutive promoters including SV40, CMV, UBC, EF1A, PGK and CAGG for mammalian systems that do not appear to be included for gene expression in rAAV in differentiated mammalian muscle cells because of lack of muscle specificity and a short duration of expression as they are silenced by host cell factors over time ((para 9 of the Schneider Decl. 2) or large size to be able to be packaged in the claimed rAAV vector which has a 4.7 kb limit (Applicants remarks page 5).
Thus, the instant specification not provide sufficient written description to support the claim to constitutive promoters like MCK and others listed in claims 58-59. Thus is not clear that the Applicant was in possession of a genus of undefined constitutive promoters that achieve expression of the AUF1 gene in differentiated muscle cells and have to be packaged by an rAAV vector which has a 4.7 kb limit before the effective filing date of the claimed invention. This is a matter of written description, not a question of what one of skill in the art would or would not have known. “The trouble is that there is no disclosure, easy though it is to imagine it.” In re Ruschig, 379 F.2d 990, 995, 154 USPQ 118, 123 (CCPA 1967); M.P.E.P. § 2163.05, part II. The material within the four corners of the as-filed specification must lead to the generic concept. If it does not, the material is new matter. Declarations and new references cannot demonstrate possession of a concept after the fact.
Claim Rejections - 35 USC § 112b
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 48-59 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 pre-AIA the applicant regards as the invention.
This rejection is supported by the disclosure of Weeratna et al. "Designing gene therapy vectors: avoiding immune responses by using tissue-specific promoters." Gene therapy 8.24 (2001): 1872-1878 (hereinafter Weeratna). This rejection is newly applied to address applicants claim amendments filed on 6/8/2026.
Claims 51-53 and by dependency claims 57-59 require a composition comprising a means for constitutively expressing exogenous AUF1 in differentiated mammalian muscle cells reciting specific species of constitutive promoters. The practitioner in the art would readily understand that the promoters recited in claims 51-53 are tissue specific promoters for differentiated mammalian muscle cells. Thus, it is unclear how a promoter can be simultaneously constitutively active and specific to differentiated mammalian muscle cells. For example, MCK is not known by one of ordinary skill in the art as a constitutive promoter and is highly restricted to striated muscle tissues as evidenced by Weeratna (Results para 1). Please note that the language of a claim must make it clear what subject matter the claim encompasses to adequately delineate its "metes and bounds", see MPEP 2173. Thus, the metes and bounds of the claims are indefinite.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any extension fee pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ALEXANDER NICOL whose telephone number is (571)272-6383. The examiner can normally be reached on M-F 8-5 EST.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Maria Leavitt can be reached on (571)272-1085. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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Alexander Nicol Patent Examiner
Art Unit 1634
/ALEXANDER W NICOL/Examiner, Art Unit 1634
/MARIA G LEAVITT/Supervisory Patent Examiner, Art Unit 1634
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