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 .
Claim Amendments
Claim 1 has been amended to specify that the adenovirus is “oncolytic”, “replicates in a YB-1 dependent manner”, and “lacking expression of E1A13S protein”. Claims 1 and 3-4 have also been amended to resolve indefiniteness. Applicant has canceled claims 2 and 18, and added claims 34-37. No new matter has been added.
Election/Restrictions
Claims 22-33 remain withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. The elected species “XVir-N-31” (as the oncolytic virus) and “palbociclib” (as the CDK4/6 inhibitor) remain in effect.
Claims 1, 3-4, 19-21, and 34-37 have been considered on the merits.
Drawings
RE: Objection to Drawings
Applicant submitted replacement drawings to correct the improper labels, as well as amended the specification to reflect the new labels. However, Figures 27 and 43 have typographical errors, which necessitate new objections to the drawings.
New objections
The drawings are objected to due to typographical errors in Figures 27 and 43: each of said figures shows two partial views identified by the same letter (two “Fig. 27B” and two “Fig. 43B”) but the amended specification indicates Figure 27 has view numbers 27A-27C while Figure 43 has view numbers 43A-43D.
Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
In addition to Replacement Sheets containing the corrected drawing figure(s), applicant is required to submit a marked-up copy of each Replacement Sheet including annotations indicating the changes made to the previous version. The marked-up copy must be clearly labeled as “Annotated Sheets” and must be presented in the amendment or remarks section that explains the change(s) to the drawings. See 37 CFR 1.121(d)(1). Failure to timely submit the proposed drawing and marked-up copy will result in the abandonment of the application.
Nucleotide and/or Amino Acid Sequence Disclosures
RE: Sequence disclosure deficiency
The substitute specification includes an incorporation-by-reference paragraph in the first page, which satisfies the requirements for sequence disclosures.
Claim Objections
RE: Objection to the claims
The minor informalities in claims 1 and 32 have been corrected. Thus, the claim objections have been withdrawn.
New objections
Claim 4 is objected to because “Poly ADP ribose polymerase” should be amended to “poly(ADP-ribose) polymerase”.
Claim 32 is objected to because of the following minor informality: the term “replication deficient” is missing a hyphen between the two words. Appropriate correction is required.
Claim 36 is objected to since “fibre” is a British term and should be spelled as “fiber” to reflect the American spelling.
Claim Rejections - 35 USC § 112
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.
RE: Rejection of claims 2-4 under 35 U.S.C. 112(b) for being indefinite
The parent claim of dependent claims 2-4 has been amended to omit “at least one further agent selected from the group consisting of… a bromodomain inhibitor and a PARP inhibitor” and retain “nutlin or a derivative of nutlin”, which makes it clear that claims 3-4 require the addition of a bromodomain inhibitor or a PARP inhibitor in the combination of claim 1.
Hence, the rejections on claims 3-4 have been withdrawn. The rejection on claim 2 is moot since said claim has been canceled.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
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.
RE: Rejection of claims 1, 3-4, and 18-21 under 35 U.S.C. 103 as being unpatentable over Holm, as evidenced by Czolk et al., in view of Parasuraman et al. and Borgstrom et al.; as well as claims 1-4 and 18-21 under 35 U.S.C. 103 as being unpatentable over Holm, as evidenced by Czolk et al., in view of Parasuraman et al. and Shangary et al.
Traversal of rejections is based on the combined teachings of Holm, Czolk et al., Parasuraman et al., and Borgstrom et al. not teaching the claimed invention. Applicant points that Holm prefers the use of dl520 as the oncolytic adenovirus and cytostatics as the anti-tumor or anti-cancer agent, with no more specific teachings regarding the latter aside from cytostatics and radiation. Referring to Holm’s Example 4 and Figure 3, applicant also states that treatment with DeloRGD alone led to better survival rate relative to the combination treatment using DeloRGD and temozolomide. In addition, applicant argues that Parasuraman et al. does not provide motivation to combine a CDK4/6 inhibitor with an oncolytic adenovirus because said prior teaches co-administering a CXCR4 inhibitor with one or more additional therapeutics, which allegedly does not include an oncolytic adenovirus. Borgstrom et al. supposedly also does not provide such motivation as compound of Formula I is taught to be utilized with a plethora of other therapeutic agents, wherein only one of the numerous listed agents is an oncolytic adenovirus. Moreover, applicant argues that Shangary et al. does not particularly teach combining nutlin or a derivative thereof with an oncolytic adenovirus and a CDK4/6 inhibitor. It is asserted that there is no motivation for a person with ordinary skill in the art to combine the teachings of Shangary et al. with Holm, Parasuraman et al., and Borgstrom et al. and arrive at the claimed invention since the essential feature of the latter secondary references (use of a CXCR4 inhibitor or the compound of Formula I, respectively, with another therapeutic agent) would have to be omitted.
All arguments have been full considered and are found unpersuasive. First, preferred embodiments do not constitute a teaching away from a broader disclosure or nonpreferred embodiments. MPEP § 2123 states that “a reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill the art, including nonpreferred embodiments”. Merck & Co. v. Biocraft Laboratories, 874 F.2d 804, 10 USPQ2d 1843 (Fed. Cir.), cert. denied, 493 U.S. 975 (1989). So even though Holm teaches dl520 as the preferred oncolytic adenovirus, this embodiment does not negate other teachings including the suitability of DeloRGD and other anti-tumor agents to kill tumor stem cells. Holm is not limited to cytostatics since it teaches the use of other anti-tumor agents such as the cytotoxic drugs CYC202 (last par., page 78), PS-341, CCI-779, and RAD001 (first par., page 79).
Second, Holm’s Example 4 show that the survival rate of mice implanted with glioma-derived tumor stem cells is greater for mice treated with either adenovirus Delo3RGD alone or in combination with temozolomide compared to those treated with temozolomide alone, indicating that said adenovirus is effective for killing tumor cells. It is respectfully submitted that these results do not mean that adenovirus alone is better than the combination treatment given that the latter exhibited greater survival at day 140 to day 170 and the same survival at day 250. The experiment also only tested one anti-tumor drug, and presumably, one concentration. A person with ordinary skill in the art would have recognized that applicant’s conclusion of Holm’s Example 4 results would be premature.
Third, Parasuraman et al. does teach an oncolytic adenovirus as an example of an additional therapeutic agent, contrary to applicant’s argument. The prior art teaches that the additional therapeutic agent can not only be an immunomodulatory drug, but can also be an oncolytic viral therapy. The third sentence in par. [0090] states “In some embodiments, the additional therapeutic agents is selected from an oncolytic viral therapy such as… enadenotucirev (NG-348, PsiOux, formerly known as ColoAd1)” (lines 2-3 and 11), which is an oncolytic adenovirus. Examiner did not “subsumes an adenovirus under the term “immunomodulatory drug inducing apoptosis” as an oncolytic virus” (second par., page 13 of Applicant Arguments/Remarks) as Parasuraman et al. clearly teaches oncolytic viral therapy as another type of additional therapeutic agent.
With regards to Borgstrom et al., it should be noted that a prior art naming a claimed species anticipates the claim regardless of the number of other named species. See MPEP § 2131.02(II) and Ex parte A, 17 USPQ2d 1716 (Bd. Pat. App. & Inter. 1990) (The claimed compound was named in a reference which also disclosed 45 other compounds. The Board held that the comprehensiveness of the listing did not negate the fact that the compound claimed was specifically taught). Thus, the listing of 169 therapeutic agents does not invalidate the applicability of oncolytic virus for treating cancer. Borgstrom et al. is cited to show support on examiner’s position that combination therapies for treatment of cancer is known and conventional in the art.
Lastly, Shangary et al. teaches that 50% of human cancers have alterations in the tumor suppressor p53 gene (last par., page 1) and that in the remaining cancers retaining wild-type p53, the function of p53 is inactivated by MDM2 (Summary Points, page 12). Among various small molecules tested, nutlin-3 was one of the two molecules found to possess desirable properties including having a high binding affinity and specificity to MDM2, as well as potent cellular activity in cancer cells. Given that nutlin has characteristics that are desirable as a MDM2 inihibtor, it would have therefore been obvious to combine the teachings of Shangary et al. with Holm, Parasuraman et al., and Borgstrom et al..
The claims are thus deemed obvious over the cited prior art. But to address the amendments and newly added claims, the rejections of record have been withdrawn and new rejections are set forth below.
New rejections
Claims 1, 4, 19-21, and 34-37 are rejected under 35 U.S.C. 103 as being unpatentable over Holm (WO 2012/022496 A2), as evidenced by Czolk et al. (International Journal of Molecular Medicine 2019, Vol. 44, pages 1484-1494) and Rognoni et al. (Cancer Gene Therapy 2009, Vol. 16, pages 753-763), in view of Parasuraman et al. (WO 2018/237158 A1), Borgstrom et al. (WO 2018/195202 A1) and Shangary et al. (Annual Review of Pharmacology and Toxicology 2009, Vol. 49, pages 223-241).
According to Holm, replication selective oncolytic viruses have been used in the treatment of tumors. These viruses lyse infect tumor cells and spread to adjacent tumor cells during replication. Since the replication capabilities are limited to tumor cells, normal tissue is spared from lysis by the viruses (last par., page 1; first par., page 2). Previous studies have shown that if the E1A protein is present in a specific deleted from or has one or more mutations, which do not affect binding of Rb/E2F and/or p107/E2F and/or p130/E2F, these viruses will not induce entry of the infected cells into the S phase and will be capable of replicating in tumor cells without functional Rb protein (last par., page 2). Various oncolytic viruses that have been developed for a more selective replication are known in the art (first to fourth par., page 3).
However, tumors harbor tumor stem cells that can lead to relapse after killing or removal of tumor cells (last par., page 4). To address this problem, Holm discloses a YB-1 dependent virus that can be used to kill tumor stem cells of a tumor (Abstract). In some aspects, the virus is replication deficient in cells that lack YB-1 in the nucleus and encodes an oncogene product such as E1A is capable or incapable of binding a functional Rb tumor suppressor gene product (page 7). A preferred embodiment of the YB1-dependent virus is dl520 (first par., page 29). Holm teaches administering the disclosed virus together with an anti-tumor or anti-cancer agent (first and second par., page 31).
In a working example, Holm teaches using AdDelo3RGD as the YB-1 dependent oncolytic adenovirus to induce cell death in tumor stem cells (Example 3, page 95). Holm also shows administering AdDelo3RGD with or without the anticancer agent temozolomide in an orthotopic mouse model bearing glioma tumor (Example 4, page 96).
Holm is comparable to the instant application’s combination for the following reasons:
Regarding claim 1: the oncolytic adenovirus like AdDelo3RGD combined with the anticancer agent temozolomide is similar to “A combination comprising an oncolytic adenovirus, a cyclin dependent kinase 4 and 6 (CDK4/6) inhibitor”, wherein “XVir-N-31” is the elected species for the adenovirus and “palbociclib” is the elected species for the CDK4/6 inhibitor.
AdDelo3RGD is the same as XVir-N-31 as evidenced by Czolk et al.. Czolk et al. states that “The YB-1-dependent oncolytic adenovirus XVir-N-31 developed by this study group, also termed Ad-Delo3-RGD…” (second par. in left col, page 1485). Czolk et al. also provides evidence that AdDelo3RGD is YB-1-dependent and replicates in tumor cells harboring nuclear YB-1 (second par. in left col., page 1485). In addition, Rognoni et al. further provides evidence regarding AdDelo3RGD’s YB-1 dependency (Abstract; Figure 2, page 756) and its lack of expression of E1A13S protein (Figure 1, page 765), thereby satisfying “wherein the adenovirus replicates in a YB-1 dependent manner and wherein the adenovirus is lacking expression of E1A13S protein”.
Holm is different from the claimed invention in that the anticancer agent combined with AdDelo3RGD is not palbociclib. It also does not teach combining “nutlin or a derivative of nutlin”.
Despite these differences, combination therapies for treating cancer or killing tumor cells is well-known and routine in the art. For example, Parasuraman et al. teaches treating cancer by administering a CXCR4 inhibitor in combination with one or more additional therapeutic agents (par. [0007]). One aspect of the one or more additional therapeutic agents is that it is selected from a group that includes a CDK4/6 inhibitor like palbociclib and a PARP inhibitor like olaparib (par. [0029], [0031], [0033]). In some embodiments, the additional therapeutic agent is an inhibitor of interaction between two primary p53 suppressor proteins MDMX and MDM2 (par. [0086]). And in other embodiments, the additional therapeutic agent is an immunomodulatory therapeutic such as an oncolytic virus (par. [0089]-[0090]). Similarly, Borgstrom et al. teaches treating a subject suffering from cancer by administering a composition comprising a compound of Formula I in combination with one or more additional agents that include oncolytic adenovirus, palbociclib, and olaparib (par. [0330]).
Since combination therapies for treatment of cancer is known and conventional in the art as shown by Parasuraman et al. and Borgstrom et al., it would have been obvious for a person with ordinary skill in the art to combine Holm’s oncolytic adenovirus like AdDelo3RGD or XVir-N-31 with other therapeutic agents including a CDK4/6 inhibitor like palbociclib and a PARP inhibitor like olaparib. It can be expected that combining these anticancer agents with AdDelo3RGD or XVir-N-31 would facilitate cancer treatment. Obviousness is based on the rationale that combining prior art elements according to known methods yields predictable results. See MPEP § 2143 and KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 415-421, 82 USPQ2d 1385, 1395-97 (2007).
Furthermore, Shangary et al. teaches that nutlin-3 is a small molecule inhibitor of the interaction between p53 and MDM2 proteins and that it has entered preclinical development or early phase clinical trials (Abstract). Nutlin-3 meets the criteria to serve as a cancer therapeutic because it has high binding affinity and specificity to MDM2, potent cellular activity in cancer cells and wild-type p53, and a highly desirable pharmacokinetic profile (second and third par., page 7). Based on the teachings of Shangary et al., it would have been obvious to further modify Holm by also incoporating nutlin-3 as an additional therapeutic agent with reasonable expectation that combining it with Holm’s oncolytic adenovirus would help treat cancer. The rationale to support obviousness is that all claimed elements were known in the prior art and their combination would have yielded nothing more than predictable results. Id.
Hence, claim 1 is obvious over Holm, as evidenced by Czolk et al., in view of Parasuraman et al., Borgstrom et al., and Shangary et al..
Regarding claim 4: olaparib is a PARP inhibitor and meets “the combination further comprises a Poly ADP ribose polymerase (PARP} inhibitor”.
Regarding claim 19: AdDelo3RGD, also known as XVir-N-31, satisfies “the adenovirus is selected from the group consisting of XVir-N-31…”.
Regarding claim 20: AdDelo3RGD is identical to “the adenovirus is XVir-N-31”.
Regarding claim 21: palbociclib is a PARP inhibitor and therefore fulfills “the CDK4/6 inhibitor is selected from the group consisting of palbociclib which is also referred to as PD-0332991…”.
Regarding claim 34: Czolk et al. (second par. in left col., page 1485) and Rognoni et al. (Abstract, page 753; Figure 2, page 756) provide evidence that AdDelo3RGD is YB-1-dependent and replicates in tumor cells with YB-1 in the nucleus, thereby satisfying “replicating in cells which have YB-1 in the nucleus”.
None of the cited prior art explicitly teaches that said adenovirus is “replication deficient in cells which lack YB-1 in the nucleus”.
However, the courts have held that an inherent feature does not have to be recognized at the relevant time. MPEP § 2112 states “[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer.” Atlas Powder Co. v. Ireco Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977).
Regarding claim 35: Rognoni et al.’s evidence that AdDelo3RGD does not express E1B19K protein (Figure 1, page 756) corresponds to “the adenovirus lacks expression of E1B 19 kDa protein”.
Regarding claim 36: According to Rognoni et al., AdDelo3RGD harbors a RGD motif in the fiber knob and expresses said motif (Abstract, page 753; Figure 1, page 756). This evidence meets the limitation “the adenovirus expresses an RGD motif at a fibre”.
Regarding claim 37: Rognoni et al. also shows that the E3 region in AdDelo3RGD is deleted (Figure 1a, page 756), which necessarily means that said region is not functionally active and satisfies “the adenovirus is lacking a functionally active adenoviral E3 region”.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
RE: Non-statutory double patenting rejections
Applicant did not submit any arguments against the double patenting rejections over co-pending Application No. 16/978048 and merely requests that said rejections be held in abeyance until all other rejections have been overcome.
The rejections of record have been modified in light of all the claim amendments.
Modified rejections
Claims 1, 3-4, 19-21, and 34-37 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 16-18 and 21-23, and 34-37 of co-pending Application No. 16/978048 in view of Shangary et al. (Annual Review of Pharmacology and Toxicology 2009, Vol. 49, pages 223-241).
The co-pending application is drawn to a combination comprising an oncolytic adenovirus and a CDK4/6 inhibitor, wherein the adenovirus is replicating in a YB-1 dependent manner and wherein the adenovirus is lacking expression of E1A13S. Claims also disclose that the adenovirus is replication deficient in cells which lack YB-1 in the nucleus, but is replication proficient in cells which have YB-1 in the nucleus, lacks expression of E1B 19 kDa protein, or expresses an RGD motif at a fibre.
In an embodiment, the adenovirus is further limited to XVir-N-31. And in another embodiment, the CDK4/6 inhibitor is selected from a group that includes palbociclib. The combination can further comprise a PARP inhibitor or a bromodomain inhibitor.
Although the co-pending application does not disclose combining nutlin or a derivative thereof to an oncolytic adenovirus and a CDK4/6 inhibitor, Shangary et al. teaches that this small molecule is also an anticancer agent that works by inhibiting the MDM2-p53 protein interaction. One with ordinary skill in the art would have thus added nutlin or a derivative thereof in the co-copending application’s combination and predict that the resulting combination would be useful for treatment of cancer.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
No claim is allowed.
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 nonprovisional extension fee (37 CFR 1.17(a)) 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 MICHELLE F PAGUIO FRISING whose telephone number is (571)272-6224. The examiner can normally be reached Monday-Friday, 8:00 a.m. - 4:00 p.m..
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Adam Weidner can be reached at (571) 272-3045. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/Michelle F. Paguio Frising/Primary Examiner, Art Unit 1651