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. 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. DETAILED ACTION This action is in response to claim amendments filed 2/7/24. Claims 1-5, 10-11, and 13-16 are pending and under examination. Specification The specification is objected to as failing to provide proper antecedent basis for the claimed subject matter. See 37 CFR 1.75(d)(1) and MPEP § 608.01(o). Correction of the following is required: the specification does not use the phrase “compounds capable of removing extraneuronal Aß plaques or deposits”, “capable of removing extraneuronal Aß plaques or deposits”, or “extraneuronal Aß plaques or deposits” as currently recited in claim 11 . Claim Interpretation The list in claim 4 concludes with “analogues of G1 or A1”. Initially, it would appear that “A1” is the last member of the list. However, this is not a reasonable interpretation as “A1” is already part of the list and, in light of the specification, this is clearly meant to indicate “analogues of G1” or “analogues of A1”. The claim is objected to on formalities but is not indefinite. Claim Objections Claims 4 is objected to because of the following informalities: Claim 4 “a small molecule compound inhibitors” contains a number agreement deficiency (“a” vs the plural “inhibitors”). Further, the list should contain “and” or “or” prior to the last element of the list. Further, “analogues of G1” and “analogues of A1” should be listed as separate members to avoid potential interpretation where “analogues” does not also modify “A1”. Claim 11 is objected to because of the following informalities: the claim recites “one or more of” as well as “and/or”. While the intention is clear—an Aß antibody (element A) , an extraneuronal Aß plaque removal compound (element B) , or both (combination AB) are administered—the use of both qualifiers creates potential confusion. For example, where the claim encompasses “and”, meaning the antibody and the compound, then there is only one “choice” in the list (AB) , which makes “one or more” confusing. The phrase “one or more” of a list of two items and the phrase “and/or” in the list of two items accomplish the same goal (A, B, or AB) and so one of the two phrases should be removed. Appropriate correction is required. 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. 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 appl icant regards as his invention. Claims 1-5, 10-11, and 13-16 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. The preamble of claim 1 uses the term “or” four times. This creates confusion as to which elements are modified by which other elements. The phrase “preventing or delaying the onset of Alzheimer’s disease” is clear that the claim is directed to both preventing Alzheimer’s disease or delaying the onset of Alzheimer’s disease. The instant claims use the nebulous phrase “or any symptoms associated therewith”, but a reasonable interpretation is that these are symptoms associated with AD, not the preventing/delaying. However, the claim continues with “or ameliorating symptoms”. This phrase is not tied to any previous recitation and so might be referring to ameliorating any symptoms the subject might have, irrespective of what those symptoms are associated with. This is further supported by the claim language that indicates the subject does not have AD (“before the onset”), though it is unclear if “or ameliorating symptoms” is meant to be a stand-alone option (ameliorating any symptom irrespective of whether or not the subject has AD) or is meant to be grouped with the next “or”. The phrase “or reducing the severity of conditions before the onset of” AD in a subject is clear that the “conditions” are not associated with AD, as the subject has no such associated condition because the subject does not have AD. It remains unclear if this phrase is meant to include “ameliorating symptoms” or not. Overall, it is unclear what the breadth of the claim encompasses with respect to the results accomplished by the method and whether or not the subject might have AD or not. Dependent claims do not correct this deficiency and are indefinite for the same reasons. Therefore, claims 1-5, 10-11, and 13-16 are indefinite. 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 1-5, 10-11, and 13-16 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 ameliorating or reducing severity of symptoms / conditions associated with Alzheimer’s disease, does not reasonably provide enablement for preventing AD, delaying the onset of AD, ameliorating non-AD symptoms, reducing severity of non-AD conditions, or ameliorating/reducing AD symptoms in a subject without AD . The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims. The claim recites “ameliorating symptoms or reducing the severity of conditions before the onset of Alzheimer’s disease in a subject in need thereof”. As above, this phrase is indefinite. One interpretation includes “ameliorating symptoms” to includes subjects with AD, interpreting “ameliorating symptoms” as separate from “reducing the severity of conditions before the onset of Alzheimer’s disease” due to the “or”, and this embodiment is partially enabled as subjects with AD may have their AD symptoms ameliorated. In the interpretation that the symptoms and conditions are unrelated to Alzheimer’s disease, the specification as a whole is directed to the treatment of AD. The specification does not disclose non-AD symptoms or conditions which the instant compounds ameliorate. Further, the specification broadly discusses the mechanism of increasing neuronal Aß42 secretion from neurons; other than AD, the specification does not disclose which non-AD conditions or symptoms benefit from increased Aß42 secretion. Rather, the breadth of “symptom or condition” encompasses any and all such symptoms and conditions regardless of their cause. It would be undue experimentation to test every possible symptom or condition arising from the numerous and varied causes of such to determine if and how the instant inhibitors are effective. There is no common cause of all symptoms and no reasonable expectation that all symptoms could be treated by inhibiting PI4IIIα. In another interpretation, where the symptoms and conditions are associated with AD, it is unclear how any treatment could reduce the severity of a condition before the onset of that condition. While symptoms may be reduced if/when the condition presents via a prophylactic administration of a therapeutic, the instant claims are directed to reduction /amelioration of a non-present symptom. Such a use is not enabled as one cannot use the instant method in this manner. The claims also recite “preventing or delaying the onset of” AD or any symptoms associated therewith. However, t he art currently does not recognize any drug or method that results in the complete prevention of Alzheimer’s disease. See for example Reitz ( IDS 11/29/23 citation C76 ) that states “as the currently available drugs only slightly affect disease severity and progression, AD remains at present effectively untreatable” (p.2 C1) and Stanford ( IDS 11/29/23 citation C91 ) that states "unfortunately, there are no currently available FDA-approved medications proven to delay or slow progression of the underlying brain degeneration and loss of synaptic connections that occurs in Alzheimer’s disease”. Where the goal is recognized as difficult and as-yet unrealized, the evidence supporting a claim that such a result is achievable must necessarily be strong. The instant specification does not provide any working examples of AD prevention nor does it provide adequate guidance on how to overcome the art-recognized difficult nature of this goal. One skilled in the art could not practice the method of the claims to achieve the result of prevention of AD as claimed. The specification uses genetic models of drosophila. The Aß drosophila demonstrate Aß accumulation and certain, specific symptoms. Complete genetic knockout of RBO is not equivalent to pharmaceutical inhibition of PI4KIIIα but is rather expected to show the greatest possible effect as the knockout equates to the protein not being expressed while a pharmaceutical inhibitor is not expected to be 100% effective. Even in this case, figure 1 demonstrates that while the rbo gene mutation ameliorates symptoms, it does not prevent those symptoms. Panel c demonstrates that the Aßarc and the two Aßarc / rbo models are similar after 16 days. After 26 days, while the Aßarc performs worse than the other two, they all appear worse than the control model, suggesting that symptoms were ameliorated, but onset was not delayed. The specification itself uses the term “ameliorates” in the various examples (paragraph 15 8 describing figure 19B; paragraph 1 57 describing figure 12; paragraph 15 3 describing figure 6; paragraph 11 5 ) but does not state that onset was delayed or prevented. Figure 8 demonstrates that tau and Aß models both perform worse than controls, which is not ameliorated by rbo ; “ rbo gene mutation could not ameliorate the lifespan shortening of flies over-expressing tau protein” (p.27), yet tau is a known AD-associated protein. Taken as a whole, the evidence observes specific aspects of AD, but not Alzheimer’s disease itself. Moreover, these results appear to be inconsistent with the conclusion that AD could be prevented or delayed. MPEP §2164 notes that in vitro and in vivo models constitute a working example when that model correlates with the claimed method. Further, art recognized models—such as those in the instant specification—should be accepted as correlating unless there is evidence otherwise. First, while flies and mice may be used as surrogate models for Alzheimer’s disease and recapitulate certain aspects of the disease, these subjects do not actually have Alzheimer’s disease. See e.g., Reardon (IDS 11/29/23 citation C74) teaching that AD does “not occur naturally in mice” (p.611 C2). Drummond (IDS 11/29/23 citation C27) describes APP/PS1 mice (the model instantly used; see remarks in parent application 15/570681 on 3/21/22 at p.9) but notes their deficiencies when it comes to recapitulating every aspect of AD (table 1; p.6) as well as being generally limited to modeling a very rare form of the disease (p.28). The instant specification suggests that AD may exist in humans and dogs (paragraph 47); however, while other animals may suffer Alzheimer’s-like pathologies, “the complete behavioral and pathologic phenotype of Alzheimer’s disease…has not yet been identified in a nonhuman species” (Walker, abstract; IDS 11/29/23 citation C97). Thus, the claims are directed to achieving certain results in humans—and arguably dogs per the guidance in the specification—but treatment of flies and mice is not a working example of treating AD but rather a correlative model suggesting efficacy in treating AD. Thus, while the in vivo data provided in the specification may correlate to the disease, they are not examples of actual treatment of Alzheimer’s, while the claims are directed to preventing the disease, delaying onset of the disease, or treating symptoms in a subject that does not have the disease. The evidence supports a conclusion that the skilled artisan would not accept the instant models as reasonably correlating to the ability to prevent, reverse, or delay onset of Alzheimer’s disease in those with or at risk of Alzheimer’s disease, e.g., humans. The results in flies and mice are not indicative of the ability to prevent, reverse, or delay onset of AD in such subjects; there is not a single therapeutic which achieves any of these goals despite decades of attempts. The art is replete with treatments that are promising in mice but then fail in humans. In addition to Reitz and Stanford, see for example Franco ( IDS 11/29/23 citation C32 ), noting that there are many successful Alzheimer’s treatments in animal models but “none in humans” (title). Vitek ( IDS 11/29/23 citation C96 ) teaches that animal models reflecting only a single aspect of AD fail because this does not mimic AD (abstract); the fly model used in the instant specification reflects only a single aspect of AD ( Aß arc expression). Drummond (IDS 11/29/23 citation C27) describes APP/PS1 mice (the mouse model instantly used) but notes their deficiencies when it comes to recapitulating every aspect of AD (table 1; p.6) as well as being generally limited to modeling a very rare form of the disease (p.28). Drummond notes that “the response of endogenous mouse proteins to human PS1 is different from that in humans” and that “the downstream pathological effects” of these AD mouse models should be “interpreted carefully” because the animal responds differently than would a human (p.14). Reardon notes that drug companies have spent billions trying to prevent or even slow the progress of Alzheimer’s disease, but “to no avail” (p.611 C1), while those skilled in the art say “we appreciate that the models we had were insufficient” (p.611 C1). Reardon further teaches “many experimental drugs that have successfully removed [amyloid] plaques from mouse brains have not lessened the symptoms of Alzheimer’s disease in people. Such a method is also unpredictable in light of others who demonstrate that PAOs—the compounds of claim 5—may induce neurodegeneration rather than preventing it. Administering PAO, which is a PI4IIIα inhibitor—to a mouse—which is a “subject”—is within the scope of the instant claims, yet WO2004080416 (claim 10; IDS 11/29/23 citation B4) teaches this method causes neurodegeneration. While Applicant has demonstrated some degree of benefit in reducing symptoms in subjects which model Alzheimer’s disease, the specification does not demonstrate any evidence that would rise to the level of prevention or delayed onset, while the art provides ample evidence demonstrating that such a result is unpredictable and, so far, unachievable. The claims encompass preventing or delaying onset of AD in any “subject”, while others have tried and failed to accomplish this goal. Taking the evidence as a whole, the results in the instant fly and mouse models are not reasonably correlated to the outcomes currently claimed, demonstrating that models of AD, particularly single aspect models such as Aß transgenics, do not correlate to the prevention or delay of AD. One skilled in the art could not practice the method of the claims to achieve the result of preventi ng or delaying onset of AD as claimed without undue experimentation . Neither could they predictably ameliorate non-AD conditions nor ameliorate AD conditions prior to having AD. Therefore, claims 1-5, 10-11, and 13-16 are not enabled for their full scope. Claim 11 is 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. In the prosecution of parent application 15/570681, now US 11766420, the record establishes that the specification is sufficient to provide written description support for the functionally defined genus of “PI4KIIIα inhibitor”; that rationale is reiterated in the conclusion of this office action. However, the specification fails to provide similar support for analogues of HSH971 , analogues of acamprosate, or analogues of edaravone . While a claim cannot be defined entirely by function (MPEP §2163(I)(A)) it is also appreciated that these are method claims. In other words, the invention is not the inhibitors themselves but rather a new use for known inhibitors. Information which is well known in the art need not be described in detail in the specification. See, e.g., Hybritech , Inc. v. Monoclonal Antibodies, Inc., 802 F.2d 1367, 1379-80, 231 USPQ 81, 90 (Fed. Cir. 1986). However, sufficient information must be provided to show that the inventor had possession of the invention as claimed . Further, the Court in Rochester ( Univ. of Rochester v. G.D. Searle & Co., 358 F.3d 916, 927, 69 USPQ2d 1886, 1894-95 (Fed. Cir. 2004 )) makes clear that the compositions used in a method must still meet the written description requirement even in a method claim, while MPEP §2163 notes that elements “auxiliary to the invention must have a corresponding written description only so specific as to lead one having ordinary skill in the art to that class of compounds. Occasionally, a functional recitation of those known compounds in the specification may be sufficient as that description”. The inhibitors in claim 11 are auxiliary to the invention as the specification does not purport to invent any new compounds but rather rests on the mechanism of action. However, when a compound is auxiliary to the invention, the written description must “lead one having ordinary skill in the art to that class of compounds”. The identified genera above are not a known “class” of compounds and there is inadequate evidence of record to convey to the skilled artisan that Applicant was in possession of these genera. Much like in Rochester , a claim to a functionally defined genus must still otherwise meet the written description requirement and the above genera do not. The specification does not use the phrase “compound capable of removing extraneuronal Aß plaques”. The support for this phrase appears to come from p.19 (paragraph 76) disclosing three embodiments that “facilitate disaggregation of Aß aggregates”. Currently, the phrase “compound capable of removing extraneuronal Aß plaques” is limited to three genera: HSH971, acamprosate, and edaravone , to include “analogues” of the three. However, of these three, there are no analogues disclosed. The specification only recites these genera twice and while the specification uses the term “analogues”, the specification does not disclose any such analogues. Where such analogues were well-known at the time of filing, the written description may also be met. However, the Examiner was unable to establish such analogues. It appears acamprosate is an analogue of GABA ( Hunter ; form 892), but that does not describe an analogue of acamprosate itself. There were no documents discovered disclosing analogues of HSH971 or edaravone as of the effective filing date . Proper written description requires more than naming a molecule by a hoped-for function. There is no portion of the parent molecule described as necessary to define the claimed analogues and the naming of “analogue” does not lead the person of ordinary skill to a known class of molecules. Therefore, claim 11 does not meet the written description requirement. Double Patenting Claims 1-5 and 13-16 are rejected on the ground of nonstatutory double patenting a s being unpatentable over claims 1-5 of U.S. Patent No. 11766420 . Although the claims at issue are not identical, they are not patentably distinct from each other because : Under the BRI of instant claim 1, the instant claims include ameliorating symptoms of AD in a subject with AD (see §112b rejection above). Reference claim 1 is directed to ameliorating AD symptoms by administering the same therapeutics as instant claims 1-5; see reference claims 1-5. Instant claims 13-16 describe downstream results or properties of the claimed therapeutics. Since the reference claims administering the same therapeutics, they must have the same properties. Chemical compounds and their properties are inseparable (In re Papesch , 315 F.2d 381, 137 USPQ 43 (CCPA1963)), as are their processes and yields (In re Von Schickh , 362 F.2d 821, 150 USPQ 300 (CCPA 1966)). Claims 10-11 are rejected on the ground of nonstatutory double patenting a s being unpatentable over claims 1-5 of U.S. Patent No. 11766420 in view of US2014035 7 648 (‘648; form 892) and CN103529182 (IDS11/29/23 citation B2). US11766420 is discussed above as applied to instant claims 1-5 and 13-16, incorporated herein. Regarding claim 11, ‘648 teaches administering acamprosate to treat AD (claims 1 and 3). Combining two known therapeutics to treat the same disease is prima facie obvious; “ It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art.” In re Kerkhoven , 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980). S ee MPEP § 2144.06(I). Similarly, regarding claim 10, ‘182 teaches inhibitors of RBO/EFR3a/EFR3b for treatment of AD (claim 8) and would be obvious to combine for the same reasons. Conclusion It is noted that claims 1, 2, and 4 define the therapeutic agent entirely by function. While a claim cannot be defined entirely by function (MPEP §2163(I)(A)) it is also appreciated that these are method claims. In other words, the invention is not the inhibitors themselves but rather a new use for known inhibitors. Information which is well known in the art need not be described in detail in the specification. See, e.g., Hybritech , Inc. v. Monoclonal Antibodies, Inc., 802 F.2d 1367, 1379-80, 231 USPQ 81, 90 (Fed. Cir. 1986). However, sufficient information must be provided to show that the inventor had possession of the invention as claimed . See also MPEP §2163, where elements “auxiliary to the invention must have a corresponding written description only so specific as to lead one having ordinary skill in the art to that class of compounds. Occasionally, a functional recitation of those known compounds in the specification may be sufficient as that description”. Such is the case, where the invention is not the inhibitors but the method of their use, e.g., the identity of the inhibitor is “auxiliary” to its function as an inhibitor in the invention of inhibiting PI4KIIIα to treat AD. Further, the class is sufficiently known in the art that direction to this class of molecules would lead the skilled artisan to a sufficient number of species to meet the written description requirement. T he specification as filed is considered sufficient to convey possession of the genus of compounds for use in the method. PAO and PAO derivatives: the specification describes numerous examples of this genus, e.g., claim 5. As such, the specification has provided a representative number of species sufficient to convey to the skilled artisan that Applicant was in possession of this genus. A1 analogues; G1 analogues : in support of this genus, the specification describes A1 (paragraph 67) and G1 (paragraph 68). However, in support of analogues, no examples of such analogues are provided, no disclosure of a conserved structure for such analogues is provided, and no reference to such analogues known in the art is provided. The specification states that synthesis methods are known (paragraph 69) and, provided with guidance that any analogue of A1 or G1 is capable of treating AD, guidance to this class of compounds is sufficient for the instant method claims. While disclosure of a potential method of making (synthesis) is insufficient for the written description requirement, the synthesis steps are sufficient to envisage the structure of the end product. Small molecule inhibitors : The specification discloses PAO and its derivatives, G1, and A1. Representative species within a genus must reflect the structural diversity of the claimed genus (MPEP §2163(II)(3)(A)(ii)) and these examples are sufficient in the instant case to provide support for the breadth of the genus. PI4KIIIα antibodies: The specification discloses antibody 4E10 and OSH2-PH2X (paragraph 72). While Amgen makes clear that an antibody per se cannot be claimed by its antigen, the target antigen coupled with examples of known antibodies is sufficient for the instant methods as other such antibodies were already known in the art at the time of filing. Thus, taken as a whole, the recitation in claim 1 of a “PI4KIIIα inhibitor” guides one to a class of compounds, represented by examples of structural diversity in the specification, sufficient to convey to the skilled artisan that Applicant was in possession of this genus for the purposes of treating AD. There are no prior art rejections. P rior art must be enabled and all prior art is presumed enabled (MPEP §2121). However, the Examiner has advanced numerous reasons why most embodiments of the instant claims are not enabled, rebutting the prima facie assumption that administering, e.g., PAO derivatives would prevent AD. The enabled embodiment—ameliorating symptoms of AD or reducing the severity of AD—is allowable over the prior art for the reasons set forth in parent application 15/570681 (now US11766420). It is noted for the record that all “subjects” would meet the limitation of “ in need of AD ” prevention or delayed onset because Alzheimer’s is a disease which is not beneficial. Further, the result of “preventing” or “delaying onset” of AD is a result which flows from the method step itself. Thus, should the claims be deemed enabled for, e.g., prevention—which is not the case currently—then administration of any PI4KIIIα inhibitor to any subject for any reason would anticipate the instant claims. For example, Snezna (US20020115713; form 892) teaches administering PAO and PAO derivatives to a mammal (claim 14). There is no disclosure or reason to suspect the claimed mammal has AD. Therefore, this is administration prior to having AD. This is the only claimed step for preventing AD. This teaching has not been set forth in a prior art rejection because there is adequate reason to presume that, much like the instant claims, this administration would not prevent or delay Alzheimer’s disease. Additional art cited but not used is: WO200243654 (IDS 11/29/23 citation B3 ) teaching treatment of AD with phenylarsine (claim 4/12) US20150051193 (form 892) teaching treating a subject by administering (claim 15) a compound (claim 1) that inhibits PI4KIIIα (claim 14). The subject is being treated for infection and there is no evidence the subject has Alzheimer’s disease. Any inquiry concerning this communication or earlier communications from the examiner should be directed to FILLIN "Examiner name" \* MERGEFORMAT ADAM M WEIDNER whose telephone number is FILLIN "Phone number" \* MERGEFORMAT (571)272-3045 . The examiner can normally be reached FILLIN "Work Schedule?" \* MERGEFORMAT M-T 9-18; W-R 9-15 . 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, FILLIN "SPE Name?" \* MERGEFORMAT Jeffrey Stucker can be reached at FILLIN "SPE Phone?" \* MERGEFORMAT 571-272-0911 . The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300. Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000. /Adam Weidner/ Primary Examiner, Art Unit 1675