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 Status
Claims 1-3, 8-9, 12, 18-19 and 21-22 are currently pending in this application.
Election/Restriction
Applicant’s election without traverse of Group I, claims 1-5, 9, and 12-16, in the reply filed on Aug. 7, 2024 is acknowledged. Claim 8 is withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected Group II, there being no allowable generic or linking claim. Pursuant to 37 CFR 1.121.c.2, markings to the claim text of a claim indicate a status of currently amended, thus it is noted that claim 8 has the status of “(withdrawn – currently amended).” Claims 1-3, 9, 12, 18-19 and 21-22 have been considered on the merits and all arguments have been fully considered
Previous Rejections
The previous claim rejections under section 112(a) and 103 are withdrawn in view of applicant’s amendments.
The previous rejection of claim 19 pursuant to 112(b) is withdrawn in view of applicant’s claim amendment.
The previous rejection of claims 5 and 20 pursuant to 112(d) are moot in view of applicant’s amendment.
Information Disclosure Statement
The listing of references in the specification is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered.
Claim Interpretation
In claim 1, the preamble phrase “animal model of non-human mammal liver fibrosis” and “animal model of liver fibrosis” merely implies the mouse or rat model has a liver which may be used to model liver fibrosis in some manner. In claim 2, the “animal model of early liver fibrosis” limits the animal model to a mouse and requires such an individual mouse of the model be capable of living until at least 5 weeks from birth, as indicated by the amended claim language “that appears in a mouse as within 5-6 weeks.”
In claim 1, the term “liver-specific” is interpreted as meaning “liver-limited” as ordinarily used in this art, meaning the gene inactivation occurs in a subset of liver cells or all liver cells but not in any non-liver cells. This is inapposite of “systemic” gene inactivation as used in the instant application and contrary to the instant application describing at pg. 4 (lines 91-4) that a neuron specific enolase-Cre can be used to make a “liver-specific” knockout mouse.
In claim 9, the term “control group” is implicitly defined in the claims and thus for clarity means the control group comprises the same animal model to which the test compound is not administered and with all other conditions being the same (see also instant pg. 6, line 26, to pg. 7, line 9).
In claim 12 viewed under a broadest reasonable interpretation, the phrase “the animal model of non-human mammal liver fibrosis survives for at least 8 weeks” encompasses wherein the animal model is a genetic lineage (e.g., inbred strain) or just a single individual of such a lineage. Further, claim 12 is interpreted as a product-by-process as limited by claim 1 whereby the resulting animal model is kept alive for at least 8 weeks. Thus, the method of making the animal model is further limited by a process comprising the additional method step of maintaining an individual animal of the model or the model itself for at least an 8-week duration. Thus, the limitation to the animal model of claim 12 confirms the presence of a capability mentioned in claim 1 merely as an intended use, but an intended use without any active method step or implied structural limitation to the animal model. Note, for patentability purposes product-by-process claims are treated foremostly as products, while, for patent infringement purposes, product-by-process claims are treated entirely as process claims. See Abbott v. Sandoz, 566 F.3d 1282 (Fed. Cir. 2009).
In claim 21, the term “hepatocyte-specific” is interpreted as meaning “hepatocyte-limited” meaning the gene inactivation occurs only in hepatocytes but not necessarily all hepatocytes.
In claim 22, the animal model of claim 12 is further described as having one or more recited characteristics; however, there is no expressly recited or implied limitation to claim 12. Thus, claim 22 is merely directed to the animal model product-by-process of claim 12 made by all processes encompassed by claim 12, which is an identical product.
Claim Rejections - 35 USC § 112(a), Written Description (new)
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 1-3, 9, 12, 18-19, and 21-22 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
When claim 1 is analyzed in light of the specification, the instant invention is directed to a method of making a mouse or rat model of liver fibrosis (currently limited to liver-specific ECM1 gene activation) wherein the method comprises (a) providing a cell of a mouse or rat, inactivating the ECM1 gene in the cell to obtain a mouse or rat cell with inactivated ECM1 gene; and (b) preparing the mouse or rat model using this cell made in step (a).
When claim 12 is analyzed in light of the specification, the instant invention is directed to a mouse or rat model of liver fibrosis made by a method according to claim 1 (currently limited to liver-specific ECM1 gene activation), and wherein the liver fibrosis encompasses any liver fibrosis known in the prior art as explained below. Similarly, claim 1 purports to be a method of preparing a model of claim 12 having the same aforementioned scope.
M.P.E.P. §2163 states “To satisfy the written description requirement, a patent specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. See, e.g., Moba, B.V. v. Diamond Automation, Inc., 325 F.3d 1306, 1319, 66 USPQ2d 1429, 1438 (Fed. Cir. 2003); Vas-Cath, Inc. v. Mahurkar, 935 F.2d at 1563, 19 USPQ2d at 1116.”.
In the instant case, the claimed methods state a mouse or rat having liver-specific ECM1 gene inactivation can be made from a cell with an inactivated ECM1 gene. The breadth of “the cell” is generic and not limited to a liver cell and, in view of the instant specification, includes an embryonic stem cell or blastocyst and may be heterozygous or homozygous for inactivated ECM1. Further, the method steps of animal model creation are recited only at a very high level of generality in “using the cell” and “preparing an animal model.” The specification fails to provide any description of a representative method capable of making a mammal having any liver-specific gene activation using a cell with an inactivated gene. Instead, there is description of methods using a mouse cell having an active ECM1 gene flanked by loxP sites (FIG. 14A). The liver-specific feature does not naturally and necessarily flow from performing the method as claimed. Does the method of claim 1 imply re-activation of the ECM1 gene outside the liver? As the claimed method does not sufficiently describe all essential steps to produce the recited “liver-specific” feature from a cell having ECM1 inactivation regardless of its relation to the liver, the skilled artisan would not find applicant was reasonably in possession of the claimed method. Dependent claims 2-3, 9, 12, 18-19, and 21-22 fail to provide the missing step(s) resulting any liver-specific ECM1 inactivation feature, e.g., deleting a portion of the ECM1 gene or editing the gene to have a selection marker or using a method comprising genetically chimeric mammals fails to remedy the deficiency.
Additionally, the breadth of claim 1 or 22 regarding the genus of “liver fibrosis” represents a broad genus. As described in the instant specification and claims, species of liver fibrosis include early liver fibrosis, non-induced spontaneous liver fibrosis, drug-induced fibrosis, nonalcoholic fatty liver (NAFLD), fibrotic damage caused by any chronic liver injury, such as alcoholic liver disease, drug-induced (e.g., CCL4), auto-immune caused (e.g., biliary tract disease), metabolic-caused (e.g., NAFLD), biliary tract disease caused, or chronic infection (e.g., hepatitis) with certain viruses like an HBV or HCV virus (claims 2 and 3; pg. 1, 2nd para.; pg. 5, lines 18-20; Example 3). The specification vaguely refers to other pathogenic liver conditions associated with liver fibrosis include alcoholic liver and fatty liver without clearly describing these as specifically being species of the liver fibrosis genus (pg. 5, lines 18-20); however, it is clear that liver fibrosis occurs in a subset of chronic cases of the aforementioned (Wallace et al., Biochem J 411: 1-18 (2008)). Furthermore, the prior art describes various additional liver fibrosis conditions and causes, including NASH, gallstone complications, cystic fibrosis, chronic HDV infection, Budd–Chiari syndrome, and Wilson disease (id. at Table 1).
In analyzing whether the written description requirement is met for genus claims, it is first determined whether a representative number of species have been described. In the instant case, the specification fails to provide any clear description of a representative number species for this genus by instead describing a single species, but not made by a method according to claim 1, a mouse model of uninduced, spontaneous, early liver fibrosis (ECM1-KO) (Examples 1-2). Although another model species is described that is instead has a hepatocyte-specific gene inactivation (Alb-cre/ECM1Flox/flox mouse), no liver fibrosis was empirical demonstrated, such as an uninduced, spontaneous, early liver fibrosis phenotype (Example 4; FIG. 14). Thus, the full scope of the claims is only prophetically described for performance on a rat or to generate mouse models achieving the full genus of liver fibrosis models.
It is unpredictable that mouse or rat models across the full scope of the liver fibrosis genus can be made by the method of claim 1, such as caused by cystic fibrosis or in putative rats with hereditary hemochromatosis or Wilson’s disease. Not a single working embodiment was shown, instead possession of claims 2 and 3 is only inferred from evidence from the systemic knockout of ECM1, which also affects the liver (Examples 1-2).
The instant application provides no nexus between the method of claim 1 and creation of any animal having liver fibrosis other than spontaneously arising early onset liver fibrosis in a mouse. Nowhere does the originally filed application describe how this method might achieve a model of liver fibrosis selected from drug-induced fibrosis, auto-immune caused fibrosis, late stage NAFLD, late stage alcoholic liver disease, metabolic-caused fibrosis, biliary tract disease caused, or chronic viral infection caused. Instead, the single species described would spontaneously exhibit liver fibrosis without any intervention, such as by drug or diet administration, viral infection, etc. This characteristic would confound attempts to analyze induced causes at the same time.
There is no description or guidance of how the method achieves the different types of liver fibrosis models when spontaneous uninduced is the sole representative species. Instead, the written description represents an invitation to the skilled artisan to experiment figure out whether different inactivation approaches for ECM1 (e.g., different liver-specific promoters) or rearing mice in different environments alters the spontaneous phenotype to some other model.
Regarding claims 9, 18-19 and 21, the genus of liver fibrosis remains unlimited, and thus lacks written description for the same reasons as claim 1. As claim 22 does not limit claim 12, the insufficient written description for claim 22 is for the same reasons above.
In conclusion, the skilled artisan could not rely upon the disclosure in the specification such that the specification would sufficiently describe that Applicant was in possession of the full scope of the broad genus of diverse liver fibrosis types described in the specification and known in the prior art.
35 USC § 112(a) – Enablement (new)
Claims 1-3, 9, 12, 18-19, and 21-22 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because claim is not enabled to produce an animal model homozygous for liver-specific ECM1 gene inactivation from a mammalian cell of the same species having an inactivated ECM1 gene. Furthermore, claims 1, 9, 12, 18-19, and 21-22 are not enabled for wherein the mouse or rat model of liver fibrosis specifically models inducible liver fibrosis as encompassed by these claims in view of dependent claim 2 or 3.
Enablement is considered in view of the Wands factors (MPEP 2164.01 (a)). The court in Wands states that "Enablement is not precluded by the necessity for some experimentation such as routine screening. However, experimentation needed to practice the invention must not be undue or unreasonable experimentation. The key word is 'undue.' Not 'experimentation;" (Wands, 8 USPQ2d 104). Clearly, enablement of a claimed invention cannot be predicated on the basis of quantity of experimentation required to make or use the invention. "Whether undue experimentation is needed is not a single, simple factual determination, but rather is a conclusion reached by weighting many factual considerations." (Wands, 8 USPQ2d 1404).
The factors to be considered when determining whether there is sufficient evidence to support a determination that a disclosure does not satisfy the enablement requirement and whether any necessary experimentation required is “undue” or unreasonable include, but are not limited to:
(A) The breadth of the claims;
(B) The nature of the invention;
(C) The state of the prior art;
(D) The level of one of ordinary skill;
(E) The level of predictability in the art;
(F) The amount of direction provided by the inventor;
(G) The existence of working examples; and
(H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure.
Furthermore, the USPTO does not have laboratory facilities to test if an invention will function as claimed when working examples are not disclosed in the specification. Therefore, enablement issues are raised and discussed based on the state of knowledge pertinent to an art at the time of the invention. And thus, skepticism raised in the enablement rejections are those raised in the art by artisans of expertise.
All of the Wands factors have been considered with regard to the instant claims, with the most relevant factors discussed below.
Nature of the invention:
The claims are directed to a method of producing a mouse or rat model of liver fibrosis, such as early liver fibrosis or non-inducible spontaneous liver fibrosis, which is currently limited to homozygous liver-specific ECM1 gene activation.
Cell with inactivated ECM1 gene
Claim 1 is directed to a method of making a mouse or rat having a liver-specific ECM1 gene inactivation comprising the steps of (a) obtaining a mouse or rat cell with inactivated ECM1 gene; and (b) preparing the animal model using the aforementioned cell. In other words, the end result of the method is liver-specific ECM1 gene inactivation somehow obtained from a non-liver cell comprising an inactivated gene and an animal model made therefrom, such as in claim 12. Similarly, claim 21 is directed to a subset of liver-specific inactivation in the form of a hepatocyte-specific ECM1 knockout mouse made by the method of claim 1 using a non-liver mouse or rat cell with inactivated ECM1 gene.
Breadth of the claims: liver fibrosis
Claim 1 is broadly directed to a method of making an animal model of mouse or rat liver fibrosis wherein the term “liver fibrosis” has an implied breadth. In view of claims 2 and 3, the genus of “liver fibrosis” in claim 1 at least encompasses (1) both early (within 5-6 mouse weeks) and non-early liver fibrosis (after 6 mouse weeks) as well as (2) both uninduced/spontaneous liver fibrosis or inducible/non-spontaneous liver fibrosis. In other words, the genus “liver fibrosis” encompasses (1) early liver fibrosis, whether spontaneous or induced, (2) non-early uninduced/spontaneous liver fibrosis or non-inducible spontaneous liver fibrosis, and (3) inducible/non-spontaneous liver fibrosis whether early or non-early (i.e., either arising before or after 6 mouse weeks). Thus, claims 1, 9, 12, 18-19, and 21-22 encompasses models of different types of liver fibrosis but made by the exact same method.
The state of the art:
The prior art teaches numerous rodent models of liver fibrosis wherein the condition must be induced, such as via diet and/or chemical-inducers (Van Herck et al., Nutrients 9: 1072 (2017) at pg. 2 last para. to pg. 7, para. 4). The prior art also teaches a method of making a homozygous Ecm1 knockout mouse exhibiting death by week 8 (Li et al., Nat Immunol 12: 178-85 (2011) at pg. 180, left col., para. 1-2; Suppl. Fig. 2; Online methods, last pg. Fig. 3-4).
However the prior art is silent as to wherein a single mouse or rat animal model having liver-specific homozygous ECM1 gene inactivation (or further hepatocyte-specific) can be created from a mouse or rat cell with inactivated ECM1 gene. The prior art is also silent as to wherein a single mouse or rat animal model having liver-specific homozygous ECM1 gene inactivation can be used to model both (1) early, spontaneous, uninduced liver fibrosis and (2) non-early uninduced/spontaneous liver fibrosis or (3) non-early inducible liver fibrosis. As the prior art does not teach or predict such a situation, these aspects must be shown to a reasonable extent so that one of the ordinary skills in the art would be able to practice the invention without any undue or unreasonable burden being on such an artisan.
The amount of direction and guidance and working examples provided by Applicant:
The instant application fails to provide a liver-specific working example, instead describing only a hepatocyte subtype specific example (parenchymatous) at Example 4 and FIG. 14 (homozygous ECM1-KO mice (Alb-cre/ECM1Flox/flox)), which may not even exhibit any type of liver fibrosis. However in light of teaching a method of making a mouse model of uninduced, spontaneous, early liver fibrosis using a liver-wide global knockout (ECM1-KO) (Examples 1-2), it is not unreasonable to conclude a liver-specific homozygous ECM1-KO mouse would develop uninduced, spontaneous, early liver fibrosis phenotypes even if the parenchymatous-specific version does not. This predictability does not apply to all diverse forms of liver fibrosis encompassed by claim 1.
The working example and guidance is silent as to how make an animal model with liver-specific and/or hepatocyte-specific gene inactivation from a cell wherein the gene is already inactivated generally.
The quantity of experimentation needed to make and/or use the invention:
Extensive experimentation would be required to determine how to make a mouse or rat homozygous for ECM1 inactivation at least in hepatocytes to reliably model the full scope of liver fibrosis conditions encompassed by claim 1 in view of claims 2 and 3. The examples provided, while extrapolatable to similar ECM1 inactivated rodents, do not provide sufficient guidance without working examples in the specification regarding a nexus between ECM1 inactivation and control of the timing of liver fibrosis whether inducible or spontaneous, e.g., before or after 6 mouse weeks. Thus, undue and unreasonable experimentation is required across the entire scope of the claims, which may never be successfully achieved for such broad types of liver fibrosis.
Extensive experimentation would be required to determine how to make a liver-specific or hepatocyte-specific ECM1 inactivation mouse or rat from a cell already having an ECM1 inactivated status, and may never be achievable. The examples and guidance provided, while extrapolatable to other liver-specific promoters and floxed ECM1 constructs, do not provide sufficient guidance without a working example of this extraordinary assertion. Thus, undue and unreasonable experimentation is required across the entire scope of the claims.
In summary, claims 1, 9, 12, 18-19, and 21-22 are rejected under 35 U.S.C. 112(a) because the specification does not reasonably provide enablement, to a person skilled in the art to which it pertains or with which it is most nearly connected to, to make/use the claimed mouse or rat model over the scope of the term “liver fibrosis.” Given the lack of working examples, the limited guidance provided in the specification, the lack of guidance in the prior art, and the broad scope of the claims with respect to the genus; undue and unreasonable experimentation would have been required for one skilled in the art to perform the claimed methods to produce the recited animal model, which may never be achieved across the entire scope of types of liver fibrosis or methods comprising using a mouse or rat cell with ECM1 already inactivated.
Claim Rejections - 35 USC § 112(b) (modified)
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 1-3, 9, 12, 18-19 and 21-22 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 pre-AIA the applicant regards as the invention.
Claim 1 recites a method of preparing a mouse or rat having liver-specific ECM1 gene activation from a mouse or rate cell having an inactivated ECM1 gene, which is incoherent as to how the liver-specific feature is placed upon the model derived from such a cell already having ECM1 “inactivated.” Claims 2-3, 9, 12, 18-19 and 21-22 are included in this rejection for depending from indefinite claim 1.
Claim 2 recites the relative term “early” with regard to a rat model of liver fibrosis. While the instant application provides a definition for “early” with regard to a mouse as within 5-6 weeks (pg. 17, line 9), neither the prior art nor the specification provides a definition or standard for measuring a requisite degree of “early” liver fibrosis for a rat, and thus, a person of ordinary skill in the art would not understand the metes and bounds of “early” in the claim.
Claim Rejections - 35 USC § 112(d) (maintained, new)
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claims 2-3 and 22 are rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
In claims 2-3, the type of liver fibrosis modelled by the non-human animal model is limited to either early liver fibrosis or non-inducible spontaneous liver fibrosis; however, as noted in a previous section, claim 1 is directed merely to a preparation method of making a model of liver fibrosis and any intended use language of using the model is not limiting if failing to provide or imply any additional active method step or narrowing of a step of the claimed method of making the animal model. Instead, the characteristics of the fibrosis phenotype(s) of the model are all considered inherent unless a particular phenotype requires an additional implied method step or structure/feature be present in the making of the model. In claim 2 or 3, nothing about the phrases model “early liver fibrosis” or ‘non-inducible spontaneous liver fibrosis” implies any additional method step or narrowing of the method steps of claim 1. The examples in the instant application show systemic ECM1 homozygous knockout mice lacking functional ECM1 in the liver spontaneously develop liver fibrosis around 6-8 weeks of age without any inducement/stimulation (FIG. 2-5; pg. 22-23).
In new claim 22, the method of making the animal model is limited to wherein the mouse or rat in step (b) has one or more recited phenotypes (characteristics), but the characteristics of the fibrosis phenotype(s) of the model are all considered inherent when performing the active method steps recited in claim 1 to obtain the animal model of claim 12, which is then provided for so as to survive for 8 weeks or more. Again, nothing about the characteristics listed in claim 22 implies any additional feature to the animal model of claim 12 or its method of creation recited in claim 1. Thus, claim 22 fails to further limit the scope of claim 12 from which it depends.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
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 ERIC J ROGERS whose telephone number is (571)272-8338. The examiner can normally be reached Monday - Friday 9:00-6:00.
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, Tracy Vivlemore can be reached on (571) 272-2914. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/ERIC J ROGERS/Examiner, Art Unit 1638
/KEVIN K HILL/Primary Examiner, Art Unit 1638