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 .
Election/Restrictions
2. Applicant's election without traverse of Group III (claims 10, 15-17, 19) on 4/1/26 is acknowledged.
Claims 1-5, 9, 20, 25-34 are withdrawn from further consideration by the Examiner, 37 CFR 1.142(b), as being drawn to a non-elected invention.
Claims 6-8, 18, and 21-24 are canceled.
Information Disclosure Statement
3. The information disclosure statement (IDS) submitted on 10/15/2025 is in compliance with the provisions of 37 CFR 1.97 and has been considered by the examiner.
Applicant is reminded of their duty to disclose to the Office all information known to the person to be material to patentability as defined in 37 CFR 1.56. As stated therein, “[e]ach individual associated with the filing and prosecution of a patent application has a duty of candor and good faith in dealing with the Office, which includes a duty to disclose to the Office all information known to that individual to be material to patentability as defined in this section”.
Claim Rejections - 35 USC § 112, first paragraph, scope of enablement
3. 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.
3a. Claims 10, 15-17, 19 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 a method for inhibiting Tau aggregates in cardiac tissue of a subject with heart failure comprising administration of an anti-Tau monoclonal antibody TOMA of monoclonal antibody clone (TOMA-1) that specifically recognizes oligomeric forms of Tau protein, does not reasonably provide enablement for a method as recited in claim 10. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to practice the invention commensurate in scope with these claims.
The claims are drawn very broadly to a method of treating a subject with heart disease characterized by misfolded proteins in cardiac tissue, or reducing the likelihood of the same, comprising delivering to said subject an antibody or antibody fragment that binds to Tau.
The specification on pages 79, recites:
“TOMA Antibody treatment. Twelve-month-old hTau mice were treated with either
IgG (12 mice, 6 male/6 female) or anti-tau-PAO structural antibodies (TOMA) (12 mice, 6 male/6 female). Mice were treated with a single intraperitoneal injection of TOMA as
previously described (Castillo-Carranza, 2014a; 2014b).”
The specification on page 80 discloses:
“ Big-tau is the human hearts isoform. The inventors tested heart samples from idiopathic dilated cardiomyopathy (iDCM) and non-failing age/sex/ethnicity matched controls as well as brain and heart tissue from four cases with medical history and pathological evidence of AD (Table S1) and matched controls (detailed in the methods section) (Troncone et al., 2016). The AD samples were previously used to describe that A3 pathology affects the heart of AD patients (Troncone et al., 2016). These new data show that tau is expressed in human hearts (Figs. lA-I). Total tau expression by SDS page was not significantly different both in the iDCM and the AD groups (Figs. 1A-E), whereas ELISA, using Tau-5, showed higher expression in both AD heart and brain (Figs. 1H-I). The lack of significance in the SDS page can be due to the semi-quantitative nature of the method and the inter-patients variability also shown in AD brains (Sjogren et al., 2001). Additionally, iDCM is a diagnosis of exclusion and the diagnosis of iDCM includes a heterogeneous group of cardiomyopathies clustered by the dilated phenotype and not the underlying pathogenesis. Thus tauopathy (as other proteinopathies (Troncone et al., 2016; Taylor et al.) may occur in a subgroup of cases. Instead, ELISA demonstrated that tau is more expressed in the heart and in the brain of AD patients compared to controls (Figs. 1H-I). Interestingly, the inventors found that the most represented isoform in the heart is the 100-110kDa isoform, known as big-tau (Georgieff et al., 1993). Immunofluorescence showed that tau is expressed inside cardiomyocytes and co-localizes with PAO stained with the structural antibody against PAO (T22) in diseases (Figs. 2A-B).
Tau phosphorylation and pathology in human hearts. Tau pathology is composed of paired helical filaments, which are primarily formed by hyper-phosphorylated tau, and tau
p-Ser396 is traditionally associated with AD tangles (Taylor et al., 2007). As in the brain, the inventors found that tau is hyperphosphorylated on Ser396 both in the soluble and insoluble fractions in iDCM hearts (Figs. 3A-C). p-Ser396 was not significantly increased in the heart of AD patients possibly due to the variability of the samples, whereas the brain signal couldn't be quantified due to saturation (Figs. 3D-F). However increased tau p-Ser396 was shown by ELISA
(Figs. 1G-I).”
On page 81, the specification discloses:
“Functional readout of cardiac tauopathy in mice. The inventors tested the pathogenic effect of cardiac tauopathy in a well-established transgenic mouse model of humanized tau (hTau). They performed the behavioral tests to compare the time course of the brain with cardiac pathology and phenotype in the same mice. As previously shown (Andorfer et al., 2003; Polydoro et al., 2009; Geizler et al., 2016; Phillips et al., 2011), cognitive performance was unaffected in the 3- and 7-months old hTau mice compared with C57B1/6J age-matched controls. The spatial learning and memory tested by Morris water maze (Figs. S1A-B) and novelty Y-maze (Fig. S1C) became significantly impaired in the 12-months-old mice while the open field test showed no significant abnormalities for ages and genotypes (Fig. S1D). Using anti-Tau-Oligo-Monoclonal-Antibodies (TOMA), the inventors confirmed an
age-dependent tau pathology in hTau mouse brain (Fig. SlE) (Andorfer et al., 2003; 2005).
Different from the brain, progressive myocardial dysfunction was present from 3- month-old hTau mice by echocardiography (Figs. 5A-J, Table S2, Fig. S2) accompanied by accumulation of tau-PAO (Figs. 5L-M; Fig. S3). Systolic function was lower, but non- significant at all ages in hTau mice with the worse values at 12 months (Fig. 5D). Diastolic function appeared progressively impaired with age in hTau mice when parameters were compiled as defined by the degrees of diastolic dysfunction (Fig. S4A). E/A ratio (Fig. 5G) wasn't significantly different, however showed an averaged reduced value at 7-month and an increased value at 12-months of age supporting a progressive worsening of diastolic function from grade-II to grade-III, as also paralleled by the mirror changes in mitral valve deceleration time (Fig. 5H). The mean left-atrial (LA) pressure was steadily higher (Fig. 5F, Table 2), in30 3-nd 7-months-old hTau mice. The increased right ventricular (RV) pressure was severe in some mice where it caused paradox septal movement (Fig. 5K) impeding the accurate hemodynamic measurements of the left ventricular end diastolic pressure (LVEDP).
The in-vivo echocardiographic findings were confirmed in cardiomyocytes isolated from 6-months-old hTau mice and C57B1/6J control hearts. Systolic function was lower, but non-significant, also in hTau cardiomyocytes (Table S3) whereas diastolic defect was confirmed as shown by i) stiffer sarcomeres revealed by higher tau value (Fig. 5P; Fig. S5, Table S3) and ii) abnormal Ca2+ homeostasis revealed by the reduced Ca2+ peak amplitude and the significant delayed rise and decay velocities (Fig. 5Q-T; Fig. S5; Table S3). An inhomogeneous accumulation of tau-PAO in the cardiomyocytes may explain the high variability of cardiomyocyte values (Figs. 5N-O; Fig.S6).”
The specification on pages 82-83, discloses:
“TOMA therapy for cardiac tauopathy. Monoclonal antibody (mAb) therapy is a recently introduced, and rapidly expanding, modality for the treatment of human diseases. To mimic the studies in the brain (Castillo-Carranza et al., 2014; 2015), same age male and female
hTau mice were injected (once) intraperitoneally with TOMA or IgG control. Mice were studied 10 and 30 days after injection by echocardiography (Fig. 6A). Whereas no significant changes were detected at the 10-day time-point, 30-days after treatment diastolic function was improved as shown by the E/e' ratio, mean LA pressure and a significant reduction in LA dimension (Figs. 6B-D, 6F, 6G). Although the measurements of filling pressure were not significant, the pseudo-normalization in the most severe dysfunction might explain the result. The degree of dysfunction based on the algorithm that includes E/A ratio, E-wave deceleration time and LA dimension showed that a grade-IV diastolic dysfunction in >1/3 of IgG-treated mice compared to TOMA-treated mice where the majority of mice (>1/3) showed grade I/II.
The functional improvement was accompanied by a reduction in the accumulation of tau-PAO (Figs. 6H, 6J), and a significant remodeling of the transverse tubule architecture corresponding to a more ordered distribution of Ca+ handling proteins as simplified by the RyRs (Fig. 6I), setting the first evidence of anti-proteotoxic mAb therapy for HF.”
Furthermore, on page 86, lines 12-15, the specification discloses:
“Here, the inventors show that anti tau-PAO antibody treatment (TOMA) reduces tau-PAO aggregates in the heart (Figs. 6H-I) and improves diastolic function one month after therapy (Figs. 6B-G; Table S4). TOMA treatment acting of both arms of the dual pathogenic mechanisms of tauopathy sets the first evidence for anti-proteotoxic immunotherapy for HF.”
However, other than this disclosure by the administration of anti-Tau-antibody (TOMA)
(see specification, page 28, lines 14-22), the specification fails to provide any guidance for the successful treatment of all heart diseases or disorders with every and all Tau antibodies as recited in claim 10.
The specification delimits the instant method to administering a specific Tau antibody for inhibiting Tau aggregation in a subject with heart failure, HF (see page 28). However, with respect to claim 10, as recited, what is claimed in the instant invention broadly encompasses a method of administering "all" Tau antibodies. The specification is non-enabling for a method of administering these unlimited and unidentified number of substances, which are encompassed by the scope of the claims. Claim 10, for example, is a single means claim (M.P.E.P. 2164.08(a)). In In re Hyatt, 708 F.2d 712, 218 USPQ 195 (Fed. Cir. 1983), the Courts have held that: A single means claim, i.e. where a means recitation does not appear in combination with another recited element of means, is subject to an undue breadth rejection under 35 U.S.C. 112, first paragraph. (A single means claim which covered every conceivable means for achieving the stated purpose was held nonenabling for the scope of the claim because the specification disclosed at most only those means known to the inventor). Since no material limitations for “Tau antibody” have been recited in the claim and only a biological activity has been recited, the claim encompasses every conceivable structure (means) for achieving the stated property (result), a fact situation comparable to Hyatt. The claimed invention encompasses a method of administering compositions not envisioned or described in the specification, and neither does the specification disclose how these compositions can be distinguished from each other. The specification only enables a method of administering TOMA, this antibody having specific characteristics and properties. These properties may differ structurally, chemically and physically from other known antibodies. By application of the factors set forth in Ex parte Forman (230 USPQ 546 (Bd. Pat. App. & Int. 1986), and reiterated in In re Wands (858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988)), which include (1) quantity of experimentation, (2) guidance presented, (3) the predictability of the art, and (4) the breadth of the claims, in the instant application, the quantity of experimentation to determine which other substances are encompassed by the scope of the claims is practically infinite and the guidance provided in the specification very little, thereby rendering the results of the methods taught in the specification unpredictable (see pages 79-82). Therefore, it would require undue experimentation to determine which Tau antibodies would be encompassed by the scope of the method claims. The disclosure of a single TOMA is clearly insufficient support under the first paragraph of 35 U.S.C. 112 for claims, which encompass a method of administering every and all Tau antibodies, including variants of such. In In re Fisher, 427 F.2d 833, 166 USPQ 18 (CCPA 1970), the Courts have held that:
"Inventor should be allowed to dominate future patentable inventions of others where those inventions were based in some way on his teachings, since some improvements while unobvious from his teachings, are still within his contribution, since improvement was made possible by his work; however, he must not be permitted to achieve this dominance by claims which are insufficiently supported and hence, not in compliance with first paragraph of 35 U.S.C. 112; that paragraph requires that the scope of the claims must bear a reasonable correlation to scope of enablement provided by specification to persons of ordinary skill in the art; in cases involving predictable factors, such as mechanical or electrical elements, a single embodiment provides broad enablement in the sense that, once imagined, other embodiments can be made without difficulty and their performance characteristics predicted by resort to known scientific law; in cases involving unpredictable factors, such as most chemical reactions and physiological activity, scope of enablement varies inversely with degree of unpredictability of factors involved."
Furthermore, the amount of embodiments corresponding to the desirable antibodies, may be several, and the enabled embodiments amount to only one. Therefore, there are substantial scientific reasons to doubt the scope of enablement, as set forth above. Reasonable correlation must exist between the scope of the claims and scope of enablement set forth. The specification does not describe administering any other antibodies other than the specific antibody recited in the specification, and since it is deemed to constitute undue experimentation to determine all the others, the disclosure is not commensurate with the scope of the claims. It is suggested that by employing conventional claim language, the method claims be amended to include the specific antibody supported by the instant specification.
Furthermore, the claims as recited encompass a method of treating every and all heart disease while the only disease enabled is the one in which there are Tau aggregates in cardiac tissue.
In re Fisher, 427 F.2d 833, 839, 166 USPQ 18, 24 (CCPA 1970) states, “The amount of guidance or direction needed to enable the invention is inversely related to the amount of knowledge in the state of the art as well as the predictability in the art.” “The “amount of guidance or direction” refers to that information in the application, as originally filed, that teaches exactly how to make or use the invention. The more that is known in the prior art about the nature of the invention, how to make, and how to use the invention, and the more predictable the art is, the less information needs to be explicitly stated in the specification. In contrast, if little is known in the prior art about the nature of the invention and the art is unpredictable, the specification would need more detail as to how to make and use the invention in order to be enabling” (MPEP 2164.03). The MPEP further states that physiological activity can be considered inherently unpredictable. Given the inherent unpredictability of physiological activity, which would include biological processes, i.e., methods of treatment, a certain amount of enablement beyond mere assertion must be required.
The CAFC decision (Genentech Inc. v. Novo Nordisk, 42 USPQ2d 1001, 1997) expressly states that:
"When there is no disclosure of any specific starting material or of any of the conditions under which a process can be carried out, undue experimentation is required; there is a failure to meet the enablement requirement that cannot be rectified by asserting that all the disclosure related to the process is within the skill of the art. It is the specification, not the knowledge of one skilled in the art, that must supply the novel aspects of an invention in order to constitute adequate enablement".
If Applicants will kindly review page 1404 of In re Wands, they will find that the factors to be considered in determining whether a disclosure would require undue experimentation include (1) the quantity of experimentation necessary, (2) the amount of direction or guidance presented, (3) the presence or absence of working examples, (4) the nature of the invention, (5) the state of the prior art, (6) the relative skill of those in the art, (7) the predictability or unpredictability of the art and (8) the breadth of the claims.
Thus, it would require undue experimentation on the part of the skilled artisan to use the claimed method of treatment as recited, in the absence of sufficient information to predict the results with an adequate degree of certainty. Therefore, a method for treating all heart diseases characterized by misfolded proteins in cardiac tissue as recited in claim 10 has not been enabled by the specification. The recitation of "heart disease" in claim 10, is not commensurate with the scope of the specification. Given the breadth of claim 10 in light of the predictability of the art as determined by the number of working examples, the level of skill of the artisan, and the guidance provided in the instant specification and the prior art of record, it would require undue experimentation for one of skill in the art to practice the claimed invention.
Claim Rejections - 35 USC § 112, first paragraph, written description
3b. Claims 10, 15-17, and 19, are rejected under 35 U.S.C. 112, first paragraph, as containing 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(s), at the time the application was filed, had possession of the claimed invention.
The claims require administration of “a Tau antibody”. The claims, however, do not require that the “Tau antibody” possess any particular conserved structure, or other distinguishing feature.
To provide adequate written description and evidence of possession of a claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of complete or partial structure, physical and/or chemical properties, functional characteristics, structure/function correlation, methods of making the claimed product, and any combination thereof. In this case, the only factor present in the claim that is sufficiently disclosed is a recitation of a desired activity. The specification does not identify any particular portion of the structure, nor does it provide a disclosure of structure/function correlation for the claimed antibody. The distinguishing characteristics of the claimed genus for the “Tau antibody” with respect to the heavy chain variable region and the light chain variable region or the three CDR’s in the heavy chain variable region and the three CDRs in the light chain variable region have not been described. Accordingly, the specification does not provide adequate written description of the claimed genus of “Tau antibody”.
To satisfy the written-description requirement, the specification must describe every element of the claimed invention in sufficient detail so that one of ordinary skill in the art would recognize that the inventor possessed the claimed invention at the time of filing. Vas-Cath, 935 F.3d at 1563; see also Lockwood v. American Airlines, Inc., 107 F.3d 1565, 1572 [41 USPQ2d 1961] (Fed. Cir. 1997) (patent specification must describe an invention and do so in sufficient detail that one skilled in the art can clearly conclude that “the inventor invented the claimed invention”); In re Gosteli, 872 F.2d 1008, 1012 [10 USPQ2d 1614] (Fed. Cir. 1989) (“the description must clearly allow persons of ordinary skill in the art to recognize that [the inventor] invented what is claimed”). Thus, an applicant complies with the written-description requirement “by describing the invention, with all its claimed limitations, not that which makes it obvious,” and by using “such descriptive means as words, structures, figures, diagrams, formulas, etc., that set forth the claimed invention.” Lockwood, 107 F.3d at 1572.
See University of Rochester v. G.D. Searle & Co., 68 USPQ2d 1424 (DC WNY 2003) and University of Rochester v. G.D. Searle & Co. et al. CAFC [(03-1304) 13 February 2004]. In University of Rochester v. G.D. Searle & Co. a patent directed to method for inhibiting prostaglandin synthesis in human host using an unspecified compound, in order to relieve pain without side effect of stomach irritation, did not satisfy written description requirement of 35 U.S.C. §112, since the patent described the compound's desired function of reducing activity of the enzyme PGHS-2 without adversely affecting PGHS-1 enzyme activity, but did not identify said compound, since invention consists of performing “assays” to screen compounds in order to discover those with desired effect. The patent did not name even one compound that assays would identify as suitable for practice of invention, or provide information such that one skilled in art could identify suitable compound. And since specification did not indicate that compounds are available in public depository, the claimed treatment method cannot be practiced without compound. Thus the inventors cannot be said to have “possessed” the claimed invention without knowing of a compound or method certain to produce compound. Thus said patent constituted an invitation to experiment to first identify, then characterize, and then use a therapeutic a class of compound defined only by their desired properties.
Therefore the full breadth of the claims fails to meet the written description provision of 35 U.S.C. §112, first paragraph. In the instant case, for example, Applicants have failed to describe which Tau antibody is to be administered in independent method claim 10. Similarly, Applicants have failed to describe administering “a Tau antibody” which has the desirable property for treatment of the heart disease recited in claim 10. Applicant is reminded that Vas-Cath makes clear that the written description provision of 35 U.S.C. §112 is severable from its enablement provision.
Claim Rejections - 35 U.S.C. § 112(b)
4. 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.
4a. Claims 10, 15-17, 19 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 10 is vague and indefinite for several reasons.
Regarding claim 10, the phrase "characterized by" in line 1, renders the claim indefinite because it is unclear whether the limitations following the phrase are part of the claimed invention. See MPEP § 2173.05(d).
Claim 10 is incorrect because it recites “misfolded proteins” and it is unclear which “misfolded proteins” are encompassed by this term. Furthermore, the metes and bounds of the term “misfolded proteins" is unclear.
Claim 10 is vague and indefinite because it is unclear whether the Tau antibody administered is "effective" in treating the claimed heart disease. Appropriate correction of the claim is requested to obviate this rejection.
Claim 10, line 2, is vague and indefinite because it recites “or reducing the likelihood of the same”. It suggested that the claim be amended to recite specifically the limitation Applicant intend to claim to obviate this rejection.
Claim 10, line 2, is vague and indefinite because it recites the term “delivering” rather than the conventional term “administering”. It is suggested that the claim be amended to recite the specific method for administering for which there is a basis in the instant specification.
Claim 10, line 3, is improper because it recites non-elected inventions. Appropriate correction of the claim is required to delete the non-elected inventions.
Claim 15 is vague and indefinite for several reasons.
Claim 15, lines 2-3, is vague and indefinite because it recites the limitation "an Fc portion mutated to alter (eliminate or enhance) FcR interactions". Firstly, it is unclear what the metes and bounds of the term “mutated" are. Secondly, the limitation in brackets is confusing and it is required that it be deleted from the claim and only the Fc mutations, for which there is a basis in the instant specification, should be recited to obviate this rejection. Thirdly, the acronym “FcR” should be spelled out at its first recitation in a claim.
In claim 15, line 3, the term “and/or” is confusing because it is unclear how therapeutic efficacy can be increased.
Regarding claim 15, the phrase "such as" in lines 4 and 5, renders the claim indefinite because it is unclear whether the limitations following the phrase are part of the claimed invention. See MPEP § 2173.05(d). This rejection can only be obviated by deleting the recitation of “such as”.
Claim 15, line 4, is vague and indefinite because it is unclear what “LALA, LALA-PG, N297, GASD/ALIE, DHS, YTE or LS mutation” are. It is suggested that these limitations be spelled out in the claim, for which there is a basis in the specification, to obviate this rejection (See pages 2-3, 6-7).
Claim 15, lines 4-7, is vague and indefinite because it recites the limitation "….LS mutation or glycan modified to alter (eliminate or enhance) FcR interactions such as enzymatic or chemical addition or removal of glycans or expression in a cell line engineered with a defined glycosylating pattern”. This recitation is extremely confusing for several reasons. Firstly, it is unclear what the metes and bounds of the term “mutation" and “modified” are and do they relate to “LALA, LALA-PG, N297, GASD/ALIE, DHS, YTE” or only to “LS”. It is required that the specific mutations or modifications be recited in the claim to obviate this rejection. Secondly, the recitation of the limitation in brackets “(eliminate or enhance)” is confusing and it is required that this limitation be deleted, in both instances, from the claim. Thirdly, the metes and bounds of the limitation “enzymatic or chemical addition or removal of glycans” is unclear. It is unclear which glycans are encompassed by the claim and how are the glycans enzymatically or chemically added. It is required that this limitation be spelled out specifically with limitations for which there is a basis in the instant specification, to obviate this rejection. Fourthly, the recitation of “expression in a cell line engineered with a defined glycosylating pattern” is unclear. Which cell line, how is it engineered, and what is the “defined glycosylation pattern” encompassed by the claim? It is required that the specific limitations, for which there is a basis in the specification, be recited in the claim to obviate this rejection.
Claim 17, line 2, is vague and indefinite because it recites the limitation “antibody….is administered multiple times” and there is no upper limit on the number of times the antibody is administered. Is the antibody administered five times, ten times, are more than that?
Claim 19, lines 2-3, is improper because it recites non-elected inventions. Appropriate correction of the claim is required to delete the non-elected inventions.
Claim 16 is rejected as vague and indefinite insofar as they depend on the above rejected claims for their limitations.
Conclusion
No claims are allowed.
Claims 10, 15-17, and 19 are rejected.
Advisory Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to PREMA MARIA MERTZ whose telephone number is (571)272-0876. The examiner can normally be reached on Monday to Thursday from 7:30am to 6:00pm.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, VANESSA FORD, can be reached at telephone number 571-272-0857. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of an application may be obtained from Patent Center. Status information for published applications may be obtained from Patent Center. Status information for unpublished applications is available through Patent Center for authorized users only. Should you have questions about access to Patent Center, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free).
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) Form at https://www.uspto.gov/patents/uspto-automated- interview-request-air-form.
/PREMA M MERTZ/ Primary Examiner, Art Unit 1674
Prosecution Insights