DETAILED ACTION
Notice of Pre-AIA or AIA Status
1. The present application is being examined under the pre-AIA first to invent provisions.
Response to Amendment and
Status of the Claims
2. Applicant’s Response, submitted September 9, 2025, has been reviewed by the examiner. No claim is amended, added, or canceled.
3. Applicant previously elected (1) the tyrosine kinase inhibitor species, nilotinib, and (2) the toxic protein species alpha-synuclein.
4. The non-elected species of tyrosine kinase inhibitors and toxic protein species remain withdrawn from consideration, with traverse.
5. Claims 1-9 are under examination with the elected species and are the subject of this office action.
Information Disclosure Statement
6. The information disclosure statements (IDS) submitted on March 13, 2025, June 13, 2025, August 7, 2025, October 21, 2025, and December 5, 2025, are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements have been considered by the examiner, please refer to the signed copies of Applicant’s PTO-1449 forms, attached herewith.
New Claim Rejections - 35 USC § 112
7. 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.
8. Claims 1-9 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.
9. Claims 1 and 6 contain the trademark/trade name "Gleevec.” Where a trademark or trade name is used in a claim as a limitation to identify or describe a particular material or product, the claim does not comply with the requirements of 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph. See Ex parte Simpson, 218 USPQ 1020 (Bd. App. 1982). The claim scope is uncertain since the trademark or trade name cannot be used properly to identify any particular material or product. A trademark or trade name is used to identify a source of goods, and not the goods themselves. In fact, the value of a trademark would be lost to the extent that it became the generic name of a product, rather than used as an identification of a source or origin of a product. Thus, the use of a trademark or trade name in a claim to describe a material or product would not only render a claim indefinite, but would also constitute an improper use of the trademark or trade name.
10. Thus, a trademark or trade name does not identify or describe the goods associated with the trademark or trade name. In the present case, the trademark/trade name is used to identify/describe imatinib mesylate and, accordingly, the identification/description is indefinite.
11. Claims 2-5 are rejected as being dependent upon and including all of the limitations of claim 1.
12. Claims 7-9 are rejected as being dependent upon and including all of the limitations of claim 6.
Previous Claim Rejections – 35 U.S.C. § 103
13. Claims 1-5 were previously rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over Davies and Conrad, U.S. 20070134724 A1, further in view of Shukla et al., Mol Pharm (2011).
14. Claims 6-9 were previously rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over Davies and Conrad, (U.S. 20070134724 A1), in view of Shukla et al., (Mol Pharm 2011), as applied to claims 1-5, and further in view of Martin et al., Annu Rev Genomics Hum Genet (2011).
15. Applicant’s arguments with respect to claims 1-5 and claims 6-9 have been considered but are moot because of the new ground of rejection, applied below.
New Claim Rejections - 35 USC § 103
16. Claims 1-5 are rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over Davies and Conrad, U.S. 20070134724 A1, further in view of Shukla et al., Mol Pharm (2011), as evidenced by Schulz et al., Pharacol Rev (2023).
Claim 1 is drawn to a method of treating Lewy body disease in a subject in need thereof, comprising: selecting a subject with Lewy body disease or at risk for Lewy body disease; and administering to the subject daily (claim 4) an effective amount (more specifically, less than about 10 mg/kg (claim 3)), of a tyrosine kinase inhibitor or a pharmaceutically acceptable salt thereof (more specifically, nilotinib (claim 2)),
wherein the tyrosine kinase inhibitor is not Gleevec, and wherein the tyrosine kinase inhibitor or a pharmaceutically acceptable salt thereof crosses the blood brain barrier.
It is noted that the disclosure of prior-filed Provisional Application No. 61/641,441 fails to provide adequate support or enablement in the manner provided by pre-AIA 35 U.S.C. 112, first paragraph for one or more claims of this application. Specifically, the limitation of treating Lewy body disease is not supported by the disclosure of Application No. 61/641,441. Accordingly, claims 1-9 are not entitled to the benefit of prior application No. 61/641,441, but are entitled to benefit of priority to U.S. Prov. Appl. No. 61/771,515, filed March 1, 2013.
17. Davies teaches the administration of abl tyrosine kinase inhibitors for treating a tauopathy or a human at risk of a taupathy, wherein a preferred inhibitor is imatinib (also known as ST1571 or Gleevec) and the tauopathy is Lewy body disease (paragraphs [0073]-[0074]). Davies recites a method of treating Lewy body disease comprising administering imatinib (ST1571) (see claims 55, 58, and 63). Although Davies does not specifically disclose a single embodiment comprising the administration of imatinib for the treatment of Lewy body disease, as recognized by In re Schaumann, 572 F.2d 312 (CCPA 1978), claims to a species are anticipated where the prior art teaches a genus embracing a limited number of members closely related to each other such that one of ordinary skill in the art could immediately envisage each member. Notably, in In re Petering, 301 F.2d 676 (CCPA 1962) the court determined that a prior art genus containing only 20 compounds anticipated a claimed species within the genus because "one skilled in [the] art would... envisage each member" of the genus (emphasis in original)). Thus, considering that the genera disclosed by Davies comprises only five compounds and seven tauopathies, the skilled artisan would have immediately envisaged selecting imatinib as the tyrosine kinase inhibitor for the treatment of Lewy body disease.
18. Davies additionally implicates the blood-brain barrier:
“Where the compound is administered peripherally such that it must cross the blood-brain barrier, the compound is preferably formulated in a pharmaceutical composition that enhances the ability of the compound to cross the blood-brain barrier of the mammal,” (paragraph [0087]).
19. As such, Davies teach a method of treating Lewy body disease comprising administering a therapeutically effective amount of the tyrosine kinase inhibitor imatinib to a subject in need thereof, wherein said administration crosses the blood brain barrier, however Davies does not teach the administration of nilotinib.
20. Yet, Shukla et al. compare the activity of tyrosine kinase inhibitors Tasigna® (nilotinib) and Gleevec (imatinib) on the abl kinase domain, wherein Tasigna (nilotinib) was rationally designed to have higher selectivity for Bcr-abl and enhanced potency over imatinib (page 2, second paragraph). Shukla et al. go on to demonstrate that Tasigna inhibits Pgp and ABCG2 transport function at the blood-brain barrier, wherein Tasigna: “maximally reduced luminal fluorescence to approximately 50% of control capillaries… [wherein] [t]he IC50 concentrations for Tasigna to inhibit efflux activity were 3.46 mM for Pgp and 93.2 nM for ABCG2, respectively,” (page 5, last paragraph-page 6, first paragraph). As such, Shukla et al. demonstrate the inhibitory activity of Tasigna against Pgp and ABCG2. And, it is clear as evidenced by Schulz et al. that “[t]he drug efflux transporters ABCB1 and ABCG2 at the blood-brain barrier limit the delivery of drugs into the brain.” Schulz et al. evidence that a strategy to overcome blood-brain barrier resistance is to develop ABCG2 transport inhibitors (see Abstract and page 824, Figure 4). Therefore, as Tasigna inhibits both Pgp and ABCG2, even if moderately, Tasigna crosses the blood brain barrier.
21. Shukla et al. teach daily Tasigna administration and teach a dosage of 400 mg, which is equivalent to a dosage of 6.45 mg/kg (assuming an average 62 kg human), which is less than 10 mg/kg, as required by claim 3 (page 8, last paragraph, last sentence).
22. Thus, one skilled in the art before the effective filing date of the claimed invention would have been motivated to substitute the abl kinase inhibitor nilotinib for imatinib in the treatment of Lewy body disease in a subject in need thereof. And, as noted by the court in In re Font, 675 F.2d 297 (CCPA 1982), an express suggestion to substitute one equivalent component (i.e., an equivalent abl tyrosine kinase inhibitor) for another is not necessary to render such substitution obvious. In the instant case, (1) the prior art element of Davies performs the function specified in the claim with only insubstantial differences; (2) the claimed component (i.e., nilotinib) and its function was known in the art; (3) a person of ordinary skill in the art would have recognized the interchangeability of the elements and could have substituted one known element for another; and (4) the results of the substitution would have been predictable, i.e. successful treatment of Lewy Body disease in a patient in need thereof. Therefore it would have been obvious to one of skill in the art before the effective filing date of the claimed invention to modify Davies by administering nilotinib to treat Lewy Body disease in a subject in need thereof, with a reasonable expectation of success.
As such, claims 1-4 are prima facie obvious.
Claim 5 is drawn to claim 1, further comprising administering a second therapeutic agent.
23. Davies additionally teaches that the presence of an additional therapeutic agent: “[p]arenteral formulations may also include antibacterial agents such as for example, benzyl alcohol or methyl parabens, antioxidants such as for example, ascorbic acid or sodium bisulfite and chelating agents such as EDTA,” (paragraph [0083]).
24. Therefore, one skilled in the art before the effective filing date of the claimed invention would have been motivated to combine the abl kinase inhibitor nilotinib with an additional therapeutic agent in the treatment of Lewy body disease in a subject in need thereof, resulting in the practice of claim 5, with a reasonable expectation of success.
25. Claims 6-9 are newly rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over Davies and Conrad, (U.S. 20070134724 A1), in view of Shukla et al., (Mol Pharm 2011), as evidenced by Schulz et al. (Pharmacol Rev 2023), as applied to claims 1-5 above, and further in view of Martin et al., Annu Rev Genomics Hum Genet (2011).
Claim 6 is directed to a method of inhibiting or preventing toxic protein aggregation (more specifically, a-synuclein aggregation (claim 8)), in a neuron of a subject with Lewy body disease, comprising contacting the neuron in the subject with an effective amount (more specifically, less than about 10 mg/kg (claim 9)), of a tyrosine kinase inhibitor or a pharmaceutically acceptable saltPage 2 of 618444237V.1Appl. No. 16/909,075Amdt. dated June 9, 2021 Preliminary Amendmentthereof (more specifically, nilotinib (claim 7)),
wherein the tyrosine kinase inhibitor is not Gleevec, and wherein the tyrosine kinase inhibitor or a pharmaceutically acceptable salt thereof crosses the blood brain barrier.
It is noted that the disclosure of prior-filed Provisional Application No. 61/641,441 fails to provide adequate support or enablement in the manner provided by pre-AIA 35 U.S.C. 112, first paragraph for one or more claims of this application. Specifically, the limitation of treating Lewy body disease is not supported by the disclosure of Application No. 61/641,441. Accordingly, claims 1-9 are not entitled to the benefit of prior application No. 61/641,441, but are entitled to benefit of priority to U.S. Prov. Appl. No. 61/771,515, filed March 1, 2013.
26. Davies in view of Shukla et al. as evidenced by Schultz et al. suggest the administration of nilotinib for treating Lewy body disease in a subject in need thereof, wherein nilotinib crosses the blood-brain barrier, however the combined prior art is silent to a-synuclein protein aggregation.
27. Yet, Martin et al. teach that Lewy body disease is characterized by α-Synuclein protein aggregation: “α-Synuclein exhibits a high propensity to aggregate in vitro and the presence of α-synuclein aggregates in Lewy bodies has led to the hypothesis that aggregation may be important to α-synuclein toxicity (Figure 2) (16),” (Page 3, last paragraph). Martin et al. go on to suggest that “[p]rotection against toxic α-synuclein aggregation is an attractive therapeutic strategy and several studies have focused on a number of small molecules that interact with α-synuclein and inhibit its aggregation in vitro (7; 30; 46; 144),” (Page 54, first full paragraph, first sentence).
28. Therefore, one of skill in the art before the effective filing date of the claimed invention would have reasonably considered that in practicing the method of Davies in view of Shukla et al. as evidenced by Schultz et al. for the successful treatment of Lewy body disease, one is necessarily reducing the aggregation of α-Synuclein protein. It would have been obvious to one of skill in the art before the effective filing date of the claimed invention to administer the abl kinase inhibitor nilotinib for treating Lewy body disease in a subject in need thereof, wherein one would reasonably expect a reduction in the aggregation of α-Synuclein protein.
29. As such, claims 6-9 are prima facie obvious.
Response to Arguments
30. Applicant traverses the previous obviousness rejection, and argues the following:
Applicant argues that Davies discloses methods of treating a subject having a tauopathy like Alzheimer's disease using Gleevec (imatinib mesylate), wherein in preferred embodiments, the formulated pharmaceutical composition enhances the ability of the compound to cross the blood brain barrier. (Davies at [0079] and [0087]). Applicant alleges that while Shukla discloses the activity of nilotinib (Tasigna), Shukla discloses that nilotinib is actively effluxed into the lumen of brain capillaries (i.e., stays within the central portion of the capillaries and does not cross the blood brain barrier). Shukla at pg. 6 left column second full paragraph. Applicant alleges that Shukla teaches away from the use of nilotinib in place of imatinib for treating Alzheimer's disease because nilotinib does not cross the blood brain barrier.
31. Applicant's arguments have been fully considered but they are not persuasive. Shukla et al. teach that Tasigna inhibits Pgp and ABCG2 transport function at the blood-brain barrier, wherein Tasigna demonstrates inhibitory activity of against Pgp and ABCG2 by: “maximally reduc[ing] luminal fluorescence to approximately 50% … [wherein] [t]he IC50 concentrations for Tasigna to inhibit efflux activity were 3.46 mM for Pgp and 93.2 nM for ABCG2, respectively,” (page 5, last paragraph-page 6, first paragraph). And, it is clear as evidenced by Schulz et al. that “[t]he drug efflux transporters ABCB1 and ABCG2 at the blood-brain barrier limit the delivery of drugs into the brain.” Schulz et al. evidence that a strategy to overcome blood-brain barrier resistance is to develop ABCG2 transport inhibitors (see Abstract and page 824, Figure 4).
Regarding Applicant’s argument that each reference teaches away from the claimed invention, the examiner refers to MPEP 2141.02 VI, Allied Erecting v. Genesis Attachments, 825 F.3d 1373,1381,119 USPQ2d 1132,1138 (Fed. Cir. 2016) ("Although modification of the movable blades may impede the quick change functionality disclosed by Caterpillar, ‘[a] given course of action often has simultaneous advantages and disadvantages, and this does not necessarily obviate motivation to combine,’" (quoting Medichem, SA. v. Rolabo, S.L., 437 F.3d 1157,1165, 77 USPQ2d 1865,1870 (Fed Cir. 2006) (citation omitted)).
And, 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). See also Upsher-Smith Labs. v. Pamlab, LLC, 412 F.3d 1319, 1323, 75 USPQ2d 1213, 1215 (Fed. Cir. 2005)(reference disclosing optional inclusion of a particular component teaches compositions that both do and do not contain that component); Celeritas Technologies Ltd. v. Rockwell International Corp., 150 F.3d 1354, 1361, 47 USPQ2d 1516, 1522-23 (Fed. Cir. 1998) (The court held that the prior art anticipated the claims even though it taught away from the claimed invention. "The fact that a modem with a single carrier data signal is shown to be less than optimal does not vitiate the fact that it is disclosed.").
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Therefore, as Tasigna inhibits both Pgp and ABCG2, even if moderately, Tasigna crosses the blood brain barrier.
Previous Double Patenting Rejections
32. 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).
33. 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).
34. The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The 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/process/file/efs/guidance/eTD-info-I.jsp.
35. Claims 1-9 remain rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3 and 5 of U.S. Patent No. 9,474,753, in view of Games et al., (The American Journal of Pathology 2013, accepted for publication November 2012).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims recite the following:
Claim 1 is drawn to a method of treating Lewy body disease in a subject in need thereof, comprising: selecting a subject with Lewy body disease or at risk for Lewy body disease; and administering to the subject daily (claim 4) an effective amount (more specifically, less than about 10 mg/kg (claim 3)), of a tyrosine kinase inhibitor or a pharmaceutically acceptable salt thereof (more specifically, nilotinib (claim 2)), wherein the tyrosine kinase inhibitor is not Gleevec, and wherein the tyrosine kinase inhibitor or a pharmaceutically acceptable salt thereof crosses the blood brain barrier.
Claim 6 is directed to a method of inhibiting or preventing toxic protein aggregation (more specifically, a-synuclein aggregation (claim 8)), in a neuron of a subject with Lewy body disease, comprising contacting the neuron in the subject with an effective amount (more specifically, less than about 10 mg/kg (claim 9)), of a tyrosine kinase inhibitor or a pharmaceutically acceptable saltPage 2 of 618444237V.1Appl. No. 16/909,075Amdt. dated June 9, 2021 Preliminary Amendmentthereof (more specifically, nilotinib (claim 7)), wherein the tyrosine kinase inhibitor is not Gleevec, and wherein the tyrosine kinase inhibitor or a pharmaceutically acceptable salt thereof crosses the blood brain barrier.
36. Claim 1 of U.S. Patent No. 9,474,753 recites a method of treating an -Synucleinopathy in a subject, comprising: selecting a subject with an -Synucleinopathy or at risk for an -Synucleinopathy; and systemically administering to the subject an effective amount of nilotinib, wherein the nilotinib is administered to the subject at a dosage of about 5 mg/kg or less. Claim 3 recites wherein the administration is daily. Claim 5 of U.S. Patent No. 9,474,753 recites a method of inhibiting toxic protein aggregation in a neuron of a subject with an a-synucleinopathy, comprising contacting the neuron with an effective amount of nilotinib, wherein the neuron is contacted with nilotinib by systemically administering nilotinib to the subject at a dosage of about 5 mg/kg or less. A dosage amount of 5 mg/kg or less meets the limitation of less than about 10 mg/kg, required by instant claims 3 and 9.
37. U.S. Patent No. 9,474,753 does not recite the treatment of Lewy body disease.
38. Yet, Games et al. teach that Lewy body disease is considered an α-synucleinopathy because it is characterized by the aggregation of abnormal deposits of the protein α-synuclein, forming Lewy bodies (see Abstract and first paragraph, page 1).
39. And, dosage amount is clearly a result effective parameter that a person of ordinary skill in the art would routinely optimize given the guidance of the prior art. It would have been obvious to one skilled in the art to optimize the dosage recited in U.S. Patent No. 9,474,753, thus resulting in the practice of claims 1 and 5, with a reasonable expectation of success.
40. Thus, it would have been obvious to one skilled in the art to employ the previously patented method of treating an -Synucleinopathy in a subject, comprising administering to the subject an effective amount of nilotinib, wherein the nilotinib is administered to the subject at a dosage of about 5 mg/kg or less.
41. Claims 1-9 remain rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 of U.S. Patent No. 10,709,704.
Although the claims at issue are not identical, they are not patentably distinct from each other. Applicant’s instant claims have been described in detail, above.
42. Claim 1 of U.S. Patent No. 10,709,704 recite a method of treating a neurodegenerative disease in a subject in need thereof, comprising: selecting a subject with a neurodegenerative disease of the central nervous system or at risk for a neurodegenerative disease of the central nervous system; and systemically administering to the subject an effective amount of a tyrosine kinase inhibitor, wherein the tyrosine kinase inhibitor crosses the blood brain barrier, wherein the effective amount of the tyrosine kinase inhibitor is less than 10 mg/kg, and wherein the effective amount of the tyrosine kinase inhibitor is lower than a chemotherapeutic dosage, wherein the tyrosine kinase inhibitor is selected from the group consisting of nilotinib, bosutinib, and a combination thereof. Claim 4 recites wherein the administration is daily. In the Specification, under the detailed description of the invention, U.S. Patent No. 10,709,704 names Lewy body disease as a neurodegenerative disease to be treated (column 17, line 48). Please refer to MPEP § 804 II.B.2(a), i.e., the specification of the reference patent may be relied upon to properly construe the scope of the reference claim, and “may be considered when addressing the issue of whether a claim in the application defines an obvious variation of an invention claimed in the patent.” See also In re Vogel, 422 F.2d 438, 441-42, 164 USPQ 619, 622 (CCPA 1970): those portions of the specification which provide support for the reference claims may also be examined and considered when addressing the issue of whether a claim in the application defines an obvious variation of an invention claimed in the reference patent or application (as distinguished from an obvious variation of the subject matter disclosed in the reference patent or application).
43. Thus, it would have been obvious to one skilled in the art to employ the previously patented method of treating a neurodegenerative disease in a subject, wherein the neurodegenerative disease is Lewy body disease, comprising administering to the subject an effective amount of nilotinib, wherein the nilotinib is administered to the subject at a dosage of about 10 mg/kg or less.
44. Applicant has not argued or responded to the double patenting rejections. Therefore, the previous double patenting rejections are maintained.
Conclusion
45. Claims 1-9 are present in the application. Claims 1-9 are rejected. No claim is presently allowable.
46. Any inquiry concerning this communication or earlier communications from the examiner should be directed to JANET L COPPINS whose telephone number is (571)272-0680. The examiner can normally be reached Monday-Friday 8:30AM-5PM EST.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Amy L Clark can be reached on 571-272-1310. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/JANET L COPPINS/Examiner, Art Unit 1628
/AMY L CLARK/Supervisory Patent Examiner, Art Unit 1628