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 .
DETAILED ACTION
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Request for Continued Examination
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.
Applicant’s submission filed on 05/12/2025 has been entered.
Claim Status
Claims 1-3, 6, 8-9, 11-13, 16 and 18-19 were pending as of Office Action from 11/14/2024.
Upon the amendment entrance, Claims 1-3, 6, 8-9, are cancelled.
Upon the amendment entrance, new Claims 23-33 were added.
Claims 11-13, 16, 18-19, and 23-33 are pending in the application.
Priority Status
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Priority was acknowledged in the previous Office Action.
Information Disclosure Statement
Examiner acknowledged IDS(s) filed for the Instant Application in a previous Office Action.
Drawings
Examiner acknowledged drawings filed for the Instant Application in a previous Office Action.
Examiner Response to Arguments
The issues raised in the previous Office Action are addressed below:
I. Response to Arguments 35 U.S.C. §102 –
Claims 1-3, 8-9, 11-13, and 18-19 are rejected under 35 U.S.C. §102(a)(1) and 35 U.S.C. §102(a)(2) as anticipated by Peng Leong, W02004/035076 Al ("Leong").
Claims 1-3, 8-9, 11-13, and 18-19 are rejected under 35 U.S.C. §102(a)(1) as anticipated by QJ Meng. "Entrainment of disrupted Cicadian behavior through inhibition of casein kinase 1 (CK1) enzymes" Proc Natl Acad Sci USA 2010 Aug 24:107, 34, 15240-5) ("Meng").
Applicant' s arguments, filed 05/12/2025, with respect to claims have been fully considered but they are not persuasive.
The amended claims of the present application are directed at methods of use of compositions containing CK1δ inhibitors to reduce total peripheral resistance in the patient to treat subarachnoid haemorrhage (claim 23), hypertension (claim 28), and other vascular and/or cardiovascular disease (claim 11).
Applicant argues “Leong does not disclose use of CK1δ inhibitors. Leong clearly articulates that CK1δ is not the same as CK1. As explained by Leong, CK1δ has only a 53% identity with CK1Ɛ in the carboxyl terminal region (SEQ ID 2 of Leong)(see Leong, p.7, line 29). Leong at p.8, lines 4-9 defines substantial similarity as in various ways, but under none of those definitions would CK1δ's 53% identity with CK1E be considered a substantial similarity.”
With respect to Applicant’s argument of the 102, the argument is not persuasive because: Leong does disclose CK1δ inhibitors having a stronger inhibitory effect. As stated in pg. 1, lns. 17-20, “CK1δ and ε isoforms share 98% identity in the kinase domain and are 53% identical in a C-terminal domain that is not present in other CKI isoforms.” Leong further discloses use of CK1 inhibitors in methods of modulating tumor necrosis factor-alpha (TNF-α) mediated pathways to treat inflammatory diseases. (See p. 7, line 21-p. 8, line 11). Leong's entire disclosure is directed at use of CK1inhibitors (See entire specification and claims).
See MPEP 2114:
I. INHERENCY AND FUNCTIONAL LIMITATIONS IN APPARATUS CLAIMS
Features of an apparatus may be recited either structurally or functionally. In re Schreiber, 128 F.3d 1473, 1478, 44 USPQ2d 1429, 1432 (Fed. Cir. 1997).
II. Response to Arguments 35 U.S.C. §103 –
With respect to Applicant’s argument of the 103, the argument is not persuasive because: Leong does disclose CK1δ inhibitors having a stronger inhibitory effect. As stated in pg. 1, lns. 17-20, “CKI-δ and ε isoforms share 98% identity in the kinase domain and are 53% identical in a C-terminal domain that is not present in other CKI isoforms.” Leong further discloses use of CK1 inhibitors in methods of modulating tumor necrosis factor-alpha (TNF-a) mediated pathways to treat inflammatory diseases. (See p. 7, line 21-p. 8, line 11). Leong's entire disclosure is directed at use of CK1 inhibitors (See entire specification and claims).
In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
III. RCE Claim Rejections -
Claim Interpretation
In the Instant Application, total peripheral resistance (TPR) is a hemodynamic parameter reflecting the overall resistance to blood flow in the systemic circulation. It is primarily determined by the diameter and tone of the small arteries and arterioles and can be affected by neural, hormonal, and local factors. TPR is central in regulating blood pressure and tissue perfusion and is often calculated as the ratio of mean arterial pressure (MAP) to cardiac output (CO).
As such, it is seen through preceding prior art, as well as prior art submitted in this RCE, that CK1δ/ε inhibition can affect total peripheral resistance, primarily by modulating the myogenic tone (pressure-induced contraction and relaxation of vascular smooth muscle in the walls of arteries and arterioles) of resistance arteries. The myogenic response in skeletal muscle resistance arteries, which significantly impacts TPR, is regulated by the circadian clock and involves casein kinase 1 (CK1).
The art is therefore good for the Instant claims, as well as its function as a “treatment of a vascular and/or cardiovascular disease comprising administering at least one casein kinase 1 delta (CK1δ) inhibitor having an inhibitory effect on CK1δ to a patient in an effective amount which reduces total peripheral resistance in the patient.”
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
A. First Rejection
Claim(s) 11-13, and 18-19 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by CR Keenan, et. al in “Casein Kinase 1 δ/Ɛ Inhibitor, PF670462 Attenuates the Fibrogenic Effects of Transforming Growth Factor-in Pulmonary Fibrosis” (pub’d 07/10/2018; hereinafter “Keenan”) as evidenced by Agrawal A, Verma I, Shah V, Agarwal A, Sikachi RR. Cardiac manifestations of idiopathic pulmonary fibrosis. Intractable Rare Dis Res. 2016 May;5(2):70-5; hereinafter “Agarwal”).
With respect to Claims 11-13, 16, 18-19, 23-33:
Keenan discloses (pg. 1, abstract) “PF670462 administered in a ‘therapeutic’ regimen…. Elevated expression and activity of CK1 δ and Ɛ in IPF and anti-fibrogenic effects of the dual CK1δ/Ɛ inhibitor, PF670462, support CK1 δ/Ɛ as novel therapeutic targets for idiopathic pulmonary fibrosis (IPF).” Reading on Claims 11-13, 23-24, and 28-29 for what the art teaches, Keenan discloses the cardiovascular diseases, IPF, which is consisting of heart failure, subarachnoid hemorrhage, and hypertension as manifestations of this disease.
Keenan further discloses“…CK1δ physically interacts with Smad3 to mediate some TGF-β signals, including upregulation of the fibrogen, plasminogen-activator inhibitor-1 CK1Ɛ shares much functional redundancy with CK1δ due to 98% homology in the kinase domains,..(pg. 2, col. 2, split para. 1; which reads on Claims 24, 29, & 33, the inhibitor of the instant claims is the same as the prior art. Thus, the claim reads on the art).
IPF leads to a cascade of cardiovascular complications (col. 1 to col. 2, para. 1). Heart failure, hypertension, and subarachnoid hemorrhage can lead to pulmonary fibrosis, through different mechanisms. Heart failure can cause pulmonary fibrosis through pulmonary hypertension (high blood pressure in the lungs) and edema, while hypertension can be a risk factor for heart failure and contribute to vascular damage. Subarachnoid hemorrhage can cause pulmonary fibrosis by triggering pulmonary edema via catecholamine discharge, a common mechanism in both heart failure and hypertension.
Keenan further discloses PF670462 (reading on Claim 16, 25, 30) is a selective inhibitor of casein kinase 1 delta and epsilon (CK1δ/ε). These kinases have been associated in the regulation of circadian rhythms and fibrogenic signaling pathways, notably those activated by transforming growth factor-beta (TGF-β).
As such, Keenan also reads on Claims 11-13, 16, 18-19, 23-33:
On pg. 4, col. 1, para. 2, Keenan discloses “Acute and chronic bleomycin mouse models were used to assess the effect of PF670462 on pulmonary fibrosis in vivo. PF670462 was administered systemically by intraperitoneal injection or locally to the lungs by inhalation of an aerosol generated using an oxygen concentrator connected to a Hudson nebulizer operating at 5L/min for 15 min” which indicates the patient was administered treatment at least once. It also reads on PF670462 (reading on Claim 16, 25, 30) is a selective inhibitor of casein kinase 1 delta and epsilon (CK1δ/ε)
More specifically, Keenan discloses “In the 3-day model, PF670462 administration commenced on day-1 (day prior to bleomycin) and continued to day 3. In the 14-day model PF670462 was administered from day 3 to day 14. In the 21-day model considered to reflect the peak of fibrosis, PF670462 administration commenced on day 8 and continued to day 21.” This indicates reading on multiple administrations to the patient, as well as before the patients bedtime (Claims 18-19, 26-27, 31-32).
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, parenchymal disease of the lung (as evidenced by Agrawal; the cardiac manifestations of IPF read on hypertension specifically pulmonary hypertension, subarachnoid hemorrhage and heart failure). Patients usually present with coughing and exertional dyspnea (shortness of breath), which can lead to acute respiratory failure. IPF has been associated with various co-morbidities such as lung cancer, emphysema, obstructive sleep apnea (OSA), GERD and multiple cardiovascular ramifications.
The art teaches the structure and one would expect that the structure is capable of performing this function. See MPEP 2114:
I. INHERENCY AND FUNCTIONAL LIMITATIONS IN APPARATUS CLAIMS
Features of an apparatus may be recited either structurally or functionally. In re Schreiber, 128 F.3d 1473, 1478, 44 USPQ2d 1429, 1432 (Fed. Cir. 1997). See also MPEP § 2173.05(g). If an examiner concludes that a functional limitation is an inherent characteristic of the prior art, then to establish a prima case of anticipation or obviousness, the examiner should explain that the prior art structure inherently possesses the functionally defined limitations of the claimed apparatus. In re Schreiber, 128 F.3d at 1478, 44 USPQ2d at 1432. See also Bettcher Industries, Inc. v. Bunzl USA, Inc., 661 F.3d 629, 639-40,100 USPQ2d 1433, 1440 (Fed. Cir. 2011). The burden then shifts to applicant to establish that the prior art does not possess the characteristic relied on. In re Schreiber, 128 F.3d at 1478, 44 USPQ2d at 1432; In re Swinehart, 439 F.2d 210, 213, 169 USPQ 226, 228 (CCPA 1971) (“where the Patent Office has reason to believe that a functional limitation asserted to be critical for establishing novelty in the claimed subject matter may, in fact, be an inherent characteristic of the prior art, it possesses the authority to require the applicant to prove that the subject matter shown to be in the prior art does not possess the characteristic relied on”).
B. Second Rejection -
Claim(s) 11-13, and 18-19 are rejected under 35 U.S.C. 102(a)(1) & 102(a)(2) as being anticipated by Peng Leong, et al (Made of Record – WO 2004/035076 A1; hereinafter “Leong”).
With respect to Claims 11-13, and 18-19, Leong discloses a composition of casein kinase 1 (CK1) inhibitor - methods comprise administering indicating inhibitor is administered at least once - to a patient (subject is human; pg. 5, lns. 1-3; pg. 7, lns. 12-13; pg. 12, lns. 24-26) a composition comprising a CKIε inhibitor in an amount sufficient to modulate a TNF-α-mediated pathway (abstract, pg. 1, lns. 8-11) for use in the treatment of vascular (pg. 2, lns. 1-6) and/or cardiovascular diseases (pg. 47, claim 20); diseases from the group of heart failure (pg. 5, lns. 11-15), advanced heart disease (pg. 32, lns. 29-31; pg. 34, lns. 3-8), abnormal heart rhythms (pg. 6, lns. 25-29); CK1 inhibitor is selective for CK1δ and/or CK1ε (pg. 7, lns. 23-30).
Claim(s) 11-13, and 18-19:
With respect to Claims 19, based on claim interpretation, the compound of casein kinase 1 (CK1) is met with the WIPO prior art of Leong above.
As stated in pg. 1, lns. 17-20, “CKI-δ and ε isoforms share 98% identity in the kinase domain and are 53% identical in a C-terminal domain that is not present in other CKI isoforms.
Any dose of a CK1 inhibitor to a subject in need to modulate the treatment of TNF-alpha disorders (as seen in Leong, which is acknowledged by Applicant. According to the Instant case Specification (pg. 3, para. [0010]), Applicant acknowledges “since CK1 family isoforms display similar substrate specificity in vitro, their distinct biological functions in vivo - e.g., chromosome segregation, spindle formation, circadian rhythms, nuclear import, Wnt pathway signaling and cell survival/apoptosis - arise almost entirely from differences in localization, docking sequences and interaction partners”) with casein kinase 1 epsilon (CK1ε) inhibitors (entire patent; title) meets the functional limitation of the claims.
Additionally, according to MPEP δ 2112.01.I:
“Where the claimed and prior art products are identical or substantially identical in structure or composition, or are produced by identical or substantially identical processes, a prima facie case of either anticipation or obviousness has been established.
In re Best, 562 F.2d 1252, 1255, 195 USPQ 430, 433 (CCPA 1977). "When the PTO shows a sound basis for believing that the products of the applicant and the prior art are the same, the applicant has the burden of showing that they are not." In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990).”
In addition, with respect to claims 19, these claims contain functional language. The art teaches the structure and one would expect that the structure is capable of performing this function.
See MPEP 2114:
I. INHERENCY AND FUNCTIONAL LIMITATIONS IN APPARATUS CLAIMS
Features of an apparatus may be recited either structurally or functionally. In re Schreiber, 128 F.3d 1473, 1478, 44 USPQ2d 1429, 1432 (Fed. Cir. 1997). See also MPEP § 2173.05(g). If an examiner concludes that a functional limitation is an inherent characteristic of the prior art, then to establish a prima case of anticipation or obviousness, the examiner should explain that the prior art structure inherently possesses the functionally defined limitations of the claimed apparatus. In re Schreiber, 128 F.3d at 1478, 44 USPQ2d at 1432. See also Bettcher Industries, Inc. v. Bunzl USA, Inc., 661 F.3d 629, 639-40,100 USPQ2d 1433, 1440 (Fed. Cir. 2011). The burden then shifts to applicant to establish that the prior art does not possess the characteristic relied on. In re Schreiber, 128 F.3d at 1478, 44 USPQ2d at 1432; In re Swinehart, 439 F.2d 210, 213, 169 USPQ 226, 228 (CCPA 1971) (“where the Patent Office has reason to believe that a functional limitation asserted to be critical for establishing novelty in the claimed subject matter may, in fact, be an inherent characteristic of the prior art, it possesses the authority to require the applicant to prove that the subject matter shown to be in the prior art does not possess the characteristic relied on”).
C. Third Rejection -
Claim(s) 11-13, and 18-19 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by QJ Meng, et. al “Entrainment of disrupted circadian behavior through inhibition of casein kinase 1 (CK1) enzymes. (Made of Record; hereinafter “Meng”) and as referenced by I. Lagunes (Made of Record; hereinafter “Lagunes”).
With respect to claims 11-13, and 18-19, Meng teaches casein kinase 1 (CK1) inhibitors (entire article) and their intended use in areas connecting cardiovascular systems.
Meng provides insight into circadian clocks and just how the disruption of circadian rhythms can lead to cardiovascular diseases, which includes heart failure. “CK1δ-selective inhibition can be used to synchronize and restore circadian rhythms in arrhythmic animals, highlighting this enzyme as an important therapeutic target” (pg. 15240, col. 2, para. full paragraph 2).
According to the Instant case Specification (pg. 3, para. [0010]), Applicant acknowledges “since CK1 family isoforms display similar substrate specificity in vitro, their distinct biological functions in vivo - e.g., chromosome segregation, spindle formation, circadian rhythms, nuclear import, Wnt pathway signaling and cell survival/apoptosis - arise almost entirely from differences in localization, docking sequences and interaction partners.”
This indicates the CK1 inhibitor of the Instant case is the same inhibitor in Meng. It also indicates the inhibitor can be administered to a patient (treatment with PF-670462 caused significant dose-dependent lengthening of the circadian period: high-dose PF-670462 extended the period in WT fibroblasts to 33 h; pg. 15241, col. 1, para. 1) indicating the inhibitor was administered at least once (eight- to 12-wk-old mice were placed under an LD lighting cycle for 7–10 d, before release into DD or LL at the initiation of drug administration. Following 21–28 d of daily administration of vehicle, PF-670462, or 10 d of PF-4800567, wheel-running activity was recorded in DD or LL for a further 14–28 d; pg. 15245, col. 1, full para. 2). The patient also claimed in the prior art is the same recognized by the Applicant in the Instant case Specification (pg. 8, para. [0027]) which can be a mammal (i.e. human patients; pg. 15245, col. 1, full para. 2; col. 1, para. 2; pg. 15244, col. 1, end of hanging para. 1).
Additionally, Meng’s teaching of the CK1 inhibitor is PF-670462 (abstract; pg. 15240, col. 1; para. 1) continues with its use of CK1’s “selectively targeted WT CK1ε and CK1δ using pharmacological inhibitors (PF-670462) alongside genetic knockout and knockdown reveal that CK1 activity is essential to molecular pacemaking” (pg. 15240, col. 1, para. 1) and as referenced by Lagunes (pg. 81, col. 1, para. 1).
With respect to claim 19, based on claim interpretation, the compound of casein kinase 1 (CK1) is met with the prior art above. Meng teaches overlapping structure and dosing to animals (active step of administering).
In addition, with respect to claim 19, these claims contain functional language. The art teaches the structure and one would expect that the structure is capable of performing this function. See MPEP 2114:
I. INHERENCY AND FUNCTIONAL LIMITATIONS IN APPARATUS CLAIMS
Features of an apparatus may be recited either structurally or functionally. In re Schreiber, 128 F.3d 1473, 1478, 44 USPQ2d 1429, 1432 (Fed. Cir. 1997). See also MPEP § 2173.05(g). If an examiner concludes that a functional limitation is an inherent characteristic of the prior art, then to establish a prima case of anticipation or obviousness, the examiner should explain that the prior art structure inherently possesses the functionally defined limitations of the claimed apparatus. In re Schreiber, 128 F.3d at 1478, 44 USPQ2d at 1432. See also Bettcher Industries, Inc. v. Bunzl USA, Inc., 661 F.3d 629, 639-40,100 USPQ2d 1433, 1440 (Fed. Cir. 2011). The burden then shifts to applicant to establish that the prior art does not possess the characteristic relied on. In re Schreiber, 128 F.3d at 1478, 44 USPQ2d at 1432; In re Swinehart, 439 F.2d 210, 213, 169 USPQ 226, 228 (CCPA 1971) (“where the Patent Office has reason to believe that a functional limitation asserted to be critical for establishing novelty in the claimed subject matter may, in fact, be an inherent characteristic of the prior art, it possesses the authority to require the applicant to prove that the subject matter shown to be in the prior art does not possess the characteristic relied on”).
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Joint Inventors
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 16 are rejected under 35 U.S.C. 103 as being unpatentable over “Leong” in view of QJ Meng, et. al “ Entrainment of disrupted circadian behavior through inhibition of casein kinase 1 (CK1) enzymes. (Made of Record; hereinafter “Meng”) as referenced by I. Lagunes (Made of Record; hereinafter “Lagunes”).
With respect to Claims 16, Leong teaches a casein kinase 1 (CK1) inhibitor and methods comprising administering to a patient a composition comprising a CKI inhibitor in an amount sufficient to modulate an immunological-mediated pathway for treatment of vascular and cardiovascular diseases.
Leong fails to teach the specific CK1 inhibitor PF-670462.
Meng teaches the CK1 inhibitor is PF-670462 (abstract; pg. 15240, col. 1; para. 1) and continues its use of CK1’s “selectively targeted WT CK1ε and CK1δ using pharmacological inhibitors (PF-670462) alongside genetic knockout and knockdown to reveal that CK1 activity is essential to molecular pacemaking” (pg. 15240, col. 1, para. 1) and as referenced by Lagunes (pg. 81, col. 1, para. 1).
Moreover, Meng teaches “treatment with PF-670462 caused significant dose-dependent lengthening of the circadian period: high-dose PF-670462 (1µM) extended the period in WT fibroblasts to 33 h.” (pg. 15240, col. 2, end para. 4 to pg. 15241, col. 1, hanging para. 1).
It would therefore be obvious to combine Leong and Meng to provide a casein kinase 1 (CK1) inhibitor and methods comprising administering to a patient a composition comprising a CKI inhibitor, in an amount sufficient to modulate an immunological-mediated pathway for treatment of vascular and cardiovascular diseases.
Based on the tenets of KSR, Prong A: “combining prior art elements according to known methods to yield predictable results” both Leong and Meng establish the prior art elements of the CK1 inhibitors and their use in treating cardiovascular diseases, according to known methods. In addition, KSR, Prong B applies – “substituting one known CK1 inhibitor for another”. Since it is known in the art the CK1 inhibitor inhibit the same isoforms I (CK1δ and CK1ε) this increases the expectation of substitution success as it has been known before.
Conclusions
Claims 11-13, 16, 18-19, and 23-33 are rejected.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Josmalen M. Ramos-Lewis whose telephone number is (571)272-0084. The examiner can normally be reached M-F 9:30-5:30 pm.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Clinton A. Brooks can be reached at (571) 270-7682. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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Josmalen M. Ramos-Lewis, Ph.D.
Patent Examiner
Art Unit 1621
/CLINTON A BROOKS/Supervisory Patent Examiner, Art Unit 1621