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 .
Priority
This Application is a 371 of PCT/CN2021/082899, filed March 25, 2021, and claims foreign priority to CN202010350632.6, filed April 28, 2020 in the People’s Republic of China.
Claim Status
Claims 1 and 19-23 are currently pending and subject to examination.
Withdrawn Rejections – Overcome by Amendment
The rejection of claims 1 and 18 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or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention is withdrawn.
The rejection of claim(s) 1 and 18 is/are rejected under 35 U.S.C. 103 as being unpatentable over “Progesterone for the Treatment of COVID-19 in Hospitalized Men” (NCT04365127, ClinicalTrials.gov, p. 1-10, April 24, 2020) (herein “Cedars-Sinai”) citing to Sun et al. (Cytokine and Growth Factor Reviews, 53, pp. 38-42, published April 25, 2020) (of record) and Hall (Doctoral dissertation, Johns Hopkins University, Nov. 2016) (of record), and further in view of Prendergast (US20090053294A1) (of record) is withdrawn.
The above rejections were overcome by amendment.
Claim Rejections – 35 USC § 112(b) – New Grounds of Rejection Necessitated by Amendment
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 23 is 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.
Claim 22 is directed towards the treatment of a subject with cytokine storm syndrome induced by SARS-CoV-2 and claim 23 is directed towards the method of claim 22, wherein the subject is a mouse injected with OKT3. One of ordinary skill in the art cannot determine the metes and bounds of the claim because a mouse inject with OKT3 is not a subject infected with SARS-CoV-2. OKT3 is an antibody used in research to induce the production of cytokines and is not a virus (Specification, p. 4, paragraph 0026).
Claim Rejections – 35 USC § 112(a) – New Matter Rejection Necessitated by Amendment
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.”
Claim 19 is rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention. This is a new matter rejection.
Claim 19 is directed towards the method of claim 1, wherein the therapeutically effective amount is from about 3 mg/kg to about 7 mg/kg. The specification provides no reference to a therapeutically effective dosage range. The specification only provides support for the specific amount of 5 mg/kg (para. [0048], [0051] and [0052]). The disclosure of one specific example within the claimed range is not sufficient to support the entirety of the claimed range of 3 mg/kg to 7 mg/kg:
The failure to meet the written description requirement of 35 U.S.C. 112(a) or pre-AIA 35 U.S.C. 112, first paragraph, commonly arises when the claims are changed after filing to either broaden or narrow the breadth of the claim limitations, or to alter a numerical range limitation or to use claim language which is not synonymous with the terminology used in the original disclosure…
With respect to changing numerical range limitations, the analysis must take into account which ranges one skilled in the art would consider inherently supported by the discussion in the original disclosure. In the decision in In re Wertheim, 541 F.2d 257, 191 USPQ 90 (CCPA 1976), the ranges described in the original specification included a range of “25%- 60%” and specific examples of “36%” and “50%.” A corresponding new claim limitation to “at least 35%” did not meet the description requirement because the phrase “at least” had no upper limit and caused the claim to read literally on embodiments outside the “25% to 60%” range, however a limitation to “between 35% and 60%” did meet the description requirement.
See also Purdue Pharma L.P. v. Faulding Inc., 230 F.3d 1320, 1328, 56 USPQ2d 1481, 1487 (Fed. Cir. 2000) (“[T]he specification does not clearly disclose to the skilled artisan that the inventors... considered the... ratio to be part of their invention.... There is therefore no force to Purdue’s argument that the written description requirement was satisfied because the disclosure revealed a broad invention from which the [later-filed] claims carved out a patentable portion”). See also General Hosp. Corp. v. Sienna Biopharmaceuticals, Inc., 888 F.3d 1368, 1372, 126 USPQ2d 1556, 1560 (Fed. Cir. 2018) (written description support for the claimed concentration is lacking where the specification discloses a range of optical densities and several discrete values in the range with no explicitly defined maximum concentration; and even if the specification may be read to convert each disclosed value into a range, there is insufficient written description for the entire claimed range where the disclosed range minimally overlaps with the claimed range). Compare Union Oil of Cal. v. Atl. Richfield Co., 208 F.3d 989, 997, 54 USPQ2d 1227, 1232-33 (Fed. Cir. 2000) (Description in terms of ranges of chemical properties which work in combination with ranges of other chemical properties to produce an automotive gasoline that reduces emissions was found to provide an adequate written description even though the exact chemical components of each combination were not disclosed and the specification did not disclose any distinct embodiments corresponding to any claim at issue. “[T]he Patent Act and this court’s case law require only sufficient description to show one of skill in the . . . art that the inventor possessed the claimed invention at the time of filing.”).
MPEP § 2163.05.
Claim Rejections - 35 USC § 103- New Grounds of Rejection Necessitated by Amendment
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.
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.
Claim(s) 1 and 19-22 is/are rejected under 35 U.S.C. 103 as being unpatentable over “Progesterone for the Treatment of COVID-19 in Hospitalized Men” (NCT04365127, ClinicalTrials.gov, p. 1-10, April 24, 2020) (herein “Cedars-Sinai”) in view of Sun et al. (Cytokine and Growth Factor Reviews, 53, pp. 38-42, published April 25, 2020) (of record), Hall (Doctoral dissertation, Johns Hopkins University, Nov. 2016) (of record), and Prendergast (US20090053294A1) (of record).
Response to Arguments
The Applicant argues that the distinguishing feature of the present invention is the use of hydroxyprogesterone caproate (Remarks, p. 4). These arguments were fully considered but are not persuasive. Cedars-Sinai teaches progesterone for the treatment of COVID-19. One of ordinary skill in the art would have a reasonable expectation of success in using HPC as the progesterone for inhibiting the cytokine storm in COVID-19 because HPC is well-known in the art to be a form of progesterone and act similarly. It is not inventive to substitute HPC for progesterone because it is prima facie obvious to substitute equivalents known for the same purpose (MPEP § 2144.06). The Applicant has not demonstrated that HPC is a superior form of progesterone in the context of the claimed invention.
The Applicant argues that the distinguishing feature of the present invention is intravenous or intraperitoneal injection (Remarks, p. 4). These arguments were fully considered but are not persuasive. One of ordinary skill in the art would have a reasonable expectation of success to administer HPC by intravenous or intraperitoneal injection because these are known routes of administration. The Applicant has not demonstrated that these routes of injection produce superior results to other routes of administration.
The Applicant argues that “it cannot be assumed that progesterone, being a well-known immunomodulator in the field, can suppress the production of inflammatory cytokines in the cytokine storm syndrome induced by SARS-CoV-2.” (Remarks, p. 7). These arguments were fully considered but are not persuasive. Cedars-Sinai teaches progesterone for the treatment of COVID-19. One of ordinary skill in the art would have a reasonable expectation of success to inhibit cytokine storm syndrome in these COVID-19 patients because it is well known in the art that moderate to severe COVID-19 causes cytokine storm syndrome characterized by high levels of inflammatory cytokines and progesterone is well known in the art to be an immunomodulator and to inhibit the production of pro-inflammatory cytokines. Cedars-Sinai is performing the clinical trial because they hypothesize that the drug treatment will be effective against COVID-19 which is well known to cause cytokine storm syndrome as demonstrated by Sun. Furthermore, both Hall and Prendergast teach that progesterone has immunomodulatory properties and should inhibit cytokine storm syndrome caused by respiratory infections. Therefore, one of ordinary skill in the art would reasonably expect that HPC would inhibit cytokine storm syndrome caused by COVID-19.
The Applicant’s experimental results do not overcome the prima facie case of obviousness. The Applicant uses an OKT3 mouse model, which is merely a model of cytokine storm syndrome, but does not clinically mimic COVID-19 infection. OKT3 is a human antibody which produces severe adverse effects in humanized severe combined immunodeficient mice (Specification, p. 4, para. [0025-0026]). This model does not have any particular relevance to cytokine storm syndrome induced by COVID-19 infection. It merely demonstrates that progesterone can suppress an immune reaction, which is well documented in the art as shown by the cited references.
Rejection
Claim(s) 1 and 19-22 is/are rejected under 35 U.S.C. 103 as being unpatentable over “Progesterone for the Treatment of COVID-19 in Hospitalized Men” (NCT04365127, ClinicalTrials.gov, p. 1-10, April 24, 2020) (herein “Cedars-Sinai”) in view of Sun et al. (Cytokine and Growth Factor Reviews, 53, pp. 38-42, published April 25, 2020) (of record), Hall (Doctoral dissertation, Johns Hopkins University, Nov. 2016) (of record), and Prendergast (US20090053294A1) (of record).
Claim 1 is directed towards a method for inhibiting a cytokine storm syndrome, comprising administering progestogen to a subject in need who already has elevated levels of IL-1β, Il-2, Il-4, Il-5, IL-6, Il-10, IFN-λ, and TNF-α cytokines, wherein the progestogen is hydroxyprogesterone caproate; wherein the cytokine storm syndrome is induced by SARS-CoV-2, wherein the hydroxyprogesterone caproate is administered intravenous injection or intraperitoneal injection in a therapeutically effective amount.
Cedars-Sinai discloses a method of treating moderate to severe COVID-19 in men by administering a therapeutically effective amount of progesterone subcutaneously:
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Cedars-Sinai, p. 2-7.
While Cedars-Sinai does not teach that the subject already has elevated levels of the claimed cytokines, one of ordinary skill in the art would have a reasonable expectation of success to inhibit cytokine storm syndrome in these patients because it is well known in the art that moderate to severe COVID-19 causes cytokine storm syndrome characterized by high levels of inflammatory cytokines and progesterone is well known in the art to be an immunomodulator and to inhibit the production of pro-inflammatory cytokines.
For example, see the teachings of Sun:
Current clinical observations indicate that SARS-CoV2 infection can range from an inapparent non-symptomatic infection, to a respiratory illness presenting with spiking fever and dry cough, accompanied by a high rate of human-human transmission. One of the most serious complications of Corona virus disease (COVID-2) is the development of an atypical upper respiratory tract pneumonia that poses a major challenge to clinicians in terms of disease management. An abnormal and uncontrolled production of cytokines has been observed in critically ill patients with COVID-19 pneumonia [1] and the ensuing uncontrolled cytokine storm in COVID-19 patients is centrally involved in the exacerbation of symptoms and disease development, and represents a major factor contributing to COVID-19 mortality. In this sense, COVID-19 disease shares similarities with other viral diseases such as SARS, MERS and influenza, where the development of a cytokine storm is a warning sign of disease escalation.
Sun, p. 38 (emphasis added);
In addition to SARSCoV2, two other novel coronaviruses have emerged as global health threats since 2002, namely severe acute respiratory syndrome coronavirus (SARS-CoV in 2002) that was transmitted to 37 countries, and the Middle East respiratory syndrome coronavirus (MERS-CoV in 2012) that was transmitted to 27 countries. Severe pneumonia caused by pathogenic human coronaviruses (HCoV) are often associated with induced hypercytokinemia, also termed cytokine storm, in immunocompetent individuals; uncontrolled overproduction of inflammatory cytokines contributes to acute lung injury and acute respiratory distress syndrome (ARDS).
Sun, p. 39;
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Sun, p. 39, Fig. 1.
Hall teaches that progesterone has immunomodulatory properties and should inhibit cytokine storm syndrome caused by respiratory infections:
Influenza A viruses cause an acute respiratory infection typically characterized by virus replication in respiratory epithelial cells, initiation of a ‘cytokine storm’ with production of IL-1b[Symbol font/0x62], TNF-a[Symbol font/0x61], IFN-a[Symbol font/0x61], IL-6 and CCL2 in the host, and long-term damage to pulmonary tissues (264, 265). This pulmonary inflammation is characterized by edema, bronchitis, lung fibrosis, diffuse alveolar damage, infiltration of immune cells and death of epithelial cells which threatens proper gas exchange and pulmonary function (153, 265-268).The typical presentation of influenza in adults and children is an abrupt onset of fever and chills along with headaches, sore throat and myalgia (143). In the most severe cases of IAV, excessive pulmonary infiltrates and hypoxemia can lead to acute respiratory distress syndrome (ARDS) which accounts for 4% of all hospitalization for respiratory failure during influenza infections (269, 270). Long after the symptoms of disease have subsided, pulmonary tissue damage can persist and increase the risk of secondary bacterial infections (265, 271). The 2009 H1N1 pandemic, in particular, was associated with increased inflammation and pulmonary tissue damage requiring extensive tissue repair (272)…
Taken together, these data suggest that the clearance and resolution of IAV infection relies on a delicate balance of pro- and anti- inflammatory mediators with any dysregulation towards exacerbated inflammation leading towards severe influenza illness and sequelae to the lungs. I hypothesize that given its anti-inflammatory role and repair role, P4 may help tilt the balance towards a dampening of inflammation, thus protecting the respiratory epithelium while inducing repair, without compromising the immune response necessary to clear the virus.
Hall, p. 27-28 (emphasis added).
Hall teaches that progesterone is beneficial in the context of infections which cause excessive inflammation leading to tissue damage:
To date, only two studies have assessed the role of progesterone or progestins on infectious diseases in the respiratory tract. The first study looked at the effect of DMPA on the outcome of a Mycobacterium tuberculosis infection and found that DMPA can increase the viral load by inducing an anti-inflammatory environment with a decrease in the production of TNF-[Symbol font/0x61], IFN-[Symbol font/0x67], and G-CSF (130). The second study is from this thesis, in which administration of P4 to ovariectomized mice prevented severe outcome from influenza A virus infection by decreasing inflammation and promoting repair of the pulmonary tissues through the epithelial growth factor amphiregulin (AREG), which is the focus of the work described in chapter 1 (131). Antibody titers and memory CD8+ T cell responses are also decreased following treatment of ovary-intact mice with either P4 or LNG, which results in greater susceptibility to a challenge with a heterologous virus and will be the focus of chapter 2 (132).
These results show that progestin can reduce inflammation in the respiratory tract, which is detrimental in the context of tuberculosis, but beneficial during influenza A virus infection. This discrepancy may depend on whether control of severe disease requires a strong proinflammatory response to clear the pathogen (e.g., tuberculosis) or causes excessive inflammation leading to tissue damage (e.g., influenza).
Hall, p. 14-15 (emphasis added).
While Cedars-Sinai does not teach that the progesterone is hydroxyprogesterone caproate (HPC), one of ordinary skill in the art would have a reasonable expectation of success in using HPC as the progesterone for inhibiting the cytokine storm in COVID-19 because HPC is well-known in the art to be a form of progesterone and act similarly. For example, see Prendergrast who teaches that progestogens, including hydroxyprogesterone caproate, have antiviral activity and reduce inflammatory cytokines:
The present invention is directed to therapeutic applications for Anti Mineralocorticoid compounds for their previously unappreciated, prophylactic and therapeutic antiviral properties and their other therapeutic properties disclosed herein.
Prendergast, Specification, paragraph 0001;
In another embodiment the Antimineralocorticoid compound is, selected from the group of progestogens with antimineralocorticoid activity consisting of progesterone, gestodene, drospirenone, dimethisterone, ethinyloestradiol, ethisterone, 11β-hydroxyprogesterone, 17α-hydroxyprogesterone, 16α-methyl progesterone, hydroxyprogesterone caproate, medroxyprogesterone acetate, proligestone and pharmaceutically acceptable salts thereof or their metabolites, analogues and mimic molecules.
Prendergast, Specification, paragraph 0039 (emphasis added);
The Antimineralocorticoid compound eliminates the virus by blocking viral-cell attachment, cellular entry and replication.
The Antimineralocorticoid compound has Immuno upregulatory properties, for example natural killer cells, and/or dendritic cells are upregulated and inflammatory cytokines are reduced.
Prendergast, Specification, paragraphs 0051-0052 (emphasis added).
Furthermore, Prendergast teaches progestogens for the treatment of coronavirus infections: “Thus virus infections that may be treated include… coronaviruses” (Prendergast, Specification, paragraph 0057).
While Cedars-Sinai teaches subcutaneous injection and not intravenous or intraperitoneal injection, one of ordinary skill in the art would have a reasonable expectation of success to administer the progestogen via these routes because it is known that these are alternative routes of administration for progestogens. For example, Prendergast teaches that suitable routes include intraperitoneal (Prendergast, Specification, paragraph 0060).
Therefore, claim 1 was prima facie obvious at the time of filing.
Claim 19 is directed towards the method of claim 1, wherein the therapeutically effective amotun is about 3 mg/kg to about 7 mg/kg. Claim 20 is directed towards the method according to claim 1, wherein wherein the therapeutically effective amount is 5mg/kg.
As shown in the rejection of claim 1, Cedars-Sinai teaches that the progesterone is administered subcutaneously at a dose of 100 mg twice daily. For a typical 80 kg adult male, this is about 1.25 mg/kg per dose or 2.5 mg/kg/day.
While Cedars-Sinai does not teach HPC administered by intraperitoneal injection at a dose of about 3 mg/kg to 7 mg/kg, specifically 5mg/kg, one of ordinary skill in the art would have a reasonable expectation of success to administer HPC intraperitoneally at a dose of about 3 mg/kg to 7 mg/kg or 5 mg/kg because this form of administration and dose is generally known in the art for progestogens such as HPC.
For example, Prendergast teaches that the ideal dosage of the compound is 400 mg/day which is about 5 mg/kg/day for an 80 kg adult male (Prendergast, Specification, paragraph 0082). Prendergast teaches that suitable routes include intraperitoneal (Prendergast, Specification, paragraph 0060).
Therefore, claims 19-20 were prima facie obvious at the time of filing.
Claim 21 is directed towards the method of claim 1, wherein the HPC is administered in an effective dose to reduce the level of at least two cytokines selected from the group consisting of IL-1β, Il-2, Il-4, Il-5, IL-6, Il-10, IFN-λ, and TNF-α.
One of ordinary skill in the art would have a reasonable expectation of success to administer HPC in an effective dose to reduce the level of at least two of the above cytokines because it is known in the art to administer progestogens in an effective amount to reduce inflammatory cytokines and treat COVID-19.
As shown in the rejection of claim 1, Cedars-Sinai teaches that the progesterone is administered subcutaneously at a dose of 100 mg twice daily. For a typical 80 kg adult male, this is about 1.25 mg/kg per dose or 2.5 mg/kg/day, which is similar to the instantly disclosed 5 mg/kg/day.
Furthermore, Prendergrast teaches that progestogens, including hydroxyprogesterone caproate, have antiviral activity and reduce inflammatory cytokines (Prendergast, Specification, paragraphs 0051-0052). Prendergast teaches that the ideal dosage of the compound is 400 mg/day which is about 5 mg/kg/day for an 80 kg adult male (Prendergast, Specification, paragraph 0082). Prendergast teaches that suitable routes include intraperitoneal (Prendergast, Specification, paragraph 0060).
Therefore, claim 21 was prima facie obvious at the time of filing.
Claim 22 is directed towards a method for inhibiting a cytokine storm syndrome, comprising administering progestogen to a subject in need who already has elevated levels of IL-1β, Il-2, Il-4, Il-5, IL-6, Il-10, IFN-λ, and TNF-α cytokines, wherein the progestogen is hydroxyprogesterone caproate; and wherein the cytokine storm syndrome is induced by SARS-CoV-2, and wherein the hydroxyprogesterone caproate is administered by intraperitoneal injection at a dose of 5 mg/kg.
The rejection of claims 1 and 20 is incorporated herein by reference which address each limitation of claim 22. Therefore, claim 22 was prima facie obvious at the time of filing.
Given the above teachings, the invention as a whole was prima facie obvious at the time of filing.
Conclusion
No claim is found to be allowable.
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 extension fee 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 date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to HEATHER DAHLIN whose telephone number is (571)270-0436. The examiner can normally be reached 9-5.
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/HEATHER DAHLIN/Examiner, Art Unit 1629
/JEFFREY S LUNDGREN/Supervisory Patent Examiner, Art Unit 1629