Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claim Status
Claims 1-12 filed on 11/15/2023 are pending and will be examined on the merits.
Information Disclosure Statement
There is no information disclosure statements (IDS) filed on the record.
Specification
The disclosure is objected to because of the following informalities:
Under “BRIEF DESCRIPTION OF THE DRAWINGS”, paragraph [0028], “FIG. 13 is a diagram confirming the expression of immune-related factors in immune tolerogenic dendritic cells according to the present disclosure by real time PCR. In FIG. 11, ** means p<0.01 and**** means p<0.0001.” should read “FIG. 13 is a diagram confirming the expression of immune-related factors in immune tolerogenic dendritic cells according to the present disclosure by real time PCR. ** means p<0.01 and**** means p<0.0001.”
Appropriate correction is required.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(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 9 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.
Claim 9 recites the immune tolerogenic dendritic cell of claim 6, wherein the immune tolerogenic dendritic cell suppresses the expression of at least one factor selected from the group consisting of TGF-beta and CCR2.
The specification of the instant case recites in paragraph [0064] (page 4), “according to an exemplary embodiment of the present disclosure, the immune tolerogenic dendritic cells may suppress the expression of at least one factor selected from the group consisting of TGF-beta and CCR2.” In Figure 13, which is “a diagram confirming the expression of immune-related factors in immune tolerogenic dendritic cells according to the present disclosure by real time PCR.” The difference between the control tDC and Antigen-tDC is shown as “ns”, which is interpreted as non-significant statistically by the examiner. The specification provides no further description to support a citrullinated vimentin antigen primed tDC to reduce the expression of TGF b. Therefore, a person with ordinary skills in the art would not recognize that the applicant has the possession of the claimed invention at the time of filing.
Claim 9 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 enablement requirement. The claim contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
The factors to be considered in determining whether undue experimentation is required
are summarized In re Wands 858 F.2d 731, 8 USPQ2nd 1400 (Fed. Cir.1988). The court in Wands states: "Enablement is not precluded by the necessity for some experimentation such as routine screening. However, experimentation needed to practice the invention must not be undue experimentation. The key word is 'undue,' not 'experimentation.'" (Wands, 8 USPQ2d 1404). Clearly, enablement of a claimed invention cannot be predicated on the basis of quantity of experimentation required to make or use the invention. "Whether undue experimentation is needed is not a single, simple factual determination, but rather is a conclusion reached by
weighing many factual considerations." (Wands, 8 USPQ2d 1404). The factors to be
considered in determining whether undue experimentation is required include: (1) the breadth of
the claims, (2) the nature of the invention, (3) the state of the prior art, (4) the relative skill of
those in the art, (5) the predictability or unpredictability of the art, (6) the amount or direction or
guidance presented, (7) the presence or absence of working examples, and (8) the quantity of
experimentation necessary. Although the quantity of experimentation alone is not dispositive in
a determination of whether the required experimentation is undue, this factor does play a central
role. For example, a very limited quantity of experimentation may be undue in a fledgling art
that is unpredictable where no guidance or working examples are provided in the specification
and prior art, whereas the same amount of experimentation may not be undue when viewed in
light of some guidance or a working example or the experimentation required is in a predictable
established art. Conversely, a large quantity of experimentation would require a
correspondingly greater quantum of guidance, predictability and skill in the art to overcome
classification as undue experimentation. In Wands, the determination that undue
experimentation was not required to make the claimed invention was based primarily on the
nature of the art, and the probability that the required experimentation would result in
successfully obtaining the claimed invention. (Wands, 8 USPQ2d 1406). Thus, a combination of
factors which, when viewed together, would provide an artisan of ordinary skill in the art with an
expectation of successfully obtaining the claimed invention with additional experimentation
would preclude the classification of that experimentation as undue. A combination of Wands
factors, which provide a very low likelihood of successfully obtaining the claimed invention with
additional experimentation, however, would render the additional experimentation undue.
Claim 9 recites the immune tolerogenic DCs generated by the method described in claim 1 suppresses the expression of at least one of TGF b or CCR2. Example 4 in the specification (page 20, paragraph [00104] and Fig. 13 supports that Antigen-tDCs expressed lower level of CCR2 compared to control-tDC. However, the difference of TGFb between Antigen-tDC and control-DC is not statistically significant.
It is well known in the art that TGF-ß cytokine is a central modulator of immune cell functions and plays a dominant role as an immunosuppressive agent. Esebanmen et al recites in "The role of TGF-beta signaling in dendritic cell tolerance." Immunologic research 65.5 (2017): 987-994, that “The importance of dendritic cells in the maintenance of central and peripheral tolerance is now well established and investigations in several animal models suggest TGF-ß signaling is essential for DC regulatory function” (Conclusion, page 992). According to Esebanmen et al, the role of TGF-ß signaling in maintaining DC tolerance has been demonstrated in several mouse models of autoimmunity. For example, Studies demonstrate that TGF-ß signaling is required for preventing the development or progression of EAE; TGF-ß signaling in DC is required for suppression of Th17 differentiation at the site of neuroinflammation. It is also known that TGF-ß mediates induction and expansion of autoantigen-specific Tregs from CD4+T cells, which in turn suppress DC costimulatory molecule expression, decreasing the ability of DCs to stimulate autoreactive T cell differentiation (page 991, column 2, paragraphs 2-3).
Choo et al, "Infarcted myocardium-primed dendritic cells improve remodeling and cardiac function after myocardial infarction by modulating the regulatory T cell and macrophage polarization." Circulation 135.15 (2017): 1444-1457 (2017) teach a method of generation of tolerogenic DCs (tDCs) to treat myocardial infarction, using similar method as the instant application with the priming agent to be infarct lysate prepared from myocardial infarction heart tissue, rather than pure antigen. Choo et al demonstrated that TGF-β-1 level is significantly increased in the infarcted myocardium from tDC treated mice compare to control (Figure 3C, page 1451-1452, page 1446, column 2, paragraph 1), which is consistent with the tolerance promoting role of TGFb.
Since the invention is designed to generate antigen specific tolerogenic DCs to treat a subject suffering heart disease post-myocardial infarction due to inflammation and excessive remodeling of heart tissue, based on the broadest reasonable interpretation of the invention and the state of the art as discussed above, one with ordinary skill in the art would predict that the tDC generated by the instant invention to increase, rather than decrease, the expression of TGF b, which is a tolerance promoting cytokine and could effectively induce antigen specific Treg cells and contribute to an inflammatory-to-reparative immune modulation. What the instant application claims in claim 9 is opposite to what’s known in the art regarding the level of TGF b in the relevant context. It would have been highly uncertain if a person with ordinary skill in the art can generate tolerogenic DCs with a method in the instant invention with reduced level of TGFb expression yet having immune-suppressive function of a tDC. Therefore, this high level of unpredictability and contradiction necessitates "undue experimentation" to get the claimed result, rendering the invention not enabled.
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.
Claims 1, 3, 4, 5, 6 and 9 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Benham et al. "Citrullinated peptide dendritic cell immunotherapy in HLA risk genotype–positive rheumatoid arthritis patients." Science translational medicine 7.290 (2015): 290ra87-290ra87.
Claim 1 recites a preparation method of immune tolerogenic dendritic cells comprising culturing immature dendritic cells in a citrullinated vimentin-containing medium.
Claim 3 recites the preparation method of the immune tolerogenic dendritic cells of claim 1, wherein the medium further comprises at least one selected from the group consisting of granulocyte macrophage colony stimulating factor (GM-CSF), interleukin-4 (IL-4) and tumor necrosis factor-α (TNF-α).
Claim 4 recites the culture in claim 1 is performed for 2-24 hours.
Claim 5 recites a method for inducing differentiation of immature dendritic cells into immune tolerogenic dendritic cells, comprising treating immature dendritic cells with citrullinated vimentin.
Claim 6 recites an immune tolerogenic dendritic cell comprising citrullinated vimentin as an antigen, prepared through the preparation method according to claim 1.
Benham et al (2015) teach a clinical study using DCs modified with Bay11-7082, an NF-kB inhibitor, and exposed to 4 citrullinated peptides, designated “Rheumavax”, in ACPA+ RA (anti–citrullinated peptide autoantibodies positive rheumatoid arthritis) patients (page 1, Abstract). The concept and schema of immunomodulatory therapy with DCs and citrullinated peptides in HLA risk genotype–positive patients with RA are illustrated in Fig. 1 (A and B) (page 3).
Autologous DCs generated ex vivo from peripheral blood monocytes in the presence of the NF-kB inhibitor Bay11-7082, IL-4 and GM-CSF, are exposed to synthetic citrullinated peptides, including collagen type II1237–1249 Cit1240, fibrinogen a chain717–725– Cit720, fibrinogen b chain433–441–Cit436, and vimentin447–455 Cit450 (page 8, column 2, last paragraph, table S4), for 3 hours, the modified autologous DCs loaded with these citrullinated peptides are then injected intradermally (I.D.) into patients, which are well tolerated and caused reduction in effector T cells and an increased ratio of regulatory to effector T cells. Rheumavax also caused a reduction in serum interleukin-15 (IL-15), IL-29, CX3CL1, and CXCL11; and reduced T cell IL-6 responses to vimentin447–455–Cit450 relative to controls. DAS28, a baseline disease activity score, decreased within 1month in Rheumavax-treated patients with active disease (Abstract, page 1), which demonstrates its immunotolerogenic activity in in vivo. Taken together, Rheumavax meets the limitations in claims 1, 3, 4, 5, and 6.
Regarding claim 9 which recites the immune tolerogenic dendritic cell of claim 6, wherein the immune tolerogenic dendritic cell suppresses the expression of at least one factor selected from the group consisting of TGF-beta and CCR2, since Rheumavax anticipates the immune tolerogenic dendritic cell described in claim 6, the characteristics, including expression of immune factors of these cells, are anticipated as well.
According to MPEP 2112.01, “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). Therefore, the prima facie case can be rebutted by evidence showing that the prior art products do not necessarily possess the characteristics of the claimed product. In re Best, 562 F.2d at 1255, 195 USPQ at 433. See also Titanium Metals Corp. v. Banner, 778 F.2d 775, 227 USPQ 773 (Fed. Cir. 1985) (Claims were directed to a titanium alloy containing 0.2-0.4% Mo and 0.6-0.9% Ni having corrosion resistance. A Russian article disclosed a titanium alloy containing 0.25% Mo and 0.75% Ni but was silent as to corrosion resistance. The Federal Circuit held that the claim was anticipated because the percentages of Mo and Ni were squarely within the claimed ranges. The court went on to say that it was immaterial what properties the alloys had or who discovered the properties because the composition is the same and thus must necessarily exhibit the properties.).”
Since the instant disclosure does not provide evidence to show that Rheumavax, which anticipates the tolerogenic DC in claim 6, as discussed above, does not have the same property in terms of its effect on CCR2 expression level, the property recited in claim 9 is considered an inherent property of Rheumavax, therefore it does not render the tDC in claim 6 patentably new to the discoverer.
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 text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
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.
Claims 1-8, 10-12 are rejected under 35 U.S.C. 103 as being unpatentable over Choo et al. "Infarcted myocardium-primed dendritic cells improve remodeling and cardiac function after myocardial infarction by modulating the regulatory T cell and macrophage polarization." Circulation 135.15 (2017): 1444-1457, in view of Mao et al. "Role of protein deimination in cardiovascular diseases: potential new avenues for diagnostic and prognostic biomarkers." Expert review of proteomics 18.12 (2021): 1059-1071.
Claim 2 recites the preparation method of immune tolerogenic dendritic cells of claim 1, wherein the medium further comprises Troponin I. Claim 6 recites an immune tolerogenic dendritic cell comprising citrullinated vimentin as an antigen, prepared through the preparation method according to claim 1. Claim 7 recites the immune tolerogenic dendritic cell of claim 6, wherein the immune tolerogenic dendritic cell further comprises Troponin I as an antigen. Claim 8 recites the immune tolerogenic dendritic cell of claim 6 increases the expression of at least one factor selected from the group consisting of Ido, IL-10, IL-12b and IL-6.
Choo et al (2017) teach a method of generation of tolerogenic DC (tDCs) by treating bone marrow–derived dendritic cells with tumor necrosis factor-α and cardiac lysate from MI (myocardial infarction) mice. These tDCs showed beneficial effect on postinfarct left ventricular
remodeling in MI mice via alteration of the immune environment in the infarcted heart, which resulted in a better wound remodeling, preserved left ventricular systolic function after myocardial tissue damage, and improved survival (page 1444, Abstract, Methods and Results).
Choo et al (2017) recites that tDCs were generated from bone marrow progenitors by culturing BM single cell suspension in the presence of 20 ng/mL recombinant murine
granulocyte-monocyte colony stimulating factor, and 2 ng/mL recombinant murine interleukin (IL)-4. After 8 days of culture, tDCs were generated by additional 4-hour incubation of tumor necrosis factor a and myocardium-derived antigens from tissue lysate of infarcted myocardium (infarct lysate; 50 µg/mL), recombinant mouse troponin I (10ng/ml) and myosin (50ug/ml), infarct lysate was custom-made from infarcted myocardium dissected from the heart within 24 hours after MI (page 144, column 2, paragraph 4).
Choo et al (2017) does not explicitly teach priming of the BM derived DCs with citrullinated vimentin.
However, Mao et al (2021) teach that arginine deimination (citrullination) is a post-translational modification catalyzed by a family of peptidyl arginine deiminase (PAD) enzymes. Overexpression or increased activity of PAD has been observed in various CVDs (cardiovascular diseases) with acute and chronic inflammation, which give rise to citrullinated proteins (page 1060, column 1, paragraph 2), including citrullinated vimentin (Table 1).
Therefore, one with ordinary skill in the art would predict that citrullinated vimentin is present in the infarct lysate prepared from infarcted myocardium tissue which has high PAD level and citrullination PTM of proteins. As such, the tDC generation method taught by Choo et al (2017) comprises incubating the BM derived DCs with a medium containing both Troponin and citrullinated vimentin for 4 hours, and the resultant tDC would have both citrullinated vimentin and Troponin I loaded. This preparation method of an immune tolerogenic DC meets the limitations in claims 1-7.
Regarding claim 8, Choo et al (2017) further teach the tolerogenic characteristics of tDCs generated by priming of the BM derived DCs with the infarct lysate, tDCs produced higher level of Il-6 than immature DCs (imDCs) (Supplemental Figure 1c) (page 1448, column 1, paragraph 1).
Regarding claims 10-12 which recites a method for preventing or treating heart diseases comprising administering to a subject immune tolerogenic dendritic cells prepared by the preparation method according to claim 1. Choo et al (2017) recites the tolerogenic DC therapy
is an anti-remodeling therapy in myocardial infarction. Using a mouse model of acute myocardial infarctions, induced by a ligation of the left anterior descending coronary artery in C57BL/6 mice, Choo et al (2017) demonstrated that the tolerogenic DC therapy discussed above successfully regulates postinfarct myocardial healing process via their control of regulatory T cells and M1/M2 macrophages. The ease of administration and feasibility of production of infarct-specific tolerogenic dendritic cells further support potential clinical translation of tolerogenic dendritic cell therapy as a new strategy for the prevention of heart failure after myocardial infarction in
humans.
Therefore, combining the teaching of Choo et al (2017) and Mao et al (2021), one with ordinary skill in the art would be motivated to generate immune tolerogenic DCs by culturing autologous immature DCs cells in the presence of GM-CSF, IL-4, and TNFa, and pulse the cells with autoantigens present in a myocardial infarction tissue such as tissue from an acute myocardial infarction, including citrullinated vimentin and troponin I, and administer these tDCs into patients who have experienced acute myocardial infarction, and expect induction of a systemic immune tolerance to these pathogenic autoantigens via upregulation of antigen specific Treg cells and an inflammatory-to-reparative macrophage shift. This method of preventing or treating a heart failure after an acute myocardial infarction meets the limitation of claims 10-12.
Double Patenting
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).
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).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual 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/apply/applying-online/eterminal-disclaimer.
Claims 1-8, 10-12 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-2 of Chang et al “Tolerogenic dendric cells for treating myocardial infarction and manufacturing method thereof”, U.S. Patent No. 9, 833,473, Dec. 5, 2017 (Herein US’473) in view of Choo et al (2017) and Mao et al (2021).
Claim 1 of US’473 recites a method of inhibiting remodeling of left ventricle after myocardial infarction comprising preparing a pharmaceutical composition comprising tolerogenic dendritic cells for treating a myocardial infarction, the method comprising culturing immature dendritic cells in a medium including TNF-a (tumor necrosis factor-a), and protein extracted from a region of a myocardial infarction of an object having a myocardial infarction or serum obtained from an object having a myocardial infarction; and administering the pharmaceutical composition comprising tolerogenic dendritic cells as an effective component to a subject in need thereof.
Claim 2 of US’473 recites the composition in the method of claim 1 has an effect on alleviating the inflammation and inhibiting the remodeling of left ventricle after a myocardial infarction.
The method of inhibiting remodeling of left ventricle after myocardial infarction by administering tolerogenic DCs generated by ex vivo culture in the presence of TNFa and protein extract from a region of a myocardial infarction is equivalent to the method of the instant application of treating a heart disease caused by excessive remodeling of left ventricle. The difference between the method in US’473 and the instant application is the form of antigen used to prime tolerogenic DCs: US’473 uses protein extract from a tissue of myocardial infarction that contains pathogenic autoantigens, similar to the infarct lysate described by Choo et al (2017), whereas the instant application uses known antigens including citrullinated vimentin and troponin I, which are taught by Mao et al (2021) and Choo et al (2017), respectively.
Therefore, it would have been obvious for a person with ordinary skill in the art to utilize known antigen citrullinated vimentin and troponin I taught by Choo and Mao to prime tolerogenic DCs and treat a subject with myocardial infarction and expect an antigen specific immune suppressive effect on alleviating the inflammation and inhibiting the remodeling of left ventricle after a myocardial infarction.
Conclusion
All claims are rejected.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Joanne Hama can be reached at (571) 272-2911. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/HONG REN/
Examiner, Art Unit 1647
/JOANNE HAMA/ Supervisory Patent Examiner, Art Unit 1647
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