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
The amendment filed July 31, 2025 in response to the Office Action of March 31, 2025 is acknowledged and has been entered.
The Declaration of Dr. Xiankai Sun filed July 31, 2025 is acknowledged and has been considered.
Claim 42 has been cancelled.
Claims 34-41, 43-51, 53, 55, and 56 are pending.
Claims 38-40, 49-51, 53, 55 and 56 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected inventions or species, there being no allowable generic or linking claim.
Claims 34-37, 41, and 43-48 are currently under consideration as drawn to the elected invention.
Information Disclosure Statement
Information Disclosure Statement (IDS) filed July 31, 2025 has been entered and considered.
MAINTAINED/MODIFIED REJECTION
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 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.
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 34-37, and 41-48 are rejected under 35 U.S.C. 103 as being unpatentable over Shimoda (Shimoda et al., Current Opinion in Physiology, Jan. 7, 2019, 7: 33-40, Publication Date: 2019-01-07, of record) in view of Dai (Dai et al., Am J Respir Crit Care Med Vol. 198, Iss 11, pp 1423-1434, Publication Date: 12/01/2018), Chen (Chen et al., Nature, vol. 539, 112-117, Publication Date: 2016-11-03, with Extended Data, of record), Ohira (Ohira et al., Journal of Nuclear Cardiology, 2015; 22:141-157, Publication Date: February 2015, of record), Donnelly (Donnelly, Seminars in Nuclear Medicine, 47:454-460, Publication Year: 2017, of record), and Leide-Svegborn (Leide-Svegborn, Radiation Protection Dosimetry, 2010, Vol. 139, No. 1-3, pp. 208-213, Publication Date: 02/18/2010).
Shimoda teaches that pulmonary hypertension (PH) is a deadly condition with limited treatment options. See Abstract. PH can be classified into 5 groups: pulmonary arterial hypertension (PAH), pulmonary hypertension due to left heart disease, pulmonary hypertension due to lung diseases and/or hypoxia, chronic thromboembolic pulmonary hypertension (CTEPH), and pulmonary hypertension with unclear multifactorial mechanisms. See Table 1.
Shimoda teaches that hypoxia-inducible factors (HIFs) contribute to the development of hypoxia induced PH. See Abstract.
Shimoda teaches that hypoxia-inducible factors (HIFs) are heterodimeric transcription factors, consisting of α and β subunits, which bind hypoxia response elements in target genes. The α subunit is highly inducible by hypoxia, and three different isoforms have been identified (HIF-1α, HIF-2α and HIF-3α); all of which interact with HIF-1β. See page 34, col. 2, para. 2.
Shimoda teaches that HIF-2 and HIF1 play important roles in oxygen sensing. See page 34, col. 2, para. 4.
Shimoda teaches that studies have generally found HIFs to be upregulated in PH. See page 35, col. 1, para. 2.
Shimoda teaches that HIF-2α shows increased expression in PAH (endothelial cells (ECs) either in vivo or in culture. See page 35, col. 1, para. 4.
Shimoda teaches that mice with partial deficiency for HIF-2α show reduced PH. See page 35, col. 2, para. 2.
Shimoda teaches that EC-specific deletion of HIF-2α, but not HIF-1α, attenuated CH-induced PH. HIF-1 and HIF-2, perhaps acting in different cell types, contribute to hypoxia-induced PH. See page 35, col. 2, para. 2, and Figure 1.
Shimoda teaches that a HIF-2 inhibitor, e.g. C76, is effective in treating PH. See page 37, col. 2, para. 2.
Shimoda teaches that overexpression of HIF-2 can lead to PH. See pages 36-37, § HIF gain-of-function and PH.
Shimoda teaches that there is considerable potential benefit for targeting HIF system in PH. And targeting HIF-2 using the small molecule inhibitor C76, was shown to be effective in reducing PH in several models. See page 37, § Targeting HIFs in PH.
Shimoda teaches that in a disease with limited treatments, careful future clinical trials will be needed to elucidate whether, and under what conditions and in which patients, HIF inhibitors might be an option for therapeutically treating, or even curing, PH. See page 37, § Conclusion.
Shimoda teaches as set forth above. However, Shimoda does not teach detecting or monitoring pulmonary hypertension in a subject not undergoing treatment with a drug that binds to an hypoxia inducible factor 2-alpha (HIF-2α) comprising a) intravenously administering to the subject a HIF-2α-specific radioactive tracer comprising a drug that binds to HIF-2α and a radioactive label, wherein the radioactive label is a positron emitting radioisotope; b) subjecting the subject to a positron emission topography (PET) scan; and c) determining an amount of the tracer, wherein an increased amount of the tracer as compared to a control indicates that the subject has pulmonary hypertension.
Dai teaches the predominant role of HIF-2a versus HIF-1a activation in the pathogenesis of PAH. HIF-2a but not HIIF-1a activation in mediating pulmonary vascular remodeling and PH. Mice lacking HIF-2a but not HIF-1a in lung endothelium were resistant to hypoxia induced PH (page 1424, col. 2, para. 1).
Donnelly teaches various ways to make small molecule PET tracers and many small molecule PET tracers (table on page 459).
Dai teaches that quantitative RT-PCR analysis HIF-2a (not HIF-1a) is upregulated in lung tissues from patients with IPAH, mainly in endothelial cells (ECs) of lung sections from patients (Fig. 1A and 1B). HIF-2a protein expression was highly induced in PAECs but not in PASMCs isolated from patients with IPAH (Fig. 1C). A marked increase in HIF-2a protein levels and its downstream target genes such as Cxcl2 and IL6 in the lungs of SuHx and MCT rats (Figs. 1D, 1E, E2A, and E2B). Thus, these data demonstrate HIF-2a activation in lung tissues of three distinct rodent PAH models, as seen in patients with IPAH (page 1425, col. 3, para. 1).
Dai teaches HIF-2a specific inhibitor C76 can inhibit obliterative vascular remodeling and right heart failure in Egln1Tie2Cre mice and reverses severe PAH and right heart failure in SuHx Rats. (pages 1426-1427). HIF-2a specific inhibitor C76 can inhibit PAH in monocrotaline-challenged rats (page 1428, cols. 1-2).
Dai teaches that targeting of HIF-2a reversed aberrant vascular remodeling and prevented right heart failure and death in the setting of severe PAH (page 1428, col. 2).
Dai teaches testing/using other selective HIF-2a inhibitors given the beneficial impact of inhibiting HIF-2a (page 1429, col. 1, para. 1; and page 1431, col. 1, para. 1).
In summary, Dai shows a marked activation of endothelial HIF-2a signaling in the lungs of three rodent models and also patients with IPAH, and provides clear evidence that targeting HIF-2a can reverse established PAH, inhibit vascular remodeling and right heart failure, and promote survival. Together, these results strongly support the concept that selective targeting of HIF-2a is a potential therapeutic strategy for effective treatment of PAH and, importantly, for promoting survival (page 1429, col. 3, para. 1).
Chen teaches that HIF-2α has a 280 Å cavity within the PAS-B domain. PT2399 and PT2385 are specific HIF-2α inhibitors (antagonist) that bind the cavity. See page 112, col. 1, para. 2.
Chen teaches method of PET/CT scan, comprising two rounds PECT/CT scan to assess tumor response to HIF-2α inhibitors therapy. See § Methods-PET/CT.
Chen teaches that PT2399 decrease tumor growth by 60% across all tumor grafts evaluated (P < 0.001) (page 112, col. 2, para. 3; Fig. 1). Tumor sensitivity to PT2399 is correlated to the expression of HIF-2α (Fig. 3a, b and Extended Data Fig. 4a).
Chen teaches that patients could acquire resistance to prolonged treatment (>120 days) with PT2399, which is associated with a mutation (G323E) preventing PT2399 access. See the bridging paragraph of pages 115-116; and Fig. 4a-4e.
Ohira teaches that early diagnosis, risk stratification, monitoring, and assessing treatment response are important clinical steps in the management of patients with pulmonary hypertension (PH). See page 154-§ FUTURE DIRECTIONS AND CONCLUSIONS.
Ohira teaches that early diagnosis, risk stratification, monitoring, and assessing treatment response are important clinical steps in the management of patients with pulmonary hypertension (PH). See page 154-§ FUTURE DIRECTIONS AND CONCLUSIONS.
Ohira teaches that new nuclear techniques using metabolic tracers or new ligands are expected to play an important role in clinical practice in the field of PH. See page 154-§ FUTURE DIRECTIONS AND CONCLUSIONS.
Ohira teaches emerging imaging techniques to study PH, including PET imaging and use of radioligands to image the site of action of drugs. See page 151-§ EMERGING IMAGING TECHNIQUES TO STUDY PH, and Table 3.
Ohira teaches that FDG-PET imaging may be useful not only to grade the severity of PH and RV dysfunction, but may also provide a prognostic marker in patients with PH. See page 149, col. 2, para. 1.
Ohira teaches that nuclear imaging with new radioligands has the potential to be a new approach to treatment in patients with PH. See page 151, col. 2, para. 4.
Ohira teaches that FDG-PET imaging may be useful not only to grade the severity of PH and RV dysfunction, but may also provide a prognostic marker in patients with PH.
Ohira teaches that FDG-PET can be used to monitor a treatment for PH. See Figure 5.
Ohira teaches SPECT scan can be used for diagnosis of PH. See Figure 3. And it is intuitive that PET-MPI can achieve similar results. See page 147, col. 2, para. 1.
Donnelly teaches that PET is a translational, noninvasive imaging technique that provides quantitative information about a potential drug candidate and its target at the molecular level. See Abstract.
Donnelly teaches that molecular imaging techniques such as PET can significantly impact productivity and lower development costs by ensuring a new drug has target engagement, proper receptor occupancy, and guides dose selection in a more rapid timeframe. See 454, col. 1, para. 1.
Donnelly teaches that generally, there are three main approaches for the use of PET tracers. The first is using a radiolabeled candidate to evaluate the distribution and pharmacokinetics of the drug candidate. For small molecules PET tracers, direct labeling with short-lived PET radionuclides such as replacing a native carbon (C-12) with carbon-11 (20-minute half-life) or a native fluorine (F19) with fluorine-18 (109.5 minute half-life) is important to keep the physiochemical properties of the molecule the same. Recent advancements in PET radiochemistry have helped make this process more feasible. The second approach is to use a radioligand with known affinity for the molecular target of interest to evaluate the PD properties of the drug candidate. Finally, a small molecule PET tracer is used as an imaging biomarker of a known biochemical, metabolic, or physiological process (such as FDG) to evaluate efficacy of a candidate drug. See page 455, § PET within Drug Discovery and Development.
Donnelly teaches that PET tracers can be used in both preclinical animal models to confirm a drug’s target engagement, receptor occupancy, dose selection, and dose ranges to provide information to plan focused human studies in early development. See page 456, col. 2, para. 3.
Donnelly teaches that small molecule PET tracers can be used in late-phase clinical development as surrogate markers of response and to show pharmacologic differentiation of an asset from a drug already on the market. Additional PET can show differentiation when a new competitor drug comes to the market. Patient selection, using PET to select the proper patient population that will benefit from the drug candidate, is a powerful technique used during full clinical development of a drug candidate. This is a personalized medicine approach and allows researchers to ask mechanism-based questions within patient populations. This approach can determine if a drug is relevant within a disease population which is key to the proposed mode of action of a drug. See page 458, § PET within Full Clinical Development.
Based on the teaching of Shimoda, it would have been prima facie obvious at the time the invention was filed given that the level of skill in the art was high for one of ordinary skill in the art to have used HIF-2α as a marker for detection of pulmonary hypertension, because HIF-2α expression in EC is generally increased in PH patients and is associated with PH and to identify the patients with increased HIF-2α expression, e.g. HIF-2α-mediated pulmonary hypertension, as suitable patients for a HIF-2α inhibitor therapy, because HIF-2α inhibitor show therapeutic activity to PH, as taught by Shimoda and Dai; and further expand the method with other specific HIF-2α inhibitor, as taught by Dai, and using inhibitors such as PT2399 or PT2385, because Chen showed that PT2399 or PT2385 are specific inhibitors to HIF-2α and bind specifically to the HIF-2α cavity. It would have been prima facie obvious to one of ordinarily skilled in the art at the time the invention was filed to combine the teachings of Shimoda, Dai, Chen, Ohira and Donnelly, to develop a radioactive PET tracer e.g. PT2399 or PT2385 labeled with 11C, to test HIF-2α expression, because Ohira teaches: 1) early diagnosis, risk stratification, monitoring, and assessing treatment response are important clinical steps in the management of PH; 2) PET imaging can be used to diagnosis and monitoring PH; 3) new radioligands has the potential to be a new approach to treatment in patients with PH, and Donnelly teaches 1) PET scan can provide quantitative information about drug target (e.g. HIF-2α) at molecular level; 2) PET scan is non-invasive; 3) PET scan with radioactive tracer is widely used in clinical settings; 4) the binding of PT2399 and PT2385 to HIF-2α is specific and well-understood; 5) direct labeling with short-lived PET radionuclides e.g. 11C (20 min half-life), is important to keep the physiochemical properties of the molecule the same; 6) PET scan can be used to screen patients suitable for a therapy. Based on the teachings from these references, one of ordinary in the art would have been motivates and known to check HIF-2α level prior to a HIF-2α targeted therapy (not undergoing treatment with a drug that binds to an HIF-2α inhibitor). One of ordinary skill in the art would have been motivated to expand the application of PT2399 or PT2385, and identify the best patient population for a HIF-2α inhibitor therapy. Because roles of HIF-2α in PH, PT2385/PT2399, radioactive labeling method, and PET scan are well known in the art, one of ordinary skill in the art would have had a reasonable expectation of success to reach the claimed method.
Regarding to intravenously administration of radioactive tracer, Leide-Svegborn teaches intravenous administration of radioactive tracers for PET scan (see Abstract). It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to use intravenous administration taught by Leide-Svegborn to reach the claimed invention. In addition, it is a routine practice for an ordinary skilled in the art to adjust administration methods based on the specific purpose to achieve optimal outcome. Given that intravenous administration of radioactive tracer is commonly used in the art, as evidenced by Leide-Svegborn, one of ordinary skilled in the art would have reasonable expectation of success to reach the claimed invention.
Regarding claims 36 and 37, Shimoda teaches that deficiency for HIF-2α can reduce PH. See page 35, col. 2, para. 2. Shimoda also teaches that increased HIF-2α expression is associated with PH and promote PH. And induction of HIF-2 or HIF-1 by hypoxia in fibroblasts increase production of factors that stimulate PASMC growth or migration. See page 37, § Mechanisms by which HIFs promote PH. HIF-2α inhibitor can be used to treat PH. Chen further teach that prolonged treatment could lead to resistance. Based on the teachings of Shimoda, Chen, Ohira and Donnelly, one of ordinary skilled would have used a HIF-2α-specific radioactive tracer, e.g. 11C PT2385, for PH detection and treatment, as set forth above, and to monitor PH development by adding second PET-scan step to check the expression level of HIF-2α, because the expression of HIF-2α is a good indicator of PH. One of ordinary skilled in the art would have been motivated to check whether a certain HIF-2α inhibitor treatment is effective for a PH patient. Since Shimoda teaches high expression of HIF-2α would indicate more severe PH compared to low expression of HIF-2α, and Shimoda, Chen, Ohira and Donnelly the method of detection HIF-2α expression with a HIF-2α-specific radioactive tracer, one of ordinary skilled in the art would have had a reasonable expectation of success to reach the claimed invention. Furthermore, since resistant mutation (such as G323E) can affect HIF-2α bind to inhibitor such as PT2399, one of ordinary skilled in the art would be motivated to monitor PH by examining a second amount of HIF-2α expression to detecting possible resistant patients.
Response to Arguments
For the rejection of claims 34-37, 41, and 43-48 under 35 U.S.C. 103 applicant argues:
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Applicant’s arguments have been fully considered but they are not persuasive.
In the Remarks filed July 31, 2025 and Declaration of Dr. Su filed July 31, 2025, applicant first argues that a skilled person would not have a reasonable expectation that HIF-2α could be targeted by PET at the time of filing and the cited references do not teach HIF-2α can be a viable PET target.
First, 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).
As set forth above, Shimoda teaches that HIF-2α shows increased expression in PAH in vivo (page 35, col. 1, para. 4). Dai teaches that HIF-2α protein expression was highly induced in the lung tissues of distinct PAH models (page 1425, col. 3, para. 1). Chen teaches that HIF-2α has a 280 Å cavity within the PAS-B domain. PT2399 and PT2385 are specific HIF-2α inhibitors (antagonist) that bind the cavity (page 112, col. 1, para. 2). Chen teaches that PT2399 decreases tumor growth by 60% across all tumor grafts evaluated (P < 0.001) (page 112, col. 2, para. 3; Fig. 1). Tumor sensitivity to PT2399 is correlated to the expression of HIF-2α (Fig. 3a, b and Extended Data Fig. 4a). Thus, one of ordinary skill in the art would have expected that HIF-2α can be targeted/bound by PT2399. Ohira teaches emerging imaging techniques to study PH, including PET imaging and use of radioligands to image the site of action of drugs (page 151-§ EMERGING IMAGING TECHNIQUES TO STUDY PH, and Table 3). Donnelly teaches various ways to make small molecule PET tracers and many small molecule PET tracers (table on page 459). Taken together, as set forth above, one of ordinary would have had a reasonable expectation that a PET tracer based on PT2399 would be able to detect HIF-2α in PH patients, because HIF-2α protein expression is high in lung tissue in vivo, PT2399 can specifically bind HIF-2α and show activity associated with HIF-2α expression in vivo. In addition, using the administration method taught by Leide-Svegborn, one of ordinary skill in the art would have a reasonable expectation that the PET-tracer can reach the area of tumor quickly, as the drug travels through the bloodstream and the binding between the PET tracer and HIF-2α would occur before degradation of radioactivity.
Applicant pointed out that the uncertainty is high (para. 7 of Declaration), difference between in vivo and in vitro assays, and an ideal PET target would have certain properties (such as (a) to (d) of para. 5 of Declaration). However, uncertainty does not equate patentability since the expectation of success need only be reasonable not absolute. Thus, given all the in vivo HIF-2α expression data, PT2399 data, and administration method as set forth above, one of ordinary skill in the art would have had a reasonable expectation of success to reach the claimed invention.
In the field of biological technology, no invention has absolute certainty of success before experimental tests. For example, the data shown in the specification and Declaration were related to detection of HIF-2α in ccRCC with PT2385 and PT2977. No data have been provided for detecting PH in a subject by determining a PET tracer (any recited compounds, e.g. PT2399) targeting HIF-2α. Thus, only a reasonable expectation of success (not absolute) would have motivated an artisan to develop the claimed method. Given the teachings from references, an ordinary skilled in the art would have would have had a reasonable expectation of success in producing the claimed invention.
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Applicant further argues that the specification showed surprising results that HIF-2α could be a viable PET target. As set forth above, the combination of recited references teaches a method of detecting PH in a subject by determining a PET tracer (such as compound based on PT2399) targeting HIF-2α. Thus, HIF-2α is used as a target for PET tracer is not essentially surprising.
In addition, the results provided by the specification and declaration are the data shown in the specification and Declaration were related to detection of HIF-2α in RCC with PT2385 and PT2977. No data have been provided for detecting PH in a subject by determining a PET tracer (any recited compounds) targeting HIF-2α.
“Whether the unexpected results are the result of unexpectedly improved results or a property not taught by the prior art, the "objective evidence of nonobviousness must be commensurate in scope with the claims which the evidence is offered to support." In other words, the showing of unexpected results must be reviewed to see if the results occur over the entire claimed range. In re Clemens, 622 F.2d 1029, 1036, 206 USPQ 289, 296 (CCPA 1980) (Claims were directed to a process for removing corrosion at "elevated temperatures" using a certain ion exchange resin (with the exception of claim 8 which recited a temperature in excess of 100C). Appellant demonstrated unexpected results via comparative tests with the prior art ion exchange resin at 110C and 130C. The court affirmed the rejection of claims 1-7 and 9-10 because the term "elevated temperatures" encompassed temperatures as low as 60C where the prior art ion exchange resin was known to perform well. The rejection of claim 8, directed to a temperature in excess of 100C, was reversed.). See also In re Peterson, 315 F.3d 1325, 1329-31, 65 USPQ2d 1379, 1382-85 (Fed. Cir. 2003) (data showing improved alloy strength with the addition of 2% rhenium did not evidence unexpected results for the entire claimed range of about 1-3% rhenium); In re Grasselli, 713 F.2d 731, 741, 218 USPQ 769, 777 (Fed. Cir. 1983) (Claims were directed to certain catalysts containing an alkali metal. Evidence presented to rebut an obviousness rejection compared catalysts containing sodium with the prior art. The court held this evidence insufficient to rebut the prima facie case because experiments limited to sodium were not commensurate in scope with the claims.)”. MPEP 716.02(d)
In this case, the claimed method is related to PH but the data are related to detecting HIF-2α in RCC. In addition, there is not data for any PET tracers for PT2399. Accordingly, the data is not commensurate in scope with the claimed invention and does not demonstrate the non-obviousness of the claimed invention.
Additionally, for the evidence of the Declaration to show the non-obviousness of the claimed invention the presented evidence must show unexpected results. See MPEP716.02(a) I-IV. However, the evidence presented in the Declaration simply shows that PT2977 and PT2385 function as claimed. The Declaration does not provide any evidence that the claimed method is superior or unexpected compared to the methods known in the art.
Further a declaration under 37 CFR 1.132 must compare the claimed subject matter with the closest prior art to be effective to rebut a prima facie case of obviousness. See MPEP 716.02(e). The declaration did not explicitly compare the claimed subject matter with the closest prior art.
Thus, Applicant’s arguments and the Declaration of Dr. Xiankai Sun are not found persuasive for the reasons set forth above and the rejection is maintained for the reasons of record.
Conclusion
No claims are allowed.
All other rejection set forth in the previous Office Action of March 31, 2025 are hereby withdrawn in view of the claim amendments and Applicant’s arguments.
THIS ACTION IS MADE FINAL. 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 nonprovisional extension fee (37 CFR 1.17(a)) 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 mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to CHENG LU whose telephone number is (571)272-0334. The examiner can normally be reached Monday-Friday 8-5.
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/CHENG LU/ Examiner, Art Unit 1642
/PETER J REDDIG/ Primary Examiner, Art Unit 1646