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
This Office Action is responsive to Applicant’s Amendment and Remarks, filed June 23, 2026. The amendment, filed June 23, 2026, is acknowledged, wherein claims 1, 18, and 21 are amended and claims 2, 6 – 8, 13, 17, and 19 are canceled.
Claims 1, 3 – 5, 9 – 12, 14 – 16, 18, and 20 – 22 are pending in this application and are currently examined.
Priority
This application is a domestic application, filed January 20, 2022, which claims benefit of provisional application 63/139,437, filed January 20, 2021.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 06/23/2026 was filed after the mailing date of the previous Office Action on February 23, 2026. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Withdrawn Rejections
The rejection of claims 1 – 3, 9 – 10, 12, 15 – 16, and 18 in the previous Office Action, dated February 23, 2026, under 35 U.S.C. 103 as being unpatentable over Kazezian et al. in view of Chen et al. has been considered and is withdrawn in view of the amended claim 1.
The rejection of claims 4 – 6, 11, 13 – 14, and 20 – 22 in the previous Office Action, dated February 23, 2026, under 35 U.S.C. 103 as being unpatentable over Kazezian et al. in view of Chen et al. as applied to claims 1 – 3, 9 – 10, 12, 15 – 16, and 18 above, and further in view of Davis et al. has been considered and is withdrawn in view of the amended claim 1.
The following are new grounds of rejection necessitated by Applicant’s Amendment, filed June 23, 2026, wherein claims 1, 18, and 21 are amended and claims 2, 6 – 8, 13, 17, and 19 are canceled. Previously and newly cited references have been used to establish the new grounds of rejection.
New 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.
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 1, 3 – 5, 9 – 12, 14 – 16, 18, and 20 – 22 are rejected under 35 U.S.C. 103 as being unpatentable over Kazezian et al. (Applied Sciences, 2020, Vol. 10, Issue 18, cited in the PTO-892 on February 23, 2026) in view of Chen et al. (Cell Death and Disease, 2016, Vol. 7, Issue 10, cited in the PTO-892 on February 23, 2026), Davis et al. (US10279079B2, cited in the PTO-892 on February 23, 2026), and Liu et al. (Advanced Healthcare Materials, 2016, Vol. 5, Issue 12, page 1513 – 1521, PTO-892).
Kazezian et al. teach that intervertebral disc (IVD) degeneration is a leading cause of low back pain worldwide. In the last few decades, hyaluronic acid (HA) has popularized due to its anti-inflammatory, analgesic and extracellular matrix enhancing properties. Thus, there is expressed interest in treating the IVD degeneration using different HA compositions. An ideal HA-based biomaterial needs to be compatible and supportive of the disc microenvironment in general and inhibit inflammation and downstream cascades leading to the innervation, vascularization and pain sensation in particular (Abstract). The following figure disclose the administration of HA hydrogel for treating IVD degeneration (page 2, Figure 1):
PNG
media_image1.png
185
496
media_image1.png
Greyscale
.
Thus, Kazezian et al. teach treating IVD degeneration by administering injectable HA hydrogel, which corresponds to the limitations “treating intervertebral disc disease”, “by injection”, and “hydrogel composition comprising hyaluronic acid” of claim 1, “a syringe” of claim 16, and “treating spinal degeneration” of claim 18. There are some studies report that the hydrophilic properties of HA is able to restore disc height (page 13, para. 2). Kazezian et al. disclose that the biochemical properties of the HA molecule are entirely dependent on its size (page 5, para. 2). High molecular weight (HMW) HA is capable of inhibiting the signaling of inflammatory cytokines and matrix-degrading enzymes (page 6, para. 2). A study discloses that use of various combinations of HMW HA and processing techniques can reduce inflammation, innervation, and pain in the disc (page 13, para. 5; page 14, para. 1). For example, HMW HA might have a molecular weight of 2 – 4 x 106 Da (page 4, para. 3). Thus, the disclosure reads on the limitation of claims 3 and 20. Another study disclosed by Kazezian et al. finds that re-herniation is deferred successfully by using HA/collagen hydrogel (page 9, Table 2). Therefore, HA-based injectable hydrogels are strong candidates as effective treatments for disc degeneration (page 14, para. 6). Kazezian et al. disclose deferral of re-herniation, which indicates that the treated disc had previously undergone herniation. Thus, Kazezian et al. suggest treatment of a subject having disc herniation, which corresponds to the limitation of claim 15. Moreover, Kazezian et al. disclose that studying IVD degeneration using human subjects is challenging, thus, different animal models emerged (page 6, para. 3). Thus, the disclosed IVD treatment is tested on animal models, but it is intended for treating human subjects, which reads on the limitations “mammal” of claim 1 and “human” of claim 12.
However, Kazezian et al. do not teach administering the hydrogel composition by injection into the nucleus pulposus; a composition comprising a poloxamer and a compound comprising amobarbital, adenosine diphosphate ribose, or metformin that reversibly inhibits respiratory enzyme complex I; a thermoresponsive hydrogel that is injectable at a temperature below body temperature and forms a gel at body temperature; or sustained release of the compound for at least 72 hours into the nucleus pulposus. Kazezian et al. do not tach the claimed poloxamer concentration of about 15% to about 20% (wt/vol). Kazezian et al. do not explicitly teach that the treated disc is a lumbar disc, as recited in claim 9, or that administration reduces ROS production in the nucleus pulposus, as recited in claim 10.
Chen et al. teach that IVD degeneration is a complicated process that involves both cellular apoptosis and senescence. The effect of metformin on IVD degeneration is investigated both in vitro and in vivo. The study shows that metformin attenuated cellular apoptosis and senescence induced by tert-butyl hydroperoxide in nucleus pulposus cells. In vivo study illustrates that metformin treatment could ameliorate IVD degeneration in a puncture-induced rat model. Thus, the study shows that metformin could protect nucleus pulposus cells against apoptosis and senescence via autophagy stimulation and ameliorate disc degeneration in vivo, revealing its potential to be a therapeutic agent for IVD degeneration (Abstract). Accordingly, Chen et al. read on the limitations requiring treatment of intervertebral disc disease in a mammal using metformin in an amount effective to treat intervertebral disc degeneration. Chen et al. further read on the nucleus pulposus-related therapeutic aspect because Chen et al. specifically evaluates metformin in nucleus pulposus cells and reports protection against apoptosis and senescence. Moreover, Chen et al. teach that, following puncture-induced intervertebral disc surgery, metformin treatment is initiated immediately after surgery (page 12, Right Col., para. 1). Because treatment begins immediately after surgery/injury, Chen et al. teach administration within four days of surgery/injury, as required by claim 11.
Davis et al. teach biocompatible composition comprising a poloxamer and one or more additives, such as hyaluronic acid for the repair of an injured spinal disc (Abstract). The biocompatible composition includes HA-gelatin-containing poloxamer hydrogel. Accordingly, Davis et al. teach the limitations requiring a hydrogel composition comprising hyaluronic acid and a poloxamer in claims 1 and 18. HA-gelatin-containing poloxamer hydrogel is liquid at low temperatures (e.g. between about 4 ⁰C and about room temperature) and transition to a gel/solid phase at higher temperatures, including body temperature (Col. 2, lines 46 – 51). Thus, Davis et al. teach the limitation requiring a thermoresponsive hydrogel that is injectable at a temperature below body temperature and forms a gel at body temperature, which corresponds to the limitations “thermoresponsive hydrogel”, “injectable at a temperature below body temperature” and “forms a gel at body temperature” of claims 1 and 18. The composition comprising 0.2 – 1.0 % w/v hyaluronic acid and 20% w/v poloxamer (Col. 3, lines 40 – 44). The disclosed hyaluronic acid concentration reads on the ranges recited in claims 4 – 5, and the disclosed 20% w/v poloxamer, as a synthetic polymer, reads on the range of about 15% to about 20% w/v recited in claims 21 – 22.
Liu et al. teach an in situ gelling drug delivery system for treatment of spinal cord injury comprising a poloxamer-407/poloxamer 188 mixture-based thermoresponsive hydrogel matrix containing an incorporated therapeutic compound, GM1. Accordingly, Liu et al. teach use of a poloxamer-containing thermoresponsive hydrogel as a local therapeutic drug delivery system. Liu et al. further teach that the GM1-containing poloxamer polymer solution is converted to a hydrogel upon administration to the injured spinal cord as a result of the increase in temperature. Thus, Liu et al. teach the temperature-responsive sol-to-gel behavior corresponding to the claimed limitation requiring a thermoresponsive hydrogel that is administered in a lower temperature solution state and forms a gel upon exposure to body temperature. Liu et al. additionally teach that the thermoresponsive hydrogel prolongs release of GM1 for approximately one month as a result of dissolution and swelling of the hydrogel matrix at body temperature. Liu et al. explain that such sustained release prolongs residence time of the therapeutic agent at the injured spinal cord and decreases the frequency of administration. Accordingly, Liu et al. teach sustained release of an incorporated therapeutic compound for a period exceeding the claimed “at least 72 hours” limitation of claims 1 and 18.
It would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to combine the injectable hyaluronic acid hydrogel taught by Kazezian et al. with the poloxamer-containing thermoresponsive hydrogen in view of Davis et al., and the metformin treatment in view of Chen et al. for the treatment of intervertebral disc degeneration because Kazezian et al. teach that HA-based injectable hydrogels are useful candidates for treatment of intervertebral disc degeneration, Davis et al. teach that incorporating poloxamer into an HA-containing hydrogel provides an injectable, biocompatible spinal disc formulation having temperature-dependent gelation, and Chen et al. teach that metformin protects nucleus pulposus cells and ameliorates intervertebral disc degeneration. One of ordinary skill in the art therefore would have had reason to incorporate the metformin of Chen et al. into the HA/poloxamer hydrogel system of Kazezian et al. and Davis et al. in order to locally deliver a known therapeutic agent to a diseased intervertebral disc using a known injectable hydrogel carrier suitable for the same anatomical environment. The combination amounts to use of known prior art elements according to the established functions to obtain the predictable result of localized treatment of intervertebral disc degeneration. One of ordinary skill in the art would have had a reasonable expectation of success because each component is known for a compatible purpose, whereas hyaluronic acid and poloxamer as biocompatible injectable disc treatment materials and metformin as a therapeutic for IVD degeneration and nucleus pulposus cells.
Regarding to “injection into a nucleus pulposus” of claims 1 and 18, Chen et al. teach that metformin acts directly on nucleus pulposus cells and protects such cells against apoptosis and senescence in the treatment of intervertebral disc degeneration. Liu et al. teach localized delivery of a therapeutic agent using an in situ-forming thermoresponsive poloxamer hydrogel. In view of these teachings, one of ordinary skill would have been motivated to locally administer the metformin-containing hydrogel to the nucleus pulposus region so that metformin is delivered directly to the cells population identified by Chen et al. as therapeutically responsive. Such local administration would have been a predictable use of the known localized thermoresponsive hydrogel drug delivery technique of Liu et al. to the known nucleus pulposus therapeutic target identified by Chen et al., with a reasonable expectation of success because Chen et al. demonstrate therapeutic activity of metformin in nucleus pulpous cells and Liu et al. demonstrate successful localized delivery of a therapeutic agent from a thermoresponsive poloxamer hydrogel.
Regarding “sustained release for at least 72 hours” of claims 1 and 18, Liu et al. teach that a thermoresponsive poloxamer hydrogel containing an incorporated therapeutic compound provides sustained release for approximately one month at body temperature. One of ordinary skill seeking to prolong local exposure to the metformin taught by Chen et la. would therefore have had reason to employ the known sustained release capability of a thermoresponsive poloxamer hydrogel in the disc treatment system of Davis et al. One of ordinary skill in the art would have been motivated to seek for prolong local exposure because it reduces the need for repeated administration. Because Liu et al. demonstrate sustained release exceeding 72 hours from the same general class of thermoresponsive poloxamer delivery system, one of ordinary skill would have had a reasonable expectation of success that such a system could be configured to provide sustained release for at least 72 hours.
Regarding claims 3 and 20, Kazezian et al. teach high molecular weight HA having a molecular weight of approximately 2 – 4 x 106 Da, which is approximately 2 – 4 MDa. This range is greater than 0.5 MDa. Accordingly, Kazezian et al. directly teach the molecular weight limitation of claims 3 and 20.
Regarding claims 4 – 5 and 21 – 22, Davis et al. teach an HA concentration of approximately 0.2 – 1.0% w/v, which falls within the broader range of claim 4 and directly corresponds to the range of claim 5. Davis et al. further teach approximately 20% w/v poloxamer, which falls within the recited range of about 15 – 20% w/v of claim 21. Because poloxamer is a synthetic polymer, the same disclosure also reads on the synthetic polymer concentration recited in claim 22. Thus, the claimed concentration limitations are taught by Davis et al.
With respect to claim 9, Kazezian et al. do not explicitly identify the treated disc as lumbar, but they teach IVD degeneration as a leading cause of low back pain. One of ordinary skill would have recognized the lumbar intervertebral discs as a conventional anatomical site associated with low back symptoms and IVD degeneration and therefore would have considered treatment of a lumbar disc to be an obvious application of the disclosed IVD treatment of Kazezian et al.
With respect to claim 10, Kazezian et al. do not explicitly teach that administration reduces ROS production in the nucleus pulposus. Chen et al., however, teach oxidative stress contributes to apoptosis and senescence of nucleus pulposus cells and that metformin protects nucleus pulposus cells against oxidative stress-induced apoptosis and senescence and ameliorates intervertebral disc degeneration. When the metformin-containing hydrogel of the combined references is administered to the nucleus pulposus in an amount effective to treat IVD degeneration, the claimed reduction in ROS production is an inherent physiological result of the metformin treatment. Thus, the functional limitation of claim 10 would necessarily be present in the method resulting from the proposed combination.
Regarding claim 11, Chen et al. employ a puncture-induced intervertebral disc degeneration model in which the surgical puncture produces injury to the intervertebral disc and initiates the degenerative process. Chen et al. administer metformin immediately following the puncture procedure. Thus, Chen et al. teach treatment initiated contemporaneously with the disc injury/surgery. In view of the teaching of Chen et al. that prompt administration of metformin following the injury-producing procedure ameliorates subsequent intervertebral disc degeneration, one of ordinary skill in the art would have been motivated to administer the claimed therapeutic composition shortly after spinal injury or surgery, including within the recited four-day period, in order to intervene during the early post-injury degenerative process. One of ordinary skill would have had a reasonable expectation of success because Chen et al. demonstrate a therapeutic benefit when metformin treatment is begun immediately following the injury-inducing surgical procedure.
Regarding claim 14, Chen et al. employ a puncture-induced model of intervertebral disc degeneration and specifically evaluate the resulting degenerative effects in nucleus pulposus cells. Thus, Chen et al. at least suggest an injured or damaged nucleus pulposus in the context of the disclosed IVD degeneration model. Accordingly, one of ordinary skill in the art would have understood the disclosed treatment to be applicable to a mammal having an injury involving the nucleus pulposus, as recited by claim 14.
Responses to Applicant’s Remarks:
Applicant’s Remarks, filed June 23, 2026, has been fully considered but are moot because the new ground(s) of rejection does not rely on the same combination of references in the prior rejection of record. However, upon further consideration, a new ground(s) of rejection is made in view of the new combination of references.
Applicant argues that Kazezian et al. and Chen et al., alone or in combination, do not teach or suggest the amended method because neither reference discloses a thermoresponsive HA/poloxamer hydrogel containing metformin or another complex I inhibitor, injection into the nucleus pulposus, or sustained release of the inhibitor for at least 72 hours. However, the argument is moot because the rejection is based on the combined teachings of Kazezian et al., Chen et al., Davis et al., and Liu et al. Kazezian et al. teach injectable HA-based hydrogels for treatment of IVD degeneration. Chen et al. teach metformin as a therapeutic agent that protects nucleus pulposus cells and ameliorates IVD degeneration. Davis et al. teach an HA/poloxamer hydrogel for spinal disc repair that is liquid at low temperature and gels at body temperature, thereby supplying the claimed thermoresponsive HA/poloxamer formulation. Liu et al. further teach that a thermoresponsive poloxamer hydrogel may serve as a local drug delivery depot and provide sustained release of an incorporated therapeutic agent for approximately one month, which exceeds the claimed period of at least 72 hours. Thus, the cited references collectively teach or suggest the recited formulation and sustained delivery features.
Applicant argues that Chen et al. administers metformin systemically by intraperitoneal injection rather than by intradiscal injection and does not deliver metformin in a hydrogel or sustained release formulation. Applicant further argues that Kazezian et al. merely review HA-based delivery platforms and does not disclose delivery of a complex I inhibitor in the claimed thermoresponsive hydrogel. However, the argument is not persuasive because obviousness does not require a single reference to disclose all limitations or the identical route and formulation. Chen et al. is relied upon for the therapeutic use of metformin in IVD degeneration and its effect on nucleus pulposus cells, while Davis et al. and Liu et al. are relied upon for the local thermoresponsive hydrogel delivery platform and prolonged release characteristics. Chen et al. is relied upon for the therapeutic use of metformin in IVD degeneration and its direct effect on nucleus pulposus cells, while Davis et al. is relied upon for the HA/poloxamer thermoresponsive hydrogel formulation and Liu et al. is relied upon for localized thermoresponsive hydrogel delivery and prolonged release characteristics. One of ordinary skill would have had reason to locally deliver the metformin taught by Chen et al. to the nucleus pulposus cells as a therapeutically responsive target, and Liu et al. teach localized delivery of an incorporated therapeutic agent from a thermoresponsive poloxamer hydrogel.
Applicant argues that the claimed formulation provides localized, sustained intradiscal delivery with functional results allegedly distinct from the prior art, including uniform distribution in the nucleus pulposus, minimal backflow through a small-bore needle, and sustained release for at least 72 hours. However, the argument is not persuasive as to the presently claimed subject matter because the cited combination already provides a basis for localized delivery and prolonged release. Davis et al. teach an injectable thermoresponsive HA/poloxamer hydrogel suitable for spinal disc repair, and Liu et al. teach use of a thermoresponsive poloxamer hydrogel as a localized drug-delivery depot providing prolonged release well beyond 72 hours. Applicant intends these asserted properties to establish unexpected results, the remarks do not appear to provide a comparative showing demonstrating that the claimed results are unexpected relative to the closest prior art or attributable to the claimed combination over the prior art systems.
Applicant argues that there is no motivation to reformulate the systemically administered metformin formulation of Chen et al. into a thermoresponsive HA/poloxamer hydrogel for intradiscal delivery and no reasonable expectation that such a formulation would sustain metformin release for at least 72 hours while retaining therapeutic activity. However, the argument is not persuasive. Kazezian et al. establish the desirability of HA-based injectable hydrogels for treatment of IVD degeneration; Chen et al. establish metformin as a therapeutic agent for the same disease and specifically for nucleus pulposus cells; Davis et al. teach an injectable thermoresponsive HA/poloxamer hydrogel for treatment of damaged spinal discs; and Liu et al. teach that thermoresponsive poloxamer hydrogels may be used to prolong local release of an incorporated therapeutic agent. A person of ordinary skill seeking to maintain a therapeutic agent locally within a diseased disc would have had reason to incorporate metformin of Chen et al. into the known injectable thermoresponsive hydrogel platform taught by Davis et al. and to employ the sustained release capability taught by Liu et al. in order to prolong local drug exposure and reduce repeated administration. The prolonged release of a therapeutic from a thermoresponsive poloxamer matrix demonstrated by Liu et al. provides a reasonable expectation that sustained delivery exceeding 72 hours is achievable.
Applicant argues that Davis et al. do not cure the deficiencies of Kazezian et al. and Chen et al. because Davis et al. do not specifically disclose metformin, amobarbital, adenosine diphosphate ribose, or other complex I inhibitor among the therapeutic agents incorporated into the hydrogel. However, the argument is not persuasive because Davis et al. is not relied upon for identifying the therapeutic agent. Chen et al. supply metformin, which his one of the compounds recited in the claims. while Davis et al. supply the HA/poloxamer thermoresponsive spinal disc delivery vehicle. It is not necessary that Davis et al. independently identify metformin where the reason for incorporating the known IVD therapeutic of Chen et al. into the known spinal disc hydrogel of Davis et al. arises from the combined teachings of the references.
Applicant further argues that Davis is primarily directed to a structural disc-nucleus implant that fills the intradiscal space and mimics the mechanical properties of the natural disc, rather than to a pharmaceutical sustained release vehicle for delivery of a complex I inhibitor. However, the argument is not persuasive because Davis et al. explicitly describe the composition as a biocompatible HA/poloxamer hydrogel and discuss drug delivery application in addition to structural disc repair. Moreover, Liu et al. independently teach use of a closely related thermoresponsive poloxamer hydrogel specifically as a prolonged local drug delivery system. Thus, the combined prior art would have suggested using the same thermoresponsive poloxamer platform as a therapeutic delivery vehicle.
Applicant argues that the prior art provides no reason to arrive at the specific combination of a complex I inhibitor, thermoresponsive HA/poloxamer hydrogel, intradiscal placement, and at least 72-hour sustained release. However, the argument is not persuasive. The rejection does not rely on knowledge of Applicant’s disclosure as the reason for combination. Instead, each modification is supported by an identified prior art teaching directed to the same general problem of treating degenerative or injured spinal tissue through localized hydrogel delivery. Kazezian et al. teach HA-based injectable treatment of IVD degeneration; Chen et al. teach metformin for IVD degeneration and nucleus pulposus protection; Davis et al. teach the thermoresponsive HA/poloxamer spinal disc hydrogel; and Liu et al. teach prolonged release from a thermoresponsive poloxamer drug delivery system. The proposed combination therefore represents the application of known therapeutic and drug delivery techniques to a closely related treatment setting for the established purposes, with predictable benefits of localized administration, in situ gel formation, and prolonged drug residence.
Applicant finally asserts that the specification demonstrates inhibition of nucleus pulposus cell apoptosis and structural disc degeneration following injury, which allegedly is not taught or suggested by the cited art. However, the argument is not persuasive because Chen et al. already teach that metformin protects nucleus pulposus cells against apoptosis and senescence and ameliorates IVD degeneration in vivo.
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 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 HOI YAN LEE whose telephone number is 571-270-0265. The examiner can normally be reached Monday - Thursday 7:30 - 17:30.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, SCARLETT GOON can be reached at 571-270-5241. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/H.Y.L./Examiner, Art Unit 1693
/JONATHAN S LAU/Primary Examiner, Art Unit 1693
Prosecution Insights