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 .
Election/Restrictions
Applicant’s election without traverse of Group I (Claims 1, 4-5, 9-14, and 16; drawn to a method facilitating neointima formation over an endovascular device) in the reply filed on May 7, 2024, is acknowledged.
Claims 17, 20-21, 25-27, 32-34, and 36 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention (Groups II and III), there being no allowable generic or linking claim.
DETAILED ACTION
The amended claims filed on December 12, 2025, have been acknowledged.
Claims 2-3, 5-8. 15, 18-19, 21-24, 28-31, 34-35, and 37-146 were cancelled. Claims 1, 17, and 32 were amended. Claims 17, 20, 25-27, 32-33, and 36 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention (Groups II and III), there being no allowable generic or linking claim. Claims 1, 4, 9-14, and 16 are pending and examined on the merits.
Priority
The applicant claims domestic priority from U.S. provisional application No. 63/146,464, filed on February 5, 2021. Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged. Claims 1, 4, 9-14, and 16 receive domestic benefit from U.S. provisional application No. 63/146,464, filed on February 5, 2021.
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.
Claims 1, 4, 9-10, and 13 are rejected under 35 U.S.C. 103 as being unpatentable over Nakazaki et al. (J Neurosurg 133: 1773-1785. 2020), Eirin et al. (Stem Cells 30: 1030-1041. 2012), Yan et al. (Adv Sci 7: 1-12. 2020), Kean et al. (Stem Cells International 2013: 1-13. 2013), and Lundberg et al. (Cell Transplantation 21: 333–343, 2012), as evidenced by Akyurekli et al. (Stem Cell Rev and Rep 11: 150-160. 2015). This is a new rejection made in response to Applicant’s amendments to claim 1 that is substantially similar to a previous rejection. Any aspect of Applicant’s traversal that is relevant to the rejection as newly written is addressed below.
Regarding claim 1, the specification fails to define the meaning of “patient” and the Applicant’s working examples are using a non-human animal (New Zealand White Rabbits) (page 9, paragraphs 3-4). As such, “patient” is interpreted to include non-human animals.
Furthermore, the Applicant does not define the comparison point for the increase in neointima formation. Therefore, any comparison is considered applicable for assessing the increase in neointima formation. For example, if the comparison is between no neointima formation, any neointima formation would be an increase compared to no neointima formation.
Nakazaki teaches a method of facilitating neointima formation over an endovascular device deployed within a vessel comprising administering mesenchymal stem cells. Nakazaki teaches that two types of bare metal stents were deployed using a porcine (mini-pig) model. One stent was implanted in the common carotid artery (CCA), which is considered quite similar to the human CCA, and the other was inserted in the superficial cervical artery (SCA), which is similar in size to the human middle cerebral artery (abstract). Fourteen days after stent implantation, the mini-pigs were infused with 1 x 108 mesenchymal stem cells (MSCs) (Figure 1). Neointimal proliferation was seen in stented CCA and SCA MSC-infused pigs (page 1780, column 1-page 1781, column 2, paragraph 2 and Figure 5). Therefore, as neointima formation occurred in the MSC infused group, this would be an increase compared to no neointima formation. Nakazaki teaches that intravenous infusion of MSCs immediately after deployment of stents prevented in-stent stenosis of the CCA and SCA (abstract).
Nakazaki does not teach wherein the mesenchymal stem cells are administered intra-arterially upstream of the endovascular device.
However, Eirin teaches a method of administering 10 x 106 MSCs intra-arterially in swine immediately after implanting a stent (abstract; page 1031, column 2, paragraph 3; and page 1039, column 2, paragraph 3). Eirin teaches that MSC were manually injected slowly through a balloon catheter placed in the renal artery (Supplementary Information page 2, paragraph 3). Eirin teaches that reno-protective strategies are needed to improve renal outcomes in patients with atherosclerotic renal artery stenosis (ARAS) (abstract). Eirin teaches that the MSCs successfully treated ARAS and improved kidney function (page 1039, column 1, paragraph 1).
Yan teaches that a major challenge facing stem cell therapeutics is the efficient delivery of cells to tissues of interest. Local injection into tissues or infusion into proximal blood vessels represents two potential delivery routes. For vascular injuries, local injection is hazardous as arterial walls are thin and pulsatile. Intra-arterial infusion is minimally invasive, enables repetitive dosing, and circumvents problems associated with secondary vascular injury and calcification (page 2, column 1, paragraph 4).
Kean teaches that engraftment efficiency of MSCs is enhanced by using intra-arterial delivery instead of intravenous delivery, thus avoiding the “first-pass” accumulation of MSCs in the lung (abstract). MSCs showed significant entrapment in the lungs when delivered IV into the tail vein. However, when delivered IA, the cells were more evenly distributed throughout the entire animal (Figure 1). Over time, there was evidence of engraftment of the MSCs at the injury site and not at noninjured sites in the arterial-delivered groups. In the tail vein-injected group, the cells dissipated from the animal after a few days and were undetectable one week after injection (page 6, column 1, paragraph 3).
Regarding the upstream administration limitation, Lundberg teaches that when transplanting a cell type that gives engraftment through intra-arterial transplantation, it is possible to increase the efficiency ratios by placement of a microcatheter just upstream of a target site (page 342, column 1, paragraph 2).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have substituted the intravenous route of administration of Nakazaki with the intra-arterial route of administration of Eirin and Lundberg to arrive at the instantly claimed invention. One of ordinary skill in the art would have been motivated to make the substitution with a reasonable expectation of success because Nakazaki and Eirin are focused on administering MSCs to subjects with stents to treat stenosis of arteries and Eirin has successfully reduced to practice that MSCs can be administered intra-arterially following stent implantation in an artery and that intra-arterial administration of MSCs successfully treated stenosis of the artery. Furthermore, Yan and Kean teach that intra-arterial administration is minimally invasive, enables repetitive dosing, and circumvents problems associated with secondary vascular injury and increases engraftment efficiency of MSCs compared to intravenous delivery by avoiding the “first-pass” accumulation of MSCs in the lung that occurs with intravenous delivery. Regarding upstream administration, Lundberg teaches that placement of a microcatheter just upstream of a target site increases the rate of engraftment of the cells. As such, it would have been obvious to administer the MSCs intra-arterially upstream of the device as intra-arterial administration avoids “first-pass” accumulation of MSCs in the lung, leading to increased engraftment and this engraftment can be further enhanced by administering the cells upstream of the target. Because the prior art teaches all of the elements of the claimed invention, there is a reasonable expectation of success.
Regarding claim 4, Nakazaki teaches that fourteen days after stent implantation, the mini-pigs were infused with 1 x 108 mesenchymal stem cells (MSCs) (Figure 1).
Regarding claims 9 and 10, Nakazaki teaches that one stent was implanted in the common carotid artery (CCA), which is considered quite similar to the human CCA, and the other was inserted in the superficial cervical artery (SCA), which is similar in size to the human middle cerebral artery (abstract).
Regarding claim 13, Akyurekli evidences that the therapeutic potential of mesenchymal stromal cells (MSCs) may be largely mediated by paracrine factors contained in microvesicles (MV) released from intracellular endosomes (abstract). Microvesicles released by MSCs were of various sizes depending on the tissue source in humans and animals (page 157, column 2, paragraph 3). As such, MSCs inherently produce microvesicles, so the MSCs of Nakazaki would also produce MSC derived microvesicles.
Response to Arguments
Applicant's arguments filed December 12, 2025, are acknowledged.
Applicant argues that the focus of Eirin was entirely on the treatment of patients with ARAS (see, for example, Eirin at Abstract), and the authors do not make any discoveries or pronouncements to the use of MSCs more generally. Notably, nowhere does Eirin teach, disclose or suggest that the intra-arterial administration of MSCs would facilitate/increase neointima formation over an endovascular device or to heal an endovascular tear. More particularly, the Applicant notes Eirin's silence throughout the report with respect to the stenting, beyond its brief mention in association with PTRA, as well as its complete silence regarding neointima, its formation, or association with endovascular devices and vascular tears. As such, the Applicant submits that, whereas Eirin did intra-arterially deliver MSCs to improve ARAS in swine models, such findings reliably pertain only to renal outcomes and are not of general application, such as those claimed in the present application (page 6, paragraph 7-page 7, paragraph 1).
Applicant's arguments have been fully considered but they are not persuasive.
As an initial matter, 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).
The rejection is made based on the combined teachings of Nakazaki, Eirin, Kean, and Lundberg and the combined teachings make the method of the instant application obvious.
As stated in the rejection above, Nakazaki and Eirin are focused on administering MSCs to subjects with stents to treat stenosis of arteries and Eirin has successfully reduced to practice that MSCs can be administered intra-arterially following stent implantation in an artery and that intra-arterial administration of MSCs successfully treated stenosis of the artery. Furthermore, Yan and Kean teach that intra-arterial administration is minimally invasive, enables repetitive dosing, and circumvents problems associated with secondary vascular injury and increases engraftment efficiency of MSCs compared to intravenous delivery by avoiding the “first-pass” accumulation of MSCs in the lung that occurs with intravenous delivery. Regarding upstream administration, Lundberg teaches that placement of a microcatheter just upstream of a target site increases the rate of engraftment of the cells. As such, it would have been obvious to administer the MSCs intra-arterially upstream of the device as intra-arterial administration avoids “first-pass” accumulation of MSCs in the lung, leading to increased engraftment and this engraftment can be further enhanced by administering the cells upstream of the target.
Although Eirin focuses on treating renal stenosis using intra-arterial administration of MSCs, it is well understood that a treatment that works in limiting stenosis in one area (e.g. renal) would provide a reasonable basis for using a similar method to treat stenosis in a different area (e.g. CCA and SCA). Furthermore, although Eirin does not examine neointima formation, they do examine and treat stenosis after stenting, which is similar to Nakazaki. Therefore, there is a common nexus between Nakazaki and Eirin that would lead one of ordinary skill to examine Eirin for potential improvements in treating stenosis. Furthermore, Eirin has successfully reduced to practice that MSCs can be administered intra-arterially following stent implantation in an artery and that intra-arterial administration of MSCs successfully treated stenosis of the artery. As identified by Yan, Kean, and Lundberg, there are distinct benefits to using intra-arterial administration of MSCs compared to intravenous administration as intra-arterial administration “first-pass” accumulation of MSCs in the lung, leading to increased engraftment and this engraftment can be further enhanced by administering the cells upstream of the target
Therefore, Applicants arguments are unpersuasive.
Furthermore, Applicant argues that none of the cited art teach, disclose or otherwise suggest a method for increasing neointima formation, as recited in the amended claims. The Applicant submits that these amendments highlight a key feature of the invention, which is that intra-arterial injection of the MSCs upstream increases neointima formation, particularly over an endovascular device or a vascular tear, rather than merely permits the presence of neointima formation, as shown in Nakazaki. More particularly, as described in Nakazaki at page 1780, column 2, first paragraph, FIG. 5 shows that "neotinimal proliferation was less observed in the MSC-infused group [relative to a control group]".
Applicant argues that the Nakazaki reference provides a theory as to why MSCs would discourage neointima proliferation and hyperplasia (see, for example, the text of page 1782, page 1783, left column, first paragraph). It is respectfully submitted that the Office Action rejections have failed to properly take into account the importance of the theory proposed by Nakazaki, as this theory fundamentally informs the conclusions the skilled person would draw from the article. Accordingly, in view of findings of Nakazaki and the theory proposed therein, the skilled person would reasonably conclude that, administration of MSCs, by reducing inflammation and preventing MMP-9 activation, would reduce the risk of neointimal hyperplasia by inhibiting neointima formation. The Applicant additionally submits that the skilled person, in view of Nakazaki, would further not conclude that MSCs could be used to increase neointima formation. Nothing in Nakazaki teaches, discloses or suggests that administration of MSCs can increase neointima formation. Conversely, in view of the disclosures, and particularly the theory provided in Nakazaki, the skilled person would likely conclude that administration of more MSCs would lead to less neointima formation, consistent with the results shown in Nakazaki's FIG. 5, which shows "less observed" neotintimal proliferation in the arteries from MSC-infused patients (page 7, paragraph 2-page 10, paragraph 5).
Applicant's arguments have been fully considered but they are not persuasive.
Regarding Applicants’ arguments regarding the reduction of neointima formation in the MSC infused group of Nakazaki compared to the control group of Nakazaki (as seen in Figure 5), it is noted the features upon which applicant relies (i.e. a specific comparison of neointima formation between an MSC infused group and a non-MSC infused control group) are not recited in the rejected claim(s). Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993). The court explained that “reading a claim in light of the specification, to thereby interpret limitations explicitly recited in the claim, is a quite different thing from ‘reading limitations of the specification into a claim,’ to thereby narrow the scope of the claim by implicitly adding disclosed limitations which have no express basis in the claim.” The court found that applicant was advocating the latter, i.e., the impermissible importation of subject matter from the specification into the claim.). See also In re Morris, 127 F.3d 1048, 1054-55, 44 USPQ2d 1023, 1027-28 (Fed. Cir. 1997) (The court held that the PTO is not required, in the course of prosecution, to interpret claims in applications in the same manner as a court would interpret claims in an infringement suit. Rather, the “PTO applies to verbiage of the proposed claims the broadest reasonable meaning of the words in their ordinary usage as they would be understood by one of ordinary skill in the art, taking into account whatever enlightenment by way of definitions or otherwise that may be afforded by the written description contained in applicant’s specification.”). See MPEP 2111]
The Applicant does not define the comparison point for the increase in neointima formation. Therefore, any comparison is considered applicable for assessing the increase in neointima formation. For example, if the comparison is between no neointima formation, any neointima formation would be an increase compared to no neointima formation.
Applicant points to one particular comparison between the control group and the MSC infused group of Figure 5 of Nakazaki to show that the MSC infused group has less neointima formation, and, therefore, does not fall within the limitations of the claims. However, the claims do not limit the increase in neointima formation to the specific comparison identified by the Applicant. As identified by Nakazaki, neointimal proliferation was seen in stented CCA and SCA MSC-infused pigs (page 1780, column 1-page 1781, column 2, paragraph 2 and Figure 5). Therefore, as neointima formation occurred in the MSC infused group, this would be an increase compared to no neointima formation.
Therefore, Applicant’s arguments are considered unpersuasive.
Claims 1, 11, 12, and 16 are rejected under 35 U.S.C. 103 as being unpatentable over Nakazaki et al. (J Neurosurg 133: 1773-1785. 2020), Eirin et al. (Stem Cells 30: 1030-1041. 2012), Yan et al. (Adv Sci 7: 1-12. 2020), Kean et al. (Stem Cells International 2013: 1-13. 2013), and Lundberg et al. (Cell Transplantation 21: 333–343, 2012) as applied to claim 1 above, and further in view of United States Patent Application No. 20020040239 (Murayama) and Gao et al. (Journal of Biomedical Materials Research A 106A: 1878-1886, 2018). This rejection is repeated with regards to the rejection in the Non-final Office action mailed on June 12, 2025. Applicant’s traversal has been addressed above.
Regarding claim 11, the teachings of Nakazaki, Eirin, Yan, Kean, and Lundberg are as discussed above.
The combined teachings of Nakazaki, Eirin, Yan, Kean, and Lundberg do not teach wherein the endovascular stent is coated with VEGF.
However, Murayama an endovascular device (claim 1) comprising a biocompatible and bioabsorbable polymer. This device may carry growth factors, such as a vascular endothelial growth factor, a basic fibroblast growth factor or a mixture of several growth factors or cytokines (paragraphs 0009-0010 and 0043). Murayama teaches that VEGF promotes wound healing (paragraph 0043).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have combined the method of neointima formation around a stent of the combined teachings of Nakazaki, Eirin, Yan, Kean, and Lundberg with the biocompatible polymer carrying VEGF of Murayama to arrive at the instantly claimed invention. One of ordinary skill in the art would have been motivated to make the combination with a reasonable expectation of success because Murayama teaches that VEGF promotes wound healing. As such, it would have been obvious to include VEGF as part of a coating around the stents to improve healing and long-term stability of the stents. Because the prior art teaches all of the elements of the claimed invention, there is a reasonable expectation of success.
Regarding claim 12, although Nakazaki teaches the mini-pigs were infused with 1 x 108 MSCs, Eirin teaches that 10 x 106 MSCs were intra-arterially administered and that this amount successfully treated arterial stenosis (abstract). Accordingly, it would have been obvious to administer about 4 x 106 MSCs, since it has been held that where the general conditions of a claim are disclosed in the prior art, discovering the optimum or workable ranges involves only routine skill in the art. In re Aller, 105 USPQ 233.
Regarding claim 16, the teachings of Nakazaki, Eirin, Yan, Kean, and Lundberg are as discussed above.
The combined teachings of Nakazaki, Eirin, Yan, Kean, and Lundberg do not teach wherein a cytokine is administered with the MSCs.
However, Murayama teaches an endovascular device (claim 1) comprising a biocompatible and bioabsorbable polymer or noncollagenous protein that promotes an intra-aneurysmal inflammatory response and healing of the aneurysms. This device may carry growth factors, such as a vascular endothelial growth factor, a basic fibroblast growth factor or a mixture of several growth factors or cytokines (paragraphs 0009-0010). Clear angiographic separation between the coil mass and parent artery 14 as seen in FIG. 2C, suggesting the development of thickened neointima, was present in 6 of 8 hybrid bioactive treated aneurysms, and in none of the metal coil aneurysms (P<=0.01). For the hybrid bioactive group, mean neointima thickness measured angiographically was 0.28±0.21 mm (mean±SD). For the metal coil group, no significant angiographical separation between coil mass and parent artery was seen (paragraph 0061). Murayama does not specifically identify that device used in the examples is carrying cytokines.
Gao teaches that excessive immune responses following the use of implantable, biomaterial-based medical devices represent a substantial challenge for treatment efficacy and patient wellbeing. Specifically, after implantation, pro-inflammatory M1 macrophages are activated by cytokines such as interferon-g (IFN-g) followed by anti-inflammatory M2 macrophages polarized by cytokines including interleukin-4 (IL-4), leading to healing and long-term stability of implants. Here, we report the loading of an immunomodulatory cytokine,IL-4, into TiO2 nanotubes (TNTs) followed by hydrogel coating on the TNTs for subsequent release of IL-4. Finally, IFN-g was added onto the gel layer to effect rapid release. In vitro testing showed that the sample could stimulate macrophage polarization from the M1 to M2 phenotype at the desired period owing to temporal release of IFN-g and IL-4 (abstract).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have combined the method of neointima formation around a stent of the combined teachings of Nakazaki, Eirin, Yan, Kean, and Lundberg with the biocompatible polymer carrying cytokines of the combined teachings of Murayama and Gao to arrive at the instantly claimed invention. One of ordinary skill in the art would have been motivated to make the combination with a reasonable expectation of success because Murayama teaches that hybrid bioactive coated stents show clear angiographic separation between the coil mass and parent artery, suggesting the development of thickened neointima, was present in 6 of 8 hybrid bioactive treated aneurysms, and in none of the non-coated metal coil aneurysms while Gao teaches that using an implant that produces rapid release IFN-g and delayed release IL-4 after implantation led to pro-inflammatory M1 macrophages being activated by interferon-g (IFN-g) and anti-inflammatory M2 macrophages were polarized by interleukin-4 (IL-4), leading to healing and long-term stability of implants. As such, it would have been obvious to include releasable cytokines as part of a coating around the stents to improve healing and long-term stability of the stents. Because the prior art teaches all of the elements of the claimed invention, there is a reasonable expectation of success.
Claims 1 and 14 are rejected under 35 U.S.C. 103 as being unpatentable over Nakazaki et al. (J Neurosurg 133: 1773-1785. 2020), Eirin et al. (Stem Cells 30: 1030-1041. 2012), Yan et al. (Adv Sci 7: 1-12. 2020), Kean et al. (Stem Cells International 2013: 1-13. 2013), and Lundberg et al. (Cell Transplantation 21: 333–343, 2012), as evidenced by Akyurekli et al. (Stem Cell Rev and Rep 11: 150-160. 2015), as applied to claim 1 above, and further in view of Hwang et al. (Int. J. Mol. Sci. 21: 1-17. 2020). This is a new rejection. Any aspect of Applicant’s traversal that is relevant to the rejection as newly written has been addressed above.
The teachings of Nakazaki, Eirin, Yan, Kean, and Lundberg are as discussed above. Nakazaki teaches that they administered human MSCs to porcine subjects (i.e. xenotransplantation) (page 1774, column 1, paragraph 6-column 2, paragraph 1 and Figure 1).
Nakazaki does not teach wherein allogeneic MSCs were administered.
Eirin teaches that they used allogeneic MSCs (page 1039, column 1, paragraph 3).
Hwang teaches that xenogeneic MSC transplantation elicits an increased immune responses compared to allogenic and autologous MSC transplantation, specifically infiltration of CD45-positive leukocytes. Such immune responses can subsequently not only affect the survival of MSCs but also the therapeutic efficacy of MSCs (page 10, paragraph 3 and Figures 3 and 7).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have substituted the xenogeneic MSCs of Nakazaki with the allogeneic MSCs of Eirin to arrive at the instantly claimed invention. One of ordinary skill in the art would have been motivated to make the substitution with a reasonable expectation of success because Hwang teaches that xenogeneic MSC transplantation can lead to an increased immune response compared to allogeneic transplantations and that this can subsequently not only affect the survival of MSCs but also the therapeutic efficacy of MSCs. Because the prior art teaches all of the elements of the claimed invention, there is a reasonable expectation of success.
Conclusion
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 KEENAN A BATES whose telephone number is (571)270-0727. The examiner can normally be reached M-F 7:30-5:00.
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, Doug Schultz can be reached on (571) 272-0763. 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.
/KEENAN A BATES/Examiner, Art Unit 1631
/JAMES D SCHULTZ/Supervisory Patent Examiner, Art Unit 1631