DETAILED ACTION
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 .
Claims Status
Claims 1-20 are pending and are under current examination.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION. —The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claim 10 and 11 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 10 recites the limitation " said angiogenic factors" in claim 8. There is insufficient antecedent basis for this limitation. Claim 8 does not recite “angiogenic factors”. Therefore, it is unclear which angiogenic factors claim 10 is referring to.
Claim 11, recited “enhanced regenerative activity”. There is insufficient antecedent basis for this. Claim 11 is dependent on claim 1 where “augmenting regenerative activity” is recited, but not “enhanced regenerative activity”. Therefore, it is not clear which “enhanced regenerative activity” claim 11 is referring to.
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claim 4 rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Claim 3 recites the limitation of regenerative activity to angiogenesis which is defined in the specification as “characterized by the protrusion and outgrowth of capillary buds and sprouts from pre-existing blood vessels” (paragraph 0047). This is interpreted to read on creation of new blood vessels. Claim 4 recites the limitation “angiogenesis comprises creation of new blood vessels” (page 1, claims). In light of this there doesn’t appear to be a difference in scope between claims 3 and 4. Therefore, claim 4 which is dependent on claim 3, fails to further limit claim 3.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Claim interpretation:
The terms ‘augmenting’ and ‘regenerative activity’ are not defined in the specification therefore the broadest possible interpretations of the terms were derived from the teachings provided by the specification. The term ‘augmenting’ is interpreted as ‘enhancing’ and the ‘regenerative activity is interpreted as the differentiation, survival, proliferation, immune modulation and angiogenesis potential of the MSCs consistent with the teachings of the specification.
Claims 12-20 recite an intended use of “utilized to treat an ischemic condition”. This intended does not carry patentable weight. The phrase “utilized to treat an ischemic condition” has been treated as “capable of” language.
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.
Claim 1 is rejected under 35 U.S.C. 103 as being unpatentable over Horwitz, Edwin M., et al. "Isolated allogeneic bone marrow-derived mesenchymal cells engraft and stimulate growth in children with osteogenesis imperfecta: Implications for cell therapy of bone." Proceedings of the National Academy of Sciences 99.13 (2002): 8932-8937 in view of Elabd, Christian, et al. "Oxytocin controls differentiation of human mesenchymal stem cells and reverses osteoporosis." Stem cells 26.9 (2008): 2399-2407.
Regarding Clam 1, Horwitz, 2002 teaches a method of obtaining a bone marrow mononuclear cell (MNC) population/aspirate (in Methods section, pages 8932-8933) and administrating the said mononuclear cell population into a human subject (in Methods section, pages 8932-8933) to stimulate bone growth in children with osteogenesis imperfecta.
Horwitz does not teach administering a concentration of oxytocin (OT) to a subject which is capable of enhancing the regenerative activity of the said MNC. However, methods of administering OT to augment regenerative activity of bone marrow MNC/aspirates were known in the art prior to the effective filing date of the invention as evidenced by Elabd et al.
Elabd et al. teaches the safe subcutaneous administration of OT into mice that were subjected to either bilateral ovariectomy (OVX) or sham surgery (control group) to reverse osteoporosis which is induced by ovariectomy in the experimental group (Methods section, under the heading ‘Animals’, page 2401, discussion, last paragraph, page 2405). Injecting OT into OVX mice, an animal model of osteoporosis reduced the marrow adiposity and restored the bone biomechanical properties (Conclusion, page 2405, figure 5, page 2404), which is interpreted to read on augmenting regenerative activity.
Elabd et al. further illustrate that the observed reversal of osteoporosis in OVX mice was due to OT stimulation of the mesenchymal stem cells in a transcriptomic analysis. They identified the oxytocin receptor pathway as a potential regulator of the osteoblast/adipocyte balance in human multipotent adipose-derived stem cells (hMADS) and human bone marrow mesenchymal stromal cells by regulating their differentiation. Where in dysregulation of osteoblast/adipocyte balance is considered a major cause for osteoporosis (Abstract, page 2399, figure 2, page 2402).
Therefore, it will be obvious to a person of ordinary skill in the art before the effective filing date of the claimed invention to utilize the above-mentioned teachings of Horwitz that teaches obtaining a bone marrow MNC population and administering it into a human subject and modify it with the teachings of Elabd to administer OT into the same subject at a concentration capable of enhancing the regenerative activity of the bone marrow MNCs. One of ordinary skill in the art would have been motivated to co-administer MNCs with OT to enhance the regenerative activity of the MNCs. There would be a reasonable expectation of success in administering MNCs with OT, because the enhanced regenerative activity of MNCs with OT administration is taught by Elabd with successful reversal of osteoporosis in OVX mice with OT injections.
Regarding claims 12-20, the intended use of treating ischemia has not been given patentable weight as noted in the claim interpretation section above. Further, the phrase “utilized to treat an ischemic condition” has been treated as “capable of” language.
Claims 2, and 5-20 are rejected under 35 U.S.C. 103 as being unpatentable over Horwitz and Elabd as applied to claim 1 above, and further in view of Noiseux, Nicolas, et al. "Preconditioning of stem cells by oxytocin to improve their therapeutic potential." Endocrinology 153.11 (2012): 5361-5372.
The teachings of Horwitz and Elabd are relied on above.
Horwitz and Elabd do not teach the regenerative activity of MNCs that comprise the generation of endothelial cells (as recited in claim 2) and angiogenesis (claim 3).
Regarding Claims 2, Noiseux teaches that preconditioning mesenchymal stem cells (MSCs) with OT enhance their therapeutic potential. OT treatment stimulated MSCs differentiation into vascular cells which include endothelial cells (background section, page 5362, paragraph 1) and Noiseux shows a significant increase in angiogenic markers in MSCs after OT treatment, detected in the culture conditioned medium (abstract, secreted factor by MSC in the results section, page 5368, Table 1, page 5370).
Regarding claim 5, Noiseux teaches OT administration enhances the MSC protection from apoptosis in both normoxic and hypoxic conditions. The study shows that OT administration stimulates the PI3K/Akt and ERK1/2 pathway which is a key transducer of antiapoptotic signaling in MSCs. (Results section, cell survival under serum starvation and hypoxic stress is improved by OT, page 5367, abstract, page 5361, table 1, page 5370, Discussion Paragraph 2, page 5369).
Regarding claim 6, Noiseux teaches that OT treatment may optimize host vasculature milieu and enhance healing by altering cellular response to ischemia, and priming MSCs with OT enhanced the cardiac repair in ischemia/reperfusion injury in a rat model (Background, paragraph 2, page 5362).
Regarding claim 7, Noiseux teaches that OT administration enhances the production of growth factors in MSCs (abstract, secreted factors by MSC in results section, page 5368, table 1, page 5370).
Regarding claim 8, Noiseux teaches that OT treatment causes MSC to produce growth factors that are capable of stimulating angiogenesis (abstract, secreted factors by MSC in results section, page 5368, table 1, page 5370).
Regarding claim 9, Noiseux teaches the growth factors capable of stimulating angiogenesis such as BDNF, bFGF, VEGF, VEGF-C (abstract, secreted factors by MSC in results section, page 5368, table 1, page 5370).
Regarding claim 10, Noiseux teaches the “angiogenic factors” produced by MSCs when stimulated with OT such as TIMPs and MMPs (abstract, secreted factors by MSC in results section, page 5368, table 1, page 5370).
Regarding claim 11, Noiseux teaches the increased expression of genes that enhance regenerative activity of MSC upon OT administration such as integrin alpha M and integrin beta 2 (table 1, page 5370). Regarding claims 12, Noiseux teaches that OT treatment enhanced the MSC’s potential for cardiac repair in a rat model of cardiac ischemia/reperfusion injury, in which the fibrosis was reduced and the cardiac function was improved when OT primed MSCs were transplanted into rat ischemic heart. They further teach that OT plays a supportive role in optimizing host vasculature milieu to promote healing by altering cell responses to ischemia. (Introduction, page 5362, paragraph 1).
Regarding claim 13, Noiseux teaches OT treatment enhanced the MSC’s potential for cardiac repair in a rat model of cardiac ischemia/reperfusion injury, in which the fibrosis was reduced and the cardiac function was improved when OT primed MSCs were transplanted into rat ischemic heart. (Introduction, page 5362, paragraph 1).
Regarding claim 14, Noiseux teaches that OT treatment enhanced the MSC’s potential for cardiac repair in a rat model of cardiac ischemia/reperfusion injury, in which the fibrosis was reduced and the cardiac function was improved when OT primed MSCs were transplanted into rat ischemic heart. (Introduction, page 5362, paragraph 1). The claim limitations disclose the intended use of the method of claim 1 to treat myocardial ischemia caused by various ailments, such as hypertension, coronary artery disease, etc. These various ailments are not known to cause clinically distinguishable forms of myocardial ischemias. Therefore, the method of treatment taught in Noiseux to treat myocardial ischemia was considered as prior art in the claim analysis, regardless of the cause.
Therefore, it will be obvious to a person of ordinary skill in the art before the effective filing date of the claimed invention to utilize the above-mentioned teachings of Horwitz that teaches obtaining a bone marrow MNC population and administering it into a human subject and modify it with the teachings of Elabd to administer OT into the same subject at a concentration capable of enhancing the regenerative activity of MNCs and further modify their teachings with Noiseux that teaches the enhanced differentiation, proliferation, immune modulation, production of angiogenic markers and reduced apoptosis to increase the therapeutic potential of MSCs upon OT treatment (abstract, Table 1 page 5370, and section secreted factors by MSC, page 5368). One of ordinary skill in the art would have been motivated to combine the teachings of Howitz, Elabd and Noiseux to co-administer MSCs with OT to enhance the regenerative activity of MSCs to achieve endothelial cell generation, increase the production of angiogenic markers and formulate an effective treatment for ischemia including myocardial ischemia. There would be a reasonable expectation of success in administering MNCs with OT, because MSCs and OT co-administration is taught by Noiseux to improve regenerative activity of MSCS and to treat myocardial ischemia.
Regarding claims 12-20, the intended use of “utilized to treat an ischemic condition” has not been given patentable weight as noted in the claim interpretation section above. Further, the phrase “utilized to treat an ischemic condition” has been treated as “capable of” language. Given the the combined teachings of Horwitz, Elabd and Noiseux it is understood that administration of MSCs and OT is capable of treating an ischemic condition.
Claims 3- 4 is rejected under 35 U.S.C. 103 as being unpatentable over Horwitz and Elabd as applied to claims 1-2 and 5-15 above, and further in view of Kim, Yong Sook, et al. "Restoration of angiogenic capacity of diabetes-insulted mesenchymal stem cells by oxytocin." BMC Cell Biology 14.1 (2013): 38.
Teaching of Howitz and Elabd are relied on above.
Howitz and Elabd do not teach the creation of blood vessels.
Claim 3 is interpreted to read on creation of blood vessels. See 112d rejection above.
Regarding claim 4, Kim et al. teaches the improved vascular tube formation upon OT treatment in diabetes mellitus (DM) induced mouse model. Diabetes is known to impair the angiogenic capacity of MSCs. When the cultures of bone-marrow MSCs derived from DM mice (DM-MSC) were pre-treated with OT, the disease associated malformation of vascular tubes was restored. (figure 2, page 4, section under the heading tube formation and KLF2 are reduced in DM-MSC and recovered by oxytocin in the results section, page 2). Also, OT- pre-treated and untreated DM-MSCs were cultured on Matrigel, and was later extracted as Matrigel plugs, and subcutaneously injected into athymic nude mice. The injected Matrigel plugs were harvested two weeks later to examine the effect of oxytocin on neovascularization. The results showed a significant improvement on red blood cell containing vascular area in the oxytocin treated assay compared to untreated DM-MSC (figure 4, page 6, section with heading “Impaired angiogenic capacity of DM-MSC is restored by oxytocin”, page 3).
Therefore, it will be obvious to a person of ordinary skill in the art before the effective filing date of the claimed invention to utilize the above-mentioned teachings of Horwitz that teaches obtaining a bone marrow MNC population and administering it into a human subject and modify it with the teachings of Elabd, to administer OT into the same subject at a concentration capable of enhancing the regenerative activity of MNCs, and further modify it with Kim which teaches the blood vessel formation capability of MSCs upon OT treatment. One of ordinary skill in the art would have been motivated to co-administer MSCs and OT in order to improve angiogenesis in disease conditions. There would be a reasonable expectation of success to achieve sufficient blood vessel formation with MSC and OT treatment, because it is taught by Kim et al.
Claim 15 is rejected under 35 U.S.C. 103 as being unpatentable over Horwitz, Elabd and Noiseux as applied to claims 1-2 and 5-14 above, and further in view of, Cunningham, Catriona J. "The therapeutic potential of the mesenchymal stem cell secretome in ischaemic stroke." Journal of Cerebral Blood Flow & Metabolism 38.8 (2018): 1276-1292.
Howitz, Elabd and Noiseux are relied on above.
Howitz, Elabd and Noiseux do not teach treating cerebral ischemia.
Regarding claim 15, Cunningham teaches the potential of MSCs as a regenerative therapy for cerebral ischemia. Cunningham teaches the paracrine action of MSCs, and the current approaches that drive the MSC secretome towards enhancing MSc’s therapeutic potential to improve recovery in preclinical models of cerebral ischemia (abstract, page 1276). The study also teaches OT priming of MSCs to obtain “trained” cells which are better able to respond to ischemic events including cerebral ischemia (Figure 1, page 1278, Molecular priming, page 1277).
Therefore, it will be obvious to a person of ordinary skill in the art before the effective filing date of the claimed invention to utilize the above-mentioned teachings of Horwitz that teaches obtaining a bone marrow MNC population and administering it into a human subject and modify it with the teachings of Elabd, to administer OT into the same subject at a concentration capable of enhancing the regenerative activity of the said MNCs and Noiseux, that further teaches the benefit of co-administering OT with MSC to enhance the regenerative potential of the treatment, and Cunningham that teaches the treatment of cerebral ischemia with MSCs. One of ordinary skill in the art would have been motivated to modify the teachings of Cunningham with the teachings of Howitz, Elabd and Noiseux to co-administer MSCs with OT in order to formulate a more effective treatment for cerebral ischemia. There would be a reasonable expectation of success in administering MNCs with OT to treat cerebral ischemia, because Noiseux teaches the successful treatment of myocardial ischemia with OT and MSCs.
Claims 16-17 are rejected under 35 U.S.C. 103 as being unpatentable over Horwitz, Elabd and Noiseux as applied to claims 1-2 and 5-14, discussed above, and further in view of, Oliva, Joan. "Therapeutic properties of mesenchymal stem cell on organ ischemia-reperfusion injury." International journal of molecular sciences 20.21 (2019): 5511.
Howitz, Elabd and Noiseux are relied on above.
Howitz, Elabd and Noiseux do not teach treatments for renal and liver ischemias. Regarding claim 16, Oliva teaches the use of therapeutic properties of MSCs on organ ischemia/reperfusion injuries. As described in this review, various animal studies have shown the efficacy of bone marrow derived-MSC (BMSC) in treating renal ischemia. The intravenous injection of BMSCs after in vivo ischemia has shown to minimize acute kidney injury, while lowering the serum creatinine and urea levels, the markers of kidney malfunction (abstract, page 1, 2.2 kidney treatment page 2).
Regarding claim 17, Oliva teaches injection of BMSC into an artery to reduce liver damage due to ischemia/reperfusion injury. Decreased apoptosis, inflammation and liver damage was seen after the treatment. (2.3 liver treatment, page 3).
Therefore, it will be obvious to a person of ordinary skill in the art before the effective filing date of the claimed invention to utilize the above-mentioned of Horwitz that teaches obtaining a bone marrow MNC population and administering it into a human subject and modify it with the teachings of Elabd, to administer OT into the same subject and Noiseux, that further teaches the increase in regenerative activity of MSCs upon OT treatment, and Oliva that teaches the treatment of renal and liver ischemia with MSCs. One of ordinary skill in the art would have been motivated to modify the teachings of Oliva with the teachings of Howitz, Elabd and Noiseux to co-administer MSCs with OT in order to formulate an effective treatment for renal and liver ischemia. There would be a reasonable expectation of success in administering MNCs with OT to treat renal and liver ischemia, because Noiseux teaches the successful treatment of myocardial ischemia with MSCs and OT.
Claim 18 is rejected under 35 U.S.C. 103 as being unpatentable over Horwitz, Elabd and Noiseux as applied to claims 1-2 and 5-14 above, and further in view of, Liew, Aaron, and Timothy O'Brien. "Therapeutic potential for mesenchymal stem cell transplantation in critical limb ischemia." Stem cell research & therapy 3.4 (2012): 28.
Regarding claim 18, Liew teaches the use of MSCs to treat limb ischemia. Skeletal muscles of the limbs are interpreted as the peripheral muscles in the claim analysis. The study teaches the myogenic potential of the MSCs and clinical trial data of the treatment (myogenic differentiation, page 4). Intravenous administration of bone-marrow derived MSCs were used in clinical trial to treat a patient with gangrene (ischemic condition) in upper and lower limbs. Revascularization of the extremities and a reduction in the necrotic area of the patient was seen after the treatment (Clinical data section, page 6).
Therefore, it will be obvious to a person of ordinary skill in the art before the effective filing date of the claimed invention to utilize the above-mentioned teachings of Horwitz that teaches obtaining a bone marrow MNC population and administering it into a human subject and modify it with the teachings of Elabd, to administer OT into the same subject at a concentration capable of enhancing the regenerative activity of the said MNCs and Noiseux, that further teaches the benefit of co-administering OT with MSC to enhance the regenerative potential of the treatment, and Liew that teaches the treatment of limb ischemia with MSCs which is a type of peripheral muscle ischemia. One of ordinary skill in the art would have been motivated to modify the teachings of Liew with the teachings of Howitz, Elabd and Noiseux to co-administer MSCs with OT in order to formulate a more effective treatment for peripheral muscle ischemia. There would be a reasonable expectation of success in administering MNCs with OT to treat renal and liver ischemia, because Noiseux teaches the successful treatment of myocardial ischemia with MSCs and OT.
Claim 19 is rejected under 35 U.S.C. 103 as being unpatentable over Horwitz, Elabd and Noiseux as applied to claims 1-2 and 5-14 above, and further in view of, Mathew, Biji, et al. "Bone-marrow mesenchymal stem-cell administration significantly improves outcome after retinal ischemia in rats." Graefe's Archive for Clinical and Experimental Ophthalmology 255.8 (2017): 1581-1592.
Regarding claim 19, Mathew teaches treatment of retinal ischemia with bone marrow MSCs in rats. Intravitreal delivery of MSCs significantly improved the recovery after retinal ischemia with reduced apoptosis, inflammation and diminished retinal vascular permeability (abstract, page 1581).
Therefore, it will be obvious to a person of ordinary skill in the art before the effective filing date of the claimed invention to utilize the above-mentioned teachings of Horwitz that teaches obtaining a bone marrow MNC population and administering it into a human subject and modify it with the teachings of Elabd, to administer OT into the same subject at a concentration capable of enhancing the regenerative activity of the said MNCs and Noiseux, that further teaches the benefit of co-administering OT with MSC to enhance the regenerative potential of the treatment while Mathew teaches the treatment of retinal ischemia with bone marrow MSC. One of ordinary skill in the art would have been motivated to modify the teachings of Mathew with the teachings of Howitz, Elabd and Noiseux to co-administer MSCs with OT in order to formulate a more effective treatment for retinal ischemia. There would be a reasonable expectation of success in administering MNCs with OT to treat retinal ischemia, because Noiseux teaches the successful treatment of myocardial ischemia with MSCs and OT.
Claim 20 is rejected under 35 U.S.C. 103 as being unpatentable over Horwitz, Elabd and Noiseux as applied to claims 1-2 and 5-14 above, and further in view of, Takahashi, Shinya, et al. "Mesenchymal stem cell-based therapy improves lower limb movement after spinal cord ischemia in rats." The Annals of Thoracic Surgery 105.5 (2018): 1523-1530.
Regarding claim 20, Takahashi teaches treatment of spinal cord ischemia in rats with MSCs. Induced spinal cord ischemia was treated with either MSCs or PBS via injection in to the left carotid artery. Injected MSCs were found in the spinal cord after 24 hrs. They observed the hind limb function to assess the efficacy of the treatment which showed significant improvement in the MSC treatment group over PBS group (abstract, page 1523).
Therefore, it will be obvious to a person of ordinary skill in the art before the effective filing date of the claimed invention to utilize the above-mentioned teachings of Horwitz that teaches obtaining bone marrow MNC population and administering it into a human subject and modify it with the teachings of Elabd, to administer OT into the same subject and Noiseux, that further teaches the co-administration of OT with MSC to enhance the regenerative potential of MNCs, and Takahashi that teaches the treatment of spinal cord ischemia with MSCs. One of ordinary skill in the art would have been motivated to modify the teachings of Cunningham with the teachings of Howitz, Elabd and Noiseux to co-administer MSCs with OT in order to formulate a more effective treatment for spinal cord ischemia. There would be a reasonable expectation of success in administering MNCs with OT to treat spinal cord ischemia, because Noiseux teaches the successful treatment of myocardial ischemia with MSCs and OT.
Conclusion
No claim is allowed.
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/HASHANTHI KOMITIGE ABEYRATNE-PERERA/Examiner, Art Unit 1632
/PETER PARAS JR/Supervisory Patent Examiner, Art Unit 1632