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 .
Status of Claims
Acknowledgement is made of the receipt and entry of the amendment to the claims filed on May 4, 2026, wherein claims 1, 4-11 and 16 are unchanged; claims 2-3 and 42 are amended; and claims 12-15 and 17-41 are cancelled.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Claims 1-11, 16 and 42 are pending and under examination.
Priority
The instant application 17/424,979 filed on July 22, 2021 is a 371 of PCT/US2020/014531 filed on January 22, 2020, which claims priority to, and the benefits of U.S. Provisional Application No. 62/795,524 filed on January 22, 2019.
Action Summary
Acknowledgement is made of the receipt and entry of the amendment to the specification filed on May 4, 2026, which corrects the typographical error on page 34, paragraph [00119]. Applicant’s amendment to the specification overcome each and every objection previously set forth in the Non-Final Office Action mailed on November 3, 2025.
Applicant’s amendment to claims 2, 3 and 42 overcome each and every objection previously set forth in the Non-Final Office Action mailed on November 3, 2025.
Applicant’s argument with respect to the objection to claims 8-9 have been fully considered and are found persuasive. Therefore, the objection of claims 8-9 have been withdrawn.
Claims 1-8, 16 and 42 rejected under 35 U.S.C. 103 as being unpatentable over Hughes et al. (J Med Genet, 2017. Vol. 54(4): 288-296 and supplemental material), in view of Bikkina et al. (JAMA, 1994. Vol. 272(1): 33-36), as evidenced by Castelli et al. (US 2016/0324839 A1; cited in the previous non-final office action mailed on April 23, 2024) are maintained, but revisited and modified in light of the claim amendments.
Claims 1-9, 16 and 42 rejected under 35 U.S.C. 103 as being unpatentable over Hughes et al. (J Med Genet, 2017. Vol. 54(4): 288-296 and supplemental material), in view of Bikkina et al. (JAMA, 1994. Vol. 272(1): 33-36) as applied to claims 1-8, 16 and 42 above, and further in view of Castelli et al. (US 2016/0324839 A1) are maintained, but revisited and modified in light of the claim amendments.
Claims 1-8, 10-11, 16 and 42 rejected under 35 U.S.C. 103 as being unpatentable over Hughes et al. (J Med Genet, 2017. Vol. 54(4): 288-296 and supplemental material), in view of Bikkina et al. (JAMA, 1994. Vol. 272(1): 33-36) as applied to claims 1-8, 16 and 42 above, and further in view of Germain et al. (N Engl J Med., 2016. Vol. 375(6): 545-55) and Swift et al. (Molecular Genetics and Metabolism, 2018. Vol. 123: S15–S153) are maintained, but revisited and modified in light of the claim amendments.
Claims 1-11, 16 and 42 provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 6-7, 9-13 and 20 of copending Application No. 17/172,846 (reference application) in view of Hughes et al. (J Med Genet, 2017. Vol. 54(4): 288-296 and supplemental material) and Bikkina et al. (JAMA, 1994. Vol. 272(1): 33-36) are maintained, but revisited and modified in light of the claim amendments.
Claims 1-9, 16 and 42 provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 201 and 203-207 of copending Application No. 18/199,120 (the reference application) in view of Hughes et al. (J Med Genet, 2017. Vol. 54(4): 288-296 and supplemental material) and Bikkina et al. (JAMA, 1994. Vol. 272(1): 33-36) are maintained, but revisited and modified in light of the claim amendments, and in light of the fact that the reference application is now an issued U.S. Patent No. 12,599,594 B2 published on April 14, 2026.
Claim Interpretation
The claims recite the term “ERT-experienced patient”, when construed in view of paragraph [0063] of the specification shown below:
PNG
media_image1.png
59
674
media_image1.png
Greyscale
, is taken to refer to a Fabry patient that was receiving ERT immediately prior to initiating migalastat therapy.
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 1-8, 16 and 42 remain rejected under 35 U.S.C. 103 as being unpatentable over Hughes et al. (J Med Genet, 2017. Vol. 54(4): 288-296 and supplemental material), in view of Bikkina et al. (JAMA, 1994. Vol. 272(1): 33-36), as evidenced by Castelli et al. (US 2016/0324839 A1; cited in the previous non-final office action mailed on April 23, 2024).
Hughes et al. teaches oral migalastat, a pharmacological chaperone, is being developed
as an alternative to enzyme replacement therapy (ERT) in the treatment of Fabry disease, which is a X-linked lysosomal storage disorder caused by GLA mutations, resulting in α-galactosidase (α-Gal) deficiency and accumulation of lysosomal subtract (see e.g., abstract; p. 293, left column, “Discussion” section, line 1). Hughes et al. further teaches migalastat stabilizes specific mutant (amenable) forms of α-Gal to facilitate normal lysosomal trafficking (see e.g., abstract). Please note the migalastat taught by Hughes et al. is a migalastat that enhance a-galactosidase A activity in patients with Fabry disease. Hughes et al. further teaches a randomized phase III ATTRACT study that compares the safety and efficacy of migalastat to ERT in male and female patients with Fabry disease and amenable mutation previously treated with ERT (see e.g., p. 289, left column, line1-4); wherein the study comprised an 18-month open-labeled comparison between oral migalastat and enzyme replacement therapy (ERT), followed by a 12-month open-labeled extension with oral migalastat shown below:
PNG
media_image2.png
823
847
media_image2.png
Greyscale
(see e.g., p. 289, left column, 1st paragraph under the “Study design and participants” section; and the title; Figure 1). Hughes et al. further teaches in the 18-month controlled period, patients previously treated with ERT (agalsidase alfa and agalsidase beta) for >12 months were randomized 1.5:1 to switch to migalastat HCl (150 mg every other day) or continue ERT (see e.g., p. 289, left column, 1st paragraph under the “Study design and participants” section). Please note the 150 mg of migalastat HCl taught by Hughes et al. is equivalent to about 123 mg of migalastat in free base, as evidenced by Castelli et al. (see e.g., [0084] and [0108]). Hughes et al. further teaches at baseline, the majority of patients with amenable mutations had multiorgan system disease shown below:
PNG
media_image3.png
441
812
media_image3.png
Greyscale
(see e.g., Table S1; p. 291, left column, line 3-5). Hughes et al. further teaches the percentage of patients who experienced renal, cardiac or cerebrovascular events during the 18-month treatment period was 0% for CBV (TIA) for migalastat and 6% for ERT in Table 4 shown below:
PNG
media_image4.png
534
570
media_image4.png
Greyscale
(see e.g., p. 292, left column, the “Composite clinical outcome assessment” section), wherein the cerebrovascular events includes stroke and transient ischemic attack (TIA) (see e.g., p. 290, left column, “Composite clinical outcome assessment” section). Hughes et al. further teaches the frequency of events noted above indicates that the effect of migalastat compares favorably to ERT in these composite clinical events (see e.g., p. 293, right column, 3rd column). Hughes et al. further teaches in patients switched from ERT to migalastat, left ventricular mass index (LVMi) decreased significantly from baseline over 18 months, and the LVMi changes were largest for patient with left ventricular hypertrophy; and plasma lyso-Gb3 levels remained low and stable in patients with amenable mutations (see e.g., p. 292, “Echocardiography” section and “Plasma lyso-Gb3” section). Hughes et al. further teaches a smaller, nonsignificant change in LVMi was observed in patient who remained on ERT (see e.g., p. 292, left column, “Echocardiography” section) Hughes et al. further teaches the LVMi is determined using echocardiography (see e.g., p. 290, left column, “Echocardiography” section; p. 292, left column, “echocardiography” section). Hughes et al. further teaches migalastat, an oral pharmacological chaperone being developed as an alternative to intravenous enzyme replacement therapy, stabilizes specific mutant (amenable) forms of α-Gal to facilitate normal lysosomal trafficking (see e.g., abstract). Hughes et al. further teaches enrolled patients were required to have responsive mutant α-Gal forms based on a preliminary HEK assay (see e.g., p. 289, “determination of amenability of GLA mutation”). Please note the patients with Fabry disease and amenable mutation, and have responsive mutant α- galactosidase forms based on a preliminary HEK assay taught by Hughes et al. is a patient with HEK
assay amenable mutation in α-galactosidase A as claimed in claim 16.
Bikkina et al. teaches a Framingham Heart Study that evaluates the association of echocardiographically determined left ventricular mass (LVM) with incidence of stroke or transient ischemic attack in an elderly cohort (see e.g., abstract). Bikkina et al. further teaches the echocardiographically determined LVM was associated with risk for cerebrovascular events in men and women; and this increased risk persisted even after adjusting for other risk factors for stroke including age, systolic blood pressure, hypertension treatment, diabetes, cigarette smoking, blood lipid levels, left atrial size, and mitral annular calcification (see e.g., p. 35, right column, “comment” section to p. 35, left column, line 1-2); wherein the cerebrovascular events includes stroke and transient ischemic attack (see e.g., abstract, “results” section). Bikka et al. further teaches the hazard ratio for stroke or transient ischemic attack was 3.08 comparing the highest and lowest quartiles of LVM-to-height ratio (see e.g., p. 35, middle section, “Association of LVM and Outcome” section, 2nd paragraph).
In Summary, Hughes et al. clearly teaches the administration of oral migalastat HCl (150 mg every other day, which is equivalent to about 123 mg of migalastat in free base, as evidenced by Castelli et al.) to the patient with Fabry disease for 18 + 12 months provides favorable results for a composite clinical endpoint of renal, cardiac, and cerebrovascular events (including stroke and transient ischemic attack); and significantly decrease left ventricular mass index. Please note the 18 +12 months taught by Hughes et al., which when calculated by:
18
+
12
=
30
m
o
n
t
h
s
30
m
o
n
t
h
s
÷
12
m
o
n
t
h
s
y
e
a
r
=
2.5
y
e
a
r
s
, gives 2.5 years. Hughes et al. further teaches the patient is previously treated with ERT for >12 month prior to initiating migalastat HCl, and that is an ERT-experienced patient having Fabry disease and a patient received ERT for at least 12 months immediately prior to initiating the administration of the
migalastat or salt thereof. Hughes et al. further teaches the majority of patients had multiorgan system disease at baseline, including central nervous system (CNS) events based on medical history findings (stroke/transient ischemic attack). It would have been prima facie obvious to one of ordinary skill in the art at the time the application was filed to administer oral migalastat HCl at 150 mg every other day (about 123 mg of migalastat in free base) for 2.5 years to an ERT-experienced patient with Fabry disease and a medical history of transient ischemic attack prior to administering the migalastat. One would have been motivated to do so, because Hughes et al. teaches the patient who switched from ERT to the migalastat significantly decrease left ventricular mass index, and has favorable results for a composite clinical endpoint of renal, cardiac, and cerebrovascular events (including stroke and transient ischemic attack) during the 18 month treatment period; and Bikkina et al. teaches increased LVM is associated with higher incidence of cerebrovascular events (including stroke and transient ischemic attack). One would have a reasonable expectation of success to arrive at the claimed invention, because one would have reasonably expected that the administration of oral migalastat HCl at 150 mg every other day (about 123 mg of migalastat in free base) for 2.5 years to an ERT-experienced patient having Fabry disease and a medical history of transient ischemic attack at baseline would have successfully provide a favorable results for the composite clinical endpoint (including cerebrovascular events) and reduce the risk of a cerebrovascular event by decreasing left ventricular mass index of said patient.
Regarding the limitation of “wherein the CBV event is selected from the group consisting of …transient ischemic attack” in claim 2, the claimed limitation simply expresses the intended outcome of the method step positively recited. It would have been prima facie obvious to one of ordinary skill in the art at the time the application was filed to reduce the risk of transient ischemic attack as the cerebrovascular event in the ERT-experienced patient having Fabry disease and a medical history of transient ischemic attack at baseline in the method of Hughes et al. and Bikkina et al. set forth above. One would have been motivated to do so, because Bikkina et al. teaches increased LVM is associated with higher incidence of cerebrovascular events, including transient ischemic attack. One would have a reasonable expectation of success to arrive at the claimed invention, because one would have reasonably expected that the administration of migalastat HCl at 150 mg every other day (about 123 mg of migalastat in free base) for 2.5 years to an ERT-experienced patient having Fabry disease and a medical history of transient ischemic attack at baseline would have successfully reduce the risk of transient ischemic attack as the cerebrovascular event by decreasing left ventricular mass index of said patient.
Regarding the limitation of “wherein the patient has an increased risk of a CBV event prior to initiating the administration of the migalastat or salt thereof” in claim 3, the claimed limitation is drawn to the characteristic of the patient that received the formulation comprising the migalastat. In this case, the patient in the method of Hughes et al. and Bikkina et al. set forth above is a patient with an increased risk of a CBV event prior to initiating the administration of the migalastat HCl, because Hughes et al. teaches 6% of the ERT-experienced patients who did not switch to the migalastat HCl and continue on ERT experienced a CNS event (transient ischemic attack) during the study, and none of the patient who switched from ERT to the migalastat HCl experienced a CNS event; and the patients who did not switched to the migalastat HCI has no change in LVMi. In other words, the fact that the patients who did not switch to migalastat HCl experienced transient ischemic attack during the study demonstrates that the patient who does not switch to the migalastat HCI has an increased risk of transient ischemic attack event, and that is the patient with as increased risk of a CBV event prior to initiating the administration of the migalastat HCl. Therefore, the teachings of Hughes et al. renders obvious the limitation instantly claimed.
Therefore, the claimed invention is prima facie obvious to one of ordinary skill in the art at the time the application was filed, absent factual evidence to the contrary.
Claims 1-9, 16 and 42 remain rejected under 35 U.S.C. 103 as being unpatentable over Hughes et al. (J Med Genet, 2017. Vol. 54(4): 288-296 and supplemental material), in view of Bikkina et al. (JAMA, 1994. Vol. 272(1): 33-36) as applied to claims 1-8, 16 and 42 above, and further in view of Castelli et al. (US 2016/0324839 A1).
Please note Castelli et al. has been cited in the previous Non-Final Office Action mailed on April 23, 2024.
The teachings of Hughes et al. and Bikkina et al. are set forth above and applied as before.
Hughes et al. and Bikkina et al. does not teach a tablet, a capsule or a solution as claimed in claim 9.
Castelli et al. teaches a method of treating Fabry disease in a patient in need thereof, the method comprising administering to the patient a formulation comprising an effective amount of 1-deoxy-galactonojirimycin or salt thereof every other day, wherein the effective amount is about 123 mg free base equivalent (see e.g., claim 14); wherein the patient is administered about 150 mg of migalastat hydrochloride every other day (see e.g., claim 17); wherein the formulation comprises an oral dosage form (see e.g., claim 18); wherein the oral dosage form comprises a tablet, a capsule or a solution (see e.g., claim 19). Castelli et al. further teaches the term “1-deoxygalactonojirimycin” is also known as migalastat (see e.g., [0108]).
The difference between the method of Hughes et al. and Bikkina et al. set forth above and the claimed method is that Hughes et al. and Bikkina et al. does not specifically teach the oral migalastat is a tablet, a capsule, or a solution. It would have been prima facie obvious for one of ordinary skill in the art at the time the application was filed to modify the method of Hughes et al. and Bikkina et al. set forth above to selectively choose to administer the oral migalastat HCI in the form of tablet, capsule or solution as the oral dosage form. One would have been motivated to do so, because Castelli et al. teaches oral migalastat in the form of a tablet, a capsule or a solution are the suitable for treating the patient with Fabry disease. One would have a reasonable expectation of success to arrive at the claimed invention, because one would have reasonably expected that the administration of the oral migalastat HCl in a form of a tablet, a capsule, or a solution to the patient with Fabry disease would successfully treat said patient.
Therefore, the claimed invention is prima facie obvious to one of ordinary skill in the art at the time the application was filed, absent factual evidence to the contrary.
Claims 1-8, 10-11, 16 and 42 remain rejected under 35 U.S.C. 103 as being unpatentable over Hughes et al. (J Med Genet, 2017. Vol. 54(4): 288-296 and supplemental material), in view of Bikkina et al. (JAMA, 1994. Vol. 272(1): 33-36) as applied to claims 1-8, 16 and 42 above, and further in view of Germain et al. (N Engl J Med., 2016. Vol. 375(6): 545-55) and Swift et al. (Molecular Genetics and Metabolism, 2018. Vol. 123: S15–S153).
Please note Germain et al. has been cited in the previous Non-Final Office Action mailed on April 23, 2024.
The teachings of Hughes et al. and Bikkina et al. are set forth above and applied as before.
Hughes et al. and Bikkina et al. does not teach the migalastat or salt thereof is administered for at least 3 years in claim 10. Hughes et al. and Bikkina et al. also does not teach the migalastat or salt thereof is administered for at least 4 years in claim 11.
Germain et al. teaches migalastat may obviate the burden of lifelong administration of enzyme-replacement infusions every 2 weeks and immunogenicity associated with enzyme-replacement therapy (see e.g., p. 546, left column, 3rd paragraph). Germain et al. further teaches the higher volume of distribution of migalastat than of recombinant [Symbol font/0x61]-galactosidase hints at the possibility of better diffusion in organs and tissues (see e.g., p. 546, left column, 3rd paragraph). German et al. further teaches migalastat may better mimic natural enzyme trafficking and result in more consistent [Symbol font/0x61]-galactosidase activity than enzyme-replacement infusions every 2 weeks (see e.g., p. 546, left column). Germain et al. further teaches Fabry’s disease patients who completed the study were eligible to enroll in the open-label study for up to 5 years (see e.g., p. 546, right column, 1st paragraph).
Swift et al. teaches a case report that describes the efficacy of long term migalastat treatment in managing Fabry disease-associated pain in a 47-year-old male patient with an amenable GLA mutation; wherein the patient was treated with migalastat 150 mg every other day for > 10 years. Swift et al. further teaches the migalastat ameliorate Fabry disease-associated pain in this patient, resulting in discontinuation of pain medications and enabling him to resume normal daily activities that were not possible prior to treatment. Swift et al. further teaches no drug related adverse events were observed; and cardiac and renal function remain stable (see e.g., p. S138, left column).
The difference between the method of Hughes et al. and Bikkina et al. set forth above and the claimed method is that the prior art administer the migalastat HCl for 2.5 years and the claimed invention administer the migalastat or salt thereof for at least 3 years or at least 4 years. It would have been prima facie obvious to one of ordinary skill in the art at the time the application was filed to modify the method of Hughes et al. and Bikkina et al. set forth above to extend the treatment duration to include the claimed years through routine experimentation. One would have been motivated to do so, because Germain et al. teaches the migalastat may be an alternative treatment option for the lifelong administration of ERT as it provides more consistent [Symbol font/0x61]-galactosidase activity, and suggests that the current study enrolled eligible patients for up to 5 years; and Swift et al. teaches the patient with Fabry disease treated with migalastat greater than 10 years successfully ameliorate Fabry disease-associated pain with no drug-related adverse events. One would have a reasonable expectation of success to arrive at the claimed invention through routine experimentation, because one would have reasonably expected that by extending the treatment duration of the oral migalastat starting from 2.5 years to up to 5 years as suggested by Bikkina et al. would successfully provide more consistent [Symbol font/0x61]-galactosidase activity compared to ERT as well as ameliorating Fabry-disease associated pain.
Therefore, the claimed invention is prima facie obvious to one of ordinary skill in the art at the time the application was filed, absent factual evidence to the contrary.
Response to Arguments
Applicant's arguments filed on May 4, 2026 have been fully considered.
Applicant's arguments filed on May 4, 2026 with respect to the rejection of claims 1-8, 16 and 42 under 35 U.S.C. 103 as being unpatentable over Hughes et al. (J Med Genet, 2017. Vol. 54(4): 288-296 and supplemental material), in view of Bikkina et al. (JAMA, 1994. Vol. 272(1): 33-36), as evidenced by Castelli et al. (US 2016/0324839 A1); the rejection of claims 1-9, 16 and 42 under 35 U.S.C. 103 as being unpatentable over Hughes et al., in view of Bikkina et al. as applied to claims 1-8, 16 and 42 above, and further in view of Castelli et al. (US 2016/0324839 A1); and the rejection of claims 1-8, 10-11, 16 and 42 under 35 U.S.C. 103 as being unpatentable over Hughes et al., in view of Bikkina et al. as applied to claims 1-8, 16 and 42 above, and further in view of Germain et al. (N Engl J Med., 2016. Vol. 375(6): 545-55) and Swift et al. (Molecular Genetics and Metabolism, 2018. Vol. 123: S15–S153) have been fully considered but they are not persuasive.
In this case, Applicant amends claim 2-3 and 42; and therefore, the rejection of record has been revisited and modified in light of the claim amendments.
In Summary, applicant argues there is no evidence in Hughes et al. that the claimed patient population was treated with migalastat. Specifically, applicant argues that even though Hughes et al. teaches 17/23 males and 12/33 females had a medical history of a CNS event, this is not synonymous with a CBV event as used in the present application. Applicant argues the “CNS events” described in Table S1 of Hughes et al. includes stroke/TIA as well as tinnitus/hearing loos, and therefore, the term CNS as used in Hughes is broader than the term CBV even as used in the present application; and there is no indication in Hughes et al. which patients had which CNS events. Applicant further argues it is uncertain whether the patients enrolled in the 12-month open-labeled extension with oral migalastat (see Figure 1 of Hughes et al.) includes any patients with a history of stroke/TIA because these patient could have been those that decline to participate in said extension. Applicant further argues none of Bikkina, Castelli, Germain or Swift teaches the administration of migalastat to the claimed patient population. Applicant further argues the teachings of Bikkina et al. is not relevant to the claimed invention, because the patient taught by Bikkina is elderly patients rather than patients with Fabry disease and evaluation is based on the LVM-to-height ratio rather than LVM alone; therefore, one would not make any conclusion on the treatment of Fabry disease with migalastat based on the study of Bikkina et al.
In response, Applicant’s arguments are not found persuasive for the reasons set forth below:
First, applicant’s argument with respect to the “CNS events” described in the baseline assessment/Table S1 of Hughes et al. is not found persuasive, because the rejection of record does not rely merely on the numerical values reported in Table S1 or Hughes et al. Rather, the rejection of record relies on the reference's express description of the baseline assessment criteria(s) immediately below Table S1, which states: "CNS involvement was based on medical history findings (Stroke/TIA, tinnitus/hearing loss).". Thus, the reference expressly identifies stroke/TIA as one of the medial history findings used to classify patients having CNS involvement at baseline. A person of ordinary skill in the art would have reasonably understood from this disclosure that the enrolled study population included patients whose medical histories included prior stroke and/or TIA. Although the reference does not separately report the exact number of patient within each CNS subgroup (e.g., TIA.), such numerical stratification is not required to establish what the reference teaches. The absence of a separate breakdown of stroke/TIA versus tinnitus/hearing loss does not negate the reference’s disclosure that stroke/TIA formed part of the baseline medical history criteria for CNS involvements.
Second, applicant’s argument with respect to the numerical numbers described in Figure 1 of Hughes et al. is not found persuasive, because the rejection of record also does not rely merely on the numerical values reported in Figure 1 or Hughes et al. Rather, the rejection of record relies on the reference's express description of Fabry disease patients who had prior enzyme replacement therapy (ERT) can enrolled in the 18 + 12 month study, in which the 18-month study compares the efficacy and safety of switching to migalastat versus continuing ERT, and the 12-month extension study continued or transitioned to migalastat for an additional 12 months. In other words, the reference not only expressly identifies stroke/TIA as one of the medial history findings used to classify patients having CNS involvement at baseline as noted above, the reference also expressly teach the patients can be treated with 18 + 12 month of oral migalastat, which is equivalent to 2.5 years (see calculation noted in the rejection above). A person of ordinary skill in the art would have reasonably understood from this disclosure that the enrolled study population included patients whose medical histories included prior stroke and/or TIA, and are treated with migalastat for 18 + 12 month.
According to MPEP 2143.02, “[c]onclusive proof of efficacy is not required to show a reasonable expectation of success. OSI Pharm., LLC v. Apotex Inc., 939 F.3d 1375, 1385, 2019 USPQ2d 379681 (Fed. Cir. 2019) ("To be clear, we do not hold today that efficacy data is always required for a reasonable expectation of success. Nor are we requiring ‘absolute predictability of success.’"); Acorda Therapeutics, Inc. v. Roxane Lab., Inc., 903 F.3d 1310, 1333, 128 USPQ2d 1001, 1018 (Fed. Cir. 2018)”. Applying the same logic to instant process case, the exact number of patients with stroke and/or TIA enrolled in the subsequent 12 month extension study is not required to show a reasonable expectation of success. If applicant contends that the method made obvious by the prior art cannot reduce the risk of cerebrovascular event in an ERT-experience patient having Fabry disease, said objective evidence is respectfully request.
In addition, applicant’s argument towards Bikkina, Castelli, Germain and Swift, respectively, are 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). For instance, applicant argues none of Bikkina, Castelli, Germain or Swift teaches the administration of migalastat to the claimed patient population; However, the rejection of record is formed using the combination of references, rather than each reference individually. It is respectfully noted that the rejection of record rely on Hughes et al. to established the administration of oral migalastat to Fabry disease patients who were previously treated with ERT for >12 months and those with medical histories of prior stroke and/or TIA.
In response to applicant’s argument that the teachings of Bikkina et al. is irrelevant, because Bikkina et al. uses elderly patients and the evaluation is based on LVM-to-height ratio rather than LVM alone. Again, the rejection of record does not rely on Bikkina et al. alone to teach the claimed invention. In this case, the rejection of record is form on the basis that Hughes et al. teaches Fabry disease patients (previously treated with ERT for >12 months) who switched from ERT to oral migalastat significantly decrease left ventricular mass (LVM) index, and has favorable results for a composite clinical endpoint of renal, cardiac, and cerebrovascular events (including stroke and transient ischemic attack) during the 18 month treatment period; and the rejection further rely on Bikkina et al. to teach increased LVM is associated with higher incidence of cerebrovascular events (including stroke and transient ischemic attack). A person of ordinary skill in the art would have reasonably understood that the Fabry disease patients of Hughes et al. prior to switching to migalastat has relatively higher left ventricular mass index, and they are associated with higher incidence of cerebrovascular events, including stroke and transient ischemic attack; and therefore, one of ordinary skill in the art would have understood the reduction in left ventricular mass index and the favorable composite clinical endpoint taught by Hughes et al. reduces the risk of cerebrovascular event. In addition, there mere fact that Bikkina et al. evaluates the association of echocardiographically determined left ventricular mass (LVM) with incidence of stroke or transient ischemic attack using the LVM-to-height ratio does not negate the fact that high left ventricular mass is associated with an increased risk of stroke.
Therefore, applicant’s argument are not found persuasive for the reasons set forth herein.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1-11, 16 and 42 remain provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 6-7, 9-13 and 20 of copending Application No. 17/172,846 (reference application) in view of Hughes et al. (J Med Genet, 2017. Vol. 54(4): 288-296 and supplemental material) and Bikkina et al. (JAMA, 1994. Vol. 272(1): 33-36).
The claims of the reference application are drawn to a method of reducing the risk of composite clinical outcomes comprising, inter alia, cerebrovascular events in an ERT-experienced female patient having Fabry disease, the method comprising administering to the female patient a formulation comprising an effective amount of migalastat or salt thereof every other day for at least 18 months, wherein the effective amount is about 100 mg to about 150 free base equivalent (FBE); wherein the cerebrovascular events comprises one or more of stroke or transient ischemic attack (see claim 1); wherein the migalastat or salt thereof enhances α-galactosidase A activity (see claim 6); wherein the female patient is administered about 123 mg FBE of the migalastat or salt thereof every other day (see claim 7); wherein the female patient is administered about 150 mg of migalastat hydrochloride every other day (see claim 9); wherein the formulation comprises an oral dosage form (see claim 10); wherein the oral dosage form comprises a tablet, a capsule, or a solution (see claim 11); wherein the migalastat or salt thereof is administered for at least 3 years (see claim 12); wherein the migalastat or salt thereof is administered for at least 4 years (see claim 13); wherein the female patient has a HEK assay amenable mutation in α-galactosidase A (see claim 20).
The claims of the reference application does not teach the patient had a first CBV even prior to initiation the administration of the migalastat or salt thereof.
Hughes et al. teaches a randomized phase III ATTRACT study that compares the safety and efficacy of migalastat to ERT in male and female patients with Fabry disease and amenable mutation previously treated with ERT (see e.g., p. 289, left column, line1-4); wherein the study comprised an 18-month open-labeled comparison between oral migalastat and enzyme replacement therapy (ERT), followed by a 12-month open-labeled extension with oral migalastat (see e.g., p. 289, left column, 1st paragraph under the “Study design and participants” section; and the title; Figure 1). Hughes et al. further teaches in the 18-month controlled period, patients previously treated with ERT (agalsidase alfa and agalsidase beta) for >12 months were randomized 1.5:1 to switch to migalastat HCl (150 mg every other day) or continue ERT (see e.g., p. 289, left column, 1st paragraph under the “Study design and participants” section). Hughes et al. further teaches at baseline, the majority of patients with amenable mutations had multiorgan system disease shown below:
PNG
media_image3.png
441
812
media_image3.png
Greyscale
(see e.g., Table S1; p. 291, left column, line 3-5). Hughes et al. further teaches the percentage of patients who experienced renal, cardiac or cerebrovascular events during the 18-month treatment period was 0% for CBV (TIA) for migalastat and 6% for ERT in Table 4 (see e.g., p. 292, left column, the “Composite clinical outcome assessment” section), wherein the cerebrovascular events includes stroke and transient ischemic attack (TIA) (see e.g., p. 290, left column, “Composite clinical outcome assessment” section). Hughes et al. further teaches the frequency of events noted above indicates that the effect of migalastat compares favorably to ERT in these composite clinical events (see e.g., p. 293, right column, 3rd column). Hughes et al. further teaches in patients switched from ERT to migalastat, left ventricular mass index (LVMi) decreased significantly from baseline over 18 months, and the LVMi changes were largest for patient with left ventricular hypertrophy; and plasma lyso-Gb3 levels remained low and stable in patients with amenable mutations (see e.g., p. 292, “Echocardiography” section and “Plasma lyso-Gb3” section).
Bikkina et al. teaches a Framingham Heart Study that evaluates the association of echocardiographically determined left ventricular mass (LVM) with incidence of stroke or transient ischemic attack in an elderly cohort (see e.g., abstract). Bikkina et al. further teaches the echocardiographically determined LVM was associated with risk for cerebrovascular events in men and women; and this increased risk persisted even after adjusting for other risk factors for stroke including age, systolic blood pressure, hypertension treatment, diabetes, cigarette smoking, blood lipid levels, left atrial size, and mitral annular calcification (see e.g., p. 35, right column, “comment” section to p. 35, left column, line 1-2); wherein the cerebrovascular events includes stroke and transient ischemic attack (see e.g., abstract, “results” section). Bikka et al. further teaches the hazard ratio for stroke or transient ischemic attack was 3.08 comparing the highest and lowest quartiles of LVM-to-height ratio (see e.g., p. 35, middle section, “Association of LVM and Outcome” section, 2nd paragraph).
In Summary, the claims of the reference application are also drawn to a method of reducing the risk of stroke or transient ischemic attack as the composite clinical outcome of cerebrovascular events in an ERT-experienced female patient having Fabry disease comprising administering to the female patient a formulation comprising an effective amount of migalastat or salt thereof every other day for at least 18 months, wherein the effective amount is about 100 mg to about 150 mg free base equivalent (FBE). The difference between the claims of the reference application and the claimed invention is that the reference application does not teach the ERT-experienced patient had a first CBV event prior to initiating the administration of the migalastat or salt thereof. It would have been prima facie obvious to one of ordinary skill in the art at the time the application was filed to modify the method of the reference application to administer the migalastat for 2.5 years, and then incorporate an ERT-experienced patient with Fabry disease and a medical history of transient ischemic attack prior to administering the migalastat. One would have been motivated to do so, because Hughes et al. teaches in the 18+12 month study, the patient who switched from ERT to the migalastat significantly decrease left ventricular mass index, and has favorable results for a composite clinical endpoint of renal, cardiac, and cerebrovascular events (including stroke and transient ischemic attack) during the 18 month treatment period; and Bikkina et al. teaches increased LVM is associated with higher incidence of cerebrovascular events (including stroke and transient ischemic attack). One would have a reasonable expectation of success to arrive at the claimed invention, because one would have reasonably expected that the administration of migalastat at about 100 mg to about 150 free base equivalent (FBE) for at least 18 months to an ERT-experienced patient having Fabry disease and a medical history of transient ischemic attack at baseline would have successfully provide a favorable results for the composite clinical endpoint (including cerebrovascular events) and reduce the risk of a cerebrovascular event by decreasing left ventricular mass index of said patient.
In the case where the claimed ranges "overlap or lie inside ranges disclosed by the prior art" a prima facie case of obviousness exists. In re Wertheim, 541 F.2d 257, 191 USPQ 90 (CCPA 1976); In re Woodruff, 919 F.2d 1575, 16 USPQ2d 1934 (Fed. Cir. 1990). In this case, the claims of the reference application clearly teaches the administration of the migalastat or salt thereof every other day for at least 18 months, at least 3 years, or at least 4 years, and each of these overlap with the treatment duration instantly claimed.
Therefore, this is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Response to Arguments
Applicant’s arguments filed on May 4, 2026 with respect to the provisional rejection of claims 1-11, 16 and 42 on the ground of nonstatutory double patenting as being unpatentable over claims 1, 6-7, 9-13 and 20 of copending Application No. 17/172,846 (reference application) in view of Hughes et al. (J Med Genet, 2017. Vol. 54(4): 288-296 and supplemental material) and Bikkina et al. (JAMA, 1994. Vol. 272(1): 33-36) have been fully considered but they are not persuasive.
In Summary, applicant argues the arguments toward the rejection(s) under 35 U.S.C. 103 are set forth above and applied as before.
In response, applicant’s arguments against the rejection under 35 U.S.C. 103 are addressed above and applied as before. Given that Applicant's arguments over the rejection(s) under 35 U.S.C. 103 is not found persuasive, the provisional rejection has been maintained, but revisited and modified in light of the claim amendments for the same reasons of record and the reasons set forth herein.
Claims 1-19, 16 and 42 remain rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 of U.S. Patent No. 12,599,594 B2 in view of Hughes et al. (J Med Genet, 2017. Vol. 54(4): 288-296 and supplemental material) and Bikkina et al. (JAMA, 1994. Vol. 272(1): 33-36).
Please note this nonstatutory double patenting rejection is the same as the provisional nonstatutory double patenting rejection over copending Application No. 18/199,120 as set forth in the
previous office action. Since the copending application is now an issued U.S. Patent No. 12,599,594 B2
published on April 14, 2026, and do not have the same claim numbers, this nonstatutory double
patenting rejection has been revisited and modified in light of the issued patent; However, this rejection should be interpretated as being the same as corresponding to the previous provisional nonstatutory double patenting rejection of record.
The claims of the reference patent is drawn to a method of reducing left ventricular mass index (LVMi) in an enzyme replacement therapy (ERT) experienced human patient having Fabry disease, the method comprising administering to the patient a formulation comprising an effective amount of 1-deoxygalactonojirimycin or salt thereof every other day, wherein the effective amount is about 123 mg free base equivalent (FBE) and wherein the patient has left ventricular hypertrophy (LVH) prior to initiating administration of the 1-deoxygalactonojirimycin or salt thereof (see claim 1); wherein the 1-deoxygalactonojirimycin or salt thereof enhances-galactosidase A activity (see claim 2); wherein the patient is administered about 123 mg of 1-deoxygalactonojirimycin every other day (see claim 3); wherein the patient is administered about 150 mg of migalastat hydrochloride every other day (see claim 4); the formulation comprises an oral dosage form (see claim 5); the oral dosage form comprises a tablet, a capsule or a solution (see claim 6). Please note the 1-deoxygalactonojirimycin taught by the reference patent is a migalastat according to paragraph [0077] of the instant specification.
The claims of the reference patent does not teach the migalastat or salt thereof is administered for at least 2 years. The claims of the reference patent also does not teach the patient had a first CBV even prior to initiation the administration of the migalastat or salt thereof. The claims of the reference patent also does not teach the migalastat or salt thereof reduce the risk of a cerebrovascular event. The claims of the reference patent also does not teach the patient has a HEK assay amenable mutation in [Symbol font/0x61]-galactosidase A.
Hughes et al. teaches a randomized phase III ATTRACT study that compares the safety and efficacy of migalastat to ERT in male and female patients with Fabry disease and amenable mutation previously treated with ERT (see e.g., p. 289, left column, line1-4); wherein the study comprised an 18-month open-labeled comparison between oral migalastat and enzyme replacement therapy (ERT), followed by a 12-month open-labeled extension with oral migalastat (see e.g., p. 289, left column, 1st paragraph under the “Study design and participants” section; and the title; Figure 1). Hughes et al. further teaches in the 18-month controlled period, patients previously treated with ERT (agalsidase alfa and agalsidase beta) for >12 months were randomized 1.5:1 to switch to migalastat HCl (150 mg every other day) or continue ERT (see e.g., p. 289, left column, 1st paragraph under the “Study design and participants” section). Hughes et al. further teaches at baseline, the majority of patients with amenable mutations had multiorgan system disease shown below:
PNG
media_image3.png
441
812
media_image3.png
Greyscale
(see e.g., Table S1; p. 291, left column, line 3-5). Hughes et al. further teaches the percentage of patients who experienced renal, cardiac or cerebrovascular events during the 18-month treatment period was 0% for CBV (TIA) for migalastat and 6% for ERT in Table 4 (see e.g., p. 292, left column, the “Composite clinical outcome assessment” section), wherein the cerebrovascular events includes stroke and transient ischemic attack (TIA) (see e.g., p. 290, left column, “Composite clinical outcome assessment” section). Hughes et al. further teaches the frequency of events noted above indicates that the effect of migalastat compares favorably to ERT in these composite clinical events (see e.g., p. 293, right column, 3rd column). Hughes et al. further teaches in patients switched from ERT to migalastat, left ventricular mass index (LVMi) decreased significantly from baseline over 18 months, and the LVMi changes were largest for patient with left ventricular hypertrophy; and plasma lyso-Gb3 levels remained low and stable in patients with amenable mutations (see e.g., p. 292, “Echocardiography” section and “Plasma lyso-Gb3” section). Hughes et al. further teaches enrolled patients were required to have responsive mutant α-Gal forms based on a preliminary HEK assay (see e.g., p. 289, “determination of amenability of GLA mutation”).
Bikkina et al. teaches a Framingham Heart Study that evaluates the association of echocardiographically determined left ventricular mass (LVM) with incidence of stroke or transient ischemic attack in an elderly cohort (see e.g., abstract). Bikkina et al. further teaches the echocardiographically determined LVM was associated with risk for cerebrovascular events in men and women; and this increased risk persisted even after adjusting for other risk factors for stroke including age, systolic blood pressure, hypertension treatment, diabetes, cigarette smoking, blood lipid levels, left atrial size, and mitral annular calcification (see e.g., p. 35, right column, “comment” section to p. 35, left column, line 1-2); wherein the cerebrovascular events includes stroke and transient ischemic attack (see e.g., abstract, “results” section). Bikka et al. further teaches the hazard ratio for stroke or transient ischemic attack was 3.08 comparing the highest and lowest quartiles of LVM-to-height ratio (see e.g., p. 35, middle section, “Association of LVM and Outcome” section, 2nd paragraph).
In Summary, the claims of the reference patent are also drawn to a method of reducing LVMi in an ERT-experienced female patient having Fabry disease comprising administering to the patient a formulation comprising an effective amount of 1-deoxygalactonojirimycin or salt thereof (equivalent to the claimed migalastat or salt thereof) every other day, wherein the effective amount is about 100 mg to about 150 mg free base equivalent (FBE). The difference between the claims of the reference patent and the claimed invention is that the reference patent does not teach the ERT-experienced patient had a first CBV event prior to initiating the administration of the migalastat or salt thereof; and does not teach the migalastat is administered for at least 2 years for reducing the risk of a cerebrovascular event. It would have been prima facie obvious to one of ordinary skill in the art at the time the application was filed to modify the method of the reference patent to incorporate an ERT-experienced patient with Fabry disease and a medical history of transient ischemic attack prior to administering the migalastat, and then administer the migalastat for 2.5 years for reducing the risk of a cerebrovascular event. One would have been motivated to do so, because Hughes et al. teaches in the 18+12 month study of migalastat (equivalent to 2.5 years), the patient who switched from ERT to the migalastat significantly decrease left ventricular mass index, and has favorable results for a composite clinical endpoint of renal, cardiac, and cerebrovascular events (including stroke and transient ischemic attack) during the 18 month treatment period; and Bikkina et al. teaches increased LVM is associated with higher incidence of cerebrovascular events (including stroke and transient ischemic attack). One would have a reasonable expectation of success to arrive at the claimed invention, because one would have reasonably expected that the administration of the migalastat for 2.5 years to an ERT-experienced patient having Fabry disease and a medical history of transient ischemic attack at baseline would have successfully provide a favorable results for the composite clinical endpoint (including cerebrovascular events) and reduce the risk of a cerebrovascular event by decreasing left ventricular mass index of said patient.
Regarding the limitation of “wherein the patient has a HEK assay amenable mutation in α- galactosidase A” in claim 16, it would have been prima facie obvious to one of ordinary skill in the art to further modify the method of the reference patent, Hughes et al. and Bikkina et al. set forth above to incorporate a patient with amenable mutation in α- galactosidase A based on a HEK assay. One would have been motivated to do so, because Hughes et al. teaches the patients with Fabry disease treated with migalastat is required to have responsive mutant α- galactosidase forms based on a preliminary HEK assay. One would have a reasonable expectation of success to arrive at the claimed invention, because one would have reasonably expected that the patient with an amenable mutation in α- galactosidase A based on a HEK assay would successfully response to the migalastat treatment.
Response to Arguments
Applicant’s arguments filed on May 4, 2026 with respect to the provisional rejection of claims 1-9, 16 and 42 on the ground of nonstatutory double patenting as being unpatentable over claims 201 and 203-207 of copending Application No. 18/199,120 (the reference application) in view of Hughes et al. (J Med Genet, 2017. Vol. 54(4): 288-296 and supplemental material) and Bikkina et al. (JAMA, 1994. Vol. 272(1): 33-36) have been fully considered, but they are not persuasive.
In Summary, applicant argues the arguments toward the rejection(s) under 35 U.S.C. 103 are set forth above and applied as before.
In response, applicant’s argument is not found persuasive. First of all, the Examiner noted that the ‘120 application is now an issued U.S. Patent No. 12,599,594 B2 published on April 14, 2026, which
does not have the same claim numbers. Therefore, the rejection of record has been amended in view of the issued patent. In addition, applicant’s arguments against the rejection under 35 U.S.C. 103 are addressed above and applied as before. Given that applicant's arguments over the rejection(s) under 35 U.S.C. 103 is not found persuasive, the provisional rejection has been maintained, but revisited and modified in light of the claim amendments and in light of the issued patent for the reasons set forth herein. It is respectfully noted that this nonstatutory double patenting rejection over U.S. Patent No. 12,599,594 B2, in view of Hughes et al. and Bikkina et al. should be interpretated as being the same as corresponding to the provisional nonstatutory double patenting rejection sets forth in the Non-Final Office Action mailed on November 3, 2025.
Conclusion
No claims are allowed.
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 Chihyi Lee whose telephone number is (571)270-0663. The examiner can normally be reached Monday - Friday 8:30 am - 5:00 pm EST.
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, Amy L. Clark can be reached at (571) 272-1310. 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.
/CHIHYI LEE/Examiner, Art Unit 1628 /JEAN P CORNET/Primary Examiner, Art Unit 1628
Prosecution Insights