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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 03/16/2026 has been entered.
Response to Amendment
The amendments received 03/16/2026 have been entered. Claims 166, 170-175, 185, and 189-190 are pending. Claims 185 and 189-190 remain withdrawn.
Priority
Examiner acknowledges that, according to the Filing receipt received 05/10/2024, that the
instant application 18/479,396 filed 10/02/2023 is a CON of 17/269,890 filed 02/19/2021 which is a 371
of PCT/US2019/013761 filed 01/16/2019 which claims benefit of U.S. provisional application 62/719,962
filed 08/20/2018.
However, the limitations of the instant claims are not adequately supported or enabled in the
manner provided by 35 U.S.C. 112(a) or pre-AIA U.S.C. 112, first paragraph by 62/719,962. More
specifically, the limitations of an α-galactosidase A mutation selected from the group consisting of:
V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, 1239M, A257V, P259Q, N320H, P323T,
E338V, P380L, and T412P are not taught or suggested in their entirety by 62/719,962. As such, all the
instant claims have been awarded the effective filing date of PCT/US2019/013761 filed 01/16/2019.
Claim Rejections - 35 USC § 102/103
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 the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
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(s) 166 and 170-175 is/are rejected under 35 U.S.C. 102(a)(1) as anticipated by or, in the alternative, under 35 U.S.C. 103 as obvious over GALAFOLD (U.S. Food and Drug Administration; August 2018).
GALAFOLD teaches the treatment of Fabry disease in adults by administering GALAFOLD (migalastat) at a dose of 123 mg orally once every other day (p. 2, section 2-3). GALAFOLD further discloses that 123 mg of migalastat is equivalent to 150 mg migalastat hydrochloride (p. 6, section 11). GALAFOLD discloses that migalastat can be administered to both male and female patients and demonstrates no pharmacokinetic differences, and has been administered to both male and female patients with amenable α-galactosidase mutations in clinical trials (p. 21, 22; Table 3, p. 23). GALAFOLD discloses amenable α-galactosidase variants of individuals with Fabry disease that can be treated with migalastat, which include: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P (Table 2, pgs. 8-19).
It is clear that subjects with Fabry disease, male or female, with α-galactosidase variants V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P may be treated with 123 mg migalastat, or 150 mg migalastat hydrochloride. However, if this showing is insufficient under 35 U.S.C. 102, these limitations are obvious under 35 U.S.C. 103.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to try, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease as set forth in a defined list of alternatives.
It would have been prima facie obvious for one of ordinary skill in the art to try to administer migalastat to a patient that is male or female. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that migalastat has been effectively administered in both male and female patients and demonstrates no pharmacokinetic differences.
Claim(s) 166 and 170-175 is/are rejected under 35 U.S.C. 102(a)(1) as anticipated by or, in the alternative, under 35 U.S.C. 103 as obvious over GALAFOLD (European Medicines Agency; 14 August 2018).
GALAFOLD teaches the treatment of Fabry disease in adults by administering GALAFOLD (migalastat) at a dose equivalent of 123 mg orally once every other day (p. 2, section 4.2). GALAFOLD further discloses that the capsule contains 150 mg migalastat hydrochloride (p. 30, section 5.2). GALAFOLD discloses that migalastat can be administered to both male and female patients and demonstrates no pharmacokinetic differences, and has been administered to both male and female patients with amenable α-galactosidase mutations in clinical trials (p. 28-29,31). GALAFOLD discloses amenable α-galactosidase variants of individuals with Fabry disease that can be treated with migalastat, which include: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P (Table 2, pgs. 8-19).
It is clear that subjects with Fabry disease, male or female, with α-galactosidase variants V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P may be treated with 123 mg migalastat, or 150 mg migalastat hydrochloride. However, if this showing is insufficient under 35 U.S.C. 102, these limitations are obvious under 35 U.S.C. 103.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to try, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease as set forth in a defined list of alternatives.
It would have been prima facie obvious for one of ordinary skill in the art to try to administer migalastat to a patient that is male or female. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that migalastat has been effectively administered in both male and female patients and demonstrates no pharmacokinetic differences.
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 166 and 170-173 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4, and 6-7 of copending Application No. 17/618,277 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims are drawn to a method of treating Fabry disease in a patient having renal impairment, wherein the patient has an HEK assay amenable α-galactosidase A mutation.
In looking to the specification to construe the scope of “amenable” α-galactosidase A mutations, Table 1 (p. 20-70) provides a description of amenable α-galactosidase A mutations determined by HEK assay, which includes V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. The aforementioned mutations are therefore within the scope of the claimed invention.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 166, 170-173, and 175 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim 31 and 38-41 of copending Application No. 17/838,820 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims are drawn to a method of treating Fabry disease in a female patient of childbearing potential comprising administering migalastat.
In looking to the specification to construe the scope of “patient”, Table 1 (p. 16-25) provides a description of amenable α-galactosidase A mutations determined by HEK assay, which includes V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. The aforementioned mutations are therefore within the scope of the claimed invention.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 166 and 170-173 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 8-10 of copending Application No. 18/315,928 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims are drawn to a method of increasing the bioavailability of migalastat in a patient.
In looking to the specification to construe the scope of “patient”, Table 1 (p. 19-50) provides a description of amenable α-galactosidase A mutations determined by HEK assay, which includes V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. The aforementioned mutations are therefore within the scope of the claimed invention.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 166 and 170-173 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 11 of copending Application No. 18/578,483 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims are drawn to a method of treating Fabry disease in a pediatric patient comprising administering migalastat.
In looking to the specification to construe the scope of “patient”, Table 1 (p. 18-50) provides a description of amenable α-galactosidase A mutations determined by HEK assay, which includes V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. The aforementioned mutations are therefore within the scope of the claimed invention.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 166 and 170-175 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3, 6, and 10-11 of copending Application No. 17/269,890 (now U.S. patent 12594268). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims are drawn to a method of treating Fabry disease in a patient comprising administering migalastat.
In looking to the specification to construe the scope of “patient”, Table 1 (p. 22--50) provides a description of novel amenable α-galactosidase A mutations determined by HEK assay, which includes V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. The aforementioned mutations are therefore within the scope of the claimed invention as a patient could also be carrying these mutations.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 166 and 170-173 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 8, and 10-11 of copending Application No. 18/069,732 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1, 8, and 10-11 of Application No. 18/069,732 are set forth below.
A method of treating Fabry disease, the method comprising administering migalastat to a patient in need thereof, wherein the patient has an α -galactosidase A protein comprising a HEK assay amenable mutation selected from the group consisting of: D55G, H125Y, Q157H, L166S, N215I, K240N, G261R, L275V, N278Y, W287L, K308E and P343T.
8. The method of claim 1, wherein the migalastat or salt thereof is administered to the patient every other day.
10. The method of claim 1, wherein the patient is administered about 150 mg of the migalastat or salt thereof every other day.
11. The method of claim 1, wherein the patient is administered about 150 mg of migalastat hydrochloride every other day.
Claim 1 does not teach that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
This is a provisional nonstatutory double patenting rejection.
Claims 166 and 170-173 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3 and 6 of copending Application No. 17/909,450 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1-3 and 6 of Application No. 17/909,450 are presented below.
1. A method for treatment of Fabry disease in a human patient in need thereof, the method comprising administering to the patient a therapeutically effective dose of migalastat or a salt thereof, wherein the patient has an u-galactosidase A mutation selected from the group consisting of: A29D, R38S, N53Y, Y88C, V124G, I133F, A143V, Y152N, F159C, A160D, D165N, F1691, L180V, D182G, R196T, W209R, A257T, P259S, G271A, S276T, M290V, A291S, I303T, I303V, L310V, G360A, G360R, G375A, L394P, G41 iS, and N419D.
2. The method of claim 1, wherein the migalastat or salt thereof is administered to the patient every other day.
3. The method of claim 1, wherein the patient is administered about 100 to about 150 mg free base equivalent of the migalastat or salt thereof every other day.
6. The method of claim 1, wherein the patient is administered about 150 mg of migalastat hydrochloride every other day.
Claim 1 does not teach that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
This is a provisional nonstatutory double patenting rejection.
Claims 166 and 170-173 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 16 of copending Application No. 17/424,979 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 19 of Application No. 17/424,979 are set forth below.
1. A method of reducing the risk of a cerebrovascular (CBV) event in a patient having Fabry disease, the method comprising administering to the patient a formulation comprising an effective amount of migalastat or salt thereof every other day for at least 2 years, wherein the effective amount is about 100 mg to about 150 mg free base equivalent (FBE).
16. The method of claim 1, wherein the patient has a HEK assay amenable mutation in a-galactosidase A.
Claim 1 does not teach a method of treating Fabry disease. Claim 16 does not teach that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, it would be reasonably understood by one of ordinary skill in the art that treatment of Fabry disease would occur regardless of the length of treatment, and that reduction of a CBV event in a patient with Fabry disease would inherently occur in a patient being treated for Fabry disease with migalastat.
This is a provisional nonstatutory double patenting rejection.
Claims 166 and 170-173 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 20 of copending Application No. 17/172,846 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 20 of Application No. 17/172,846 are shown below.
1. A method of reducing the risk of composite clinical outcomes (CCO) comprising renal events, cardiac events, cerebrovascular events and death 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 mg free base equivalent (FBE).
20. The method of claim 1, wherein the female patient has a HEK assay amenable mutation in a-galactosidase A.
Claim 1 does not teach the treatment of Fabry disease. Claim 20 does not teach that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, it would be reasonably understood by one of ordinary skill in the art that treatment of Fabry disease would occur regardless of the length of treatment, and that reduction of the risk of CCO events in a patient with Fabry disease would inherently occur in a patient being treated for Fabry disease with migalastat.
This is a provisional nonstatutory double patenting rejection.
Claims 166, 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 12-15 of U.S. Patent No. 11,357,784 B2. Although the claims at issue are not identical, they are not patentably distinct from each other because the claims are drawn to a method of treating Fabry disease in a pregnant patient comprising administering migalastat.
In looking to the specification to construe the scope of “patient”, Table 1 (cols. 12-21) provides a description of amenable α-galactosidase A mutations determined by HEK assay, which includes V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. The aforementioned mutations are therefore within the scope of the claimed invention.
Claims 166 and 170 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 3 of U.S. Patent No. 11,833,164 B2. Although the claims at issue are not identical, they are not patentably distinct from each other because the claims are drawn to a method of treating Fabry disease in a patient comprising administering migalastat to the patient, wherein the patient is identified to have two or more mutations selected from a list of α-galactosidase A mutations that include V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. The aforementioned mutations are therefore within the scope of the claimed invention.
Claims 166 and 170-175 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 15-20 of U.S. Patent No. 12,109,205 B2 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 15-20 of the ‘205 patent are directed toward a method of treating Fabry disease in a patient with renal impairment.
Claim 1 does not teach that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
This is a provisional nonstatutory double patenting rejection.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 15, and 18 of U.S. Patent No. 11,666,564 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1, 15, and 18 of U.S Patent No. 11,666,564 are below.
1. A method of treating Fabry disease, the method comprising administering migalastat to a patient in need thereof, wherein the patient has an a -galactosidase A protein comprising a HEK assay amenable mutation selected from the group consisting of A13T, A15T, W24R, N34T, M42K, L54F, P60T, P60S, E87D, L89F, R112G, Y123C, H125L, I133M, K140T, F145S, P146R, Y152H, D165G, p.M187_S188dup, V199G, M208R, I219L, Q221P, N224T, Q250R, G261C, G271D, W277G, W277C, M284V, R301L, I303F, S304N, D322N, G325R, K326N, G334E, E358Q, E358D, G361E, G375E, T412N and M421V.
15. The method of claim 1, wherein the migalastat or salt thereof is administered to the patient every other day.
18. The method of claim 1, wherein the patient is administered about 150 mg of migalastat hydrochloride every other day.
Claim 1 does not teach that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3, and 6 of U.S. Patent No. 11,389,437 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1, 3, and 6 of U.S. Patent No. 11,389,437 are below.
1. A method of treating a Fabry patient, the method comprising administering migalastat to a Fabry patient having an α-galactosidase A protein comprising a HEK assay amenable mutation selected from the group consisting of D33G, L36W, Q57L, M96I, R112G, C174R, M187I, I253S, G258R, G271S/D313Y, D313Y, D322E, G325R, and R356Q.
3. The method of claim 1, wherein the migalastat or salt thereof is administered to the patient every other day.
6. The method of claim 1, wherein the patient is administered about 150 mg of migalastat hydrochloride every other day.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 6-7 of U.S. Patent No. 11,357,763 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 6-7 of U.S. Patent No. 11,357,763 are set forth below.
1. A method of treating Fabry disease in an ERT-experienced female patient with normal renal function with an eGFR of at least 90 mL/min/1.73 m.sup.2 and with a HEK assay amenable mutation in α-galactosidase A, the method comprising administering to the patient about 100 mg to about 150 mg free base equivalent (FBE) of migalastat at a frequency of once every other day.
6. The method of claim 1, comprising administering about 123 mg FBE of migalastat at a frequency of every other day.
7. The method of claim 6, comprising administering about 150 mg of migalastat hydrochloride at a frequency of every other day.
Claim 1 does not teach that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would recognize that treatment of Fabry disease would occur in a patient with Fabry disease regardless of specific parameters of the patient population.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 16 of U.S. Patent No. 11,278,537 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 16 of U.S. Patent No. 11,278,537 are set forth below.
1. A method of stabilizing renal function in a Fabry patient with moderate or severe renal impairment with an eGFR less than 60 mL/min/1.73 m2 and with a HEK assay amenable α-galactosidase A mutation, the method comprising: administering to the patient about 100 mg to about 150 mg free base equivalent (FBE) of migalastat at a frequency of once every other day, wherein the administration is effective to (i) increase the mean white blood cell (WBC) α-galactosidase A activity in the patient, and (ii) provide a mean annualized rate of change in eGFRCKD-EPI of greater than −1.0 mL/min/1.73 m2.
16. The method of claim 1, comprising administering about 150 mg of migalastat hydrochloride.
Claim 1 does not teach that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would recognize that treatment of Fabry disease would occur in a patient with Fabry disease regardless of specific parameters of the patient population.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 16 of U.S. Patent No. 11,357,761 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 16 of U.S. Patent No. 11,357,761 are delineated below.
1. A method of treating Fabry disease in a human patient in need thereof, the method comprising administering to the patient a therapeutically effective dose of migalastat or salt thereof at a frequency of once every other day, wherein the therapeutically effective dose is about 100 mg to about 150 mg free base equivalent (FBE), and wherein the patient has a mutation in α-galactosidase A that has been determined to be HEK assay amenable and that has been determined to be disease-causing, wherein the patient is an enzyme replacement therapy (ERT)-experienced patient.
16. The method of claim 1, wherein the therapeutically effective dose is about 150 mg of migalastat hydrochloride.
Claim 1 does not teach that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would recognize that treatment of Fabry disease would occur in a patient with Fabry disease regardless of specific parameters of the patient population.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 16 of U.S. Patent No. 11,278,538 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 16 of U.S. Patent No. 11,278,538 are set forth below.
1. A method of stabilizing renal function in a Fabry patient with moderate or severe renal impairment with an eGFR less than 60 mL/min/1.73 m2 and with a HEK assay amenable α-galactosidase A mutation, the method comprising: administering to the patient about 100 mg to about 150 mg free base equivalent (FBE) of migalastat at a frequency of once every other day, wherein the administration is effective to (i) reduce mean globotriaosylceramide (GL-3) accumulated in an organ of the patient, (ii) reduce mean plasma globotriaosylsphingosine (lyso-Gb3) in the patient, and (iii) stabilize mean renal function in the patient.
16. The method of claim 1, comprising administering about 150 mg of migalastat hydrochloride.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the method of stabilization of renal function in a Fabry patient would inherently occur alongside treatment of Fabry disease in a Fabry patient.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 16 of U.S. Patent No. 11,278,540 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 16 of U.S. Patent No. 11,278,540 are delineated below.
1. A method of stabilizing renal function in a Fabry patient with moderate or severe renal impairment with an eGFR less than 60 mL/min/1.73 m2 and with a HEK assay amenable α-galactosidase A mutation, the method comprising: administering to the patient about 100 mg to about 150 mg free base equivalent (FBE) of migalastat at a frequency of once every other day, wherein the administration is effective to (i) reduce left ventricular mass index (LVMi) in the patient, and (ii) provide a mean annualized rate of change in eGFRCKD-EPI of greater than −1.0 mL/min/1.73 m2.
16. The method of claim 1, comprising administering about 150 mg of migalastat hydrochloride.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the method of stabilization of renal function in a Fabry patient would inherently occur alongside treatment of Fabry disease in a Fabry patient.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim1 and 16 of U.S. Patent No. 11,278,539 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
Claims 1 and 16 of U.S. Patent No. 11,278,539 are delineated below.
1. A method of stabilizing renal function in a Fabry patient with moderate or severe renal impairment with an eGFR less than 60 mL/min/1.73 m2 and with a HEK assay amenable α-galactosidase A mutation, the method comprising: administering to the patient about 100 mg to about 150 mg free base equivalent (FBE) of migalastat at a frequency of once every other day, wherein the administration is effective to (i) reduce mean globotriaosylceramide (GL-3) accumulated in an organ of the patient, (ii) reduce mean plasma globotriaosylsphingosine (lyso-Gb3) in the patient, (iii) increase mean white blood cell (WBC) α-galactosidase A activity in the patient, (iv) reduce mean left ventricular mass index (LVMi) in the patient and (v) stabilize mean renal function in the patient.
16. The method of claim 1, comprising administering about 150 mg of migalastat hydrochloride.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the method of stabilization of renal function in a Fabry patient would inherently occur alongside treatment of Fabry disease in a Fabry patient.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 16 of U.S. Patent No. 11,278,536 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 16 of U.S. Patent No. 11,178,536 are set forth below.
1. A method of stabilizing renal function in a Fabry patient with moderate or severe renal impairment with an eGFR less than 60 mL/min/1.73 m2 and with a HEK assay amenable α-galactosidase A mutation, the method comprising: administering to the patient about 100 mg to about 150 mg free base equivalent (FBE) of migalastat at a frequency of once every other day, wherein the administration is effective to (i) reduce a mean plasma globotriaosylsphingosine (lyso-Gb3) in the patient, and (ii) provide a mean annualized rate of change in eGFRCKD-EPI of greater than −1.0 mL/min/1.73 m2.
16. The method of claim 1, comprising administering about 150 mg of migalastat hydrochloride.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the method of stabilization of renal function in a Fabry patient would inherently occur alongside treatment of Fabry disease in a Fabry patient.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 17 of U.S. Patent No. 11,357,762 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 17 of U.S. Patent No. 11,357,762 read as follows.
1. A method of stabilizing renal function in a Fabry patient with moderate or severe renal impairment with an eGFR less than 60 mL/min/1.73 m2 and with a HEK assay amenable α-galactosidase A mutation, the method comprising: administering to the patient about 100 mg to about 150 mg free base equivalent (FBE) of migalastat at a frequency of once every other day, wherein the administration is effective to (i) reduce globotriaosylceramide (GL-3) accumulated in the patient's organs, and (ii) provide a mean annualized rate of change in eGFRCKD-EPI of greater than −1.0 mL/min/1.73 m2, wherein the organs comprise the kidney, heart, and optionally the liver.
17. The method of claim 1, comprising administering about 150 mg of migalastat hydrochloride.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the method of stabilization of renal function in a Fabry patient would inherently occur alongside treatment of Fabry disease in a Fabry patient.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 13, and 16 of U.S. Patent No. 11,633,388 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1, 13, and 16 of U.S. Patent No. 11,633,388 are as follows.
1. A method of treating Fabry disease, the method comprising administering migalastat to a patient in need thereof, wherein the patient has an α-galactosidase A protein comprising a HEK assay amenable mutation selected from the group consisting of: A13P, A20D, Q57L, G80D, P146S, D175E, K213R, K213M, I242F, M267T, A309V, V316I, V316G, P323R, A352G, R356P, T385A, V390M, and G395A.
13. The method of claim 1, wherein the migalastat or salt thereof is administered to the patient every other day.
16. The method of claim 1, wherein the patient is administered about 150 mg of migalastat hydrochloride every other day.
Claim 1 does not teach that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 8, and 11 of U.S. Patent No. 11,642,334 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1, 8, and 11 of U.S. Patent No. 11,642,334 are set forth below.
1. A method of treating Fabry disease, the method comprising administering migalastat to a patient in need thereof, wherein the patient has an α-galactosidase A protein comprising a HEK assay amenable mutation selected from the group consisting of: D55G, H125Y, Q157H, L166S, N215I, K240N, G261R, L275V, N278Y, W287L, K308E and P343T.
8. The method of claim 1, wherein the migalastat or salt thereof is administered to the patient every other day.
11. The method of claim 1, wherein the patient is administered about 150 mg of migalastat hydrochloride every other day.
Claim 1 does not teach that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 15 of U.S. Patent No. 10,874,656 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 15 of U.S. Patent No. 10,874,656 are as follows.
1. A method of stabilizing renal function in enzyme replacement therapy (ERT)-experienced patients diagnosed with Fabry disease and having renal impairment, the method comprising: administering to a group of Fabry disease patients having renal impairment and a HEK assay amenable α-galactosidase A mutation, about 100 mg to about 150 mg free base equivalent (FBE) of migalastat at a frequency of once every other day, wherein the administration is effective to (i) increase the mean white blood cell (WBC) α-galactosidase A activity in the patients, and (ii) provide a mean annualized rate of change in eGFRCKD-EPI of greater than −1.0 mL/min/1.73 m2.
15. The method of claim 1, comprising administering about 150 mg of migalastat hydrochloride.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the method of stabilization of renal function in a Fabry patient would inherently occur alongside treatment of Fabry disease in a Fabry patient and would be effective regardless of specific parameters of the patient population with Fabry disease.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 12 of U.S. Patent No. 10,792,279 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 12 of U.S. Patent No. 10,792,279 are as follows.
1. A method of stabilizing renal function in enzyme replacement therapy (ERT)-experienced patients diagnosed with Fabry disease and having mild renal impairment with an eGFR of 60 to 90 mL/min/1.73 m2, the method comprising: administering, to a group of Fabry disease patients having mild renal impairment and a HEK assay amenable α-galactosidase A mutation, about 100 mg to about 150 mg free base equivalent (FBE) of migalastat at a frequency of once every other day; wherein the administration is effective to (i) reduce mean globotriaosylceramide (GL-3) accumulated in an organ of the patients, (ii) reduce mean plasma globotriaosylsphingosine (lyso-Gb3) in the patients, (iii) increase mean white blood cell (WBC) α-galactosidase A activity in the patients, (iv) reduce mean left ventricular mass index (LVMi) in the patients, and (v) stabilize mean renal function in the patients; and wherein administration of a single dose of the migalastat to the patients is effective to provide (i) a mean plasma migalastat increase in AUC 0 of about 1.2-fold compared to healthy control subjects, and (ii) no increase in mean plasma migalastat Cmax compared to healthy control subjects.
12. The method of claim 7, comprising orally administering about 150 mg of migalastat hydrochloride for at least 28 days, wherein the migalastat hydrochloride is in solid dosage form.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the method of stabilization of renal function in a Fabry patient would inherently occur alongside treatment of Fabry disease in a Fabry patient and would be effective regardless of specific parameters of the patient population with Fabry disease, the dosage form of migalastat, or the length of treatment.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 7 of U.S. Patent No. 10,849,890 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 7 of U.S. Patent No. 10,849,890 are as follows.
1. A method of stabilizing renal function in enzyme replacement therapy (ERT)-experienced patients diagnosed with Fabry disease and having mild renal impairment with an eGFR of 60 to 90 mL/min/1.73 m2, the method comprising: administering to, a group of Fabry disease patients having mild renal impairment and a HEK assay amenable α-galactosidase A mutation, about 100 mg to about 150 mg free base equivalent (FBE) of migalastat at a frequency of once every other day; wherein the administration is effective to (i) reduce mean globotriaosylceramide (GL-3) accumulated in organs of the patients, (ii) reduce mean plasma globotriaosylsphingosine (lyso-Gb3) in the patients, and (iii) stabilize mean renal function in the patients; and wherein administration of a single dose of the migalastat to the patients is effective to provide (i) a mean plasma migalastat increase in AUC 0 by about 1.2-fold compared to healthy control subjects, and (ii) no increase in mean plasma migalastat Cmax compared to health control subjects.
7. The method of claim 2, comprising orally administering the migalastat as a salt comprising about 150 mg of migalastat hydrochloride for at least 28 days, wherein the migalastat hydrochloride is in solid dosage form.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the method of stabilization of renal function in a Fabry patient would inherently occur alongside treatment of Fabry disease in a Fabry patient and would be effective regardless of specific parameters of the patient population with Fabry disease, the dosage form of migalastat, or the length of treatment.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 14 of U.S. Patent No. 10,792,278 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 14 of U.S. Patent No. 10,792,278 are delineated below.
1. A method of stabilizing renal function in a patient diagnosed with Fabry disease and having severe renal impairment with an eGFR less than 30 mL/min/1.73 m2, the method comprising: administering to the patient about 100 mg to about 150 mg free base equivalent (FBE) of migalastat at a frequency of once every other day, wherein administration of a single dose of the migalastat to subjects provides an increase in plasma migalastat AUC 0 of about 4.5-fold compared to a healthy control subject, and wherein the administration of the migalastat is effective to stabilize renal function in the patient and wherein the patient has a HEK assay amenable mutation in α-galactosidase A.
14. The method of claim 1, comprising administering about 150 mg of migalastat hydrochloride at a frequency of every other day.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the method of stabilization of renal function in a Fabry patient would inherently occur alongside treatment of Fabry disease in a Fabry patient.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 13 of U.S. Patent No. 10,857,142 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 13 of U.S. Patent No. 10,857,142 are as follows.
1. A method of stabilizing renal function in an enzyme replacement therapy (ERT)-experienced patient diagnosed with Fabry disease and having mild renal impairment with an eGFR of 60 to 90 mL/min/1.73 m2, the method comprising: administering to the patient about 100 mg to about 150 mg free base equivalent (FBE) of migalastat at a frequency of once every other day, wherein administration of a single dose of the migalastat to the subject provides an increase in plasma migalastat AUC 0, of about 1.2-fold compared to a healthy control subject, and wherein the administration of the migalastat is effective to stabilize renal function in the patient and wherein the patient has a HEK assay amenable mutation in α-galactosidase A.
13. The method of claim 1, wherein comprising administering about 150 mg of migalastat hydrochloride at a frequency of every other day.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the method of stabilization of renal function in a Fabry patient would inherently occur alongside treatment of Fabry disease in a Fabry patient and would be effective regardless of specific parameters of the patient population with Fabry disease.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 15 of U.S. Patent No. 10,874,657 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 15 of U.S. Patent No. 10,874,657 are delineated below.
1. A method of stabilizing renal function in enzyme replacement therapy (ERT)-experienced patients diagnosed with Fabry disease and having renal impairment, the method comprising: administering, to a group of Fabry disease patients having renal impairment and a HEK assay amenable α-galactosidase A mutation, about 100 mg to about 150 mg free base equivalent (FBE) of migalastat at a frequency of once every other day, wherein the administration is effective to (i) reduce left ventricular mass index (LVMi) in the patient, and (ii) provide a mean annualized rate of change in eGFRCKD-EPI of greater than −1.0 mL/min/1.73 m2.
15. The method of claim 1, comprising administering about 150 mg of migalastat hydrochloride.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the method of stabilization of renal function in a Fabry patient would inherently occur alongside treatment of Fabry disease in a Fabry patient and would be effective regardless of specific parameters of the patient population with Fabry disease.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 15 of U.S. Patent No. 10,799,491 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 15 of U.S. Patent No. 10,799,491 are as follows.
1. A method of stabilizing renal function in a patient diagnosed with Fabry disease and having moderate renal impairment with an eGFR of 30 to 59 mL/min/1.73 m.sup.2, the method comprising: administering to the patient about 100 mg to about 150 mg free base equivalent (FBE) of migalastat at a frequency of once every other day, wherein administration of a single dose of the migalastat to the subject provides an increase in plasma migalastat AUC.sub.0-∞ of about 1.8-fold compared to a healthy control subject, and wherein the administration of the migalastat is effective to stabilize renal function in the patient and wherein the patient has a HEK assay amenable mutation in α-galactosidase A.
15. The method of claim 1, comprising administering about 150 mg of migalastat hydrochloride at a frequency of every other day.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the method of stabilization of renal function in a Fabry patient would inherently occur alongside treatment of Fabry disease in a Fabry patient and would be effective regardless of specific parameters of the patient population with Fabry disease.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 15 of U.S. Patent No. 10,857,141 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 15 of U.S. Patent No. 10,57,141 are set forth below.
1. A method of stabilizing renal function in enzyme replacement therapy (ERT)-experienced patients diagnosed with Fabry disease and having renal impairment, the method comprising: administering to a group of Fabry disease patients having renal impairment and HEK assay amenable α-galactosidase A mutation, about 100 mg to about 150 mg free base equivalent (FBE) of migalastat at a frequency of once every other day, and reducing plasma globotriaosylsphingosine (lyso-Gb3) in the patient, wherein the administration is effective to (i) reduce the mean plasma globotriaosylsphingosine (lyso-Gb3) in the patients, and (ii) provide a mean annualized rate of change in eGFRCKD-EPI of greater than −1.0 mL/min/1.73 m2.
15. The method of claim 1, comprising administering about 150 mg of migalastat hydrochloride.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the method of stabilization of renal function in a Fabry patient would inherently occur alongside treatment of Fabry disease in a Fabry patient and would be effective regardless of specific parameters of the patient population with Fabry disease.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of U.S. Patent No. 10,849,889 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claim 1 of U.S. Patent No. 10,849,889 are as follows.
1. A method of stabilizing renal function in an enzyme replacement therapy (ERT)-experienced patient diagnosed with Fabry disease and having renal impairment, the method comprising: a. administering to the patient an effective amount of migalastat at a frequency of once every other day, and b. reducing globotriaosylceramide (GL-3) accumulated in the patient's organs, wherein the effective amount is about 100 mg to about 150 mg free base equivalent (FBE), wherein the administration of the migalastat is effective to stabilize renal function in the patient and wherein the patient has a HEK assay amenable mutation in α-galactosidase A.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the method of stabilization of renal function in a Fabry patient would inherently occur alongside treatment of Fabry disease in a Fabry patient and would be effective regardless of specific parameters of the patient population with Fabry disease.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 15 of U.S. Patent No. 10,874,655 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 15 of U.S. Patent No. 10,874,655 are set forth below.
1. A method of treating Fabry disease in a human patient having moderate renal impairment with an eGFR of 30 to 59 mL/min/1.73 m.sup.2, the method comprising administering to the patient a therapeutically effective dose of migalastat at a frequency of once every other day, wherein the therapeutically effective dose is about 100 mg to about 150 mg free base equivalent (FBE), wherein the patient has a HEK assay amenable mutation in α-galactosidase A, and wherein the dose is not adjusted relative to a patient without renal impairment.
15. The method of claim 1, wherein the therapeutically effective dose is about 150 mg of migalastat hydrochloride.
Claim 1 does not teach that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the treatment of Fabry disease in a Fabry patient and would be effective regardless of specific parameters of the patient population with Fabry disease.
Claims 166 and 170-173 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 21 of U.S. Patent No. 10,251,873 in view of GALAFOLD (U.S. Food and Drug Administration; August 2018).
The limitations of claims 1 and 21 of U.S. Patent No. 10,251,873 are set forth below.
1. A method of stabilizing renal function in a patient diagnosed with Fabry disease and having renal impairment, the method comprising administering to the patient an effective amount of migalastat or salt thereof at a frequency of once every other day, wherein the effective amount is about 100 mg to about 150 mg free base equivalent (FBE) wherein the administration of the migalastat or salt thereof is effective to stabilize renal function in the patient and wherein the patient has a HEK assay amenable mutation in α-galactosidase A.
21. The method of claim 1, wherein the effective amount is about 150 mg of migalastat hydrochloride.
Claim 1 does not teach a method of treating Fabry disease or that the HEK amenable mutations are V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. However, this is obvious over GALAFOLD.
GALAFOLD teaches as described in the above rejections.
It would have been prima facie obvious to one of ordinary skill in the art to administer migalastat to a patient with an α-galactosidase mutation selected from: V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P for the treatment of Fabry disease. One would have been motivated to do so, with reasonable expectation of success, because GALAFOLD teaches that the above mutations are amenable by migalastat for the treatment of Fabry disease.
Furthermore, one of ordinary skill in the art would reasonably recognize that the method of stabilization of renal function in a Fabry patient would inherently occur alongside treatment of Fabry disease in a Fabry patient and would be effective regardless of specific parameters of the patient population with Fabry disease.
Response to Arguments
Applicant's arguments filed 03/16/2026 have been fully considered but they are not persuasive.
35 U.S.C. 102/103 and NSDP
Regarding the rejections under 35 U.S.C. 102/103, Applicant attempts to disqualify both GALAFOLD references as prior art. This is not persuasive.
Applicant first attempts to disqualify both GALAFOLD references pursuant 35 U.S.C. 102(b)(1)(A). However, Applicant’s arguments are improper and require filing of an affidavit or declaration. See MPEP 717 and 37 CFR 1.130. First, Applicant states that the cited Galafold references (US FDA 2018 and EMA 2018) are manufactured for subsidiaries of the present Applicant named on the instant application, and that the inventor is an employee of the Applicant (p. 5 of Remarks) and further concludes that “the relevant portions of these disclosures regarding the claimed mutations were publicly disclosed directly or indirectly from the inventor” (p. 5 of Remarks). This is not persuasive. Neither the FDA or EMA GALAFOLD documents cite an author of their disclosed subject matter, nor does the presence of Amicus Therapeutics U.S., Inc. or Amicus Therapeutics UK Ltd., which are allegedly subsidiaries of the Applicant of the instant invention, clearly establish who (whether that be the inventor, or another) disclosed the subject matter of the prior art documents. Moreover, Applicant’s arguments cannot take the place of evidence where evidence is necessary, such as allegations in an attempt to disqualify prior art. MPEP 716.01(c) and 2155.01.
Applicant also attempts to disqualify both GALAFOLD references on the grounds that the prior art documents fall within the 1-year grace period under 35 U.S.C. 102(b)(1)(A) and the inventor’s oath filed 10/02/2023 establishes that Elfrida Benjamin is the inventor of the present application. This is not persuasive. While Elfrida Benjamin is the only named inventor on the instant application, Examiner additionally points to U.S. patent 11,833,164 B2 which names both Elfrida Benjamin and Xiaoyang Wu as co-inventors, where the claims a method of treating Fabry disease in a patient comprising administering migalastat to the patient, wherein the patient is identified to have two or more mutations selected from a list of α-galactosidase A mutations that include V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. All of these amenable mutations are recited in the instant claims as well, but it is unclear in the case of the ‘164 patent whether the subject matter that overlaps with the instant invention was invented only by Elfrida Benjamin, or by Xiaoyang Wu, as an oath has also been filed for both inventors in the ‘164 patent. Additionally, as evidenced by the above non-statutory double patenting rejections, there are many applications and patents that disclose and claim subject matter overlapping with the instant invention (U.S. patent 11,357,784; applications 17/618,277; 17/838,820; 18/315,928; and 18/578,483) including the claimed mutations, which either name at least one other inventor or do not name Elfrida Benjamin as an inventor at all. At present, the record is not yet clear that Elfrida Benjamin both invented the claimed invention and disclosed, either directly or indirectly, the subject matter referred to in the GALAFOLD references. The rejection is maintained. For the same reasons, the non-statutory double patenting rejections that rely on the US FDA GALAFOLD reference are also maintained.
Regarding the additional rejections under non-statutory double patenting, Applicant has submitted no arguments against the rejections over the claims of co-pending applications 17/618,277; 17/838,820; 18/315,928; and 18/578,483. These rejections are therefore maintained. Additionally, Applicant argues that the scope of the amenable α-galactosidase mutations for U.S. Patent No. 11,833,164 is much broader than the claims of the instant application, and that the claims of U.S. Patent No. 11,357,784 do not mention any of the mutations of the instant claims. This is not persuasive. Per MPEP 804(II)(B)(1), the specification of a reference patent may be used to construe the scope of the claims in order to give the claims their broadest reasonable construction in light of the specification as interpreted by one of ordinary skill in the art. Phillips v. AWH Corp., 415 F.3d 1303, 1316, 75 USPQ2d 1321, 1329 (Fed. Cir. 2005) (en banc) (quoting In re Am. Acad. of Sci. Tech. Ctr., 367 F.3d 1359, 1364, 70 USPQ2d 1827, 1830 (Fed. Cir. 2004). Thus, in looking to the specification of U.S. Patent No. 11,357,784 to construe the scope of what patients with Fabry disease may be treatable by administration of migalastat, one of ordinary skill in the art would recognize that patients with the amenable mutations listed in Table 1 (cols. 12-21) would be treatable within the scope of the claims and would reasonably try to treat a patient with mutations such as V22G, N34H, G80V, Q107R, Y152D, A156S, L189F, W204L, S238G, I239M, A257V, P259Q, N320H, P323T, E338V, P380L, and T412P. The same would be true for U.S. Patent No. 11,833,164, wherein while the ‘164 claims are broader than the instant claims, one of ordinary skill in the art would reasonably try to treat patients with a listed amenable mutation that is within the scope of the claims and could arrive at the mutations of the instant invention.
The rejections are therefore maintained.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to MADELINE E BRAUN whose telephone number is (703)756-4533. The examiner can normally be reached M-F 8:30am-5:00pm ET.
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/M.E.B./Examiner, Art Unit 1624 04/28/2026
/BRENDA L COLEMAN/Primary Examiner, Art Unit 1624
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