Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
DETAILED ACTION
This office action is in response to applicant's request for continued examination filed on October 15, 2025.
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.
Status of Claims
Claims 9, 11, 15, 18-19 and 68-69 are currently pending and are the subject of this office action.
Claims 9, 11, 15, 18-19 and 68-69 are presently under examination.
The following species is under examination:
(S)-Quinuclidin-3-yl-(2-(2-(4-fluorophenyl)-thiazol-4-yl)-propan-2-yl)-carbamate:
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Priority
The present application is a CON of 15/946,355 (ABN) filed on 04/05/2018, which is a CON of 15/108,686 (ABN) filed on 06/28/2016, which is a 371 of PCT/US14/069338 filed on 12/09/2014, and claims priority to provisional application No. 61/914,842 filed on 12/11/2013.
Rejections and/or Objections and Response to Arguments
Rejections and/or objections not reiterated from previous office actions are hereby withdrawn. The following rejections and/or objections are either reiterated (Maintained Rejections and/or Objections) or newly applied (New Rejections and/or Objections, Necessitated by Amendment or New Rejections and/or Objections not Necessitated by Amendment). They constitute the complete set presently being applied to the instant application.
Responses to Applicant’s arguments have been addressed immediately after the corresponding rejections, or in the section: Withdrawn Rejections and/or Objections, if the rejection was withdrawn.
Claim Rejections - 35 USC § 103 (Maintained Rejection).
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.
Claim(s) 9, 11, 15, 18-19 and 68-69 stand rejected under 35 U.S.C. 103 as being unpatentable over Bourque et. al. (WO 2012/129084, 09-2012, cited in previous office action) in view of Palling (US 2010/0113517, cited in previous office action) and Hollak et. al. (Expert Opinion Ther. Targets (2007) 11:821-833, cited by Applicant, cited in previous office action).
For claims 9 and 19, Bourque teaches a method of treating Fabry disease comprising administering to a subject having Fabry disease a composition comprising an effective amount of a compound of formula I or a pharmaceutically acceptable salt thereof (see for example claims 1 and 258-261, see also page 2, line 6 and page 66, one paragraph before last):
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which is identical to the general formula I of claim 9, and more specifically with compound:
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(Venglustat, Ibiglustat, GCS452 or its 2-hydrosuccinate salt: GZ452; see for example page 64, last paragraph through page 66, one paragraph before last, claim 268 and Figure 2A) which anticipates the general formula I of claim 1 and it is identical to the compound of claim 19.
Bourque does not teach that:
1- the subject (i.e., the Fabry patient) has increased GL-3 as compared to healthy cardiomyocytes or has accumulated GL-3, and
2- the subject (i.e., the Fabry patient) is suffering from a cardiac manifestation of Fabry disease.
However, regarding topic 1- above, the prior art teaches that Fabry patients inherently have increased Gl-3 compared to healthy cardiomyocytes:
For example, Bourque teaches:
“As noted previously, Fabry’s disease is caused by the deficiency of the lysosomal enzyme alpha-galactosidase A. The enzymatic defect leads to systemic deposition of glycosphingolipids having terminal alpha-galactosyl moieties, predominantly globotriaosylceramide (GL3 or Gb3)” (See page 144, under Fabry).
Palling teaches:
“Fabry disease is a glycosphingolipid (GSL) storage disease caused by an X-linked inherited deficiency of lysosomal alpha-galactosidase A (alpha-Gal A), an enzyme responsible for the hydrolysis of terminal alpha-galactosyl residues from glycosphingolipids. A deficiency in the enzyme activity results in a progressive deposition of neutral glycosphingolipids, predominantly globotriaosylceramide (GL-3), in vascular endothelial cells causing renal failure along with premature myocardial infarction and strokes in patients with this condition” (see [0003]). Palling also teaches:
“As non-limiting examples, surrogate markers of Fabry disease include decreased lysosomal alpha.-Gal A activity in cells (e.g., fibroblasts) and tissue; cellular deposition of GL-3; increased plasma concentrations of homocysteine and vascular cell adhesion molecule-1 (VCAM-1); GL-3 accumulation within myocardial cells and valvular fibrocytes, leading to cardiac hypertrophy (especially of the left ventricle), valvular insufficiency, and arrhythmias; proteinuria; increased urinary concentrations of lipids such as CTH, lactosylceramide, ceramide, and decreased urinary concentrations of glucosylceramide and sphingomyelin” (see [0049]).
Finally, Hollak also teaches that in patients with Fabry disease there is accumulation of GL-3 in cardiomyocytes. For example, Hollak states:
“The main glycosphingolipid that is stored in Fabry disease is globotriaosylceramide (GL-3). Globotriaosylceramide (GL-#) accumulates in various cell types of Fabry patients. Extensive storage occurs in arterial walls, especially in endothelial and smooth muscle cells. In the kidney, extensive storage occurs in the podocytes, with less storage in mesangial and endothelial cells. In the heart, storage occurs in the lysosomes of cardiomyocytes, although secondary changes, such as hypertrophy, account for the increase in cardiac mass” (see page 821 under Introduction).
Regarding topic 2- above, Palling teaches: “This disorder (Fabry disease) is classified by clinical manifestations into two groups: a classic form with generalized vasculopathy, and a typical variant form, with clinical manifestations limited to cardiac tissue” (see last sentence of paragraph [0003]). In other words, a subgroup of subjects suffering from Fabry disease suffer from cardiac manifestations.
Since Bourque teaches a method of treating Fabry disease) comprising administering to a patient suffering from Fabry disease (that inherently have increased GL-3 as compared to healthy cardiomyocytes) a composition comprising an effective amount of a composition comprising the compound GZ452, and since Palling teaches that some Fabry patients suffer from cardiac manifestations, before the effective filing date of the invention, it would have been prima facie obvious for a person of ordinary skill in the art to: treat Fabry disease in the subgroup of Fabry patients, also suffering from cardiac manifestations, comprising administering an effective amount of a composition comprising the compound GZ452, with a reasonable expectation of success, since the subpopulation of Fabry patients suffering from cardiac manifestations are expected to benefit from such treatment (treatment of Fabry disease) that has already proven to be effective for the larger population of subjects suffering from Fabry disease.
The prior art is silent regarding: “reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a human subject in need thereof, having Fabry disease that is suffering from a cardiac manifestation”
However, Bourque further teaches that the compound GZ452 reduces the accumulation of Gb3 (globotriaosylceramide or GL-3; i.e., reduces GL-3) in the heart of the subject (see page 76 Figure 3, see also Example 111 on pages 236-239 and more specifically, page 238, lines 4-8). Cardiomyocytes are hearth muscle cells.
Further, the statement: “reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease that is suffering from a cardiac manifestation” will naturally flow from the teachings of the prior art, since the same compound (GS452 or GZ452) is being administered to the same subjects (subjects suffering from Fabry disease who suffer from a cardiac manifestation, all of which inherently have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes). In other words, products of identical composition cannot exert mutually exclusive properties when administered under the same or similar circumstances.
In other words, even though the prior art might be silent regarding “reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease that is suffering from a cardiac manifestation”, by practicing the method made obvious by the prior art: “treating Fabry disease comprising administering to a subject having Fabry disease and suffering from a cardiac manifestation (which inherently have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes) a composition comprising an effective amount of a compound of formula I or more specifically GS452 or a pharmaceutically acceptable salt (GZ45)2 thereof ", one will also be “reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease that is suffering from a cardiac manifestation (which inherently have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes)”, even though the prior art was not aware of it.
Apparently, Applicant has discovered a new property or advantage ("reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease that is suffering from a cardiac manifestation (which inherently have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes)”) of the method made obvious by the prior art (“treating Fabry disease comprising administering to a subject having Fabry disease that is suffering from a cardiac manifestation (which inherently have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes) a composition comprising an effective amount of a compound of formula I or more specifically GS452 or a pharmaceutically acceptable salt (GZ452) thereof ").
MPEP 2145 II states: “The fact that Applicant has recognized another advantage which would flow naturally from following the suggestion of the prior art, cannot be the basis for patentability when the differences would otherwise be obvious”. Ex parte Obiaya, 227 USPQ 58, 60. (FP 7.37.07, MPEP 707.07(f)).
All this will result in the practice of claims 9 and 19 with a reasonable expectation of success.
For claim 11, as evidenced by Palling, in patients with Fabry disease there is accumulation of GL-3 in lysosomes of the heart (see [0038]). Also as evidenced by Hollak: “In the heart, storage occurs in the lysosomes of cardiomyocytes, although secondary changes, such as hypertrophy, account for the increase in cardiac mass” (see page 821 under Introduction).
Bourque also teaches that the method reduces GL-3 in lysosomes (See page 66, last two lines through page 67 through page 68 fourth paragraph).
All this will result in the practice of claim 11 with a reasonable expectation of success.
The statement in claim 15: “wherein administration of the compound reduces GL-3 levels in the lysosome of the cardiomyocytes” does not require additional steps to be performed and simply expresses the intended result of carrying the process made obvious by the prior art: “a method of treating Fabry disease comprising administering to a subject having Fabry disease that suffers from a cardiac manifestation (which inherently have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes) a composition comprising an effective amount of a compound of formula I or more specifically GS452 or a pharmaceutically acceptable salt (GZ452) thereof ".
MPEP 2114.04 states: “Claim scope is not limited by claim language that suggests or makes optional but does not require steps to be performed, or by claim language that does not limit a claim to a particular structure. However, examples of claim language, although not exhaustive, that may raise a question as to the limiting effect of the language in a claim are:
(A) “ adapted to ” or “adapted for ” clauses;
(B) “ wherein ” clauses; and
(C) “ whereby ” clauses.
The determination of whether each of these clauses is a limitation in a claim depends on the specific facts of the case. In Hoffer v. Microsoft Corp., 405 F.3d 1326, 1329, 74 USPQ2d 1481, 1483 (Fed. Cir. 2005), the court held that when a “whereby’ clause states a condition that is material to patentability; it cannot be ignored in order to change the substance of the invention.” Id. However, the court noted (quoting Minton v. Nat ’l Ass ’n of Securities Dealers, Inc., 336 F.3d 1373, 1381, 67 USPQ2d 1614, 1620 (Fed. Cir. 2003)) that a “whereby clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited.” (Emphasis added).
In the instant case “reducing GL-3 levels in the lysosome of the cardiomyocytes” appears to be the result of the process made obvious by the prior art: “a method of treating Fabry disease comprising administering to a subject having Fabry disease that is suffering from cardiac manifestations (which inherently have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes) a composition comprising an effective amount of a compound of formula I or more specifically GS452 or a pharmaceutically acceptable salt (GZ452) thereof ", e. g. the intended result of a process step positively recited.
As such, this limitation in the instantly claimed method has not been given any weight.
Further, as mentioned above, Bourque teaches that the compound GZ452 reduces the accumulation of Gb3 (globotriaosylceramide or GL-3; i.e., reduces GL-3) in the heart of the subject (see page 76 Figure 3, see also Example 111 on pages 236-239 and more specifically, page 238, lines 4-8). Cardiomyocytes are hearth muscle cells.
All this will result in the practice of claim 15 with a reasonable expectation of success.
For claim 18, Bourque explicitly teaches that the compounds of the invention inhibit glucosylceramide synthase (GCS) activity (see for example page 67, one paragraph before last).
All this will result in the practice of claim 15 with a reasonable expectation of success.
For claims 68-69, Palling teaches that some of the cardiac manifestations encompass: left-ventricular hypertrophy (see [0005]), thus resulting in the practice of claims 68-69 with a reasonable expectation of success.
Response to Applicant’s arguments related to the above rejection
Applicant's arguments have been fully considered but are not persuasive.
NOTE: apparently Applicant did not present arguments against the above 103 rejection, instead Applicant responded to the second 103 rejection (see below). The difference between these two 103 rejections is that in the above one, it is assumed that all Fabry patients inherently have increased GL-3 as compared to healthy cardiomyocytes and that only a subset of Fabry patients suffer from cardiac manifestations, while in the second one it is assumed that a subset of Fabry patients that both: have increased GL-3 as compared to healthy cardiomyocytes and also suffer from cardiac manifestations.
Examiner’s response:
First, Bourque teaches:
“A method of treating a subject diagnosed as having a lysosomal storage disease, comprising administering to the subject an effective amount of the compound according to claim 1 (GZ452), wherein the lysosomal disease is Fabry” (see claims 259-261).
Second, Bourque further teaches:
that the compound GZ452 reduces the accumulation of Gb3 (globotriaosylceramide or GL-3; i.e., reduces GL-3) in the heart of the subject (see page 76 Figure 3, see also Example 111 on pages 236-239 and more specifically, page 238, lines 4-8). Cardiomyocytes are hearth muscle cells.
Third, it is clear from the above rejection that based on Bourque, Palling and Hollak, that all Fabry patients inherently have increased GL-3 in the cardiomyocytes.
Apparently, the subjects “in need” of Bourque are the same as the subjects “in need” of the instant claims. Both suffer from Fabry disease, and apparently, all inherently have increased GL-3 in the cardiomyocytes as evidenced by Palling, Hollak and by Bourque, and some suffer from a cardiac manifestation.
So, when the same drug (GZ452) is administered to the same patients ((subjects suffering from Fabry disease who suffer from a cardiac manifestation, all of which have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes).), the same results are expected: reduction of GL-3 in the cardiomyocytes of the patient, whether the prior art was aware of it or not.
The fact that GL-3 accumulation can also happen in other cell-types (besides cardiomyocytes) is irrelevant, since what is relevant is that GL-3 accumulation definitively occurs in cardiomyocytes. So, there is no need for the skilled in the art to know where GL-3 accumulation occurs, or if it occurs in which cell types will occur, since as stated above the same drug (GZ452) is administered to the same population (subjects suffering from Fabry disease who suffer from a cardiac manifestation, all of which inherently have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes).
As stated in the above rejection:
“Reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease that is suffering from a cardiac manifestation” will naturally flow from the teachings of the prior art, since the same compound (GS452 or GZ452) is being administered to the same subjects (subjects suffering from Fabry disease who suffer from a cardiac manifestation, all of which inherently have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes). In other words, products of identical composition cannot exert mutually exclusive properties when administered under the same or similar circumstances.
In other words, even though the prior art might be silent regarding “reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease that is suffering from a cardiac manifestation”, by practicing the method made obvious by the prior art: “treating Fabry disease comprising administering to a subject having Fabry disease and suffering from a cardiac manifestation (which inherently have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes) a composition comprising an effective amount of a compound of formula I or more specifically GS452 or a pharmaceutically acceptable salt (GZ45)2 thereof ", one will also be “reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease that is suffering from a cardiac manifestation (which inherently have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes)”, even though the prior art was not aware of it.
Apparently, Applicant has discovered a new property or advantage ("reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease that is suffering from a cardiac manifestation (which inherently have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes)”) of the method made obvious by the prior art (“treating Fabry disease comprising administering to a subject having Fabry disease that is suffering from a cardiac manifestation (which inherently have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes) a composition comprising an effective amount of a compound of formula I or more specifically GS452 or a pharmaceutically acceptable salt (GZ452) thereof ").
MPEP 2112 I states: “[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer.” Atlas Powder Co. v. Ireco Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus, the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977).”
Claim Rejections - 35 USC § 103 (Maintained Rejection).
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.
Claim(s) 9, 11, 15, 18-19 and 68-69 stand rejected under 35 U.S.C. 103 as being unpatentable over Bourque et. al. (WO 2012/129084, 09-2012, cited in previous office action) in view of Palling (US 2010/0113517, cited in previous office action) and Hollak et. al. (Expert Opinion Ther. Targets (2007) 11:821-833, cited by Applicant, cited in previous office action).
For claims 9 and 19, Bourque teaches a method of treating Fabry disease comprising administering to a subject having Fabry disease a composition comprising an effective amount of a compound of formula I or a pharmaceutically acceptable salt thereof (see for example claims 1 and 258-261, see also page 2, line 6 and page 66, one paragraph before last):
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which is identical to the general formula I of claim 9, and more specifically with compound:
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(Venglustat, Ibiglustat, GCS452 or its 2-hydrosuccinate salt: GZ452; see for example page 64, last paragraph through page 66, one paragraph before last) which anticipates the general formula I of claim 1 and it is identical to the compound of claim 19.
Bourque does not teach that:
1- the subject (i.e., the Fabry patient) has increased GL-3 as compared to healthy cardiomyocytes or has accumulated GL-3, and
2- the subject (i.e., the Fabry patient) is suffering from a cardiac manifestation of Fabry disease.
However, regarding topic 1- above, the prior art teaches that some Fabry patients have increased Gl-3 compared to healthy cardiomyocytes:
For example, Bourque teaches:
“As noted previously, Fabry’s disease is caused by the deficiency of the lysosomal enzyme alpha-galactosidase A. The enzymatic defect leads to systemic deposition of glycosphingolipids having terminal alpha-galactosyl moieties, predominantly globotriaosylceramide (GL3 or Gb3)” (See page 144, under Fabry).
Palling teaches:
“Fabry disease is a glycosphingolipid (GSL) storage disease caused by an X-linked inherited deficiency of lysosomal alpha-galactosidase A (alpha-Gal A), an enzyme responsible for the hydrolysis of terminal alpha-galactosyl residues from glycosphingolipids. A deficiency in the enzyme activity results in a progressive deposition of neutral glycosphingolipids, predominantly globotriaosylceramide (GL-3), in vascular endothelial cells causing renal failure along with premature myocardial infarction and strokes in patients with this condition” (see [0003]). Palling also teaches:
“As non-limiting examples, surrogate markers of Fabry disease include decreased lysosomal alpha.-Gal A activity in cells (e.g., fibroblasts) and tissue; cellular deposition of GL-3; increased plasma concentrations of homocysteine and vascular cell adhesion molecule-1 (VCAM-1); GL-3 accumulation within myocardial cells and valvular fibrocytes, leading to cardiac hypertrophy (especially of the left ventricle), valvular insufficiency, and arrhythmias; proteinuria; increased urinary concentrations of lipids such as CTH, lactosylceramide, ceramide, and decreased urinary concentrations of glucosylceramide and sphingomyelin” (see [0049]).
Finally, Hollak also teaches that in patients with Fabry disease there is accumulation of GL-3 in cardiomyocytes. For example, Hollak states:
“The main glycosphingolipid that is stored in Fabry disease is globotriaosylceramide (GL-3). Globotriaosylceramide (GL-#) accumulates in various cell types of Fabry patients. Extensive storage occurs in arterial walls, especially in endothelial and smooth muscle cells. In the kidney, extensive storage occurs in the podocytes, with less storage in mesangial and endothelial cells. In the heart, storage occurs in the lysosomes of cardiomyocytes, although secondary changes, such as hypertrophy, account for the increase in cardiac mass” (see page 821 under Introduction).
Regarding topic 2- above, Palling teaches: “This disorder (Fabry disease) is classified by clinical manifestations into two groups: a classic form with generalized vasculopathy, and a typical variant form, with clinical manifestations limited to cardiac tissue” (see last sentence of paragraph [0003]).
In other words, some subjects suffering from Fabry disease also suffer from cardiac manifestations.
Since Bourque teaches a method of treating Fabry disease) comprising administering to a patient suffering from Fabry disease a composition comprising an effective amount of a composition comprising the compound GZ452, and since Bourque, Palling and Hollak teach that some Fabry patients have accumulation of GL-3 in the cardiomyocytes, and since Palling teaches that some Fabry patients suffer from cardiac manifestations, before the effective filing date of the invention, it would have been prima facie obvious for a person of ordinary skill in the art to: treat Fabry disease in the subgroup of Fabry patients that 1-suffer from GL-3 accumulation in their cardiomyocytes and 2- also suffer from cardiac manifestations, comprising administering an effective amount of a composition comprising the compound GZ452, with a reasonable expectation of success, since the subpopulation of Fabry patients suffering from 1- GL-3 accumulation in their cardiomyocytes and 2- also suffering from cardiac manifestations, are expected to benefit from such treatment (treatment of Fabry disease) that has already proven to be effective for the larger population of subjects suffering from Fabry disease.
The prior art is silent regarding: “reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a human subject in need thereof, having Fabry disease that is suffering from a cardiac manifestation”
However, Bourque further teaches that the compound GZ452 reduces the accumulation of Gb3 (globotriaosylceramide or GL-3; i.e., reduces GL-3) in the heart of the subject (see page 76 Figure 3, see also Example 111 on pages 236-239 and more specifically, page 238, lines 4-8). Cardiomyocytes are hearth muscle cells.
Further, the statement: “reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease that is suffering from a cardiac manifestation” will naturally flow from the teachings of the prior art, since the same compound (GS452 or GZ452) is being administered to the same subjects (a subset of Fabry patients who suffer from a cardiac manifestation, and suffer from increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes). In other words, products of identical composition cannot exert mutually exclusive properties when administered under the same or similar circumstances.
In other words, even though the prior art might be silent regarding “reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease that is suffering from a cardiac manifestation”, by practicing the method made obvious by the prior art: “treating Fabry disease comprising administering to a subject having Fabry disease and suffering from a cardiac manifestation that also suffers from increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes, a composition comprising an effective amount of a compound of formula I or more specifically GS452 or a pharmaceutically acceptable salt (GZ45)2 thereof ", one will also be “reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease that is suffering from a cardiac manifestation and also suffering from increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes”, even though the prior art was not aware of it.
Apparently, Applicant has discovered a new property or advantage ("reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease that is suffering from a cardiac manifestation and have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes”) of the method made obvious by the prior art (“treating Fabry disease comprising administering to a subject having Fabry disease that is suffering from a cardiac manifestation and suffering from increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes, a composition comprising an effective amount of a compound of formula I or more specifically GS452 or a pharmaceutically acceptable salt (GZ452) thereof ").
MPEP 2112 I states: “[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer.” Atlas Powder Co. v. Ireco Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus, the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977).”
All this will result in the practice of claims 9 and 19 with a reasonable expectation of success.
For claim 11, as evidenced by Palling, in patients with Fabry disease there is accumulation of GL-3 in lysosomes of the heart (see [0038]). Also as evidenced by Hollak: “In the heart, storage occurs in the lysosomes of cardiomyocytes, although secondary changes, such as hypertrophy, account for the increase in cardiac mass” (see page 821 under Introduction).
Bourque also teaches that the method reduces GL-3 in lysosomes (See page 66, last two lines through page 67 through page 68 fourth paragraph).
All this will result in the practice of claim 11 with a reasonable expectation of success.
The statement in claim 15: “wherein administration of the compound reduces GL-3 levels in the lysosome of the cardiomyocytes” does not require additional steps to be performed and simply expresses the intended result of carrying the process made obvious by the prior art: “a method of treating Fabry disease comprising administering to a subject having Fabry disease that has increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes and also suffers from cardiac manifestations, a composition comprising an effective amount of a compound of formula I or more specifically GS452 or a pharmaceutically acceptable salt (GZ452) thereof ".
MPEP 2114.04 states: “Claim scope is not limited by claim language that suggests or makes optional but does not require steps to be performed, or by claim language that does not limit a claim to a particular structure. However, examples of claim language, although not exhaustive, that may raise a question as to the limiting effect of the language in a claim are:
(A) “ adapted to ” or “adapted for ” clauses;
(B) “ wherein ” clauses; and
(C) “ whereby ” clauses.
The determination of whether each of these clauses is a limitation in a claim depends on the specific facts of the case. In Hoffer v. Microsoft Corp., 405 F.3d 1326, 1329, 74 USPQ2d 1481, 1483 (Fed. Cir. 2005), the court held that when a “whereby’ clause states a condition that is material to patentability; it cannot be ignored in order to change the substance of the invention.” Id. However, the court noted (quoting Minton v. Nat ’l Ass ’n of Securities Dealers, Inc., 336 F.3d 1373, 1381, 67 USPQ2d 1614, 1620 (Fed. Cir. 2003)) that a “whereby clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited.” (Emphasis added).
In the instant case “reducing GL-3 levels in the lysosome of the cardiomyocytes” appears to be the result of the process made obvious by the prior art: “a method of treating Fabry disease comprising administering to a subject having Fabry disease that has increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes and also suffers from cardiac manifestations, a composition comprising an effective amount of a compound of formula I or more specifically GS452 or a pharmaceutically acceptable salt (GZ452) thereof ", e. g. the intended result of a process step positively recited.
As such, this limitation in the instantly claimed method has not been given any weight.
Further, as mentioned above, Bourque teaches that the compound GZ452 reduces the accumulation of Gb3 (globotriaosylceramide or GL-3; i.e., reduces GL-3) in the heart of the subject (see page 76 Figure 3, see also Example 111 on pages 236-239 and more specifically, page 238, lines 4-8). Cardiomyocytes are hearth muscle cells.
All this will result in the practice of claim 15 with a reasonable expectation of success.
For claim 18, Bourque explicitly teaches that the compounds of the invention inhibit glucosylceramide synthase (GCS) activity (see for example page 67, one paragraph before last), thus resulting in the practice of claim 18 with a reasonable expectation of success.
For claims 68-69, Palling teaches that some of the cardiac manifestations encompass: left-ventricular hypertrophy (see [0005]), thus resulting in the practice of claims 68-69 with a reasonable expectation of success.
Response to Applicant’s arguments related to the above rejection
Applicant's arguments have been fully considered but are not persuasive.
NOTE: apparently Applicant only presented arguments against this 103 rejection, but not to the first 103 rejection. The difference between these two 103 rejections is that in the first one, it is assumed that all Fabry patients inherently have increased GL-3 as compared to healthy cardiomyocytes and that a subset of Fabry patients suffer from cardiac manifestations., while in this one it is assumed that a subset of Fabry patients both: have increased GL-3 as compared to healthy cardiomyocytes and also suffer from cardiac manifestations.
Examiner’s response:
First, Bourque teaches:
“A method of treating a subject diagnosed as having a lysosomal storage disease, comprising administering to the subject an effective amount of the compound according to claim 1, wherein the lysosomal disease is Fabry” (see claims 259-261).
Second, Bourque further teaches:
that the compound GZ452 reduces the accumulation of Gb3 (globotriaosylceramide or GL-3; i.e., reduces GL-3) in the heart of the subject (see page 76 Figure 3, see also Example 111 on pages 236-239 and more specifically, page 238, lines 4-8). Cardiomyocytes are hearth muscle cells.
Third, it is clear from the above rejection that based on Bourque, Palling and Hollak, that most Fabry patients have increased GL-3 in the cardiomyocytes.
Apparently, the subjects “in need” of Bourque are the same as the subjects “in need” of the instant claims. Both suffer from Fabry disease, both suffer from a cardiac manifestation and apparently, most have increased GL-3 in the cardiomyocytes as taught by Palling and Hollak and also by Bourque.
So, when the same drug (GZ452) is administered to the same patients (subjects suffering from Fabry disease who suffer from a cardiac manifestation and have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes) the same results are expected: reduction of GL-3 in the cardiomyocytes of the patient, whether the prior art was aware of it or not.
The fact that GL-3 accumulation can also happen in other cell-types (besides cardiomyocytes) is irrelevant, since what is relevant is that GL-3 accumulation definitively occurs in cardiomyocytes. So, there is no need for the skilled in the art to know if GL-3 reduction will occur, or if it occurs in which cell types will occur, since as stated above the same drug (GZ452) is administered to the same population (subjects suffering from Fabry disease who suffer from a cardiac manifestation and have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes).
As stated in the above rejection:
“Reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease that is suffering from a cardiac manifestation” will naturally flow from the teachings of the prior art, since the same compound (GS452 or GZ452) is being administered to the same subjects (subjects suffering from Fabry disease who suffer from a cardiac manifestation, all of which have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes). In other words, products of identical composition cannot exert mutually exclusive properties when administered under the same or similar circumstances.
In other words, even though the prior art might be silent regarding “reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease that is suffering from a cardiac manifestation”, by practicing the method made obvious by the prior art: “treating Fabry disease comprising administering to a subject having Fabry disease, having increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes and suffering from a cardiac manifestation a composition comprising an effective amount of a compound of formula I or more specifically GS452 or a pharmaceutically acceptable salt (GZ45)2 thereof ", one will also be “reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease, having increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes and that is suffering from a cardiac”, even though the prior art was not aware of it.
Apparently, Applicant has discovered a new property or advantage ("reducing globotriaosylceramide (GL-3) in the cardiomyocytes of a subject having Fabry disease that is suffering from a cardiac manifestation and have increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes”) of the method made obvious by the prior art (“the administration of PBA to patients that suffer from ocular GVHD after bone marrow transplantation"). art (“treating Fabry disease comprising administering to a subject having Fabry disease that is suffering from a cardiac manifestation and suffering from increased GL-3 in cardiomyocytes as compared to healthy cardiomyocytes, a composition comprising an effective amount of a compound of formula I or more specifically GS452 or a pharmaceutically acceptable salt (GZ452) thereof ").
MPEP 2145 II states: “The fact that Applicant has recognized another advantage which would flow naturally from following the suggestion of the prior art, cannot be the basis for patentability when the differences would otherwise be obvious”. Ex parte Obiaya, 227 USPQ 58, 60. (FP 7.37.07, MPEP 707.07(f)).
Though new properties of a compound or their mechanism of action are no doubt important contributions to scientific and pharmaceutical development, the assessment of patentability is based upon the therapeutic applications and effects of the compounds, not the mechanism or properties by which they exert such a therapeutic effect.
MPEP 2145 states: “Mere recognition of latent properties in the prior art does not render non-obvious an otherwise known invention. In re Wiseman, 201 USPQ 658 (CCPA 1979). Granting a patent on the discovery of an unknown but inherent function would remove from the public that which is in the public domain by virtue of its inclusion in, or obviousness from, the prior art. In re Baxter Travenol Labs, 21 USPQ2d 1281 (Fed. Cir. 1991)
Double Patenting (Maintained Rejections).
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) 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 USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The 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/process/file/efs/guidance/eTD-info-I.jsp.
1) Claims 9, 11, 15, 18-19 and 68-69 stand rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of U.S. Patent No. 9,139,580. Although the claims at issue are not identical, they are not patentably distinct from each other because the ‘580 patent teaches the same compound, which according to the specification of the ‘580 patent, are effective in treating Fabry disease, and reduce the accumulation of GL-3.
See MPEP § 804(II)(B)(2)(a) (“In AbbVie Inc. v. Kennedy Institute of Rheumatology Trust, 764 F.3d 1366, 112 USPQ2d 1001 (Fed. Cir. 2014), the court explained that it is also proper to look at the disclosed utility in the reference disclosure to determine the overall question of obviousness in a nonstatutory double patenting context. See Sun Pharm. Indus., Ltd. v. Eli Lilly & Co., 611 F.3d 1381, 95 USPQ2d 1797 (Fed. Cir. 2010); Pfizer, Inc. v. Teva Pharm. USA, Inc., 518 F.3d 1353, 86 USPQ2d 1001 (Fed. Cir. 2008); Geneva Pharmaceuticals Inc. v. GlaxoSmithKline PLC, 349 F3d 1373, 1385-86, 68 USPQ2d 1865, 1875 (Fed. Cir. 2003).”). See also Sun Pharmaceutical Industries v. Eli Lilly and Co., 611 F. 3d 1381, 1385 (CAFC 2010) (“Our prior obviousness-type double patenting decisions in Geneva and Pfizer … we found claims of a later patent invalid for obviousness-type double patenting where an earlier patent claimed a compound, disclosing its utility in the specification, and a later patent claimed a method of using the compound for a use described in the specification of the earlier patent”).
2) Claims 9, 11, 15, 18-19 and 68-69 stand rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of U.S. Patent No. 9,126,993. Although the claims at issue are not identical, they are not patentably distinct from each other because the ‘993 patent teaches the same compound, which according to the specification of the ‘993 patent, are effective in treating Fabry disease, and reduce the accumulation of GL-3.
See MPEP § 804(II)(B)(2)(a) (“In AbbVie Inc. v. Kennedy Institute of Rheumatology Trust, 764 F.3d 1366, 112 USPQ2d 1001 (Fed. Cir. 2014), the court explained that it is also proper to look at the disclosed utility in the reference disclosure to determine the overall question of obviousness in a nonstatutory double patenting context. See Sun Pharm. Indus., Ltd. v. Eli Lilly & Co., 611 F.3d 1381, 95 USPQ2d 1797 (Fed. Cir. 2010); Pfizer, Inc. v. Teva Pharm. USA, Inc., 518 F.3d 1353, 86 USPQ2d 1001 (Fed. Cir. 2008); Geneva Pharmaceuticals Inc. v. GlaxoSmithKline PLC, 349 F3d 1373, 1385-86, 68 USPQ2d 1865, 1875 (Fed. Cir. 2003).”). See also Sun Pharmaceutical Industries v. Eli Lilly and Co., 611 F. 3d 1381, 1385 (CAFC 2010) (“Our prior obviousness-type double patenting decisions in Geneva and Pfizer … we found claims of a later patent invalid for obviousness-type double patenting where an earlier patent claimed a compound, disclosing its utility in the specification, and a later patent claimed a method of using the compound for a use described in the specification of the earlier patent”).
3) Claims 9, 11, 15, 18-19 and 68-69 stand rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-2 of U.S. Patent No. 11,008,316. Although the claims at issue are not identical, they are not patentably distinct from each other because the ‘316 patent teaches the same compound, which according to the specification of the ‘316 patent, are effective in treating Fabry disease, and reduce the accumulation of GL-3
See MPEP § 804(II)(B)(2)(a) (“In AbbVie Inc. v. Kennedy Institute of Rheumatology Trust, 764 F.3d 1366, 112 USPQ2d 1001 (Fed. Cir. 2014), the court explained that it is also proper to look at the disclosed utility in the reference disclosure to determine the overall question of obviousness in a nonstatutory double patenting context. See Sun Pharm. Indus., Ltd. v. Eli Lilly & Co., 611 F.3d 1381, 95 USPQ2d 1797 (Fed. Cir. 2010); Pfizer, Inc. v. Teva Pharm. USA, Inc., 518 F.3d 1353, 86 USPQ2d 1001 (Fed. Cir. 2008); Geneva Pharmaceuticals Inc. v. GlaxoSmithKline PLC, 349 F3d 1373, 1385-86, 68 USPQ2d 1865, 1875 (Fed. Cir. 2003).”). See also Sun Pharmaceutical Industries v. Eli Lilly and Co., 611 F. 3d 1381, 1385 (CAFC 2010) (“Our prior obviousness-type double patenting decisions in Geneva and Pfizer … we found claims of a later patent invalid for obviousness-type double patenting where an earlier patent claimed a compound, disclosing its utility in the specification, and a later patent claimed a method of using the compound for a use described in the specification of the earlier patent”).
4) Claims 9, 11, 15, 18-19 and 68-69 stand rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-24 of U.S. Patent No. 9,518,049. Although the claims at issue are not identical, they are not patentably distinct from each other because the ‘049 patent teaches the same compound, which according to the specification of the ‘049 patent, are effective in treating Fabry disease, and reduce the accumulation of GL-3
See MPEP § 804(II)(B)(2)(a) (“In AbbVie Inc. v. Kennedy Institute of Rheumatology Trust, 764 F.3d 1366, 112 USPQ2d 1001 (Fed. Cir. 2014), the court explained that it is also proper to look at the disclosed utility in the reference disclosure to determine the overall question of obviousness in a nonstatutory double patenting context. See Sun Pharm. Indus., Ltd. v. Eli Lilly & Co., 611 F.3d 1381, 95 USPQ2d 1797 (Fed. Cir. 2010); Pfizer, Inc. v. Teva Pharm. USA, Inc., 518 F.3d 1353, 86 USPQ2d 1001 (Fed. Cir. 2008); Geneva Pharmaceuticals Inc. v. GlaxoSmithKline PLC, 349 F3d 1373, 1385-86, 68 USPQ2d 1865, 1875 (Fed. Cir. 2003).”). See also Sun Pharmaceutical Industries v. Eli Lilly and Co., 611 F. 3d 1381, 1385 (CAFC 2010) (“Our prior obviousness-type double patenting decisions in Geneva and Pfizer … we found claims of a later patent invalid for obviousness-type double patenting where an earlier patent claimed a compound, disclosing its utility in the specification, and a later patent claimed a method of using the compound for a use described in the specification of the earlier patent”).
5) Claims 9, 11, 15, 18-19 and 68-69 stand rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of U.S. Patent No. 9,682,975. Although the claims at issue are not identical, they are not patentably distinct from each other because the ‘975 patent teaches the same compound, which according to the specification of the ‘975 patent, are effective in treating Fabry disease, and reduce the accumulation of GL-3
See MPEP § 804(II)(B)(2)(a) (“In AbbVie Inc. v. Kennedy Institute of Rheumatology Trust, 764 F.3d 1366, 112 USPQ2d 1001 (Fed. Cir. 2014), the court explained that it is also proper to look at the disclosed utility in the reference disclosure to determine the overall question of obviousness in a nonstatutory double patenting context. See Sun Pharm. Indus., Ltd. v. Eli Lilly & Co., 611 F.3d 1381, 95 USPQ2d 1797 (Fed. Cir. 2010); Pfizer, Inc. v. Teva Pharm. USA, Inc., 518 F.3d 1353, 86 USPQ2d 1001 (Fed. Cir. 2008); Geneva Pharmaceuticals Inc. v. GlaxoSmithKline PLC, 349 F3d 1373, 1385-86, 68 USPQ2d 1865, 1875 (Fed. Cir. 2003).”). See also Sun Pharmaceutical Industries v. Eli Lilly and Co., 611 F. 3d 1381, 1385 (CAFC 2010) (“Our prior obviousness-type double patenting decisions in Geneva and Pfizer … we found claims of a later patent invalid for obviousness-type double patenting where an earlier patent claimed a compound, disclosing its utility in the specification, and a later patent claimed a method of using the compound for a use described in the specification of the earlier patent”).
6) Claims 9, 11, 15, 18-19 and 68-69 stand rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of U.S. Patent No. 10,065,949. Although the claims at issue are not identical, they are not patentably distinct from each other because the ‘949 patent teaches the same compound, which according to the specification of the ‘949 patent, are effective in treating Fabry disease, and reduce the accumulation of GL-3
See MPEP § 804(II)(B)(2)(a) (“In AbbVie Inc. v. Kennedy Institute of Rheumatology Trust, 764 F.3d 1366, 112 USPQ2d 1001 (Fed. Cir. 2014), the court explained that it is also proper to look at the disclosed utility in the reference disclosure to determine the overall question of obviousness in a nonstatutory double patenting context. See Sun Pharm. Indus., Ltd. v. Eli Lilly & Co., 611 F.3d 1381, 95 USPQ2d 1797 (Fed. Cir. 2010); Pfizer, Inc. v. Teva Pharm. USA, Inc., 518 F.3d 1353, 86 USPQ2d 1001 (Fed. Cir. 2008); Geneva Pharmaceuticals Inc. v. GlaxoSmithKline PLC, 349 F3d 1373, 1385-86, 68 USPQ2d 1865, 1875 (Fed. Cir. 2003).”). See also Sun Pharmaceutical Industries v. Eli Lilly and Co., 611 F. 3d 1381, 1385 (CAFC 2010) (“Our prior obviousness-type double patenting decisions in Geneva and Pfizer … we found claims of a later patent invalid for obviousness-type double patenting where an earlier patent claimed a compound, disclosing its utility in the specification, and a later patent claimed a method of using the compound for a use described in the specification of the earlier patent”).
7) Claims 9, 11, 15, 18-19 and 68-69 stand rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of U.S. Patent No. 10,604,518. Although the claims at issue are not identical, they are not patentably distinct from each other because the ‘518 patent teaches the same compound, which according to the specification of the ‘518 patent, are effective in treating Fabry disease, and reduce the accumulation of GL-3
See MPEP § 804(II)(B)(2)(a) (“In AbbVie Inc. v. Kennedy Institute of Rheumatology Trust, 764 F.3d 1366, 112 USPQ2d 1001 (Fed. Cir. 2014), the court explained that it is also proper to look at the disclosed utility in the reference disclosure to determine the overall question of obviousness in a nonstatutory double patenting context. See Sun Pharm. Indus., Ltd. v. Eli Lilly & Co., 611 F.3d 1381, 95 USPQ2d 1797 (Fed. Cir. 2010); Pfizer, Inc. v. Teva Pharm. USA, Inc., 518 F.3d 1353, 86 USPQ2d 1001 (Fed. Cir. 2008); Geneva Pharmaceuticals Inc. v. GlaxoSmithKline PLC, 349 F3d 1373, 1385-86, 68 USPQ2d 1865, 1875 (Fed. Cir. 2003).”). See also Sun Pharmaceutical Industries v. Eli Lilly and Co., 611 F. 3d 1381, 1385 (CAFC 2010) (“Our prior obviousness-type double patenting decisions in Geneva and Pfizer … we found claims of a later patent invalid for obviousness-type double patenting where an earlier patent claimed a compound, disclosing its utility in the specification, and a later patent claimed a method of using the compound for a use described in the specification of the earlier patent”).
8) Claims 9, 11, 15,18-19 and 68-69 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 273-280 of copending Application No. 17/242,016 in view of Palling (US 2010/0113517, cited in previous office action) and Hollak et. al. (Expert Opinion Ther. Targets (2007) 11:821-833, cited by Applicant, cited in previous office action).
The ’016 application teaches (like Bourque in the above 103 rejections) a method of treating Fabry disease comprising the administration of the same or similar compounds as in the instant application including compound GCS452 or its 2-hydrosuccinate salt: GZ452 (see claim 279).
The ‘016 application does not teach that:
1- the subject (i.e., the Fabry patient) has increased GL-3 as compared to healthy cardiomyocytes or has accumulated GL-3, and
2- the subject (i.e., the Fabry patient) is suffering from a cardiac manifestation of Fabry disease.
However, as disclosed in the above 103 rejections, based on the teachings of Palling and Hollak, it will be further obvious to treat the subset of Fabry patients that have increased GL-3 compared to healthy cardiomyocytes and suffer from a cardiac manifestation comprising the administration of the instantly claimed compounds.
This is a provisional nonstatutory double patenting rejection.
Response to Applicant’s arguments related to the above rejection
Applicant's arguments have been fully considered but are not persuasive.
Examiner’s response:
For the same reasons explained above 103 rejections above, the ODP rejections will stand.
Conclusion
No claims are allowed.
Correspondence
Any inquiry concerning this communication or earlier communications from the examiner should be directed to MARCOS L SZNAIDMAN whose telephone number is (571)270-3498. The examiner can normally be reached Flexing M-F 7 AM-7 PM.
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/MARCOS L SZNAIDMAN/
Primary Examiner, Art Unit 1628
October 17, 2025.