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
Request for Continued Examination
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 08/19/2025 has been entered.
Review of Claim Status
Claims 1-2, 4-5, 7-8, 11-18, 21-22 were examined in prior Office Action.
Upon RCE Amendment entry, Claims 3, 6, 19-20 remain withdrawn.
Upon RCE Amendment entry, Claims 1 was amended.
Claims 1-2, 4-5, 7-8, 11-18, 21-22 are currently pending investigation.
Priority
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Applicant claims NO priority; therefore the effective filing date is 10/14/2022.
Information Disclosure Statements
All references have been considered in the one (1) IDS(s) filed on 08/19/2025 unless marked with a strikethrough.
Review of Restriction Election
Applicant elected the following species: fasudil as the rho kinase inhibitor (see below) and SOD mutations as the genetic mutation. Claims 1-2, 4-5, and 7-18 encompass the elected species. The elected specie was found in the art (please see 102 and 103 rejections below).
Examiner Responses to Amendments/Arguments
The issues raised in the Office Action are addressed below:
I. Claim Amendments –
Independent Claim 1 has the following added limitation: A method of treating a human patient diagnosed with familial amyotrophic lateral sclerosis (ALS), comprising orally administering a therapeutically effective amount of fasudil or hydroxyfasudil (M3), or a pharmaceutically acceptable salt thereof, to the patient.
II. Claim Rejections –
a. Rejections Under 35 U.S.C. 102
Applicant' s arguments, filed 08/19/2025, with respect to the claims have been fully considered but they are not persuasive for the following reason(s):
Applicant has stated that Lingor is not an enabling reference.
Applicant further states:
“Lingor doesn't anticipate the claims because it is not enabled for treating SOD1 mice or humans with familial ALS with oral fasudil at any dose without undue experimentation.”
“Lingor doesn't enable treating an ALS patient with orally administered fasudil (or hydroxyfasudil). Although Lingor discloses treating familial ALS, i.e., ALS patients with SOD1 mutations, Lingor's claims are supported only by experiments in the SOD1 G93A-transgenic mouse model of ALS - not ALS patients.”
Examiner disagrees.
In response to the Applicant’s argument that the reference is not enabling:
As seen in col. 2, lns. 40-45, Lingor states “The inventors decided to evaluate the therapeutic potential of the ROCK inhibitor Fasudil in the chronic SOD1 G93A mouse model of ALS ((B6SJL-TgN (SOD1-G93A) 1Gur), that reflects the evolution of ALS disease clinically very well over a period of up to 22 weeks.” This statement is also supported by the evidentiary reference of Gunther for reading on the claims.
According to MPEP 2121: Prior art is presumed to be operable/enabling.
When the reference relied on expressly anticipates or makes obvious all of the elements of the claimed invention, the reference is presumed to be operable. Once such a reference is found, the burden is on applicant to provide facts rebutting the presumption of operability. In re Sasse, 629 F.2d 675, 207 USPQ 107 (CCPA 1980).
US patents are presumed to be enabled. According to 35 U.S.C. § 282, it states: “A patent shall be presumed valid.”
In response to Applicant's addition of the limitation: of treating a human patient diagnosed with familial amyotrophic lateral sclerosis (ALS).
With respect to the added limitation of ‘human’ to Claim 1. Amyotrophic lateral sclerosis (ALS) is called Lou Gehrig's disease after the American baseball player Lou Gehrig. This background, with the prior art discussing dosing suggests human patients.
The evidentiary reference explicitly states the model uses human SOD (Günther - title; abstract; pg. 1 to pg. 2-col. 1, para. 2). Further, as evidenced by The Jackson Laboratory, SOD1-G93A transgenic mice express a mutant form of human SOD1 (superoxide dismutase 1), not a mouse form. Specifically, these mice are genetically engineered to carry and express multiple copies of the human SOD1 gene containing a glycine-to-alanine substitution at position 93 (G93A).
As seen in col. 2, lns. 40-45, Lingor states “The inventors decided to evaluate the therapeutic potential of the ROCK inhibitor Fasudil in the chronic SOD1 G93A mouse model of ALS ((B6SJL-TgN (SOD1-G93A) 1Gur), that reflects the evolution of ALS disease clinically very well over a period of up to 22 weeks.”
Therefore, given that the model is for humans, and that the common name of the disease is human, and that the background infers human patients. The amendment to a ‘human’ patient population has been considered but is not found to be persuasive.
In response to applicant's argument that the references fail to show certain features of the invention, it is noted that the features upon which applicant relies (i.e., ALS patients with SOD1 mutations, Lingor's claims are experiments in the SOD1 experiments, more specifically to mouse model of ALS) and geared to humans.
It must be noted that the US 9,980,972 B2 patent teaches (col. 7, lns. 54-60): “The subject may be a mammal, such as a mouse, rat, guinea pig, dog, cat, pig, sheep, horse, or cow. Preferably, the subject is a primate, and most preferably a human. As it can be taken from the experimental section, the invention is preferably effective in females. Accordingly, in a preferred embodiment of the invention, the subject is a female.”
As seen in col. 2, lns. 40-45, Lingor states “The inventors decided to evaluate the therapeutic potential of the ROCK inhibitor Fasudil in the chronic SOD1 G93A mouse model of ALS ((B6SJL-TgN (SOD1-G93A) 1Gur), that reflects the evolution of ALS disease clinically very well over a period of up to 22 weeks.”
Further, the prior art is good for all it wholly teaches. Although the models are for mice, the art explicitly teaches that humans are a preferred patient population, through its use of these transgenic mice. They are genetically engineered to carry and express multiple copies of the human SOD1 gene containing a glycine-to-alanine substitution at position 93 (G93A), therefore it teaches the claims. Correspondingly (col. 10, lns. 57-67), Lingor continues teaching “dose translation from one animal to another animal or from an animal to human studies is well known in the art, - Reagan-Shaw et al. (2007), which is incorporated herewith by reference, in particular FIG. 1 and Table 1.”
Similarly, Lingor teaches a pharmaceutical composition, comprising or consisting of 1-(5-isoquinolinesulfonyl) homopiperazine (fasudil), or a fasudil derivative for use in the treatment of a subject suffering or prone to suffer from sporadic or familial ALS, which is the scope of Applicant’s claims.
Additionally (col. 22, lns. 28-36), “Reactive astrogliosis represents another parameter in the evaluation of histologic manifestation of ALS disease. In human ALS patients, the clinical progression of this neurodegenerative disease seems to be associated with changes in astrocytic cell infiltration in the spinal cord. Therefore, the inventors evaluated the extent of astrogliosis in the lumbar spinal cord by counting the number of GFAP positive astroglial cells in the ventral horn and normalized values to area (FIG. 12).
As such, the functional language is met for the claims. The Applicants argument is not persuasive.
b. Rejections Under 35 U.S.C. 103
Applicant states: “The claims are not obvious over Lingor, combined with any of the other cited references, either. Because Lingor's results show no treatment effects of fasudil on symptomatic SOD] transgenic mice, and because Lingor's human trials of ALS patients failed, Lingor fails to provide the requisite reasonable expectation of success of treating familial ALS patients with orally administered fasudil.”
Examiner disagrees.
With respect to the added limitation of ‘human’ to Claim 1. Amyotrophic lateral sclerosis (ALS) is called Lou Gehrig's disease after the American baseball player Lou Gehrig. This background, with the prior art discussing dosing suggests human patients.
The evidentiary reference explicitly states that the model uses human SOD (Günther - title; abstract; pg. 1 to pg. 2-col. 1, para. 2). Further, as evidenced by The Jackson Laboratory, SOD1-G93A transgenic mice express a mutant form of human SOD1 (superoxide dismutase 1), not a mouse form. Specifically, these mice are genetically engineered to carry and express multiple copies of the human SOD1 gene containing a glycine-to-alanine substitution at position 93 (G93A).
Therefore, given that the model is for humans, and that the common name of the disease is human, and that the background infers human patients. The amendment to a ‘human’ patient population has been considered but is not found to be persuasive.
According to MPEP 2131, it states that “Extra References and Extrinsic Evidence Can Be Used To Show the Primary Reference Contains an “Enabled Disclosure”.
When the claimed composition or machine is disclosed identically by the reference, an additional reference may be relied on to show that the primary reference has an “enabled disclosure.” In re Samour, 571 F.2d 559, 197 USPQ 1 (CCPA 1978) and In re Donohue, 766 F.2d 531, 226 USPQ 619 (Fed. Cir. 1985)”
So in response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
Additionally, Lingor teaches a pharmaceutical composition, comprising or consisting fasudil, or a fasudil derivative for use in the treatment of a subject suffering or prone to suffer from sporadic or familial ALS, which is the scope of Applicant’s claims. As such, the functional language is met for the claims. A recitation of the intended use of the claimed invention must result in a structural difference between the claimed invention and the prior art in order to patentably distinguish the claimed invention from the prior art. If the prior art structure is capable of performing the intended use, then it meets the claim.
Independently, the Applicant has not shown the criticality of the use of the “a method of treating a human patient diagnosed with familial amyotrophic lateral sclerosis (ALS), comprising orally administering a therapeutically effective amount of fasudil or hydroxyfasudil (M3), or a pharmaceutically acceptable salt thereof, to the patient” that would differ from that seen already in the art.
In the weight of this evidence, Examiner still states it is obvious with this combination, if the composition and patient population are the same, then the functional readout would necessitate similar results.
The Applicants argument is not persuasive.
The 35 USC § 102 & 103 Rejections are maintained.
III. Maintained Rejections -
Claim Rejections - 35 USC § 102
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.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1-2, 4-5, 8, 11-12, 18, 21-22 are rejected under 35 U.S.C. 102(a)(1) & 102(a)(2) as being anticipated by P. Lingor, et. al in US 9,980,972 B2 (hereinafter “Lingor”) as evidenced by R. Günther, in “Rho Kinase Inhibition with Fasudil in the SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis—Symptomatic Treatment Potential after Disease Onset (Front. Pharmacol. 8:17, 2017; hereinafter “Günther”) and Chemical supplier The Jackson Company.
This rejection relates to the elected specie.
With respect to Claim 1, Lingor teaches a method of treating a patient with familial amyotrophic lateral sclerosis (ALS) comprising orally administering a therapeutically effective (col. 5, lns. 17-18) amount of a fasudil (col. 3, lns. 1-5) or hydroxyfasudil (M3), or a pharmaceutically acceptable salt thereof, to the patient (the chemical name for fasudil is 1-[5-isoquinolinesulfonyl]homopiperazine; col. 3, lns. 6-8).
With respect to the added limitation of ‘human’ to Claim 1. Amyotrophic lateral sclerosis (ALS) is called Lou Gehrig's disease after the American baseball player Lou Gehrig. This background, with the prior art discussing dosing suggests human patients.
The evidentiary reference explicitly states that the model uses human SOD (Günther - title; abstract; pg. 1 to pg. 2-col. 1, para. 2). Given that the model is for humans, and that the common name of the disease is a human, and that the background infers human patients.
Further, as evidenced by The Jackson Laboratory, SOD1-G93A transgenic mice express a mutant form of human SOD1 (superoxide dismutase 1), not a mouse form. Specifically, these mice are genetically engineered to carry and express multiple copies of the human SOD1 gene containing a glycine-to-alanine substitution at position 93 (G93A).
Therefore, given that the model is for humans, and that the common name of the disease is human, and that the background infers human patients.
As seen in col. 2, lns. 40-45, Lingor states “The inventors decided to evaluate the therapeutic potential of the ROCK inhibitor Fasudil in the chronic SOD1 G93A mouse model of ALS ((B6SJL-TgN (SOD1-G93A) 1Gur), that reflects the evolution of ALS disease clinically very well over a period of up to 22 weeks.”
Claim 2: wherein the patient has a mutation in superoxidase dismutase gene 1 (SOD1) (col. 2, lns. 58-60).
Claim 4: wherein the patient has only lower motor neuron involvement (paragraph teaches the earliest symptoms of ALS in a patient, as well as diagnostic signs whether in the upper or lower motor neurons which indicated signs of ALS with further criteria as how to detection criteria; col. 8, lns. 20-42)
Claim 5: wherein the patient has only upper motor neuron involvement (paragraph teaches the earliest symptoms of ALS in a patient, as well as diagnostic signs whether in the upper or lower motor neurons which indicated signs of ALS with further criteria as how to criteria of detection; col. 8, lns. 20-42).
Claim 8: wherein the treatment results in reduced muscle wasting and reduced paralysis of voluntary muscles (col. 8, lns. 20-42).
Claim 11: wherein the patient is treated with fasudil hydrochloride (1-(5-isoquinoline
sulfonyl)homopiperazine, fasudil, or a pharmaceutically acceptable salt thereof, for use in the treatment of a subject suffering from ALS; col. 2, lns. 65-67 to col. 3, lns. 1-2; col. 6, lns. 13-15).
Claim 12: wherein the isoquinoline is treated with hydroxyfausdil, M3 (…the fasudil derivative is 1-(6-hydroxyl-5-iso-quinolinesulfonyl)homopiperazine, hydroxyl-fasudil; col. 3, lns. 1-5; as such is executed in its intended use throughout the prior art).
Claim 18: wherein the fasudil is administered in a sustained release formulation (col. 12, lns. 30-35).
Claim 21: wherein the fasudil is fasudil hydrochloride hemihydrate (col. 5, lns 59 to col. 6, lns. 1-3).
Claim 22: wherein the fasudil is fasudil hydrochloride hemihydrate (col. 5, lns 59 to col. 6, lns. 1-3).
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Joint Inventors
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) 7 is rejected under 35 U.S.C. 103 as being unpatentable over P. Lingor, et. al in US 9,980,972 B2 (hereinafter “Lingor”) as evidenced by R. Günther, in “Rho Kinase Inhibition with Fasudil in the SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis—Symptomatic Treatment Potential after Disease Onset (Front. Pharmacol. 8:17, 2017; hereinafter “Günther”) and Chemical supplier The Jackson Company, and in view of Cedarbaum, et. al titled “The ALSFRS-R: a revised ALS functional rating scale…” (hereinafter “Cedarbaum”).
The teachings of Lingor is disclosed above and at least those teachings are incorporated by reference herein.
Lingor fails to teach the treatment results in 50% reduction in the decline over at least three months as measured on the revised ALS Functional Rating Scale (ALSFRS-R).
Cedarbaum teaches the ALS Functional Rating Scale (ALSFRS) is a validated rating instrument for monitoring the progression of disability in patients with amyotrophic lateral sclerosis (ALS). The ALSFRS test accurately tracks progression of patients’ disability in ALS. Inclusion of assessments of ADL function such as the ALSFRS is an essential element of the design of ALS clinical trials. The ALSFRS-R was a stronger predictor than the original scale, with a larger likelihood ratio chi-square than for the ALSFRS, 5.3 for the ALSFRS-R compared with 4.0 for the ALSFRS in a model that also included baseline FVC% and the patient’s age Fig. 3 (pg. 20; 9-month survival rates) shows the predicted values of the logistic regression model for 9-month survival based on the baseline ALSFRS-R score.
It would therefore be obvious to one skilled in the art to combine Lingor and Cedarbaum since Lingor teaches each component individually (referenced above) and known as components of the method of treating a patient with familial amyotrophic lateral sclerosis (ALS). Cedarbaum teaches how to understand the results of the ALSFRS-R score and its importance in understanding the progression of the disease but to also see how the treatment results would show reduction in the decline of the disease.
Lingor and Cedarbaum teaches one in the art would have been motivated by the specific examples (experimental results) just how effective the use of fasudil hydrochloride is in protecting again cell death resulting from SOD1 damage, which teaches to the same utility as the Instant Application.
Claims 13-15 are rejected under 35 U.S.C. 103 as being unpatentable over P. Lingor, et. al in US 9,980,972 B2 (hereinafter “Lingor”) as evidenced by R. Günther, in “Rho Kinase Inhibition with Fasudil in the SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis—Symptomatic Treatment Potential after Disease Onset (Front. Pharmacol. 8:17, 2017; hereinafter “Günther”) and Chemical supplier The Jackson Company..
The teachings of Lingor is disclosed above and at least those teachings are incorporated by reference herein.
Lingor fails to explicitly teach the ranges and points within the ranges as asserted in the Instant Claims 13-15.
However Lignor does teach: Claim 13: where the patient is treated with a daily dose of 90 to 240 mg/day (col. 10, lns. 44-67; col. 11, lns. 1-14-Table 1) teaches “Dose translation from one animal to another animal or from an animal to human studies is well known in the art, cf. Reagan-Shaw et al. (2007), which is incorporated herewith by reference, in particular FIG. 1 and Table 1. Accordingly, the human equivalent dose (HED; mg per kg body weight) may be calculated as follows: HED (mg/kg)=Animal dose (mg/kg)x(Animal Km/Human Km). As such fasudil is to be administered in a dosage of 2-4 mg/kg for a 60 kg adult body weight per day is 120-240 mg/day; which reads within the claimed range”.
Claim 14: wherein the daily dose is 180 mg/day (col. 10, lns. 44-67; col. 11, lns. 1-14-Table 1) teaches “Dose translation from one animal to another animal or from an animal to human studies is well known in the art, cf. Reagan-Shaw et al. (2007), which is incorporated herewith by reference, in particular FIG. 1 and Table 1. Accordingly, the human equivalent dose (HED; mg per kg body weight) may be calculated as follows: HED (mg/kg)=Animal dose (mg/kg)x(Animal Km/Human Km). As such fasudil is to be administered in a dosage of 1.5 - 6 mg/kg for a 60 kg adult body weight per day is 90 -360 mg/day; which reads on the claim point of 180 mg/kg; col. 12, lns. 30-35).
Claim 15: wherein the daily dose is 240 mg/day (col. 10, lns. 44-67; col. 11, lns. 1-14-Table 1) teaches “Dose translation from one animal to another animal or from an animal to human studies is well known in the art, cf. Reagan-Shaw et al. (2007), which is incorporated herewith by reference, in particular FIG. 1 and Table 1. Accordingly, the human equivalent dose (HED; mg per kg body weight) may be calculated as follows: HED (mg/kg)=Animal dose (mg/kg)x(Animal Km/Human Km). As such fasudil is to be administered in a dosage of 1.5 -6 mg/kg for a 60 kg adult body weight per day is 90 -360 mg/day; which reads on the claim point of 180 mg/kg; col. 12, lns. 30-35).
However, it would have been prima facie obvious to one having ordinary skill in the art to arrive at an overlapping range because according to MPEP 2144.05
Overlapping ranges:
In the case where the claimed ranges “overlap or lie inside ranges disclosed by the prior art” a prima facie case of obviousness exists. In re Wertheim, 541 F.2d 257, 191 USPQ 90 (CCPA 1976); In re Woodruff, 919 F.2d 1575, 16 USPQ2d 1934 (Fed. Cir. 1990) (The prior art taught carbon monoxide concentrations of “about 1-5%” while the claim was limited to “more than 5%.” The court held that “about 1-5%” allowed for concentrations slightly above 5% thus the ranges overlapped.); In re Geisler, 116 F.3d 1465, 1469-71, 43 USPQ2d 1362, 1365-66 (Fed. Cir. 1997) (Claim reciting thickness of a protective layer as falling within a range of “50 to 100 Angstroms” considered prima facie obvious in view of prior art reference teaching that “for suitable protection, the thickness of the protective layer should be not less than about 10 nm [i.e., 100 Angstroms].” The court stated that “by stating that ‘suitable protection’ is provided if the protective layer is ‘about’ 100 Angstroms thick, [the prior art reference] directly teaches the use of a thickness within [applicant’s] claimed range.”).
Claim(s) 16-17 are rejected under 35 U.S.C. 103 as being unpatentable over P. Lingor, et. al in US 9,980,972 B2 (hereinafter “Lingor”) as evidenced by R. Günther, in “Rho Kinase Inhibition with Fasudil in the SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis—Symptomatic Treatment Potential after Disease Onset (Front. Pharmacol. 8:17, 2017; hereinafter “Günther”) and Chemical supplier The Jackson Company, and in view of M. Takata in “Fasudil, a rho kinase inhibitor, limits motor neuron loss in experimental models of amyotrophic lateral sclerosis” (hereinafter “Takata”).
The teachings of Lingor is disclosed above and at least those teachings are incorporated by reference herein.
Lingor fails to teach the equal portions of a dose measured in two or three equal portions.
Takata teaches amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder with no effective treatment. Fasudil hydrochloride (fasudil), a potent rho kinase (ROCK) inhibitor and its experimental study teaches to:
Claim 16: wherein the dose is administered in three equal portions throughout the day (pg. 343, col. 2, para. 1; the prior art uses two doses of fasudil hydrochloride: 30 - a low dose - and 100 mg·kg−1 - a high dose - in drinking water implicitly teaching that the dose is being administered at 2 and 3 equal portions depending on the amount of drinking water)
Claim 17: wherein the dose is administered in two equal portions throughout the day (pg. 343, col. 2, para. 1; the prior art uses two doses of fasudil hydrochloride: 30 - a low dose - and 100 mg·kg−1 - a high dose - in drinking water implicitly teaching that the dose is being administered at 2 and 3 equal portions depending on the amount of drinking water)
It would therefore be obvious to one skilled in the art to combine Lingor and Takata since Lingor teaches each component individually (referenced above) and known as components of the method of treating a patient with familial amyotrophic lateral sclerosis (ALS). Takata teaches amyotrophic lateral sclerosis (ALS) where the dose is administered. Lingor and Takata teaches one in the art would have been motivated by the specific examples (experimental results) and just how effective the use of fasudil hydrochloride is in protecting again cell death resulting from SOD1 damage, which teaches to the same utility as the Instant Application.
Conclusion
Claims 1-2, 4-5, 7-8, 11-18, 21-22 are rejected.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Josmalen M. Ramos-Lewis whose telephone number is (571)272-0084. The examiner can normally be reached M-F 9:30-5:30 pm.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Clinton A. Brooks can be reached on (571) 270-7682. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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Josmalen M. Ramos-Lewis, Ph.D.
Patent Examiner
Art Unit 1621
/CLINTON A BROOKS/Supervisory Patent Examiner, Art Unit 1621
Prosecution Insights