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 .
Response to Amendment
The amendment filed 06/08/2026 is acknowledged. Claims 1-6 and 8-16 are amended and claims 7 and 17 are newly canceled. Claims 1-6 and 8-16 are under examination.
Priority
Applicant’s amendment has incorporated the limitations of now canceled claim 7 into the independent claims. Since the subject matter in claims 7 is not supported by the ‘538 provisional (see p. 4 of the Office action mailed 01/07/2026, the effective filing date of claims 1-6 and 8-16 is 06/04/2021.
Objections/Rejections Withdrawn
Any previous rejections over claims 7 and 17 are hereby withdrawn in response to Applicant’s cancelation of those claims.
Drawings
The drawings were received on 06/08/2026. These drawings are accepted. Further, the objection to the drawings because of blurriness is withdrawn in response to Applicant’s amendment of the drawings filed 06/08/2026.
Specification
The objection to the disclosure because it contains an embedded hyperlink and/or other form of browser-executable code is withdrawn in response to Applicant’s amendment of p. 17 of the instant specification deleting the embedded hyperlink.
Claim Objections
The objection to claims 2-6, 8, 9, 14 and 16 for minor informalities is withdrawn in response to Applicant’s amendment of the claim correcting grammatical and typographical errors.
Claim Rejections - 35 USC § 112(b)
The rejection of claims 2-6, 10-12 and 16 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention is withdrawn in response to Applicant’s amendment. Specifically, claim 2-6 and 16 have been amended to recite “wherein the ligand is activin” after “ACVR1”; claim 11 no longer recites a trademark; and claim 16 recites the limitation has been amended to correct the antecedent basis issue, thereby rendering the claims definite.
Claim Rejections - 35 USC § 112(a)
The rejection of claims 1 and 8-16 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, for scope of enablement is withdrawn in response to Applicant’s amendment of claim 1 to recite known inhibitors.
The rejection of claims 1 and 8-16 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement is withdrawn in response to Applicant’s amendment of claim 1 to recite known inhibitors.
Claim Rejections - 35 USC § 102
The rejection of claims 1 8-10 and 12-15 under 35 U.S.C. 102(a)(1) as being anticipated by Karni et al. (WO 2013186777) is withdrawn in response to Applicant’s amendment of the claims to delete reference to the inhibitor LDN-193189.
The rejection of claims 1, 8 and 9 under 35 U.S.C. 102(a)(1) as being anticipated by Izrael et al. (WO 2015/186128) is withdrawn in response to Applicant’s amendment of the claims to delete reference to the inhibitor LDN-193189.
Claim Rejections - 35 USC § 103
The following rejections under 35 U.S.C. 103 are withdrawn in response to Applicant’s amendment of claim 1 to delete reference to the ACVR1 inhibitor LDN-193189.
The rejection of claims 1-6 and 8-15 as being unpatentable over Karni et al. (WO 2013186777—cited above) in view of Barber (WO2008039514).
The rejection of claims 1-6, 8-10 and 12-16 as being unpatentable over (WO 2013186777—cited above) in view of Gromada et al. (WO 2015017576) is withdrawn in response to Applicant’s amendment of the claims to delete reference to the ACVR1 inhibitor LDN-193189.
The rejection of claim 17 as being unpatentable over Karni et al. and Gromada et al. as applied to claims 1-10 and 12-16 above, and further in view of Latres et al. (Nature Communications 8: 15153; DOI: 10.1038/ncomms15153).
Rejections Maintained/New Rejections
Claim Rejections - 35 USC § 112(a)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
The rejection of claims 2-6 for scope of enablement is maintained for reasons of record and the following. Applicant’s amendment to the independent claims to recite particular ACVR1 inhibitors and to remove the language of prevention overcomes those issues. Nevertheless, claims 2-6 are still broad with respect to modulators of the ACVR1 ligand. The added limitation of modulators of activin is broad because there are many signaling pathways through which activin may be modulated. Further, as noted at p. 9 of the Office action mailed 01/07/2026, “modulate” encompasses both up- and down-regulation. See Figure 1 at pages 740-741 of Bloise et al. (PhysiolRev99:739–780,2019), which provides a schematic for activin “receptor binding and downstream signaling”. The breadth and complexity in the development of activin antagonists and agonists is outlined at pages 765-766 of Bloise et al., who conclude “[t]his ubiquitous, albeit precise, distribution of activin A creates, at the same time, vast opportunities and huge challenges to translate the accumulated knowledge of activin physiology from bench to bedside.” In summary, the evidence in the art and the instant specification is not commensurate with the broad scope of the recited activin modulators for treating neurodegenerative disease.
Response to Arguments
Applicant argues at p. 9 that the claims have been amended to remove prevention language and specifically enumerate the ACVR1 inhibitors.
This argument has been fully considered, but is not found persuasive. While Applicant’s amendment has addressed the issues raised with regard to prevention and the ACVR1 inhibitors, the claims remain broad with respect to modulators of activin for the reasons explained in the preceding paragraph, hereby incorporated.
The rejection of claims 2-6 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement is maintained for reasons of record and the following. Applicant’s amendment to the independent claims to recite particular ACVR1 inhibitors and to remove the language of prevention overcomes those issues. Nevertheless, claims 2-6 recite modulators of the ACVR1 ligand. Further, as noted at p. 13 of the Office action mailed 01/07/2026, “modulate” encompasses both up- and down-regulation. While the claims have been amended to add the limitation of modulators of activin, there are many signaling pathways through which activin may be modulated. The instant specification discloses a single activin modulator, the anti-activin antibody, namely, REGN2477. The single species disclosed in the instant application as originally filed is not representative the genus of activin modulators capable of treating neurodegenerative disease, promoting remyelination, ameliorating demyelination or decreasing differentiation of progenitors to astrocytes. See Figure 1 at pages 740-741 of Bloise et al. (PhysiolRev99:739–780,2019), which provides a schematic for activin “receptor binding and downstream signaling”. The skilled artisan cannot envision the detailed chemical structure of the encompassed activin modulators, and therefore conception is not achieved until reduction to practice has occurred, regardless of the complexity or simplicity of the method of isolation.
Response to Arguments
Applicant argues at p. 10 that the claims have been amended to recite the disclosed species of ACVRI1 inhibitors, therefore, the written description requirement is satisfied.
This argument has been fully considered, but is not found persuasive. While Applicant’s amendment has addressed the issues raised with regard to the ACVR1 inhibitors, the claims encompass a genus of modulators of activin, which is not described in the application as originally filed. See the preceding paragraph, hereby incorporated.
Notice for all US Patent Applications filed on or after March 16, 2013: 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.
Claim Rejections - 35 USC § 102
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 rejections under 35 U.S.C. 102(a)(1) are maintained for reasons of record and the following. Applicant has amended the claims to delete reference to LDN-193189 as an ACVR1 inhibitor, however, claims 2-6 also recite administering to the mammal an effective amount of an agent that modulates a ligand for ACVR1, wherein the ligand is activin. The small molecule LDN-193189 modulates activin.
The rejection of claims 2-6 as being anticipated by Karni et al. (WO 2013186777).
The rejection of claims 2-6 under 35 U.S.C. 102(a)(1) as being anticipated by Izrael et al. (WO 2015/186128).
Response to Arguments
Applicant argues at pages 10-11 that Karni et al. and Izrael et al. do not teach any of the agents recited in amended claim 1.
This argument has been fully considered, but is not found persuasive. Claims 2-6 are independent claims that read on administration of an agent that “modulates a ligand for ACVR1, wherein the ligand is activin”, in the alternative. According to Horbelt et al. (JBC, 2015, 290: 3390-3404) LDN-193180 by inhibiting GDF8 signaling, also modulates the activin receptors (ActRIIA and ActRIIB), and therefore, activin (see p. 3391, left column, 3rd paragraph):
Here, we report that dorsomorphin and LDN-193189 activities, even within the TGF-family, are not restricted to type I receptors but extend also to the type II receptors ActRIIA and ActRIIB…
See also p. 3393, right column, which teaches that LDN-193189 binds ActRIIA. The MPEP 2131.01 states that evidentiary references are proper in anticipation rejections when they illustrate that a characteristic not disclosed in the reference is inherent. In summary, LDN-193189 is an activin modulator.
New Claim Rejections - 35 USC § 102
Claims 1-6, 8 and 9 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Shi (WO2017/223241). This rejection was necessitated by amendment. Shi teaches a method of treating a neurodegenerative disease comprising administering a small molecule such as LDN-212854, wherein the subject is human (see claims 11-17). Since the document by Shi teaches treating a neurodegenerative disease, it flows therefrom it treats neurodegeneration, thus meeting limitations set forth in claims 1, 2, 8 and 9. Shi teaches that the contemplated neurodegenerative diseases include multiple sclerosis (paragraph [0006]; [0043]), a condition known to be characterized by demyelination, wherein the patient population is in need of promoting myelination, thus it flows therefrom that Shi meets the limitations set forth in claims 3-5. Moreover, because Shi teaches administration of the same agent to ameliorate neurodegenerative disease and demyelination in the same patient population, the same clinically significant improvements as recited in claims 1-6 regarding treatment, promoting myelination and decreasing differentiation of progenitors to astrocytes, is inherent to their teachings (see Ex parte Novitski, 26 USPQ2d 1389 (BPAI 1993); see also Integra LifeSciences I Ltd. V. Merck KGaA, (DC SCalif) 50 USPQ2d 1846)). The treatment methods set forth in the Shi document must, by definition, achieve the same clinically significant improvements as recited in claims 1-6 absent evidence to the contrary.
Claims 1-6, 8 and 9 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Albers (WO 2017173451). This rejection was necessitated by amendment. Albers teaches methods of treating neurodegenerative disease, such as Alzheimer's disease, amyotrophic lateral sclerosis, frontotemporal dementia and others comprising administering small molecule inhibitors such as momelotinib (see claims 5-8). Since human diseases are contemplated, it flows therefrom that treatment of humans is contemplated (see also pages 41-45, Example 1 of Albers, which describes experiments performed in human neurons). Because Albers teaches administration of the same agent to treat a patient population suffering from neurodegenerative disease, the same clinically significant improvements as recited in claims 1-6 regarding treatment, promoting myelination and decreasing differentiation of progenitors to astrocytes, is inherent to their teachings (see Ex parte Novitski, 26 USPQ2d 1389 (BPAI 1993); see also Integra LifeSciences I Ltd. V. Merck KGaA, (DC SCalif) 50 USPQ2d 1846)). The treatment methods set forth in the Albers document must, by definition, achieve the same clinically significant improvements as recited in claims 1-6 absent evidence to the contrary.
New Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1-6, 8-10 and 12-15 are rejected under 35 U.S.C. 103 as being unpatentable over Shi (WO2017/223241) in view of Karni et al. (WO 2013186777—of record). This rejection was necessitated by amendment. The first factor to consider when making a rejection under 35 U.S.C. 103(a) is to determine the scope and contents of the prior art. Shi teaches a method of treating a neurodegenerative disease comprising administering a small molecule such as LDN-212854, wherein the subject is human (see claims 11-17). Shi teaches that the neurodegenerative diseases may include Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS—see paragraph [0043]). Since the document by Shi teaches treating a neurodegenerative disease, it flows therefrom it treats neurodegeneration, thus meeting limitations set forth in claims 1, 2, 8 and 9. Further, since Shi teaches that the contemplated neurodegenerative diseases include multiple sclerosis (paragraph [0006]; [0043]), a condition known to be characterized by demyelination, wherein the patient population is in need of promoting myelination, it flows therefrom that Shi meets the limitations set forth in claims 3-5.
Moreover, because Shi teaches administration of the same agent to ameliorate neurodegenerative disease and demyelination in the same patient population, the same clinically significant improvements as recited in claims 1-6 are inherent. The recited effects of the LDN-212854 on the patient population are part of to the understandings and expectations disclosed in the prior art of the Shi document. The method of treatment comprising administering LDN-212854 was part of the disclosure of the prior art, so the effects upon the body of the patients are inherent. Further, for the record, the express, implicit, and inherent disclosures of a prior art reference may be relied upon in the rejection of claims under 35 U.S.C. 103. “The inherent teaching of a prior art reference, a question of fact, arises both in the context of anticipation and obviousness.” In re Napier, 55 F.3d 610, 613, 34 USPQ2d 1782, 1784 (Fed. Cir. 1995) (affirmed a 35 U.S.C. 103 rejection based in part on inherent disclosure in one of the references). See also In re Grasselli, 713 F.2d 731, 739, 218 USPQ 769, 775 (Fed. Cir. 1983). See also MPEP 2112. Thus, Shi teaches the limitations of claims 1-6, 8 and 9.
The second factor to consider is to ascertain the differences between the prior art and the instant claims. Shi does not teach treatment with additional agents as recited in claims 10 and 12-15. Karni et al. teach treating neurodegenerative diseases, including MS, Alzheimer’s disease, Parkinson’s disease and ALS (claims 20-35) and that when treating various neurodegenerative diseases, additional agents “may be required” (see p. 35, 3rd-6th paragraphs; p. 40, 2nd paragraph; claims 36 and 37). Specifically, Karni et al. teach co-administering with their inventive composition: (1) donepezil, galantamine, rivastigmine or memantine when treating Alzheimer’s disease, (2) pramipexole, ropinirole, selegiline or rasagiline when treating Parkinson’s disease, (3) the promyelinating agent, benztropine and (4) glatiramer acetate, interferon-beta, natalizumab, fingolimod, mitoxantrone, dimethyl fumarate, teriflunomide or alemtuzumab when treating MS (see p. 31, 2nd paragraph; p. 35, last paragraph; p. 36, 1st line and 2nd paragraph), thereby meeting limitations of claims 10 and 12-15.
It would have been obvious to the person of ordinary skill in the art at the time of the filing of the invention to modify the teachings of Shi by co-administering agents to treat Alzheimer’s, Parkinson’s and MS, as taught in Karni because these agents were part of the standard treatment of these particular neurodegenerative diseases. The person of ordinary skill in the art would have been motivated to try all known treatments for these conditions because they are progressive and ultimately incurable. Furthermore, the person of ordinary skill in the art could have reasonably expected success because Karni et al. suggest that “[a] person skilled in the art in the field of the invention (e.g. a physician) will know how to identify an "additional therapeutic agent" that will be suitable for the treatment of any of the… neurodegenerative disease[s] or CNS damage encompassed by the present disclosure”.
Thus, the claims do not contribute anything non-obvious over the prior art.
Claims 1-6 and 8-15 are rejected under 35 U.S.C. 103 as being unpatentable over Shi and Karni et al. as applied to claims 1-6, 8-10 and 12-15 above, and further in view of Barber (WO2008039514—of record). This rejection was necessitated by amendment. The first factor to consider is to ascertain the differences between the prior art and the instant claims. While Karni et al. disclose that the single approved medicine for ALS is riluzole (see paragraph bridging pages 31 and 32), the combined teachings of Shi and Karni do not explicitly teach co-administering riluzole with LDN-212854. Barber teaches co-administering riluzole with their inventive compound in order to treat ALS (see claims 1-6).
It would have been obvious to the person of ordinary skill in the art at the time of the filing of the invention to co-administer riluzole because even though it is not curative, it is the only approved medicine for treating ALS. The person of ordinary skill in the art would have been motivated to co-administer riluzole because ALS is “rapidly progressive [and] invariably fatal”, and co-administering it with other agents may improve its efficacy (see paragraphs [0015] and [0025] of Barber). There is also a normal desire of those having ordinary skill in the art to use all possible methods of treatment to treat such a devastating disease. Furthermore, the person of ordinary skill in the art could have reasonably expected success because Karni et al. suggest that “[a] person skilled in the art in the field of the invention (e.g. a physician) will know how to identify an "additional therapeutic agent" that will be suitable for the treatment of any of the… neurodegenerative disease[s] or CNS damage encompassed by the present disclosure”, and he or she would be aware that riluzole is the sole approved medicine available for treatment of ALS.
Thus, the claims do not contribute anything non-obvious over the prior art.
Claims 1-6, 8-10 and 12-16 are rejected under 35 U.S.C. 103 as being unpatentable over Shi and Karni et al. as applied to claims 1-6, 8-10 and 12-15 above, and further in view of Gromada et al. (WO 2015017576—of record) and Latres et al. (Nature Communications 8: 15153; DOI: 10.1038/ncomms15153—of record). This rejection was necessitated by amendment. The first factor to consider when making a rejection under 35 U.S.C. 103(a) is to determine the scope and contents of the prior art. The combined teachings of Shi and Karni et al. and how they meet the limitations of claims 1-6, 8-10 and 12-15 are outlined above in the preceding rejection and are hereby incorporated. The second factor to consider is to ascertain the differences between the prior art and the instant claims. The combined teachings of Shi and Karni et al. do not teach that the agent that modulates the ligand activin is an REGN2477 antibody.
Gromada et al. teach antibodies that bind activin A for the treatment of diseases associated with decreased muscle mass or strength, which include MS, ALS and Parkinson’s disease (see abstract; paragraphs [0034] and [00115]; claims 34 and 35). As with Gromada et al., Latres et al. teach that inhibition of activin A with anti-activin A antibodies is a viable co-therapy for muscle wasting conditions and specifically characterizes the anti-activin antibody, REGN2477 (see abstract; p. 2, right column).
It would have been obvious to the person of ordinary skill in the art at the time of the filing of the invention to modify the combined teachings of Shi and Karni et al. by also administering REGN2477 to treat MS, ALS or Parkinson’s disease because these conditions are characterized by loss of muscle mass and strength and Gromada et al. and Latres et al. provide methods for ameliorating conditions associated with decreased “muscle mass and strength” (see paragraph [0033]-[0034] of Gromada and colleagues and p. 4, Figure 2 of Latres and colleagues). The person of ordinary skill in the art would have been motivated to treat conditions associated with loss of muscle with anti-activin antibodies such as REGN2477 because there is a motivation in the art to treat symptoms of these conditions, including muscle loss, and administration resulted in increased muscle in a mouse model (see p. 52 of Gromada and colleagues and p. 4, Figure 2 of Latres and colleagues). Furthermore, given the success in REGN2477 increasing muscle force in the experiments disclosed in Latres et al., the person of ordinary skill in the art could have reasonably expected success.
Response to Arguments
Applicant’s argument regarding the rejections under 35 USC 103 address now-withdrawn rejections. Nevertheless, some of the issues are still relevant and will be addressed herein.
Applicant argues at p. 11 of the Remarks that Karni’s generic disclosure would not have a reasonable expectation of success in substituting the specific ACVR1 selective inhibitors of the amended claims because the specification teaches that dorsomorphin and LDN-212854 produce opposite effects on OPC differentiation.
This argument has been fully considered, but is not found persuasive. The primary reference by Shi teaches a method of treating a neurodegenerative disease comprising administering a small molecule such as LDN-212854, wherein the subject is human (see claims 11-17). Shi also teaches that the neurodegenerative diseases may include Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS—see paragraph [0043]). The secondary reference by Karni and colleagues was relied upon for its teaching of co-administering (1) donepezil, galantamine, rivastigmine or memantine when treating Alzheimer’s disease, (2) pramipexole, ropinirole, selegiline or rasagiline when treating Parkinson’s disease, (3) the promyelinating agent, benztropine and (4) glatiramer acetate, interferon-beta, natalizumab, fingolimod, mitoxantrone, dimethyl fumarate, teriflunomide or alemtuzumab when treating MS (see p. 31, 2nd paragraph; p. 35, last paragraph; p. 36, 1st line and 2nd paragraph). There is no need to for Karni et al. to teach substituting LDN-212854 for dorsomorphin, since the primary reference by Shi already taught administering LDN-212854. 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).
Incidentally, while Applicant asserts the specification teaches that dorsomorphin and LDN-212854 produce opposite effects on OPC differentiation, there is no indication of where this is disclosed. Rather, the instant specification explicitly discloses that the ACVR1 inhibitors may be dorsomorphin or LDN-193189 (see p. 3, lines 5-8).
Applicant argues at pages 11-12 that Gromada et al. is focused is muscle wasting and merely mentions MS, ALS and Parkinson’s in passing as conditions that may involve muscle loss. Applicant argues the person having ordinary skill in the art would not combine the teachings of Karni et al. and Gromada et al. because they are directed to different mechanistic targets and therapeutic goals.
This argument has been fully considered but is not found persuasive. Irrespective of the mouse model used to study muscle wasting in Gromada et al., neurodegenerative diseases such as Parkinson’s, MS and ALS are known to be characterized by muscle wasting (see [0005]). Further, Latres et al. conclude that their study shows that REGN2477 “support the use of…REGN2477 for muscle atrophy and wasting diseases” (see p. 10, right column, 1st paragraph). The person having ordinary skill in the art would be motivated to treat the symptoms of muscle wasting in conditions associated therewith.
Applicant argues at pages 12-13 that Latres et al. do not disclose or suggest use of REGN2477 to treat neurodegenerative disease, but rather concerns muscle related wasting disorders.
This argument has been fully considered, but is not found persuasive. Since the primary reference by Shi already teaches a method of treating neurodegenerative disease such as Parkinson’s disease, MS and ALS comprising administering LDN-212854 (see claims 11-17; paragraph [0043]), there is no need for the supporting references to teach this as well. Latres et al. was relied upon for its teachings of the potential benefits of REGN2477 in treatment of muscle wasting diseases, and Parkinson’s, MS and ALS were known to be associated with muscle wasting (see paragraph [0005] of Gromada and colleagues). 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).
Conclusion
No claim is allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/CHRISTINA M BORGEEST/Primary Examiner, Art Unit 1675
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