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 .
Amendments
In the reply filed 2/24/2026, Applicant has amended Claims 1-2, 6, 11-15, cancelled claims 8-10, and added new claims, Claims 25-26.
Claims 16-19 are pending but withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a non-elected invention, there being no allowable generic or linking claim.
Claims 1-7, 11-15, 20-21, and 25-26 are under consideration.
Withdrawn Objection to Drawings
The objection to Figure 3b (DNA sequences) of the Specification has been withdrawn due to Applicant’s amended Figure to use “SEQ ID NO:”.
Withdrawn Claim Objections
The objection to Claims 1, 6 and 13 have been withdrawn due to Applicant’s amendments to use “SEQ ID NO:”.
Withdrawn 35 USC § 112(a)
The prior rejection of Claims 1-7, 11-15, and 20-21 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, is withdrawn in light of Applicant’s amendments of Claim 1 to describe an agent comprising a nucleic acid that is capable of expressing p38g or a variant thereof in order to elevate activity
Withdrawn 35 USC § 112(b)
The prior rejection of Claims 11 and 12 under 35 U.S.C. 112(b), as being indefinite is withdrawn in light of Applicant’s amendments of instant claims to describe the SEQ ID NOs.
New Claim Rejections - 35 USC § 112(b)
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 7 and 20 are rejected 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 pre-AIA the applicant regards as the invention.
Claims 7 and 20 recite the limitation "the tauopathy" in regard to Claim 1. There is insufficient antecedent basis for this limitation in the claim because Claim 1 has been amended to no longer recite a tauopathy, thereby rendering instant claims indefinite. Appropriate correction is required.
Withdrawn 35 USC § 112(d)
The prior rejection of Claim 15 under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form is withdrawn in light of Applicant’s amendments of instant claim to describe the SEQ ID NO.
Withdrawn Claim Rejections - 35 USC § 102
The prior rejection of Claims 1-7, 13-14, and 20-21 under 35 U.S.C. 102(a)(1)/(a)(2) as being anticipated by Ittner et al., (WO2017/147654, filed 3/01/2017, published 9/08/2017 see IDS filed 3/22/2022) is withdrawn in light of Applicant’s amendments of claim to change the subject from one with tauopathy, to one with a disease mediated by hyperphosphorylation of tau, which is a limitation not taught by Ittner.
Withdrawn 35 USC § 103
The prior rejection of Claim 12 under 35 U.S.C. 103 as being unpatentable over Ittner et al., (WO2017/147654, filed 3/01/2017, published 9/08/2017), in view of Danos et al. (US 2021/0010025, with priority to PCT US2018/056343 filed 10/17/2018) is withdrawn in light of Applicant’s amendment of Claim 12 to limit the p38g to comprising the amino acid sequence of SEQ ID NO: 3, which is a limitation neither Ittner nor Dano teach. Specifically, Danos makes obvious a p38g nucleic acid sequence corresponding to at least 60% identity to SEQ ID NO:2.
The prior rejection of Claims 15 under 35 U.S.C. 103 as being unpatentable over Ittner et al., (WO2017/147654, filed 3/01/2017, published 9/08/2017), in view of GenBank CR456515 (Homo sapiens MAPK12 full ORF cDNA, published 10/16/2008). is withdrawn in light of Applicant’s amendment of Claim 15 to limit the p38gCA comprises the amino acid sequence of SEQ ID NO: 4, which is a limitation neither Ittner nor GenBank teach. Specifically, GenBank CR456515 makes obvious the p38g of SEQ ID NO:3.
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 of this title, 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 set forth in Graham v. John Deere Co., 383 U.S. 1, 148 USPQ 459 (1966), that are applied 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 1-7, 12-14, and 20-21 are rejected under 35 U.S.C. 103 as being unpatentable over Ittner et al., (WO2017/147654, filed 3/01/2017, published 9/08/2017), in view of Grueninger et al. (Neuro Disease, 37, 294-306 (2010).
With respect to claim 1, Ittner teaches methods of treating Alzheimer’s disease in a subject by gene therapy comprising administering a nucleic acid agent that encodes p38g and promotes phosphorylation of tau at threonine corresponding to T205 of human tau (see Claims 1-3, 14 and 51 of Ittner).
Ittner teaches that upon transfection of wild-type (WT) p38g or constitutively active (CA) p38g, tau is predominantly phosphorylated on T205, but virtually not at S396 and S404 (p. 16, 5th para., see Fig. 5A)
Ittner teaches that AAV transduction of wild-type (WT) p38g or constitutively active (CA) p38g, reduced toxicity induced by amyloid-beta in hippocampal neurons (p. 17, 6th para., see Fig. 5H) and improved and prevented spatial working memory deficits in APP23 transgenic mouse model of Alzheimer’s disease (pgs. 22-23, see Figs. 16-18 and 20, as well as pgs. 28-29, see Fig. 34, see also pgs.30-31, see Fig. 39).
However, Ittner is silent to treating a disease mediated by hyperphosphorylation of tau, such as in a APP23 transgenic mouse further comprising the human mutations of the PSEN2 gene and a human tau gene.
Grueninger teaches a TauPS2APP mouse model of Alzheimer’s disease comprising not only the human mutations of the APP gene, but also the human mutation in the PSEN2 gene, and human tau (p. 295, Transgenic mice).
Gurenginer teaches the TauPS2APP mouse develop amyloid plaques, NFTs, and not just hyperphosphorylated Tau, but abnormally phosphorylated Tau (i.e., the typical manifestations of abnormally phosphorylated Tau that are observed in AD) (p. 304, Discussion, first para., p. 305, Discussion, last para.). Thus, TauPS2APP mouse exhibit a disease mediated by hyperphosphorylation of tau.
Accordingly, it would have been prima facie obvious to one of ordinary skill in the art at the time of filing to have practiced the method of treating a disease mediated by amyloid beta toxicity and the tau-dependent signaling complex such as in the Alzheimer’s APP23 mouse model comprising administering a nucleic acid encoding p38g as taught by Ittner, and to substitute the Alzheimer’s TauPS2APP mouse model as taught by Gruenginer with a reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so as taught by Gruenginer because the TauPS2APP mouse develop amyloid plaques, NFTs, and abnormally phosphorylated Tau observed in Alzheimer’s disease.
In regard to claims 2 and 21, as stated supra, Gurenginer teaches the TauPS2APP mouse exhibits cognitive impairment, and Ittner teaches p38g gene therapy improved spatial working memory deficits in the single APP23 transgenic mice (pgs. 22-23, see Figs. 16-18 and 20, as well as pgs. 28-29, see Fig. 34, see also pgs.30-31, see Fig. 39). Thus, there would have been a reasonable expectation of success in improving spatial memory in the mice of Gurenginer after p38g gene therapy.
In regard to claims 3-5, as stated supra, Gurenginer teaches the TauPS2APP mouse develop amyloid plaques, NFTs, and abnormally phosphorylated Tau. Furthermore, Gureninger disloses the “amyloid hypothesis” of AD, that Tau pathology is a consequence of upstream APP misprocessing (p. 294, Introduction, 1st para.), and concludes there is a clear correlation between amyloidosis and Tau phosphorylation at the phosphor-Tau S422 epitope (p. 305, Discussion, last para). Since, Ittner teaches p38g gene therapy reduced toxicity induced by amyloid-beta in hippocampal neurons (p. 17, 6th para., see Fig. 5H), there was a reasonable expectation of success that the p38g treatment of Ittner would reduce S422 phosphorylation and tau aggregation in the mice of Gurenginer.
In regard to claims 6-7, as stated supra, Gurenginer teaches the TauPS2APP mouse comprises a copy of human tau, and Ittner teaches that co-expression of p38g and tau demonstrated predominant phosphorylation at the threonine in the sequence of SEQ ID NO:7, alias “T205” in the human form (p. 86, last para., see Fig. 5A and 45). Furthermore, Ittner demonstrates that crossing between APP23 mice and p38g knock-out mice resulted in reduced phosphorylation at the mouse equivalent of T205. Thus, Ittner concludes T205 is the primary site in tau phosphorylated by p38g (p. 87, 1st para.). Furthermore, SEQ ID NO: 7 is conserved in both human and mice. Thus, there would have been a reasonable expectation of success that this threonine would have been phosphorylated in mice comprising a copy of human tau administered the p38g vector.
In regard to claims 12-14, as stated supra, Ittner teaches administering the CA variant of p38g, which comprises the 367 amino acid sequence of SEQ ID NO:3 (see Fig. 44, see also nucleic acid sequence of Fig. 49), which is about 96% identical to the 357 amino acid sequence of instant SEQ ID NO:3, and also comprises the C-terminal amino acid sequence “ETPL” of SEQ ID NO:9.
In regard to claim 20, as stated supra, Gurenginer teaches the TauPS2APP mouse is a model of advanced Alzheimer’s as evidenced by NFTs and hyperphosphorylated tau.
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
RESPONSE TO ARGUMENTS
Applicant's arguments filed on 2/24/2026 are acknowledged.
Applicant argues that the amended claims are directed to a method of treating or preventing a disease mediated by hyperphosphorylation of tau, which is a subject not disclosed by Ittner. Applicant argues that the hyperphosphorylation of tau is associated with late-stage Alzheimer’s disease, and is a distinct pathological driver from the earlier-stage tau dependent signalling of Ittner. Applicant argues that Ittner teaches tau phosphorylation is causative of pathological aggregation, and Ittner provides no motivation to modify a method to further increase the phosphorylation of tau to treat a disease mediated by hyperphosphorylation of tau, such as advanced Alzheimer’s. Applicant argues that one of ordinary skill in the art would avoid the methods of Ittner to treat a disease mediated by tau hyperphosphorylation because further tau phosphorylation would be detrimental in such a disease.
Furthermore, Applicant argues that the inventors have unexpectedly shown that phosphorylation of T205 of tau reduces phosphorylation of S422, a late-stage disease epitope, and reduces or reverses symptoms associated with hyperphosphorylated tau aggregation. Specifically, Applicant argues S422 is a late-stage Alzheimer’s disease and is strongly correlated with NFT formation and cognitive decline, and Applicant’s demonstration that the claimed treatment reduced S422 phosphorylation directly targeted aggregation-mediated pathology, not tau-dependent signalling complexes as shown by Ittner. For example, Applicant argues that Fig. 1 demonstrates that AAV38gCA to 13-month old APP23 mice resulted in improved cognitive performance when assessed 2 months post treatment, thereby demonstrating that the claimed method treated advanced Alzheimer’s.
Applicant's arguments have been fully considered but they are found partially persuasive.
In regard to Applicant’s first arguments regarding Ittner not teaching the treatment of a disease that is mediated by the hyperphosphorylation of tau, the Examiner concedes this point and has withdrawn the rejections by Ittner. However, as noted the revised rejection, Grueninger makes obvious the treatment of a subject comprising a disease mediated by hyperphosphorylation of tau.
In regard to Applicant’s arguments that Ittner teaches aberrantly phosphorylated tau lead to NFTs, Ittner makes clear that “contrary to teaching in the art, phosphorylation of tau at particular amino acid residues” can be therapeutic (Summary, 1st para.). Furthermore, Ittner demonstrates that as Alzheimer’s disease advances, there are markedly reduced levels of p38g (p. 24, 3rd. para., p. 83, lines 25-27, see Fig. 23), and Ittner claims the taught method “can be used to treat or prevent neurological conditions mediated by a tau-dependent signalling complex, such as AD” (p 34, Detailed Description, 1st para.). Thus, a person of ordinary skill would have understood from reading Ittner that p38g MAP kinase phosphorylation of tau on T205 was a reasonable method to pursue for the treatment of AD.
In response to Applicant’s second arguments that the inventors have unexpectedly discovered that p38g phosphorylation of tau at T205 reduced phosphorylation of S422, a late-stage AD epitope, and reduced or reversed symptoms associated with hyperphosphorylated tau aggregation, as a first matter, the scope of the claims are not commensurate with the purported unexpected results. Specifically, the claimed method not only encompasses treating but “preventing” a disease associated with hyperphosphorylation of tau, and the genus of diseases claimed do not require elevated S422 phosphorylation or NFT formation as in a late-stage Alzheimer’s patient.
Furthermore, it is not clear from Applicant’s disclosure that the claimed method achieved the purported unexpected results. Specifically, although Fig. 1 demonstrates that AAV-p38g-CA improved spatial memory in aged APP transgenic APP23 mice, and Fig. 5 demonstrates that p38g-CA transgenesis improved spatial memory in APP23 mice, which accordingly to Applicant the APP23 mice do not exhibit tau hyperphosphorylation, much less elevated S422 phosphorylation or NFT formation. In other words, Applicant has not demonstrated that the APP23 mouse is a model for late-stage Alzheimer’s disease.
[AltContent: textbox ([img-media_image1.png])]Moreover, although Figs. 2 and 7, demonstrate that the knock-out of p38g worsens spatial memory in tau transgenic Alz17 mice, this does not necessarily equate to improving spatial memory by administering p38g gene therapy, much less doing so in a subject with elevated S422 phosphorylation and/or NFTs. In fact, Applicant has presented a single figure that demonstrates reduced S422 phosphorylation after p38g gene therapy (see Fig. 19 excerpt adjacent), which has no quantification and the reductions of pTau S422 are highly variable and phosphorylation levels are also reduced in the control AAV-GFP samples.
Applicant is reminded that a showing of unexpected results must be based on evidence, not argument or speculation. In re Mayne, 104 F.3d 1339, 1343-44, 41 USPQ2d 1451, 1455-56 (Fed. Cir. 1997) (conclusory statements regarding unusually low immune response or unexpected biological activity that were unsupported by comparative data held insufficient to overcome prima facie case of obviousness).
Claims 11 and 15 are rejected under 35 U.S.C. 103 as being unpatentable over Ittner et al., (WO2017/147654, filed 3/01/2017, published 9/08/2017), in view of Grueninger et al. (Neuro Disease, 37, 294-306 (2010), as applied to claims 1 and 14, in further view of GenBank CR456515 (Homo sapiens MAPK12 full ORF cDNA, published 10/16/2008).
As discussed previously, Ittner et al. suggest methods of treating a disease mediated by hyperphosphorylation of tau in a subject by gene therapy, comprising administering an p38g encoding nucleic acid that promotes T205 phosphorylation of human tau.
Specifically, in regard to claims 11 and 15, Ittner teaches that either the wild-type human p38g or the constitutive active (CA) human p38g comprising a D to A mutation in its regulatory loop can be used (p. 38, 2nd para., p. 45, 1st para., see also Figs. 43 and 44).
However, Ittner is silent to the human p38g comprising the amino acid sequence of SEQ ID NO:3 or the constitutively active human p38g variant comprising the D to A mutation in the amino acid sequence of SEQ ID NO:3 (i.e., SEQ ID NO: 4).
Nevertheless, Collins et al. deposited a cDNA sequence as GenBank CR456515.1 that encodes the following human p38g amino acid sequence that is 100% identical to SEQ ID NO:3. Note the “D” position in the regulatory loop is highlighted, which corresponds to the D to A mutation in the amino acid sequence of SEQ ID NO:4.
MSSPPPARSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYRPFQSELFAKRAYRELRLLKHMRHENVIGLLDVFTPDETLDDFMDFYLVMPFMGTDLGKLMKHEKLGEDRIQFLVYQMLKGLRDLKPGNLAVNEDCELKILDFGLARQADSEMTGYVVTRWYRAPEVILNWMRYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMKVTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDAEQRVTAGEALAHPYFESLHDTEDEPQVQKYDDSFDDVDRTLDEWKRVTYKEVLSFKPPRQLGARVSKETPL
Accordingly, it would have been prima facie obvious to one of ordinary skill in the art at the time of filing to have practiced the method of treating a disease mediated by hyperphosphorylation of tau in a subject comprising administering a nucleic acid encoding human p38g or constitutive active human p38g comprising the D to A mutation as taught by Ittner, and to choose the nucleic acid encoding human wild-type p38g that translates into the amino acid sequence of SEQ ID NO:3 or human CA p38g variant comprising the D to A of SEQ ID NO:3 (i.e., SEQ ID NO:4) as taught by the GenBank deposit of Collins with a reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so as the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA as provided by Ittnar, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art as provided by the deposit of Collins. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
RESPONSE TO ARGUMENTS
Applicant's arguments filed on 2/24/2026 are acknowledged and have been addressed above.
Claim 25 is rejected under 35 U.S.C. 103 as being unpatentable over Ittner et al., (WO2017/147654, filed 3/01/2017, published 9/08/2017), in view of Grueninger et al. (Neuro Disease, 37, 294-306 (2010), as applied to claim 1, in further view of of Danos et al. (US 2021/0010025, with priority to PCT US2018/056343 filed 10/17/2018).
As discussed previously, Ittner et al. suggest methods of treating a disease mediated by hyperphosphorylation of tau in a subject by gene therapy, comprising administering an p38g encoding nucleic acid that promotes T205 phosphorylation of human tau.
In regard the variant of p38g comprising a nucleic acid sequence that it at least 60% identical to the nucleic acid sequence of SEQ ID NO:2, Ittnar teaches the human p38g nucleic acid sequence of SEQ ID NO:1. Importantly, SEQ ID NO:1 of Ittnar shares about a 95% sequence identity with the first half of instant SEQ ID NO:2.
However, instant SEQ ID NO:2 comprises two copies of the human p38g transgene and is about twice as long as the nucleic acid of SEQ ID NO:1 of Ittnar.
Nevertheless, Dano teaches methods of gene therapy for human diseases and teaches “double dose” constructs, wherein two tandem copies of the same transgene is inserted into the expression construct [0022, 0181, 0234, 0305].
Accordingly, it would have been prima facie obvious to one of ordinary skill in the art at the time of filing to have practiced the method of treating a disease mediated by hyperphosphorylation of tau in a subject comprising administering the p38g construct of SEQ ID NO:1 as taught by Ittner, and to provide two tandem copies of SEQ ID NO:1 as taught by Danos with a reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so as taught by Danos because this two copy form of the expression vector provides a double dose for increasing p38g activity. Importantly, the combination of two tandem copies of SEQ ID NO:1 would have been about 95% identical to SEQ ID NO:2.
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
RESPONSE TO ARGUMENTS
Applicant's arguments filed on 2/24/2026 are acknowledged and have been addressed above.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory obviousness-type 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); and 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 a nonstatutory double patenting ground provided the conflicting application or patent either is shown to be commonly owned with this application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement.
Effective January 1, 1994, a registered attorney or agent of record may sign a terminal disclaimer. A terminal disclaimer signed by the assignee must fully comply with 37 CFR 3.73(b).
Claims 1-7, 13-14, and 20-21 are provisionally rejected on the grounds of nonstatutory double patenting as being unpatentable over claims 60-63, 65-70 of copending Application No. 17/931,229. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented
The subject matter claimed in the instant application is disclosed in the referenced application as follows: the method of treating or preventing a condition mediated by a tau dependent signaling complex in the neurons of a subject cited application anticipates the method of instant application. It is clear that elements of the cited application claims are to be found in instant claims. The difference between the cited application claims and the instant claims lies in the fact that the cited application claims are much more specific with respect to the p38 gamma sequence. Thus the invention of said claims of the cited application are in effect “species” of the “generic” invention of the instant claim. It has been held that the generic invention is “anticipated” by the “species”. See In re Goodman, 29 USPQ2d 2010 (Fed. Cir. 1993).
Since the instant application claims are anticipated by and/or obvious over cited application claims, said claims are not patentably distinct.
RESPONSE TO ARGUMENTS
Applicant's arguments filed on 2/24/2026 are acknowledged.
Again, Applicant argues that the patients comprising a neurological condition mediated by tau-dependent signaling of copending Application are patentably distinct from the patients of instant Application wherein the conditions is mediated by tau hyperphosphorylation.
Applicant’s arguments have been fully considered but are not found persuasive.
Although the preambles of copending claims are different with respect the nature of tau, the active method steps claimed are the same, and the patients claimed are the same (e.g., Parkinson’s).
The court in Integra Life Sciences I Ltd. v. Merck KGaA, 50 USPQ2d 1846 (DC SCalif, 1999) held that a reference teaching a process may anticipate claims drawn to a method comprising the same process steps, despite the recitation of a different intended use in the preamble or the later discovery of a particular property of one of the starting materials or end products. In the instant case, the only active method step is the administration of a nucleic acid that is capable of expressing p38g to a Parkinson’s patient, which is exactly what is claimed by cited application.
Allowable subject matter
Claim 26 is objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims.
Specifically, the prior art does not teach nor reasonably suggest the nucleic acid sequence of SEQ ID NO:2, which encodes two tandem copies of human p38g MAP kinase with accompanying 5’ and 3’ UTR sequences.
Conclusion
Applicant's amendment necessitated the amended/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 extension fee 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 date of this final action.
No claims are allowed.
Examiner Contact Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ARTHUR S LEONARD whose telephone number is (571)270-3073. The examiner can normally be reached on Mon-Fri 9am-5pm.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, James Doug Schultz can be reached on 571-272-0763. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/ARTHUR S LEONARD/Examiner, Art Unit 1631
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