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
RESPONSE TO AMENDMENT
Status of Application/Amendments/claims
2. Applicant’s amendment filed October 14, 2025 is acknowledged. Claims 1-59, 61, 64, 72, 75 and 77 are cancelled. Claims 60, 62-63, 65, 68-71, 73-74, 76 and 79-81 are amended. Claim 83 is newly added. Claims 60, 62-63, 65-71, 73-74, 76, 78-82 and new claim 83 are pending in this application and under examination in this office action.
3. Applicant’s arguments filed on October 14, 2025 have been fully considered but they are not deemed to be persuasive for the reasons set forth below.
Drawings
4. The objection to the drawing 44 is withdrawn in response to Applicant’s arguments on p. 8 of the response. However, the drawings 43 and 45 stand objected to because the sequence listings of SEQ ID NOs: are included in the specification and cannot not be duplicated in the drawings. See 37 C.F.R. §1.58(a) and §1.83(a). Appropriate correction is required. See MPEP § 608.02-I Drawing requirements.
Claim Rejections/Objections Withdrawn
5. The objection to claims 60-68, 71-75 and 79-81is withdrawn in response to Applicant’s amendment to the claims.
The rejection of claims 60-82 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite is withdrawn in response to Applicant’s amendment to the claims and cancelation of claims 61, 64, 72, 75 and 77.
The rejection of claims 61, 64, 72, 75 and 77 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, lack of scope of enablement is moot because the claims are canceled.
The rejection of claims 61, 64, 72, 75 and 77 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 moot because the claims are canceled.
The provisional rejection of claims 61, 64, 72, 75 and 77 on the ground of nonstatutory double patenting as being unpatentable over claims 1-21 of copending Application No. 17/754047 is moot because the claims are canceled.
Claim Rejections/Objections Maintained
In view of the amendment filed on October 14, 2025, the following rejections are maintained.
Claim Rejections - 35 USC § 112
6. 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.
Claims 60, 62-63, 65-71, 73-74, 76 and 78-83 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for rescuing memory deficits in APP23-AAVp38γCA by AAV-mediated p38γCA expression in APP23 mice (mice carrying K670N/M671L mutant APP) as compared to those of APP23-AAVGFP mice based on Morris-water maze tests and mitigating the toxic effects of Aβ in hippocampal neurons by increasing p38γ activity in the neurons and decreasing progression of PTZ-induced seizures by AAV-p38γ (SEQ ID NO:4) or AAV-p38γCA (constitutively active: SEQ ID NO:2 with a substitution of D179A), does not reasonably provide enablement for a method for treating including curing all forms of undefined neurological conditions mediated by a tau-dependent signaling complex including AD using the claimed p38g or variant of p38g comprising a PDZ interaction motif comprising EPTL (SEQ ID NO:8) or ETAL (SEQ ID NO:32) as broadly claimed. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims. In addition, the specification does not enable the invention of claims 60, 62-63 and 65-70 that is directed to a method of curing. The rejection is maintained for the reasons of record and the reasons set forth below.
Claims 60, 62-63, 65-70 and 83 as amended are drawn to a method of treating a neurological condition mediated by a tau-dependent signaling complex in neurons of a subject, comprising administering to the subject an agent which promotes phosphorylation of threonine at position 205 of Tau (T205) in the neuron of the subject, wherein the agent comprises p38g or a variant of p38g, or a nucleic acid capable of expressing p38g or a variant of p38g, and wherein the variant of p38g comprises a PDZ interaction motif comprising EPTL (SEQ ID NO:8) or ETAL (SEQ ID NO:32).
Claims 71, 73-74, 76 and 78-82 as amended are drawn to a method of disrupting a signaling complex comprising PSD-95, tau and FYN in a neuron, comprising contacting the neuron with an agent which promotes phosphorylation of threonine at position 205 of Tau (T205) in the neuron including in vitro and in vivo; wherein the agent comprises p38g or a variant of p38g, or a nucleic acid capable of expressing p38g or a variant of p38g, and wherein the variant of p38g comprises a PDZ interaction motif comprising EPTL (SEQ ID NO:8) or ETAL (SEQ ID NO:32).
Response to Arguments
On p. 12-14 of the response, Applicant argues that i) claim 60 has been amended to recite “an agent which promotes phosphorylation of threonine at position 205 of Tau (T205) in the neurons of the subject” and “wherein the agent comprises p38g or a variant of p38g or a nucleic acid capable of expressing p38g or a variant of p38g”; ii) the inventors identified a new means of disrupting tau-dependent signaling complexes such as PSD-95/tau/FYN receptor complexes, which involve and mediate neuronal excitotoxicity and the progression of AD and other neurodegenerative diseases; iii) the specification provides support for the claimed methods and cites paragraphs [0162], Examples of [0254]-[0255] in support of the arguments; iv) the specification provides support for the claimed variant of p38g and cites paragraph [0170] in support of the arguments.
Applicant's arguments have been fully considered but they are not found persuasive. Contrary to Applicant's arguments, the examiner asserts that based on MPEP §2164, MPEP §§2164.01-2164.06(b) & 2164.08, neither the specification nor the prior art provides sufficient guidance to enable a skilled artisan to practice the full scope of the claimed invention without undue experimentation because of the following:
i. The claims 60, 62-63, 65-70 and 83 as amended also encompass a method of curing a neurological disease-mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms in view of paragraph [0241] of the instant specification.
[0241] As used herein, “treating” means affecting a subject, tissue or cell to obtain a desired pharmacological and/or physiological effect and includes inhibiting the condition, i.e. arresting its development; or relieving or ameliorating the effects of the condition i.e. cause reversal or regression of the effects of the condition.
Based on paragraph [0241] of the instant specification, the definition of “treating” encompass curing the claimed neurological disease-mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms. However, as previously made of record, there is no cure for the claimed neurological disease-mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms by any given agent. Neither the specification nor the prior art provides sufficient guidance or support that administration of the claimed p38g or variant of p38g to a subject can cure the claimed neurological disease-mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms. The specification provides no working examples for curing AD or any claimed neurological disease-mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms. There is no guidance or evidence to demonstrate that Applicant can cure the claimed neurological disease-mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms as instantly claimed. Thus, it is unpredictable whether administration of the claimed p38g or variant of p38g can cure the claimed neurological disease-mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms, indicating that undue experimentation is required by a skilled artisan to perform while practicing the claimed invention.
ii. The specification provides no well-established correlation among different forms of neurological disease mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms.
There is no well-established correlation between the claimed neurological disease mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms and APP23 mice (mice carrying K670N/M671L mutant APP) or wild type mice challenged with PTZ.
The specification provides no well-established structural and functional relationship between rescuing memory deficits in APP23 mice (mice carrying K670N/M671L mutant APP) or decreasing progression of PTZ-induced seizures in hippocampal neurons in wild type mice challenged with PTZ by AAV-p38g (SEQ ID NO:2) or AAV-p38γCA (constitutively active: SEQ ID NO:2 with a substation of D179A) in and the treatment of neurological disease mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms by the claimed agent comprising p38g or a variant of p38g.
iii. There is no well-established structural and functional relationship between AAV-p38g (SEQ ID NO:2) or AAV-p38γCA and the claimed variant of p38g comprisng a PDZ interaction motif comprising the sequence of SEQ ID NO:8 or 32.
The specification provides no guidance or support to demonstrate that a variant of p38g comprising a PDZ interaction motif comprising the sequence of SEQ ID NO:8 or 32 only can promote phosphorylation of T205 and thereby treating the claimed neurological diseases mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms. Note that a single amino acid change on a molecule or protein can abolish the binding ability or activity of the molecule or protein as taught by Burgess et al. (J of Cell Bio. 1990, 111:2129-2138, cited previously). Further, the conformation for binding is dependent upon surrounding residues. In addition to a core determinant sequence, the protein-protein interaction also relies on the flanking or noncontiguous residues (see p. 445 the second column, first paragraph, Pawson et al. 2003, Science 300:445-452, cited previously). The optimal binding motif for a domain is not necessarily suitable for physiological or in vivo interaction. The predictive data always need to be validated by actual analyses in cells (see p. 445, the third column, second paragraph, Pawson et al. 2003, Science 300:445-452, cited previously).
The specification fails to teach what other amino acid sequences and features are required by the claimed variant of p38g and what amino acid sequences can or cannot included or changed in the claimed variant of p38g in order to preserve the activity of AAV-p38g (SEQ ID NO:2) or AAV-p38γCA in rescuing memory deficits in APP23 mice (mice carrying K670N/M671L mutant APP) or decreasing progression of PTZ-induced seizures in hippocampal neurons in wild type mice challenged with PTZ. Thus, a skilled artisan cannot contemplate what other amino acid sequences and features and what amino acid sequences can or cannot included or changed in the claimed variant of p38g in order to preserve the activity of AAV-p38g (SEQ ID NO:2) or AAV-p38γCA.
Note that the scope of the claims must bear a reasonable correlation with the scope of enablement (In re Fisher, 166 USPQ 19 24 (CCPA 1970)). Without such guidance, it is unpredictable whether all forms of the claimed neurological disease mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms can be treated by the claimed agent comprising p38g or the claimed variant of p38g; and thus the experimentation left to those skilled in the art is extensive and undue. See Ex parte Forman, 230 USPQ 546 (Bd. Pat. App. & Int. 1986). Thus, the skilled artisan cannot readily know how to use the claimed invention as currently claimed without further undue experimentation. In re Marzocchi, 439 F.2d 220, 223-24, 169 USPQ 367, 369-70 (CCPA 1971)” See MPEP § 2164.03.
Therefore, in view of the breadth of the claims, the lack of guidance in the specification, limited working examples, the unpredictability of inventions, and the current status of the art, undue experimentation would be required by a skilled artisan to perform in order to practice the claimed invention as it pertains to a method for treating neurological disease mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms by administration of the claimed agent comprising p38g or the claimed variant of p38g.
Accordingly, the rejection of claims 60, 62-63, 65-71, 73-74, 76 and 78-83 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, lack of scope of enablement is maintained.
Claim Rejections - 35 USC § 112
7. Claims 60, 62-63, 65-71, 73-74, 76 and 78-83 are rejected 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. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention. The rejection is maintained for the reasons of record and the reasons set forth below.
Claims 60, 62-63, 65-71, 73-74, 76 and 78-83 also encompass using p38g or a genus of variant of p38g comprising a PDZ interaction motif comprising the amino acid sequence of SEQ ID NO:8 or SEQ ID NO:32 for treating a genus of neurological conditions mediated by a tau-dependent signaling complex in neurons or disrupting a signaling complex comprising PSD-95, tau and FYN in a neuron in vitro and in vivo in all possible conditions. Claims 63, 65, 74, 76, 79 encompass using a genus of variant of p38g comprising the amino acid sequence represented by SEQ ID NO:31 and at least 80% identical to the amino acid sequence of SEQ ID NO:2 or comprising an amino acid sequence that is at least 85%, 90%, 95% or 95% identical to SEQ ID NO:2 and comprising a PDZ interaction motif.
Applicant has not disclosed sufficient species for using p38g for treating a genus of neurological conditions mediated by a tau-dependent signaling complex in the neuron. Applicant also has not disclosed sufficient species for using the broad genus of variant of p38g comprising a PDZ interaction motif comprising SEQ ID NO:8 or 32 for promoting phosphorylation of T205 in the neurons, the broad genus of variant of p38g comprising the amino acid sequence represented by SEQ ID NO:31 and at least 80% identical to the amino acid sequence of SEQ ID NO:2 or comprising an amino acid sequence that is at least 85%, 90%, 95% or 95% identical to SEQ ID NO:2 and comprising the PDZ interaction motif for treating a genus of neurological conditions mediated by a tau-dependent signaling complex or disrupting a signaling complex comprising PSD-95, tau and FYN in a neuron in vitro and in vivo in all possible conditions.
Response to Arguments
On p. 14 of the response, Applicant argues that the rejection has been overcome in view of amendment to the claims and for the same reasons set forth above.
Applicant's arguments have been fully considered but they are not found persuasive. Contrary to Applicant's arguments, the examiner asserts that based on MPEP §2163, MPEP §§2163.01-2163.03, the specification fails to provide sufficient description or information or evidence to demonstrate that Applicant is in possession of using p38g for treating a genus of neurological conditions mediated by a tau-dependent signaling complex in the neuron or using the claimed genus of variant of p38g for treating a genus of neurological conditions mediated by a tau-dependent signaling complex in neurons or disrupting a signaling complex comprising PSD-95, tau and FYN in a neuron in vitro and in vivo because of the following:
i. There is no well-established correlation among different forms of neurological disease mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms.
There is no well-established correlation between the claimed neurological disease mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms and APP23 mice (mice carrying K670N/M671L mutant APP) or wild type mice challenged with PTZ.
The specification provides no well-established structural and functional relationship between rescuing memory deficits in APP23 mice (mice carrying K670N/M671L mutant APP) or decreasing progression of PTZ-induced seizures in hippocampal neurons in wild type mice challenged with PTZ by AAV-p38g (SEQ ID NO:2) or AAV-p38γCA (constitutively active: SEQ ID NO:2 with a substation of D179A) in and the treatment of neurological disease mediated by a tau-dependent signaling complex including AD, FTD, ALS, HD, PD, stroke and epilepsy caused by any possible mechanisms by the claimed agent comprising p38g or a variant of p38g.
ii. There is no well-established structural and functional relationship between AAV-p38g (SEQ ID NO:2) or AAV-p38γCA and the claimed variant of p38g comprising a PDZ interaction motif comprising the sequence of SEQ ID NO:8 or 32.
The specification provides no information to demonstrate that Applicant is in possession of using the claimed genus of variant of p38g comprising a PDZ interaction motif comprising the sequence of SEQ ID NO:8 or 32 or comprising the amino acid sequence represented by SEQ ID NO:31 and at least 80% identical to the amino acid sequence of SEQ ID NO:2, or comprising an amino acid sequence that is at least 85%, 90%, 95% or 95% identical to SEQ ID NO:2 and comprising the PDZ interaction motif for promoting phosphorylation of T205 and thereby treating a genus of neurological conditions mediated by a tau-dependent signaling complex or disrupting a signaling complex comprising PSD-95, tau and FYN in a neuron in vitro and in vivo in all possible conditions.
The specification fails to teach what other amino acid sequences and features are required by the claimed variant of p38g and what amino acid sequences can or cannot included or changed in the claimed variant of p38g in order to preserve the activity of AAV-p38g (SEQ ID NO:2) or AAV-p38γCA in rescuing memory deficits in APP23 mice (mice carrying K670N/M671L mutant APP) or decreasing progression of PTZ-induced seizures in hippocampal neurons in wild type mice challenged with PTZ. Thus, a skilled artisan cannot contemplate what other amino acid sequences and features and what amino acid sequences can or cannot included or changed in the claimed variant of p38g in order to preserve the activity of AAV-p38g (SEQ ID NO:2) or AAV-p38γCA.
Since the common characteristics/features of other variant of p38g and other neurological conditions mediated by a tau-dependent signaling complex are unknown, a skilled artisan cannot envision the functional correlations of the genus with the claimed invention in view of Burgess et al. (J of Cell Bio. 1990, 111:2129-2138, cited previously) and Pawson et al. (see p. 445 the second column, first paragraph, Pawson et al. 2003, Science 300:445-452, cited previously).
Accordingly, in the absence of sufficient recitation of distinguishing identifying characteristics, the specification does not provide adequate written description of the genus of variants of p38g and the genus of neurological conditions mediated by a tau-dependent signaling complex.
Based on MPEP § 2161.01 and §2163, “to satisfy the written description requirement, a patent specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. See, e.g., Moba, B.V. v. Diamond Automation, Inc., 325 F.3d 1306, 1319, 66 USPQ2d 1429, 1438 (Fed. Cir. 2003); Vas-Cath, Inc. v. Mahurkar, 935 F.2d at 1563, 19 USPQ2d at 1116”.
Vas-Cath Inc. v. Mahurkar, 19USPQ2d 1111, clearly states “applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the ‘written description’ inquiry, whatever is now claimed.” (See page 1117.) The specification does not “clearly allow persons of ordinary skill in the art to recognize that [he or she] invented what is claimed.” (See Vas-Cath at page 1116).
As discussed above, the skilled artisan cannot envision the detailed chemical structure of the encompassed genus of variants of p38g and the genus of neurological conditions mediated by a tau-dependent signaling complex, and therefore conception is not achieved until reduction to practice has occurred, regardless of the complexity or simplicity of the method of isolation. Adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method of isolating it. The compound itself is required. See Fiers v. Revel, 25 USPQ2d 1601 at 1606 (CAFC 1993) and Amgen Inc. v. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016. One cannot describe what one has not conceived. See Fiddes v. Baird, 30 USPQ2d 1481 at 1483 and Centocor v. Abbott, 636 F.3d1341 (Fed. Cir. 2011) and AbbVie v. Janssen, 759 F.3d 1285 (Fed. Cir.2014). One cannot describe what one has not conceived. See Fiddes v. Baird, 30 USPQ2d 1481 at 1483.
Therefore, the claimed methods have not met the written description provision of 35 U.S.C. §112, first paragraph. Applicant is reminded that Vas-Cath makes clear that the written description provision of 35 U.S.C. §112 is severable from its enablement provision (see page 1115). Applicant is directed to the Guidelines for the Examination of Patent Applications Under the 35 U.S.C. 112, ¶ 1 "Written Description" Requirement. See MPEP § 2161.01 and 2163.
Accordingly, the rejection of claims 60, 62-63, 65-71, 73-74, 76 and 78-83 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.
Double Patenting
8. The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 60, 62-63, 65-71, 73-74, 76 and 78-83 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-21 of copending Application No. 17/754047 (the ‘047 Application). The rejection is maintained for the reasons of record and the reasons set forth below.
On p. 15 of the response, Applicant requests the rejection be held in abeyance until the instant application or the ‘047 is allowed.
In response, the provisional rejection of claims 60, 62-63, 65-71, 73-74, 76 and 78-83 on the ground of nonstatutory double patenting as being unpatentable over claims 1-21 of the ‘047 Application is maintained of record until a terminal disclaimer is filed.
Conclusion
9. NO CLAIM IS ALLOWED.
10. The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
WO2008132464 teaches a method of diagnosing a neurodegenerative disease or a method of identifying compounds that activates MEK5/ERK5/MEF using
by measuring the level of human mitogen activated protein kinase 12 comprising the amino acid sequence of instant SEQ ID NO:2 (see the sequence alignment below).
SEQ ID NO:2
ATS79850
ID ATS79850 standard; protein; 367 AA.
XX
AC ATS79850;
XX
DT 05-FEB-2009 (first entry)
XX
DE Human Mitogen activated protein kinase 12.
XX
KW diagnostic test; prognosis; drug screening; protein therapy;
KW Alzheimers disease; neuroprotective; nootropic; Parkinsons disease;
KW antiparkinsonian; dementia; prion disease; growth-disorder-gen.; atrophy;
KW motor neuron disease; frontotemporal dementia;
KW Stress activated protein kinase-3; BOND_PC;
KW mitogen-activated protein kinase 12; stress-activated protein kinase 3;
KW mitogen-activated protein kinase 3; MAPK12; ERK3; ERK6; SAPK3; PRKM12;
KW SAPK-3; P38GAMMA; mitogen-activated protein kinase 12, isoform CRA_b;
KW stress-activated protein kinase-3; GO166; GO287; GO4674; GO4707; GO5515;
KW GO5524; GO5737; GO6975; GO7049; GO7050; GO7165; GO7517; GO16740; GO45445;
KW GO165; GO4682; GO4691; GO4713; GO16910; GO45786.
XX
OS Homo sapiens.
XX
CC PN WO2008132464-A2.
XX
CC PD 06-NOV-2008.
XX
CC PF 25-APR-2008; 2008WO-GB001469.
XX
PR 26-APR-2007; 2007GB-00008075.
XX
CC PA (UYNO-) UNIV NOTTINGHAM.
XX
CC PI Mayer JR, Chan WC, Rezvani ZN;
XX
DR WPI; 2009-B32078/08.
DR SWISSPROT; P53778.
DR PC:NCBI; gi48255970.
DR PC:SWISSPROT; P53778.
DR PC:BIND; 231957.
XX
CC PT Diagnosing a neurodegenerative disease by measuring the level of
CC PT components or activator of mitogen activated protein kinase kinase
CC PT 5/extracellular signal regulated kinase 5/myocyte enhancer factor
CC PT (MEK5/ERK5/MEF) module.
XX
CC PS Disclosure; Page 15; 94pp; English.
XX
CC The present invention relates to a method for diagnosing
CC neurodegenerative disease by measuring the level of components or
CC activator of mitogen activated protein kinase kinase 5/extracellular
CC signal regulated kinase 5/myocyte enhancer factor (MEK5/ERK5/MEF) module.
CC The invention also provides: i) a method of determining the
CC susceptibility of an individual to developing a neurodegenerative disease
CC by measuring the level of one or more components of the MEK5/ERK5/MEF
CC module, or an activator of the MEK5/ERK5/MEF module, or the level of one
CC or more components of the MEK3/p38 MAPK module, in a sample of body fluid
CC or tissue from the patient; ii) a method for detecting compounds useful
CC for the treatment of neurodegenerative disease comprising contacting a
CC test compound with one or more component(s) of the MEK5/ERK5/MEF module
CC and assaying for activation of the MEK5/ERK5/MEF module component(s);
CC iii) a method of detecting compounds useful for the diagnosis,
CC monitoring, or imaging of neurodegenerative disease by contacting a test
CC compound with one or more component(s) of the MEK5/ERK5/MEF module (or
CC MEK1 module) and assaying for binding to, activation, or inhibition of
CC the MEK5/ERK5/MEF module (or MEK1 module) component(s); iv) a compound
CC detected from the methods above for use in medicine; v) a pharmaceutical
CC composition comprising the compound and an excipient; vi) a kit of parts
CC useful for diagnosing or monitoring neurodegenerative disease comprising
CC a material which is capable for use in determining the level of one or
CC more components of the MEK5/ERK5/MEF module or an activator of the
CC MEK5/ERK5/MEF module or one or more components of the MEK3/p38 MAPK
CC module; vii) a method of treating an individual suffering from a
CC neurodegenerative disease comprising supplying to the individual an
CC amount of the compound detected from the method above. The method of the
CC invention is useful for treating neurodegenerative diseases e.g,
CC Alzheimer's disease, Parkinson's disease, dementia with Lewy bodies,
CC prion diseases, progressive supranuclear palsy, multisystem atrophy,
CC motor neuron disease (amyotrophic lateral sclerosis), or frontotemporal
CC dementia. The present sequence is Mitogen activated protein kinase 12
CC used in the invention.
CC
CC Revised record issued on 09-DEC-2008 : Enhanced with precomputed
CC information from BOND.
XX
SQ Sequence 367 AA;
ALIGNMENT:
Query Match 100.0%; Score 1915; Length 367;
Best Local Similarity 100.0%;
Matches 367; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 MSSPPPARSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 MSSPPPARSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 60
Qy 61 PFQSELFAKRAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 PFQSELFAKRAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 120
Qy 121 KHEKLGEDRIQFLVYQMLKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 KHEKLGEDRIQFLVYQMLKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 180
Qy 181 EMTGYVVTRWYRAPEVILNWMRYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 EMTGYVVTRWYRAPEVILNWMRYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 240
Qy 241 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDAEQRV 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDAEQRV 300
Qy 301 TAGEALAHPYFESLHDTEDEPQVQKYDDSFDDVDRTLDEWKRVTYKEVLSFKPPRQLGAR 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 301 TAGEALAHPYFESLHDTEDEPQVQKYDDSFDDVDRTLDEWKRVTYKEVLSFKPPRQLGAR 360
Qy 361 VSKETPL 367
|||||||
Db 361 VSKETPL 367
WO9942592 teaches methods for designing inhibitors of serine/threonine kinases including ERK6 mutant comprising the amino acid sequence that is 96.9% identical to instant SEQ ID NO:2 (see the sequence alignment below).
SEQ ID NO:2
AAY42412
(NOTE: this sequence has 5 duplicates in the database searched.
See complete list at the end of this report)
ID AAY42412 standard; protein; 367 AA.
XX
AC AAY42412;
XX
DT 02-DEC-1999 (first entry)
XX
DE Extracellular signal Regulated Kinase (ERK)6 mutant.
XX
KW mitogen activated protein; MAP kinase; apoptosis; cancer; inflammation;
KW intracellular signal transduction pathway; inhibitor; wildtype; ERK;
KW extracellular signal regulated kinase; pyridinyl-imidazole.
XX
OS Homo sapiens.
XX
FH Key Location/Qualifiers
FT Misc-difference 109
FT /note= "Met can be substituted by an amino acid with a
FT small side chain, for example alanine or threonine"
XX
CC PN WO9942592-A1.
XX
CC PD 26-AUG-1999.
XX
CC PF 16-FEB-1999; 99WO-US003181.
XX
PR 18-FEB-1998; 98US-00025580.
XX
CC PA (VERT-) VERTEX PHARM INC.
XX
CC PI Su MS, Fox E, Wilson KP, Germann UA;
XX
DR WPI; 1999-540310/45.
XX
CC PT Method of designing Ser/Thr or Tyr kinase inhibitor useful for treating,
CC PT example breast cancer, restenosis, asthma or hypertension.
XX
CC PS Example 6; Page 48-49; 71pp; English.
XX
CC This is the amino acid sequence of ERK6. Substitution of methionine with
CC an amino acid with a small side chain, such as alanine and threonine will
CC create a mutant kinase which can theoretically bind to a pyridinyl-
CC imidazole inhibitor of p38. (MAP) 1 kinase. MAP 1 kinases mediate
CC intracellular signal transduction pathways and so have a role in many
CC diverse human diseases. For example, kinases have been implicated in cell
CC entry into apoptosis, cancer, Alzheimer's disease, angiotensin II and
CC hematopoietic cytokine receptor signal transduction, oncoprotein
CC signalling and mitosis, inflammation and infection, etc. Members of the
CC MAP kinase family share sequence similarity and conserved structural
CC domains, and include the extracellular-signal regulated kinases (ERKs),
CC Jun N-terminal kinases (JNKs) and p38 kinases. The invention relates to
CC methods for designing inhibitors of serine/threonine kinases,
CC particularly MAP kinases, and tyrosine kinases through the use of ATP-
CC binding site mutants of these kinases. The methods of this invention take
CC advantage of the fact that the mutant kinases are capable of binding
CC inhibitory compounds of other kinases with greater affinity than the
CC corresponding wild-type kinase
XX
SQ Sequence 367 AA;
Query Match 96.9%; Score 1855; Length 367;
Best Local Similarity 96.7%;
Matches 355; Conservative 5; Mismatches 7; Indels 0; Gaps 0;
Qy 1 MSSPPPARSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 60
|||||| |||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 MSSPPPTRSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 60
Qy 61 PFQSELFAKRAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 120
||||||||| ||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 PFQSELFAKLAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 120
Qy 121 KHEKLGEDRIQFLVYQMLKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 180
|||||||||||||||||:||||||||||||||||||||||||||||||||||||||||||
Db 121 KHEKLGEDRIQFLVYQMMKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 180
Qy 181 EMTGYVVTRWYRAPEVILNWMRYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 240
||||||||||||||||||||: ||||||||||||||||||||||||||||||||||||||
Db 181 EMTGYVVTRWYRAPEVILNWIAYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 240
Qy 241 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDAEQRV 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||: |:
Db 241 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDADIRL 300
Qy 301 TAGEALAHPYFESLHDTEDEPQVQKYDDSFDDVDRTLDEWKRVTYKEVLSFKPPRQLGAR 360
|||| |:|||||||||||||||||||||||| |||||||||||||||||||||||||||
Db 301 TAGEFLSHPYFESLHDTEDEPQVQKYDDSFDYFDRTLDEWKRVTYKEVLSFKPPRQLGAR 360
Qy 361 VSKETPL 367
|||||||
Db 361 VSKETPL 367
WO2004038003 teaches a nucleic acid molecule comprising a
CC polynucleotide sequence or its complement that encodes a polypeptide that is 96.9% identical to instant SEQ ID NO:2 (see the sequence alignment below).
SEQ ID NO:2
ADN99642
ID ADN99642 standard; protein; 839 AA.
XX
AC ADN99642;
XX
DT 29-JUL-2004 (first entry)
XX
DE Novel human protein sequence #458.
XX
KW anti-inflammatory; dermatological; neuroprotective; immunomodulator;
KW antibacterial; virucide; antipsoriatic; cytostatic; gene therapy;
KW vaccine; inflammatory; CNS; immune disorder; cancer; psoriasis; diabetes;
KW early aging; hormonal imbalance; ischemic heart disease;
KW ulcerative colitis.
XX
OS Homo sapiens.
XX
CC PN WO2004038003-A2.
XX
CC PD 06-MAY-2004.
XX
CC PF 24-OCT-2003; 2003WO-US033947.
XX
PR 25-OCT-2002; 2002US-0421061P.
PR 25-OCT-2002; 2002US-0421080P.
PR 25-OCT-2002; 2002US-0421552P.
PR 25-OCT-2002; 2002US-0421614P.
PR 30-OCT-2002; 2002US-0422177P.
PR 30-OCT-2002; 2002US-0422178P.
PR 15-NOV-2002; 2002US-0426355P.
PR 15-NOV-2002; 2002US-0426384P.
PR 15-NOV-2002; 2002US-0426394P.
PR 15-NOV-2002; 2002US-0426430P.
PR 15-NOV-2002; 2002US-0426916P.
PR 27-NOV-2002; 2002US-0429224P.
PR 27-NOV-2002; 2002US-0429275P.
PR 27-NOV-2002; 2002US-0429302P.
PR 27-NOV-2002; 2002US-0429326P.
PR 27-NOV-2002; 2002US-0429651P.
PR 04-DEC-2002; 2002US-0430645P.
PR 04-DEC-2002; 2002US-0430651P.
PR 04-DEC-2002; 2002US-0430657P.
PR 04-DEC-2002; 2002US-0430663P.
PR 04-DEC-2002; 2002US-0430668P.
PR 04-DEC-2002; 2002US-0430684P.
PR 05-DEC-2002; 2002US-0430937P.
PR 05-DEC-2002; 2002US-0430965P.
PR 05-DEC-2002; 2002US-0431458P.
PR 12-DEC-2002; 2002US-0433251P.
PR 12-DEC-2002; 2002US-0433500P.
PR 13-DEC-2002; 2002US-0433316P.
PR 13-DEC-2002; 2002US-0433318P.
PR 23-DEC-2002; 2002US-0436236P.
PR 03-JAN-2003; 2003US-0437914P.
PR 17-JAN-2003; 2003US-0440820P.
PR 17-JAN-2003; 2003US-0440821P.
PR 18-APR-2003; 2003US-0463700P.
PR 18-APR-2003; 2003US-0463708P.
PR 18-APR-2003; 2003US-0463716P.
PR 18-APR-2003; 2003US-0463732P.
PR 02-MAY-2003; 2003US-0467199P.
PR 02-MAY-2003; 2003US-0467201P.
PR 02-MAY-2003; 2003US-0467203P.
PR 02-MAY-2003; 2003US-0467230P.
PR 19-MAY-2003; 2003US-0471306P.
PR 19-MAY-2003; 2003US-0471336P.
PR 22-MAY-2003; 2003US-0472420P.
PR 22-MAY-2003; 2003US-0472430P.
PR 09-JUN-2003; 2003US-0476609P.
PR 09-JUN-2003; 2003US-0476621P.
PR 09-JUN-2003; 2003US-0476632P.
PR 09-JUN-2003; 2003US-0476641P.
PR 08-JUL-2003; 2003US-0485217P.
PR 08-JUL-2003; 2003US-0485218P.
PR 08-JUL-2003; 2003US-0485223P.
PR 08-JUL-2003; 2003US-0485224P.
PR 08-JUL-2003; 2003US-0485325P.
PR 08-JUL-2003; 2003US-0485359P.
PR 14-JUL-2003; 2003US-0486446P.
PR 14-JUL-2003; 2003US-0486480P.
PR 15-JUL-2003; 2003US-0486891P.
PR 15-JUL-2003; 2003US-0486960P.
PR 08-AUG-2003; 2003US-0493341P.
PR 08-AUG-2003; 2003US-0493370P.
PR 08-AUG-2003; 2003US-0493573P.
PR 08-AUG-2003; 2003US-0493577P.
XX
CC PA (FIVE-) FIVE PRIME THERAPEUTICS INC.
XX
CC PI Williams LT, Chu K, Lee E, Hestir K, Beaurang PA, Behrens D;
CC PI Halenbeck RF, Kothakota S, Lin H, Linnemann T, Pierce K, Wang Y;
CC PI Wong JGP, Wu G, Zhang H, Zeng C;
XX
DR WPI; 2004-365511/34.
DR N-PSDB; ADN98858.
XX
CC PT New nucleic acid molecules, useful in preparing a composition for
CC PT treating or preventing e.g. inflammatory, CNS, bacterial or viral
CC PT disorders, cancer, psoriasis, diabetes, ischemic heart disease or
CC PT ulcerative colitis.
XX
CC PS Claim 14; SEQ ID NO 1242; 532pp; English.
XX
CC The invention relates to a nucleic acid molecule comprising a
CC polynucleotide sequence or its complement that encodes a polypeptide. The
CC nucleic acid is useful in preparing a composition for treating or
CC preventing inflammatory, CNS, immune, bacterial or viral disorder,
CC cancer, psoriasis, diabetes, early aging, hormonal imbalance, ischemic
CC heart disease or ulcerative colitis. This sequence corresponds to a
CC protein of the invention.
XX
SQ Sequence 839 AA;
ALIGNMENT:
Query Match 96.9%; Score 1855.5; Length 839;
Best Local Similarity 94.2%;
Matches 360; Conservative 0; Mismatches 3; Indels 19; Gaps 1;
Qy 5 PPARSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYRPFQS 64
||| |||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 458 PPAGRGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYRPFQS 517
Qy 65 ELFAKRAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLMKHEK 124
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 518 ELFAKRAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLMKHEK 577
Qy 125 LGEDRIQFLVYQMLKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADSEMTG 184
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 578 LGEDRIQFLVYQMLKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADSEMTG 637
Qy 185 YVVTRWYRAPEVILNWMRYTQTVDIWSVGCIMAEMITGKTLFKGSDH------------- 231
||||||||||||||||||||||||||||||||||||||||||||||
Db 638 YVVTRWYRAPEVILNWMRYTQTVDIWSVGCIMAEMITGKTLFKGSDRILQPQGGTRGGCV 697
Qy 232 ------LDQLKEIMKVTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAV 285
||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 698 PDLGADLDQLKEIMKVTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAV 757
Qy 286 NLLEKMLVLDAEQRVTAGEALAHPYFESLHDTEDEPQVQKYDDSFDDVDRTLDEWKRVTY 345
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 758 NLLEKMLVLDAEQRVTAGEALAHPYFESLHDTEDEPQVQKYDDSFDDVDRTLDEWKRVTY 817
Qy 346 KEVLSFKPPRQLGARVSKETPL 367
||||||||||||||||||||||
Db 818 KEVLSFKPPRQLGARVSKETPL 839
US2003232772 teaches a method for identifying antisense compound targeting to human ERK6 comprising the amino acid sequence that is 96.9% identical to instant SEQ ID NO:2 (see the sequence alignment below).
SEQ ID NO:2
ADH44535
ID ADH44535 standard; protein; 367 AA.
XX
AC ADH44535;
XX
DT 15-JUN-2007 (revised)
DT 25-MAR-2004 (first entry)
XX
DE Human extracellular-signal-regulated kinase-6.
XX
KW Antisense therapy; human; extracellular-signal-regulated kinase-6;
KW hyperproliferative disorder; cancer; inflammatory disorder;
KW neurodegenerative disorder; Alzheimer's disease; infection; inflammation;
KW tumour formation; cytostatic; antiinflammatory; neuroprotective;
KW nootropic; antibacterial; enzyme; BOND_PC;
KW extracellular signal regulated kinase;
KW extracellular signal regulated kinase [Homo sapiens]; GO165; GO166;
KW GO287; GO4674; GO4682; GO4691; GO4707; GO5515; GO5524; GO5737; GO6975;
KW GO7049; GO7050; GO7165; GO7517; GO16740; GO16910; GO45445; GO45786.
XX
OS Homo sapiens.
XX
CC PN US2003232772-A1.
XX
CC PD 18-DEC-2003.
XX
CC PF 17-JUN-2002; 2002US-00174465.
XX
PR 17-JUN-2002; 2002US-00174465.
XX
CC PA (ISIS-) ISIS PHARM INC.
XX
CC PI Bennett CF, Dobie KW;
XX
DR WPI; 2004-052189/05.
DR N-PSDB; ADH44468.
DR PC:NCBI; gi1486363.
DR PC:SWISSPROT; P53778.
XX
CC PT New antisense compound targeted to a nucleic acid molecule encoding
CC PT extracellular-signal-regulated kinase-6, useful for modulating expression
CC PT of extracellular-signal-regulated kinase-6 or treating cancer.
XX
CC PS Disclosure; Page 32-33; 45pp; English.
XX
CC The present invention relates to antisense compounds targeted to a
CC nucleic acid encoding extracellular-signal-regulated kinase-6. The
CC antisense compound comprises an antisense oligonucleotide that
CC specifically hybridises with the nucleic acid and inhibits the expression
CC of extracellular-signal-regulated kinase-6. The antisense oligonucleotide
CC is a chimeric oligonucleotide. The antisense oligonucleotide comprises at
CC least one modified internucleoside linkage, preferably a phosphorothioate
CC linkage. It also comprises at least one modified sugar moiety, preferably
CC a 2'-O-methoxyethyl (2'-MOE) sugar moiety. The antisense oligonucleotide
CC further comprises at least one modified nucleobase, preferably a 5-
CC methylcytosine. The antisense oligonucleotides are useful for the
CC treatment of diseases such as hyperproliferative disorders, preferably
CC cancer, inflammatory disorders, and neurodegenerative disorders,
CC preferably Alzheimer's disease. The antisense compound can also be used
CC as prophylaxis, e.g. to prevent or delay infection, inflammation or
CC tumour formation. The present sequence represents human extracellular-
CC signal-regulated kinase-6.
CC
CC Revised record issued on 15-JUN-2007 : Enhanced with precomputed
CC information from BOND.
XX
SQ Sequence 367 AA;
ALIGNMENT:
Query Match 96.9%; Score 1855; Length 367;
Best Local Similarity 96.7%;
Matches 355; Conservative 5; Mismatches 7; Indels 0; Gaps 0;
Qy 1 MSSPPPARSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 60
|||||| |||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 MSSPPPTRSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 60
Qy 61 PFQSELFAKRAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 120
||||||||| ||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 PFQSELFAKLAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 120
Qy 121 KHEKLGEDRIQFLVYQMLKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 180
|||||||||||||||||:||||||||||||||||||||||||||||||||||||||||||
Db 121 KHEKLGEDRIQFLVYQMMKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 180
Qy 181 EMTGYVVTRWYRAPEVILNWMRYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 240
||||||||||||||||||||: ||||||||||||||||||||||||||||||||||||||
Db 181 EMTGYVVTRWYRAPEVILNWIAYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 240
Qy 241 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDAEQRV 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||: |:
Db 241 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDADIRL 300
Qy 301 TAGEALAHPYFESLHDTEDEPQVQKYDDSFDDVDRTLDEWKRVTYKEVLSFKPPRQLGAR 360
|||| |:|||||||||||||||||||||||| |||||||||||||||||||||||||||
Db 301 TAGEFLSHPYFESLHDTEDEPQVQKYDDSFDYFDRTLDEWKRVTYKEVLSFKPPRQLGAR 360
Qy 361 VSKETPL 367
|||||||
Db 361 VSKETPL 367
US2003232778 teaches a method for identifying antisense compound targeting to human ERK6 comprising the amino acid sequence that is 96.9% identical to instant SEQ ID NO:2 (see the sequence alignment below).
SEQ ID NO:2
ADJ32678
ID ADJ32678 standard; protein; 367 AA.
XX
AC ADJ32678;
XX
DT 15-JUN-2007 (revised)
DT 22-APR-2004 (first entry)
XX
DE Human extracellular-signal-regulated kinase-6 (ERK-6).
XX
KW Extracellular-signal-regulated kinase-6; ERK-6;
KW hyperproliferative disorder; cancer; inflammatory disorder;
KW neurodegenerative disorder; Alzheimer's disease; angiogenesis;
KW tubular formation; matrix degradation; human; therapy; enzyme; BOND_PC;
KW extracellular signal regulated kinase;
KW extracellular signal regulated kinase [Homo sapiens]; GO165; GO166;
KW GO287; GO4674; GO4682; GO4691; GO4707; GO5515; GO5524; GO5737; GO6975;
KW GO7049; GO7050; GO7165; GO7517; GO16740; GO16910; GO45445; GO45786.
XX
OS Homo sapiens.
XX
CC PN US2003232778-A1.
XX
CC PD 18-DEC-2003.
XX
CC PF 17-JAN-2003; 2003US-00348431.
XX
PR 17-JUN-2002; 2002US-00174465.
XX
CC PA (MARC/) MARCUSSON E G.
CC PA (BENN/) BENNETT C F.
CC PA (DOBI/) DOBIE K W.
XX
CC PI Marcusson EG, Bennett CF, Dobie KW;
XX
DR WPI; 2004-061312/06.
DR N-PSDB; ADJ32611.
DR PC:NCBI; gi1486363.
DR PC:SWISSPROT; P53778.
XX
CC PT New compound targeted to a nucleic acid molecule encoding extracellular-
CC PT signal-regulated kinase-6, useful for treating angiogenic,
CC PT hyperproliferative (cancer), inflammatory or neurodegenerative disorders
CC PT (Alzheimer's disease).
XX
CC PS Disclosure; SEQ ID NO 72; 47pp; English.
XX
CC The invention relates to antisense compounds, compositions and methods
CC for modulating the expression of extracellular-signal-regulated kinase-6
CC (ERK-6). The compound is useful in treating an animal having a disease or
CC condition associated with ERK-6, e.g. a hyperproliferative disorder
CC (especially cancer), an inflammatory disorder or a neurodegenerative
CC disorder (especially Alzheimer's disease). It is also useful for
CC inhibiting angiogenesis, for preventing tubular formation of blood
CC vessels, and for preventing degradation of extracellular matrix for new
CC blood vessel formation. The present sequence is human ERK-6 protein. This
CC sequence is used to illustrate the method of the invention.
CC
CC Revised record issued on 15-JUN-2007 : Enhanced with precomputed
CC information from BOND.
XX
SQ Sequence 367 AA;
ALIGNMENT:
Query Match 96.9%; Score 1855; Length 367;
Best Local Similarity 96.7%;
Matches 355; Conservative 5; Mismatches 7; Indels 0; Gaps 0;
Qy 1 MSSPPPARSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 60
|||||| |||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 MSSPPPTRSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 60
Qy 61 PFQSELFAKRAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 120
||||||||| ||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 PFQSELFAKLAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 120
Qy 121 KHEKLGEDRIQFLVYQMLKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 180
|||||||||||||||||:||||||||||||||||||||||||||||||||||||||||||
Db 121 KHEKLGEDRIQFLVYQMMKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 180
Qy 181 EMTGYVVTRWYRAPEVILNWMRYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 240
||||||||||||||||||||: ||||||||||||||||||||||||||||||||||||||
Db 181 EMTGYVVTRWYRAPEVILNWIAYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 240
Qy 241 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDAEQRV 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||: |:
Db 241 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDADIRL 300
Qy 301 TAGEALAHPYFESLHDTEDEPQVQKYDDSFDDVDRTLDEWKRVTYKEVLSFKPPRQLGAR 360
|||| |:|||||||||||||||||||||||| |||||||||||||||||||||||||||
Db 301 TAGEFLSHPYFESLHDTEDEPQVQKYDDSFDYFDRTLDEWKRVTYKEVLSFKPPRQLGAR 360
Qy 361 VSKETPL 367
|||||||
Db 361 VSKETPL 367
US6579972 teaches an antibody against human ERK5 comprising the amino acid sequence that is 90.0% identical to instant SEQ ID NO:2 (see the sequence alignment below).
SEQ ID NO:2
ADC64457
(NOTE: this sequence has 1 duplicate in the database searched.
See complete list at the end of this report)
ID ADC64457 standard; protein; 404 AA.
XX
AC ADC64457;
XX
DT 18-DEC-2003 (first entry)
XX
DE Human extracellular signal regulated kinase (hERK)-5, #2.
XX
KW Human; antibody; extracellular signal regulated kinase-5; hERK-5; ERK;
KW mitogen activated protein kinase; MAP kinase; hybridoma;
KW diabetes mellitus; Alzheimer's disease; peripheral neuropathy;
KW gene therapy; antidiabetic; neuroprotective; enzyme.
XX
OS Homo sapiens.
XX
CC PN US6579972-B1.
XX
CC PD 17-JUN-2003.
XX
CC PF 09-SEP-1999; 99US-00393212.
XX
PR 19-MAR-1993; 93US-00029404.
PR 02-JUN-1995; 95US-00459953.
XX
CC PA (PLAC ) MAX PLANCK GES FOERDERUNG WISSENSCHAFTEN.
XX
CC PI Lechner C, Moller NP, Ullrich A;
XX
DR WPI; 2003-634515/60.
XX
CC PT New antibody, useful for preparing a composition for treating
CC PT extracellular signal regulated kinase - 5-associated diseases in a mammal
CC PT e.g., diabetes mellitus, Alzheimer's disease or peripheral neuropathies.
XX
CC PS Disclosure; SEQ ID NO 7; 40pp; English.
XX
CC The invention discloses a new antibody comprising a specific binding
CC affinity to the human extracellular signal regulated kinase (hERK)-5
CC protein. ERKs are also referred to as mitogen activated protein (MAP)
CC kinases. The hybridoma that produces the monoclonal antibody is also
CC claimed. The antibody is useful for preparing a composition for treating
CC hERK-5-associated diseases e.g. diabetes mellitus, Alzheimer's disease or
CC peripheral neuropathies in a mammal. The polynucleotide encoding the
CC protein is also useful for treating these diseases using gene therapy
CC techniques. The sequence presented is the human ERK-5 protein.
XX
SQ Sequence 404 AA;
Query Match 90.0%; Score 1724; Length 404;
Best Local Similarity 96.5%;
Matches 329; Conservative 5; Mismatches 7; Indels 0; Gaps 0;
Qy 1 MSSPPPARSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 60
|||||| |||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 12 MSSPPPTRSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 71
Qy 61 PFQSELFAKRAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 120
||||||||| ||||||||||||||||||||||||||||||||||||||||||||||||||
Db 72 PFQSELFAKLAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 131
Qy 121 KHEKLGEDRIQFLVYQMLKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 180
|||||||||||||||||:||||||||||||||||||||||||||||||||||||||||||
Db 132 KHEKLGEDRIQFLVYQMMKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 191
Qy 181 EMTGYVVTRWYRAPEVILNWMRYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 240
||||||||||||||||||||: ||||||||||||||||||||||||||||||||||||||
Db 192 EMTGYVVTRWYRAPEVILNWIAYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 251
Qy 241 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDAEQRV 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||: |:
Db 252 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDADIRL 311
Qy 301 TAGEALAHPYFESLHDTEDEPQVQKYDDSFDDVDRTLDEWK 341
|||| |:|||||||||||||||||||||||| ||||||||
Db 312 TAGEFLSHPYFESLHDTEDEPQVQKYDDSFDYFDRTLDEWK 352
WO9421781 teaches a method for identifying agonist or antagonists of human ERK5 comprising the amino acid sequence that is 89.7% identical to instant SEQ ID NO:2 (see the sequence alignment below).
SEQ ID NO:2
AAR60700
(NOTE: this sequence has 1 duplicate in the database searched.
See complete list at the end of this report)
ID AAR60700 standard; protein; 393 AA.
XX
AC AAR60700;
XX
DT 25-MAR-2003 (revised)
DT 25-JUN-1995 (first entry)
XX
DE Human ERK-5.
XX
KW Extracellular signal-related kinase; diabetes mellitus; skeletal; muscle;
KW Alzheimer's disease; peripheral neuropathies.
XX
OS Homo sapiens.
XX
CC PN WO9421781-A2.
XX
CC PD 29-SEP-1994.
XX
CC PF 18-MAR-1994; 94WO-IB000089.
XX
PR 19-MAR-1993; 93US-00029404.
XX
CC PA (PLAC ) MAX PLANCK GES FOERDERUNG WISSENSCHAFTEN.
XX
CC PI Lechner C, Moller NPH, Ullrich A;
XX
DR WPI; 1994-317002/39.
DR N-PSDB; AAQ73592.
XX
CC PT Extracellular signal regulated kinase (ERK-5) polypeptide - useful for
CC PT detecting agonists or antagonists for treating e.g. diabetes mellitus,
CC PT skeletal muscle diseases or Alzheimer's disease.
XX
CC PS Claim 7; Page 43; 61pp; English.
XX
CC The sequence is that of the human extracellular signal-related kinase ERK
CC -5, which was obtained using a human skeletal muscle cDNA library and
CC probes based on the rat ERK-3 sequence. The protein can be used to treat
CC diabetes mellitus, skeletal muscle diseases, Alzheimer's disease or
CC peripheral neuropathies. (Updated on 25-MAR-2003 to correct PN field.)
XX
SQ Sequence 393 AA;
Query Match 89.7%; Score 1717; Length 393;
Best Local Similarity 96.2%;
Matches 328; Conservative 5; Mismatches 8; Indels 0; Gaps 0;
Qy 1 MSSPPPARSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 60
|||||| ||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 MSSPPPGGSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 60
Qy 61 PFQSELFAKRAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 120
||||||||| ||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 PFQSELFAKLAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 120
Qy 121 KHEKLGEDRIQFLVYQMLKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 180
|||||||||||||||||:||||||||||||||||||||||||||||||||||||||||||
Db 121 KHEKLGEDRIQFLVYQMMKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 180
Qy 181 EMTGYVVTRWYRAPEVILNWMRYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 240
||||||||||||||||||||: ||||||||||||||||||||||||||||||||||||||
Db 181 EMTGYVVTRWYRAPEVILNWIAYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 240
Qy 241 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDAEQRV 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||: |:
Db 241 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDADIRL 300
Qy 301 TAGEALAHPYFESLHDTEDEPQVQKYDDSFDDVDRTLDEWK 341
|||| |:|||||||||||||||||||||||| ||||||||
Db 301 TAGEFLSHPYFESLHDTEDEPQVQKYDDSFDYFDRTLDEWK 341
US2003229209 teaches a method for identifying agonist or antagonists of human ERK5 comprising the amino acid sequence that is 90.0% identical to instant SEQ ID NO:2 (see the sequence alignment below)
SEQ ID NO:2
ADG98193
ID ADG98193 standard; protein; 404 AA.
XX
AC ADG98193;
XX
DT 11-MAR-2004 (first entry)
XX
DE Human extracellular signal regulated kinase ERK5 #2.
XX
KW enzyme; human; ERK5; signal transduction pathway abnormality;
KW muscular dystrophy; extracellular signal regulated kinase.
XX
OS Homo sapiens.
XX
CC PN US2003229209-A1.
XX
CC PD 11-DEC-2003.
XX
CC PF 16-JUN-2003; 2003US-00461402.
XX
PR 19-MAR-1993; 93US-00029404.
PR 02-JUN-1995; 95US-00459953.
PR 09-SEP-1999; 99US-00393212.
XX
CC PA (PLAC ) MAX PLANCK GES FOERDERUNG WISSENSCHAFTEN.
XX
CC PI Lechner C, Moller NP, Ullrich A;
XX
DR WPI; 2004-052037/05.
XX
CC PT New extracellular signal regulated kinase, useful in diagnosing or
CC PT treating a disorder associated with an abnormality in signal transduction
CC PT pathway, e.g., muscle dystrophy.
XX
CC PS Disclosure; SEQ ID NO 7; 42pp; English.
XX
CC The invention relates to a new isolated, enriched or purified ERK5
CC polypeptide. The polypeptide is useful in diagnosing or treating a
CC disorder associated with an abnormality in signal transduction pathway,
CC e.g., muscular dystrophy. The present sequence represents the amino acid
CC sequence of the human extracellular signal regulated kinase ERK5 #2.
XX
SQ Sequence 404 AA;
ALIGNMENT:
Query Match 90.0%; Score 1724; Length 404;
Best Local Similarity 96.5%;
Matches 329; Conservative 5; Mismatches 7; Indels 0; Gaps 0;
Qy 1 MSSPPPARSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 60
|||||| |||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 12 MSSPPPTRSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 71
Qy 61 PFQSELFAKRAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 120
||||||||| ||||||||||||||||||||||||||||||||||||||||||||||||||
Db 72 PFQSELFAKLAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 131
Qy 121 KHEKLGEDRIQFLVYQMLKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 180
|||||||||||||||||:||||||||||||||||||||||||||||||||||||||||||
Db 132 KHEKLGEDRIQFLVYQMMKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 191
Qy 181 EMTGYVVTRWYRAPEVILNWMRYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 240
||||||||||||||||||||: ||||||||||||||||||||||||||||||||||||||
Db 192 EMTGYVVTRWYRAPEVILNWIAYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 251
Qy 241 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDAEQRV 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||: |:
Db 252 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDADIRL 311
Qy 301 TAGEALAHPYFESLHDTEDEPQVQKYDDSFDDVDRTLDEWK 341
|||| |:|||||||||||||||||||||||| ||||||||
Db 312 TAGEFLSHPYFESLHDTEDEPQVQKYDDSFDYFDRTLDEWK 352
US6030822 teaches a method for identifying agonist or antagonists of human ERK5 comprising the amino acid sequence that is 89.7% identical to instant SEQ ID NO:2 (see the sequence alignment below).
SEQ ID NO:2
AAY80297
ID AAY80297 standard; protein; 393 AA.
XX
AC AAY80297;
XX
DT 01-JUN-2000 (first entry)
XX
DE Human extracellular signal regulated kinase 5 SEQ ID NO:2.
XX
KW Human; extracellular signal regulated kinase; ERK-5; antidiabetic;
KW nootropic; neuroprotective; diabetes mellitus; skeletal muscle disease;
KW Alzheimer's disease; peripheral neuropathy.
XX
OS Homo sapiens.
XX
CC PN US6030822-A.
XX
CC PD 29-FEB-2000.
XX
CC PF 02-JUN-1995; 95US-00459953.
XX
PR 19-MAR-1993; 93US-00029404.
XX
CC PA (PLAC ) MAX PLANCK GES FOERDERUNG WISSENSCHAFTEN.
XX
CC PI Moller NP, Ullrich A, Lechner C;
XX
DR WPI; 2000-205206/18.
DR N-PSDB; AAZ95360.
XX
CC PT Isolated extracellular signal regulated kinase (ERK) polypeptide, useful
CC PT for treating diabetes mellitus and Alzheimer's disease.
XX
CC PS Claim 4; Fig 1; 39pp; English.
XX
CC The present sequence represents human ERK-5 (extracellular signal
CC regulated kinase). ERK-5 has antidiabetic, nootropic and neuroprotective
CC activities. Agonists and antagonists of ERK5 are useful for treating
CC diabetes mellitus, skeletal muscle diseases, Alzheimer's disease, and
CC peripheral neuropathies
XX
SQ Sequence 393 AA;
ALIGNMENT:
Query Match 89.7%; Score 1717; Length 393;
Best Local Similarity 96.2%;
Matches 328; Conservative 5; Mismatches 8; Indels 0; Gaps 0;
Qy 1 MSSPPPARSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 60
|||||| ||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 MSSPPPGGSGFYRQEVTKTAWEVRAVYRDLQPVGSGAYGAVCSAVDGRTGAKVAIKKLYR 60
Qy 61 PFQSELFAKRAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 120
||||||||| ||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 PFQSELFAKLAYRELRLLKHMRHENVIGLLDVFTPDETLDDFTDFYLVMPFMGTDLGKLM 120
Qy 121 KHEKLGEDRIQFLVYQMLKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 180
|||||||||||||||||:||||||||||||||||||||||||||||||||||||||||||
Db 121 KHEKLGEDRIQFLVYQMMKGLRYIHAAGIIHRDLKPGNLAVNEDCELKILDFGLARQADS 180
Qy 181 EMTGYVVTRWYRAPEVILNWMRYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 240
||||||||||||||||||||: ||||||||||||||||||||||||||||||||||||||
Db 181 EMTGYVVTRWYRAPEVILNWIAYTQTVDIWSVGCIMAEMITGKTLFKGSDHLDQLKEIMK 240
Qy 241 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDAEQRV 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||: |:
Db 241 VTGTPPAEFVQRLQSDEAKNYMKGLPELEKKDFASILTNASPLAVNLLEKMLVLDADIRL 300
Qy 301 TAGEALAHPYFESLHDTEDEPQVQKYDDSFDDVDRTLDEWK 341
|||| |:|||||||||||||||||||||||| ||||||||
Db 301 TAGEFLSHPYFESLHDTEDEPQVQKYDDSFDYFDRTLDEWK 341
11. THIS ACTION IS MADE FINAL. 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.
12. Any inquiry concerning this communication or earlier communications from the examiner should be directed to Chang-Yu Wang whose telephone number is (571)272-4521. The examiner can normally be reached on Monday-Thursday, 7:00am-5:30pm EST.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Jeffrey Stucker, can be reached on 571-272-0911. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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Chang-Yu Wang
February 11, 2026
/CHANG-YU WANG/Primary Examiner, Art Unit 1675