DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Election/Restrictions and Claim Status
Applicants amendments, arguments and affidavit filed 8/26/26 are acknowledged.
The affidavit under 37 CFR 1.130(a) filed on 8/26/26 is sufficient to overcome the rejection of claims based on Cho et al. (see pages 10-11 of office action of 4/14/26).
Any other objection or rejection that is not addressed below is withdrawn based on the amendments.
Previously, peptide TGN-2 (SEQ ID NO:6) was elected.
Claims 2-13 have been canceled.
Claims 1 and 14-17 are being examined.
Priority
The priority information is found in the filing receipt dated 12/18/23.
Claim Rejections - 35 USC § 103
Claims were previously rejected based on the references cited below. Since the claims have been amended, the rejections are updated to correspond to the instant claims.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claim(s) 1, 14 and 16-17 is/are rejected under 35 U.S.C. 103 as being unpatentable over Lee et al. (US 2016/0340396; ‘Lee’).
Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1). Lee teach that blocking of PTEN activity is known to be effective in axon regeneration after nerve injury (section 0112). Lee recites details about the peptide (claims 2-8). Lee teach the peptide TGN-2 of sequence RRRRRRRR-HYRYpSDTTDpSDPENEPFDEDQHTQITKV-amide where pS is phosphorylated serine (figure 1b and section 0047). Lee teach that TGN-2 promote neurite outgrowth as well as delayed neurite degeneration and is thus useful as a therapeutic agent for nerve regeneration after CNS injury (section 0007 and figure 4 and example 2.4). Lee teach that the nerve injury is in the central nervous system (claim 9). Lee teach spinal cord injury (section 0020). Lee teach neurons involved in motor control (sections 0056, 0073, 0077 and 0079). Lee teach movements necessary for coordinated movement (sections 0070, 0073 and 0075).
Lee does not teach a specific example with administration after a spinal cord injury.
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of Lee based on the specific teachings and suggestions of Lee. Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1). Lee teach that the nerve injury is in the central nervous system (claim 9). Lee teach spinal cord injury (section 0020). Lee teach neurons involved in motor control (sections 0073, 0077 and 0079). Lee teach movements necessary for coordinated movement (sections 0070, 0073 and 0075). Thus, one would have been motivated to use the method of Lee as suggested – after a spinal cord injury. Since Lee teach that TGN-2 promote neurite outgrowth as well as delayed neurite degeneration and is thus useful as a therapeutic agent for nerve regeneration after CNS injury (section 0007 and figure 4 and example 2.4) one would have been motivated to use such peptide with a reasonable expectation of success. Further, one would have had a reasonable expectation of success since the mechanism of action was known - Lee teach that blocking of PTEN activity is known to be effective in axon regeneration after nerve injury (section 0112).
In relation to the spinal cord injury recited in claims 1, Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1) and specifically teach that the nerve injury is in the central nervous system (claim 9) and recite spinal cord injury (section 0020).
In relation to the motor function of claims 1 and 16, Lee teach neurons involved in motor control (sections 0056, 0073, 0077 and 0079).
In relation to the movement of claims 1 and 17, Lee teach movements necessary for coordinated movement (sections 0070, 0073 and 0075).
In relation to the administration of a PTEN inhibiting peptide of claims 1 and 14, Lee teach administering a peptide (claim 1). Lee recites details about the peptide (claims 2-8). Lee teach the peptide TGN-2 of sequence RRRRRRRR-HYRYpSDTTDpSDPENEPFDEDQHTQITKV-amide where pS is phosphorylated serine (figure 1b and section 0047) and RRRRRRRR is a PTD. This sequence is the elected sequence (SEQ ID NO:6). Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1).
Claim(s) 1 and 14-17 is/are rejected under 35 U.S.C. 103 as being unpatentable over Lee et al. (US 2016/0340396; ‘Lee’) in view of Lee et al. (‘Nerve regeneration restores supraspinal control of bladder function after complete spinal cord injury’ The Journal of Neuroscience v33(26) June 26 2013 pages 10591-10606; ‘Lee2013’).
Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1). Lee teach that blocking of PTEN activity is known to be effective in axon regeneration after nerve injury (section 0112). Lee recites details about the peptide (claims 2-8). Lee teach the peptide TGN-2 of sequence RRRRRRRR-HYRYpSDTTDpSDPENEPFDEDQHTQITKV-amide where pS is phosphorylated serine (figure 1b and section 0047). Lee teach that TGN-2 promote neurite outgrowth as well as delayed neurite degeneration and is thus useful as a therapeutic agent for nerve regeneration after CNS injury (section 0007 and figure 4 and example 2.4). Lee teach that the nerve injury is in the central nervous system (claim 9). Lee teach spinal cord injury (section 0020). Lee teach neurons involved in motor control (sections 0056, 0073, 0077 and 0079). Lee teach movements necessary for coordinated movement (sections 0070, 0073 and 0075).
Lee does not teach a specific example with administration after a spinal cord injury.
Lee2013 teach that urinary dysfunction is attributable to a lack of regeneration of supraspinal pathways that control the bladder and can occur after spinal cord injury (abstract). Lee2013 specifically refers to the Cameron reference whose title refers to neurogenic bladder (page 10604 references section).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of Lee based on the specific teachings and suggestions of Lee. Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1). Lee teach that the nerve injury is in the central nervous system (claim 9). Lee teach spinal cord injury (section 0020). Lee teach neurons involved in motor control (sections 0056, 0073, 0077 and 0079). Lee teach movements necessary for coordinated movement (sections 0070, 0073 and 0075). Thus, one would have been motivated to use the method of Lee as suggested – after a spinal cord injury. Since Lee teach that TGN-2 promote neurite outgrowth as well as delayed neurite degeneration and is thus useful as a therapeutic agent for nerve regeneration after CNS injury (section 0007 and figure 4 and example 2.4) one would have been motivated to use such peptide with a reasonable expectation of success. Further, since Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1) and Lee2013 teach that urinary dysfunction after spinal cord injury can be attributable to a lack of regeneration of supraspinal pathways that control the bladder one would have been motivated to specifically administer to those as taught by Lee2013. One would have had a reasonable expectation of success since the mechanism of action was known - Lee teach that blocking of PTEN activity is known to be effective in axon regeneration after nerve injury (section 0112).
In relation to the spinal cord injury recited in claims 1, Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1) and specifically teach that the nerve injury is in the central nervous system (claim 9) and recite spinal cord injury (section 0020).
In relation to the motor function of claims 1 and 16, Lee teach neurons involved in motor control (sections 0056, 0073, 0077 and 0079).
In relation to the movement of claims 1 and 17, Lee teach movements necessary for coordinated movement (sections 0070, 0073 and 0075).
In relation to neurogenic bladder of claim 1 and 15, Lee2013 teach that urinary dysfunction is attributable to a lack of regeneration of supraspinal pathways that control the bladder and can occur after spinal cord injury (abstract). Lee2013 specifically refers to the Cameron reference whose title refers to neurogenic bladder (page 10604 references section).
In relation to the administration of a PTEN inhibiting peptide of claims 1 and 14, Lee teach administering a peptide (claim 1). Lee recites details about the peptide (claims 2-8). Lee teach the peptide TGN-2 of sequence RRRRRRRR-HYRYpSDTTDpSDPENEPFDEDQHTQITKV-amide where pS is phosphorylated serine (figure 1b and section 0047) and RRRRRRRR is a PTD. This sequence is the elected sequence (SEQ ID NO:6). Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1).
Response to Arguments – 103
Applicant's arguments filed 8/26/26 have been fully considered but they are not persuasive with respect to the rejections set forth above.
Although applicants argue that Lee does not mention the bladder, claim 1 is not limited to the bladder as it recites ‘loss of motor function, or loss of movement coordination’.
Although applicants argue that the claims have been amended, the amended claims are addressed above.
Although applicants argue that Lee2013 is drawn to a different intervention, the rejection based on Lee2013 is a multiple reference 103 rejection and as such any single reference does not necessarily anticipate the claims.
Although applicants argue about predictability, Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1). Lee teach that blocking of PTEN activity is known to be effective in axon regeneration after nerve injury (section 0112). Lee recites details about the peptide (claims 2-8). Lee teach the peptide TGN-2 of sequence RRRRRRRR-HYRYpSDTTDpSDPENEPFDEDQHTQITKV-amide where pS is phosphorylated serine (figure 1b and section 0047). Lee teach that TGN-2 promote neurite outgrowth as well as delayed neurite degeneration and is thus useful as a therapeutic agent for nerve regeneration after CNS injury (section 0007 and figure 4 and example 2.4). Lee2013 refers to ‘complete spinal cord injury’ (abstract) which is not required by the instant claims.
Although applicants argue that Lee2013 does not teach a peptide as claimed, the rejection based on Lee2013 is a multiple reference 103 rejection and as such any single reference does not necessarily anticipate the claims.
Double Patenting
Claims were previously rejected based on the patent/references cited below. Since the claims have been amended, the rejections are updated to correspond to the instant claims.
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 1, 14 and 16-17 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-10 of U.S. Patent No. 10,584,153 (153) in view of Lee et al. (US 2016/0340396; ‘Lee’).
153 recites a method of regenerating a nerve at a site of nerve injury comprising administering a PTEN inhibiting peptide that can be SEQ ID NO:6 (claim 1). SEQ ID NO:6 is recited in column 9 lines 62-65.
153 does not specifically recite spinal cord injury.
Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1). Lee teach that blocking of PTEN activity is known to be effective in axon regeneration after nerve injury (section 0112). Lee recites details about the peptide (claims 2-8). Lee teach the peptide TGN-2 of sequence RRRRRRRR-HYRYpSDTTDpSDPENEPFDEDQHTQITKV-amide where pS is phosphorylated serine (figure 1b and section 0047). Lee teach that TGN-2 promote neurite outgrowth as well as delayed neurite degeneration and is thus useful as a therapeutic agent for nerve regeneration after CNS injury (section 0007 and figure 4 and example 2.4). Lee teach that the nerve injury is in the central nervous system (claim 9). Lee teach spinal cord injury (section 0020). Lee teach neurons involved in motor control (sections 0056, 0073, 0077 and 0079). Lee teach movements necessary for coordinated movement (sections 0070, 0073 and 0075).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of 153 because SEQ ID NO:6 of 153 is the same as TGN-2 of Lee. Thus, one would have been motivated to use SEQ ID NO:6 as taught by the prior art. Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1). Lee teach that the nerve injury is in the central nervous system (claim 9). Lee teach spinal cord injury (section 0020). Lee teach neurons involved in motor control (sections 0056, 0073, 0077 and 0079). Lee teach movements necessary for coordinated movement (sections 0070, 0073 and 0075). Thus, one would have been motivated to use the method of Lee as suggested – after a spinal cord injury. Since Lee teach that TGN-2 promote neurite outgrowth as well as delayed neurite degeneration and is thus useful as a therapeutic agent for nerve regeneration after CNS injury (section 0007 and figure 4 and example 2.4) one would have been motivated to use such peptide with a reasonable expectation of success. Further, one would have had a reasonable expectation of success since the mechanism of action was known - Lee teach that blocking of PTEN activity is known to be effective in axon regeneration after nerve injury (section 0112).
In relation to the spinal cord injury recited in claims 1, Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1) and specifically teach that the nerve injury is in the central nervous system (claim 9) and recite spinal cord injury (section 0020).
In relation to the motor function of claims 1 and 16, Lee teach neurons involved in motor control (sections 0056, 0073, 0077 and 0079).
In relation to the movement of claims 1 and 17, Lee teach movements necessary for coordinated movement (sections 0070, 0073 and 0075).
In relation to the administration of a PTEN inhibiting peptide of claims 1 and 14, Lee teach administering a peptide (claim 1). 153 recites a method of regenerating a nerve at a site of nerve injury comprising administering a PTEN inhibiting peptide that can be SEQ ID NO:6 (claim 1). SEQ ID NO:6 is recited in column 9 lines 62-65 which is the instant elected species. Lee recites details about the peptide (claims 2-8). Lee teach the peptide TGN-2 of sequence RRRRRRRR-HYRYpSDTTDpSDPENEPFDEDQHTQITKV-amide where pS is phosphorylated serine (figure 1b and section 0047) and RRRRRRRR is a PTD. This sequence is the elected sequence (SEQ ID NO:6). Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1).
Claims 1 and 14-17 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-10 of U.S. Patent No. 10,584,153 (153) in view of Lee et al. (US 2016/0340396; ‘Lee’) in view of Lee et al. (‘Nerve regeneration restores supraspinal control of bladder function after complete spinal cord injury’ The Journal of Neuroscience v33(26) June 26 2013 pages 10591-10606; ‘Lee2013’).
153 recites a method of regenerating a nerve at a site of nerve injury comprising administering a PTEN inhibiting peptide that can be SEQ ID NO:6 (claim 1). SEQ ID NO:6 is recited in column 9 lines 62-65.
153 does not specifically recite spinal cord injury.
Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1). Lee teach that blocking of PTEN activity is known to be effective in axon regeneration after nerve injury (section 0112). Lee recites details about the peptide (claims 2-8). Lee teach the peptide TGN-2 of sequence RRRRRRRR-HYRYpSDTTDpSDPENEPFDEDQHTQITKV-amide where pS is phosphorylated serine (figure 1b and section 0047). Lee teach that TGN-2 promote neurite outgrowth as well as delayed neurite degeneration and is thus useful as a therapeutic agent for nerve regeneration after CNS injury (section 0007 and figure 4 and example 2.4). Lee teach that the nerve injury is in the central nervous system (claim 9). Lee teach spinal cord injury (section 0020). Lee teach neurons involved in motor control (sections 0056, 0073, 0077 and 0079). Lee teach movements necessary for coordinated movement (sections 0070, 0073 and 0075).
Lee2013 teach that urinary dysfunction is attributable to a lack of regeneration of supraspinal pathways that control the bladder and can occur after spinal cord injury (abstract). Lee2013 specifically refers to the Cameron reference whose title refers to neurogenic bladder (page 10604 references section).
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the teachings of 153 because SEQ ID NO:6 of 153 is the same as TGN-2 of Lee. Thus, one would have been motivated to use SEQ ID NO:6 as taught by the prior art. Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1). Lee teach that the nerve injury is in the central nervous system (claim 9). Lee teach spinal cord injury (section 0020). Lee teach neurons involved in motor control (sections 0056, 0073, 0077 and 0079). Lee teach movements necessary for coordinated movement (sections 0070, 0073 and 0075). Thus, one would have been motivated to use the method of Lee as suggested – after a spinal cord injury. Since Lee teach that TGN-2 promote neurite outgrowth as well as delayed neurite degeneration and is thus useful as a therapeutic agent for nerve regeneration after CNS injury (section 0007 and figure 4 and example 2.4) one would have been motivated to use such peptide with a reasonable expectation of success. Since 153 and Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1) and Lee2013 teach that urinary dysfunction after spinal cord injury can be attributable to a lack of regeneration of supraspinal pathways that control the bladder one would have been motivated to specifically teach those as taught by Lee2013. Further, one would have had a reasonable expectation of success since the mechanism of action was known - Lee teach that blocking of PTEN activity is known to be effective in axon regeneration after nerve injury (section 0112).
In relation to the spinal cord injury recited in claims 1, Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1) and specifically teach that the nerve injury is in the central nervous system (claim 9) and recite spinal cord injury (section 0020).
In relation to the motor function of claims 1 and 16, Lee teach neurons involved in motor control (sections 0056, 0073, 0077 and 0079).
In relation to the movement of claims 1 and 17, Lee teach movements necessary for coordinated movement (sections 0070, 0073 and 0075).
In relation to neurogenic bladder of claim 1 and 15, Lee2013 teach that urinary dysfunction is attributable to a lack of regeneration of supraspinal pathways that control the bladder and can occur after spinal cord injury (abstract). Lee2013 specifically refers to the Cameron reference whose title refers to neurogenic bladder (page 10604 references section).
In relation to the administration of a PTEN inhibiting peptide of claims 1 and 14, Lee teach administering a peptide (claim 1). 153 recites a method of regenerating a nerve at a site of nerve injury comprising administering a PTEN inhibiting peptide that can be SEQ ID NO:6 (claim 1). SEQ ID NO:6 is recited in column 9 lines 62-65 which is the instant elected species. Lee recites details about the peptide (claims 2-8). Lee teach the peptide TGN-2 of sequence RRRRRRRR-HYRYpSDTTDpSDPENEPFDEDQHTQITKV-amide where pS is phosphorylated serine (figure 1b and section 0047) and RRRRRRRR is a PTD. This sequence is the elected sequence (SEQ ID NO:6). Lee teach a method of regenerating nerve or attenuating degeneration of nerve at a site of nerve injury comprising administering at a site of nerve injury an amount of a PTEN inhibiting peptide (claim 1).
Response to Arguments – Double Patenting
Applicant's arguments filed 8/26/26 have been fully considered but they are not persuasive with respect to the rejections set forth above.
Although applicants argue that 153 and Lee do not mention the bladder, claim 1 is not limited to the bladder as it recites ‘loss of motor function, or loss of movement coordination’.
Although applicants argue about reasons above, the arguments are addressed above and not found persuasive.
Although applicants argue about use of a specification, the reference cited above is US 2016/0340396 which is a prior art reference.
Although applicants refer to preparing a terminal disclaimer, no terminal disclaimer is of record.
Conclusion
Applicant's amendment necessitated any new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to RONALD T NIEBAUER whose telephone number is (571)270-3059. The examiner can normally be reached M - F 6:30 - 2:30 EST.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Melissa Fisher can be reached at 571-270-7430. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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RONALD T. NIEBAUER
Primary Examiner
Art Unit 1658
/RONALD T NIEBAUER/Examiner, Art Unit 1658
