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 .
Claim Status
1. The amendment filed 03/30/2026 has been entered. Claims 1 – 20 remain pending and are under consideration.
Election/Restrictions
2. Applicant’s election without traverse of Group I (claims 1 – 20) in the reply filed on 10/06/2025 is acknowledged.
3. Claims 21 – 22 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 10/06/2025.
Priority
4. This application is the U.S. national stage entry of PCT/US2021/040178 filed 07/01/2021, which claims priority to U.S. provisional patent application No. 63/047697 filed 07/02/2020.
Information Disclosure Statement
5. The information disclosure statement (IDS) submitted on 04/23/2026 is acknowledged. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Withdrawn Drawings Objection
6. The objection to the drawings for description of color figures without showing those figures in color is withdrawn in view of Applicant’s amendment to the specification to remove reference to color.
Withdrawn Claim Objections
7. The objections to claims 1, 18, and 19 are withdrawn in view of Applicant’s amendment to these claims.
Withdrawn Claim Rejections
8. The rejection of claims 1 – 12 and 16 – 20 under 35 U.S.C. 112(b) is withdrawn in view of Applicant’s amendment to claim 1.
9. The rejection of claim 18 under 35 U.S.C. 112(d) is withdrawn in view of Applicant’s amendment to claim 1 and 18.
10. The rejection of claims 1 – 3, 5 – 9, 11 – 13, and 16 – 20 under 35 U.S.C. 102(a)(1) is withdrawn in view of Applicant’s amendment to claim 1.
11. The rejection of claims 1 – 20 under 35 U.S.C. 103 is withdrawn in view of Applicant’s amendment to claim 1.
Claim Interpretation
12. For the purpose of applying prior art, “human stem cells are obtained from a human embryo” of claim 4 is interpreted as the human stem cells of claim 1 are human embryonic stem cells because Example 1 of Applicant’s specification cultures hESCs (page 25, para. 00072).
13. For the purpose of applying prior art, claim 19 is interpreted as a portion of the spinal dI4 progenitor cells of step (b) further differentiate into spinal GABA interneurons by culturing in any culture medium because the claim does not recite any active method steps or any requirements for a culture medium for differentiating spinal dI4 progenitors into spinal GABA interneurons.
Rejections Necessitated by Amendment
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
14. Claim(s) 1 – 20 are rejected under 35 U.S.C. 103 as being unpatentable over Chen (CN-109554342-A; Filed 10/23/2018; Published 04/02/2019; previously cited), hereinafter Chen in view of Du (Du, Zhong-Wei, et al. Nature communications 6.1 (2015): 6626; previously cited), which is cited on the IDS filed 04/14/2023 in view of Ogura (Ogura, Takenori, et al. Development 145.16 (2018): dev162214.), hereinafter Ogura in view of Glasgow (Glasgow, Stacey M., et al. (2005): 5461-5469.), hereinafter Glasgow. A machine translation of CN1095543342A was previously provided. The translation was performed on 12/09/2025 of pages 2 – 6 of the original document.
Regarding step (a) of claim 1 – 3 and claims 5 – 7 and 11 – 12, Chen teaches a method comprising a first step of culturing human induced pluripotent stem cells (“human stem cells” of claim 1; claim 2; “human induced pluripotent stem cells” of claim 3) in a medium comprising CHIR99021, SB431542, and DMH for 7 days (“step (a)” of claim 1; “CHIR99021” of claim 5; “DMH-1” of claim 6; “SB431542” of claim 7; “7 days” of claims 11 – 12) to form neuronal epithelial cells wherein the resulting cells express Sox1 and Hoxa3 (“at least 95% of the population of cells generated are Sox1+/Hoxa3+ spinal neuroepithelia progenitors”) (page 3, para. 2 – 3; page 3, last para.; page 4, para. 8; page 5, para. 2 and last para.; Figure 1, 2a, and 2b of the original document).
Regarding step (b) of claim 1 and claims 8, 9, 13, 16, and 17, Chen teaches the method further comprises a second step of adding cyclopamine at 5 nM and retinoic acid at 1 nM to the medium for continuous induction of differentiation for an additional 7 days (“step (b)” of claim 1; “retinoic acid” of claim 8; “cyclopamine” of claim 9; claim 13; “7 days” of claims 16 – 17) to form spinal cord interneuron precursor cells (page 1, claim 3; page 3, para. 2 – 4; page 4, para. 1 and para. 7 – 8; page 5, para. 2 – 5; page 6, para. 1; Figure 1, 2a and 2b of the original document). Chen does not teach “about 0.01 µM -2 µM” of retinoic acid or “about 0.1 µM-2µM” of cyclopamine. However, Chen teaches a molar ratio of cyclopamine to retinoic acid is 5:1 (page 3, para. 8). Chen teaches the method uses CHIR99021, SB431542, and DMH1 and then cyclopamine and retinoic acid to obtain a spinal cord-derived GABAergic interneuron where the culture media is animal-free and the interneurons are clinical grade (page 4, para. 6 – 8).
Regarding claim 10, Chen teaches 3 µM CHIR99021, 2 µM SB431542, and 2 µM DMH1 (page 1, claim 2; page 3, para. 7).
Regarding claim 14, Chen teaches 3 µM CHIR99021, 2 µM SB431542, and 2 µM DMH1, cyclopamine at 5 nM and retinoic acid at 1 nM (page 1, claim 2; page 3, para. 7). Chen does not teach “about 0.01 µM -2 µM RA, and about 0.1 µM -2µM cyclopamine”.
Regarding claim 15, Chen teaches 3 µM CHIR99021, 2 µM SB431542, and 2 µM DMH1, cyclopamine at 5 nM and retinoic acid at 1 nM (page 1, claim 2; page 3, para. 7). Chen does not teach 0.1 µM retinoic acid or 0.5 µM cyclopamine.
Regarding claim 19, Chen teaches further differentiating the cells after day 14 to form GABAergic spinal interneurons (page 3, para. 5; page 5, para. 6 – 11; page 6, para. 2 – 3; Figure 1 and 4 of the original document).
Chen does not teach “about 0.01 µM -2 µM” of retinoic acid or “about 0.1 µM-2µM” of cyclopamine of claim 1 or “the human stem cells are obtained from a human embryo” of claim 4 or “about 0.01 µM -2 µM RA, and about 0.1 µM -2µM cyclopamine” of claim 14 or 0.1 µM retinoic acid or 0.5 µM cyclopamine of claim 15. However, Chen teaches a molar ratio of cyclopamine to retinoic acid is 5:1 (page 3, para. 8). Chen teaches spinal cord injury is a common traumatic disease that causes a range of motor and psychological problems that are common in people under the age of 30 (page 2, para. 1 of Background technique). Chen teaches nearly 40% - 50% of patients have neuropathic pain in 1 year and later converted to chronic pain, affecting the recovery of patients (page 2, para. 1 of Background technique). Chen teaches at present, the clinical treatment of pain mainly includes drug treatment and physical factor treatment, but the systemic side effects of drug treatment are obvious, while the remission period of physical factor treatment is short, and the ideal therapeutic effect is not achieved, and new treatment methods need to be sought (page 2, para. 3 of Background technique). Chen teaches the use of pluripotent stem cells to differentiate into high-purity spinal GABAergic interneurons for the treatment of pain and the method can quickly and efficiently obtain high-purity spinal GABAergic interneurons (page 3, para. 1 – 17).
Regarding “about 0.01 µM -2 µM” of a retinoic acid signaling agonist of claim 1, Du teaches a method comprising culturing human pluripotent stem cells in a culture media comprising 3 µM CHIR99021, 2 µM DMH1, and 2 µM SB431542 to form neuroepithelial progenitors (NEPs) (page 7, right col. para. 4; Supplementary Figure 3; Figure 1a). Du teaches >98% of the NEPs were SOX1+/HOXA3 (page 2, right col. para. 1). Du teaches then culturing the NEPs in a medium comprising 1 µM CHIR99021, 2 µM SB431542, 2 µM DMH1, 0.1 µM retinoic acid (“about 0.01 µM -2 µM”) and 0.5 µM Purmorphamine to form motor neuron progenitors (MNPs) (Supplementary Figure 3; page 7, right col. para. 4.).
Regarding “about 0.1 µM-2µM of a SHH signaling inhibitor” of claim 1 and “about 0.01 µM -2 µM RA, and about 0.1 µM -2µM cyclopamine” of claim 14 and 0.1 µM retinoic acid or 0.5 µM cyclopamine of claim 15, Du teaches then culturing the NEPs in a medium comprising 1 µM CHIR99021, 2 µM SB431542, 2 µM DMH1, 0.1 µM retinoic acid (“about 0.01 µM -2 µM” of claim 1 and claim 14; “0.1 µM” of claim 15) and 0.5 µM Purmorphamine to form motor neuron progenitors (MNPs) (Supplementary Figure 3; page 7, right col. para. 4.). Du teaches replacing the Purmorphamine with cyclopamine to produce progenitors that could be further differentiated to GABA neurons (page 5, left col.; Supplementary Figure 3a). Du does not teach the concentration of cyclopamine. However, as Chen teaches a molar ratio of cyclopamine to retinoic acid is 5:1 (page 3, para. 8) with 3 µM CHIR99021, 2 µM SB431542, and 2 µM DMH1 (page 1, claim 2; page 3, para. 7), and Du teaches 0.1 µM retinoic acid, it would have been obvious to use 0.5 µM cyclopamine because Du teaches replacing 0.5 µM Purmorphamine with cyclopamine and Chen teaches the molar ratio of cyclopamine to retinoic acid is 5:1 to produce spinal cord interneuron precursor cells. Therefore, a culture medium of step (b) comprising 3 µM CHIR99021, 2 µM SB431542, and 2 µM DMH1, 0.1 uM retinoic acid, and 0.5 uM cyclopamine would be expected to produce spinal dI4 progenitor cells with a reasonable expectation of success as both Chen and Du teach 3 µM CHIR99021, 2 µM SB431542, and 2 µM DMH1, retinoic acid, and cyclopamine where Chen teaches a molar ratio of cyclopamine to retinoic acid is 5:1 to produce spinal cord interneuron precursor cells and Du teaches a ratio of 5:1 of purmorphamine to retinoic acid where purmorphamine is replaced with cyclopamine.
Regarding claim 4, Du teaches human embryonic stem cells were used in the method (page 7, para. 3; Supplementary Table 1).
Regarding “wherein at least 90% of the population of cells generated are spinal dI4 progenitor cells that express at least one gene selected from PTF1A, PAX7, and ASCL1, or a combination” of claim 1 and “at least 90% of the population of the spinal dI4 progenitor cells of step (b) are PTF1A+/PAX7/ASCL1+ spinal dI4 progenitor cells” of claim 18, Du teaches the method guides human embryonic stem cells to a near-pure population (>95%) of motor neuron progenitors (MNPs) in 12 days, and an enriched population (>90%) of functionally mature motorneurons (MNs) in an additional 16 days (Abstract). Du does not teach the cells are positive for these markers.
Du teaches degeneration of MNs is implicated in a number of devastating diseases (page 2, left col. para. 2). Du teaches iPSCs have been generated from patients with diseases such as SMA, ALS, Charcot-Marie-Tooth, and poliomyelitis disease to identify disease-related phenotypes but efforts are hindered by the inability to produce pure or highly enriched MNs with consistent quality (page 2, left col. para. 2). Du teaches there is a critical need to develop new methods that enable generation of highly pure and functionally mature MNs with consistent quality and in a short time (page 2, left col. para. 2). Du teaches deriving MNs and GABA neurons from iPSCs from SMA patients and in both neurons, survival motor neuron (SMN) mRNA was decreased (page 5). Du teaches MNs showed lower SMN than GABA neurons (page 5, right col.; Figure 4a). Du teaches deriving MNs and GABA neurons from ALS patients and there was reduced expression of NEFL in MNs with the D90A mutation but not in GABA neurons (page 5, right col.; Figure 4b). Du teaches correction of the D90A mutation restored NEFL expression in Figure 4b. Du teaches enriched MNs generated from patient iPSCs using the method enable identification of disease-related phenotypes and for drug screening and suggest its potential for identifying disease-specific targets (page 6; page 7, left col. para. 1). Du teaches the method enables generation of large quantities of MNs with consistency and high purity, providing a basis for modelling MN diseases in vitro and for drug discovery (page 7, right col. para. 2). Du does not teach the spinal GABA interneurons express at least one gene selected from PAX2 and LHX1/5 of claim 20. One would have been motivated to combine the teachings of Chen and Du as both teach methods for the formation of spinal dI4 progenitor cells and GABA neurons by culturing human pluripotent cells in a medium comprising CHIR99021, SB431542, DMH1, cyclopamine and retinoic acid.
Regarding “PAX7” of claims 1 and 18 and “PAX2 and LXH1/5” of claim 20, Ogura teaches a method of differentiating human pluripotent stem cells (hPSCs) to dorsal spinal cord-like tissues that express PAX7 (claim 1 and 18) that can be further differentiated to form dI4 GABAergic neurons that is positive for PAX2 and Lhx1 (claim 20) comprising culturing hPSCs in media comprising CHIR99021, SB431542, and retinoic acid (page 6, right col. last para.; page 8, left col. para. 2; Figure S8; Figure 1A; Figure 3B; Figure 4C; Figure 6A, K, L). Ogura teaches expression of PAX6 and PAX7 suggested the generation of dorsal progenitor domains (page 2, left col. para. 4; Figure 1I,L). Ogura teaches activating Shh signaling produces intermediate and ventral spinal cord-like tissues and after dissociation of these tissues, spinal motor neurons are detected (Abstract; page 1, right col. para. 1). Ogura teaches the induction of the spinal cord as a whole tissue has not been achieved and their method recapitulates patterning of the developing dorsal spinal cord and enables the generation of four types of dorsal interneuron marker-positive cell populations (Abstract). Ogura teaches the derivation of a 3D spinal cord equivalent would allow better understanding of spinal cord development and contribute to the generation of valid in vitro disease models (page 1, right col. para. 2). Ogura does not teach PTF1A or ASCL1 of claim 18. One would have been motivated to combine the teachings of Chen, Du, and Ogura because each teach methods of generating spinal motor neurons.
Regarding PTF1A and ASCL1 of claim 18, Glasgow teaches Ptf1a and Mash1 (ASCL1) are present in precursors to GABAergic neurons (Abstract; page 5462, right col. last para.; Figure 1; page 5463, left col. para. 1; page 5467, right col. para. 1; page 5468, left col. last para.). Glasgow teaches Ptf1a is required to generate dI4 interneurons (page 5463, left col. para. 2 and right col. para. 1 – 2; Figure 2J). Glasgow teaches in the absence of Ptf1a, Pax2 was completely lost and Lhx1/5 was dramatically reduced (page 5464, left col. para. 2). Glasgow teaches Ptf1a is required for Pax2 expression leading to the formation of GABAergic neurons (page 5461, right col.; page 5462, left col. para. 1; page 5465, left col. para. 2; page 5467, left col. para. 1; Figure 5I). Glasgow teaches the spinal cord dorsal horn largely consists of glutamatergic excitatory and GABAergic inhibitory neurons that modulate somatosensory inputs from the periphery, including pain (page 5461, right col. para. 1). Glasgow teaches GABAergic neurons produce inhibition of primary sensory afferents, and thus represent a major gatekeeper for the strength of sensory input to the spinal cord (page 5466, right col. para. 3).
It would have been obvious prior to the effective filing date of the invention as claimed for the person of ordinary skill in the art to combine the teachings of Chen regarding a method of producing spinal cord interneuron precursor cells and GABA neurons from human pluripotent stem cells with the teachings of Du regarding a method of producing spinal cord interneuron precursor cells and GABA neurons from human pluripotent stem cells with the teachings of Ogura regarding a method of producing dorsal spinal cord-like tissues that express PAX7 and GABAergic neurons that express PAX2 from human pluripotent stem cells with the teachings of Glasgow regarding Ptf1a is required to generate dI4 interneurons and Ptf1a and Mash1 (ASCL1) are present in precursors to GABAergic neurons to arrive at the claimed method of generating a population of spinal dorsal interneuron domain 4 (dl4) progenitor cells from human stem cells, the method comprising: (a) culturing the human stem cells in a culture medium comprising a Wnt signaling pathway agonist, a BMP signaling pathway inhibitor, and a TGFβ signaling pathway inhibitor, to generate a population of cells comprising spinal neuroepithelia progenitors, wherein at least 95% of the population of cells generated are Sox1 +/Hoxa3+ spinal neuroepithelia progenitors; and (b) culturing the spinal neuroepithelia progenitors of step (a) in a medium additionally comprising a Wnt signaling pathway agonist, a BMP signaling pathway inhibitor, a TGFβ signaling pathway inhibitor, about 0.01 μM-2 μM of a retinoic acid (RA) signaling agonist and about 0.1 μM-2 μM of a SHH signaling inhibitor, to generate a population of cells comprising spinal [[dl4]] dl4 progenitor cells, wherein at least 90% of the population of cells generated are spinal dl4 progenitor cells that express at least one gene selected from PTF1A PAX7, and ASCL 1, or a combination thereof. One would have been motivated to combine the teachings of Chen, Du, Ogura, and Glasgow in a method of producing spinal dI4 progenitor cells and GABAergic neurons for treating pain in patients, modeling spinal disease, and drug discovery as Chen teaches at present, the clinical treatment of pain mainly includes drug treatment and physical factor treatment, but the systemic side effects of drug treatment are obvious, while the remission period of physical factor treatment is short, and the ideal therapeutic effect is not achieved, and new treatment methods need to be sought and Chen teaches the use of pluripotent stem cells to differentiate into high-purity spinal GABAergic interneurons for the treatment of pain and Du teaches there is a critical need to develop new methods that enable generation of highly pure and functionally mature spinal motor neurons with consistent quality in a short time and Du teaches enriched MNs generated from patient iPSCs using the method enable identification of disease-related phenotypes and for drug screening and suggest its potential for identifying disease-specific targets. One would have a reasonable expectation of success in combining the teachings as Chen teaches the method can quickly and efficiently obtain high-purity spinal GABAergic interneurons and Du teaches the method enables generation of large quantities of MNs with consistency and high purity, providing a basis for modelling MN diseases in vitro and for drug discovery.
Applicant’s Arguments/Response to Arguments
15. Applicant Argues: On page 9, para. 2 and page 13 – 16, Applicant asserts that because claim 14 is not subject to the rejection under 102(a)(1), amended claim 1 which incorporates elements of claim 14 is also not anticipated by Chen as evidenced by Xu and there is no motivation to combine Chen and Du.
Response to Argument: The previous rejection of claim 1 as being anticipated by Chen is withdrawn in view of Applicant’s amendment to the claim. A new rejection is set forth above in which claims 1 – 20 are obvious over the combined teachings of Chen, Du, Ogura, and Glasgow.
Applicant Argues: On page 9, para. 5 – 7 and page 10 – 12, Applicant asserts that there is not prima facie obviousness because not all claim elements are disclosed by the cited references because Du does not expressly recite 0.5 µM cyclopamine and Chen and Du do not demonstrate that the method is able to generate a population of cells comprising spinal dI4 progenitor cells wherein at least 90% of the population of cells express at least one of PTF1A, PAX7, and ASCL1. Applicant asserts that the effects of CpdE used in Du are unknown and therefore, it is unknown whether the claimed 90% of cells generated in Du are positive for PTF1A/PAX7/ASCL1. Applicant asserts that neither Chen nor Du teach or suggest generating a nearly pure population of dI4 GABA neurons. On pages 13 – 16, Applicant asserts there is no motivation to combine Chen and Du.
Response to Argument: This is not found persuasive because in the new rejection set forth above, Du teaches then culturing the NEPs in a medium comprising 1 µM CHIR99021, 2 µM SB431542, 2 µM DMH1, 0.1 µM retinoic acid and 0.5 µM Purmorphamine to form motor neuron progenitors (MNPs) (Supplementary Figure 3; page 7, right col. para. 4.). Du teaches replacing the Purmorphamine with cyclopamine to produce progenitors that could be further differentiated to GABA neurons (page 5, left col.; Supplementary Figure 3a). Du does not teach the concentration of cyclopamine. However, as Chen teaches a molar ratio of cyclopamine to retinoic acid is 5:1 (page 3, para. 8) with 3 µM CHIR99021, 2 µM SB431542, and 2 µM DMH1 (page 1, claim 2; page 3, para. 7), and Du teaches 0.1 µM retinoic acid, it would have been obvious to use 0.5 µM cyclopamine because Du teaches replacing 0.5 µM Purmorphamine with cyclopamine and Chen teaches the molar ratio of cyclopamine to retinoic acid is 5:1 to produce spinal cord interneuron precursor cells. Therefore, a culture medium of step (b) comprising 3 µM CHIR99021, 2 µM SB431542, and 2 µM DMH1, 0.1 µM retinoic acid, and 0.5 µM cyclopamine would be expected to produce spinal dI4 progenitor cells with a reasonable expectation of success as both Chen and Du teach 3 µM CHIR99021, 2 µM SB431542, and 2 µM DMH1, retinoic acid, and cyclopamine where Chen teaches a molar ratio of cyclopamine to retinoic acid is 5:1 to produce spinal cord interneuron precursor cells and Du teaches a ratio of 5:1 of purmorphamine to retinoic acid where purmorphamine is replaced with cyclopamine. Additionally, Chen teaches further differentiating the cells after day 14 to form GABAergic spinal interneurons (page 3, para. 5; page 5, para. 6 – 11; page 6, para. 2 – 3; Figure 1 and 4 of the original document). Therefore, as Du and Chen teach identical method of step (a) of claim 1 and Du teaches >98% of the NEPs were SOX1+ and HOXA3, and Chen teaches the method further comprising culturing with cyclopamine and retinoic acid produces GABAergic neurons, and Du teaches the method further comprising culturing with cyclopamine and retinoic acid produce GABAergic progenitors, one would have a reasonable expectation of success that combining the teachings of Chen and Du would produce spinal dI4 progenitors that express PTF1A, PAX7, and/or ASCL1 that can be further differentiated to GABA interneurons. Further, in the new rejection set forth above, Glasgow teaches Ptf1a is required for Pax2 expression leading to the formation of GABAergic neurons (page 5461, right col.; page 5462, left col. para. 1; page 5465, left col. para. 2; page 5467, left col. para. 1; Figure 5I). Therefore, the progenitors of Chen and Du produced with CHIR99021, SB5431542, DMH1, retinoic acid, and cyclopamine would be expected to express Ptf1a because Chen and Du’s progenitors are capable of producing GABA neurons and Du teaches >95% of a near-pure population of progenitors (Abstract).
Regarding Applicant’s arguments of CpdE of Du, Du teaches CpdE is used with retinoic acid to produce GABA neurons from progenitors (Supplementary Figure 3) and not the claimed spinal dI4 progenitors of claim 1.
Conclusion
No claims allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/Z.M.B./Examiner, Art Unit 1632
/MARCIA S NOBLE/Primary Examiner, Art Unit 1632
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