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 .
Claim Status
Applicant’s reply filed on 01/22/2026 is acknowledged. Claim 46 is cancelled.
Claims 1, 5, 9, 15-18, 21-22, 25, 28-29, 32, 34, 40, 44-45 and 47-48 are pending and under examination.
Rejections Withdrawn
The rejection of claim 46 in the office action dated 10/23/2025 is withdrawn in view of claim cancellation.
Rejections Maintained
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claims 1, 5, 9, 15, 17-18, 21-22, 25, 28-29, 32, 34, 40, 44-45 and 48 remain rejected under 35 U.S.C. 103 as being unpatentable over Adusumilli (US 2017/0081405 A1, published 03/23/2017, PTO-892 01/16/2024) in view of Jiang (Front Immunol. 2017 Jan 11;7:690, PTO-892 01/16/2024) and Zeng (J Exp Med. 2005 Jan 3;201(1):139-48, PTO 12/04/2024).
The disclosure of Adusumilli is generally related to immune cells comprising CARs that target mesothelin (a tumor-specific antigen) that have enhanced immune-activating properties (Abstract). Adusumilli discloses modification of the immune cells with at least one exogenous cytokine selected from the list consisting of IL-2, IL-3, IL-6, IL-7, IL-11, IL-12, IL-15, IL-17, and IL-21 ([0013], Lines 9-13).
Regarding claim 1, pertaining to an isolated T cell that comprises a CAR that targets GPC3, wherein said cell comprises two or more disclosed recombinant interleukins and wherein the interleukins are secretable IL-15 and secretable IL-21, Adusumilli discloses immunoresponsive T cells that express tumor antigen-specific CARs ([0089], Lines 8-13) and discloses embodiments wherein the immunoresponsive cell further comprises at least one exogenous cytokine selected from a list comprising IL-15 and IL-21 ([0013], Lines 9-13). The exemplary recombinant cytokine of Adusumilli’s disclosure was secreted IL-12 ([0395], Lines 1-2).
Regarding claim 5, wherein the CAR is expressed from a recombinant nucleic acid, Adusumilli teaches a method of introducing a nucleic acid that encodes a CAR into cells ([0018], Lines 4-6) and diagrams the nucleic acid construct in Figure 2A.
Regarding claims 9 and 15, wherein the secretable IL-15, IL-21 or combination are expressed from a recombinant nucleic acid (claim 9) and wherein the tumor-antigen specific CAR and interleukins are expressed on the same recombinant molecule (claim 15), Adusumilli teaches that the interleukin can be covalently joined to the 3’ terminus of the intracellular domain of the mesothelin tumor antigen M28z ([0199], Lines 11-14, construct shown in Figure 24E).
Regarding claims 17 and 18, wherein the tumor antigen specific CAR comprises one, two or three costimulatory domains selected from the group listed in claim 18, Adusumilli discloses embodiments that comprise at least one costimulatory signaling region wherein the at least one costimulatory signaling region comprises CD28, 4-1BB, OX40, and ICOS ([0010], Lines 3-7).
Regarding claims 21 and 22, wherein the T cells are virus specific and selected from the group listed in claim 22, Adusumilli teaches that the engineered cell further comprises an antigen recognizing receptor that recognizes an antigen from a cytomegalovirus infected cell ([0013), Lines 23-26 and 33).
Regarding the population of cells of claim 25, Adusumilli discloses a cell population comprising the disclosed immunoresponsive CAR-expressing cells. ([0255], Lines 8-11).
Regarding claims 28 and 29, pertaining to a composition comprising the population of cells of claim 25 (claim 28) and wherein the pharmaceutical composition is in a pharmaceutically acceptable excipient (claim 29), Adusumilli discloses pharmaceutical compositions comprising an effective amount of the disclosed immunoresponsive cells and a pharmaceutically acceptable carrier ([0020], Lines 1-4).
Regarding claim 32, a method comprising the step of providing a therapeutically effective amount of the plurality of the claimed cells, Adusumilli discloses the method of reducing tumor burden in a subject comprising administered an effective amount of disclosed immunoresponsive cells to the subject ([0014], Lines 3-7) and provides a schema for administration (Figure 10E).
Regarding claim 48, Adusumilli teaches the transduced T cells are human T cells ([0471], Lines 4-6) isolated from the blood of healthy volunteer donors ([0477], Lines 1-2).
Adusumilli does not teach (1) the specific tumor antigen GPC3 as required in the isolated T cell of independent claim 1 and the methods of independent claims 40, 44, and 45, (2) that the composition that targets the specific cancer cells listed in claim 34, or (3) that the T cell expresses IL-15 and IL-21 as required in the isolated T cell of independent claim 1 and the methods of independent claims 40, 44, and 45.
These deficiencies are taught by Jiang and Zeng.
The disclosure of Jiang is generally directed to evaluating tumor suppression of anti-GPC3 CAR T cells in a patient-derived xenograft model of hepatocellular carcinoma (HCC) (see Abstract).
Regarding the limitation of claims 1, 40, 44, and 45 where in the T cell comprises a CAR that targets GPC3, Jiang teaches CAR T cells comprising anti-GPC3 scFv (Fig. 2A).
Regarding the tumor types listed in claim 34, Jiang teaches that GPC3 is expressed in HCC tissues and is thus a suitable target for CAR therapy in HCC tumors (Page 2, First Column, Paragraph 3, Lines 1-4). Jiang’s data demonstrate that GPC3-specific CAR T cells efficiently suppress HCC tumor growth in vivo in the xenograft model (Page 140, First column, Full Paragraph 1, Lines 7-10, and Figure 5A-D).
The disclosure of Zeng is directed to exploring the actions of IL-21 and how it integrates its signals with other γc-dependent cytokines, including IL-15 (Pg. 140, Left column, Full paragraph 1, Lines 8-10).
Regarding the limitation of claims 1, 40, and 44-45, pertaining to methods of enhancing T cell therapy by modifying T cells to express secretable IL-15 and IL-21, Zeng teaches that IL-15 and IL-21 have a synergistic effect on CD8+ T cell proliferation in culture, as the combination of low concentrations of the two cytokines (10 or 50 ng/ml) was more potent than the effect of either cytokine alone at a concentration of 50 or 100 ng/ml (Pg. 140, right column, Lines 15-20 and Fig. 1C, lane 9 vs. 4 and 7, and lane 13 vs. 5 and 8). Zen further teaches that IL-15 and IL-21 cooperatively enhance the function of memory-phenotype CD8+ T cells by showing evidence that the combination of IL-15 and IL-21 resulted in a marked increase in the number of CD8+ T cells, with an increase in the percent of IFN-γ-producing cells as compared with that seen in cells expanded with IL-15 alone or IL-21 alone (Fig. 3C) As shown in Fig. 3D, the combination of IL-15 and IL-21 greatly increased the total number of IFN-γ–producing CD8+ T cells. Zeng concludes that IL-21 has a cooperative effect with IL-15 on the expansion of memory-phenotype CD8+ T cells as well as on their effector function.
Regarding the limitation of claim 40 wherein after the claimed modification, the T cells are protected from apoptosis and/or wherein the T cells have enhanced in vivo expansion and persistence compared to unmodified T cells, this limitation describes the inherent results of the modifications recited in the method steps. Likewise, the limitations of claim 44 wherein the modified T cells are protected from apoptosis and claim 45 wherein the modified T cells have increased expansion and persistence also describe inherent properties that result from performing the claimed method steps.
It would have been obvious to one having ordinary skill at the time of filing to modify the engineered immune cell of Adusumilli by (1) targeting the tumor antigen GPC3 as taught by Jiang, (2) using the composition to target the specific cancer cells listed in claim 34 as taught by Jiang and (3) expressing IL-15 and IL-21 as taught by Zeng. It would have been obvious to do so because Jiang teaches (1) that GPC3 is a well-known cancer antigen expressed in HCC and provides evidence that targeting GPC3 results in tumor suppression and (2) GPC3 is expressed in HCC tissues and is thus a suitable target for CAR therapy in HCC tumors, and Zeng teaches that (3) IL-21 has a cooperative effect with IL-15 on the expansion of memory-phenotype CD8+ T cells as well as on their effector function. The combination of the components would predictably result in engineered cells that effectively target HCC tumors. As the ability to produce recombinant nucleic acids that encode the anti-GPC3 CAR of Jiang as well encode the cytokines as taught by Adusumilli and Zeng was practiced at the time of filing, one would have a reasonable expectation of success in combining the disclosed elements to obtain predictable results.
Claims 1, 5, 9, 15-18, 21-22, 25, 28-29, 32, 34, 40, 44-45, and 48 remain rejected under 35 U.S.C. 103 as being unpatentable over Adusumilli, Jiang, and Zeng as applied to claims 1-2, 4-5, 9, 15, 17-18, 21-22, 25, 28-29, 32, 34, 40, 44-45, and 48 above, and further in view of Liu (Sci Rep. 2017 May 19;7(1):2193, PTO-892 01/16/2024).
The combined disclosures of Adusumilli, Jiang, and Zeng teach engineered cells that express an anti-GPC3 CAR that can further express IL-21 and IL-15 encoded on the same recombinant nucleotide as described above.
Regarding claim 16, the combined teachings of Adusumilli, Jiang, and Zeng do not teach the use of a cleavable linker in between the CAR and interleukin constructs.
This deficiency is taught by Liu.
The disclosure of Liu is generally directed to comparison of several 2A “self-cleaving” peptides that allow for the cloning of multiple genes in a single vector (Abstract, Lines 1-4). Regarding the cleavable linker of the instant claims, Liu teaches that 2A peptides such as T2A can be used in multigene co-expression strategies because they mediate “cleavage” of polypeptides during translation in eukaryotic cells via ribosome skipping (Page 1, Paragraph 1, Lines 4-12).
It would have been obvious to one having ordinary skill in the art at the time of filing to include a self-cleaving linker such as those taught by Liu to the multigene construct of Adusumilli, Jiang, and Zeng because Liu teaches self-cleaving peptides allow for relatively high levels of downstream protein expression compared to other strategies for multigene co-expression (Page 1, Paragraph 1, Lines 19-20). As the ability to create recombinant nucleotides encoding the GCP3 CAR and recombinant interleukins of Adusumilli, Jiang, and Zeng as well as the self-cleaving linker of Liu, there would be a reasonable expectation of success in combing the disclosed components.
Declaration Under 37 C.F.R. § 1.132
The declaration under 37 CFR 1.132 of Dr. Andras Heczey filed 01/22/2026 is insufficient to overcome the rejection of claims 1-2, 4-5, 9, 15-18, 21-22, 25, 28-29, 32, 34, 40, 44-45, and 48 based upon 35 USC § 103 as set forth in the last Office action.
The Declaration addresses the following arguments:
I. The Declaration contrasts the teaching of Patent ‘762 regarding the safety profile of secreted IL-15 and IL-21 with the results of the instant disclosure. The decalaration states: “We showed surprising results by engineering CAR T cells to express secretable IL-15 and secretable IL-21. Interestingly, the combination resulted in CAR T cells that were safe to use and showed augmented anti-tumor activity in preclinical models.” (Declaration, Pg. 2, paragraph 5). Dr. Heczey adds that their team has treated eight human patients with IL-15 and IL-21 expressing CAR T cells and only one had severe cytotoxicity due to cytokine release syndrome, concluding “Our clinical data in humans show that the co-expression of IL15 and IL21 in CAR T cells are not inducing toxicities specific to their co-expression in their secreted form” (Declaration, Pg. 2, paragraph 6).
In response, the scope of the declaration is not commensurate with the scope of the claimed invention. Claim 1 is directed to an isolated T cell that comprises a CAR that targets GPC3, wherein said cell comprises two or more recombinant interleukins, wherein the interleukins comprise secretable IL-15 and secretable IL-21.
The scope of the claim includes:
Any T cell, including T cells of all phenotypes, origin, and ex vivo culture conditions.
Any CAR construct that targets GPC3, and is not limited only to the 15.21.GBBz construct of the instant disclosure.
Two or more recombinant interleukins, wherein the interleukins comprise at a minimum IL-15 and IL-21, but can also include any number of additional interleukins that could drastically affect the phenotype and function of the T cells away from the embodiments presented in the disclosure.
Pertaining specifically to the comparison that the instant invention is unexpectedly safe compared to the prior art, the evidence provided is not reasonably commensurate with the scope of the claimed invention because the unexpected results do not apply to the full scope of the claimed product invention. It is not clear if the declarant is stating that each any every CAR T cell expressing two or recombinant interleukins including secretable IL-15 and IL-21 is unexpectedly safe for use in humans or if the unexpected results are unique to the specific conditions of the applicant’s specific disclosure. In short, the finding of unexpected safety profile would only be relevant if each and every embodiment of the claimed invention is unexpectedly safe for use in humans. MPEP 2145 states: “…to be entitled to substantial weight, the applicant should establish a nexus between the rebuttal evidence and the claimed invention, i.e., objective evidence of nonobviousness must be attributable to the claimed invention.”
Importantly, the declaration does not take into account that the scope of the claimed invention includes means of mediating the safety of CAR T cells that secrete cytokines which were known in the art at the time of filing. As an example, Hoyos (Leukemia. 2010 Jun;24(6):1160-70, IDS 12/04/2024) is directed to CD19 CAR T cells engineered to express IL-15, teaching the use of suicide genes to prevent cytokine release syndrome. As embodiments that incorporate safety measures fall within the scope of the claimed invention then the claims as written are not directed to an invention that is unexpectedly safe.
II. The Declaration states a combination of cytokines can have unpredictable effects on a cell and the instant disclosure shows that the engineering of cells to express a secretable form of IL-15 and IL-21 demonstrates unexpected synergy. The declarant cites Kishida et al., Mol Ther. 2003, 8(4):552-8, for showing that IL-15 and IL-21 had no effect on cytotoxic T lymphocyte ("CTL") killing activity, concluding that the properties of cytokines make it very difficult, if not impossible, to predict how certain cells may react to genetic engineering to produce different versions of cytokines (Declaration Pg. 2-3, paragraph 9). The instant disclosure shows that the engineering of the cells to express a secretable form of IL-15 and a secretable form of IL-21 provides the cell with synergistic properties. Their experimental controls show that cells engineered with only the CAR, or IL-15 with a CAR, or IL-21 with a CAR gave poor results compared to the cells with IL-15, IL-21 and the CAR ("15.21.GBBz"), as shown at least in Exhibit 2 and Exhibit 3. (Declaration, Pg. 3, paragraph 11).
In response, in weighing the totality of the prior art the art that teaches synergy of the cytokines Il-21 and IL-15, the synergistic results of the instant disclosure would not be unexpected to a person having ordinary skill in the art. To this end, the references cited in previous office actions are presented below:
Zeng (J Exp Med. 2005 Jan 3;201(1):139-48) teaches that IL-15 and IL-21 have a synergistic effect on CD8+ T cell proliferation in culture, as the combination of low concentrations of the two cytokines (10 or 50 ng/ml) was more potent than the effect of either cytokine alone at a concentration of 50 or 100 ng/ml (Pg. 140, right column, Lines 15-20 and Fig. 1C, lane 9 vs. 4 and 7, and lane 13 vs. 5 and 8). Zeng further teaches that IL-15 and IL-21 cooperatively enhance the function of memory-phenotype CD8+ T cells by showing evidence that the combination of IL-15 and IL-21 resulted in a marked increase in the number of CD8+ T cells, with an increase in the percent of IFN-γ-producing cells as compared with that seen in cells expanded with IL-15 alone or IL-21 alone (Fig. 3C) As shown in Fig. 3D, the combination of IL-15 and IL-21 greatly increased the total number of IFN-γ–producing CD8+ T cells. Zeng concludes that IL-21 has a cooperative effect with IL-15 on the expansion of memory-phenotype CD8+ T cells as well as on their effector function.
Strengell (J Immunol. 2003 Jun 1;170(11):5464-9) teaches the synergistic effect of IL-15 and IL-21 on primary T cell IFN-γ production after cytokine stimulation in vitro (Fig 1A, bottom graph and Fig 2, bottom blot).
Pouw (Cancer Immunol Immunother. 2010 Jun;59(6):921-31) teaches that T cells treated with a combination of IL-15 and IL-21 in culture show enhanced antigen-specific cytotoxicity (Fig. 2).
The preponderance of the evidence under different conditions suggests a synergistic effect on T cells by combining IL-15 and IL-21 which not only establishes the obviousness of making the claimed invention, but also teaches the resulting synergistic effect in the instant disclosure is not unexpected.
Response to Applicant’s Arguments
Applicant's arguments filed 01/22/2026 have been fully considered but they are not persuasive.
The arguments not previously addressed in the response to the declaration are included below:
I. The state of the art at the time filing taught away from the claimed invention. The applicant states the ‘762 patent which shows that soluble IL-15 and IL-21 induced high levels of IL-5, while tethered version did not. The applicant states a person of ordinary skill in the art would be “led in a path divergent from the path that was taken by the Applicants” by not using secreted cytokines and concludes that secreted IL-15 and IL-21 are toxic, thus rendering the prior art invention being modified unsatisfactory for its intended purpose (Remarks, Pg. 8).
In response, the art at the time of filing provided multiple examples of CAR T cell embodiments engineered to secrete interleukins to enhance persistence and efficacy of CAR T cell therapy. Adusumilli (US 2017/0081405 A1) from the 35 U.S.C. 103 rejection above is an example.
Importantly, the scope of the claimed invention includes means of mediating the safety of CAR T cells that secrete cytokines, which are known in the art at the time of filing. As cited in the response to the Declaration above, Hoyos (Leukemia. 2010 Jun;24(6):1160-70) is directed to a CD19 CAR T cell engineered to express IL-15, teaching the use of suicide genes to prevent cytokine release syndrome. As embodiments that incorporate safety measures fall within the scope of the claimed invention then the claims as written are not directed to an invention that is unexpectedly safe.
Thus, not only does the prior art teach the use of secreted cytokines to augment the efficacy of T cell therapy, it additionally provides measure for increasing the safety of this methodology.
II. There is a lack of motivation combine Adusumilli, Jiang and Zeng. The applicant states a POSITA would lack motivation to generate T cells as claimed because Kishida (Mol Ther. 2003 Oct;8(4):552-8) teaches that IL-15 and IL-21 had a synergistic effect on NK cells, but not T cells. The applicant concludes that a skilled artisan, regardless of whether they could, would lack a motivation to combine the references as proposed by the Office to generate engineered T cells that express IL- 15 and IL-21 because Kishida teaches that there is no significant effect on T cells (Remarks, Pg. 9).
In response, notwithstanding evidence from Kishida’s studies that they did not have a synergistic effect, a large body of evidence under various conditions suggests that there is a synergistic effect on T cells. Those reference are provided in the response to the Declaration above. Furthermore, synergy is not required for a finding of obviousness. As the effect of each cytokine individually was known at the time of filing, combining IL-15 and IL-21 amounts to combining prior art elements according to known methods to yield predictable results (See MPEP 2143 (I)). There is no evidence in the art that a combination of the two cytokines is contraindicated or renders them inoperable. On the contrary, multiple references cited herein point to the benefits of combining the two cytokines.
III. The claimed invention yields surprising results. The applicant maintains that the claimed invention gave surprising results because T cell expressing both IL-21 and IL-15 (21.15.GBBz T cell) possessed a statistically significant superior ability proliferate compared to cells expressing only IL-15 or IL-21 (21.GGBz and 15.GBBz). (Remarks, Pgs. 9-10).
In response, as described in the response to the Declaration above, the office maintains that a synergistic effect of combining IL-15 and IL-21 would not be unexpected to one having ordinary skill in the art at the time of filing.
IV. There exist secondary considerations of non-obviousness. The applicant asks the office to weigh objective indicia such as long-felt but unsolved need, commercial success, industry or
expert praise, copying, and unexpected results, must be considered as part of the obviousness
analysis and can rebut a prima facie case of obviousness. See MPEP § 2141. The applicant puts forth the peer-reviewed NIH R01 grant stating that peer-reviewed competitive funding of this magnitude is addresses a long-felt need in the field of the claimed technology and reflects expert recognition and praise by skilled reviewers. (Remarks, Pgs. 11-12)
In response, in order to overcome obviousness on the basis of a long-felt but unresolved need MPEP 716.04 states three requirements:
First, the need must have been a persistent one that was recognized by those of ordinary skill in the art. In re Gershon, 372 F.2d 535, 539, 152 USPQ 602, 605 (CCPA 1967)
Second, the long-felt need must not have been satisfied by another before the invention by the inventor. Newell Companies v. Kenney Mfg. Co., 864 F.2d 757, 768, 9 USPQ2d 1417, 1426 (Fed. Cir. 1988).
Third, the invention must in fact satisfy the long-felt need. In re Cavanagh, 436 F.2d 491, 168 USPQ 466 (CCPA 1971)
Pertaining to this long-felt need, the Declaration filed 01/22/2026 provides evidence that of eight patients treated with a specific embodiment of the claimed invention, one had severe toxicities due to cytokine release syndrome and one of the patients presenting with aggressive, metastatic liver cancer has been in complete remission for seven months to the date of the declaration.
To the first point, the office concedes there is a long felt-need for safe and effective cancer treatments. To the second point, many research groups have satisfied this long-felt need to a degree that is commensurate with what the instant applicants have provided. As an example, Jaspers (Pharmacol Ther. 2017 Oct;178:83-91) reviews a substantial body of work available at the time of filing directed to optimizing the antitumor efficacy and safety of CAR T cells by addressing the following shortcomings: ‘on-target, off-tumor’ toxicity, antigen escape, short CAR T cell persistence, deficient CAR T cells expansion, trafficking to the tumor and inhibition of T cell activity by an inhibitory tumor microenvironment (see Abstract). To the third point, the R01 grant is evidence of promising preliminary data and a strong overarching hypothesis for addressing the long-felt need, but is not evidence that the instant applicants have met the need. Safe and effective cancer treatments continue to be pursued by various research groups using various methodologies. As the claims are directed broadly to any T cell expressing a GPC3 CAR and two or more interleukins wherein two of the interleukins are secretable IL-15 and IL-21, the weight of the prior art in support of a finding of obviousness outweighs the provided secondary considerations.
V. Claim 48 is independently patentable. The applicant argues pre-clinical studies in animal models and human trials can produce inconsistent results. While one product may be safe to use in mice, it may be unsafe to use in humans. Similarly, while mouse cells may show certain effects, human cells may show different effects. Because the art establishes species-dependent and clinically-determinative differences in cytokine-engineered cell behavior, a POSITA would lack a motivation and reasonable expectation of success in translating murine teachings to obtain the claimed human cell composition. (Remarks, Pg. 13).
In response, the primary reference (“Adusumilli”) of the above 35 U.S.C. 103 rejection provides embodiments comprising transducing human T cells with the chimeric antigen receptor of the disclosure ([0471], Lines 4-6) isolated from the blood of healthy volunteer donors ([0477], Lines 1-2). To this end, the primary reference anticipated that the T cells of the disclosure would be human cells and no obviousness rationale was required.
However, in the interest of addressing the provided arguments pertaining to the obviousness of translating murine studies to humans, at the time of filing the United States Food and Drug Administration required the use of animal models for initial scientific and safety validation of preclinical therapeutics in order to proceed to phase 1 clinical trials. While acknowledging difficulties in translating animal data to humans, Zushin (J Clin Invest. 2023 Nov 1;133(21):e175824) teaches the requirement for animal testing spanned from 1938 to 2022 with preclinical testing serving as a crucial gateway for bridging scientific discovery with tangible patient outcome (Pg. 3, far right column, “Conclusion”).
Allowable Subject Matter
Claim 47 is objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims.
Conclusion
No claims are allowed.
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.
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/CAROL ANN CHASE/Examiner, Art Unit 1646
/HONG SANG/Primary Examiner, Art Unit 1646
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