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
Acknowledgement is hereby made of receipt and entry of the communication filed on June 30, 2026. Claims 1, 3-7, 9-15, 22-24, 26-29 and 33-37 are pending and are currently examined.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION. —The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
(Previous rejection- withdrawn) Claims 1-21 and 23-32 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
This rejection is withdrawn in view of the amendment filed on June 30, 2026.
(New rejection) Claim 27 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
The amended claim 27 recites a phrase “the innate NK cells are γδ T cells” that renders the claim indefinite. Based in the instant specification, it discloses that the innate cells can be γδ T cells (See e.g., [0061], [0176]) but not discloses that the innate NK cells are γδ T cells. It is unclear what the difference and similarity between the claimed “the innate NK cells are γδ T cells” and the disclosure of the instant specification at “the innate cells comprise γδ T cells”.
Accordingly, one of ordinary skill in the art will not know the metes and bounds of the claims. Therefore, claim 27 is not included in the 103 rejection in the current office action.
Claim Rejections - 35 USC § 112 (Scope of Enablement)
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.
(Previous rejection- withdrawn) Claims 1-28 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 to use LV encoding HER2-CAR.CD3~.2A. iMC to transduce NK cells by adding the Inhibitors BX795, MRT67307, and Amlexanox, does not reasonably provide enablement for a method for transducing cells comprising contacting any cells with any compositions such as any viral particles and any TBK1/IKK£ inhibitor with any substituted N-(3-((2-((3-(aminomethyl) phenyl) amino)-5-methylpyrimidin-4-yl) amino propyl) acetamide analogue.
This rejection is withdrawn in view of the amendment filed on June 30, 2026.
(New Rejection-necessitated by amendment) Claims 1, 3-7, 9-15, 22-24, 26-29 and 33-37 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 to use LV encoding HER2-CAR.CD3~.2A. iMC to transduce NK cells by adding the Inhibitors BX795, MRT67307, and Amlexanox, does not reasonably provide enablement for a method for transducing cells comprising any other virus particles.
The base claim 1 is directed to method for transducing natural killer (NK) cells, the method comprising contacting NK cells with (i) a virus particle; and (ii) a TBK1/IKK£ inhibitor selected from the claimed formula, thereby transducing the NK cells.
The instant specification discloses that the method is for transduction of cells with a transduction composition comprising contacting cells with a TBK1/IKKɛ inhibitor and a transduction composition, e.g., a virus particle comprising a VSG-G LV. In one aspect, the disclosure relates to methods for transduction of NK cells with VSG-G LV comprising contacting cells with a TBK1/IKK£ inhibitor and a virus particle, e.g., a virus particle comprising a VSG-G LV (See [0060] and[0061]). In an example, applicant discloses the method for generating the lentiviral vectors and study the transduction efficiency in Fig. 1C (See [0015] and [0191]). However, the specification does not provide evidence to support a method for transducing NK cells using any other virus particles as claimed, thus it does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to practice the invention commensurate in scope with these claims.
To be enabling, the specification of the patent must teach those skilled in the art how to make and use the full scope of the claimed invention without undue experimentation. In re Wriqht, 999 F.2d 1557, 1561 (Fed. Cir. 1993). Explaining what is meant by "undue experimentation," the Federal Circuit has stated:
The test is not merely quantitative, since a considerable amount of experimentation is permissible, if it is merely routine, or if the specification in question provides a reasonable amount of guidance with respect to the direction in which the experimentation should proceed to enable the determination of how to practice a desired embodiment of the claimed invention. PPG v. Guardian, 75 F.3d 1558, 1564 (Fed. Cir. 1996).1
The factors that may be considered in determining whether a disclosure would require undue experimentation are set forth by In re Wands, 8 USPQ2d 1400 (CAFC 1988) at 1404 where the court set forth the eight factors to consider when assessing if a disclosure would have required undue experimentation. Citing Ex parte Forman, 230 USPQ 546 (BdApls 1986) at 547 the court recited eight factors:1) the nature of the invention, 2) the state of the prior art, 3) the breadth of the claims, 4) the amount of guidance in the specification, 5) the presence or absence of working examples, 6) the relative skill of those in the art, 7) the predictability or unpredictability of the art, and 8) and the quantity of experimentation necessary. Id. While it is not essential that every factor be examined in detail, those factors deemed most relevant should be considered.
M.P.E.P. §2164.03 [R-2] states: [I]n applications directed to inventions in arts where the results are unpredictable, the disclosure of a single species usually does not provide an adequate basis to support generic claims. In re Soil, 97 F.2d 623,624, 38 USPQ 189, 191 (CCPA 1938). In cases involving unpredictable factors, such as most chemical reactions and physiological activity, more may be required. In re Fisher, 427 F.2d 833,839, 166 USPQ 18, 24 (CCPA 1970). See also In re Wright, 999 F.2d 1557, 1562, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993); In re Vaeck, 947 F.2d 488,496, 20 USPQ2d 1438, 1445 (Fed. Cir. 1991). A conclusion of lack of enablement means that, based on the evidence regarding each of the above factors, the specification, at the time the application was filed, would not have taught one skilled in the art how to make and/or use the full scope of the claimed invention without undue experimentation. In re Wright, 999 F.2d 1557,1562, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993).
Therefore, the specification does not provide sufficient guidance to allow one skilled in the art to practice the claimed invention on the full scope with a reasonable expectation of success and without undue experimentation. In the absence of such guidance and evidence of working examples, the specification fails to provide an enabling disclosure commensurate in scope with the claims.
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.
(New Rejection-necessitated by amendment) Claims 1, 3-7, 9-12, 22-24, 26, 28-29 and 33-37 are rejected under 35 U.S.C. 103 as being unpatentable over Sutlu et al. (Hum Gene Ther. 2012 Oct;23(10):1090-100. Epub 2012 Sep 10, hereinafter, “Sutlu”) in view of Deretic et al. (US11878018 B1, patented on Jan. 23, 2024, filed on Dec. 19, 2019) as evidenced by Sigma (https://www.sigmaaldrich.com/US/en/product/mm/506306?utm_source=bing&utm_medium=cpc&utm_campaign=all+product_dsa_NA_%28bing+ebizpfs%29&utm_id=420627782&utm_content=1170981841679455&msclkid=98bf0d30bdce1886201164f35ff0222f&utm_term=%2Fproduct%2F) and Ogawa et al. (WO2021141020A1, published on July 15, 2021, priority date is Jan. 06, 2020)
The base claim 1 is directed to a method for transducing natural killer (NK) cells, the method comprising contacting NK cells with (i) a virus particle; and [ii} a TBKI/IKKe inhibitor selected from the claimed formula, thereby transducing the NK cells.
Sutlu studies the inhibition of intracellular antiviral defense mechanisms augments lentiviral transduction of human natural killer cells: implications for gene therapy and teaches that their study demonstrates that stimulation of NK cells with interleukin (IL)-2 and IL-21 supports efficient transduction using a VSV-G pseudotyped lentiviral vector. Moreover, they have identified that inhibition of innate immune receptor signaling greatly enhances transduction efficiency. They were able to boost the efficiency of lentiviral genetic modification on average 3.8-fold using BX795, an inhibitor of the TBK1/IKKɛ complex acting downstream of RIG-I, MDA-5, and TLR3. They have also observed that the use of BX795 enhances lentiviral transduction efficiency in a number of human and mouse cell lines, indicating a broadly applicable, practical, and safe approach that has the potential of being applicable to various gene therapy protocols (See Abstract). Here Fig. 4 of Sutlu teaches the effect of stimulation time on genetic modification efficiency of NK cell transduction (See page 1095 and below).
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Accordingly, Sutlu teaches a method for Lentiviral transduction of NK cell with the TBK1/IKKɛ inhibitor BX795, which also teaches the claim 3 for a lentiviral vector. Here Sutlu teaches the use of BX795, an inhibitor of the signaling molecule TBK1/IKKɛ greatly enhances lentiviral transduction efficiency in NK cells, however, Sutlu does not explicitly point out a chemical structure as claimed.
Deretic teaches a method of therapeutically treating cancer in a patient in need, the method comprising administering to said patient an effective amount of a TBK-1 inhibitor and an inhibitor of Syntaxin 17 phosphorylation to said patient, wherein said TBK-1 inhibitor is BX795, MRT67307, Bl-B206, Dl-Dl00, Fl-F-160, amlexanox or a mixture thereof and said inhibitor of Syntaxin 17 phosphorylation is Tyrphostin AG1478 and/or Tyrphostin AG1024 (See column 59, lines 1-9), where BX796 and MRT67307 are the most preferable TBK inhibitor (See column 3, lines 21-35), where the chemical structure of MRT67307 teaches one of the structures as claimed as :
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This can be evidenced by Sigma. Sigma teaches that MRT67307 is a IKKε/TBK1 Inhibitor II, N-(3-(5-Cyclopropyl-2-(3-(morpholinomethyl) phenylamino) pyrimidin-4-ylamino) propyl) cyclobutanecarboxamide (See page 1) and the GAS number 1190378-57-4 and having a structure below.
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At the same time, Ogawa teaches a method comprising treating cells with at least two TBK1/IKKɛ inhibitors, BX795 and / or MRT67307 (See Claims, page 1), where the MRT-67307 is N- [3-[[5-cyclopropyl-2- [[3- (4-morpholinylmethyl) phenyl]amino] -4-pyrimidi-nyl] amino] propyl]-cyclobutanecarboxamide, CAS 1190378- 57-4 (See page 3, paragraph 1). Based on the chemical structure described above, Ogawa also teaches the substituted N-(3-((2-((3-(aminomethyl) phenyl) amino)-5-methylpyrimidin-4-yl) amino) propyl) acetamide analogue. Ogawa further teaches that an agent for improving the efficiency of nucleic acid introduction into cells comprises Amlexanox and is used in combination with BX795 and / or MRT67307 (See page 2).
It would have been prima facie obvious for one having ordinary skill in the art before the effective filing date of the claimed invention to introduce the TBK1/IKKɛ inhibitor of Deretic and Ogawa, MRT67307, into Sutlu’s study to arrive at an invention as claimed. One of skill in the art would be motivated to substitute one TBK1/IKKɛ inhibitor for another (See MPEP 2144.06: Substituting equivalents known for the same purpose). There would be a reasonable expectation of success to develop such a method for transducing cells as claimed.
In addition, the above description also teaches claim 22, which requires the TBK1/IKKɛ inhibitor has the same chemical structure as MRT67307.
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Thus, the invention as a whole was clearly prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention.
Regarding claims 4-5, they require a transgene with specific range of base pairs from 100 base pairs to 5,000 base pairs. Sutlu teaches that the lentiviral vectors are lentiviral ‘‘gene ontology’’ (LeGO)-G2 plasmid expressing eGFP under the influence of SFFV promoter (See page 1091, left column, paragraph 5; page 1092, right column, paragraph 4), where the eGFP can be considered as a transgene (Claim 4), and it is common knowledge in the art that the sequence size of GFP about 720 base pair (teach claim 5).
Regarding claim 6, Sutlu teaches that the virus particle is a vesicular stomatitis virus G (VSV -G) pseudotyped lentivirus (LV) particle (See page 1091, left column, paragraph 3).
Regarding claims 7, 9-11, they require a specific percentage for the transduced cells. Fig. 4 of Sutlu teaches the transduced cells with GFP positive can reach from 20% to 60% under the presence of BX795 (See page 1095, left column and below).
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Regarding claim 12, it requires a specific MOI at 1 to 100. Sutlu teaches that the cells were transduced with the VSV-G pseudotyped LeGO-G2 (Weber et al., 2008) vector (expressing eGFP under the influence of SFFV promoter) at a multiplicity of infection (MOI) of 20.
Regarding claims 23-24 and 36-37, they require a method that does not utilize a toll-like receptor inhibitor and a cationic additive (claims 23-24 and 36), the TBK1/IKKɛ inhibitor is the only TBK1/IKKɛ inhibitor with which the cells are contacted. Sutlu teaches that they have identified that inhibition of innate immune receptor signaling greatly enhances transduction efficiency. They were able to boost the efficiency of lentiviral genetic modification on average 3.8-fold using BX795, an inhibitor of the TBK1/IKK£ complex acting downstream of RIG-I, MDA-5, and TLR3 (See Abstract), where the BX795 is not an inhibitor for a toll-like receptor. Therefore, Sutlu’s study does not indicate that the method utilizes a toll-like receptor inhibitor and a cationic additive. Sutlu only discloses one inhibitor, BX796, is added into the NK cells. Thus, Sutlu teaches claims 23-24 and claims 36-37.
Regarding claim 26, it requires the cells are innate NK cells (claim 26). Sutlu teaches that NK cells are cytotoxic lymphocytes of the innate immune system that have the capacity to kill virus-infected or malignant cells that display signs of cellular stress (See page 1090, left column).
Regarding claim 28, Sutalu teaches that methods of transient genetic modification such as transfection, electroporation, nucleofection, and adenoviral infection are under constant development and have come a long way from applications on NK cell lines to GMP-compatible protocols for primary NK cells (See page 1097, left column, paragraph 2).
Regarding claim 29, it requires a kit comprising a TBK1/IKK£ inhibitor; and instructions for transducing NK cells, lentiviral vector, NK cells, and the instructions, where the TBK1/IKK£ inhibitor is one of the claimed chemical structures.
Based on the description above, Sutlu in view of Deretic and Ogawa teaches the claimed TBK1/IKK£ inhibitor such as MRT67307 with the claimed chemical structure as claimed, a lentiviral vector and NK cells.
Although Sutlu does not specifically point out a term “kit”, however, the concept of packaging components into a kit is well known and routine in the art. For example, Sutlu, Deretic and Ogawa disclose a detailed protocol for how to grow NK cells and construct the lentiviral vector, and how to use the TBK1/IKK£ inhibitors. It would have been obvious to one of ordinary skill in the art at the time the invention was made to package components into a kit. One would be motivated to do this for commercial exploitation of the invention by providing convenience for the end user. Thus, the claimed invention is obvious over Li’s research.
Also, according to MPEP § 2112.01(III), “Where the only difference between a prior art product and a claimed product is printed matter that is not functionally related to the product, the content of the printed matter will not distinguish the claimed product from the prior art. In re Ngai, ** > 367 F.3d 1336, 1339, 70 USPQ2d 1862, 1864 (Fed. Cir. 2004) < (Claim at issue was a kit requiring instructions and a buffer agent. The Federal Circuit held that the claim was anticipated by a prior art reference that taught a kit that included instructions and a buffer agent, even though the content of the instructions differed.). See also In re Gulack, 703 F.2d 1381, 1385-86, 217 USPQ 401, 404 (Fed. Cir. 1983)( "Where the printed matter is not functionally related to the substrate, the printed matter will not distinguish the invention from the prior art in terms of patentability….[T]he critical question is whether there exists any new and unobvious functional relationship between the printed matter and the substrate." ).”
Regarding claims 33-35, Sutlu in view of Deretic and Ogawa teaches the TBK1/IKK£ inhibitor such as MRT67307, which is evidenced by Sigma having a structure as claimed:
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(New Rejection-necessitated by amendment) Claims 13-15 are rejected under 35 U.S.C. 103 as being unpatentable over Sutlu in view of Deretic as evidenced by Sigma, and Ogawa as applied to claims 1, 3-7, 9-12, 22-24, 26, 28-29 and 33-37 above and further in view of Li et al. (J Transl Med. 2020 Sep 23;18(1):363, submitted in IDS filed on 11/28/2023, hereinafter “Li”).
Regarding claims 13-15, they require the MOI is 1-10 (claim 13), 2 to 7 (claim 14) and MOI 1-5 (claim 15).
Sutlu teaches a MOI is 20. Although Sutlu does not explicitly teach the specific MOI ranges as claimed, these ranges are routine experimentation since the MOI of 20 worked for Sutlu.
Nevertheless, Li teaches to assess the relationship between virus dose and infection efficiency when BX795 is used, lentiviral vectors were added to human primary T cells with different MOIs. In an experiment, the first virus LdCK MOI is fixed at 10, only the second virus CAR-TEV is tested with different MOIs. For RB-340-1F, they tested CAR-TEV MOI 5, 10, and 20, combined with BX795 treatment and the data is shown at Fig. 6 (See page 8, right column, paragraph 2; Fig. 6, page 9 and above) that shows the tested MOI is from 1.25 to 80, which teaches the ranges of MOI as claimed.
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It would have been prima facie obvious for one having ordinary skill in the art before the effective filing date of the claimed invention to introduce the dose of MOI of lentiviral vectors into Sutlu’s study to arrive at an invention as claimed. One of skill in the art would be motivated to do so because both Sutlu and Li teach that lentiviral transduction of human primary T cells and NK cells with BX795 treatment is viral dose dependent (See Li: page 8, right column, paragraph 2; Sutlu: page 1093, right column, paragraph 4). There would be a reasonable expectation of success to develop a method for transducing NK cells with viral particles as claimed.
Responses to Applicant’s Remarks
Applicant’s arguments filed on June 30, 2026, have been received and fully considered.
Applicant’s amendment regarding the rejection under 35 U.S.C. § 112(b) is considered. The rejection is withdrawn.
Applicant’s amendment regarding the rejection under 35 U.S.C. §112(a) is considered and the rejection is withdrawn.
Based on applicant’s amendment and argument, the reference Li is not applied as a primary reference in the current office action. The argument regarding Li is moot.
Applicant argued that the claimed method is surprisingly superior for transducing NK Cells as superior and unexpected results (See Remarks, pages 21-22).
Applicant’s argument is not persuasive.
1). Applicant’s alleged unexpected result is based on the data of MRT67307. However, the instant base claim 1 claims a serial of substituted N-(3-((2-((3-
(aminomethyl)phenyl)amino)-5-methylpyrimidin-4-yl)amino)propyl)acetamide analogues (See instant SPEC, [0068]). Therefore, applicant’s alleged unexpected results are not commensurate with the scope of the claims.
In addition, the instant application does not limit the mechanism of the role of TBK1/IKKɛ inhibitor as the remarks allegedly argued at” Given that MRT67307 is more selective for TBKl/lKKɛ and less active against other kinases (see as filed application at paragraph [0198]) than BX795…” (See Remarks, page 21).
2). Sutlu in view of Deretic and Ogawa teaches the same structure of NK cell, virus particle and the TBK1/IKKɛ inhibitor, thus, the achieved efficiency of MRT67307 for NK cell transduction should be same.
3). Applicant claims that the “the improvement in potency was 25-fold” (See Remarks, page 22). However, this enhancement is based on a specific concentration of the MRT67307 such as 1.1 uM and is compared with a specific reagent, amlexanox, with 24. 8μM.
4). Sutlu teaches they were able to boost the efficiency of lentiviral genetic modification on average 3.8-fold using BX795 (See Abstract), Deretic teaches that both BX795 or MRT67307 can be a TBK 1 inhibitor (See claims 11-20), and Ogawa teaches that in one preferred embodiment, the at least two TBK1/IKKɛ inhibitor preferably include a combination of Amlexanox and BX795, or a combination of Amlexanox and MRT67307. These combinations exert a synergistic effect on nucleic acid transfer action, as demonstrated in the examples. For example, as shown in Fig. 3, BX795 increased the gene transfer efficiency by about 5 times compared with the case without addition, but the addition of BX795 and Amlexa showed an increase of about 22 times. Amlexanox alone showed only about a 4-fold increase, demonstrating that the increase with the addition of the two agents synergistic effect of the two (See page 4, claim 3). Here the results teach a comparable result as the alleged claimed unexpected results of the “25-fold”.
5). As an initial matter, “the burden of showing unexpected results rests on one who asserts them. Thus, it is not enough to show that results are obtained which differ from those obtained in the prior art: that difference must be shown to be an unexpected difference.” In re Klosak, 455 F.2d 1077, 1080 (CCPA 1972) (citation omitted). Moreover, “[i]t is well settled that unexpected results must be established by factual evidence. Mere argument or conclusory statements in the specification does not suffice.” In re De Blauwe, 736 F.2d 699, 705 (Fed. Cir. 1984) (citation omitted). Moreover, “[i]t is well settled that unexpected results must be established by factual evidence. Mere argument or conclusory statements in the specification does not suffice.” In re De Blauwe, 736 F.2d 699, 705 (Fed. Cir. 1984) (citation omitted). Applicant’s attention is directed to MPEP 716.02(b)-(e) for how unexpected results can be established. E.g., to evaluate if the claimed invention produces unexpected results, one must consider if the results produced by the claimed invention are commensurate in scope with the claims and how the results compare with the closest prior art. See MPEP Section 716.02(d) and (e).
Accordingly, applicant has not provided sufficient information for the Office to consider if the results produced by the claimed invention are commensurate in scope with the claims and how the results compare with the closest prior art.
Conclusion
No claims are 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 extension fee pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to RUIXUE WANG whose telephone number is (571)272-7960. The examiner can normally be reached Monday-Friday 8:00 am-5:00 pm, EST.
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/RUIXUE WANG/Examiner, Art Unit 1672
/NICOLE KINSEY WHITE/Primary Examiner, Art Unit 1672
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