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 .
Status of the Claims
Claims 1 – 6, 8, 11 – 13, 16, 18 – 27, and 29 were pending. Claims 1, 16, 22, and 23 have been amended. Claims 1 – 6, 8, 11 – 13, 16, 18 – 27, and 29 are currently pending and are the subject of this Office Action.
Claim Rejections - 35 USC § 112
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Previous rejection, withdrawn: claims 19 and 29 were rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
In view of the art and after further consideration, this rejection is withdrawn.
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, maintained: claims 1 – 6, 8, 11 – 13, 16, 18 – 24, and 29 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.
On page 8 – 9 of the reply of 05/12/2025, under the heading “35 U.S.C. & 112(b)“, Applicant argues that “the term "NK-92®" or "NK92" is intended to refer to the original NK-92® cell lines as well as NK-92® cell lines, clones of NK-92® cells, and NK-92® cells that have been modified (e.g., by
introduction of exogenous genes)”. However, because the NK-92 cells’ modification is not fully defined and can be modified by any exogenous gene, the description in the reply of 05/12/2025 does not provide a definite structure of the modified NK-92 cells of the present claims, and thus, the structure remains unclear. See MPEP 608.01(v)(I).
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.
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.
Previous rejection, maintained: claims 1, 3 – 6, 8, 11 – 13, 16, 18, 20, 21, 26, and 27 are rejected under 35 U.S.C. 103 as being unpatentable over WILLIAMS (Williams BA, et al. CD16+NK-92 and anti-CD123 monoclonal antibody prolongs survival in primary human acute myeloid leukemia xenografted mice. Haematologica. 2018 Oct;103(10):1720-1729; an IDS reference submitted 05/18/2021) in view of WU (US 2007/0224201 A1, published 09/27/2007; see PTO-892: Notice of References Cited of 02/12/2025).
The present application is directed to a population of modified NK-92® cells expressing CD16 (SEQ ID NO:1), wherein the modified NK-92® cells do not express IL-2, and wherein the population comprises one or more of the modified NK-92® cells, wherein the expression level of CD16 does not decrease or decreases no more than 20% when the cells are activated as compared to expression level of CD 16 on the cells before activation.
According to the present specification, “CD16 is an Fc receptor which recognizes and binds to the Fc portion of an antibody to activate NK cells for the ADCC effector mechanism. Because they lack CD16 receptors, unmodified NK-92 cells are unable to lyse target cells via the ADCC mechanism” (page 1, paragraph 4 of the specification). Thus, “modified NK-92 cells” are understood to consist of CD16 and the presence of CD16 on the NK-92 cells causes the activation of CD16-expressing NK-92 cells.
WILLIAMS is directed to NK cell lines, NK-92 and CD16+ NK-92, as a treatment for acute myeloid leukemia (AML). CD16+ NK-92 cells express CD16. See abstract. WILLIAMS also discloses “the new haNK platform (CD16+IL-2+NK-92)” implying that CD16+ NK-92 does not express IL-2. See p. 1728, left column.
Thus, WILLIAMS discloses a population of modified NK-92 cells expressing CD16 but do not express IL-2.
However WILLIAMS does not disclose the sequence of SEQ ID NO: 1. WU is directed to compositions of matter useful for the diagnosis and treatment of tumor in mammals and to methods of using those compositions. See abstract. WU discloses The primary cells for mediating ADCC, NK cells, express FcγRIII (CD16). See paragraphs 6455 and 6504. Finally, WU discloses the sequence of present SEQ ID NO: 1.
Regarding claim 1, WILLIAMS discloses a population of modified NK-92 cells expressing CD16 but not expressing IL-2, and WU’s SEQ ID NO: 506 is identical to present SEQ ID NO: 1.
Regarding “the expression level of CD16 does not decrease or decreases no more than 20% when the cells are activated as compared to expression level of CD 16 on the cells before activation” of claim 1, while WILLIAMS does not expressly state that the disclosed CD16+ NK-92 cells would result in an expression level of CD16 does not decrease or decreases no more than 20% when the cells are activated as compared to expression level of CD 16 on the cells before activation, WILLIAMS’ CD16+ NK-92 cells express CD16 which causes the activation of NK-92 cells and thus WILLIAMS’ CD16+ NK-92 cells anticipate this claimed observation and therefore WILLIAMS’ CD16+ NK-92 cells would inherently achieve an expression level of CD16 that does not decrease or decreases no more than 20% when the cells are activated as compared to expression level of CD 16 on the cells before activation.
Because WILLIAMS discloses CD16+ NK-92 cells which express CD16 but not IL-2 that are effective at treating tumors and WU discloses a CD16 polypeptide sequence that is effective in activating cytotoxicity for the treatment of tumors, it would have been obvious to one having ordinary skill in the art to produce the population of modified NK-92 cells expressing CD16 (SEQ ID NO:1), wherein the modified NK-92 cells do not express IL-2, of claim 1. There would have been a reasonable expectation of success given that CD16 -expressing NK-92 cells without IL-2 have been shown to successfully treat tumors as evidenced by the applied prior art.
Regarding claim 3, WILLIAMS discloses that Natural killer cells typically express CD16 and are able to mediate ADCC against antibody-coated targets, enabling both adaptive and innate immune responses. See p. 1721, left column, second paragraph.
Regarding claims 4 – 6, WILLIAMS discloses that CD16 mediate antibody-dependent cell-mediated cytotoxicity (ADCC) (see Introduction, p. 1721, left column) which then destroys cancer cells. Although WILLIAMS does not expressly disclose that the modified NK-92 cells maintain a steady state of cytotoxicity for at least 5 hours from the initiation of the activation, WILLIAMS discloses a significant survival rate increase in acute myeloid leukemia (AML) xenografted mice. See Figure 7B, p. 1728. Because the CD16+ NK-92 cells of WILLIAMS and WU renders the population of modified NK-92 cells claim 1 obvious as discussed above, they would inherently maintain a steady state of cytotoxicity as recited in claim 4, express higher levels of CD16 than NK cells from the donor as recited in claim 5, and have a percentage of cells that are positive for CD16 that decreases no more than 20% after the cells are activated as compared to the cells before activation of claim 6.
Regarding claims 8 and 16, according to the present specification, “CD16 is an Fc receptor which recognizes and binds to the Fc portion of an antibody to activate NK cells for the ADCC effector mechanism. Because they lack CD16 receptors, unmodified NK-92® cells are unable to lyse target cells via the ADCC mechanism” (paragraph [0004]). WILLIAMS discloses that CD16 negative NK-92 parental line was genetically modified to express the high affinity Fc gamma receptor, enabling antibody-dependent cell-mediated cytotoxicity (see abstract), suggesting that the NK-92 cells disclosed by WILLIAMS are activated. When the prior art discloses a product which reasonably appears to be either identical with or only slightly different than a product claimed in a product-by-process claim, a rejection based alternatively on either section 102 or section 103 of the statute is eminently fair and acceptable. See MPEP 2113 (III).
Regarding claim 11, WILLIAMS discloses the modified NK-92 cells are K562 cells. See Methods: Cell lines and primary samples, p. 1721, left column.
Regarding claims 12 and 13, although WILLAIMS does not expressly state that the disclosed CD16+ NK-92 cells results in a CD16 expression that decreases no more than 10% (of claim 12) or 5% (of claim 13) as compared to the modified NK-92 cells before the activation, WILLIAMS’ CD16+ NK-92 cells anticipate this claimed observation and therefore WILLIAMS’ CD16+ NK-92 cells would inherently achieve a CD16 expression that decreases no more than 10% (of claim 12) or 5% (of claim 13) as compared to the modified NK-92 cells before the activation.
Regarding claim 18, WILLIAMS discloses E:T ratios of 1:1, 5:1, 10:1, and 25:1. See Figure 1, p. 1722.
Regarding claim 20, WILLIAMS discloses NK-92 cytotoxicity of about 80% at an effector to target ratio of 5:1. See Figure 2A.
Regarding claim 21, WILLIAMS discloses that the gene-modified CD16+NK-92 cells disclosed by WILLIAMS demonstrate ADCC. See Introduction, first and second paragraphs, p. 1721, left column. Regarding “wherein the modified NK-92 cells have ADCC activity of at least 40%” of claim 21, although WILLAIMS does not expressly state that the disclosed CD16+ NK-92 cells results in an ADCC activity of at least 40%, WILLIAMS’ CD16+ NK-92 cells anticipate this claimed observation and therefore WILLIAMS’ CD16+ NK-92 cells would inherently achieve a CD16 expression with an ADCC activity of at least 40%.
Regarding claim 26, WU discloses pharmaceutically acceptable excipients. See paragraph 6424. Because WILLIAMS discloses CD16+NK-92 cells that may be administered to subjects and WU discloses pharmaceutically acceptable excipients, it would have been obvious to one having ordinary skill in the art to formulate WILLIAMS’ NK-92 cells with WU’s pharmaceutical excipients.
Regarding claim 27, WILLIAMS discloses the administration of the NK-92 cells to mice. See Animals, p. 1721, right column.
Response to Arguments
On page 11 of the reply of 05/12/2025, Applicant argues that “[a]s an initial matter, the Examiner alleges that Williams' modified NK-92 cells would "inherently achieve an expression level of CD 16 that does not decrease or decrease more than 20% when the cells are activated" simply because Williams' cells were modified to express CD16. Office Action, page 8. Applicant respectfully submits that this assumption is incorrect. As disclosed in the current specification, CD 16 expression levels in a cell can drop, or at least fluctuate, as a result of CD 16 degradation.” Applicant’s argument has been fully considered but not found persuasive because WILLIAMS discloses the structure of the cells of the present claims, and thus WILLIAMS’ cells inherently function as described in the present claims.
According to the present specification, “examples of haNK® cells include IL2 Dependent haNK® cells ("haNK003 cells") and IL2 Dependent haNK® cells the former additionally express recombinant IL-2 and the latter do not. As used herein, the term "NK cells" refer to a) donor derived NK cells, b) NK-92.176V- CD16.ERIL2 cells (i.e., IL2 Independent haNK® cells) and c) NK-92.176V-CD16 cells (i.e., IL2 Dependent haNK® cells)” (p. 10, end of fourth paragraph). Thus, the population of modified NK-92 cells expressing CD 16 (SEQ ID NO: 1), wherein the modified NK-92 cells do not express IL-2 of the present claims are NK-92.176V-CD16 cells. WILLIAMS discloses gene-modified CD16NK-92 cells (NK-92.176V) (see Introduction, second paragraph).
Furthermore, the present specification state that SEQ ID NO: 1 is FcγRIIIa/CD16a (p. 6, third paragraph, first sentence), and WILLIAMS teaches that “[s]ince the parental NK-92 cell line lacks CD16, and cannot mediate ADCC, a high-affinity allelic variant (valine at position 176 instead of phenylalanine) of the CD16A Fcγ receptor was transduced into the NK-92 cell line” (see Introduction, second paragraph). Thus, the present specification and WILLIAMS disclose NK-92 cells with similar structures. Because WILLIAMS’s cells have the physical properties of present claim 1, they would inherently have an expression level of CD 16 that does not decrease or decreases no more than 20% when the cells are activated as compared to expression level of CD 16 on the cells before activation.
Previous rejection, maintained: claims 2 and 22 – 25 are rejected under 35 U.S.C. 103 as being unpatentable over WILLIAMS in view of WU as applied to claims 1, 3 – 6, 8, 11 – 13, 16, 18, 20, 21, 26, and 27 above, and further in view of KLINGEMANN (WO 2018165291 A1, filed 03/07/2018; see PTO-892 of 02/12/2025).
The teachings of WILLIAMS and WU with regard to claim 1, from which claim 2 depends, are discussed above and are fully incorporated here.
Although WILLIAMS and WU render the population of NK-92 cells expressing CD16 (SEQ ID NO: 1) of present claim 1 obvious as discussed above, and WU discloses the amino acid sequence of SEQ ID NO: 1, neither WILLIAMS nor WU discloses the nucleic acid encoding CD16 (SEQ ID NO: 2) of present claims 2 and 22. However, KLINGEMANN discloses the sequence of present SEQ ID NO: 2.
KLINGEMANN is directed to modified NK-92 cells, compositions and kits comprising the cells, and methods of making and using the populations of cells. See abstract. KLINGEMANN discloses that although NK-92 cells do not typically express CD16, KLINGEMANN’s disclosed NK-92 cells do express CD16. See p. 1, lines 19 – 20 and claim 1.
Regarding claim 2, KLINGEMANN discloses the sequence of SEQ ID NO: 2. KLINGEMANN’s SEQ ID NO: 3 is identical to present SEQ ID NO: 2 of present claim 2.
Because WILLIAMS discloses that NK-92 cells expressing CD16 is effective at treating cancer and WU discloses an amino acid sequence of CD16 (whose nucleic acid sequence is disclosed in KLINGEMANN) that is effective in the treatment of cancer, it would have been obvious to one having ordinary skill in the art to modify WILLIAMS’ NK-92 cells with WU’s CD16 (which is encoded by KLINGEMANN’s CD16 nucleic acid).
Regarding claim 22, KLINGEMANN discloses a method of producing a population of modified NK-92 cells that are capable of maintaining expression of CD16 during activation, wherein the method comprises introducing CD16 (SEQ ID NO:2). See Example 1, p. 23. Regarding “expression of CD16 on the activated modified NK-92 cells is no less than 50% of the CD16 expression on the modified NK-92 cells before the activation” of claim 22, although none of the cited references expressly state that expression of CD16 on the activated modified NK-92 cells is no less than 50% of the CD16 expression on the modified NK-92 cells before the activation, the NK-92 cells of the cited references anticipate this claimed observation and therefore the disclosed NK-92 cells would inherently achieve an expression of CD16 on the activated modified NK-92 cells of no less than 50% of the CD16 expression on the modified NK-92 cells before the activation.
Regarding claim 23, KLINGEMANN discloses methods for transformation include . . . retroviral infection . . . of DNA directly into cells. See p. 14, second paragraph.
Regarding claim 24, KLINGEMANN discloses populations of modified NK-92 cells and compositions and kits comprising the cells. See abstract.
Regarding claim 25, KLINGEMANN discloses that the kit further comprises an antibody. See claim 13.
Response to Arguments
On page 12 of the reply, second to last paragraph, Applicant argues that “[i]n contrast to current claims 1 and 22, Klingemann teaches modified NK-92 cells that express a specific form of IL-2 that is bound to the endoplasmic reticulum.” Applicant’s argument has been fully considered but not found persuasive because WILLIAMS in view of WU renders modified NK-92 cells expressing CD 16 (SEQ ID NO: 1), wherein the modified NK-92 cells do not express IL-2 obvious, and KLINGEMANN discloses the CD16 sequence of SEQ ID NO: 2 (of present claims 2 and 22 – 25) on NK-92 cells as discussed above and of record. Thus, it would have been obvious to modify WILLIAMS’ NK-92 cells (which do not express IL-2) with KLINGEMANN’s CD16 sequence.
Previous rejection; maintained: claims 19 and 29 are rejected under 35 U.S.C. 103 as being unpatentable over WILLIAMS in view of WU as applied to claims 1, 3 – 6, 8, 11 – 13, 16, 18, 20, 21, 26, and 27 above, and further in view of MA (US 2018/0187149 A1, published 07/05/2018; see PTO-892 of 02/12/2025).
The teachings of WILLIAMS and WU with regard to claim 1, from which claim 19 and 29, either directly or indirectly depend, are discussed above and are fully incorporated here.
Although WILLIAMS and WU render the population of NK-92 cells expressing CD16 (SEQ ID NO: 1) of present claim 1 obvious as discussed above, and WU discloses the amino acid sequence of SEQ ID NO: 1, neither WILLIAMS nor WU discloses that the modified NK-92 cells additionally express a chimeric antigen receptor (CAR) and/or a suicide gene.
However, MA discloses NK-92 cells that express a CAR and/or a suicide gene. MA is directed to an engineered cell comprising a first CAR and a second CAR wherein the engineered cells is an NK-92 cell. See claims 1 and 12.
Regarding claims 19 and 29, MA discloses that the engineered cell includes an inducible suicide gene (“safety switch”) which greatly increases safety profile and limits on-target or off-tumor toxicities of the compound CARs. The “safety switch” may be an inducible suicide gene, such as, without limiting, caspase 9 gene, thymidine kinase, cytosine deaminase (CD) or cytochrome P450. See paragraph 0134.
Because WILLIAMS discloses CD16+ NK-92 cells which express CD16 but not IL-2 that are effective at treating tumors and WU discloses a CD16 polypeptide sequence that is effective in activating cytotoxicity for the treatment of tumors, and MA discloses that the NK-92 cells may further include a CAR and suicide gene for improved efficacy and safety for the subject, it would have been obvious to one having ordinary skill in the art to modify WILLIAMS and WU’s CD16+ NK-92 cells with MA’s CAR and suicide gene.
Response to Arguments
On page 13, fourth paragraph of the reply, Applicant argues that “Ma does not remedy the deficiencies of Williams and/or Wu.” Applicant’s arguments have been fully considered but not found persuasive because WILLIAMS in view of WU renders a population of modified NK-92 cells expressing CD 16 (SEQ ID NO: 1), wherein the modified NK-92 cells do not express IL-2 obvious as discussed above and of record, and MA discloses NK-92 cells that express a CAR and/or a suicide gene. Thus, it would have been obvious to one having ordinary skill in the art to add a CAR and/or a suicide gene, which MA teaches, to WILLIAMS and WU’s modified NK-92 cells.
Double Patenting
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.
Previous rejection, maintained: claims 1 – 6, 8, 11 – 13, 16, 18 – 27, and 29 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 7, 12 – 16, and 19 - 21 of copending Application No. 17/115,360 (reference application).
Although the claims at issue are not identical, they are not patentably distinct from each other because copending claim 1 recites a method for generating a clonal population of transfected NK-92 cells, comprising: transfecting NK-92 cells with a multi-cistronic nucleic acid vector comprising a positive selection marker and at least one transgene, wherein the positive selection marker is endoplasmic-reticulum IL2 (ER-IL2) having the sequence recited in SEQ ID NO: 1, or endoplasmic-reticulum IL 15 (ER-IL15) having the sequence recited in SEQ ID NO: 2; culturing the transfected NK-92 cells in a cell culture medium in absence of IL-2; diluting the cultured NK-92 cells by clonal dilution, in absence of IL-2, . . ..
Copending claim 4 recites wherein the at least one transgene encodes an Fc Receptor . . .
Copending claim 5 recites that the Fc Receptor is CD 16.
Thus, the present claims are anticipated by the copending claims.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
Claims 1 – 6, 8, 11 – 13, 16, 18 – 27, and 29 are rejected.
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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/ESTELLA M. GUSTILO/Examiner, Art Unit 1646 /JOANNE HAMA/Supervisory Patent Examiner, Art Unit 1647