DETAILED ACTION
Applicant’s amendment and Arguments/Remarks received on 09 December 2025 have been entered. Claims 1-4, 6, 8-10, 12-13, 22-23, 26, 35, 38-39, and 50-51 were previously pending in the application and remain pending in the application. Claims 1, 26, 35, 38, and 39 are independent claims.
Claims 1-4, 6, 8-10, 12-13, 22-23, 26, 35, 38-39, and 50-51 are currently pending and under examination in the instant application. An action on the merits follows.
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA . The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Priority
The present application is a 35 U.S.C. 371 national stage filing of International Application No. PCT/US201950850, filed 12 September 2019, which claims priority to US Provisional Application No. 62/730,387, filed 12 September 2018.
Thus, the earliest possible priority for the instant application is 12 September 2018.
Information Disclosure Statement
The information disclosure statement filed 09 December 2025 has been considered by the Examiner. Examiner notes the filing of IDS Size Fee assertions for the IDS filed 09 December 2025, as required under 37 CFR 1.98, indicating that no IDS size fee is required under 37 CFR 1.17(v) at this time.
Specification
The objection to the specification of the disclosure for containing an embedded hyperlink is maintained in view of the amendment to the specification which has replaced the hyperlink with the exact same text comprising the full web address including the prefix “http://” which makes it executable. Note that in the prior action indicated that Applicant is required to delete the embedded hyperlink and/or other form of browser-executable code; references to websites should be limited to the top-level domain name without any prefix such as http:// or other browser-executable code. See MPEP § 608.01.
Applicant asserts that the specification has been amended to remove any hyperlinks or browser-executable code. However, this is not agreed. Applicant has merely replaced the hyperlinks with identical text without removing the prefix “http://”. As such, Applicant has not corrected the specification to overcome the objection.
The objection to the specification of the disclosure for reciting trade names and/or marks used in commerce is withdrawn in view of the amendment to the specification adding the appropriate symbols indicating use in commerce.
37 CFR 1.121(c)
Examiner notes that the current claim listing no longer recites “FCN1” which was formerly both underlined and stricken-through.
Claim Rejections - 35 USC § 112(b)
The rejection of Amended, previously presented, and original claims 1-4, 6, 8-10, 12-13, 22-23, 26, 35, 38-39, and 50-51 under 35 U.S.C. 112(b) as failing to particularly point out and distinctly claim the subject matter which the inventor(s) regards as the invention for:
claims 1, 26, and 35 reciting “slow cycling” in “slow cycling cell (SCC)”, which is a relative term which renders the claim indefinite;
claim 12 reciting the limitation "the SSC transcriptome RNA" in line 1 and “SSC” without first writing out the term for which “SSC” is an abbreviation;
is maintained in part in view of Applicant’s amendments to the claims such that claim 12 has been amended to recite “SCC” instead of “SSC”, but claims 1, 26, and 35 still recite “slow cycling” without providing a standard for ascertaining the requisite degree, therefore it is still unclear which of all possible cells would be encompassed by the phrase “slow cycling cell”.
Applicant argues that one skilled in the art would be reasonably apprised of the metes and bounds of the term “slow cycling cell” when the claims are read in light of the specification and considered in view of the understanding in the field.
However, this is not agreed.
Applicant refers to a definition for “slow-cycling cells” provided in the instant specification, which reads, “as used herein, the term “slow-cycling cells” or “SCCs” refers to tumor or cancer cells that proliferate at a slow rate. In exemplary aspects, the SCCs have a doubling time of at least 50 hours.” [00104]. This definition defines the cells as tumor or cancer cells, but does not set metes or bounds on the doubling time of the cells. The definition uses a relative term “slow” to describe the proliferation rate of the “slow-cycling cells” without providing bounds for the relative term “slow”. The following sentence provides only exemplary aspects of slow cycling cells, and as such, the descriptors therein are merely exemplary and are not a limiting definition. Similarly, Applicant refers to the paper cited within the specification, Deleyrolle et al., to provide additional descriptors for slow cycling cells. The specification refers to Deleyrolle for teaching “SCCs display increased tumor-initiation properties and are stem cell like”. However, these are also relative aspects which do not have clearly defined bounds. “increased” is a relative term without even a reference as to what they are increased relative to. Additionally, “stem cell like” does not require that they are stem cells and as such it is unclear to what extent they are “like” stem cells. Therefore, Applicant’s arguments do not provide defined bounds for the definition of “slow-cycling cells” which would allow an ordinarily skilled artisan to understand the full scope of the term, and as such the metes and bounds of the claims still cannot be determined.
Claim Rejections - 35 USC § 112(a)
The rejection of amended claim 39 under 35 U.S.C. 112(a) for being enabling for:
A method of treating glioblastoma, the method comprising administering the composition of claim 1 to a subject with glioblastoma;
wherein the composition comprises a liposome comprising a cationic lipid and RNA consisting essentially of slow cycling cell (SCC) total transcriptome RNA, wherein the RNA comprises total tumor mRNA (TTmRNA), wherein the liposome is prepared by:
isolating slow cycling cells (SCCs) from a mixed tumor cell population obtained from the subject,
extracting total tumor-derived RNA (TTRNA) from the isolated SCCs,
generating and amplifying a total tumor-derived complimentary DNA (TTcDNA) library from the extracted TTRNA from step b, wherein the TTcDNA sequences incorporate a T7 RNA polymerase promoter sequence,
producing a final TTmRNA product by using a T7 RNA polymerase to in vitro transcribe the amplified cDNA library, and
mixing the TTmRNA from step d with a cationic lipid to make a liposome composition;
wherein the composition comprises TTmRNA molecules encoded by all of the about 580 genes selected from the list of genes recited in claim 1; and
wherein the administering is performed by intravenous injection of the composition into said subject,
does not reasonably provide enablement for any method of treating glioblastoma comprising administering the composition of claim 1 to any subject with glioblastoma, wherein the composition comprises a liposome comprising a cationic lipid and RNA consisting essentially of any slow cycling cell transcriptome RNA, wherein the RNA comprises RNA molecules encoded by all of the about 580 genes recited in claim 1;
is withdrawn in view of Applicant’s amendments to the claims such that claim 39 now recites, “wherein the composition comprises autologous RNA molecules encoded by all of the genes recited in claim 1”.
Claim Rejections - 35 USC § 112(d)
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
**The following new rejection is necessitated by amendments to the claims.**
Previously presented claim 22 is newly rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Previously presented claim 22 recites, “The composition of claim 1, comprising RNA molecules encoded by all of the genes of claim 1”, which does not further limit the invention of claim 1. Independent claim 1 was amended to recite “wherein the RNA comprises RNA molecules encoded by all of the following genes”. As such, the recitation in claim 22 that the composition comprises RNA molecules encoded by all of the genes of claim 1 is merely repeating the limitation already included in amended independent claim 1 and does not further limit the claim upon which it depends.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Claim Rejections - 35 USC § 103
The rejection of amended, previously presented, and original claims 1-4, 6, 8-10, 12-13, 22-23, 26, 35, 38-39, and 50-51 under 35 U.S.C. 103 as being unpatentable over Sayour et al. 2017, Oncoimmunology, Vol. 6(1), e1256527, 1-14, published 03 January 2017, IDS, cited in a prior action; in view of Vik-Mo et al. 2013, Cancer Immunology & Immunotherapy, Vol. 62, 1499-1509, cited in a prior action; Moore et al. 2012, Stem Cells and Development, 21(10), 1822-1830, IDS; Batlle & Clevers 2017, Nature Medicine, 23(10), 1124-1134; Sen et al. 2018, Glioblastoma: Methods and Protocols, Methods in Molecular Biology, Vol. 1741, 151-170, published 2 February 2018, cited in a prior action, Patel et al. 2014, Science, Vol. 344(6190), 1396-1401, IDS, cited in a prior action, and Wang et al. 2018, Frontiers in Pharmacology, Vol. 9, 1-14, published 5 September 2018, cited in a prior action, is maintained. Applicant's amendments to the claims and arguments have been fully considered but have not been found persuasive in overcoming the rejection for reasons of record as discussed in detail below.
Applicant amended independent claim 1 to recite “all of the following genes”. However, this limitation was already addressed in the rejection of record in the prior office action in that the limitation was previously recited in previously presented dependent claim 22.
Applicant also amended independent claim 39 to recite, “wherein the composition comprises autologous RNA molecules”, which was also addressed in the prior action. Vik-Mo was cited for teaching a DC-based vaccine targeting cancer stem cells in glioblastoma in which cancer stem cell total mRNA was isolated from glioblastoma stem cells (GSCs) (which had been isolated and expanded as tumorspheres) and transfected into autologous DCs [abstract]; that the immune response induced by the autologous DCs transfected with autologous glioblastoma stem cells (GSCs) mRNA is targeted against the patient’s own GSCs and further that the matured DCs which have been loaded with the GSC mRNA express glioblastoma stem cell antigens [column 2 ¶ 3, Figure 1]; and that that glioblastomas are highly heterogenous both within tumors and between individual patients, and that the use of autologous GSC antigens may stimulate immunity against antigens unique to the patient, such that use of an individualized therapeutic approach may be very important when targeting GSC, as tumors may be derived from a range of different progenitor cells [column 13 ¶ 2]. Therefore, an ordinarily skilled artisan at the time of filing the instant application would have been motivated to formulate a cancer vaccine with autologous total mRNA derived from an isolated autologous cancer stem cell population, such as GSCs, for the treatment of cancer, such as glioblastoma, to extend progression free survival.
Accordingly, Applicant’s amendments do not overcome a finding of obviousness under 35 USC 103 over Sayour, Vik-Mo, Moore, Batlle, Sen, Patel, and Wang.
Applicant argues that:
Sayour does not teach a composition comprising RNA wherein the RNA consists essentially of slow cycling cells transcriptome RNA wherein the RNA comprises RNA molecules encoded by all the genes recited in amended claim 1;
Vik-Mo does not teach or suggest slow cycling cells in that an isolated cancer stem cell population, such as glioblastoma stem cells, is not necessarily a slow cycling cell population and is not predictive of slow cycling cells;
Slow cycling cells are distinct from cancer stem cells in that they have a unique and distinguishable lineage which is not equivalent to the class of cancer stem cells, such that SCCs are isolated based on functional and metabolic criteria rather than surface marker expression by which cancer stem cells are typically isolated and that SCCS display distinct phenotypic, transcriptomic, and behavioral properties compared to cancer stem cells, as evidenced by Yang et al.’s teachings of single cell RNA sequencing results showing SCCs constitute a non-overlapping population relative to canonical CSCs;
Isolating cells based on any property other than being slow cycling would not necessarily isolate the distinct population of slow cycling cells and, by extension, would not generate RNA payload that consists essentially of slow cycling cells transcriptome RNA wherein the RNA comprises RNA molecules encoded by the genes recited in amended claim 1;
Moore fails to cure the deficiencies of Vik-Mo and Sayour by merely teaching general methods for labeling slow-dividing tumor cells and not suggesting that SCCs are distinct from cancer stem cells;
Batlle fails to cure the deficiencies of Moore, Vik-Mo, and Sayour in that the Office has not established why or how one of ordinary skill in the art would look to Sen to modify the method of Sayour in view of the teachings of Vik-Mo, Moore, and Batlle to generate a composition comprising a liposome comprising a cationic lipid and RNA consisting essentially of slow cycling cell transcriptome RNA, wherein the RNA comprises RNA molecules encoded by all of the genes of amended claim 1;
The office has not established that the cells of any of the cited references necessarily express the list of genes as recited by amended claim 1 in that SCCs are a distinct cellular population from cancer stem cells, and as such total mRNA isolated from a cancer stem cells as allegedly taught by any of the cited references will not necessarily consist essentially of slow cycling cell transcriptome RNA as recited by amended claim 1;
The SCC transcriptome RNA of the present application is isolated specifically from glioblastoma slow cycling cells which are not taught by the combination of the cited references, and that the term “slow-cycling cell” as defined by the specification provides bounds for which cells constitute “slow cycling cells” and the specification teaches one skilled in the art exactly how to isolate RNA consisting essentially of slow cycling cells transcriptome RNA, wherein the RNA comprises RNA molecules encoded by all the genes recited in amended claim 1;
Wang fails to cure the deficiencies of Sayour in that Wang does not teach a liposome comprising a cationic lipid and RNA that consists essentially of SCC transcriptome RNA.
However, this is not agreed.
In response to applicant’s arguments against the references individually, it is noted that the test for obviousness is not whether the features of a secondary reference may be bodily incorporated into the structure of the primary reference; nor is it that the claimed invention must be expressly suggested in any one or all of the references. Rather, the test is what the combined teachings of the references would have suggested to those of ordinary skill in the art. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981). One cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). Further, the examiner recognizes that obviousness may be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so found either in the references themselves or in the knowledge generally available to one of ordinary skill in the art. See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007). In addition, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
Specifically, regarding Applicant’s argument 1), that Sayour does not teach a composition comprising RNA wherein the RNA consists essentially of slow cycling cells transcriptome RNA wherein the RNA comprises RNA molecules encoded by all the genes recited in amended claim 1; note that as discussed above, Applicant has not provided a limiting definition of “slow-cycling cells” which would differentiate the SCC transcriptome RNA of the present invention from the slow cycling tumor stem cell transcriptome RNA taught by the prior art. Sayour was cited for teaching a composition comprising a liposome comprising a cationic lipid (e.g., DOTAP) and RNA consisting essentially of tumor-derived transcriptome RNAs (e.g., B16F0, B16F10, or KR158B-luc tumor cells) for use as a cancer vaccine which peripherally activates T cells against tumor antigens to target the destruction of tumor cells [column 1 ¶ 1, column 7 ¶ 1, column 9 ¶ 2- column 10 ¶ 1, Figure 3]. Vok-Mo was cited for teaching the motivation to formulate a cancer vaccine with total mRNA derived from an isolated cancer stem cell population, such as GSCs, for the treatment of cancer, such as glioblastoma, to extend progression free survival. Sen was cited for teaching that a slow-cycling cell population within a patient-derived glioblastoma cell culture contains cells with stem-like properties and differential gene expression between the slow-cycling and --fast-cycling cells, including the expression of FST and RNF150 in the FACS-isolated dye-retaining slow cycling cells [page 154 ¶ 3, page 165 ¶ 5, Figure 2-3]. As discussed in the prior action, claim 1 recites a list of genes which encode mRNAs that are a part of the slow cycling cell transcriptome. The expression of genes by a cell is an inherent property of the cell. As such, any cell which meets all of the other limitations of the recited “slow cycling cell (SCC)” as set forth in claim 1 is presumed, absent evidence to the contrary, to express the same genes. Reliance upon inherency is not improper even though rejection is based on Section 103 instead of Section 102. In re Skoner, et al. 186 USPQ 80 (CCPA). As stated in MPEP 2112, The express, implicit, and inherent disclosures of a prior art reference may be relied upon in the rejection of claims under 35 U.S.C. 102 or 103."The inherent teaching of a prior art reference, a question of fact, arises both in the context of anticipation and obviousness." In re Napier, 55 F.3d 610, 613, 34 USPQ2d 1782, 1784 (Fed. Cir. 1995). See also In re Grasselli, 713 F.2d 731,739, 218 USPQ 769, 775 (Fed. Cir. 1983). The broadest reasonable interpretation of the “slow cycling cells” according to claim 1 is any tumor cell population which progresses through the cell cycle more slowly than any other cell population and which, as a population, collectively and inherently express the genes recited in claim 1. Therefore, the combination of cited references provides the teaching and motivation for a composition comprising RNA wherein the RNA consists essentially of slow cycling cells transcriptome RNA wherein the RNA comprises RNA molecules encoded by all the genes recited in amended claim 1.
Specifically, regarding Applicant’s argument 2), that Vik-Mo does not teach or suggest slow cycling cells in that an isolated cancer stem cell population, such as glioblastoma stem cells, is not necessarily a slow cycling cell population and is not predictive of slow cycling cells, as discussed above, Sen was cited for teaching that a slow-cycling cell population within a patient-derived glioblastoma cell culture contains cells with stem-like properties and differential gene expression between the slow-cycling and --fast-cycling cells, including the expression of FST and RNF150 in the FACS-isolated dye-retaining slow cycling cells [page 154 ¶ 3, page 165 ¶ 5, Figure 2-3]. Additionally, Patel teaches that glioblastomas contain a primitive subpopulation of stemlike cells (GSCs) which exhibit a stemlike phenotype, divide at lower overall rates, have low expression of cell cycle signature genes, and express stemness genes, including the expression of GRIA2 in the glioblastoma stem cells [column 11 ¶ 2-column 13 ¶ 2, Figure 3]. Therefore, Sen and Patel are teaching specifically to use a slow cycling cell population.
Specifically, regarding Applicant’s argument 3), that slow cycling cells are distinct from cancer stem cells in that they have a unique and distinguishable lineage which is not equivalent to the class of cancer stem cells, such that SCCs are isolated based on functional and metabolic criteria rather than surface marker expression by which cancer stem cells are typically isolated and that SCCS display distinct phenotypic, transcriptomic, and behavioral properties compared to cancer stem cells, as evidenced by Yang et al.’s teachings of single cell RNA sequencing results showing SCCs constitute a non-overlapping population relative to canonical CSCs, again note that both Sen and Patel are specifically teaching slow cycling cell populations. The extent to which general cancer stem cell populations may differ from a slow cycling cell population is moot in that the cited references specifically teach slow cycling cell populations, and the claims as written do not differentiate the claimed slow-cycling cells from the slow cycling cells taught by the prior art.
Specifically, regarding Applicant’s argument 4), that isolating cells based on any property other than being slow cycling would not necessarily isolate the distinct population of slow cycling cells and, by extension, would not generate RNA payload that consists essentially of slow cycling cells transcriptome RNA wherein the RNA comprises RNA molecules encoded by the genes recited in amended claim 1; note that Applicant has not claimed an isolation procedure in the current claims as written. Neither the claims nor the specification teach that slow cycling cells are a distinct cellular population from cancer stem cells. As such, the claims as written are not limited by a particular isolation protocol, but merely that the cells are “slow cycling”, which are taught by the cited art. Independent claim 1 has not recitation of any isolation of the slow cycling cells. Independent claim 26 recites “isolating slow cycling cells (SCCs) from a mixed tumor cell population to produce a cell population consisting essentially of SCCs”, but does not limit the isolation procedure to any particular method. As such, any isolation of a cell population which meets the limitation of being “a cell population consisting essentially of SCCs” will satisfy the claim as written.
Specifically, regarding Applicant’s argument 5), that Moore fails to cure the deficiencies of Vik-Mo and Sayour by merely teaching general methods for labeling slow-dividing tumor cells and not suggesting that SCCs are distinct from cancer stem cells, note that Moore, along with Batlle, was relied on for teaching the motivation to specifically target a slow cycling cell population of cancer stem cells for the treatment of cancers such as glioblastoma. Moore was not relied on to teach every aspect of the claimed invention not taught by Sayour.
Specifically, regarding Applicant’s argument 6), that Batlle fails to cure the deficiencies of Moore, Vik-Mo, and Sayour in that the Office has not established why or how one of ordinary skill in the art would look to Sen to modify the method of Sayour in view of the teachings of Vik-Mo, Moore, and Batlle to generate a composition comprising a liposome comprising a cationic lipid and RNA consisting essentially of slow cycling cell transcriptome RNA, wherein the RNA comprises RNA molecules encoded by all of the genes of amended claim 1, note again that Sayour was cited for teaching a composition comprising a liposome comprising a cationic lipid (e.g., DOTAP) and RNA consisting essentially of tumor-derived transcriptome RNAs (e.g., B16F0, B16F10, or KR158B-luc tumor cells) for use as a cancer vaccine which peripherally activates T cells against tumor antigens to target the destruction of tumor cells [column 1 ¶ 1, column 7 ¶ 1, column 9 ¶ 2- column 10 ¶ 1, Figure 3]. Vok-Mo was cited for teaching the motivation to formulate a cancer vaccine with total mRNA derived from an isolated cancer stem cell population, such as GSCs, for the treatment of cancer, such as glioblastoma, to extend progression free survival. Moore and Battle were cited for teaching the motivation to specifically target a slow cycling cell population of cancer stem cells for the treatment of cancers such as glioblastoma. Sen was specifically cited for teaching that a slow-cycling cell population within a patient-derived glioblastoma cell culture contains cells with stem-like properties and differential gene expression between the slow-cycling and --fast-cycling cells, including the expression of FST and RNF150 in the FACS-isolated dye-retaining slow cycling cells [page 154 ¶ 3, page 165 ¶ 5, Figure 2-3]. As such, Sen was cited for teaching that the slow cycling cells have stem cell-like properties and that they are a distinct population of cells with distinct gene expression, thereby teaching that use of a slow cycling cell population transcriptome is distinct from using a total tumor cell transcriptome, further reinforcing the motivation for isolating and using the specific slow cycling cell population.
Specifically, regarding Applicant’s argument 7), that the office has not established that the cells of any of the cited references necessarily express the list of genes as recited by amended claim 1 in that SCCs are a distinct cellular population from cancer stem cells, and as such total mRNA isolated from a cancer stem cells as allegedly taught by any of the cited references will not necessarily consist essentially of slow cycling cell transcriptome RNA as recited by amended claim 1; note again that both Sen and Patel are specifically teaching slow cycling cell populations. The extent to which general cancer stem cell populations may differ from a slow cycling cell population is moot in that the cited references specifically teach slow cycling cell populations, not just total tumor mRNA, and the claims as written do not differentiate the claimed slow-cycling cells from the slow cycling cells taught by the prior art.
Specifically, regarding Applicant’s argument 8), that the SCC transcriptome RNA of the present application is isolated specifically from glioblastoma slow cycling cells which are not taught by the combination of the cited references, and that the term “slow-cycling cell” as defined by the specification provides bounds for which cells constitute “slow cycling cells” and the specification teaches one skilled in the art exactly how to isolate RNA consisting essentially of slow cycling cells transcriptome RNA, wherein the RNA comprises RNA molecules encoded by all the genes recited in amended claim 1; Applicant is reminded that the slow cycling cells as taught by the prior art fall within the scope of “slow cycling cells” as recited in the claims as written. Applicant has not provided a limiting definition of SCCs which differentiates the claimed cells from the cells taught by the cited art. Additionally, the claims as written do not recited isolation methods which would differentiate the claims cells from the cells taught by the prior art.
Specifically, regarding Applicant’s argument 9), that Wang fails to cure the deficiencies of Sayour in that Wang does not teach a liposome comprising a cationic lipid and RNA that consists essentially of SCC transcriptome RNA, note that Wang was not cited for teaching the specific RNA composition within the liposomes. Wang was cited for teaching liposome compositions with zeta potentials of 50 mV and liposome-mRNA compositions with zeta potentials of 40 mV [column 13 ¶ 1, Figure 3], and that high zeta potential of about 35 mV can better target human and murine dendritic cells to induce significant antitumor responses and that cationic liposomes comprising nucleic acids with zeta potentials of greater than 30 mV exert excellent in vitro targeted genome editing and in vivo antitumor effects [column 23 ¶ 1], thereby teaching the motivation to generate liposomes comprising a cationic lipid and nucleic acids wherein the liposome has a zeta potential of about 30 mV to at least about 50 mV or of about 40 mV to about 50 mV. Wang was not relied on for teaching the specific cell population from which the RNA was to be derived.
Therefore, Applicant’s arguments do not overcome a finding of obviousness under 35 USC 103 over Sayour, Vik-Mo, Moore, Batlle, Sen, Patel, and Wang, and the rejection is maintained.
Conclusion
No claim is 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Dr. KATIE L PENNINGTON whose telephone number is (703)756-4622. The examiner can normally be reached M-Th 8:30 am - 5:30 pm, Friday 8:30 am - 12:30 pm CT.
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DR. KATIE L. PENNINGTON
Examiner
Art Unit 1634
/KATIE L PENNINGTON/Examiner, Art Unit 1634
Dr. A.M.S. Wehbé
/ANNE MARIE S WEHBE/Primary Examiner, Art Unit 1634