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 .
Response to Amendment
The Amendment filed 07/14/2025 in which claims 1-3, 14 and 29 were amended, and claim 28 was canceled, has been entered. Claims 20-22, and 24-25 were previously withdrawn. Claims 5-6, 19, 23, 26-27 were previously canceled.
Claims 1-4, 7-18 and 29 are currently under examination on the merits.
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 of this title, 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.
(Previous rejection, withdrawn as to claim 28, maintained and modified as necessitated by amendment as to claims 1, 4, 8, 12-18) Claims 1, 4, 8, 12-18 are rejected under 35 U.S.C. 103 as being unpatentable over Kiem in view of Derdak, as evidenced by Esensten et al. (prior art of record).
See claims 1, 4, 8, 12-18 as submitted on 07/14/2025.
The previous rejections of claim 28 is moot in view of Applicant’s cancelation of this claim.
Regarding claim 1, it is noted that the amendment filed on 07/14/2025 did not introduced any new limitations to the multicistronic vector beacuase the claim as previosuly submitted on 03/17/2025 already required the vector elements in (a), (b) and (c) to be “operatively liked to at least one promoter” and the elements (a), (b), and (c) were already recited in multiple orders. Accordingly, the rejection under 35 U.S.C. 103 set forth in the previous Non-Final Office Action mailed on 04/18/2025 still applies to amended claim 1.
As previously explained, Kiem teaches a cocal envelope pseudotyped lentiviral vector encoding additional polypeptides linked by 2A self-cleaving polypeptides (Abstract; paras. [0004]-[0005], [0007]; Fig. 1; Exemplary embodiments 1-3). Specifically, a hygromycin resistance gene and an envelope encoding gene (cocal or VSV-G) were expressed from the same promoter using a 2A self-cleaving polypeptide to ensure that hygromycin resistance cells will concomitantly express the envelope proteins (para. [0040]). Kiem further teaches that the lentiviral vectors may include or encode therapeutic proteins such as CD40, Fas L, or antibodies, among other therapeutic proteins (Exemplary embodiments 8-9). Kiem also specifically teaches that produced particles can be used to deliver a gene of interest to any appropriate target cell (e.g., T. cells; para. [0032]). Kiem also teaches a multicistronic vector, ppRRLSIN.C4b17_P2A_aWPRE-1, which encodes the alpha and beta chains of WT-1 specific TCR C4 separated by a P2A element (para. [0035]). Kiem further teaches that cocal pseudotyped lentiviruses can be produced in packaging cell lines when transfer and packaging plasmids are stably expressed, and that stable expression has some advantages to traditional, transient transfection of said plasmids (paras. [0004]-[0005]; Exemplary embodiments 1-13).
Kiem does not teach the limitations under (b) of claim 1, i.e., an anti-CD3 antibody or anti-CD3 scFv and (c) a CD28 ligand.
However, Derdak teaches direct stimulation of T lymphocytes by virus-like particles that express a CD3 ligand (OKT3 scFv) and costimulatory CD80 (Derdak, generally; Abstract). Derdak teaches that the single-chain variable fragment of the OKT3 hybridoma (recognizing CD3 epsilon) can be expressed on the cell surface of HEK-293, wherein the OKT3 scFv is fused to the GPI-anchored molecule CD14, for effective targeting to lipid rafts and consequently to virus-like particles (Page 13145, col. 1., paras. 2-3). As evidenced by Esensten et al., CD80 is a ligand of CD28, therefore Derdak teaches the limitations of (b) and (c).
It would have been prima facie obvious to a person of ordinary skill in the art before the effective filing date to have included the teachings of Derdak about VLP expression of a surrogate T cell receptor comprising an anti-CD3 antibody or anti-CD3scFv as well as a costimulatory CD80 molecule into the multicistronic vector as taught by Kiem, for the benefit of delivering a gene of interest to any appropriate target cell (e.g., T cells). Further, Kiem teaches polycistronic plasmids wherein COCVG glycoprotein is separated from another gene by a P2A element (para. [0035]). Accordingly, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date that the COCVG could be separated from the anti-CD3 OKT3 scFv and CD80 taught by Derdak by a P2A element, as shown in instant claim 1.
One of ordinary skill in the art would have had a reasonable expectation of success for introducing the anti-CD3 OKT3 scFv and CD80 taught by Derdak to the multicistronic vector of Kiem given that the methods of VLP cloning and expression are known, successfully demonstrated, and commonly used as evidenced by the applied prior art.
Regarding claim 4, as indicated above and previously, Kiem further teaches that the lentiviral vectors may include or encode therapeutic surface proteins such as CD40, Fas L, or antibodies, among other therapeutic proteins (Exemplary embodiments 8-9).
Regarding claim 8, as previously explained, Derdak teaches the anti-CD3scFv. Therefore, the limitations of amended claim 8 are met by the teachings of Derdak in combination with Kiem.
Regarding claims 12 and 13, as indicated above and previously, Kiem teaches a multicistronic cocal envelope pseudotyped lentiviral vector (Abstract; paras. [0004]-[0005], [0007]; Fig. 1; Exemplary embodiments 1-3), wherein cocal pseudotyped COCV lentiviruses can be produced in packaging cell lines when transfer and packaging plasmids are stably expressed, and that stable expression has some advantages to traditional, transient transfection of said plasmids (paras. [0004]-[0005]; Exemplary embodiments 1-13).
Regarding claim 14, it is noted that the amendment of 07/14/2025 did not introduced any new limitations because the claim already recited a cell comprising no polynucleotide encoding (a) or (b) other than the multicistronic vector. The new recitation of “transcripts” falls within a polynucleotide. As indicated above and previously, Kiem teaches a cell multicistronic cocal envelope pseudotyped lentiviral vector, wherein the packaging cell is the human embryonic kidney (HEK) 293T cells (Exemplary Embodiment 9; claim 9) and will not otherwise encode (a) or (b) other than the multicistronic vector (paras. [0004]-[0005]; Exemplary embodiments 1-13).
Regarding claim 15, as indicated above and previously, Kiem teaches packaging of surface-engineered lentiviral particles (paras. [0004]-[0005]; Exemplary embodiments 1-13).
Regarding claim 16, as indicated above and previously, Kiem teaches surface-engineered lentiviral particles wherein the lentiviral particle is pseudotyped by the COCVG (Abstract; paras. [0004]-[0005], [0007]; Fig. 1; Exemplary embodiments 1-3).
Regarding claim 17, as indicated above and previously, Kiem teaches surface-engineered lentiviral particles (Abstract; paras. [0004]-[0005], [0007]; Fig. 1; Exemplary embodiments 1-3), and Derdak teaches expression of a CD3 ligand (OKT3 scFv) and costimulatory CD80 (Derdak, generally; Abstract), wherein OKT3 scFv and CD80 (“(a)” and “(b)” as recited in claim 1) are expressed on the surface of the viral particle (Page 13145, col. 1., paras. 2-3).
Regarding claim 18, as previously explained, Kiem further teaches the cocal lentiviral particles can be produced at high titers and are suited for generating large-scale, clinical grade lentiviral particles (paras. [0004]-[0005], [0026]).
The rejection is maintained for reasons of record.
(Previous rejection, maintained and modified as necessitated by amendment as to claim 2) Claim 2 is rejected under 35 U.S.C. 103 as being unpatentable over Kiem in view of Derdak, as evidenced by Esensten, as applied to claims 1, 4, 8, and 12-18 above, and further in view of Yang, prior art of record.
See claim 2 as submitted on 07/14/2025.
Regarding claim 2, it is noted that amended claim 2 recites a new limitation of “wherein the COCVG or functional variant thereof and the anti-CD3 antibody or anti-CD3 scFv are joined by a the 2A peptide”. A previously explained, the combination of Kiem in view of Derdak already teach this limitation. Specifically, Kiem teaches polycistronic plasmids wherein COCVG glycoprotein is separated from another gene by a P2A element (para. [0035]) and Derdak teaches an anti-CD3 scFv. Further, as previously explained, Yang teaches systems and methods for generation of lymphocytes having unique antigen specificity, including viral vectors including 2A elements, or specifically a P2A sequence (SEQ ID NO: 9), which is identical to the instant SEQ ID NO: 14. Alignment of record.
It would have been prima facie obvious to one of ordinary skill in the art to modify the teachings of Kiem and Derdak to incorporate the specific P2A sequence taught by Yang. One of ordinary skill in the art would have been motivated to do so to utilize an effective cleavage linker.
One of ordinary skill in the art would have had a reasonable expectation of success for introducing the P2A sequence taught by Yang to the multicistronic vector of Kiem in view of Derdak given that the methods of VLP cloning and expression are known, successfully demonstrated, and commonly used as evidenced by the applied prior art.
The rejection is maintained for reasons of record.
(Previous rejection, maintained and modified as necessitated by amendment as to claim 3) Claim 3 is rejected under 35 U.S.C. 103 as being unpatentable over Kiem in view of Derdak, as evidenced by Esensten, as applied to claims 1, 4, 8, 12-18 above, and further in view of de Felipe, prior art of record.
Regarding claim 3, it is noted that amended claim 3 recites a new limitation of “wherein the COCVG or functional variant thereof and the anti-CD3 antibody or anti-CD3 scFv are joined by a the 2A peptide”. A previously explained, the combination of Kiem in view of Derdak already teach this limitation. Specifically, Kiem teaches polycistronic plasmids wherein COCVG glycoprotein is separated from another gene by a P2A element (para. [0035]) and Derdak teaches an anti-CD3 scFv. Further, as previously explained, de Felipe teaches that where 2A oligopeptide sequence occur within ORFs, the formation of the glycyl-prolyl peptide bond at the C-terminus of each 2A does not occur (Abstract) and that 2A and “2A-like” oligopeptide sequences are widely used in biotechnology and biomedicine to co-express multiple different proteins within the same cell (Page 213, col. 1, para. 1). de Felipe further teaches that a number of studies suggest that cleavage efficiency may be improved by adding a flexible Gly-Ser-Gly sequence to the 2A sequence (Pages 220-221, bridging paragraph).
It would have been prima facie obvious to one of ordinary skill in the art to have modified with reasonable expectation of success the teachings of Kiem in view of Derdak to incorporate a flexible Gly-Ser-Gly sequence to the 2A sequence. One of ordinary skill in the art would have been motivated to do so to improve the cleavage efficiency of the 2A sequence by adding the flexible Gly-Ser-Gly sequence to the polypeptides encoded by the multicistronic vector as taught by de Felipe.
The rejection is maintained for reasons of record.
(Previous rejection, maintained and modified as necessitated by amendment as to claims 7, 9-11, 29) Claims 7, 9-11, and 29 is rejected under 35 U.S.C. 103 as being unpatentable over Kiem in view of Derdak, as evidenced by Esensten, as applied to claims 1, 4, 8, 12-18 above, and further in view of Du (prior art of record.)
See claims 7, 9-11, and 29 as submitted on 07/14/2025.
Regarding claim 7, it is noted that no amendments were introduced to claim 7 in the amendment filed on 07/14/2025. As previously explained, the multicistronic vector of claim 1 was rendered prima facie obvious by the teachings of Kiem in view of Derdak, as explained above. As previously explained, Kiem further teaches that the lentiviral vectors may include or encode therapeutic proteins such as CD40, Fas L, or antibodies, among other therapeutic proteins (Exemplary embodiments 8-9). Kiem also specifically teaches that produced particles can be used to deliver a gene of interest to any appropriate target cell (e.g., T. cells; para. [0032]). Kiem further teaches a multicistronic vector, ppRRLSIN.C4b17_P2A_aWPRE-1, which encodes the alpha and beta chains of WT-1 specific TCR C4 separated by a P2A element (para. [0035]). Kiem further teaches that cocal pseudotyped lentiviruses can be produced in packaging cell lines when transfer and packaging plasmids are stably expressed, and that stable expression has some advantages to traditional, transient transfection of said plasmids (paras. [0004]-[0005]; Exemplary embodiments 1-13).
Kiem does not teach the co-stimulatory molecules human CD137L, or a functional variant or combination thereof.
However, Du teaches expression of co-stimulatory genes CD137L (also called 4-1BBL) and CD86, among other agents, and anti-CD3 antibody and additional cytokines (Abstract, Fig. 1) for the benefit of T cell expansion wherein the expanded T cells can efficiently target tumor cells (Fig. 3).
It would have been prima facie obvious to a person of ordinary skill in the art at the time of filing to have included the teachings of Du about the human CD137L gene expression into the multicistronic vector of Kiem in view of Derdak for the benefit of T cell expansion and activation for further adoptive immunotherapy clinical applications such as efficient target of tumor cells. Further, Kiem teaches polycistronic plasmids wherein COCVG glycoprotein is separated from another gene by a P2A element (para. [0035]). Accordingly, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date that the human CD137L gene can be joined to COCVG or the anti-CD3 OKT3 scFv or CD80 by a P2A element, as recited in claim 7.
One of ordinary skill in the art would have had a reasonable expectation of success for introducing the co-stimulatory ligand CD137L (also called 4-1BBL) into the vector as taught by Kiem in view of Derdak given that the methods of viral particle or VLP cloning and expression are known, successfully demonstrated, and commonly used as evidenced by the applied prior art.
Regarding claim 9, it is noted that no amendments were introduced to claim 9 in the amendment filed on 07/14/2025. As previously explained, the teachings of Kiem and Derdak in combinations teach the limitations of claim 8, which amended claim 9 depends on. As indicated above, Du further teaches expression of co-stimulatory genes CD137L (also called 4-1BBL) and CD86, among other agents, and anti-CD3 antibody and additional cytokines (Abstract, Fig. 1) for the benefit of T cell expansion wherein the expanded T cells can efficiently target tumor cells (Fig. 3). As evidenced by Esensten et al. CD86 is a ligand of CD28, therefore Du teaches a CD28 ligand comprising CD86 and human CD137L. Accordingly, the limitations of claim 9 are met by the teachings of Du in combination with Kiem and Derdak.
Regarding claims 10 and 11, it is noted that no amendments were introduced to claims 10 and 11 in the amendment filed on 07/14/2025. As previously explained, the teachings of Kiem, Derdak and Du in combinations teach the limitations of claim 9, which claim 10 depends on. In view of the teachings of Kiem, Derdak and Du described above, the polynucleotides recited in claim 10 are obvious embodiments of the multicistronic vector of claim 9. As indicated above, Kiem teaches a multicistronic vector comprising therapeutic proteins separated by a P2A element to deliver a gene of interest to any appropriate target cell (para. [0032], [0035], Exemplary embodiments 8-9), while Derdak teaches expression of a CD3 ligand termed OKT3 scFv (for effective targeting to lipid rafts and consequently to virus-like particles Page 13145, col. 1., paras. 2-3), and Du teaches co-stimulatory genes CD137L (also called 4-1BBL) and CD86 (a CD28 ligand). Further, it is noted that the different gene configurations shown in clauses “a”-“m” in claim 10 are considered to be those determined by routine optimization according to one of ordinary skill in the art in view of the teachings of Kiem, Derdak and Du. See MPEP 2144.07. The selection of a known material based on its suitability for its intended use supported a prima facie obviousness determination in Sinclair & Carroll Co. v. Interchemical Corp., 325 U.S. 327, 65 USPQ 297 (1945). Further, it is noted that there is no indication that any particular gene configuration of those recited in claim 10 presents advantageous features over any other configuration, because independent claim 1 requires that all of the components encoded in the multicistronic vector be operatively linked to a promoter.
Regarding claim 29, it is noted that the amendments were introduced to claim 29 in the amendment filed on 07/14/2025 recites “at least one promoter…”. As previously explained, Du already teaches a CMV promoter for expression of genes of interest including scFv sequences (page 4, para 3). Therefore the limitations of claim 29 are met by the teachings of Du which include a CMV promoter as recited in claim 29.
The rejection is maintained for reasons of record.
Response to Arguments
Applicant's arguments filed 07/14/2025 have been fully considered but they are not persuasive.
Applicant contends on page 8 of the Remarks: Claim 1 is not prima facie obvious because the alleged motivation to combine the references is speculative and lacks a factual basis. The only reason provided by the Office Action for combining the polynucleotide encoding a Cocal envelope protein (in Kiem) with genes encoding an anti-CD3 scFv and the CD28 ligand CD80 (in Derdak) is "for the benefit of delivering a gene of interest to any appropriate cell (e.g., T cells)." Office Action, p. 5.
This statement assumes the person having ordinary skill in the art (PHOSITA) would read the teaching of Derdak that virus-like particles expressing an anti-CD3 scFv and a CD28 ligand activate T cells and make a series of inferences-such as:
Stimulation of T cells with anti-CD3 scFv and a CD28 ligand would increase transduction by a viral particle pseudotyped with a cocal virus G protein (COCVG), not just activate the T cells' immune function, which is what Derdak discusses.
A surface-engineered viral particle would provide a stimulatory effect similar to the VLP/immunosome of Derdak.
Co-expression of anti-CD3 scFv and a CD28 ligand with COCVG would result in effective packaging of all three elements into the viral particle.
It would be desirable to have a single viral particle engineered to provide the stimulation, rather than a second agent, like a VLP/immunosome.
It is merely speculative to suggest that the PHOSITA would make interferes like these, or others, that would lead to a motivation to combine the references.
In response: 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 response to Applicant’s argument that the motivation to combine the references, namely “for the benefit of delivering a gene of interest to any appropriate target cell (e.g., T cells)” is speculative and lacks a factual basis, it is noted that this argument is unpersuasive at least for the following reasons. Expression of an anti-CD3 antibody or anti-CD3scFv as well as a costimulatory CD80 molecule for the benefit of targeting a T cell is neither speculative nor lacks a factual basis. Derdak teaches and experimentally demonstrates precisely that, specifically Derdak shows direct targeting and stimulation of T lymphocytes by virus-like particles (VLP) upon surface expression of an anti-CD3scFv as well as a costimulatory CD80 molecule. Further, pseudotyping a lentiviral particle or a VLP to change cell tropism by expression of surface proteins with specificity for a particular target cell is well known and widely practiced in the art (See Kiem, Derdak, Du). In the instant case, one of ordinary skill in the art would have been motivated and had a reasonable expectation of success to use expression of surface proteins known in the art, anti-CD3scFv and a costimulatory CD80 ligand, to specifically target T cells and stimulate them as taught and demonstrated by the cited prior art.
With respect to Applicant’s alleged inferences first bullet point, it is noted that instant claims do not recite an “increase of transduction by a viral particle pseudotyped with a cocal virus G protein (COCVG)”. Therefore, a person of ordinary skill in the art would not need to consider increased transduction to arrive at the claimed invention simply because “increased transduction” is not a limitation of the claimed invention. Further, since the claimed invention already bears a COCV-G protein, and Kiem et al. already teach that a cocal pseudotyped lentivirus particle has broad tropism and is more resistant to inactivation by human serum (see Kiem, para. [0005]), a person of ordinary skill in the art would reasonably conclude that a lentivirus particle bearing a COCV-G on the surface is capable of efficient transduction.
With respect to Applicant’s alleged inferences second bullet point, stimulation of a T lymphocyte is modulated by the an anti-CD3scFv, a costimulatory CD80 molecule (see Derdak), as well as other costimulatory genes such as CD137L (also called 4-1BBL) and CD86, among other agents (see Du above, Abstract, Fig. 1). Both, a viral particle and a VLP expressing such elements on the surface would be capable of stimulating a T lymphocyte, as taught by the cited prior art. Hence, a person of ordinary skill in the art would not need to make such inference because it is already taught by the prior art.
With respect to Applicant’s alleged inferences third bullet point, there is no evidence to teach nor suggest that packaging of a lentiviral particle would not work with all three elements. Kiem already teaches that produced particles can be used to deliver genes of interest to any appropriate target cell (e.g., T. cells; para. [0032]). Further, lentiviral vectors are a routinely used in the art to express a wide range of viral and non-viral genes. In fact, lentiviral vectors are one of the most common vectors used for gene delivery (see Kiem). Further, it is well known in the art that packaging of lentiviral particles is mediated by the viral gag gene which is present in lentiviral backbone genome (see Kiem). Hence, a person of ordinary skill in the art would not need to make such inference because it is already taught by the prior art.
With respect to Applicant’s alleged inferences fourth bullet point, there is no evidence to teach or suggest that a single viral particle could not provide the stimulation alone. Again, lentiviral vectors are one of the most common vectors used for gene delivery and they are capable of expressing a wide variety of genes (see Kiem). Hence, a person of ordinary skill in the art would not need to make such inference because it is already taught by the prior art.
Accordingly, Applicant’s argument that the motivation to combine the references, namely “for the benefit of delivering a gene of interest to any appropriate target cell (e.g., T cells)” is speculative and lacks a factual basis is unpersuasive.
Applicant contends on page 10 of the Remarks: This disclosure in Du does not make up for the deficiencies of the other cited references. For example, such disclosure has no bearing on encoding (a), (b) and (c) as claimed, and operably linking them to at least one promoter. Further, a description about the use of certain genes in feeder cells and the other disclosure of Du would not have motivated a person of ordinary skill to put these genes in the entirely different systems of the other references, and it would not have made sense to incorporate these additional genes into a nucleic acid all operably linked to the same promoter for reasons further described above. Even if a motivation could be found, there would have been no reasonable expectation of success, based on disclosure about feeder cells, that the same genes would work in a useful manner within the combined system of the other references.
In response: Applicant's arguments against the references individually are not persuasive because 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). Du was not cited for teaching the multicistronic vector of claim 1 comprising elements (a), (b), and (c). As explained above and previously, Du was cited for teaching expression of co-stimulatory genes CD137L (also called 4-1BBL) and CD86, among other agents, and anti-CD3 antibody and additional cytokines (Abstract, Fig. 1) for the benefit of T cell expansion wherein the expanded T cells can efficiently target tumor cells (Fig. 3). It would have been prima facie obvious to a person of ordinary skill in the art to have included with reasonable expectation of success the teachings of Du about the human CD137L gene expression into the multicistronic vector of Kiem in view of Derdak. One of ordinary skill in the art would have been motivated to do so for the benefit of T cell expansion and activation, as taught by Du. Further, Kiem already teaches that the lentiviral vectors may include or encode therapeutic proteins such as CD40, Fas L, or antibodies, among other therapeutic proteins (Exemplary embodiments 8-9). Therefore, the prior art provides clear teachings, suggestions and motivation to combine all elements of the claimed invention into a single vector, as recited in instant claims. Accordingly, the claimed vector represents an obvious embodiment of the teachings of the cited prior art. See MPEP 2144.07. The selection of a known material based on its suitability for its intended use supported a prima facie obviousness determination in Sinclair & Carroll Co. v. Interchemical Corp., 325 U.S. 327, 65 USPQ 297 (1945).
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to MARLENE V BUCKMASTER whose telephone number is (703)756-5371. The examiner can normally be reached M-F 8-5.
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/MARLENE V BUCKMASTER/Examiner, Art Unit 1671
/THOMAS J. VISONE/Supervisory Patent Examiner, Art Unit 1671