DETAILED ACTION
Claims 30-46 are pending and under examination in the instant application. The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA . An action on the merits follows.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 9/11/25, 1/21/25, and 6/24/24 are in compliance with the provisions of 37 CFR 1.97 and 1.98. Accordingly, the information disclosure statements have been considered by the examiner, and initialed and signed copies of the 1449s are attached to this action. Note that duplicate references have been lined through as indicated.
Claim Interpretation
The following claim interpretation has been applied to claim 34. Claim 34 recites the composition of claim 30 wherein the NKT cells are “autologous, syngeneic, allogeneic, or xenogeneic in relation to an individual”. Since the claims are product claims, not method claims for delivery to an individual, the identification of the cells as “autologous, syngeneic, allogeneic, or xenogeneic in relation to an individual” is subjective as the meaning of those words require delivery and place no actual structural limitation on the actual composition itself. As such, the product of claim 34 has been interpreted based solely on the actual structural elements claimed which are a composition comprising isolated CD62L-positive natural killer T (NKT) cells, recombinant human interleukin-2 (rhIL-2), and alpha-galactosylceramide (aGalCer).
The following claim interpretation has been applied to claim 44. Claim 44 depends on claim 40. Claim 40 recites the composition of claim 30, “further comprising OKT3 monoclonal antibody (mAb), 6B11, APCs, or a combination thereof”. Claim 44 recites the composition of claim 40, “wherein the OKT3 mAb is at 20 ng/ml or 1 ug/ml”. However, while claim 44 limits the concentration of OKT3 mAb, it does not limit the composition to a composition comprising the OKT3 mAb. claim 40 recites the presence of OKT3 monoclonal antibody (mAb), 6B11, APCs, or a combination thereof in the alternative, and claim 44 does not recite that the composition comprises the OKT3 mAb. As such, the limitations of claim 44 will be met by a composition according to claim 30 further comprising one of 6B11 or APCs, instead of the OKT3 mAb.
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.
Claims 30-46 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.
Independent claim 30 is drawn to, “[a] composition comprising isolated CD62L-positive natural killer T (NKT) cells, recombinant human interleukin-2 (rhIL-2), and alpha-galactosylceramide (aGalCer)”. Claim 32 depends on claim 30 and recites, “wherein the NKT cells are: 1) a mixed population of CD62L-positive and CD62L-negative cells; 2) CD4-positive and CD62L-positive; 3) CD3-positive and Va24Ja18-positive; and/or 4) type 1 NKT cells”. Claim 33, which depends on claim 32, further recites “wherein the NKT cells comprise a majority of CD62L-positive NKT cells”. Alternative 1) of claim 32, where the NKT cells are a mixed population of CD62L-positive and CD62L-negative cells, and the limitation of claim 33 which refers to a majority of CD62L-positive NKT cells, are confusing as independent claim 30 recites that the composition comprises isolated CD62L-positive NKT cells. Thus, the only NKT cells referred to in claim 1 are identified as CD62L positive NKT cells. As such, the recitation in claims 32 and 33 that the NKT cells are mix of CD62L+ and CD62L- NKT cells, and where the CD62L+ NKT cells are the majority of the NKT cells, conflicts with the limitation in claim 30 that the NKT cells are CD62L+ NKT cells. Thus, the metes and bounds of claims 30, 32, and 33 cannot be determined as it unclear whether the composition of claim 30 is intended to further include additional NKT cells which are CD62L- NKT cells. Claims 31, and 34-46 depend on claim 30 and thus are included in this rejection.
In the interests of compact prosecution, claim 30 has been given its broadest reasonable interpretation as reading on a composition which may contain a separate population of NKT cells which are CD62L- in addition to the recited isolated CD62L+ NKT cells.
Claim 33 is further indefinite in that it is unclear what NKT cell population is intended to be limited to “a majority of CD62L-positive NKT cells” and how that relates to the composition as whole. As noted above, claim 33 depends on claim 32 which depends on claim 30. Claim 30 only refers to isolated CD62L+ NKT cells as being present in the composition. Claim 32 recites four different alternate NKT cell populations. Thus, it is unclear what population of NKT cells comprises a “majority” of CD62L+ NKT cells, is it the composition itself as a whole, or a portion of the composition that comprises NKT cells which could be separate from or possibly including the CD62L+ cells recited in claim 30, or one of the particular populations set forth as 1), 2), 3), or 4) in claim 32. Further, the phrase “a majority of” is a subjective quantitative term. The specification does not actually recite the phrase “a majority of” in reference to the number of CD62L positive NKT cells present in a composition or any subpopulation of NKT cells, or provide any definition of what amount or percentage of cells in a composition or cell population need to be CD62L-positive Type I human NKT cells in order to be considered the “majority” of cells in the composition. In addition, the dictionary definition of the term “majority”, which according to the Cambridge Dictionary means, “ the larger number or part of something”, does not help to refine what number of cells would qualify as a “majority” in a pharmaceutical composition as claimed (Cambridge Dictionary, https://dictionary.cambridge. org/us/dictionary/english/majority, definition of “majority”). For example, using the Cambridge dictionary definition, it is possible that a majority of cells in a mixed population would encompass the cell population that is larger than the others, where the largest cell population could be 20 or 30% of the total population, as opposed to other cell populations present in composition which constitute individually less than 20 or 30%. Thus, for all the reasons set forth above, the metes and bounds of claim 33 cannot be determined.
In the interests of compact prosecution, claim 33 has been given its broadest reasonable interpretation as comprising CD62L+ NKT cells.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale or otherwise available to the public before the effective filing date of the claimed invention.
Claims 31-35, 38-40, and 44-46 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by WO 2015/051247 (April 9, 2015), hereafter referred to as Webb et al.
Webb et al. teaches NKT cells stimulated using ligands for the TCR complex and CD28 on NKT cells. Specifically, Webb et al. teaches to stimulate NKT cells using either irradiated PBMCs pulsed with a-GalCer or beads or nanoparticles coated with CD1d-IG and anti-CD28, molecules that bind the TCR and CD28 on NKT cells, and loaded with a-GalCer wherein the NKT cells are then expanded following stimulation (Webb et al., pages 4, 6-8, 19-20, and ). Webb et al. further teaches that CD62L is present on at least 20% of CD4+ human Type I CD1d V24+ NKT cells (Webb et al., page 13, Table I). Specifically, Webb et al. teaches isolation of NKT cells from human PBMC, and stimulation and expansion of the isolated NKT cells in the presence of alphaGalCer loaded APCs/aAPCs and hIL-2 for at least 14-28 days, where the IL-2 is present at a concentration of 100 U/ml (Webb et al., pages 19-20). Webb et al. teaches that after two rounds of expansion in the presence of alphaGalCer and IL-2 it was possible to obtain greater than 1X10-7 Type I NKT cells and up to at least 5X10-8 Type I NKT cells (Webb et al., page 20, Table I). According to applicant’s specification, Figure 1A, human PBMC derived NKT cells stimulated and cultured under the same conditions as taught by Webb et al. generated an NKT cell composition comprising 64.5% CD62L+ V24+ NKT cells. Thus, by stimulating NKT cells derived from human PBMC with alphaGalCer and IL-2 for 14-21 days, Webb et al. inherently produced a composition of isolated CD62L+ NKT cells, alphaGalCer, and IL-2 as claimed.
Applicant is reminded that "[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art's functioning, does not render the old composition patentably new to the discoverer." Atlas Powder Co. v. Ireco Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977). >In In re Crish, 393 F.3d 1253, 1258, 73 USPQ2d 1364, 1368 (Fed. Cir. 2004).
The applicant is further reminded that there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the time of invention, but only that the subject matter is in fact inherent in the prior art reference. Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003)
Thus, by teaching a composition that includes all the limitations of the claims as written, Webb et al. anticipates the instant invention as claimed.
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.
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.
Claims 1-36, 38-40, and 44-46 are rejected under 35 U.S.C. 103 as being unpatentable over WO 2015/051247 (April 9, 2015), hereafter referred to as Webb et al., in view of Heczey et al. (2014) Blood, Vol. 124(18), 2824-2833.
Webb et al. teaches methods of isolating, stimulating, and expanding Type I NKT cells using ligands for the TCR complex and CD28 on NKT cells. Specifically, Webb et al. teaches to stimulate Type I NKT cells using artificial antigen presenting cells (aAPC) comprising beads or nanoparticles coated with CD1d-IG and anti-CD28, molecules that are recognized by TCR and CD28 on NKT cells respectively, and pulsed with alpha-GalCer, in the presence of hIL-2, wherein the NKT cells expand following stimulation (Webb et al., pages 6-8, and 11-13). In particular, Webb et al. teaches that the IL-2 is present at a concentration of 100U/ml (Webb et al., page 19). Webb et al. further teaches that the ex vivo expanded stimulated Type I NKT cells can be administered to patient for immunotherapy of cancer, such as treatment of a tumor or metastatic tumors (Webb et al., pages 8 and 10). Webb et al. further teaches that CD62L is present on at least 20% of CD4+ human Type I CD1d V24+ NKT cells (Webb et al., page 13, Table I). It is also noted that Webb et al. teaches to stimulate and expand Type I NKT cells which express CD62L (Webb et al., pages 13-14). In addition, Webb et al. teaches gene transfer of tumor specific TCR genes or chimeric antigen receptors to the NKT cells (Webb et al., page 14).
While Webb et al. teaches to genetically modify the NKT cells to express a chimeric antigen receptor (CAR), Webb et al. does not specific any particular CAR. Heczey et al. supplements Webb et al. by demonstrating that Type I NKT cells are a safe and effective platform for CAR-directed cancer immunotherapy (Heczey et al., page 2824). Specifically, Heczey et al. teaches the introduction of a retrovirus encoding a CAR specific for GD2 into expanded Type I NKT cells, followed by their administration to mice bearing tumors resulting in prolonged survival of the tumor bearing mice without inducing GVHD (Heczey et al. 2825-26 and 2830). Therefore, in view of the motivation to administer stimulated and expanded Type I NKT cells, particularly T cells expressing CD62L, to subjects in order to treat disease such as cancer provided by Webb et al., and further the motivation to genetically modify the NKT cells to express a tumor specific TCR or CAR and to use these cells for adoptive immunotherapy of cancer provided by both Webb et al. and Heczey et al., it would have been prima facie obvious to the skilled artisan at the time of filing to provide a stimulated population of NKT cells comprising CD62L NKT cells for use in the methods of adoptive immunotherapy taught by both Webb et al. and Heczey et al. in which the NKT cells are genetically modified to express a tumor specific TCR or CAR specific for GD2 with a reasonable expectation of success.
Claims 30-35, 37-40, and 43-46 are rejected under 35 U.S.C. 103 as being unpatentable over Rogers et al. (2004) J. Immunol. Methods, Vol. 285, 197-214, in view of WO 2015/051247 (April 9, 2015), hereafter referred to as Webb et al.
Rogers et al. teaches the activation and expansion of human NKT cells isolated from human PBMCs, where the human NKT cells are isolated by MACs columns using biotinylated anti-Va24 antibody and streptavidin microbeads, or by FACs sorting with antibodies to human Va24, and where the expansion comprises culture of the human NKT cells with autologous irradiated PBMC pulsed with a-GalCer (referred to as KRN7000 by Rogers) and either IL-2, IL-2 and IL-7, IL-2 and IL-15, IL-2 and IL-7 and IL-15, IL-7, IL-15, or IL-7 and IL-15, and wherein the expansion of the human NKT cells is greater than 2 fold in the presence of each of the cytokine or cytokine combinations (Rogers et al., pages 198-200, 202, and Figure 1). In particular, Rogers et al. teaches that the APCs are pulsed with a-GalCer by adding a-GalCer to the culture at a concentration of 100 ng/ml (Rogers et al., pages 199-200). Rogers et al. further teaches to add IL-2 at a concentration of between 10-90 ng/ml (Rogers et al., page 200). Note that 10-90 ng/ml encompasses concentrations of 100U/ml or 200 U/ml as 100U/ml of IL-2 corresponds approximately to 20-30 ng/ml.
Webb et al. supplements Rogers et al. by teaching methods of stimulating and expanding human NKT cells ex vivo comprising contacting isolated NKT cells from human peripheral blood with either irradiated PBMCs pulsed with a-GalCer or artificial antigen presenting cells coated with CDld-IG and anti-CD28 (aAPCs), and further loaded with a-GalCer, in the presence of IL-2, (Webb et al., pages 4, 6-8, and 19-20, and Figure 9). Webb et al. teaches that the NKT cells are isolated using magnetic beads and further that the NKT cells undergo at least two rounds of expansion (Webb et al., pages 19-20). Webb et al. also teaches that additional cytokines can be added to cultures of NKT cells and aAPCs in order to modulate NKT cell function and Th1 and/or Th2 polarization (Webb et al., page 32). Webb et al. further teaches that the ex vivo expanded stimulated NKT cells can be administered to a patient for immunotherapy of cancer, such as treatment of a tumor or metastatic tumors (Webb et al., pages 8 and 10). It is further noted that Webb et al. teaches to stimulate and expand NKT cells which express CD62L (Webb et al., pages 13-14). In addition, Webb et al. teaches gene transfer of tumor specific TCR genes or chimeric antigen receptors (CARs) to the NKT cells (Webb et al., page 14). Thus, in view of the teachings and motivation provided by both Roger et al. and Webb et al. for expanding human NKT cells in culture using either autologous PBMC pulsed with a-GalCer or artificial APCs pulsed with a-GalCer and cytokines such as IL-2, IL-7, or IL-15 or combinations thereof, and the teachings of Webb et al. to stimulate and expand CD62L NKT cells and to further genetically modify the NKT cells to express tumor specific TCR genes or CARs, it would have been prima facie obvious to the skilled artisan at the time of filing to use either autologous irradiated PBMC pulsed with a-GalCer or artificial APCs pulsed with a-GalCer in combination with one or more cytokines, especially, IL-2, IL-7, or IL-15, to expand human NKT cells comprising CD62L NKT cells in culture by at least two fold with a reasonable expectation of success. In particular, Webb et al. teaches to culture the NKT cells in the presence of a-GalCer pulsed APC in the presence of 100 U/ml IL-2 (Webb et al., page 19).
Therefore, in view of the teachings of both Rogers et al. and Webb et al. to activate and expand human NKT cells by combining the NKT cells, APCs or aAPCs, a-GalCer, and IL-2 in culture, the teachings of Rogers et al. to use 100ng/ml a-GalCer, the teachings of Webb et al. to use 100 U/ml hIL-2, the teachings of both Rogers et al. and Webb et al. to add a second cytokine to the culture such as IL-7 or IL-15, and the teachings of Webb et al. that NKT cells are naturally approximately 20% positive for CD62L expression, it would have been prima facie obvious to the skilled artisan at the time of filing to combine in a culture a composition comprising isolated CD62L+ NKT cells, an aAPC or APC, 100 ng/ml a-GalCer, 100 U/ml, and a second cytokine such as IL-7 or IL-15 with a reasonable expectation of success.
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 USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The 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/process/file/efs/guidance/eTD-info-I.jsp.
Claims 30-46 are rejected on the ground of nonstatutory double patenting as being unpatentable over 1) claims 1-35 of U.S. Patent No. 11,458,168, hereafter referred to as the ‘168 patent, OR 2) claims 1-31 of U.S. Patent No. 12,048,716, hereafter referred to as the ‘716 patent. Although the claims at issue are not identical, they are not patentably distinct from each other for the following reasons. While the ‘168 patent claims and the ‘716 patent claims each recite method claims, not product claims, both the ‘168 patent claims and the ‘716 patent claims each individually recite methods of preparing NKT cells for immunotherapy where the recited method steps utilize a culture composition comprising CD62L+ NKT cells, IL-2, APCs, or aAPCs, and aGalCer- see claim 1 of each patent. The dependent claims of the ‘168 and ‘716 patents each individually recite all the limitations of the components present in the culture as recited in instant claims 31-46. Thus, each of the ‘168 and ‘716 patent claims, by reciting a culture step comprising all of the components recited in the instant claims, individually render obvious the instant composition claims.
Claims 30-46 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-28 in U.S. Patent No. 11,266,689, hereafter referred to as the ‘689 patent, in view of WO 2015/051247 (April 9, 2015), hereafter referred to as Webb et al.
The ‘689 patent claims are drawn to a pharmaceutical composition comprising a CD62L-positive Type I human NKT cells comprising at least one chimeric antigen receptor (CAR) expression construct. While the ‘689 patent claims broadly encompass the additional elements recited in the instant claimed composition, such as IL-2, aGalCer, and an APC or aAPC, the ‘689 patent claims do not specifically recite these additional elements. However, it is noted that the specification of the ‘689 patent and the instant specification are identical and fully disclose that the composition comprising the CD62L-positive Type I human NKT cells comprising at least one chimeric antigen receptor (CAR) expression construct are stimulated and expanded in the presence of IL-2, aGalCer and the various APCs and aAPCs recited in the instant claims. The MPEP 804(II)(2)(a) sets forth instances where it is acceptable to utilize the disclosure of a U.S. patent document in conjunction with its claims for obvious-type double patenting rejections. In particular, the MPEP notes that the portion of the specification that supports the patent claims may be considered. See In AbbVie Inc. v. Kennedy Institute of Rheumatology Trust, 764 F.3d 1366, 112 USPQ2d 1001 (Fed. Cir. 2014). The court explained that it is also proper to look at the disclosed utility in the reference disclosure to determine the overall question of obviousness in a nonstatutory double patenting context. See Pfizer, Inc. v. Teva Pharm. USA, Inc., 518 F.3d 1353, 86 USPQ2d 1001 (Fed. Cir. 2008); Geneva Pharmaceuticals Inc. v. GlaxoSmithKline PLC, 349 F3d 1373, 1385-86, 68 USPQ2d 1865, 1875 (Fed. Cir. 2003). In particular, those portions of the specification which provide support for the reference claims may be examined and considered when addressing the issue of whether a claim in the application defines an obvious variation of an invention claimed in the reference patent or application (as distinguished from an obvious variation of the subject matter disclosed in the reference patent or application). In re Vogel, 422 F.2d 438, 441-42, 164 USPQ 619, 622 (CCPA 1970). The court in Vogel recognized “that it is most difficult, if not meaningless, to try to say what is or is not an obvious variation of a claim,” but that one can judge whether or not the invention claimed in an application is an obvious variation of an embodiment disclosed in the patent or application which provides support for the claim. According to the court, one must first “determine how much of the patent disclosure pertains to the invention claimed in the patent” because only “[t]his portion of the specification supports the patent claims and may be considered.” The court pointed out that “this use of the disclosure is not in contravention of the cases forbidding its use as prior art, nor is it applying the patent as a reference under 35 U.S.C. 103, since only the disclosure of the invention claimed in the patent may be examined.” In AbbVie Inc. v. Kennedy Institute of Rheumatology Trust, 764 F.3d 1366, 112 USPQ2d 1001 (Fed. Cir. 2014). The MPEP gives the example that if the reference patent discloses several species within the scope of the reference genus claim, that portion of the disclosure should be analyzed to properly construe the reference patent claim and determine whether it anticipates or renders obvious the claim in the application being examined. Because that portion of the disclosure of the reference patent is an embodiment of the reference patent claim, it may be helpful in determining the full scope and obvious variations of the reference patent claim. Thus, based on the portions of the specification that describe compositions of CD62L-positive Type I human NKT cells, the further presence of IL-2, APCs or aAPCs, and aGalCer in the composition of CD62L-positive Type I human NKT cells represents and obvious variant of the ‘689 patent claims.
In addition, or alternatively, the inclusion of these elements in a composition of CD62L-positive Type I human NKT cells was further taught in the prior art. Webb et al. supplements Rogers et al. by teaching methods of stimulating and expanding human NKT cells ex vivo comprising contacting isolated NKT cells from human peripheral blood with either irradiated PBMCs pulsed with a-GalCer or artificial antigen presenting cells coated with CDld-IG and anti-CD28 (aAPCs), and further loaded with a-GalCer, in the presence of IL-2, (Webb et al., pages 4, 6-8, and 19-20, and Figure 9). Webb et al. teaches that the NKT cells are isolated using magnetic beads and further that the NKT cells undergo at least two rounds of expansion (Webb et al., pages 19-20). Webb et al. also teaches that additional cytokines can be added to cultures of NKT cells and aAPCs in order to modulate NKT cell function and Th1 and/or Th2 polarization (Webb et al., page 32). Webb et al. further teaches that the ex vivo expanded stimulated NKT cells can be administered to a patient for immunotherapy of cancer, such as treatment of a tumor or metastatic tumors (Webb et al., pages 8 and 10). It is further noted that Webb et al. teaches to stimulate and expand NKT cells which express CD62L (Webb et al., pages 13-14). In addition, Webb et al. teaches gene transfer of tumor specific TCR genes or chimeric antigen receptors (CARs) to the NKT cells (Webb et al., page 14). Thus, based on the teachings of Webb concerning the culture and expansion of NKT cells in the presence of at least IL-2 and aGalCer, it would have been obvious to the skilled artisan at the time of filing to include these components in the compositions set forth in the ‘689 patent claims with a reasonable expectation of success.
No claims are allowed.
Any inquiry concerning this communication from the examiner should be directed to Anne Marie S. Wehbé, Ph.D., whose telephone number is (571) 272-0737. If the examiner is not available, the examiner’s supervisor, Maria Leavitt, can be reached at (571) 272-1085. For all official communications, the technology center fax number is (571) 273-8300. Please note that all official communications and responses sent by fax must be directed to the technology center fax number. For informal, non-official communications only, the examiner’s direct fax number is (571) 273-0737. For any inquiry of a general nature, please call (571) 272-0547.
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Dr. A.M.S. Wehbé
/ANNE MARIE S WEHBE/Primary Examiner, Art Unit 1634
Prosecution Insights