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 .
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.
DETAILED ACTION
Election/Restrictions
Applicant’s election of Group I (method of treating cancer) and the species of polynucleotide, combination CXCL9/CXCL10, vector introduced into dendritic cell, lentiviral vector, PD-1 inhibitor, pembrolizumab, and autologous in the reply filed on 7/28/25 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)).
Note that Applicant elected “polynucleotide” and not “a cell comprising the polynucleotide” for the first species. Applicant then elected “vector is introduced into a dendritic cell which is then administered”, which is a cell comprising the polynucleotide. As such, examination of the claims has covered the polynucleotide comprised in a cell, which meets the limitations of the instant claims and appears consonant with the election.
Further, the examination of the combination therapy necessarily includes examination of the individual elements. As such, the species election between CXCL9, CXCL10, or both is withdrawn.
Claims 1-6, 8-11, 14, 17-18, 23-24, 32-33, 41, are 62 are pending.
Claim 62 is withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Claims 4, 6, 8, 11, are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected species, there being no allowable generic or linking claim.
Election was made without traverse in the reply filed on 7/28/25.
Claims 1-3, 5, 9-10, 14, 17-18, 23-24, 32-33, and 41 are under examination.
Specification
The use of several trademarks/tradenames has been noted in this application. The terms should be accompanied by the generic terminology; furthermore the term should be capitalized wherever it appears or, where appropriate, include a proper symbol indicating use in commerce such as ™, SM , or ® following the term.
Although the use of trade names and marks used in commerce (i.e., trademarks, service marks, certification marks, and collective marks) are permissible in patent applications, the proprietary nature of the marks should be respected and every effort made to prevent their use in any manner which might adversely affect their validity as commercial marks.
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 24, 32, 33, and 41 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.
The terms “high” and “low” in claims 24 and 33 are relative terms which renders the claim indefinite. The terms are not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention.
Claims 24 and 33 are methods limited to a population that has either a high or low mutational burden tumor. Further, this burden is “used” to initiate, prescribe, and monitor “therapy” in claims 32 and 41.
MPEP § 2173.02 (II) states that one of the purposes of examination under 35 USC § 112, second paragraph is to determine whether the claim apprises one of ordinary skill in the art of its scope and, therefore, serves the notice function required by 35 U.S.C. 112, second paragraph, by providing clear warning to others as to what constitutes infringement of the patent. See, e.g., Solomon v. Kimberly-Clark Corp., 216 F.3d 1372, 1379, 55 USPQ2d 1279, 1283 (Fed. Cir. 2000). See also In re Larsen, No. 01-1092 (Fed. Cir. May 9, 2001) (unpublished). If the language of the claim is such that a person of ordinary skill in the art could not interpret the metes and bounds of the claim so as to understand how to avoid infringement, a rejection of the claim under 35 U.S.C. 112, second paragraph, would be appropriate. See Morton Int’l, Inc. v. Cardinal Chem. Co., 5 F.3d 1464, 1470, 28 USPQ2d 1190, 1195 (Fed. Cir. 1993). In this case, others must have fair warning as to the mutational burden a tumor must possess that defines “high” vs. “low” in order to determine both which subjects are within the scope of claims 24 and 33 as well as how these numbers are meant to be used in claims 32 and 41.
The specification uses the terms several times but these terms are never associated with any values or criteria for determining high vs low mutation burden tumor. For example, paragraph 93 notes how the burden might be determined but does not provide an example of a value for that burden. In contrast, Chabanon teaches there is no clear threshold for “high” or “low” and in many cases there is overlap between the terms when addressing immunotherapy (p.4311 C2). Thus, the scope of these terms is unclear and indefinite.
Further, claims 32 and 41 provides for the use of the mutational load (potentially of the tumor; see below) but since the claim does not set forth any steps involved in the method/process, it is unclear what method/process applicant is intending to encompass. There are no steps or other criteria claimed for how this information is meant to be “used” and a claim is indefinite where it merely recites a use without any active, positive steps delimiting how this use is actually practiced; see MPEP §2173.05(q).
Finally, claims 32 and 41 recite “the somatic mutational load and tumor-associated neoantigens”. There is insufficient antecedent basis for these phrases. The claims from which these claims depend (24 and 33, respectively) recite “a…mutational burden tumor”, i.e., a tumor with a high/low mutational burden. However, claims 32 and 41 refer to “the somatic mutational load”. A mutational burden tumor necessarily has a mutational load; however, this is not set forth clearly as a somatic mutational load in claims 24 and 33. Further, the use of “load” rather than “burden” creates additional confusion as to whether or not “the somatic mutational load” is meant to refer to “a mutational burden”. Moreover, there is no previous recitation of “tumor-associated neoantigens” and so the phrase lacks clear antecedent basis for this phrase.
Therefore, claims 24, 32, 33, and 41 are indefinite.
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.
Claims 32 and 41 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
In the alternative, claims 32 and 41 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for initiating, prescribing, and monitoring cancer therapy, does not reasonably provide enablement for any and all possible therapies as claimed. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
Note that this rejection sets forth both an enablement and scope of enablement rejection. Given the indefiniteness of “use” in the claims (see above), both analyses are set forth below to support compact prosecution.
There are many factors considered when determining if the disclosure satisfies the enablement requirement and whether any necessary experimentation is undue. These factors include, but are not limited to: 1) nature of the invention, 2) breadth of claims, 3) amount of direction or guidance by the inventor, 4) relative skill of those in the art, 5) level of predictability in the art, 6) state of the prior art, 7) existence of working examples, and 8) quantity of the experimentation needed to make or use the invention. In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988).
Regarding the scope of enablement rejection:
The nature of the invention is using a mutational load and neoepitopes in a tumor to make decisions regarding therapy. As claimed, this is any therapy because the specification provides a definition of therapy on p.10: “therapeutic treatment, including prophylactic or preventative measures, wherein the object is to prevent or slow down (lessen) an undesired physiological change associated with a disease or condition”. Since this explicit definition is “a disease or condition”, it is clear that the term “therapy” includes all diseases or conditions and not just those disclosed by the specification. However, even when looking to the specification for examples of this phrase, many different potential therapies are disclosed: cancer therapy, chemo-immunotherapy, PD1/PDL1 immunotherapy, TK1 therapy, checkpoint inhibitor therapy, CXCL9/10 therapy, cell-based therapy, etc.
In contrast, the specification provides examples of cancers. The specification does not provide any guidance as to how mutation burden in a tumor is meant to inform non-tumor therapy decisions. It is left to others to determine if and how this information might be “used” to initiate or monitor non-cancer therapies. This would require undue experimentation because it would require testing all potential therapies to determine their relevance to tumor mutational burden with no expectation that there is any particular correlation.
Regarding the enablement rejection:
Even limited to cancer therapies such as chemotherapy, the specification lacks clear guidance as to how the mutational load and tumor neoantigens are meant to be “used” to arrive at the claimed decisions. The only use of the term “initiate” is in paragraphs 94 and 97 and only in the same context and with the same specificity as the claim. These paragraphs do not provide any information on how the mutational load is meant to arrive at any particular decision regarding therapy nor is there any guidance as to the difference between how a high or low mutational load may be “used”. Other than indicating neoantigens might be determined, there is also no guidance in the specification as to how such tumor-associated neoantigens are used to make therapy decisions. It is left to others to determine for themselves the importance of these levels and how these levels relate to different therapies, such as chemotherapy, cell-based therapy, or checkpoint therapy. Additionally, therapies such as chemotherapy and checkpoint therapy are not expected to alter the number of somatic mutations and the specification lacks guidance as to how to use these levels to, e.g., monitor these therapies.
The standard of an enabling disclosure is not the ability to make and test if the invention worked but one of the ability to make and use with a reasonable expectation of success.
"[T]o be enabling, the specification, must teach those skilled in the art how to make and use the full scope of the claimed invention without 'undue experimentation.'" Wright, 999 F.2d at 1561, 27 USPQ2d at 1513 (emphasis added), quoted in Genentech, Inc. v. Novo Nordisk, A/S, 108 F.3d 1361, 1365, 42 USPQ2d 1001, 1004 (Fed. Cir. 1997). Thus, "there must be sufficient disclosure, either through illustrative examples or terminology, to teach those of ordinary skill how to make and how to use the invention as broadly as it is claimed." In re Vaeck, 947 F.2d 488, 496 & n. 23, 20 USPQ2d 1438, 1445 & n. 23 (Fed. Cir. 1991), quoted in Enzo Biochem, Inc. v. Calgene, lnc., 188 F.3d 1362, 1372, 52 USPQ2d 1129, 1138 (Fed. Cir. 1999).
"Patent protection is granted in return for an enabling disclosure..., not for vague intimations of general ideas that may or may not be workable." Genentech, 108 F.3d at 1365, 42 USPQ2d at 1005. "Tossing out the mere germ of an idea does not constitute enabling disclosure. While every aspect of a generic claim certainly need not have been carried out by an inventor, or exemplified in the specification, reasonable detail must be provided in order to enable members of the public [skilled in the art] to understand and carry out the invention." Id. at 1366, 42 USPQ2d at 1005 (emphasis added).
In this case, the specification provides no more than a vague indication that somatic mutations and tumor-neoepitopes may somehow be used to initiate, prescribe, or monitor some unclaimed therapy. Even considering only cancer therapies, this guidance does not amount to an enabling disclosure because how to use these values is left entirely to others with no reasonable predictability as to how therapy might be beneficially altered based on these values. In the claim, regardless of the mutational load, the subject is always administered a CXCL9 or CXCL10 peptide/nucleotide. Therefore, the specification lacks adequate guidance as to how the mutational load is meant to determine “initiating” or “prescribing” treatment as there does not appear to be any room in the claim to not initiate treatment, the treatment is claimed and so the information does not appear inform the prescription decision, nor is there guidance in the specification to suggest, e.g., that CXCL9 is initiated with high mutation and CXCL10 is initiated with low mutation or that there is variation within the claimed therapy that is based on the mutational load/neoepitopes. Moreover, the claim requires the mutational load and neoantigens “before, during, and after treatment” to make decisions on initiating or prescribing the therapy. One could not use information gained after the therapy has been initiated to make determinations regarding initiating or prescribing the therapy. Further, since the therapies do not alter the number of mutations, the specification lacks adequate guidance on how the mutational load is used to monitor therapy or what a high vs low mutational load means for such a decision.
The art does not provide what the specification lacks. Rather, the art establishes that even after the instant effective filing date, tumor mutation load and neoantigens remain an unpredictable and unreliable marker for treatment decisions. Gurjaro (form 892) states “we find little evidence that [tumor mutation burden] is predictive of response to [immune checkpoint blockade]” and that “the use of TMB in clinical practice is not supported by available data and can deprive patients of treatments to which they are likely to respond”. McGrail (form 892) states that a high mutation burden fails to predict therapy response and that “our analysis failed to support application of [high tumor mutation burden] as a biomarker for treatment with ICB in all solid cancer types”, noting that the type of cancer also plays a significant and unpredictable role in how tumor mutation burden can be used to inform therapy decisions. Chabanon (form 892) teaches there is no clear threshold for “high” or “low” mutational burden and that subjects may respond to immune checkpoint therapy with either high or low mutational burden. Chabanon also states that “all formed neoantigens may not be immunologically relevant”, leaving the determination of which neoantigens are useful and how they might be used up to others with no reasonable predictability, which is undue experimentation.
Taking the evidence as a whole, every aspect of the “use” portion of the instant claims is left to others to determine how this information can be used to inform those decisions with no guidance in the specification regarding any of the specifics nor any predictability in the correlation between a high vs low burden, neoepitopes, prescription/initiation of CXCR therapy/other therapy, or monitoring of those therapies.
Therefore, claims 32 and 41 are not enabled.
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.
Claim(s) 1-3, 5, 9-10, 14, 17-18 and 23 are rejected under 35 U.S.C. 103 as being unpatentable over Spranger (form 892) in view of Beech (US20160089398; form 892) and further in view of Dubinett (US 20180194825; form 892).
Spranger teaches dendritic cells (DCs) produce CXCL9 and CXCL10 (abstract). Spranger also teaches that T cells are effective to recognize and kill cancer cells but that lack of both CXCL9 and CXCL10 leads to a failure to recruit effector T cells into tumors (abstract). Spranger concludes that the lack of DCs leads to immune escape of tumors. Spranger states that DCs—producing CXCL9 and CXCL10—are necessary for T cell recruitment to tumors and by extension necessary for the anti-cancer effectiveness of T cells (p.720 C2). Spranger also teaches that increased T cell infiltration correlates to checkpoint blockade immunotherapy (p.720 C2), where this increased infiltration is also correlated to the expression of CXCL9 and CXCL10 (p.720-721). Spranger does not teach genetically modifying DCs to express these polypeptides.
Given the importance of CXCL9 and CXCL10 in DCs to the effectiveness of treating cancer by DCs, one of ordinary skill in the art at the time of filing would have been motivated to genetically engineer DCs to promote expression of these important polypeptides. Beech teaches a method for genetically engineering cells to produce specific polypeptides. Beech teaches a vector which allows a cell to produce IL-12 and PD-L1 (claim 1). This lentiviral vector (claim 3) is introduced into a human dendritic cell (claims 8 and 9). These cells are administered to treat tumors (claim 22), IL-12 being known to contribute to the protective immune response, suppression of tumorigenesis (paragraph 6), and supportive activity on T cells (paragraph 7).
Thus, at the time of filing, it would have been obvious to substitute the IL-12 polynucleotide with a combination of CXCL9 and CXCL10 polynucleotides, which meets the limitations of a cell (dendritic cell) comprising CXCL9 and CXCL10 polynucleotides. Both IL-12 and CXCL9/10 are involved in anti-cancer therapy and support T cell anticancer effects. Further, one would choose dendritic cells because Spranger teaches the importance of CXCL9/10 to the effectiveness of this cell type. One would have had a reasonable expectation of success because dendritic cells are amenable to genetic inclusion of a polynucleotide vector which expresses an anticancer, T cell supporting polypeptide (Beech) and Spranger teaches the DCs express CXCL9/10, indicating that expression of these polypeptides by the cell would be expected to achieve similar results.
This combination does not explicitly suggest including an immune checkpoint inhibitor. Dubinett is also concerned with treating cancer (claim 1). Dubinett teaches administering a dendritic cell (claim 12) which comprises a vector (claims 11 and 8), wherein the vector comprises a polynucleotide encoding a tumor inhibitor (claim 1; abstract). Dubinett also teaches this dendritic cell is administered in combination with a checkpoint inhibitor (abstract; claim 1).
Thus, at the time of filing, it would have been obvious to include administration of a checkpoint inhibitor in the method of Spranger/Beech, arriving at the instant method of claim 1. Spranger/Beech makes obvious administering a dendritic cell encoding CXCL9/10 to treat cancer. Dubinett also administers vector-containing DCs to treat cancer and teaches they are effective when combined with a checkpoint inhibitor, suggesting the inclusion of said checkpoint inhibitor in the anti-cancer treatment. Further, Spranger notes that the T cell activation—supported by the DCs as described above—is correlated to checkpoint blockade effectiveness (see above), providing further motivation to include such treatment. The combination of these references would have made instant claim 1 obvious at the time of filing.
Regarding claims 2, 3, and 5, Dubinett teaches the checkpoint inhibitor is Pembrolizumab (claim 5; paragraph 22). Pembrolizumab is recited by instant claim 5, is a PD-1 inhibitor recited by instant claim 3 (see Dubinett paragraph 22), and is a monoclonal antibody recited by instant claim 2 (see Dubinett paragraph 145). As it would have been obvious to include a checkpoint inhibitor given the teachings above, including Dubinett, it would have been obvious to select an effective checkpoint inhibitor taught by Dubinett, including Pembrolizumab.
Regarding claim 9, introducing a polynucleotide encoding CXCL9/10 into a vector and in turn introducing that vector into a DC would have been obvious as above. Further, Dubinett teaches administration intratumorally (paragraphs 164, 173; claim 16). Beech also teaches intratumoral administration (claim 22; paragraph 9). It would have been obvious to select a route known in the art, such as the preferred intratumoral route of both Beech and Dubinett, which meets the limitations of “to the tumor site”. As the combination is an anti-cancer therapeutic, it would have further been obvious to administer it to the subject which has the tumor in order to treat the tumor, meeting the limitations of “to the subject”.
Regarding claim 10, Beech claims the polynucleotide introduced into a lentiviral vector (claim 3), rendering such a choice obvious.
Regarding claim 14, Beech teaches the dendritic cells may be autologous (paragraph 455) as does Dubinett (claim 13), making the choice of autologous DCs obvious.
Regarding claim 17, intratumoral administration is addressed above. Further, Beech teaches the method as applied to treat a solid tumor (paragraph 545) as does Dubinett (paragraph 16).
Regarding claim 18, Dubinett teaches the combination cancer treatment is effective to treat NSCLC (paragraph 30), rending it obvious to administer the known effective checkpoint inhibitor in combination with the dendritic cell (Dubinett) enhanced with the CXCL9/10 vector with a reasonable expectation of success as this treatment is taught as effective and the genetic modification is expected to increase the efficacy of the cells for reasons above. Beech also teaches the treatment for NSCLC (paragraph 454).
Regarding claim 23, administration intratumorally is addressed above. Further, Dubinett, which teaches the combination of DC and checkpoint inhibitor therapy, teaches specifically the cells (DCs) are administered intratumorally (claim 16). Dubinett exemplifies one method of administration where the checkpoint inhibitor is administered intravenously while the cells are administered intratumorally (paragraph 174). This would have made obvious such dosing routes at the time of filing.
Therefore, claims 1-3, 5, 9-10, 14, 17-18 and 23 would have been obvious.
Claim(s) 24, 32-33, and 41 is/are rejected under 35 U.S.C. 103 as being unpatentable over Spranger/Beech/Dubinett as applied to claims 1-3, 5, 9-10, 14, 17-18 and 23 above, and further in view of Chabanon (form 892).
The discussion of Spranger/Beech/Dubinett is set forth above and incorporated herein. This combination does not explicitly describe the subjects as having either a high or low mutational burden nor does the combination address “using” this information to make decisions on treatment.
Chabanon teaches that immune checkpoint therapy is not a universal treatment (abstract). Chabanon suggests using “mutational load and neoantigens” for clinical implementation (abstract). Chabanon teaches there is no clear threshold for “high” or “low” and that subjects with both high mutational burden as well as nearly no burden at all may still respond to immune checkpoint treatment (p.4311 C2). Chabanon also teaches tumor-specific antigens (i.e., neoantigens) generally associate with clinical efficacy of immune blockade (p.4311 C2).
Regarding claims 24 and 33, at the time of filing, it would have been obvious to administer the cancer treatment of Spranger/Beech/Dubinett to subjects with both high or low mutational burden because Chabanon teaches that mutational burden is not indicative of the efficacy of immune checkpoint inhibitors nor does Chabanon provide any reasoning why these would be indicative of treatment with the DCs. Thus, one of ordinary skill in the art would be motivated to administer this therapy to both populations as the DC treatment would have had a reasonable expectation of success and the art teaches the DCs improve the efficacy of checkpoint inhibitors, so would have included such treatment.
Regarding claims 32 and 41, Chabanon “uses” mutational load and neoantigens to demonstrate that neoantigens in particular are broadly correlated with clinical efficacy of immune checkpoint inhibitors. While Chabanon does not teach any specific neoantigen is useful, the overall correlation provides a reasonable expectation that those with increased neoantigens will correlate to increased antitumor T cell activation (such as that caused by the administration of the DCs above) and increased immune checkpoint efficacy, such as by pembrolizumab above. Given the breadth of “used”, the Examiner believes these teachings meet the limitations set forth in claims 32 and 41, rendering these claims obvious.
Therefore, claims 24, 32-33, and 41 would have been obvious.
Conclusion
It is noted that the inventors/applicants have numerous patents and patent applications, many of which are in the same inventive area, e.g., cancer treatment, CXCL9/10, etc. However, no patent or co-pending application appears to be patentably indistinct from the instant claims. For example, 18/872496 is a corona virus vaccine, not a cancer treatment. 18/867634 observes levels of CXCL9 and CXCL10 but does not administer those proteins. 18/848224 is a method of treating wounds, not cancer. 18/264314 administers PD-1 immunotherapy but only observes the effects on CXCL9/10 expression and does not administer them. In reviewing the patents and co-pending applications, there does not appear to be a double patenting rejection warranted at this time.
A §101 rejection was considered for claims 32 and 41. However, while a natural correlation is implied, a proper §101 rejection requires the claim actually set forth the correlation (“drawn to”). The claims merely assert that some information is used in some unclaimed way to make a decision; there is no requirement that the biomarkers are in any way correlated to that decision as noted in the enablement rejection as that information could still be “used”. As set forth above, it is not clear that there is even a natural correlation and unless the claims set forth such, a §101 rejection would not be proper.
The prior art made of record and not relied upon is considered pertinent to applicant's disclosure:
Krathwohl (IDS 1/28/22 citation 1) teaches CXCL10 (also known as IP-10), which is a CXCR3-binding chemokine, administered to elicit a protective immune response (abstract). CXCL10 promoted the maturation of dendritic cells (DCs), which in turn enabled DCs to form conjugates with T cells and stimulate T-cell proliferation and that overall survival of DCs is improved with CXCL10 administration (paragraph 26).
Li (IDS 8/9/23 citation 2) also teaches a dendritic cell genetically modified with a CXCL10 vector.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ADAM M WEIDNER whose telephone number is (571)272-3045. The examiner can normally be reached M-T 9-18; W-R 9-15.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Jeffrey Stucker can be reached at 571-272-0911. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/Adam Weidner/ Primary Examiner, Art Unit 1675