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 .
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 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.
Priority
The instant application, filed 12/22/2022, is a continuation of US application 16/633,132, filed 01/22/2020, which is a 371 filing of PCT/EP2018/070856, filed 08/01/2018, and claims foreign priority to EP17184277.6, filed 08/01/2017.
Status of Application, Amendments, and/or Claims
Applicant’s response of 10/06/2025 is acknowledged. No claims are amended, cancelled or new.
Claims 106-119 and 122-125 are currently pending and are examined on the merits herein.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 10/06/2025 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement has been considered by the examiner.
The following rejections are maintained.
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 106-109, 112, 115-116, 119, and 122-125 are rejected under 35 U.S.C. 103 as being unpatentable over Weisberg, E. et al (2011) Reversible resistance induced by FLT3 inhibition: A novel Resistance Mechanism in mutant FLT3-expressing cells PLos ONE 6(9) e25351; 1-12 in view of WO 2017/053889 A2 (Devine, S., et al) 30 March 2017 and WO 2015/142675 A2 (Loew, A., et al) 24 SEPT 2015.
Weisberg teaches that over-expression of FLT3 protein in response to kinase inhibitors may be part of a novel mechanism that could contribute to clinical resistance (abstract, Results and Conclusions). Weisberg teaches that a constitutively activated, mutated version of the class III receptor tyrosine kinase, FLT3, is expressed in approximately 30% of acute myeloid leukemia (AML) patients and a subset of ALL patients. The most prevalent form of mutant FLT3, present in approximately 20-25% of AML patients occurs as internal tandem duplications (ITD) within the juxtamembrane domain (page 1, left column, paragraph 1). Thus, mutant FLT3 represents an attractive target for the therapy of AML. Several FLT3 inhibitors, including the N-indolocarbazole PKC412, also known as midostaurin, have shown sufficient efficacy and safety profiles to warrant further studies in combination with standard therapies in advanced clinical trials. However, inhibitors of FLT3 have generally elicited partial and transient clinical responses in early trials. The observed suboptimal clinical responses, coupled with detection of drug-resistant leukemic blast cells in FLT3 inhibitor-treated AML patients, have made understanding clinical resistance to FLT3 inhibitors a priority (page 1, right column, paragraph 1).
Weisberg teaches that in a phase II trial of the FLT3 inhibitor lestaurtinib (CEP701) in patients with both mutated and wild-type FLT3-expressing AML, most of the patients in which blast surface FLT3 expression was able to be measured showed an elevation in blast surface FLT3 expression while treatment with lestaurtinib ensued. Authors of the study speculated that this up-regulation of FLT3 receptor expression might have contributed to the limited clinical benefit and, therefore, might represent a potential mechanism of resistance (page 2, left column, paragraph 1).
Weisberg used two structurally distinct FLT3 kinase inhibitors, PKC412 and the novel type II ATP competitive inhibitor HG-7-85-01, to generate resistant cell lines using the human AML cell line MOLM-13 which expresses FLT3-ITD. The cell lines obtained were cross-resistant and, in both cases, resistance was associated with a striking over-expression of the mutant FLT receptor, a finding reflective of the previously observed up-regulation of surface FLT3 receptor expression in FLT3 inhibitor-treated patients (page 2, left column, paragraph 3; page 2, left column, paragraph 5). Weisberg found that MOLM13 cells readily developed cross-resistance when exposed to either midostaurin or HG-7-85-01 and resistance in both lines was associated with dramatically elevated levels of cell surface FLT3. The increase in FLT3-ITD expression was at least in part due to reduced turnover of the receptor with prolonged half-life. Importantly, the drug-resistant phenotype could be rapidly reversed upon withdrawal of either inhibitor (abstract, results and conclusions). Weisberg teaches that the findings suggest that there may be benefit to the use of combination therapy as a way to enhance the efficacy of FLT3 inhibitors and override drug resistance. The data presented points towards the potential use of FLT3 antibodies or other FLT3 target-specific therapies as a way to override drug-resistance (page 9, right column, paragraph 3).
The teachings of Weisberg differ from the instantly claimed invention in that Weisberg does not disclose that the FLT3 target-specific therapy is an immune cell expressing a CAR that binds to the extracellular domain of FLT3 or that the kinase inhibitor is administered at least once or multiple times concurrently with or at least once or multiple times after the FLT3 targeting CAR.
WO’889 teaches that despite a broad understanding of the molecular and genetic complexities of AML, only allogeneic hematopoietic stem cell transplant (HSCT) provides significant improvements in the clinical outcome of patients. However, elderly patients may not be eligible for HSCT and this approach is also associated with complications that can result in significant morbidity and mortality, such as GVHD. Moreover, patients with a FLT3 internal tandem duplication (ITD) mutation have an especially adverse prognosis and high probability of relapse (pages 1-2, [0005]).
WO’889 teaches that CAR engineered T cells graft the specificity of the monoclonal antibody with specific antitumor activity of cytotoxic T lymphocytes (CTL) to acquire the activity of recognizing tumor surfaced antigen and killing specific malignant tumors once the genetically modified T cell is activated. WO’889 teaches that FLT3 is a highly expressed surface protein in leukemia, especially in AML (page 2, [0007]). WO’889 discloses a CAR comprising the antigen binding domain of a FLT3 antibody that binds FLT3 (page 4, [0011]; page 38, [0129]). As WO’889 teaches that the antibody in CARs recognize tumor surface antigens and that the antibody binds FLT3, an ordinarily skilled artisan would reasonably envision that the CAR binds to the extracellular domain of FLT3 which is the part of the antigen that is exposed on the surface of the tumor cells.
WO’889 further teaches compositions comprising the CAR T cells (page 6, [0025]). WO’889 teaches that a “composition” intends a combination of the active agent and carriers as well as adjuvants (page 20, [0073]).
WO’889 studied the use of the FLT3-specific T cells to kill primary AML cells in studies using the MOLM-13 cell line and teaches that the FLT3 CAR T cells robustly lysed the MOLM-13 cells tested (page 69, [0229]; Figure 3).
WO’675 teaches compositions and methods for treating diseases associated with expression of cancer associated antigens including the administration of genetically modified T cells that express a CAR (abstract). WO’675 teaches immune effector cells, such as T cells or NK cells, that are engineered to express a FLT3 CAR for the treatment of cancer cells that express FLT3, such as AML (page 183, [00720]). WO’675 further teaches that in some embodiments, the CAR is administered in combination with an agent that increases the efficacy of the immune effector cell, for example a kinase inhibitor (page 20, [0070]). A CAR-expressing cell and the at least one additional therapeutic agent can be administered simultaneously, in the same or separate compositions, or sequentially. For sequential administration, the CAR-expressing cell can be administered first, and the additional agent can be administered second, or the order of administration can be reversed (pages 206-207, [00869]).
It would have been prima facie obvious to one of ordinary skill in the art prior to the effective filing date of the claimed invention to have modified the method disclosed by Weisberg to use the FLT3 targeting CAR T cells of WO’889 as the FLT3 target-specific therapy for use in combination with a FLT3 kinase inhibitor that increases FLT3 expression. It would have further been obvious to administer the kinase inhibitor in the same or separate compositions and sequentially with either the CAR expressing cell before or after the kinase inhibitor as disclosed by WO’675. An ordinarily skilled artisan would have been motivated to use the FLT3 targeting CAR T cells of WO’889 as WO’889 demonstrates that FLT3 CAR T cells are able to robustly lyse AML cells by combining the specificity of an antibody with the antitumor activity of a T cell. An ordinarily skilled artisan would have had a reasonable expectation of success as Weisberg demonstrates that FLT3 TKIs increase the surface expression of FLT3 on FLT3-ITD AML cells and, based on this increased expression, suggests the use of FLT3 targeting agents, agents which encompass the FLT3 targeting CAR of WO’889. Additionally, WO’889 demonstrates that the FLT3 targeting CAR T cells were able to robustly lyse the MOLM-13 AML cell line, which is one of the same cell line used in the studies performed by Weisberg.
It would have been obvious to an ordinarily skilled artisan to administer the kinase inhibitor at least once in the same or separate compositions, or sequentially, as WO’675 demonstrates that these methods of administration were known in the art for the treatment of cancer using CARs and additional agents such as kinase inhibitors. Additionally, Weisberg motivates administration of the FLT3 kinase inhibitor either at the same time or following CAR administration by teaching that increases in FLT3-ITD expression was at least in part due to reduced turnover of the receptor with prolonged half-life but that such phenotype could be rapidly reversed upon withdrawal of either midostaurin or HG-7-85-01 inhibitors. As the CARs of WO’889 target FLT3, an ordinarily skilled artisan would be motivated to maintain or initiate increased levels of FLT3 for targeting through concurrent or post administration of the FLT3 KI. An ordinarily skilled artisan would have had a reasonable expectation of success as WO’675 teaches methods of co-administering CARs and agents that increase the efficacy of CARs, such as kinase inhibitors, which are the same type of therapeutics taught by Weisberg and WO’889.
Claims 110-111 and 117-118 are rejected under 35 U.S.C. 103 as being unpatentable over Weisberg, E. et al (2011) Reversible resistance induced by FLT3 inhibition: A novel Resistance Mechanism in mutant FLT3-expressing cells PLos ONE 6(9) e25351; 1-12 in view of WO 2017/053889 A2 (Devine, S., et al) 30 March 2017 and WO 2015/142675 A2 (Loew, A., et al) 24 SEPT 2015 as applied to claims 106 and 116 above and in further view of Larrosa-Garcia, M. and M.R. Baer (2017) FLT3 inhibitors in acute myeloid leukemia: Current status and future directions Mol Cancer Ther 16(6); 991-1001, published June 2017.
The combination of Weisberg, WO’889, and WO’675 teach the method of claim 106 and the composition of claim 116 as discussed above.
The combination of Weisberg, WO’889, and WO’675 differ from the instantly claimed invention in that the combination of applied references does not disclose that the FLT3 kinase inhibitor is crenolanib or quizartinib.
Larrosa-Garcia teaches that FLT3 is involved in regulating survival, proliferation, and differentiation of hematopoietic stem/progenitor cells and is expressed on AML cells in most patients. Patients with AML with FLT3-ITD mutations have a high relapse rate and short relapse-free and overall survival after chemotherapy and after transplant. A number of inhibitors of FLT3 signaling have been identified and are in clinical trials, both alone and with chemotherapy, with the goal of improving clinical outcomes in patients with AML and FLT3 mutations.
Larrosa-Garcia teaches that the primary approach in inhibiting FLT3 signaling to produce cytotoxicity and clinical response has been identification and testing of small molecule inhibitors of FLT3 signaling and that some work has also focused on developing internalizing fully human antagonistic antibodies directed against FLT3 (page 2, paragraph 3). A number of FLT3 inhibitors have been studied and are classified into first- and second- generation based on their specificity for FLT3 and into type I and type II based on their mechanism of interaction with FLT3 (page 3, paragraph 4). Larrosa-Garcia provides a summary of FLT3 inhibitors in clinical trial for AML in Table 1 including midostaurin, lestaurtinib, crenolanib, and quizartinib.
It would have been prima facie obvious to one of ordinary skill in the art prior to the effective filing date of the claimed invention to have substituted the FLT3 TKIs taught in the method and composition disclosed by the combination of Weisberg, WO’889, and WO’675 with the kinase inhibitors disclosed by Larrosa-Garcia, including crenolanib or quizartinib. It would have been obvious to an ordinarily skilled artisan to substitute crenolanib or quizartinib as the FLT3 kinase inhibitors as Larrosa-Garcia teaches that they were known FLT3 kinase inhibitors that were being tested in clinical trial for the treatment of AML. One of ordinary skill in the art would have had a reasonable expectation of success that these FLT3 kinase inhibitors would upregulate cell surface expression of FLT3 as Weisberg demonstrates that FLT3 TKIs increase the surface expression of FLT3 on FLT3-ITD AML cells. As crenolanib or quizartinib are also FLT3 TKIs targeting the same pathway as the FLT3 TKIs of Weisberg, an ordinarily skilled artisan would reasonably expect that these FLT3 TKIs would result in the same upregulation of surface expression of FLT3. Additionally, Weisberg teaches that the over-expression of FLT3 was observed in two cell lines made resistant to two structurally-unrelated FLT3 inhibitors suggesting that differently structured inhibitors would still be expected to increase FLT3 expression.
This conclusion of obviousness is further supported by KSR (E) obvious to try. See MPEP 2143. In this case, the prior art recognized the transient outcomes of AML treatment with FLT3 TKIs and in the case of FLT3-ITD mutated AML, suggests the use of FLT3 targeting agents in combination with FLT3 TKIs to treat the cancer. The prior art also recognized a finite number of FLT3 TKIs. An ordinarily skilled artisan would have been able to pursue these known FLT3 TKIs with the reasonable expectation that targeting FLT3 in FLT3-ITD mutated AML with TKIs would result in the increased surface expression of FLT3 allowing for targeting with FLT3 targeting agents, such as the CAR T cells of WO’889.
Response to Arguments
Applicant’s arguments in the response filed 10/06/2025 have been fully considered, but were not persuasive.
With regards to the rejections under 35 USC 103, applicant argues that Weisberg does not disclose or suggest that a FLT3 targeting agent can be administered in combination or prior to a FLT3-kinase inhibitor; that WO’889 does not teach the co-administration of a TKI; and that WO’675 claims a broad range of agents to be administered in combination with CAR T cells.
These arguments are not persuasive. Applicant argues the teachings of each reference individually and what each reference fails to teach. The rejections of the instant office action; however, are based on a combination of the applied references and what the combination would have suggested to one of ordinary skill in the art. See MPEP 2145 (IV).
In this case, administration of the FLT3 targeting agent in combination with or prior to a FLT3 kinase inhibitor is further supported in the rejection by WO’675, which teaches FLT3 CAR expressing cells and also teaches that CARs can be administered in combination with agents that increase efficacy, including kinase inhibitors, with simultaneous administration or sequential administration where the CAR expressing cells can be administered first. WO’889 is not required to teach co-administration of a TKI because this limitation is taught by Weisberg and WO’675. While WO’675 teaches different agents that could be used to boost CAR efficacy, WO’675 does teach kinase inhibitors and their use is also motivated by Weisberg which teaches that FLT3 KIs increase expression of FLT3 due to reduced turnover of the receptor and prolonged half-life.
With regards to Weisberg, applicant argues that the examples of Weisberg indicate that the development of drug resistance to kinase inhibitors, which include the upregulation of FLT3, does not appear to be a rapid response. Applicant argues that in order to generate resistant cells in the examples, the cells were incubated with the kinase inhibitors at increasing doses for nearly 14 weeks citing Weisberg (page 2, right column, first paragraph). Applicant argues that an ordinarily skilled artisan would expect that to achieve the resistance phenotype, which includes FLT3 upregulation, the FLT3 kinase inhibitor would need to precede the CAR cells by several weeks.
While Weisberg studied FLT3 kinase inhibitor resistance, and how FLT3 upregulation contributed to such resistance, the instant claims do not require that the cancer be FLT3 kinase inhibitor resistant, only that the FLT3 kinase inhibitor upregulate cell surface expression of FLT3 on cancer cells. Additionally, while the claims require that the FLT3 kinase inhibitor be administered at least once or multiple times concurrently with the FLT3 targeting CAR or once or multiple times after administering the FLT3 targeting CAR, the claims use “comprising” language with regards to the claimed method. In the absence of a limiting definition by applicants in the specification for the transitional phrase, the term “comprising” is interpreted per MPEP 2111.03 I., which defines comprising as being inclusive or open-ended and not excluding additional, unrecited elements or method steps. Based on this, the claim encompasses a scope in which the FLT3 kinase inhibitor is administered before the FLT3 targeting CAR cells, so long as it is also administered concurrently with or after administration of the FLT3 targeting CAR cells. Therefore, even if Weisberg suggested administration prior to the CAR cells, such administration would still meet the instant claim limitations so long as administration either continued concurrently to administration of the FLT3 target CAR cells or at least once after the FLT3 targeting CAR cells.
That said, the teachings of Weisberg do not suggest that it takes several weeks to increase FLT3 expression with the kinase inhibitor, rather, applicant is discussing the time that Weisberg cultured the cells in order to establish resistance. For instance, Weisberg teaches that “FLT3 inhibitor treatment might contribute to an increase in target protein that- over time- lowers drug sensitivity of mutant FLT3-expressing cells (while patients are still being treated, even if this might be reversible upon withdrawal of the drug) could be proposed as one possible reason why FLT3 inhibitors might not be as clinically effective as one might predict seeing that development of clinical inhibitors of mutant FLT3 is biorationally-speaking a promising approach.” (page 9, right column, paragraph 4). These teachings of Weisberg suggest that the increased FLT3 expression over time leads to resistance, not that it takes 14 weeks, or any extended time, to increase FLT3 expression. Weisberg also teaches that no significant evidence of FLT3 gene amplification, kinase domain mutations, or elevated levels of mRNA was observed, suggesting that protein turnover may be part of an autoregulatory pathway initiated by FLT3 kinase activity (abstract, results and conclusions). As Weisberg teaches that elevated FLT3 surface expression was at least in part due to reduced turnover of the receptor, with a prolonged half-life, one of ordinary skill in the art would reasonably expect that the inhibition of the FLT3 kinase pathway would result in reduced turnover and the increased expression, even without resistance.
Furthermore, the rejection does not rely solely on the teachings of Weisberg to demonstrate that administration concurrently with and after would have been obvious. In the rejection, WO’675 is also applied to demonstrate that these methods of administering, including concurrent in the same or separate compositions, or sequentially, were known in the prior art for use with CAR expressing cells and additional agents, including kinase inhibitors.
With regards to WO’889, applicant argues that WO’889 teaches that FLT3 is a highly expressed surface protein in leukemia, especially in AML. Applicant argues that, therefore, one of ordinary skill in the art would not consider adding an FLT3 TKI treatment step to CAR T cell therapy, as the main teaching of the document suggests that there is already sufficient FLT3 expressed on the tumor itself to allow effective CAR T cell therapy. Applicant argues that one of ordinary skill in the art would not combine WO’889 and Weisberg without hindsight knowledge.
In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, 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).
Furthermore, the obvious rational in rejection relies on the use of the FLT3 targeting CAR of WO’889 as the FLT3 targeting therapy in the method taught by Weisberg, not the addition of an FLT3 TKI to the methods of WO’889. That said, one of ordinary skill in the art would reasonably recognize that increasing expression of FLT3 would increase the target of the FLT3 targeting CAR.
With regards to WO’675, applicant argues that the disclosure includes a broad range of agents to be administered in combination with CAR T cells and cites a list in which WO’675 states that the CAR cells can be administered with a protein phosphate inhibitor; a kinase inhibitor; a cytokine; an inhibitor of an immune inhibitory molecule; or an agent that decreases the level of activity of a TR G cell. Applicant further argues that different kinase inhibitors have different effects because kinases are involved in a variety of cellular processes. Applicant argues that WO’675 does not teach or disclose FLT3 kinase inhibitors.
As discussed in detail above, the rejection of record is based on the combination of applied references and what the combination would have suggested to one of ordinary skill in the art. As such, WO’675 is not required to teach each and every limitation of the claimed method. For instance, even if WO’675 does not teach FLT3 kinase inhibitors for use in combination therapy with CAR cells, WO’675 is not required to teach this limitation as the rejection relies on Weisberg for the teaching of FLT3 kinase inhibitors in combination with FLT3 targeting therapies. Rather, WO’675 is applied in the rejections of record in order to further support the administration of the FLT3 kinase inhibitors taught by Weisberg concurrently and/or following CAR T cell therapy. As discussed in detail in the rejection, WO’675 teaches the administration of CAR cells with agents that increase efficacy of the immune cells, including kinase inhibitors, and teaches that administration can be concurrently or sequential.
Applicant further argues that, based on the examples of WO’675, one of ordinary skill in the art would only consider the simultaneous administration of CAR T cells and kinase inhibitors if the kinase inhibitors directly affected the immune cells positively. Applicant argues that a skilled person would not consider combining the kinase inhibitors described in Weisberg, which are not known or described to have a positive effect on immune cells with the methods described in WO’675. Applicant argues that a skilled person may even assume that the kinase inhibitors described in Weisberg can affect the CAR T cells in a different, unknown manner, which is not necessarily positive and would, therefore, be discouraged from administering the FLT-KI in combination with CAR T cells.
The examples of WO’675 discussed by applicant studied mTOR-Inhibitor RAD001 and Diacylglycerol kinase (DGK) inhibition, neither of which are FLT3 KIs suggested by the teachings of Weisberg. Furthermore, at no point does WO’675 directly, or even indirectly, suggest that coadministration is limited only to agents that act directly on the immune cells as suggested by applicant. WO’675 does not directly discourage, criticize, or discredit the solution claimed and; therefore, WO’675 does not teach away from the claimed invention. See MPEP 2123 (II). While applicant argues that an ordinarily skilled artisan “may even assume” that the FLT3 kinase inhibitors of Weisberg may affect the CAR T cells in a different not necessarily positive way, applicant provides no evidence to support such speculation.
Conclusion
No claims are allowed.
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any extension fee pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/AUDREY L BUTTICE/Examiner, Art Unit 1647
/SCARLETT Y GOON/Supervisory Patent Examiner
Art Unit 1693