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 .
DETAILED ACTION
Claims 1-10, 14-20, 22, 23 and 26 are currently pending and under prosecution.
Claim Objections
Claims 5 and 10 are objected to because of the following informalities: the names of the antibodies do not need to be capitalized. Appropriate correction is required.
Claim Rejections - 35 USC § 112
Claims 1-10, 14-20, 22, 23 and 26 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 written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention. This is a WRITTEN DESCRIPTION rejection.
Claim 1 recites a method for treating a hyperproliferative disorder in a mammal in need thereof comprising, administering to the mammal a combination of: (a) an anti-cancer antibody, and (b) a T-cell activating agent for the prophylactic or therapeutic treatment of the hyperproliferative disorder. Dependent claim 4 recites that the anti-cancer antibody is a monospecific antibody. Dependent claims 6-8 recite that the T-cell activating agent activates CD4+ T cells, and that it is a bispecific antibody, a chimeric antigen receptor T (CAR-T) cells, and/or a vaccine that induces a T-cell response. There is no structure of the anti-cancer antibody or the T-cell activating agent recited.
The instant specification discloses the following:
Anti-cancer antibody: The instant specification discloses that the anti-cancer antibodies mediate antibody-dependent cellular cytotoxicity (ADCC), and that they are monoclonal antibodies. The instant specification discloses a list of 20 monoclonal antibodies that can be used in combination the “T-cell activating agent” [see pgs 12-13] No sequences or other examples of the anti-cancer antibody is recited in the instant specification.
T-cell activating agent: The instant specification discloses that the T-cell activating agents are bispecific agents, CAR-T cells, or vaccines, and that they may be anti-CD3 x anti-tumor antibodies, and lists two examples of these bispecific antibodies. [pg 11, lines 31-35 – pg 12, lines 1-7]
The instant specification describes 20 anti-cancer antibodies, and 2 T-cell activating agents. The specification does not provide any examples of CARs or vaccines as “T-cell activating agents”. Thus, the specification fails to disclose any other antibodies, or structural sequences required of either the anti-cancer antibodies that function as claimed.
Antibodies/CAR:
By the time of the filing of the instant application, it was well established in the art that the formation of an intact antigen-binding site in an antibody usually required the association of the complete heavy and light chain variable regions of a given antibody, each of which consists of three “complementarity determining regions” (“CDRs”) which provide the majority of the contact residues for the binding of the antibody to its target epitope. E.g., Almagro & Fransson, Frontiers in Bioscience 2008; 13:1619-33; (see Section 3 “Antibody Structure and the Antigen Binding Site” and Figure 1). Humanized antibodies comprise only the CDRs, or in some cases an abbreviated subset of residues within the CDRs, of a parental rodent antibody in the context of human framework sequences. Id. at Section 4. All of the CDRs of the heavy and light chain, in their proper order of CDR1, then 2, then 3, and in the context of framework sequences which maintain their required conformation are generally required to produce a humanized antibody in which the heavy and light chains associate to form an antigen-binding region that binds the same antigen as the parental rodent antibody. Id. at Section 4.
Antibody binding to the same antigen, or even the same epitope on that antigen, can be accomplished with an impressively wide variety of antibody structures, even when the antibodies are limited to those from a particular source (Gershoni et al., Epitope Mapping, Biodrugs 2007; 21 (3): 145-156 page 146 section 1.1). The skilled artisan therefore understood that antibodies from a variety of different sources may bind the same antigen and even mediate the same functional effects, but differ widely in the details of the structure of their antigen-binding sites, particularly in the amino acid sequence and length of VH-CDR3.
Further, it is not possible to predict the amino acid sequence when an epitope is recited, because there are many different epitope arrangements, such as linear and discontinuous epitopes that is dictated by the unique interaction between an antibody and its cognate epitope (Blythe et al., Benchmarking B cell epitope prediction: Underperformance of existing methods, Protein Science (2005), 14:246–248 pg. 246) . 3D structural analyses of antibody-epitope binding highlighting that the deficiency in the ability to predict the structural features of an antibody when the epitope is disclosed (Schreiber et al.,3D-Epitope-Explorer (3DEX): Localization of Conformational Epitopes within Three-Dimensional Structures of Proteins, Wiley Interscience, 2005 42–44, 60596, page 879).
To provide adequate written description and evidence of possession of the claimed composition antibody genus, the instant specification can structurally describe representative antibodies, that function as claimed, or describe structural features common to the members of the genus, which features constitute a substantial portion of the genus. Alternatively, the specification can show that the claimed invention is complete by disclosure of sufficiently detailed, relevant identifying characteristics, functional characteristics when coupled with a known or disclosed correlation between function and structure, or some combination of such characteristics (see University of California v. Eli Lilly and Co., 119 F.3d 1559, 43 USPQ2d 1398 (Fed. Cir. 1997) and Enzo Biochem, Inc. V. Gen-Probe Inc.). A disclosure that does not adequately describe a product itself logically cannot adequately describe a method of using that product.
Although Applicants may argue that it is possible to screen for antibodies that function as claimed, the court found in (Rochester v. Searle, 358 F.3d 916, Fed Cir., 2004) that screening assays are not sufficient to provide adequate written description for an invention because they are merely a wish or plan for obtaining the claimed chemical invention. “As we held in Lilly, “[a]n adequate written description of a DNA … ‘requires a precise definition, such as by structure, formula, chemical name, or physical properties,’ not a mere wish or plan for obtaining the claimed chemical invention.” 119 F.3d at 1566 (quoting Fiers, 984 F.2d at 1171). For reasons stated above, that requirement applies just as well to non-DNA (or RNA) chemical inventions.” Knowledge of screening methods provides no information about the structure of any future antibodies yet to be discovered that may function as claimed. The term “anti-cancer” provides no information about the structure of an antibody.
Given the lack of representative examples to support the full scope of the claimed antibodies, and lack of reasonable structure-function correlation with regards to the unknown sequences in the variable domains or CDRs of the antibodies that function as claimed, the present claims lack adequate written description. Thus, the specification does not provide an adequate written description of antibodies that is required to practice the claimed invention. Since the specification fails to adequately describe the product to which the claimed method uses, it also fails to adequately describe the method.
Vaccines:
The written description is on treatment of the vaccine as recited by the claims above. It has been interpreted that one of skill in the art cannot construct a cancer vaccine without knowing what the structure or the target of the vaccine. It is not clear how one can make and administer a cancer vaccine without knowing the structure of the vaccine It has been interpreted that the cancer vaccine must be capable of inducing an immune response in a patient, as well as treatment function. The definition of a vaccine in the online Merriam-Webster on-line dictionary is a preparation that is administered (as by injection) to stimulate the body’s immune response against a specific infectious agent or disease.
The instant specification does not disclose any example of any vaccine used in the claimed method.
The MPEP further states that if a biomolecule is described only by a functional characteristic, without any disclosed correlation between function and structure of the sequence, it is “not sufficient characteristic for written description purposes, even when accompanied by a method of obtaining the claimed sequence.” MPEP 2163. The MPEP does state that for generic claim the genus can be adequately described if the disclosure presents a sufficient number of representative species that encompass the genus. MPEP 2163. If the genus has a substantial variance, the disclosure must describe a sufficient variety of species to reflect the variation within that genus. See MPEP 2163. Although the MPEP does not define what constitute a sufficient number of representative, the Courts have indicated what do not constitute a representative number species to adequately describe a broad generic. In Gosteli, the Court determined that the disclosure of two chemical compounds within a subgenus did not describe that subgenus. In re Gosteli, 872 F.2d at 1012, 10 USPQ2d at 1618.
The specification does not provide adequate written description of the claimed invention. The legal standard for sufficiency of a patent's (or a specification's) written description is whether that description "reasonably conveys to the artisan that the inventor had possession at that time of the. . .claimed subject matter", Vas-Cath, Inc. V. Mahurkar, 19 USPQ2d 1111 (Fed. Cir. 1991). In the instant case, the specification does not convey to the artisan that the Applicant had possession at the time of invention of the claimed invention, the cancer vaccine.
The Federal Circuit addressed the application of the written description requirement to DNA-related inventions in University of California v. Eli Lilly and Co., 119 F.3d 1559, 43 USPQ2d 1398 (Fed. Cir. 1997). The court stated that “[a] written description of an invention involving a chemical genus, like a description of a chemical species, requires a precise definition, such as by structure, formula, [or] chemical name, of the claimed subject matter sufficient to distinguish it from other materials.” Id. At 1567, 43 USPQ2d at 1405. The court concluded that “naming a type of material generally known to exist, in the absence of knowledge as to what that material consists of, is not a description of that material.” Id.
In this case, the specification does not describe the genus of that are capable of functioning in a vaccine that satisfies either the Lilly or Enzo standards. The instant specification does not recite any example of a vaccine. The instant claims attempt to claim every type of cancer vaccine and do not limit it to the specific type of cancer vaccine that is recited in the claims. A search of the art demonstrates the complexity and challenges of utilizing cancer vaccines. Gracia-Grijo et al. (Frontiers in Immunology 2019 10 1-19) teaches the complications of cancer vaccines targeting neoantigens. Gracia-Grijo teaches although clinical trials testing vaccines targeting neoantigens have demonstrated they are safe and well tolerated, whether individualized immunotherapies targeting neoantigens can mediate effective antitumor responses in a broader patient population, remains an open question. Gracia-Grijo teaches that despite all the technological innovation and development of novel screening assays, the rapid and precise identification of the bona fide neoantigens in any given patient remains a major hurdle that will need to be overcome to translate the potential of neoantigen targeting into effective therapies for patients with cancer. [Conclusion, pg 14] Hu et al (Nature Reviews Immunology 2018 18, 168–182) teaches the complications of cancer vaccine production and use, including but not limited to, tumor heterogeneity between and within tumors is a major challenge to the development of cancer immunology. [pg 3, building cancer vaccines] Although the specification provides an example of one cancer vaccine, it does not provide enough support for the full scope of cancer vaccines as claimed. Thus, out of an unknown and likely very large number of structures and targets capable of being used in a vaccine, the specification only discloses one example of a cancer vaccine. The specification does not disclose sufficient examples of cancer vaccines that are capable of treating cancer.
Thus, the specification does not provide an adequate written description of the genus of cancer vaccines that is required to practice the claimed invention. The instant disclosure does not adequately describe the scope of the claimed genus, which encompasses a substantial variety of subgenera. Since the disclosure fails to provide sufficient relevant identifying characteristics, and because the genus is highly variant, one of skill in the art would reasonably conclude that the disclosure fails to provide a representative number of species to describe the genus as broadly claimed.
Claims 1-10, 14-20, 22, 23 and 26 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 the combination of rituximab and blinatumomab for treatment of a hyperproliferative disorder, does not reasonably provide enablement for (1) the combination of any “anti-cancer antibody” and any T-cell activating agent for the treatment of a hyperproliferative disorder. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to practice the invention commensurate in scope with these claims.
BREADTH OF THE CLAIMS: Claim 1 recites a method for treating a hyperproliferative disorder in a mammal in need thereof comprising, administering to the mammal a combination of: (a) an anti-cancer antibody, and (b) a T-cell activating agent for the prophylactic or therapeutic treatment of the hyperproliferative disorder.
STATE OF THE ART: It is well known that the art of anti-cancer therapy is highly unpredictable, for example, Gura (Science, 1997, 278:1041-1042) teaches that researchers face the problem of sifting through potential anticancer agents to find ones promising enough to make human clinical trials worthwhile and teach that since formal screening began in 1955, many thousands of drugs have shown activity in either cell or animal models that only 29 have actually been shown to be useful for chemotherapy See p. 1041, see 1st and 2nd para. Furthermore, Kaiser (Science, 2006, 313: 1370) teaches that 90% of tumor drugs fail in patients. See 3rd col., 2nd to last para. Additionally, Chames et al (British J. of Pharmacology, 2009, 157, 220-233) teach that there are several challenges to development therapeutic antibodies. These challenges include functional limitations such as inadequate pharmacokinetics, tissue accessibility and impaired interactions with the immune system (Abstract). Additionally, Chames teaches several limitations of therapeutic antibodies such as affinity between the antibody and its antigen, competition with patient’s IgG, and efficiency issues in triggering the immune response (pages 224-225).
PRESENCE OR ABSENCE OF EXAMPLES: The instant specification discloses the following: Example 1 describes the use of rituximab, an anti-CD20 monoclonal antibody, and the long-term effects on Natural Killer cell responses and effects of T-cells. Example 2 describes use of rituximab or trastuzumab to determine effects on NK cells. Thus, Examples 1 and 2 demonstrate the effects of just an anti-cancer antibody. Example 3 demonstrates use of a bispecific antibody, blinatumomab and rituximab, these agents were cultured in target Raji cells for one week and the results demonstrate that small numbers of T cells activated by blinatumomab enhanced RTX-mediated ADCC and NK cell number. No other examples in the specification are disclosed that demonstrate the claimed method of other anti-cancer antibodies and T-cell activating agents.
PREDICTABILITY: The specification lacks the critical steps necessary in presenting some type of predictable response in a population of hosts deemed necessary to treat hyperproliferative disorders with any anti-cancer antibody and any T-cell engaging agent. The amount of experimentation to required to formulate such guidance would be enormous; one would have to demonstrate the efficacy of the combination in several models across several different types of cancers and determine the appropriate regimen (doses and frequency) for use of the combination or composition in a treatment setting.
Thus, considering the high level of skill in the art, the state of the art, the level of predictability, and the guidance and examples provided, the experimentation required to enable the full scope of the claimed invention would not be reasonable.
QUANTITY OF EXPERIMENTATION: Undue experimentation would be required to determine what anti-cancer antibody and what T-cell activating agent predictably treat a hyperproliferative disease as claimed. MPEP 2164.01 recites that “The test of enablement is not whether any experimentation is necessary, but whether, if experimentation is necessary, it is undue. In re Angstadt, 537 F.2d 498, 504, 190 USPQ 214, 219 (CCPA 1976)”. The experimentation needed to practice this method is undue and unreasonable as it requires determining whether the claimed agents treat what hyperproliferative disorder. A person skilled in the art will not be able to use the invention without undue experimentation. (In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988))
Accordingly, the instant claims do not comply with the enablement requirement of §112, since to practice the invention claimed in the patent a person of ordinary skill in the art would have to engage in undue experimentation, with no assurance of success.
Claims 1-10, 14-20, 22, 23 and 26 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 the combination of rituximab and blinatumomab for treatment of a hyperproliferative disorder, does not reasonably provide enablement for the combination of rituximab and blinatumomab for prophylactic treatment of a hyperproliferative disorder The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to practice the invention commensurate in scope with these claims.
BREADTH OF THE CLAIMS: Claim 1 recites a method for treating a hyperproliferative disorder in a mammal in need thereof comprising, administering to the mammal a combination of: (a) an anti-cancer antibody, and (b) a T-cell activating agent for the prophylactic or therapeutic treatment of the hyperproliferative disorder.
STATE OF THE ART: A search of relevant art, does not reveal any demonstration that an anti-cancer antibody and a T-cell activating agent can be used to prophylactically treat a hyperproliferative disorder, such as cancer. Cancer has a wide variety of causes, from environmental and/or developmental exposure to ionizing radiation and/or chemical exposure in addition to some types viral and bacterial exposure (Lichtman MA et al. The Oncologist 2017; 22(5); 542–548). Even though cancer is featured by the infinite cell proliferation, its pathogenesis is extremely complex and related to many mechanisms. In general, the hallmarks of cancer consist of ten biological capabilities during the development of cancers, namely sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, tumor-promoting inflammation, genome instability and mutation, evading immune destruction and reprogramming energy metabolism (Hanahan D et al. Cell 2011 144(5) p646-674, Figures 1 and 3). More than 100 types of cancer have been identified which are typically termed for the organs or tissues where they occur. Hanahan taught over the past decade, tumors have increasingly been recognized as organs whose complexity approaches and may even exceed that of normal healthy tissues (page 661, right column second to last paragraph). Hanahan taught many human tumors are histopathologically diverse, containing regions demarcated by various degrees of differentiation, proliferation, vascularity, inflammation, and/or invasiveness (page 662, left column, first paragraph). Szabo et al (Selecting targets for cancer prevention: where do we go from here? Nat Rev Cancer 6, 867–874; 2006) teaches the intricacies and complications of cancer prevention. Szabo teaches that in addition to efficacy and toxicity concerns of cancer drugs targeting functions, there are a number of practical issues that should be considered, including drug formulation and dosing schedule to ensure adherence, as well as the cost. Szabo also teaches that in some cases the targets selected for drug therapy may even cause harm. [Whole document]
Clinical trials aimed at proving preventative cancer activity attributable to a specific intervention are largely infeasible, due to the impossibly large number of subjects and an equally impossible long timeframe. Although cancer is a common disease, specific types of cancer are still relatively infrequent events in an otherwise healthy population. Therefore, trials with cancer incidence as endpoints would necessarily involve several thousands of subjects followed for several decades. Such logistic difficulties have precluded cancer prevention trials with cancer incidence as an endpoint in all but a selected few malignancies for treatments such as tamoxifen and finasteride (Lee KW et al. Nature Reviews Cancer 2011 11 211-218, page 211, left column last paragraph)
PRESENCE OR ABSENCE OF EXAMPLES: The instant specification does not provide any examples of prophylactic treatment methods. Example 1 describes the use of rituximab, an anti-CD20 monoclonal antibody, and the long-term effects on Natural Killer cell responses and effects of T-cells. Example 2 describes use of rituximab or trastuzumab to determine effects on NK cells. Example 3 demonstrates use of a bispecific antibody, blinatumomab and rituximab, these agents were cultured in target Raji cells for one week and the results demonstrate that small numbers of T cells activated by blinatumomab enhanced RTX-mediated ADCC and NK cell number. No examples of prophylactic or prevention methods were described in the specification.
PREDICTABILITY: The specification lacks the critical steps necessary in presenting some type of predictable response in a population of hosts deemed necessary to prevent cancer with the instantly claimed combination. There is no evidence in the instant application or the art that as noted in the prior that demonstrate that a drug that treats cancer would prevent the onset of cancer in subjects as claimed. The amount of experimentation to required to formulate such guidance would be enormous; one would have to demonstrate the efficacy of the combination in several models across several different types of cancers and determine the appropriate regimen (doses and frequency) for use of the combination or composition in a preventative setting. Further, one would have to conduct population analysis to identify definitive characteristics which indicate that a subject is at risk of developing any cancer to a degree that would outweigh potential adverse effects of treatment with the claimed combination or composition.
Thus, considering the high level of skill in the art, the state of the art, the level of predictability, and the guidance and examples provided, the experimentation required to enable the full scope of the claimed invention would not be reasonable.
QUANTITY OF EXPERIMENTATION: Undue experimentation would be required to determine what anti-cancer antibody and what T-cell activating agent predictably prevent a hyperproliferative disease as claimed. MPEP 2164.01 recites that “The test of enablement is not whether any experimentation is necessary, but whether, if experimentation is necessary, it is undue. In re Angstadt, 537 F.2d 498, 504, 190 USPQ 214, 219 (CCPA 1976)”. The experimentation needed to practice this method is undue and unreasonable as it requires determining whether the claimed agents prevents hyperproliferative disorders. A person skilled in the art will not be able to use the invention without undue experimentation. (In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988))
Accordingly, the instant claims do not comply with the enablement requirement of §112, since to practice the invention claimed in the patent a person of ordinary skill in the art would have to engage in undue experimentation, with no assurance of success.
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.
Claim(s) 1-10, 14-20, 22, 23 and 26 are rejected under 35 U.S.C. 103 as being unpatentable over d'Argouges et al (Combination of rituximab with blinatumomab (MT103/MEDI-538), a T cell-engaging CD19-/CD3-bispecific antibody, for highly efficient lysis of human B lymphoma cells. Leuk Res. 2009 Mar;33(3):465-73), in view of Oak et al (2015). (Blinatumomab for the treatment of B-cell lymphoma. Expert Opinion on Investigational Drugs, 24(5), 715–724)
d'Argouges teaches a method for treating a hyperproliferative disorder, cancer, comprising administering a combination of (a) an anti-cancer antibody and (b) aT-cell activating agent, for the treatment of cancer. Regarding claims 2-5, d'Argouges teaches that the anti-cancer antibody is, rituximab which targets CD20 (monospecific) and exerts its therapeutic effect via antibody-dependent cellular toxicity, which requires the presence of natural killer cells. [pg 465, 2nd column, 2nd paragraph] Regarding claims 7-10, d'Argouges teaches that the T-cell activating agent, blinatumomab, activates T-cells, and is a bispecific antibody that binds to CD19xCD3. Regarding claims 14 and 15, d'Argouges teaches that the hyperproliferative disorder is cancer, and that the cancer is B-cell lymphoma. [Abstract] Regarding claim 16, d'Argouges teaches that the combination of the two agents resulted in maintained ADCC. [section 3.5-3.7] d'Argouges teaches that the cytotoxic activity induced by blinatumomab with T cells is considerably higher than ADCC by rituximab, and teaches that there is a strong rationale to combine rituximab with blinatumomab. [Discussion] Regarding claims 17 and 18, d'Argouges teaches that the agents were administered together at the same time. [pg 467, 2.7]
However, d'Argouges does not specifically teach: (1) a method of treatment in mammals, (2) the dosing regimen as recited in claims 19-20 and 22-23, and (3) the kit comprising the two agents.
Oak teaches a method for treating cancer, B-cell lymphoma, comprising administering blinatumomab. Oak teaches that blinatumomab activates CD4+ T-cells and is used in clinical trials in human subjects. Oak teaches that blinatumomab is administered intravenously in weekly or monthly cycles, at a dose of 5 micrograms. [pg 719] Oak also teaches that a combination of rituximab and blinatumomab, and teaches this combination is a potent therapy that redirects T-cells to sweep for both CD20+ and CD19+ cells. [pg 718, 2nd column]
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to treat a human subject with cancer, comprising administering an anti-cancer antibody, such as rituximab, and a T-cell activating agent, such as blinatumomab, at the claimed dosing regimen. One would have been motivated, and have a reasonable expectation of success, because: (1) d'Argouges teaches a method for treating a hyperproliferative disorder, cancer, comprising administering a combination of (a) an anti-cancer antibody and (b) aT-cell activating agent, for the treatment of cancer, and teaches that (a) may be rituximab, and (b) may be blinatumomab, (2) d'Argouges teaches that these agents were administered together, and that the cytotoxic activity induced by blinatumomab with T cells is considerably higher than ADCC by rituximab, and teaches that there is a strong rationale to combine rituximab with blinatumomab, (3) Oak teaches a method for treating cancer comprising administering both agents, and teaches blinatumomab is administered intravenously in weekly or monthly cycles, at a dose of 5 micrograms, and (4) Oak teaches that a combination of rituximab and blinatumomab, and teaches this combination is a potent therapy that redirects T-cells to sweep for both CD20+ and CD19+ cells. Given the known need to treat hyperproliferative disorders, such as cancer, given the known method for combining an anti-cancer antibody, such as rituximab, and a T-cell activating agent, such as blinatumomab, and given the known doses and dosing regimens of the T-cell activating agent, one of skilled in the art could have pursued treating “mammals” with the instantly claimed combination, with a reasonable expectation of success.
It is noted that claim 26 requires a kit comprising a T-cell activating agent, a container, and a package insert, or label indicating the administration of the T-cell activating agent with an anti-cancer antibody. One would have been motivated to, and have a reasonable expectation of success, because the prior art teaches the combination of a T-cell activating agent and an anti-cancer antibody for the treatment of a hyperproliferative disorder. Given the known uses of kits, and given the known use of other agents comprised in a kit, one of skill in the art could have put together a kit with the claimed combination, with a reasonable expectation of success.
Conclusion
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/SARAH A ALSOMAIRY/ Examiner, Art Unit 1646
/Zachariah Lucas/ Supervisory Patent Examiner, Art Unit 1600