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 .
Election/Restrictions
Applicant's election with traverse of Group I, claims 1-12 in the reply filed on 04/23/2026 is acknowledged. The traversal is on the ground(s) that the Office has not shown that a serious burden would be required to examine all the claims. This is not found persuasive because inventions I-III as claimed have materially different design, mode of operation, function, or effect. Invention I requires administering to a patient both an asparaginase and a G6PD inhibiting agent, not required by Inventions II-III. Invention II requires receiving the results of an assay that identifies a subject as having a deficiency in G6PD and administering an asparaginase, not required by Inventions I and III. Invention III requires obtaining a biological sample from a subject having cancer; assaying the sample and identifying a deficiency in G6PD before administering an asparaginase to a subject, not required by Inventions I-II.
The requirement is still deemed proper and is therefore made FINAL.
Claims 13-25 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 04/23/2026.
Priority
The instant application claims benefit to US Provisional Application No. 63349638, filed on 06/07/2022 and is acknowledged. The instant claims herein are examined using the effective filing date of 06/07/2022 for the basis of any prior art rejections.
Specification
The use of the term Elspar, Oncaspar, and Erwinaze (see para 14, 96, 98-99 and 163), which is a trade name or a mark used in commerce, has been noted in this application. The term 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(b)
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.
Claim 8 is 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.
Claim 8 contains the trademark/trade name Elspar, Oncaspar, and Erwinaze. Where a trademark or trade name is used in a claim as a limitation to identify or describe a particular material or product, the claim does not comply with the requirements of 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph. See Ex parte Simpson, 218 USPQ 1020 (Bd. App. 1982). The claim scope is uncertain since the trademark or trade name cannot be used properly to identify any particular material or product. A trademark or trade name is used to identify a source of goods, and not the goods themselves. Thus, a trademark or trade name does not identify or describe the goods associated with the trademark or trade name. In the present case, the trademark/trade name is used to identify/describe an asparaginase (enzyme), and, accordingly, the identification/description is indefinite.
Claim 8 also recites “wherein the asparaginase is selected from the group consisting of: L-asparaginase (Elspar), pegaspargase (PEG-asparaginase; Oncaspar), SC-PEG asparaginase (Calaspargase pegol, and Erwinia asparaginase (Erwinaze)”. The use of parentheses renders the claims indefinite because it is unclear whether the limitations within the parentheses are part of the claimed invention, or if the species within the parentheses are exemplary embodiments of the claimed asparaginases.
Claim Rejections - 35 USC § 112(a)
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 1-3, and 6-12 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 decreasing tumors in G6PD deficient mice models displaying colorectal cancer (i.e., treatment of colorectal cancer in mice using asparaginase and G6PD inhibitor) and treatment of leukemias does not reasonably provide enablement for the treatment of any and all cancers using asparaginase and a G6PD inhibitor. 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.
There are many factors to be considered when determining whether there is sufficient evidence to support a determination that a disclosure does not satisfy the enablement requirement and whether any necessary experimentation is “undue.” These factors include, but are not limited to:
• (A) The breadth of the claims;
• (B) The nature of the invention;
• (C) The state of the prior art;
• (D) The level of one of ordinary skill;
• (E) The level of predictability in the art;
• (F) The amount of direction provided by the inventor;
• (G) The existence of working examples; and
• (H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure.
In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988).
All Wands factors listed above have been considered with regard to the instant claims, with the relevant factors discussed below:
The breadth of the claims and the nature of the invention: Instant claim 1-3, and 5-12 are broadly drawn to recite “A method for treating cancer, the method comprising: administering to a subject having cancer an asparaginase and an agent that inhibits glucose 6 phosphate dehydrogenase (G6PD)”. Dependent claim 2 recites that the cancer is selected from the list consisting of: a carcinoma, a melanoma, a sarcoma, a myeloma, a leukemia, and a lymphoma, the cancer is a solid tumor (claim 3), the cancer is resistant or not resistant to an asparaginase (claim 6-7), the asparaginase is selected from the group consisting of: L-asparaginase (Elspar), pegaspargase (PEG-asparaginase; Oncaspar), SC-PEG asparaginase (Calaspargase pegol, and Erwinia asparaginase (Erwinaze) (claim 8), the agent that inhibits G6PD is selected from the group consisting of a small molecule, an antibody, a peptide, a genome editing system, an antisense oligonucleotide, and an RNAi (claim 9), the RNAi is a microRNA, an siRNA, or a shRNA (see claim 10), the inhibiting G6PD is inhibiting the expression level and/or activity of G6PD (see claim 11), and the expression level and/or activity of G6PD is inhibited by at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, or more as compared to an appropriate control (claim 12).
The specification defines “treating” as, inter alia, “therapeutic treatments, wherein the object is to reverse, alleviate, ameliorate, inhibit, slow down or stop the progression or severity of a condition associated with cancer, e.g., leukemia, or colon cancer. The term "treating" includes reducing or alleviating at least one adverse effect or symptom of cancer. Treatment is generally "effective" if one or more symptoms or clinical markers are reduced. Alternatively, treatment is "effective" if the progression of a disease is reduced or halted. That is, "treatment" includes not just the improvement of symptoms or markers, but also a cessation of, or at least slowing of, progress or worsening of symptoms compared to what would be expected in the absence of treatment” (see para 0027). The claims are broad in scope, as the claims have been interpreted to broadly encompass the treatment of any and all cancers (ovarian, lung, brain, stomach, throat, esophageal, leukemia, melanomas, skin, etc.) via delivering to a subject an asparaginase and any agent that inhibits glucose 6 phosphate dehydrogenase.
The level of one of ordinary skill: The level of ordinary skill in the art is high. This would include Ph.D. level scientists.
The state and level of predictability in the prior art: The claims broadly embrace the treatment of any and all cancers using an asparaginase and an agent that inhibits glucose 6 phosphate dehydrogenase. However, it is not known or unpredictable if all cancers as encompassed by the broad scope of the instant claims can be treated using asparaginase and an agent that inhibits glucose 6 phosphate dehydrogenase.
Art recognized treatments of various disease states as encompassed by the claims:
Bourre (Genetic Abnormality Spectrum in Hematologic Cancers - Crown Bioscience. 7 March 2019; retrieved from https://blog.crownbio.com/blood-cancer-genetics-models) evidences the genetic abnormality spectrum in hematological cancers (title). Bourre evidences the various differences in genetic abnormalities across the range of hematologic malignancies, the variety of targeted agents developed, and the preclinical models to assess potential new therapeutics (pg. 2, paragraph 1). Multiple myeloma (MM) affects plasma cells within bone marrow responsible for the production of antibodies, and plasma cells accumulate in the marrow and damage or weaken the bone, inducing bone pain (pg. 2, paragraph 2). The cause of MM is not clearly identified, but the most commonly reported genetic changes are in KRAS, NRAS, TP53, FAM46C, BRAF, DIS3, ATM, and CCND1 (pg. 2, paragraph 3). Common treatments for MM include chemotherapy, corticosteroids, immunomodulating agents, proteasome inhibitors, HDAC inhibitors, and monoclonal antibodies (pg. 2, paragraph 4).
Bourre also evidences that leukemia is caused by excessive production of abnormal white blood cells in bone marrow that circulate into the blood (pg. 2, paragraph 5). It is categorized into multiple subtypes including acute lymphocytic leukemia (ALL), acute myeloid leukemia (AML), chronic lymphocytic leukemia (CLL), and chronic myeloid leukemia (CML) (pg. 2, paragraph 5). The primary genetic lesions that cause the vast majority of ALL are still unknown. The main treatment for ALL in adults is typically long-term combination chemotherapy, tyrosine kinase inhibitor targeted therapy (e.g. imatinib, dasatinib, nilotinib, ponatinib, bosutinib), blinatumomab targeting CD19, the monoclonal antibody inotuzumab ozogamicin against CD22, or the CAR-T cell therapy tisagenlecleucel targeting CD19 (pg. 3, paragraph 2-3), while CLL is treated using chemotherapy, radiation therapy, monoclonal antibodies targeting CD20, or CD52, or CD22, BTK inhibitors, PI3 inhibitors, Bcl-2 inhibitors, and autologous stem cell transplantation (pg. 3, paragraph 7), and targeted therapy for chronic myeloid leukemia uses tyrosine kinase inhibitors (imatinib, dasatinib, nilotinib, ponatinib, bosutinib) as the standard treatment, as well as chemotherapy or interferon therapies (pg. 4, paragraph 2). This reference evidences treatments associated with various forms of cancers and evidences a lack of overlapping treatment modalities, demonstrating the unpredictability in the art/lack of known treatments that are capable of treating all hematological cancers with the same compound.
Matulonis et al (Nat Rev Dis Primers. 2016 Aug 25;2:16061; hereinafter “Matulonis”) evidences that ovarian cancer can be subdivided into different histological subtypes that have different identifiable risk factors, cells of origin, molecular compositions, clinical features and treatments (pg. 2, paragraph 1). Histological subtypes include epithelial cancers that account for ~90% of ovarian cancers and include serous, endometrioid, clear-cell and mucinous carcinomas (pg. 2, paragraph 1, Fig. 1, Table 1). The most commonly diagnosed ovarian cancer is high-grade serous carcinoma, and histologically and clinically, low-grade endometrioid carcinoma and low-grade serous carcinoma (LGSC) are different compared with their high-grade counterparts (pg. 2, paragraph 1). Some ovarian cancers originate from sites outside of the ovary; for example, many ovarian HGSCs probably originate in the fallopian tube, and some subsets of ovarian cancer have been shown to arise from the peritoneum (pg. 2, paragraph 2). Clear-cell and endometreoid carcinomas can originate from endometrial tissue outside the uterus (pg. 2, paragraph 2). The most active therapeutic agents against newly diagnosed ovarian cancer are platinum analogues (either cisplatin or carboplatin), with the addition of a taxane (either paclitaxel or docetaxel) (pg. 2, paragraph 4). Treatment paradigms for first-line management of newly diagnosed ovarian cancer includes surgical tumor debulking followed by combination platinum-based chemotherapy or neoadjuvant chemotherapy followed by interval surgical cytoreduction and additional chemotherapy after surgery (pg. 2, paragraph 4). This reference evidences the genetic mutations associated with ovarian cancers, as well as current treatment techniques used. It also evidences the varying molecular compositions, clinical features, and subtypes of ovarian cancers. This reference is silent to the association of similar/overlapping treatment modalities for the treatment of other cancers, demonstrating the unpredictability in the art and lack of a nexus between treatment of different diseases with the same treatment compound(s).
Hinze et al. (Exploiting the Therapeutic Interaction of WNT Pathway Activation and Asparaginase for Colorectal Cancer Therapy. Cancer Discov. 2020 Nov;10(11):1690-1705. doi: 10.1158/2159-8290.CD-19-1472. Epub 2020 Jul 23) evidences “solid tumors are thought to be asparaginase-resistant via de novo asparagine synthesis. In leukemia, GSK3 α -dependent protein degradation, a catabolic amino acid source, mediates asparaginase resistance. We found that asparaginase is profoundly toxic to colorectal cancers with WNT-activating mutations that inhibit GSK3. Aberrant WNT activation can provide a therapeutic vulnerability in colorectal cancer.” (see pg. 1 abstract, throughout document). This reference evidences the use of asparaginase as a potential therapeutic for colorectal cancer, but is silent to its use for treatment of any and all cancers.
Hinze et al. (Synthetic Lethality of Wnt Pathway Activation and Asparaginase in Drug-Resistant Acute Leukemias. Cancer Cell. 2019 Apr 15;35(4):664-676.e7; hereinafter “Hinze2”) evidences “Asparaginase, an exogenous enzyme that deaminates the nonessential amino acid asparagine, has long been recognized to have activity against aggressive hematopoietic neoplasms. Asparaginase dose-intensification has improved outcomes for T-cell and B-cell acute lymphoblastic leukemias (T-ALL and B-ALL). This enzyme also has therapeutic activity in acute myeloid leukemias (AML) and in some non-Hodgkin lymphomas. The development of resistance to asparaginase-based treatment regimens has a poor prognosis, and effective therapeutic options are lacking for many of these patients. The sensitivity of acute leukemia cells to asparaginase is due, at least in part, to low expression of asparagine synthetase (ASNS) in these cells, resulting in their dependence on exogenous asparagine.”
The art above shows various treatment of different cancers and the potential of treating leukemia and colorectal cancer with apsaraginase, but all the references are silent to the ability to treat all the above disease states with the same treatment. Different types of cancers have different etiologies and treatment modalities, even cancers within the same broad category (e.g., leukemias), and thus cannot all be treated the same way. Simply put, there is no single, end-all-be-all treatment capable of treating the broad genus of any and all cancers encompassed by the instant claims. The art available at the time of filing fails to evidence the efficacy or predictability of a single product against all these cancers generally.
Thus, the state of the art suggests the unpredictability of the treatment of any and all cancers as encompassed by the broad scope of the instant claims.
The amount of direction provided by the inventor and the existence of working examples: The instant specification only discloses a single example involving (see Example 1).
There is no evidence, direction, or working examples from the specification the treatment of any and all cancers, apart from the speculative embodiments through the disclosure, as broadly encompassed by the claimed invention. It is therefore unknown if the asparaginase and shRNA G6PD inhibitor molecule as disclosed in the specification, would reliably be considered a treatment method for all cancers as broadly encompassed by the claimed invention. As such, there is a lack of reasonable direction in the specification to support the scope encompassed by the claims for the treatment of any cancers based on the disclosure.
Quantity of experimentation needed to make or use the invention based on the content of the disclosure: Given the state of the art regarding various related and unrelated cancers, and treatments associated with those cancers, the lack of a connection between overlapping or a single treatment modality capable of treating them, and Applicant’s lack of working examples, one of ordinary skill would not have been able to practice the instantly claimed invention without undue experimentation. For example, it is highly unknown or unpredictable if the asparaginase and G6PD inhibitor molecules would be capable of effectively treating ovarian cancer, melanomas, Hodgkin lymphoma, glioblastoma, testicular cancer, etc. Nothing in the specification remotely demonstrates or suggests that the claimed compositions would have any efficacy against all of these exemplified disease states, because the specification does not have any data suggesting that the compositions were ever administered to a subject or subjects having the diseases (other than colorectal cancer) broadly encompassed by the instant claims.
Though not controlling, the lack of working examples is, nevertheless, a factor to be considered in a case involving both physiological activity and an underdeveloped art. When a patent applicant chooses to forego exemplification and bases utility on broad terminology and general allegations, they run the risk that unless one of ordinary skill in the art would accept the allegations as obviously valid and correct, the PTO may, properly, ask for evidence to substantiate them. Ex parte Sudilosky, 21 USPQ2d 1702, 1705 (BPAI 1991); In re Novak, 134 USPA 335 (CCPA 1962); In re Fouche, 169 USPQ 429 (CCPA 1971).
The essential elements toward validation of a therapeutic is the ability to test the drug on subjects monitored during clinical symptoms of various cancers, and link those results with subsequent histological confirmation of the presence, decrease, or absence of symptomology. This irrefutable link between antecedent drug and subsequent knowledge of treatment of the reaction is the essence of a valid treatment agent. All of this underscores the criticality of providing workable examples which are not disclosed in the specification for any and all disorders as instantly claimed.
In essence, the specification merely presents an idea of, and leaves it entirely up to the practitioner to determine how to carry out the claimed methods. It has been established by legal decision that a patent is not a hunting license. It is not a reward for the search, but compensation for its successful conclusion. Tossing out the germ of an idea does not constitute an enabling disclosure. While every aspect of a generic claim need not have been carried out by an inventor or exemplified in the specification, reasonable detail must be provided in order to enable one of ordinary skill to understand and carry out the invention. It is true that a specification need not disclose what is well known in the art. However, that general, oft-repeated statement is merely a rule of supplementation, not a substitute for a basic enabling disclosure. It means that the omission of minor details does not cause a specification to fail to meet the enablement requirement under 35 U.S.C. 112(a) or 35 U.S.C. 112, first paragraph.
Therefore, 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 the claims.
Examiner’s Note
The claims have been rejected under 35 USC 112(a) for being enabled for treatment of colorectal cancer and leukemia in mice using asparaginase and G6PD inhibitor. Please note that the prior art rejections below reflect the scope of enablement rejection made above.
Claim Rejections - 35 USC § 103
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.
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 1-4, 6, and 8-12 are rejected under 35 U.S.C. 103 as being unpatentable over Hinze in view of Polat et al ((2021). Glutamine Modulates Expression and Function of Glucose 6-Phosphate Dehydrogenase via NRF2 in Colon Cancer Cells. Antioxidants, 10(9), 1349; hereinafter “Polat”).
Hinze teaches the treatment of solid subcutaneous colorectal cancer tumors in immunodeficient nude mice using asparaginase, an antileukemic enzyme that degrades the nonessential amino acid asparagine in mice (abstract, pg. 1695, col 2). Hinze also teaches that “once tumors engrafted (defined as growth to a volume >100 mm3), mice were randomized to treatment with vehicle or a single dose of asparaginase (Fig. 3A) (a method of treating cancer comprising administering to a subject having cancer an asparaginase as in claim 1). Asparaginase had little effect on Apc-deficient tumors, but had significant therapeutic activity against Rspo3 fusion tumors. Indeed, asparaginase therapy not only markedly delayed disease progression in Rspo3 fusion tumors (Fig. 3B), but also induced tumor regression in most treated mice (Fig. 3C), and prolonged progression-free survival (Fig. 3D), without inducing appreciable weight loss” (see pg. 1695, col 2 and Figs.).
Hinze does not explicitly teach an agent that inhibits glucose-6-phosphate dehydrogenase.
However, Polat teaches treatment of colon cancer using G6PD inhibitors (see title, abstract). Specifically, Polat teaches “enhanced glutamine metabolism and increased glucose 6-phosphate dehydrogenase (G6PD) expression have been related to a malignant phenotype in tumors. Both inhibition of G6PD and glutamine deprivation decrease the proliferation of colon cancer cells and induce cell cycle arrest and apoptosis” (see abstract; throughout). Polat also teaches that transfection of colon cancer cell lines using siRNAs reduces G6PD gene expression by more than 90%, decreased in cancer proliferation by about 25% (see pg. 11).
Therefore, it would have been prima facie obvious to one of ordinary skill at the time of filing to modify the method of treating colorectal cancer as taught by Hinze by including a G6PD inhibitor as taught by Polat to arrive at the claimed invention. One of ordinary skill would have been motivated to make the modification because Polat explicitly teaches that G6PD inhibitor molecules (such as siRNAs) are advantageously capable of decreasing the proliferation of colon cancer cells and induce cell cycle arrest and apoptosis.
Regarding claim 2-4, both references teach treating colorectal cancer, a solid tumor carcinoma, and leukemias (see above).
Regarding claim 6, Hinze teaches that solid tumors (like colorectal cancer tumors) are resistant to asparaginase (see abstract).
Regarding claim 8, Hinze teaches use of pegasparaginase/Oncaspar® (see pg. 1700).
Regarding claim 9-10, Polat teaches use of RNAi, specifically siRNA (see above).
Regarding claim 11-12, Polat teaches inhibiting expression level and activity of G6PD by 90% (see above).
Accordingly, the claimed invention was prima facie obvious to one of ordinary skill at the time of filing, especially in the absence of evidence to the contrary.
Second rejection
Claim 5 and 7 are rejected under 35 U.S.C. 103 as being unpatentable over Hinze and Polat as applied to claims 1-4, 6, and 8-12 above, and further in view of Hinze2.
As discussed above, the claims were rendered prima facie obvious over the combined teachings of Hinze and Polat.
Neither reference explicitly teaches treatment of ALL, CLL, CML, and AML.
However, Hinze2 teaches “Asparaginase, an exogenous enzyme that deaminates the nonessential amino acid asparagine, has long been recognized to have activity against aggressive hematopoietic neoplasms. Asparaginase dose-intensification has improved outcomes for T-cell and B-cell acute lymphoblastic leukemias (T-ALL and B-ALL). This enzyme also has therapeutic activity in acute myeloid leukemias (AML) and in some non-Hodgkin lymphomas. The development of resistance to asparaginase-based treatment regimens has a poor prognosis, and effective therapeutic options are lacking for many of these patients. The sensitivity of acute leukemia cells to asparaginase is due, at least in part, to low expression of asparagine synthetase (ASNS) in these cells, resulting in their dependence on exogenous asparagine.”
Therefore, it would have been prima facie obvious to one of ordinary skill at the time of filing to modify the method of treating colorectal cancer as taught by Hinze and Polat by treating AML, CLL, and ALL as taught by Hinze2 to arrive at the claimed invention. One of ordinary skill would have been motivated to make the modification because Hinze2 explicitly teaches that asparaginases are advantageously capable of improving outcomes for T-cell and B-cell acute lymphoblastic leukemias (T-ALL and B-ALL), and has therapeutic activity in acute myeloid leukemias (AML) and in some non-Hodgkin lymphomas.
Regarding claim 7, Hinze2 teaches asparaginase has activity against aggressive hematopoetic neoplasms such as ALL and AML (i.e., cancers not resistant to aparaginase) as these acute leukemia cells have low expression of asparagine synthase (see pg. 3, paragraph 1)
Accordingly, the claimed invention was prima facie obvious to one of ordinary skill at the time of filing, especially in the absence of evidence to the contrary.
Conclusion
NO CLAIMS ALLOWED.
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/G.C.R./Examiner, Art Unit 1651
/THOMAS J. VISONE/Supervisory Patent Examiner, Art Unit 1672
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