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 .
Status of the Claims
The status of the claims are as follows:
Claims 29-47 are pending.
Claims 29-35, 38-40, 42-43 and 45-47 are rejected
Claims 30, 35-37, 40-41, and 43-44 are objected to.
Priority
Acknowledgement is made that Instant Application 18/865,113, filed on 11/12/2024, is a National Stage Entry of PCT/EP2023/065610, filed on 06/12/2023, which claims Foreign Priority from EP22020284.0, filed on 06/13/2022.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 11/12/2024 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Claim Rejections - 35 USC § 112
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.
Claim 34 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. Specifically, the claim is directed to a method for treating an inflammatory disease and/or a genetic disorder wherein said disease or disorder is a result of or is mediated by overactive RAS-signaling by administering to the subject a compound of Formula I.
There is insufficient written description for this claim limitation in the disclosure. M.P.E.P. § 2163 states:
"An applicant shows possession of the claimed invention by describing the claimed invention with all of its limitations using such descriptive means as words, structures, figures, diagrams, and formulas that fully set forth the claimed invention...one must define a compound by 'whatever characteristics sufficiently distinguish it'. A lack of adequate written description issue also arises if the knowledge and level of skill in the art would not permit one skilled in the art to immediately envisage the product claimed from the disclosed process."
To provide adequate written description of a claimed genus, the specification must describe sufficient distinguishing identifying characteristics of treating an inflammatory disease and/or a genetic disorder, wherein said disease or disorder is a result of or is mediated by overactive RAS-signaling by administering a compound of Formula I. The factors to be considered include disclosure of complete or partial structure, physical and/or chemical properties, structure/function correlation, methods of making the claimed compounds or any combination thereof. In the instant case, no description of methods of treating said disease and/or disorder is disclosed.
The Instant Specification fails to define an “inflammatory disease” and further fails to define a “genetic disorder”. By broadest reasonable interpretation, the claim is directed to treating all inflammatory diseases and all genetic disorders, wherein said disease or disorder is a result of or is mediated by overactive RAS-signaling. It is generally accepted in the art that many RAS-mediated inflammatory diseases and genetic disorders (RASopathies) are etiologically distinct. For example, hyperactivation of RAS is generally triggered by mutations on codons 12, 13, or 61 (see Khan, RAS-Mediated Oncogenic Signaling Pathways in Human Malignancies. Seminars in Cancer Biology, 2019, 54, 1-13. Doi: 10.1016/j.semcancer.2018.03.001). Said mutation leads to inflammation by triggering persistent activation of various inflammatory mediators including TFs, inflammatory cells, cytokines, chemokines, and growth factors. Alternatively, Noonan syndrome is a paradigmatic, multisystem RASopathy that leads to distinctive craniofacial features, postnatal short stature, and a high prevalence of congenital cardiac defects, with pulmonary valve stenosis and hypertrophic cardiomyopathy being the hallmark lesions (see Calcaterra, Noonan Syndrome: A Comprehensive Review from Clinical Delineation to the Molecular Era of RASopathies and Lifelong Cardiologic Managemenet. Cardiogenetics, 2026, 16(2). Doi: 10.3390/cardiogenetics16020011). Most Noonan syndrome cases are caused by a mutation of the PTPN11 gene, causing gain-of-function of the SHP-2 protein, which leads to excessive dephosphorylation of RAS and irregular downstream effects. As such, one of ordinary skill in the art would recognize that a treatment option for a RAS-mediated inflammatory disease caused by, for example, a codon 12, 13, or 61 mutation, is unlikely to also treat a RAS-mediated genetic disorder, such as Noonan syndrome.
While it is recognized that adequate written description of a limitation is not required to be stated in haec verba in the specification or claims as originally filed, adequate written support for all claim limitations must arise from either an explicit or an implicit suggestion by the disclosure to show that such a concept as now claimed was actually in possession of the Applicant at the time of the invention.
The Instant Specification provides working examples of inhibiting KRAS mutations but fails to provide any working examples for treating an inflammatory disease and/or its etiology and also fails to provide any working examples for treating a genetic disorder and/or its etiology by administering to the subject a compound of Formula I. The lack of examples is not considered representative of the exceedingly vast number of possible disease states that are encompassed by the claims.
The description requirement of the patent statue requires a description of an invention, not an indication of a result that one might achieve if one made that invention. See In re Wilder, 736, F.2d 1516, 1521, 222 USPQ 369, 372-73 (Fed. Cir. 1984) (affirming rejection because the specification does “little more than outlin[e] goals appellants hope the claimed invention achieves and the problems the invention will hopefully ameliorate.”) Accordingly, it is deemed that the specification fails to provide adequate written description for the genus of the claims and does not reasonably convey to one skilled in the relevant art that the inventor(s), at the time the application was filed, had possession of the entire scope of the claimed invention.
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 31 recites the limitation "secondary mutation". Neither the claim itself nor the claim from which it depends refer to a primary mutation. Therefore, there is insufficient antecedent basis for this limitation in the claim.
Claim Rejections - 35 USC § 102
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 the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claim(s) 29-30, 32, 34-35, 38-39, and 40 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Preston (Mutational Analysis of K-Ras Codon 12 in Blood Samples of Patients with Acute Myeloid Leukemia. Leukemia Research, 2010, 34, 883-891. Doi:10.1016/j.leukres.2010.02.023).
Claim 29 is directed to a method of inhibiting RAS protein activation in a subject comprising administering to the subject a compound of Formula I or a pharmaceutically acceptable salt thereof
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wherein
R1-R4 are independently selected as H or C1-C4 alkyl; and
n is 1, 2, or 3.
Preston teaches acute myeloid leukemia (AML) comprises a number of activating and loss-of-function mutations including alterations in three closely related Ras genes –N-ras, K-ras, and, less frequently, H-ras (page 883, left column, paragraph 1). Naturally occurring alterations in the Ras genes on codon 12 lead to a constant activity of the Ras protein which can cause uncontrolled cell proliferation and escape from apoptosis (page 883, left column, paragraph 1). Blood samples were taken from 31 patients with AML at variable time points before and during treatment to detect the prevalence of K-ras codon 12 mutations (page 884, left column, paragraph 1). Nine of the 31 patients were found to have a K-ras mutation (page 890, left column, paragraph 2). A combination of high dose cytarabine and mitoxantrone were administered to 13 of the 31 patients (page 885, Table 2). Patients 7, 15, 23, and 28-29 were administered the mitoxantrone combination and also had a K-ras mutation (page 885, Table 2). The most common K-ras mutation observed was G12V, found in 7 of the 9 patients with K-ras mutation (page 890, left column, paragraph 3), while the exact K-ras mutation of the final two patients could not be determined.
The administered compound mitoxantrone is shown below and reads on Instant Formula I when R1-R4 is selected as H and n is 2.
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Therefore, claim 29 is anticipated by the teaching of Preston, wherein nine patients were administered a compound of Formula I to inhibit RAS protein activation.
Claim 30 is directed to the method of claim 29, wherein said subject has a mutation in a RAS protein selected from the group consisting of KRAS G12V, NRAS G12V, HRAS G12V, KRAS G12A, KRAS G12C, KRAS G12D, KRAS G12C/Y96D, KRAS G12C/Y96C, KRAS G12C/Y96S, KRAS G13C, KRAS G13D, KRAS G13S, KRAS Q61H, KRAS Q61R and KRAS Q61K.
Preston teaches the G12V mutation was found in seven of the nine patients with K-ras mutation (page 890, left column, paragraph 3), and further teaches patients 7, 15, 23, and 28-29 tested positive for a K-ras mutation and were administered the composition comprising mitoxantrone (page 885, Table 2).
Preston does not explicitly state which of patients 7, 15, 23, and 28-29 had the G12V mutation. However, one of ordinary skill in the art could at once envisage at least three of those patients had the G12V mutation because the exact K-ras mutation could not be determined for only two patients (page 890, left column, paragraph 3).
Claim 32 is directed to the method of claim 29, wherein the compound is compound A or a pharmaceutically acceptable salt thereof.
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Preston teaches 9 patients with K-ras mutations were administered mitoxantrone, which is compound A.
Claim 34 is directed to a method for treating a proliferative disorder, an inflammatory disease, and/or a genetic disorder, wherein said disease or disorder is a result of or is mediated by overactive RAS-signaling, in a subject in need thereof comprising administering to the subject a compound of Formula I or pharmaceutically acceptable salt thereof
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wherein
R1-R4 are independently selected as H or C1-C4 alkyl; and
n is 1, 2, or 3.
Preston teaches treating the proliferative disorder acute myeloid leukemia (AML) by administering to patients in need a pharmaceutical composition comprising mitoxantrone. As discussed above, AML occurs through alterations in the Ras genes on codon 12 that lead to constant activity of the Ras protein which can cause uncontrolled cell proliferation and escape from apoptosis (page 883, left column, paragraph 1).
Claim 35 is directed to the method of claim 34, wherein said subject has a mutation in a RAS protein selected from the group consisting of KRAS G12V, NRAS G12V, HRAS G12V, KRAS G12A, KRAS G12C, KRAS G12D, KRAS G12C/Y96D, KRAS G12C/Y96C, KRAS G12C/Y96S, KRAS G13C, KRAS G13D, KRAS G13S, KRAS Q61H, KRAS Q61R and KRAS Q61K.
Preston teaches the G12V mutation was found in seven of the nine patients with K-ras mutation (page 890, left column, paragraph 3), and further teaches patients 7, 15, 23, and 28-29 tested positive for a K-ras mutation and were administered the composition comprising mitoxantrone (page 885, Table 2).
Preston does not explicitly state which of patients 7, 15, 23, and 28-29 had the G12V mutation. However, one of ordinary skill in the art could at once envisage at least three of those patients had the G12V mutation because the exact K-ras mutation could not be determined for only two patients (page 890, left column, paragraph 3).
Claims 38-39 are directed to claim 34, wherein R1-R4 is H or C1-C2 alkyl and n is 2, or wherein said compound is compound A or a pharmaceutically acceptable salt thereof.
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Preston teaches patients suffering from AML were administered a combination therapy comprising mitoxantrone, which is compound A.
Claim 40 is directed to the method of claim 39, wherein said subject has a mutation in a RAS protein selected from the group consisting of KRAS G12V, NRAS G12V, HRAS G12V, KRAS G12A, KRAS G12C, KRAS G12D, KRAS G12C/Y96D, KRAS G12C/Y96C, KRAS G12C/Y96S, KRAS G13C, KRAS G13D, KRAS G13S, KRAS Q61H, KRAS Q61R and KRAS Q61K.
Claim(s) 37 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Preston as evidenced by Rubinson (Sotorasib Is a Pan-RASG12C Inhibitor Capable of Driving Clinical Response in NRASG12C Cancers. Cancer Discovery, 2024, 14(5), 727-726. Doi: 10.1158/2159-8290.CD-23-1138).
Claim 37 is directed to the method of claim 34, wherein said disorder or disease is resistant to treatment with a RAS mutation specific inhibitor different from compounds of Formula I.
The teaching of Preston is discussed above and incorporated herein by reference.
A RAS mutation specific inhibitor, sotorasib, is designed for G12C mutations, whereby it covalently binds to the cysteine residue, locking the protein in the inactive state and blocking downstream oncogenic signaling (see Rubinson). The patients of Preston who have a G12V mutation inherently lack the necessary nucleophile to effectively interact with, e.g., sotorasib. Accordingly, Preston teaches patients whose disorder is resistant to treatment with at least the RAS mutation specific inhibitor sotorasib.
Claim(s) 47 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Turan-Zitouni (Synthesis and Evaluation of Bis-Thiazole Derivatives as New Anticancer Agents. Eur. J. Med. Chem. 2016, 107, 288-294. Doi 10.1016/j.ejmech.2015.11.002), as evidenced by ATCC (Cell Lines by Gene Mutation. 2022) and evidenced by Cellosaurus (5RP7, entry created 04/04/2012. https://www.cellosaurus.org/CVCL_5490).
Claim 47 is directed to a method of inhibiting proliferation of a cell population sensitive towards inhibiting RAS activation in vitro or ex vivo, the method comprising contacting the cell population with at least one compound of Formula I.
Turan-Zitouni teaches new bis-thiazole derivatives and tested the cytotoxic effects of lead compound, compound 5 (not shown), against A549 human lung adenocarcinoma, C6 rat glioma, 5RP7 H-ras oncogene transformed rat embryonic fibroblast and NIH/3T3 mouse embryonic fibroblast cell lines in MITT assay (abstract). Mitoxantrone was used as the positive control against each cell line, as shown in the table from the graphical abstract:
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The A549 lung adenocarcinoma cell line carries a K-ras G12S mutation (see ATCC).
The 5RP7 cell line carries a H-ras G12V mutation (see Cellosaurus).
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 text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
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.
Claim(s) 33 and 42 is/are rejected under 35 U.S.C. 103 as being unpatentable over Preston in view of Berge (Pharmaceutical Salts. J. Pharm. Sci. 1977, 66(1), 1-19).
Claim 33 is directed to the method of claim 32 wherein the pharmaceutically acceptable salt is compound B or a pharmaceutically acceptable salt thereof
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Claims 32 and 29, from which claim 33 depends, are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Preston. The teaching of Preston are discussed above and incorporated herein by reference.
The difference between the teaching of Preston and the Instant Application is that Preston fails to teach wherein patients are treated with the dihydrochloride salt of mitoxantrone.
However, Berge teaches a variety of salt forms approved for use by the Food and Drug Administration (FDA) (page 2, Table 1), such as, inter alia, the hydrochloride salt.
One of ordinary skill in the art could have applied prong (E) of the KSR rationale, in which choosing from a finite number of identified, predictable solutions, with a reasonable expectation of success, it would have been prima facie obvious to identify the hydrochloride salt of mitoxantrone as a suitable option for treating patients with AML, thus arriving at the current invention.
Claim 42 is directed to the method of claim 34, wherein said compound is compound B of a pharmaceutically acceptable said thereof.
Claim 34, from which claim 42 depends, is rejected under 35 U.S.C. 102(a)(1) as being anticipated by Preston. The teaching of Preston is discussed above and incorporated herein by reference.
The difference between the teaching of Preston and the Instant Application is that Preston fails to teach wherein patients are treated with the dihydrochloride salt of mitoxantrone.
However, as discussed above, Berge renders obvious HCl salts of mitoxantrone.
Claim 43 is directed to the method of claim 42, wherein said subject has a mutation in a RAS protein selected from the group consisting of KRAS G12V, NRAS G12V, HRAS G12V, KRAS G12A, KRAS G12C, KRAS G12D, KRAS G12C/Y96D, KRAS G12C/Y96C, KRAS G12C/Y96S, KRAS G13C, KRAS G13D, KRAS G13S, KRAS Q61H, KRAS Q61R and KRAS Q61K.
The teaching of Preston is discussed above and incorporated herein by reference. Specifically, Preston teaches administering mitoxantrone to patients with KRAS G12V.
The difference between the teaching of Preston and the Instant Application is that Preston fails to teach wherein mitoxantrone is in the 2HCl salt form.
However, as discussed above, Berge renders obvious HCl salts of mitoxantrone.
Claim(s) 45-46 is/are rejected under 35 U.S.C. 103 as being unpatentable over Preston in view of Turan-Zitouni as evidenced by ATCC and motivated by White (A Phase II Trial of High-Dose Cytarabine and Cisplatin in Previously Untreated Non-Small Cell Carcinoma of the Lung. Cancer. 1990, 65(8) 1700-1703. Doi: 10.1002/1097-0142(19900415)65:8<1700::aid-cncr2820650806>3.0.co;2-5).
Claims 45-46 are directed to the method of claim 34, wherein the subject has a proliferative disorder, wherein the proliferative disorder is a cancer selected from the provided group, and wherein administration inhibits growth, proliferation, or metastasis of cancer cells in said subject.
Claim 34, from which claims 45-46 depend, is rejected under 35 U.S.C. 102(a)(1) as being anticipated by Preston. The teachings of Preston and the teaching of Turan-Zitouni as evidenced by ATCC are discussed above and incorporated herein by reference.
The difference between the teaching of Preston and the Instant Application is that Preston teaches administering a compound of Formula I to patients with AML who also tested positive for K-ras mutations and fails to teach administering a compound of Formula I to patients with a proliferative disorder, wherein the proliferative disorder is a cancer, and wherein administration of the compound inhibits growth, proliferation, or metastasis of cancer cells.
However, Turan-Zitouni teaches mitoxantrone has an IC50 of 15.7 ± 4 µM against A549 lung adenocarcinoma cell line. The A549 lung adenocarcinoma cell line contains a K-ras G12S mutation (see ATCC)
One of ordinary skill in the art would have been motivated to combine the above teachings because they teach the same field of endeavor of treating proliferative disorders with underlying K-ras mutations. The combined teachings would have led to a method of treating lung cancer by administering a combination of cytarabine and mitoxantrone. Said artisan would have been further motivated to do so through the teaching of White, wherein a combination comprising cytarabine and cisplatin produced synergistic myelotoxicity in patients (page 1703, left column, paragraph 1), 17 of which had adenocarcinoma (page 1702, Table 1). Therefore, said skilled artisan would have found it prima facie obvious to administer a combination comprising cytarabine and mitoxantrone to patients to treat adenocarcinoma.
Claim Objections
Claims 30, 35, 40, and 43 are objected to containing a minor informality. Each of the claims contain the phrase “KRASG13S” which should be correctly rewritten as “KRAS G13S”. Appropriate action is required.
Claim 35 is objected to because the number “35” is in a different font than the rest of the Application. Appropriate action is required.
Claim 41 is objected to for containing a minor informality. The claim recites the limitation “wherein said subject a mutation in a RAS protein” which should be corrected to “wherein said subject has a mutation in a RAS protein.” Appropriate action is required.
Claims 36, 41, and 44 are objected to as being dependent upon a rejected base claim but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims.
The claims are directed to methods of administering a compound of Formula I to a subject to inhibit RAS protein activation, wherein said subject has a mutation in a RAS protein selected from the group consisting of KRAS G12C/Y96D, KRAS G12C/Y96C and/or KRAS G12C/Y96S, for the treatment of a disorder or disease that is resistant to treatment with a RAS mutation specific inhibitor that is different from compounds of Formula I.
The KRAS Y96 mutation is an acquired resistance mechanism to covalent KRAS G12C inhibitors, such as AMG510 (sotorasib), the mechanism of action of which was only recently solved (see Zhuang, Mechanistic Insights Into The Clinical Y96D Mutation With Acquired Resistance to AMG510 in The KRASG12C. Front. Oncol. 2022, 12:915512). Accordingly, treatment options for KRAS Y96 mutations are currently limited. The instantly claimed compounds of Formula I, for example mitoxantrone, are not common in the art for treating KRAS-mutant cancers; however, few select examples exist (e.g., KRAS G12V in treating AML). The art is silent on any compound of Formula I used to inhibit RAS protein with KRAS Y96 mutations. Therefore, one of ordinary skill in the art would not have found it obvious to overcome treatment resistance caused by KRAS Y96 mutation by administering compounds of Formula I.
Conclusions
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/P.A./
Examiner, Art Unit 1621
/CLINTON A BROOKS/Supervisory Patent Examiner, Art Unit 1621
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