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
Claims 1-17 are currently pending and under examination.
Priority
Acknowledgment is made of applicant’s claim for foreign priority under 35 U.S.C. 119 (a)-(d). The certified copy has been filed in parent Application No. PCT/CN2021/136336, filed on December 8 2021. No. PCT/CN2022/095857, filed on May 30 2022. No. PCT/CN2022/123120, filed on September 30 2022.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 09/4/2024. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Specification
The disclosure is objected to because of the following informalities:
On page 40, line 11, the specification recites “same of different,”. The language should be corrected to same or different.
On page 3, lines 22, the specification recites “one or more one or more oxo,” which contains a duplicated phrase, the language should be corrected to one or more oxo.
One page 5, line 4, the specification recites “wherein the C1-C6 alky,”. The language should be corrected to wherein the C1-C6 alkyl.
Appropriate correction is required.
Claim Objections
Claim 1-2, 11, 14, and 16 are objected to because of the following informalities:
Claim 1 recites “a stereoisomer thereof, or a pharmaceutically acceptable salt, solvates and prodrugs thereof”, The plural terms “solvates” and “prodrugs” are inconsistent with the singular phrase “a pharmaceutically acceptable” in lines 5-6, p. 2. The language should be corrected to a stereoisomer thereof, or a pharmaceutically acceptable salt, solvate or prodrug thereof. Alternatively, if plural forms are intended, the language should be corrected to a stereoisomer thereof, a pharmaceutically acceptable salt, solvates and prodrugs thereof.
In claim 1, “Wherein” and “Each” in lines 8-9, p. 2. These should be corrected to lowercase wherein and each.
Claim 2 recites “a stereoisomer thereof, or a pharmaceutically acceptable salt, solvates and prodrugs thereof”, The plural terms “solvates” and “prodrugs” are inconsistent with the singular phrase “a pharmaceutically acceptable” in lines 27-28, p. 3. The language should be corrected to a stereoisomer thereof, or a pharmaceutically acceptable salt, solvate or prodrug thereof. Alternatively, if plural forms are intended, the language should be corrected to a stereoisomer thereof, a pharmaceutically acceptable salt, solvates and prodrugs thereof.
In claim 11, “Wherein” in line 8, p. 7. It should be corrected to lowercase wherein.
In claim 14, “Wherein” in line 7, p. 14. It should be corrected to lowercase wherein.
Claim 14 recites “one or more one or more oxo,” which contains a duplicated phrase, the language should be corrected to one or more oxo. Claim 14 also recites “wherein the C1-C6 alky ”. The language should be corrected to wherein the C1-C6 alkyl.
In claim 16, “Wherein” in line 2, p. 18. It should be corrected to lowercase wherein.
Claim 16 recites “—N((Rg)S(O)2Rg,”. The language appears to be intended as —N(Rg)S(O)2Rg.
Appropriate correction is required.
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.
Claims 1-17 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.
Instant claims recite compounds of Formula VI, Formula VII, Formula VII-1, and Formula VIII, including “solvates and prodrugs thereof.” However, the specification does not reasonably convey possession of the full scope of the claimed prodrugs and solvates.
Adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method for isolating it. See Fiers v. Revel, 25 USPQ2d 1601, 1606 (CAFC 1993) and Amgen Inc. v. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016.
According to MPEP 2163 I, “[t]o satisfy the written description requirement, a patent specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. See, e.g., Moba, B.V. v. Diamond Automation, Inc., 325 F.3d 1306, 1319, 66 USPQ2d 1429, 1438 (Fed. Cir. 2003); Vas-Cath, Inc. v. Mahurkar, 935 F.2d at 1563, 19 USPQ2d at 1116”. Additionally, according to MPEP II-A-3-a-ii, “[t]he written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, reduction to drawings, or by disclosure of relevant, identifying characteristics, i.e., structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the inventor was in possession of the claimed genus. See Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406”; “[a] ‘representative number of species’ means that the species which are adequately described are representative of the entire genus. Thus, when there is substantial variation within the genus, one must describe a sufficient variety of species to reflect the variation within the genus. See AbbVie Deutschland GmbH & Co., KG v. Janssen Biotech, Inc., 759 F.3d 1285, 1300, 111 USPQ2d 1780, 1790 (Fed. Cir. 2014).”; and “’[a] patentee will not be deemed to have invented species sufficient to constitute the genus by virtue of having disclosed a single species when … the evidence indicates ordinary artisans could not predict the operability in the invention of any species other than the one disclosed.’ In re Curtis, 354 F.3d 1347, 1358, 69 USPQ2d 1274, 1282 (Fed. Cir. 2004)”
With respect to prodrugs, the specification defines a prodrug broadly as any compound that converts into a compound of the present invention when administered to a subject, for example upon metabolic processing (see p. 42, line 6). The specification does not identify representative prodrug structures, does not identify specific promoieties for the claimed chromenone PI3Kα inhibitor compounds, does not provide synthetic examples of prodrugs, and does not provide data or structural guidance showing which derivatives would convert to the parent compounds in vivo. The working examples instead describe preparation and characterization of parent compounds, typically by LC-MS and/or NMR.
Although some ester intermediates appear in the synthetic schemes, those compounds are used as intermediates and are converted to the corresponding final acid compounds. For example, a tert-butyl benzoate intermediate is treated with TFA and purified to give the corresponding benzoic acid product (see p. 53, line 1). Such disclosure of synthetic intermediates does not demonstrate possession of the broad genus of pharmaceutically acceptable prodrugs, because the specification does not identify those intermediates as prodrugs, does not show administration or metabolic conversion to the parent compound, and does not provide a structure–function correlation for prodrug conversion.
With respect to solvates, the specification states only that a solvate is formed by treating a compound in a solvent and that hydrates are formed when water is used (see p. 42, line 4). The specification does not disclose representative isolated solvate species, does not identify particular solvents, stoichiometries, crystal forms, hydrate levels, preparation conditions, or characterization data for solvates of the claimed compounds. The examples use solvents for synthesis, purification, and dosing formulations, but use of a solvent during synthesis or formulation does not itself demonstrate possession of isolated solvate forms across the full claimed genus. For example, the specification describes dosing solutions prepared in DMSO/HP-β-CD/water for PK testing (see p. 218, line 10), but this is a formulation disclosure, not a disclosure of isolated solvates.
Accordingly, the specification reasonably supports the specifically disclosed parent compounds and any properly supported narrow forms thereof, but does not reasonably convey possession of the full scope of all prodrugs and solvates encompassed by claims 1–17. The claims therefore exceed the scope of applicant’s described invention.
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 and 13 are rejected under 35 U.S.C. §103 as being unpatentable over Anderson et al. (WO2022235574A1, hereinafter "WO’574").
WO’574 teaches allosteric chromenone inhibitors of PI3K useful for treating PI3K-associated diseases, including cancers (see e.g., p. 1, [1]). WO’574 teaches chromenone PI3K inhibitors having the same general medicinal-chemistry framework as the presently claimed Formula VII compounds, including a chromenone core, 6-methyl substitution, a chiral ethylamino linker, a benzoic acid/anthranilic acid region, and a 2-aryl substituent (see e.g., p. 5). WO’574 discloses Example 22, 2-[[(1R)-1-(6-methyl-4-oxo-2-phenyl-chromen-8-yl)ethyl]amino]benzoic acid
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(see e.g. p. 220, [571]). WO’574 also discloses related chromenone PI3K inhibitor compounds, including Example 164
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(see e.g., p. 253).
Claim 1 is directed to Formula VII compounds, including stereoisomers, pharmaceutically acceptable salts, solvates, and prodrugs thereof. WO’574 teaches a Formula VII-type anthranilic acid-aminoethyl-chromenone PI3K inhibitor having a chromenone core, 6-methyl substitution, chiral ethylamino linker, carboxylic acid-containing aryl group, and 2-phenyl substituent. Therefore, WO’574 teaches the closest base scaffold and reads on at least the 2-phenyl Formula VII species encompassed by claim 1.
Claim 13 lists specific Formula VII species. WO’574 teaches at least the phenyl-substituted anthranilic acid chromenone species corresponding to Example 22, having a 6-methyl-4-oxo-2-phenyl-chromen-8-yl core linked through a chiral ethylamino group to benzoic acid. Therefore, to the extent claim 13 reads on the elected 2-phenyl species, claim 13 would have been obvious over WO’574.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to select and use the chromenone PI3K inhibitor compounds taught by WO’574 as PI3K-associated disease inhibitors, because WO’574 expressly teaches the same allosteric chromenone PI3K inhibitor scaffold and the same PI3K-associated disease use. A reasonable expectation of success would have existed because WO’574 provides working chromenone PI3K inhibitor examples in the same structural class.
Claims 1–13 are rejected under 35 U.S.C. §103 as being unpatentable over Anderson et al. (WO2022235574A1, hereinafter "WO’574"), in view of Anderson et al. (WO2022235575A1, hereinafter "WO’575").
As set forth above, WO’574 teaches the anthranilic acid-aminoethyl-chromenone PI3K inhibitor scaffold of claim 1 and at least the 2-phenyl Formula VII species of claim 13. WO’574 provides a close 2-phenyl chromenone lead compound. However, WO’574 does not expressly teach the full scope of Formula VII, including every heteroaryl 2-position substituent and every heteroaryl species recited in claims 2-13.
WO’575 teaches closely related allosteric chromenone PI3K inhibitors and shows that the chromenone 2-position may contain heteroaryl substituents (see e.g., p. 5, last line). WO’575 teaches pyridyl, pyrimidinyl, triazolyl, and related heteroaryl chromenone analogs (see e.g., pp. 5-6). WO’575 discloses working examples including Example 57, a triazolyl-substituted chromenone analog
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(see e.g., p. 260, [532]), Example 142, a pyridyl-substituted chromenone analog
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(see e.g., p. 260, [535]), Example 14
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(see e.g., p. 230), and Example 47
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(see e.g., p. 238). WO’575 also teaches PI3K-alpha kinase activity testing against wild-type and H1047R mutant PI3Kalpha (see e.g., p. 273, [537]).
WO’575 fills the deficiency of WO’574 for claims 1-13 because it teaches replacing or modifying the 2-phenyl substituent of the chromenone scaffold with heteroaryl groups, including pyridyl, pyrimidinyl, and triazolyl groups, while retaining PI3Kalpha inhibitory activity. These teachings correspond to the heteroaryl substituent alternatives and heteroaryl species recited in claims 1-13.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify the 2-phenyl chromenone lead compound of WO’574 using the heteroaryl substituents taught by WO’575 to obtain additional Formula VII PI3Kalpha inhibitors. One of ordinary skill in the art would have been motivated to make such substitutions to optimize potency, selectivity, mutant PI3Kalpha activity, and physicochemical properties within a known allosteric chromenone PI3Kalpha inhibitor scaffold. A reasonable expectation of success would have existed because WO’575 provides working heteroaryl-substituted chromenone analogs and PI3Kalpha WT/H1047R activity testing.
Claims 2-12 further limit Formula VII substituents, ring atoms, linkers, Ring B, R groups, and Formula VII-1 subgenera. The limitations of claims 2-12 are within the predictable structural modifications taught by WO’574 and WO’575 for the same allosteric chromenone PI3K inhibitor platform. Therefore, claims 2-12 would have been obvious over WO’574 in view of WO’575.
Claim 13 lists specific Formula VII species. To the extent claim 13 reads on an elected heteroaryl-substituted species, the claimed species would have been obvious because WO’574 teaches the same anthranilic acid-aminoethyl-chromenone PI3K inhibitor framework and WO’575 teaches replacement of the 2-phenyl group with heteroaryl groups, including triazolyl and pyridyl groups, while maintaining PI3Kalpha inhibitory activity.
Claims 1–15 are rejected under 35 U.S.C. §103 as being unpatentable over Anderson et al. (WO2022235574A1, hereinafter "WO’574"), in view of Anderson et al. (WO2022235575A1, hereinafter "WO’575"), and further in view of Anderson et al. (WO2022251482A1, hereinafter "WO’482").
As set forth above, WO’574 teaches the closest anthranilic acid-aminoethyl-chromenone PI3K inhibitor scaffold of claim 1 and at least the 2-phenyl species of claim 13. WO’575 teaches heteroaryl 2-position substitution, including pyridyl, pyrimidinyl, and triazolyl chromenone analogs, and provides PI3Kalpha WT/H1047R activity testing. However, WO’574 and WO’575 do not expressly teach every fused heteroaryl, bicyclic heteroaryl, oxindole, indazole, benzodioxole, or substituted aryl/heteroaryl 2-position substituent shown in the species claims, and do not fully address the Formula VI species of claims 14-15.
WO’482 teaches allosteric chromenone PI3K inhibitors in the same field and provides additional structurally close examples in which the chromenone is substituted with bicyclic or fused heteroaryl groups and substituted aryl or heteroaryl groups (see e.g., p. 476, claim 1). WO’482 discloses examples including Example 31
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(see e.g., p. 409, [806]), Example 1
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(see e.g., p. 376, [796]), Example 46
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(see e.g., p. 415), Example 91
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(see e.g., p. 419), Example 30
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(see e.g., p. 406, [799]), and Example 54
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(see e.g., p. 383), which include indazole, oxindole, benzodioxole, fused heteroaryl, and heteroaryl-type chromenone analogs. WO’482 also reports PI3Kalpha wild-type and H1047R mutant biochemical IC50 data for allosteric chromenone PI3K inhibitors (see e.g., p. 458, [847]).
WO’482 fills the remaining deficiencies of WO’574 and WO’575 for claims 1-15 by teaching additional fused heteroaryl, bicyclic heteroaryl, oxindole, indazole, benzodioxole, and substituted aryl or heteroaryl 2-position groups in the same allosteric chromenone PI3K inhibitor class, along with PI3Kalpha activity data. These teachings correspond to the additional 2-position substituent patterns recited in claims 1-13 and the specific Formula VI species recited in claims 14-15.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify the 2-phenyl or heteroaryl chromenone lead compounds taught by WO’574 and WO’575 using the fused heteroaryl, bicyclic heteroaryl, oxindole, indazole, benzodioxole, and substituted aryl or heteroaryl substituents taught by WO’482 to obtain additional Formula VII and Formula VI PI3Kalpha inhibitors. One of ordinary skill in the art would have been motivated to make such substitutions to optimize potency, selectivity, mutant PI3Kalpha activity, and physicochemical properties. A reasonable expectation of success would have existed because WO’575 and WO’482 disclose working chromenone analogs and PI3Kalpha WT/H1047R activity testing.
Claim 14 is an independent claim directed to Formula VI compounds. Formula VI retains the same allosteric chromenone PI3K inhibitor platform, including an acid-containing aryl or heteroaryl region, chiral linker, chromenone core, and varied terminal aryl, heteroaryl, fused heteroaryl, or bicyclic heteroaryl substituent at the chromenone 2-position. The differences between Formula VI and the cited examples are predictable linker, ring, and 2-position substituent variations within the same PI3Kalpha inhibitor scaffold. Therefore, claim 14 would have been obvious over WO’574 in view of WO’575 and WO’482.
Claim 15 lists specific Formula VI species. To the extent claim 15 reads on the elected species, the claimed species would have been obvious because WO’574 provides a close chromenone PI3K lead, WO’575 teaches heteroaryl substitution at corresponding positions, and WO’482 teaches specific chromenone PI3K inhibitors having indazole, oxindole, benzodioxole, fused heteroaryl, or related heteroaryl-type 2-position substituents with PI3Kalpha WT/H1047R activity data.
Claims 1–17 are rejected under 35 U.S.C. §103 as being unpatentable over Anderson et al. (WO2022235574A1, hereinafter "WO’574"), in view of Anderson et al. (WO2022235575A1, hereinafter "WO’575"), further in view of Anderson et al. (WO2022251482A1, hereinafter "WO’482"), and further in view of Anderson et al. (WO2021202964A1, hereinafter "WO’964").
As set forth in the preceding rejection, WO’574, WO’575, and WO’482 teach the subject matter of claims 1-15, including the allosteric chromenone PI3K inhibitor scaffold, the anthranilic acid-aminoethyl linker region, and aryl, heteroaryl, fused heteroaryl, bicyclic heteroaryl, oxindole, indazole, benzodioxole, and substituted aryl or heteroaryl 2-position substituents. Claims 16-17 require an additional teaching because claim 16 is directed to Formula VIII compounds and the G group recited in claim 16 is not limited to carboxylic acid. WO’574, WO’575, and WO’482 do not expressly teach all of the non-carboxylic acid G groups recited in claim 16.
WO’964 teaches allosteric chromenone PI3K inhibitors useful for PI3K modulation (see e.g., p. 1, [2]). WO’964 expressly states that the compounds modulate PI3K, including PI3Kalpha (see e.g., p. 3, [11]). WO’964 further teaches substituent alternatives corresponding to acid replacements or acid bioisosteres, including amide, sulfonamide, tetrazole, phosphonate/phosphonic acid, and boron-containing groups. For example, WO’964 teaches hydroxamic acid, N-sulfonyl acetamide, and tetrazolyl analogs (see e.g., p. 413, Examples 418-423; p. 271, Examples 19-22) and boronic acid analogs (see e.g., p. 355, Example 356, [1252]) in the same allosteric chromenone PI3K inhibitor class.
WO’964 fills the remaining deficiency for claims 16-17 by teaching that, in the same allosteric chromenone PI3K inhibitor class, the acid-containing region may be replaced or modified with non-carboxylic acid G groups and acid bioisosteres, including hydroxamic acid, amide, sulfonamide, tetrazole, phosphonate/phosphonic acid, and boron-containing groups. These teachings correspond to the G group alternatives recited in claim 16 and the species recited in claim 17.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify the acid-containing region of the chromenone PI3K inhibitor lead compounds of WO’574, WO’575, and WO’482 using the non-carboxylic acid G groups taught by WO’964 to obtain additional Formula VIII PI3Kalpha inhibitors. One of ordinary skill in the art would have been motivated to make such modifications to maintain the interaction pattern of the acid-containing region while optimizing acidity, permeability, metabolic stability, potency, selectivity, and pharmacokinetic properties. A reasonable expectation of success would have existed because WO’964 teaches these non-carboxylic acid groups in the same allosteric chromenone PI3K inhibitor class, and WO’482 further confirms that the class had measurable PI3Kalpha WT/H1047R activity.
Claim 17 lists specific Formula VIII species. To the extent claim 17 reads on the elected species, the claimed species would have been obvious because WO’574, WO’575, and WO’482 teach the allosteric chromenone PI3K inhibitor scaffold and 2-position aryl, heteroaryl, fused heteroaryl, bicyclic heteroaryl, oxindole, indazole, benzodioxole, and substituted aryl or heteroaryl modifications, while WO’964 teaches replacement or modification of the corresponding acid-containing region with non-carboxylic acid G groups in the same allosteric chromenone PI3K inhibitor class.
Therefore, claims 1-17 are unpatentable under 35 U.S.C. §103.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to GENBIN SHI whose telephone number is (571)272-8796. The examiner can normally be reached Mon-Fri, 8:00am-5pm.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Amy Clark can be reached at (571) 272-1310. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/G.S./ Examiner, Art Unit 1628 /AMY L CLARK/Supervisory Patent Examiner, Art Unit 1628
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