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, 8-11, 22-23, 40-43, 50-53, 66-69, 139-140, 145, 147, 149, 155 and 157 are pending in the instant application and subject to examination herein.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 03/26/2024 and 03/02/2026 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements are being considered by the examiner.
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.
Claims 1, 8-11, 22-23, 40-43, 50-53, 66-69, 140, 145, 147, 149, 155 and 157 are 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 1 is drawn to a genus of bifunctional compounds of Formula (I), shown below:
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Claim 1 further defines elements R1, R2, R3, U, V, X, Y, XE, YE and ZE in specific chemical terms, while defining the element L only with the statement that “L is a linker”. No structure is provided in claim 1 with regard to the “linker” L.
The instant Specification includes the word “linker” 13 times (pages 26, 73 and 112-113). On page 26, the structure of Formula (I) is provided in the same manner as instant claim 1, with only the proviso that “L is a linker” (paragraph [0061]). On pages 73 and 112-113, the Specification provides that “In certain embodiments, L is a linker having the structure of -ZL-(RL-ZL)-“, with further definitions of the elements ZL and RL provided therein (paragraphs [00143] and [00201]). Given that the definition is only provided for “certain embodiments”, a person of ordinary skill in the art would not assume that these limitations apply to instant claim 1.
The term “linker”, in the instant invention, is understood in the context of proteolysis-targeting chimeras (PROTACs), which are compounds used to direct proteins-of-interest (POIs) toward degradation by cellular proteolysis, as taught, for example, by Yang (Yang, et al.; Journal of Medicinal Chemistry, v62, pp9471-9487; 2019). Yang teaches a study on the effects of tuning the structure of a PROTAC linker, and therein teaches that “A typical PROTAC small-molecule degrader consists of three essential components: a ligand that binds the protein of interest, a second ligand that binds to and recruits an E3 ligase degradation complex, and a linker tethering the two ligands together” (page 9471). While the instant Specification does not include the words “PROTAC” or “E3 ligase”, a person of ordinary skill in the art (POSITA) would at once recognize that the compounds of the instant invention are PROTAC compounds, based on the following evidence:
A ligand for binding the protein SOS1 (son of sevenless homolog 1) is found at one end of instantly disclosed compounds, consisting of a benzylamine-substituted dialkoxyquinazoline core, and would be recognized by a POSITA in comparison to Applicant’s disclosure of known art in the field of SOS1-inhibition (“Hillig, et al., Proc. Nat. Acad. Sci. 2019, 114, 2551-60”1 on Specification page 2), which discloses SOS1 inhibitors bearing this scaffold (examples: Hillig’s compounds 15 and 16):
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;
The well-known glutarimide moiety found at the opposite end of the instantly disclosed compounds, which Yang teaches is a binding moiety for cereblon, an E3-ligase, with the glutarimide2 portion of lenalidomide engaging in a hydrogen bond with cereblon in a crystal structure of the bound cereblon-lenalidomide complex (page 9477);
The disclosure in the instant Specification that the invention regards SOS1 protein degraders (paragraph [0002]).
Thus, a POSITA would understand Applicant’s invention as a genus of PROTAC compounds, and would understand claim 1 as claiming a genus of PROTAC compounds having a defined ligand for E3-ligase binding and a defined ligand for SOS1-binding, and an undefined linker. Given that the linker can be any molecule that accomplishes a molecular linkage between the two ligands, claim 1 is rendered indefinite because a POSITA would not be able to surmise what structure is not within the scope of a linker for claim 1, and therefore what overall molecular structure(s) is/are not in scope of the genus of Formula (I) of claim 1. Claims 8-11, 22-23, 40-43, 50-53, 66-69, 140, 145, 147, 149, 155 and 157 depend directly or indirectly from claim 1 and each of these claims is indefinite because none of these claims provides structure for the linker “L”.
Claims 8-11 further limit claim 1, each to a narrower genus defined by a specific formula, and each of these claims modifies Formula (I) of claim 1 in a particular manner, specifically to modify the original element R2 to a sp3 carbon with substituents R2a, R2b and R2c, without providing structure for any of R2a, R2b and R2c. A person of ordinary skill in the art would understand that the sp3 carbon with substituents R2a, R2b and R2c, in each of the genera of claims 8-11, must, as a whole group, fall within the scope of the original substituent R2; however, a person of ordinary skill in the art would not understand whether and/or how each of the genera of claims 8-11 will further limit the genus of claim 1 with regard to the complete structure when the variables R2a, R2b and R2c are undefined. The instant Specification provides structure for R2a and R2b for “certain embodiments” only, and only in one instance: in paragraph [00104], R2a is defined as “hydrogen, methyl, or ethyl” and R2b is hydrogen. A person of ordinary skill in the art could not assume that these limitations apply to claims 8-11. The substituent R2c is not given any limitations anywhere in the instant Specification. Claims 22-23, 40-43, 50-53 and 66-69 depend directly or indirectly from claim 1 and each of these claims is indefinite because, while these claims do replace the variable substituent R2c with defined structural moiety(s), none of these claims provide structure for substituents R2a and R2b.
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 145, 147, 149, 155 and 157 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.
The Invention in General:
Applicant has disclosed an invention in the field of directed protein degradation using bifunctional small molecules, commonly referred to as “PROTAC” compounds.
The Claimed Invention:
Claim 1 is drawn to a genus of compounds of Formula (I), bearing a glutarimide3 (or derivative thereof) at one terminus, a quinazoline (or derivative thereof) at the other terminus, and an undefined “linker” connecting the two termini:
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(instant Formula (I) of claim 1).
Claims 145, 147, 149, 155 and 157 further limit claim 1, each to a distinct method that comprises administering a compound of claim 1 to a subject or contacting a cell or protein with an effective amount of a compound of claim 1. The methods are directed as follows:
Claim 145: Treating, preventing, or ameliorating a disorder, disease or condition mediated by a son of sevenless homolog 1 (SOS1) in a subject.
Claim 147: Treating, preventing, or ameliorating a disorder, disease or condition mediated by a Ras in a subject.
Claim 149: Treating, preventing or ameliorating one or more symptoms of a proliferative disease.
Claim 155: Inhibiting the growth of a cell.
Claim 157: Inducing degradation of an SOS1.
The Instant Disclosure:
Applicant discloses that oncogenic mutations in RAS proteins impair their ability for GTP hydrolysis, resulting in the accumulation of GTP-bound active RAS and hyperactivation of downstream signaling cascades that lead to uncontrolled cell proliferation and survival, and Applicant also discloses that SOS1 is a guanine nucleotide exchange factor (GEF) that binds to RAS to promote nucleotide exchange and formation of GTP-bound active RAS (page 2). Applicant discloses that small molecule SOS1 inhibitors have been shown to be effective in downregulating active RAS in tumor cells with wild-type KRAS as well as tumor cells bearing a KRAS mutation, and that by preventing formation of the KRAS-SOS1 complex, the SOS1 inhibitors block reloading of KRAS with GTP, leading to antiproliferative activity (page 2). Further, Applicant discloses that small molecule SOS1 inhibitors are known in the field of art, for example in the teaching of Hillig (Hillig, et al., Proc. Nat. Acad. Sci. 2019, 114, 2551-60)4 (page 2). Applicant’s disclosed reference of Hillig teaches SOS1 inhibitors bearing this scaffold (examples: Hillig’s compounds 15 and 16), which corresponds to one of the termini of instant Formula (I):
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Thus, a person of ordinary skill in the art would understand that compounds of the instant invention will bind to SOS1. Additionally, Applicant discloses that the invention regards SOS1 protein degraders (paragraph [0002]). Thus all of claims 145, 147, 149, 155 and 157 are methods of inhibiting SOS1 by directing SOS1 proteins toward degradation, the inherent consequences of such SOS1 inhibition being expressed in the differently disclosed methods of these claims.
As discussed in the 112(b) rejection above, the instant Specification includes the word “linker” 13 times, on pages 26, 73 and 112-113. On page 26, the structure of Formula (I) is provided in the same manner as instant claim 1, with only the proviso that “L is a linker” (paragraph [0061]). On pages 73 and 112-113, the Specification provides that “In certain embodiments, L is a linker having the structure of -ZL-(RL-ZL)-“, with further definitions of the elements ZL and RL provided therein (paragraphs [00143] and [00201]). Given that the definition is only provided for “certain embodiments” of the invention, a person of ordinary skill in the art would not assume that these limitations apply to instant claim 1. Thus, a person of ordinary skill in the art would understand that the structure of the linker “L” of instant claim 1 is limited only to the extent that is a bivalent structure that connected simultaneously to the quinazoline moiety and the “ZE” element of the glutarimide moiety, with no other requirement to the size or structure of the linker moiety.
The State of the Art and Predictability in the Field of Art:
The glutarimide moiety found at the opposite end of the instantly disclosed compounds from the SOS1-binding terminus is well-known in the field of directed protein degradation using bifunctional small molecules commonly designated as proteolysis-targeting chimeras (PROTACs), which are compounds used to direct proteins-of-interest (POIs) toward degradation by cellular proteolysis, as taught, for example, by Yang (Yang, et al.; Journal of Medicinal Chemistry, v62, pp9471-9487; 2019). Yang teaches a study on the effects of tuning the structure of a PROTAC linker, and therein teaches that “A typical PROTAC small-molecule degrader consists of three essential components: a ligand that binds the protein of interest, a second ligand that binds to and recruits an E3 ligase degradation complex, and a linker tethering the two ligands together” (page 9471). While the instant Specification does not include the words “PROTAC” or “E3 ligase”, a person of ordinary skill in the art (POSITA) would at once recognize that the compounds of the instant invention are PROTAC compounds, because they contain a ligand for binding a target protein (SOS1) at one end, and a glutarimide moiety at the other end, separated by a linker. Yang teaches that glutarimide is a binding moiety for cereblon, an E3-ligase, with the glutarimide portion of lenalidomide engaging in a hydrogen bond with cereblon in a crystal structure of the bound cereblon-lenalidomide complex (page 9477).
Yang further teaches a study on the effects of tuning the structure of a PROTAC linker, and therein shows that the structure of a linker is essential to the function of PROTAC molecules. Yang shows that a simple structural modification of a bona fide PROTAC degrader of mouse double minute 2 homolog (MDM2), designated as MD-222 and shown in the image below, said modification being an alteration of the linker, converts the MD-222 PROTAC into the compound MD-277, which functions not as a PROTAC but rather as a “molecular glue” that promotes binding between the E3 ligase cereblon and a different protein than MDM2, specifically GSPT1 (G1 to S phase transition protein), and thereby promotes degradation of GSPT1 rather than MDM2 (Abstract, page 9471):
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Thus, Yang teaches that the structure of the linker is so essential to PROTAC function that a change in the linker structure can not only diminish the degradation of the protein-of-interest (POI), it can completely alter the target of protein degradation. A person of ordinary skill in the art, knowing the teaching of Yang, would understand that PROTAC function cannot be reasonably predicted for PROTAC compounds that do not have a specifically known linker structure that has demonstrated success in protein degradation function of the overall molecular structure.
Claim Rejections - 35 USC § 102
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.
Claims 1, 8, 140, 145, 147, 149 and 155 are anticipated by Chan.
Claims 1, 8, 140, 145, 147, 149 and 155 are rejected under 35 U.S.C. 102 (a)(1) and 102(a)(2) as being anticipated by Chan (U.S. Patent No. 9,938,302 B2)5.
Claim 1 is drawn to a genus of compounds of Formula (I), bearing a glutarimide (or derivative thereof) at one terminus, a quinazoline (or derivative thereof) at the other terminus, and an undefined “linker” connecting the two termini:
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(instant Formula (I) of claim 1).
Chan discloses chimeric compounds that modulate protein function as well as modulating protein-mediated diseases and methods of treatment, amelioration, or prevention of protein-mediated diseases, disorders, and conditions, including cancer (Abstract). Chan specifically discloses “Compound 59”6 that anticipates the genus of instant Formula (I), as shown in the table below (Cols. 141-142, lines 14-43, and claim 26):
Claim Number(s) of Instant Application
Instant Application
Chan
1
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wherein:
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Thus, claim 1 is anticipated by the disclosure of Chan.
Claim 8 further limits claim 1 to wherein the linker “L” is attached at the “X” position of the quinazoline ring and the R2 substituent is a carbon atom bearing 3 undefined substituents R2a, R2b and R2c. Chan’s compound 59 meets the limitations of claim 8, wherein R2a, R2b and R2c, taken together, form a phenyl ring further bearing chloro and fluoro substituents.
Claims 145, 147 and 149 further limit claim 1, each to a distinct method that comprises administering a compound of claim 1 to a subject in need thereof. The methods are directed as follows:
Claim 145: Treating, preventing, or ameliorating a disorder, disease or condition mediated by a son of sevenless homolog 1 (SOS1) in a subject.
Claim 147: Treating, preventing, or ameliorating a disorder, disease or condition mediated by a Ras in a subject.
Claim 149: Treating, preventing or ameliorating one or more symptoms of a proliferative disease.
Regarding diseases “mediated by SOS1” in a subject or “mediated by a Ras” in a subject, the instant Specification discloses that cancer, which is a proliferative disease, meets both of these limitations (page 2).
Chan discloses a method of treating a disease, disorder or condition associated with an interkeukin, aiolos, Ikaros, TNF-alpha, CK1-alpha, or a combination of any of the foregoing comprising administering a therapeutically effective amount of a compound of Chan’s Formula (II) (Col. 16, lines 35-50):
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wherein one of R1 or R2 is L-Y, wherein Y is selected from a Markush group that includes the following structure, which a person of ordinary skill in the art would recognize as a terminal moiety of Chan’s compound 59, shown in the table above (Cols. 16-17, bridging paragraph and Col. 18, lines 15-25):
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Chan discloses that elevated levels of TNF-alpha have been implicated in several pathological conditions including cancer (Col. 1, lines 52-54) and that expression of aiolos in lung and breast cancers predicts significantly reduced patient survival (Col. 2, lines 45-46). Thus, cancer is a disease within scope of Chan’s method of treatment comprising administering a compound of Chan’s Formula (II), which includes in its scope Chan’s compound 59.
Thus, the disclosure of Chan anticipates the limitations of claims 145, 147 and 149.
Claims 1, 9, 140, 145, 147, 149, 155 and 157 are anticipated by Ye.
Claims 1, 9, 140, 145, 147, 149, 155 and 157 are rejected under 35 U.S.C. 102(a)(2) as being anticipated by Ye (US 2024/0261418 A1)7.
The limitations of claims 1, 145, 147 and 149 are discussed in the rejection above and hereby incorporated into the instant rejection.
Ye discloses a genus of compounds as SOS1 degrading agents that can degrade and/or inhibit SOS1 protein in cells, and can be used for the treatment and/or prevention of an SOS1-mediated disease or disorder, or a disease or disorder caused by the interaction of SOS1 with Ras (Abstract). Ye specifically discloses many compounds that anticipate the genus of instant Formula (I), including Ye’s “Example 1”8 shown in the table below (paragraphs [1365]-[1389]), which falls within Ye’s formula I (paragraphs [0006]-[0011]):
Claim Number(s) of Instant Application
Instant Application
Ye
1
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wherein:
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Thus, claim 1 is anticipated by the disclosure of Ye.
Claim 9 further limits claim 1 to wherein the linker “L” is attached at the “V” position of the quinazoline ring and the R2 substituent is a carbon atom bearing 3 undefined substituents R2a, R2b and R2c. Ye’s Example 1 meets the limitations of claim 9, wherein R2a, R2b and R2c, can be arbitrarily assigned among hydrogen, methyl and 1-(4-(2-chloro-6-((dimethylamino)methyl)phenyl)thien-2-yl)methyl substituents.
Claim 140 further limits claim 1 to a pharmaceutical composition comprising a compound of claim 1, or an enantiomer, a mixture of enantiomers, a diastereomer, a mixture of two or more diastereomers, a tautomer, a mixture of two or more tautomers, or an isotopic variant thereof; or a pham1aceutically acceptable salt, solvate, or hydrate thereof; and a pharmaceutically acceptable excipient. Ye discloses a pharmaceutical composition comprising a therapeutically effective amount of the compound of Ye’s formula I, and/or the stereoisomer, the enantiomer, the diastereomer, the deuteride, the hydrate, the solvate, the metabolite, the prodrug and/or the pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable carrier, diluent, or excipient (paragraph [0890]).
Thus, claims 9 and 140 are anticipated by the disclosure of Ye.
Regarding claims 145, 147 and 149, Ye discloses that the invention disclosed therein “provides a method for treating or preventing an SOS1-mediated disease or disorder, comprising administering to a patient in need thereof a therapeutically effective amount of the compound of Ye’s formula I” (paragraph [0899], and that the invention disclosed therein “provides a method for treating or preventing a disease or disorder (e.g., cancer) regulated by the interaction of SOS1 with Ras (e.g., KRAS) or SOS1 with Ras (e.g., KRAS), comprising administering to a patient in need thereof a therapeutically effective amount of the compound of formula I” (paragraph [0900]).
Thus, claims 145, 147 and 149 are anticipated by the disclosure of Ye.
Claim 155 further limits claim 1 to a method of inhibiting the growth of a cell, comprising contacting the cell with an effective amount of a compound of claim 1. Ye discloses “Test Example 4”, wherein growth of cell lines associated with KRAS mutations was assayed under exposure of compounds disclosed therein for SOS1 inhibition/degradation, including Ye’s “Example 1” compound shown above (paragraphs [2211]-[2212]). Results, shown in Ye’s “Table 2”, demonstrate that Ye’s Example 1 compound showed potent inhibition of NCI-H358 cells associated with non-small cell lung cancer (e.g., when IC50≤50 nM).
Claim 157 further limits claim 1 to a method of inducing degradation of an SOS1 protein, comprising contacting the SOS1 with an effective amount of a compound of claim 1. Ye discloses “Test Example 2”, wherein SOS1 degradation was assayed by dosing various KRAS mutant cell lines with compounds disclosed therein, including Ye’s Example 1 compound, and assaying for degraded SOS1 protein (paragraphs [2207]-[2209]). The results, shown in Ye’s Table 1, demonstrate that Ye’s Example 1 compound exhibits potent degradation (e.g., when DC50≤50 nM) of SOS1 across all the tested cell lines (page 327).
Thus, claims 155 and 157 are anticipated by the disclosure of Ye.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1 and 8 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 26 of U.S. Patent No. 9,938,302 B2 (hereafter referred to as “Chan”). Although the claims at issue are not identical, they are not patentably distinct from each other because Chan’s claim 26 claims a compound that anticipates the genera of instant claims 1 and 8.
The limitations of claims 1 and 8 are discussed in the rejections above and hereby incorporated into the instant rejection.
Chan’s claim 26 discloses Chan’s “compound 59” 9 (Cols. 141-142, lines 14-43, and claim 26), by structural representation, as shown in the table below:
Claim Number(s) of Instant Application
Instant Application
Chan’s claim 26
1
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wherein:
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Thus, instant claims 1 and 8 are anticipated by Chan’s claim 26.
Claims 1 and 10 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 23 of U.S. Patent No. 12,419,962 B2 (hereafter referred to as “Erdman”). Although the claims at issue are not identical, they are not patentably distinct from each other because Erdman’s claim 23 claims multiple compounds that anticipate the instant Formula (I) of claim 1, for example Erdman’s compound “201”10 shown in the table below (Col. 233, lines 17-20):
Claim Number(s) of Instant Application
Instant Application
Erdman’s claim 23
1
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wherein:
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Thus, instant claim 1 is anticipated by Erdman’s claim 23.
Claim 10 further limits claim 1 to wherein the linker “L” is attached at the “Y” position of the quinazoline ring and the R2 substituent is a carbon atom bearing 3 undefined substituents R2a, R2b and R2c. Erdmans’s compound A201 meets the limitations of claim 10, wherein R2a, R2b and R2c, can be arbitrarily assigned among hydrogen, methyl and 1-(3-(1,l-difluoro-2-hydroxyethyl)phenyl)methyl substituents.
Thus, instant claim 10 is anticipated by compound A201 of Erdman’s claim 23.
Allowable Subject Matter
Claim 139 is 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.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to W. JUSTIN YOUNGBLOOD whose telephone number is (703)756-5979. The examiner can normally be reached on Monday-Thursday from 8am to 5pm. The examiner can also be reached on alternate Fridays.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Jeffrey S. Lundgren, can be reached at telephone number (571) 272-5541. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/W.J.Y./Examiner, Art Unit 1629
/JEFFREY S LUNDGREN/Supervisory Patent Examiner, Art Unit 1629
1 Cited in Applicant’s Information Disclosure Statement dated 03/23/2024.
2 2,6-piperidine-dione.
3 2,6-piperidine-dione.
4 Cited in Applicant’s Information Disclosure Statement, dated 03/23/2024.
5 Cited in Applicant’s Information Disclosure Statement dated 03/23/2024.
6 (S)-2-((3-([4-((3-Chloro-4-fluorophenyl)amino)-6-(3-morpholinopropoxy)quinazolin-7-yl)oxy)propylamino)-N-(2- (2,7-dioxoazepan-3-yl)-1,3-dioxoisoindolin-4-yl)acetamide
7 Effective Filing Date: 04/23/2021.
8 l-(2-chloro-5-(9-((4-((1R,4R)-4-(4-(((R)-1-(4-(2-chloro-6-((dimethylamino)methyl)phenyl)thien-2-yl)ethyl)amino)-7-methoxy-2-methylquinazolin-6-yl)cyclohexane-l-carbonyl)piperazinl-yl)methyl)-3-azaspiro[5.5]undecane-3-carbonyl)phenyl)dihydropyrimidine-2,4(1H,3H)-dione
9 (S)-2-((3-([4-((3-Chloro-4-fluorophenyl)amino)-6-(3-morpholinopropoxy)quinazolin-7-yl)oxy)propylamino)-N-(2- (2,7-dioxoazepan-3-yl)-1,3-dioxoisoindolin-4-yl)acetamide
10 3-(7-(2-(4-(4-(4-(((R)-1-(3-(1,1-Difluoro-2-hydroxyethyl)phenyl)ethyl)amino)-6,7-dimethoxy-2-methylquinazolin-8-yl)butyl)piperazin-1-yl)-2-oxoethoxy)-1-methyl-1H-indazol-3-yl)piperidine-2,6-dione
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