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 .
Priority
This Application is a 371 National Stage Entry of PCT/KR2022/009037 filed on June 24, 2022. Acknowledgment is made of Applicant’s claim for foreign priority under 35 U.S.C. 119 (a)-(d). A certified copy in a Republic of Korea Application No. KR10-2021-0082699 filed on June 24, 2021, is on record.
Information Disclosure Statement
Three information disclosure statements (IDS) submitted on 12/11/2023, 12/06/2024 and 02/21/2025 are acknowledged and have been considered.
Status of the Application
Acknowledgement is made of the claims in the filed Application 18/569,149; Claims 1-6 and 8 (amended), claim 7 (original), and claims 9 -14 (new). No new matter was introduced.
Thus, claims 1-14 are currently under examination.
Claim Rejections - 35 USC § 112b
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 14 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.
The claim is drawn towards “A method for inhibiting the activity of at least one of c-MET and RON receptors comprising administering to a subject in need thereof…” (emphasis added). While the limitation is drawn to a method for inhibiting the activity of the receptors as recited, it does not clearly define who would be a subject in need thereof. It is understood that c-MET and RON receptors are expressed in many tissues, for example, in all humans. It’s therefore unclear the scope claimed by “a subject in need thereof”. Applicant should make the necessary amendment to clearly define the metes and bounds of the claimed invention.
Claim Rejections - 35 USC § 112a
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 10-13 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for inhibiting for RON in vitro, does not reasonably provide enablement for protein kinase-mediated disease, RON-mediated disease, cancer and immune related disease there is no named disease for the protein kinase-mediated disease, RON-mediated disease, and immune related disease, and the term ‘cancer’ is a broad term that encompasses all types of cancers. The specification does not enable a person skilled in the art to which it pertains, or with which it is most nearly connected, to make the invention commensurate in scope with these claims.
To be enabling, the specification of the patent application must teach those skilled in the art how to make and use the full scope of the claimed invention without undue experimentation. In re Wright, 999 F.2d 1557, 1561 (Fd. Cir. 1993). Explaining what is meant by "undue experimentation," the Federal Circuit has stated that:
The test is not merely quantitative, since a considerable amount of experimentation is permissible, if it is merely routine, or if the specification in question provides a reasonable amount of guidance with respect to the direction in which experimentation should proceed to enable the determination of how to practice a desired embodiment of the claimed invention. PPG v. Guardian, 75 F.3d 1558,1564 (Fed. Cir. 1996). As pointed out by the court in In re Angstadt, 537 F.2d 498 at 504 (CCPA 1976), the key word is "undue", not experimentation".
The factors that may be considered in determining whether a disclosure would
require undue experimentation are set forth In re Wands, 8 USPQ2d 1400 (CAFC 1988) at 1404 wherein, citing Ex parte Forman, 230 USPQ 546 (Bd. Apls. 1986) at 547 the court recited eight factors:
1- the nature of the invention,
2- the breadth of the claims,
3- the state of the prior art,
4- the predictability of the art,
5- the relative skill of those in the art,
6- the amount of direction or guidance provided,
7- the presence or absence of working examples and
8- the quantity of experimentation necessary to make or use the invention.
These factors are always applied against the background understanding that scope
of enablement varies inversely with the degree of unpredictability involved. In re Fisher, 57 CCPA 1099, 1108, 427 F.2d 833, 839, 166 USPQ 18, 24 (1970). Undue experimentation is required by one skilled in the art to determine enablement of the instant disclosure as claimed due to the following:
The nature of the invention (1) and the breath of the claims (2):
With regards to the nature of the invention and breath of the claims, the instant claims (10-13) are drawn to intended use; methods of treating a protein kinase-mediated disease (claim 10), treating a RON-mediated disease (claim 11), treating cancer (claim 12) and treating an immune related disease (claim 13).
The breath of the claims is unlimited, because there is no named disease for the protein kinase-mediated disease, RON-mediated disease, and immune related disease, while the term ‘cancer’ is broad and encompasses all types of cancers.
The state of the prior art (3), predictability in the art (4) or lack thereof and relative skill level (5):
MPEP § 2164.05(a) states that if a publication demonstrates that those of ordinary skill in the art would not find that a particular invention was not enabled after the filing date, the publication would be evidence that the claimed invention was not possible at the time of filing.
Regarding the state of the prior art and predictability or lack thereof; Fabbro et al., 2015, (Fabbro et al., “Ten things you should know about protein kinases: IUPHAR Review 14”, British Journal of Pharmacology (2015), Vol. 172, page 2675-2700; Published 20 January 2015), hereon after, Fabbro, provides a review on protein kinases.
Fabbro illustrates Figure 1 and Table 1 (page 2677-78), showing protein kinases targeted by different inhibitory compounds for treatment of various diseases. Further, Fabbro teaches there are different mechanisms for inhibiting protein kinases (page 2681-6). Fabbro discusses methods for discovering kinase inhibitors and reveals approaches that involve in vitro biochemical and cellular assays followed by in vivo efficacy studies; The reference teaches there are a variety of biochemical protein kinase assays (2787-9). Thus, the state of the prior art reveals there are different mechanisms for inhibiting protein kinases, a variety of protein kinases assays and pharmacological art involves screening in vitro and in vivo to determine if a compound exhibits the desired pharmacological activities and what specific diseases by what mechanism.
In addition, Yao et al., 2013, (Yao et al. “MSP-RON signalling in cancer: pathogenesis and therapeutic potential.” Nature Reviews Cancer, Vol. 13, page 466-481; Published 24 June 2013), hereon after Yao, teaches on MSP-RON signalling in cancer. Figure 1 in Yao’s teaching shows that overexpression of RON in breast cancer samples and cell lines based on reviewed studies to be about 40% (page 468). Further, Yao teaches immunohistochemical (IHC) staining routinely detects wild-type RON expression in cancerous tissues but there are findings that show wild-type RON is not universally expressed in different types of tumors. The reference reveals that data from different breast cancer studies was found to vary; in one study RON was abnormally high in about 50% of the cases, a second study, RON was overexpressed in 56% cases, while in a third study RON was positive but not overexpressed in 32% cases, and a fourth study RON was detected (positive) in 86% cases and yet another study RON was 100% positive. Notably, Yao states there are discrepancies in different studies (page 474). Thus, prior art reveals unpredictability.
Regarding RON and immune disease, Benight and Waltz, 2012 (Benight N. and Waltz S., “RON receptors tyrosine kinase signaling as therapeutic target”. Expert Opinion on Therapeutic Targets, 16(9), page 921-931; Published, 26 July 2012), hereon after, Benight, teach on RON and innate immunity (page 926); Notably, Benight teaches that RON activation in macrophages leads to inhibition of inflammatory response; The reference teaches that in the context of inflammation and cancer, studies have shown that RON plays differential roles. Benight reveals RON has numerous signaling pathways as displayed in Figure 1 (page 923-924). Benight concludes by informing artisans that the complex nature of RON’s signaling paradigm necessitates additional studies to understand the pathways by which RON is functioning and how these differ in inflammation and cancer (Expert Opinion - Abstract). As such, based on prior art there is nothing obvious or predictable in the art.
Therefore, while the relative skill of those in the art is high, that of an MD or PhD, that factor is outweighed by the unpredictable nature of the art as illustrated in the prior art discussed above. There is no absolute predictability even in view of the seemingly high level of skill in the art. Prior art teaches discovering kinase inhibitors requires approaches that involve screening in vitro and in vivo to determine if the compound exhibits the desired pharmacological activities and what specific diseases by what mechanism. Further as illustrated in prior art RON overexpression is not predictable in all cancers and the role of RON in the immune/ inflammatory disorders.
The amount of direction or guidance provided (6), presence or absence of working examples (7) and quantity of experimentation necessary (8):
Regarding the amount of direction or guidance provided; The specification provides a broad / general overview of protein kinase and RON receptors (para [(0006 and 0010]) and further states that pharmaceutical composition of the instant invention may be useful for the prevention or treatment of protein kinase-mediated disease and RON-mediated disease but does not name any disease ([0066-0067]). For cancer, the specification simply states, “in an embodiment, the disease may be cancer selected from the group consisting of”, the types as listed in para [0069] but not limited thereto; In respect to the immune disease, the specification states, “in another embodiment, the disease may be an immune disease selected from the group consisting of an inflammatory disorder”, as recited in para [0070], but not limited thereto. The specification discusses the effective dosage of the pharmaceutical composition of compound of formula (I) when the administered for a clinical purpose that “may generally be” as recited in para [0078].
Regarding the presence or absence of working examples, the specification provides examples of only two assays: for RON inhibition and c-MET activity ([00391]) with IC50 of the different claimed compounds.
As illustrative of the state of art, the examiner cites that while applicant demonstrated evaluation of the two aforementioned inhibition assays, given the complexity of RON signaling in different pathways for different conditions, applicant failed to show any other assays for example biochemical protein kinase assays, or disease-specific cell line assays or RON inhibition assays using disease-relevant cell lines. Additionally, examiner contends that based on the above-discussed prior art, the various conditions claimed by applicant; treating a protein kinase-mediated disease, treating a RON-mediated disease, treating a cancer and treating an immune related disease, have different causative agents, different cellular mechanism, different signaling pathways and different mechanisms of inhibition. Consequently, the different conditions differ in their treatment protocol, and the different compounds of formula (I) may have different responses in different assays.
Thus, the specification provides no direction or guidance for the use of a variety of compounds of formula (I) to treat a protein kinase-mediated disease, a RON-mediated disease, a cancer and an immune related disease (instant claims 10-13). Examiner notes that besides the claimed method of treatment in claims 10-13 and the two RON and MET inhibitory enzymatic assays in the disclosure, there is no reasonably specific guidance provided in the disclosure, it lacks a variety of assays to show enablement for all the claimed conditions and thus useful therapeutic protocols for all the disclosed compounds. Based on complexity of RON signaling discussed in prior art, the instant disclosure provides no evidence to suggest the two exemplified assays can be extrapolated to all the conditions claimed in claims 10-13 thus does not meet the “how to use” prong of 35 USC 112, first paragraph with regard thereto.
Regarding the quantity of experimentation necessary; Because of the known unpredictability of the art, and in the absence of experimental evidence, no one skilled in the art would accept the assertion that every single compound of formula (I) could be predictably used for the treatment of all and every single disease in existence; protein-mediated disease, RON-mediated disease, cancer, and immune related disease as inferred by the instant claims and contemplated by the specification.
Determining if compounds of formula (I) would be therapeutic for any of the claimed diseases would require careful analysis and replicability of a composition a compound of formula (I), formulation into a suitable dosage form, relevant assay testing to correlate clinical efficacy, identify off-targets, subjecting to animal trials and subjecting to clinical trials. All this is undue experimentation given the limited guidance and direction provided by applicant.
Accordingly, the instant claims do not comply with the enablement requirement of §112, since to practice the invention claimed in the patent a person of ordinary skill in the art would have to engage in undue experimentation with no assurance of success.
Double Patenting
A rejection based on double patenting of the “same invention” type finds its support in the language of 35 U.S.C. 101 which states that “whoever invents or discovers any new and useful process... may obtain a patent therefor...” (Emphasis added). Thus, the term “same invention,” in this context, means an invention drawn to identical subject matter. See Miller v. Eagle Mfg. Co., 151 U.S. 186 (1894); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Ockert, 245 F.2d 467, 114 USPQ 330 (CCPA 1957).
A statutory type (35 U.S.C. 101) double patenting rejection can be overcome by canceling or amending the claims that are directed to the same invention, so they are no longer coextensive in scope. The filing of a terminal disclaimer cannot overcome a double patenting rejection based upon 35 U.S.C. 101.
Claims 1-6, 8-9, and 11-14 are provisionally rejected under 35 U.S.C. 101 as claiming the same invention as that of claims 1-6, 8-9 and 11-16 of copending Application No. 18/569,157 (reference application). This is a provisional statutory double patenting rejection since the claims directed to the same invention have not in fact been patented.
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 7 and 10 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 7, 11 and 14 of copending Application No. 18/569,157, (hereon after ‘157) alone or in view of Benight and Waltz, 2012 (Benight N. and Waltz S., “RON receptors tyrosine kinase signaling as therapeutic target”. Expert Opinion on Therapeutic Targets, 16(9), page 921-931; Published, 26 July 2012), hereon after Benight, teach on RON and innate immunity (page 926) hereon after Benight.
The instant claim 7 recites compounds, whose structures are also provided in the specification Table 1 (para [0062] – instant application). Likewise, claim 7 in the copending application, ‘157, recites compounds whose structures are shown in Table 1 (para [0065] in ‘157, pages 14-26). As shown below, the compounds in the copending application, ‘157 differ from the instant claim by the type ring bonded to nitrogen – i.e. the fourth ring (Ring B in the instant genus compound).
Instant Application
Copending application ‘157
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Instant claim - example 65
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‘157 - example 62
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Instant claim – example 45
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‘157 - example 52
Whereas the copending application has an aryl (phenyl) ring, the instant claim has a heteroaryl ring, e.g. pyridinyl or pyrimidinyl ring. In addition, the substituents in the aryl/ heteroaryl rings in both applications are similar or in some of the examples, the heteroaryl rings in the claimed compounds are just isomers of each other. Thus, disclosed compounds in the copending application ‘157, namely Example #s 2, 3, 5, 11, 12, 15, 16, 23, 29, 36, 37, 43, 46-47, 49, 52-53, 57, 62-63 render obvious the instant claimed compounds, namely Example #s 1-2, 4-10, 12-23, 25-26, 28-38, 42-52, 56-57, 59-63.
Per MPEP § 2144.09 a prima facie case of obviousness can be made when chemical compounds have very close structural similarities and similar utilities. A skilled artisan would be motivated to modify an aryl ring for a heteroaryl or make an isomer if the other is known, expecting similar results. Additionally, position isomers are generally considered sufficiently similar in structure, and one isomer would render the other obvious.
Thus, while the claims are not identical, they are not patentably distinct from each other. Accordingly, claim 7 in the copending application ‘157, renders obvious claim 7 in the instant application.
Regarding instant claim 10; claim 11 in the copending application ‘157 is drawn to a method of treating a disease associated with overexpression of RON comprising administering the claimed compound(s) and claim 14 is drawn to a method of inhibiting the activity of RON receptors comprising administering a therapeutic effective amount of the claimed compound(s) to a subject in need thereof. Benight teaches RON is a tyrosine kinase receptor that plays a critical role in disease, for example, in cancer progression and metastasis through activation of multiple pathways including P13K/Akt and MAPK which are known protein kinases (page 922); In addition, RON signaling pathways occurs through a variety of downstream protein kinase pathways including JNK, SRC, FAK, among several others (Figure 1, page 924). Instant claim is drawn towards treating a protein kinase-mediated disease by administering a therapeutic effective amount of the claimed compound(s) to a subject in need thereof.
Thus, although the claims are not identical, they are not patentably distinct from each other because a method for treating a disease associated with overexpression of RON disease or a method of inhibiting the activity of RON receptors would be functioning via protein kinase-mediated pathways. It is understood that administering a therapeutic amount of the claimed compound for treating a disease associated with RON overexpression or method of inhibiting the activity of RON receptors would concomitantly be treating a protein kinase-mediated disease, as recited in instant claim 10. That is because the activity induced or resulting from the administration of the compound is happening through pathways that are inseparable.
Therefore, claims 11 and 14 in the copending application ‘157 render obvious the instant claim 10 alone or in view of Benight.
This is a provisional nonstatutory double patenting rejection.
Claims 1-14 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-8 of copending Application No. 19/139,709, (hereon after ‘709), alone or in view of Wermuth et al. 2008 ( “The Practice of Medicinal Chemistry” (Fourth Edition) Chapter 8: Molecular Variations Based on Isosteric Replacements. Academic Press, 2008, Pages 181-241, ISBN 978-0-12-417205-0), hereon after Wermuth and Benight and Waltz, 2012 (Benight N. and Waltz S., “RON receptors tyrosine kinase signaling as therapeutic target”. Expert Opinion on Therapeutic Targets, 16(9), page 921-931; Published, 26 July 2012), hereon after Benight, teach on RON and innate immunity (page 926) hereon after Benight.
Regarding instant claims 1-4; Claims 1-4 in the copending application ‘709, are drawn to the genus compound of formula 1 (claim 1), shown below, and further limitations as recited (claim 2-4).
Instant Application
Copending Application 19/139,709 (‘709)
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W - is N or CH (identical position as X in ‘709)
X - is O (linker between the rings)
Z - is selected from Hydrogen, halogen, NR2NR3, (R2 and R3 defined independently H, among others), C1-C6 alkyl, among other variables that overlap
Y is selected from H, halogen, C1-C6 alkyl and C3-C6 cycloalkyl
R1 is H or C1-C6 alkyl (identical position as R2 in’709)
Ring A – substituted or unsubstituted 5-membered heteroaryl containing one to four atoms consisting of nitrogen, among others.
Ring B – substituted or unsubstituted C3-C10 and other overlapping groups as defined for Ring A in ‘709.
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X is N or C
Oxygen linker between the rings
Z is selected from H, halogen, alkyl and other variables that overlap
Y1 and Y2 -each independently selected from H, halogen substituted and unsubstituted alkyl or substituted or unsubstituted cycloalkyl
R2 is -selected from H, and substituted or unsubstituted alkyl
Has a 5-membered heteroaryl (pyrazole) with a substitution R1
Ring A –is selected from a group that includes, substituted and unsubstituted aryl and heteroaryl among overlapping other groups as defined for instant application Ring B
The copending genus compound and defined variables overlap significantly with the instant genus compound of formula 1 (instant claim 1), sub-genus compound of formula 2 (instant claim 2); in addition, there are overlaps in other limitations as recited in instant claims 3-4. Therefore, copending genus claim reads on instant genus compound in the instant application. Furthermore, exemplified embodiments in the copending application read on the instant genus compound of formula I. Thus, while the claims are not identical, they are not patentably distinct from each other. Accordingly, claims 1-4 in the instant application anticipate or render obvious claims 1-4 in the copending application ‘709.
Regarding instant claim 5-6 and 8-9; Claim 6 in the copending application ‘709, is drawn to pharmaceutical composition of the claimed compounds or pharmaceutically acceptable salt and a pharmaceutically acceptable carrier. The instant claims are drawn to pharmaceutically acceptable salt wherein Y is F (instant claim 5) and wherein R1 is hydrogen (instant claim 6); a pharmaceutical composition of compound of claim 1 or pharmaceutically acceptable salt or pharmaceutically acceptable carrier (instant claim 8), and a pharmaceutical composition of compound of claim 2 or a pharmaceutically acceptable salt or pharmaceutically acceptable carrier (instant claim 9). The copending application ‘709, exemplifies embodiments wherein Y is F and R1 is hydrogen, as illustrated in the examples shown above. In addition, copending application ‘709, claim 6 reads on instant claims 8 and 9 (or vice versa). Therefore, while the instant claims 5-6 and 8-9 and copending ‘709 claim 6 are not exactly identical, they are not patentably distinct from each other. Accordingly, instant claims 5-6 and 8-9 anticipate or render obvious the copending application, ‘709, claim 6.
Regarding instant claim 7; Claim 5 in the copending application ‘709, recites compounds exemplified in para [112] (Table 1, page 18 – ‘709). The compounds in the copending application differ from compounds the instant application (Table 1 (para [0062] – instant application) as shown and further discussed below.
Instant Application
Copending - 19/139,709 (‘709)
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Instant application -example 4
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‘709 – example 4
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‘709 – example 5
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Instant application – example 28
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‘709 – example 15
The compounds in copending application ‘709, have two substituted fluorine atoms in the second ring, while the instant application only has one substituted fluorine atom in the second ring. Wermuth teaches fluorine-hydrogen isosterism; fluorine mimics hydrogen because it is considerable smaller than other halogens; fluorine being the most electronegative halogen particularly forms very stable bonds with carbon; it is rarely ionized or displaced and in addition it has no d-orbitals. Wermuth reveals that the chemical inertia of fluorine explains why fluoro derivatives are more resistant to metabolic degradation and thus, the F-H isosterism serves to give analogues that have improved properties and more resistant to metabolic degradation (Wermuth et. al 2008, pages 226-227).
Accordingly, compounds in the copending application, 709’, namely Example #s 1-18 while not identical, they are not patentably distinct from instant claimed compounds namely, Example #s 1-2, 4-11, 13-14, 16-22, 25-26, 28-32, 35-38, 43-45, 50-52, 56-67 and 59-63. The compounds differ in F-H substitution in the second ring, and as discussed previously, there is aryl/ heteroaryl substitution in the fourth ring and similar substituents. While the claims are not identical, they are not patentably distinct from each other. Accordingly, claim 7 in the instant application renders obvious claim 5 in the copending application ‘709, alone or in view of Wermuth.
Regarding instant 10; Claim 7 in the copending application ‘709, is drawn to a method for preventing or treating a RON-mediated disease comprising administering the compound or pharmaceutically acceptable salt of the claimed compound(s). As discussed previously, Benight teaches that RON signaling pathways occur through a variety of downstream protein kinase pathways. Therefore, treating a RON- mediated disease would also be targeting or functioning through protein kinase pathways and thus would amount to also be treating a protein kinase-mediated disease as recited in the instant claim 10. While the claims are not identical, they are not patentably distinct from each other. It is understood that treating a RON-mediated disease by administering similar compounds would also be treating a protein kinase-mediated disease because the pathways are connected. Therefore, claim 7 in the copending application ‘709 renders obvious the instant claim 10 (or vice versa), alone or in view of Benight.
Regarding instant claim 11-13; Claims 7 and 8 in the copending application ‘709, are drawn to a method of preventing or treating a RON-mediated disease (claim 7) and a method of treating cancer or immune disease (claim 8), comprising administering the compound or pharmaceutically acceptable salt thereof of the claimed compound to a subject in need thereof. The instant claims are drawn to a method for treating a RON-mediated disease (instant claim 11), a method for treating cancer (instant claim 12), and method for treating an immune related disease (instant claim 13), comprising administering the compound or pharmaceutically acceptable salt thereof of the claimed compound to a subject in need thereof.
While the instant claims 11, 12 and 13 and copending application ‘709, claims 7 and 8 are not identical, they are not patentably distinct from each other. Thus, instant claims 11, 12 and 13 anticipate or render obvious copending application ‘709, claims 7 and 8 (or vice versa).
Regarding instant claim 14; Claim 7 in the copending application ‘709 is drawn to a method of preventing or treating a RON-mediated disease. The instant claim is drawn to a method for inhibiting the activity of at least one of c-MET and RON receptors (instant claim 14). From Benight’s teachings, RON is tyrosine kinase receptor of the MET proto-oncogene family and Benight highlights RON and MET are the only two members of this receptor tyrosine family (page 921). Furthermore, in relation to targeting RON for therapy, Benight notes that inhibitors that were constructed to target MET were also found to have potency against RON; for example, antibody foretinib designed to inhibit both proliferation and angiogenesis, is an inhibitor of both MET and RON. Benights adds this is not surprising given that the majority of kinase inhibitors target the active conformation of the kinase and structural similarities between RON and cMET (page 925).
Therefore, while the copending application ‘709, claim 7 and instant claim 14 are not exactly identical, they are not patentably distinct from each other. Inhibiting the activity of least one of c-MET and RON receptors by administering the claimed compound(s), is directed towards a similar outcome as a method of preventing or treating a RON-mediated disease. In addition, both are accomplished using similar compounds whose activity is occurring through these inseparable pathways, and as such not patentably distinct. Therefore, instant claim 14 anticipates or renders obvious the copending application ‘709 claim 7, alone or in view of Benight.
This is a provisional nonstatutory double patenting rejection.
Conclusion
Claims 1-14 are rejected.
Communication
Any inquiry concerning this communication or earlier communications from the examiner should be directed to PAULINE ONDACHI whose telephone number is (571)272-9419. The examiner can normally be reached Mon - Fri 8:00 am - 5:00 pm EST.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Kortney L. Klinkel can be reached at (571)270-5239. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/P.O./Examiner, Art Unit 1627
/Kortney L. Klinkel/Supervisory Patent Examiner, Art Unit 1627
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