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 .
Claim Status
This Office Action is in response to Applicant’s Response to Restriction Requirement filed, 10 June 2026.
Applicant's election without traverse of Group I (claims 1-2, 10, 12-14) in the reply filed on
10 June 2026 is acknowledged. Applicant provisionally elected Example 42 on 17 June 2026; however, Example 42 does not fall into Formula (I) (see Interview Summary mailed 27 July 2026).
Accordingly, a second telephone conversation occurred with Joseph Murphy on 13 July 2026, a provisional election was made to prosecute the invention of Example 41 (
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), which is new claim 45. Mapping shown below:
18/546,285 Formula (I)
18/546,285 components
Example 41
X
N
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42
49
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Y
CH
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42
49
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Z
CH
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42
49
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R2
Amino(C3-7)cycloalkyl: amino(C5)cyclopentyl
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42
57
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R3
Substituted phenyl
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52
68
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R4
Substituted phenyl
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60
93
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Affirmation of this election must be made by applicant in replying to this Office action.
Claims 1-2, 10, 12-14, and 45-46 are pending.
Claims 14 and 46 are withdrawn from further consideration by the Examiner, 37 CFR 1.142(b), as being drawn to a non-elected invention (species). Claim 14 specifies R4 is a (C0-C5alkyl)2amino(C2-5)alkyloxy, a (C0-C5alkyl)2amino(C2-5)alkyl, a heterocyclyl (C2-5)alkyloxy, or a substituted or unsubstituted pyrrolidinoethyloxy or pyrrolidinopropyloxy, which does not read on the elected species. Claim 46 specifies Example 42, which does not read on the elected species.
Claims 1-2, 10, 12-13, and 45 are under consideration in the instant office action.
Claim Interpretation
For clarity, the Examiner notes that claim 1 recites that R2 is an amino(C3-7)cycloalkyl or (C1-5alkyl)2amino(C3-7)cycloalkyl, and the specification defines cycloalkyl to be a non-aromatic carbon-containing ring but does not specify that all of the ring must be carbon. Accordingly, the Examiner interprets claim 1 to include nitrogen-containing non-aromatic heterocycles (i.e. amino(C5)cycloalkyl includes piperidine).
Claim Suggestion
For clarity, the Examiner suggests that Applicant amend claim 45 to recite “A compound of Formula (I) that is Example 41 of the following structure:
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.”
Claim Rejections - 35 USC § 112
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.
1. Claim 45 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 45 recites a compound having the formula of Example 41 in Table 1, and thus references the specification. Where possible, claims are to be complete in themselves. Incorporation by reference to a specific figure or table "is permitted only in exceptional circumstances where there is no practical way to define the invention in words and where it is more concise to incorporate by reference than duplicating a drawing or table into the claim. Incorporation by reference is a necessity doctrine, not for applicant’s convenience." Ex parte Fressola, 27 USPQ2d 1608, 1609 (Bd. Pat. App. & Inter. 1993) (citations omitted). Accordingly, claim 45 should be amended to recite the structure of Example 41.
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.
2. Claim(s) 1-2, 10, 12-13, and 45* are rejected under 35 U.S.C. 103 as being unpatentable over Cassel (Biochimie, 2012, 94, 1974-1981) in view of Koul (WO 2015/088045, published 18 June 2015) and Lee (Nature Communications¸ 2015, 6(5791), 1-14) as evidenced by Kalescky (J. Phys. Chem. A, 2013, 117, 8981-8995), Schnider (ChemBioChem¸2020, 21, 212-234), and Wikipedia (“Lipinski’s Rule of 5,” Wikipedia¸ 2026, <en.wikipedia.org/wiki/Lipinski%27s_rule_of_five>, accessed 15 July 2026).
*While Applicant elected Example 41 after a second telephonic call, this art is also applicable to Example 42 as Cassel teaches the northern fragment R2 (Compound 1, page 1978, Table 1) and Koul teaches R4 is a phenyl ring substituted with a methylated piperazine (Compound C2, page 253).
Cassel teaches 4-aminoquinoline TDP-43 inhibitors of general formula:
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(page 1978, Table 1). Cassel teaches that trans-activating response (TAR) DNA binding protein (TDP-43) is primarily expressed in the nucleus and in cytoplasmic granules, where it functions as a regulator of gene transcription and splicing as well as RNA stabilization and subcellular localization (page 1974, column 1, paragraph 1). Cassel teaches that TDP-43 has been implicated in neurodegenerative diseases, such as frontotemporal lobar degeneration and amyotrophic lateral sclerosis (ALS; page 1974, column 2, paragraph 2). Cassel teaches that aggregation of phosphorylated and ubiquitinylated C-terminal fragments (CTFs) in ALS patients is accompanied by a decrease in TDP-43, but the mechanism is not completely understood (page 1974, column 2, paragraph 2). Cassel teaches that the CTF aggregates are the result of abnormal overexpression of TDP-43 with subsequent metabolism by caspases leading to CTF aggregates (page 1975, column 1, paragraph 1). Cassel teaches that it is unclear if the toxicity is due to gain of function resulting from high levels of TDP-43 or loss of function due to increased metabolism with subsequent sequestration of CTF aggregates (page 1975, column 1, paragraph 1). Cassel further teaches that transgenic mice overexpressing TDP-43 exhibit relatively selective degeneration in layer V cortical neurons and spinal motor neurons, consistent with ALS (page 1975, column 1, paragraph 1). Cassel teaches that overexpression of TDP-43 as well as RNAi knockdown result in cytotoxicity suggesting that the levels of TDP-43 are tightly regulated (page 1975, column 1, paragraph 2). Cassel further teaches that caspase cleavage and subsequent generation of TDP-43 CTFs may be a compensatory mechanism whereby the cell attempts to attenuate toxicity associated with overexpression of full length TDP-43 (page 1975, column 1, paragraph 2). Cassel hypothesizes that binding to TDP-43 might induce a conformational change and in turn effect the rate of caspase cleavage (page 1975, column 1, paragraph 2). Cassel teaches the inhibitors are mixed inhibitors of TDP-43 and actually stimulate caspase-7 mediated cleavage of TDP-43 (page 1975, column 1, paragraph 2). Cassel specifically teaches compounds 2 and 8:
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:
Compound #
R1
R2
IC50 (mM, TDP-43)
Stimulation of caspase-7 cleavage of TDP-43 (%) at 10 uM
2
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52
114
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OMe
5.6
123 ± 20
8
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45
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OMe
24
9 ± 4
Regarding claim 1, Cassel fails to teach Example 41:
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.
Koul teaches TLR7, TLR8, TLR7/8, TLR7/9, and TLR7/8/9 inhibitors for treating autoimmune and inflammatory diseases (abstract). Koul teaches that toll-like receptors (TLRs) are conserved membrane pattern recognition receptors of innate immunity responsible for clearing microbial pathogens ([0002]). Koul teaches that TLRs are expressed in many immune and non-immune cells and detect pattern recognition motifs that recognize both microbial products and endogenous ligands resulting from cellular insult due to inflammatory response and cell death ([0002]). Koul teaches that TLR7 and TLR8 recognize ssRNA ([0002]). Koul additionally teaches that engagement of a cognate ligand to TLRs induces conformational changes allowing of homo-or heteromeric interactions within TLRs and recruitment of adaptor proteins and that TLR7 and TLR9 activate NF-κB and IRF7 to induce proinflammatory cytokines (TNFα, IL-1β, IL-6; [0004]). Koul teaches that there are TLR-7/8/9, and TLR7/9, and TLR9 antagonists based upon a 4-aminoquinoline scaffold ([0010]). Koul teaches Compounds A35 and A42:
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and
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(pages 186 and 191). Koul teaches that Compound A35 has hTLR9 and mTLR9 IL-6 inhibitory activity (% at 1 mM) of 96.3 % and 100% (page 269-270). Koul teaches that Compound A42 has hTLR9 and mTLR9 IL-6 inhibitory activity (% at 1 mM) of 96 % and 84% (page 269-270).
Lee teaches that in vivo depletion of TDP-43 leads to a dramatic reduction in the RNA processing and protein levels of IL-6 in serum (abstract). Lee teaches cytokines are proteins that act as signaling molecules to regulate immune responses and modulate cellular activities such as growth, survival and differentiation and that interleukin (IL)-6 is a pluripotent cytokine that is involved in multiple pro- and anti-inflammatory processes (page 2, column 1, paragraph 2). Lee teaches that the TDP-43-mediated interleukin-6 and -10 splicing activating compartment (InSAC) as the essential nuclear site of IL-6 or IL-10 mRNA production and stability and that TDP-43 acts as a scaffold in the INSAC that interacts with IL-6 and IL-10 RNA, which facilitates pre-mRNA processing and prevents its degradation (page 2, column 1, paragraph 4). Lee also explores whether TLR-agonist specificity is involved in TDP-43-mediated IL-6 pre-mRNA processing via measuring cytokine production (page 4, column 2, paragraph 1). Lee teaches that cytokine production in purified bone marrow-derived macrophages exposed to CpG-DNA activates the TLR9 signaling cascade and that in TDP-43-depeted bone marrow-derived macrophages, IL-6 production was attenuated but not TNF-α (page 4, column 2, paragraph 1). Lee teaches that that TDP-43 must interact with IL-6 pre-mRNA to play a role in its RNA processing and that TDP-43 is essential for IL-6 pre-mRNA processing and stability (page 5, column 1, paragraph 2).
It would have been obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention to modify Compound 2 of Cassel to 1) incorporate a piperidine (another six-membered heterocycle akin to the piperazine of Compound 8 of Cassel that would not result in an unstable N-N single bond as evidenced by Kalescky; page 8981, Figure 1) while maintaining the amide-alkyl kinked orientation and length that is visible in Compound 2:
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to optimize activity as compounds (with p-methoxyphenyl at R2) having that conformation performed better as taught by Cassel (Page 1978, Table 1);
2) incorporate a piperidine (which is a privileged scaffold as evidenced by Schnider: page 212, column 1, paragraph 1) akin to the combination of Compounds 2 and 8 of Cassel (page 1978, Table 1) to modulate lipophilicity as evidenced by Wikipedia (page 2, bullet point 1) and to incorporate more sp3 character while maintaining length as evidenced by Schnider (page 213, column 1, paragraph 1); 3) incorporate the phenyl-piperazine of Compound A42 (
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) of Koul (page 191), which performed well at inhibiting TLR9, which is related to TDP-43 as taught by Lee (page 5, column 1, paragraph 2) in order to optimize activity; 4) trim the quinoline bicycle of Cassel and azaindole bicycle of Koul to the common core, pyridine, to decrease molecular weight as evidenced by Wikipedia (page 1, bullet point 3) and escape from flatland as evidenced by Schnider (page 213, column 1, paragraph 1); 5) incorporate the methyl of Compound A35 (
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) of Koul (page 186), which performed well at inhibiting TLR9, which is related to TDP-43, as taught by Lee (page 5, column 1, paragraph 2) in order to optimize activity and decrease the number of hydrogen bond donors as evidenced by Wikipedia (page 1, bullet point 1). One of ordinary skill in the art would have been motivated to make such a selection, with a reasonable expectation of success, because:
-Cassel teaches 4-aminoquinoline TDP-43 inhibitors of general formula:
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;
-Cassel teaches that trans-activating response (TAR) DNA binding protein (TDP-43) that is primarily expressed in the nucleus and in cytoplasmic granules, where it functions as a regulator of gene transcription and splicing as well as RNA stabilization and subcellular localization;
-Cassel teaches that TDP-43 has been implicated in neurodegenerative diseases, such as frontotemporal lobar degeneration and amyotrophic lateral sclerosis (ALS),
-Cassel teaches that aggregation of phosphorylated and ubiquitinylated C-terminal fragments (CTFs) in ALS patients is accompanied by a decrease in TDP-43, but the mechanism is not completely understood;
-Cassel teaches that the CTF aggregates are the result of abnormal overexpression of TDP-43 with subsequent metabolism by caspases leading to CTF aggregates;
-Cassel teaches that it is unclear if the toxicity is due to gain of function resulting from high levels of TDP-43 or loss of function due to increased metabolism with subsequent sequestration of CTF aggregates;
-Cassel further teaches that transgenic mice overexpressing TDP-43 exhibit relatively selective degeneration in layer V cortical neurons and spinal motor neurons, consistent with ALS;
-Cassel teaches that overexpression of TDP-43 as well as RNAi knockdown result in cytotoxicity suggesting that the levels of TDP-43 are tightly regulated;
-Cassel further teaches that caspase cleavage and subsequent generation of TDP-43 CTFs may be a compensatory mechanism whereby the cell attempts to attenuate toxicity associated with overexpression of full length TDP-43;
-Cassel hypothesizes that binding to TDP-43 might induce a conformational change and in turn effect the rate of caspase cleavage;
-Cassel teaches the inhibitors are mixed inhibitors of TDP-43 and actually stimulate caspase-7 mediated cleavage of TDP-43;
-Cassel specifically teaches compounds 2 and 8:
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:
Compound #
R1
R2
IC50 (mM, TDP-43)
Stimulation of caspase-7 cleavage of TDP-43 (%) at 10 mM
2
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114
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OMe
5.6
123 ± 20
8
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45
76
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OMe
24
9 ± 4
-Koul teaches TLR7, TLR8, TLR7/8, TLR7/9, and TLR7/8/9 inhibitors for treating autoimmune and inflammatory diseases,
-Koul teaches that toll-like receptors (TLRs) are conserved membrane pattern recognition receptors of innate immunity responsible for clearing microbial pathogens,
-Koul teaches that TLRs are expressed in many immune and non-immune cells and detect pattern recognition motifs that recognize both microbial products and endogenous ligands resulting from cellular insult due to inflammatory response and cell death,
-Koul teaches that TLR7 and TLR8 recognize ssRNA,
-Koul additionally teaches that engagement of a cognate ligand to TLRs induces conformational changes allowing of homo-or heteromeric interactions within TLRs and recruitment of adaptor proteins and that TLR7 and TLR9 activate NF-kB and IRF7 to induce proinflammatory cytokines (TNFα, IL-1β, IL-6),
-Koul teaches that there are TLR-7/8/9, and TLR7/9, and TLR9 antagonists based upon a 4-aminoquinoline scaffold,
-Koul teaches Compounds A35 and A42:
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and
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,
-Koul teaches that Compound A35 has hTLR9 and mTLR9 IL-6 inhibitory activity (% at 1 mM) of 96.3 % and 100%,
-Koul teaches that Compound A42 has hTLR9 and mTLR9 IL-6 inhibitory activity (% at 1 mM) of 96 % and 84%,
-Lee teaches that in vivo depletion of TDP-43 leads to a dramatic reduction in the RNA processing and protein levels of IL-6 in serum,
-Lee teaches cytokines are proteins that act as signaling molecules to regulate immune responses and modulate cellular activities such as growth, survival and differentiation and that interleukin (IL)-6 is a pluripotent cytokine that is involved in multiple pro- and anti-inflammatory processes,
-Lee teaches that the TDP-43-mediated interleukin-6 and -10 splicing activating compartment (InSAC) as the essential nuclear site of IL-6 or IL-10 mRNA production and stability and that TDP-43 acts as a scaffold in the INSAC that interacts with IL-6 and IL-10 RNA, which facilitates pre-mRNA processing and prevents its degradation,
-Lee also explores whether TLR-agonist specificity is involved in TDP-43-mediated IL-6 pre-mRNA processing via measuring cytokine production,
-Lee teaches that cytokine production in purified bone marrow-derived macrophages exposed to CpG-DNA activates the TLR9 signaling cascade and that in TDP-43-depeted bone marrow-derived macrophages, IL-6 production was attenuated but not TNF-α, and
-Lee teaches that that TDP-43 must interact with IL-6 pre-mRNA to play a role in its RNA processing and that TDP-43 is essential for IL-6 pre-mRNA processing and stability.
Accordingly, the combination of Cassel, Koul, and Lee as evidenced by Kalescky, Schnider, and Wikipedia teaches a compound of Formula (I):
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(Example 41).
Regarding claim 2, Cassel teaches Compound 2:
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(page 1978, Table 1), wherein X is N and Z is CH. Koul teaches Compound A35:
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(page 186), wherein X is N and Y is CH. Thus, the combination of Cassel and Koul teaches that X is N, Y is CH, and Z is CH.
Regarding claim 10, Cassel teaches Compounds 2 and 8:
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, wherein R1 is
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and R2 is OMe (Compound 2) and R1 is
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and R2 is OMe (Compound 8; page 1978, Table 1), which suggests incorporating a piperidine (another six-membered heterocycle akin to the piperazine of Compound 8 of Cassel but would not result in an unstable N-N single bond as evidenced by Kalescky; page 8981, Figure 1) while maintaining the amide-alkyl kinked orientation and length that is visible in Compound 2:
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to optimize activity as compounds (with p-methoxyphenyl at R2) having that conformation performed better as taught by Cassel (Page 1978, Table 1). Additionally, piperidine incorporation akin to the combination of Compounds 2 and 8 of Cassel would modulate lipophilicity as evidenced by Wikipedia (page 2, bullet point 1) and incorporate a privileged scaffold while increasing sp3 character as evidenced by Schnider (page 212, column 1, paragraph 1; page 213, column 1, paragraph 1). Accordingly, Cassel as evidenced by Wikipedia and Schnider teaches R2 is an amino(C3-C7)cyclopalkyl group: aminocyclopentyl.
Regarding claim 12, Cassel teaches Compound 2: Compound 2:
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(page 1978, Table 1), wherein R3 is a substituted phenyl.
Regarding claim 13, Cassel teaches Compound 2: Compound 2:
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(page 1978, Table 1), wherein R3 is a methoxyphenyl.
Regarding claim 45, Cassel teaches Compound 2:
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(page 1978, Table 1), wherein X is N and Z is CH. Koul teaches Compound A35:
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(page 186), wherein X is N and Y is CH. Cassel teaches Compounds 2 and 8:
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, wherein R1 is
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and R2 is OMe (Compound 2) and R1 is
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and R2 is OMe (Compound 8; page 1978, Table 1), which suggests incorporating a piperidine (another six-membered heterocycle akin to the piperazine of Compound 8 of Cassel but would not result in an unstable N-N single bond as evidenced by Kalescky; page 8981, Figure 1) while maintaining the amide-alkyl kinked orientation and length that is visible in Compound 2:
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to optimize activity as compounds (with p-methoxyphenyl at R2) having that conformation performed better as taught by Cassel (Page 1978, Table 1). Additionally, piperidine incorporation akin to the combination of Compounds 2 and 8 of Cassel would modulate lipophilicity as evidenced by Wikipedia (page 2, bullet point 1) and incorporate a privileged scaffold and add more sp3 character while maintaining length as evidenced by Schnider (page 212, column 1, paragraph 1; page 213, column 1, paragraph 1). Additionally, Cassel teaches R3 is p-methoxyphenyl (Compounds 2 and 8, page 1978, Table 1). Koul teaches Compound A42:
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(page 186), wherein R4 is a substituted phenyl. Koul teaches Compound A42 performed well at inhibiting TLR9, which is related to TDP-43 as taught by Lee (page 5, column 1, paragraph 2) in order to optimize activity. Koul also teaches Compound A35:
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(page 186), wherein the amine is not a secondary amine but is a tertiary amine and methylated. Koul teaches Compound A35 performed well at inhibiting TLR9, which is related to TDP-43, as taught by Lee (page 5, column 1, paragraph 2) in order to optimize activity and decrease the number of hydrogen bond donors as evidenced by Wikipedia (page 1, bullet point 1). Thus, the combination of Cassel, Koul, and Lee as evidenced by Kalescky, Schnider, and Wikipedia teaches Example 41:
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.
Conclusion
No claim is allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Madeline M Dekarske whose telephone number is (571)272-1789. The examiner can normally be reached Monday - Thursday 10am - 4pm.
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/MADELINE M. DEKARSKE/Examiner, Art Unit 1622
/JAMES H ALSTRUM-ACEVEDO/Supervisory Patent Examiner, Art Unit 1622
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