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 .
Election/Restrictions
Applicant’s election without traverse of Group I, drawn to a method of promoting oligodendrocyte precursor cell differentiation, comprising administering to one or more oligodendrocyte precursor cells an effective amount of a compound of formula (IV) or a pharmaceutically acceptable salt thereof; and compound number CN045 having the structure of:
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as the elected compound species of formula (IV) are maintained.
Expansion of Election of Species Requirement
A reasonable and comprehensive search of the elected species conducted by the Examiner
discover a prior art by Rapacz et al. that anticipates the claimed invention, wherein the prior art teaches
compound 19; and also discover a prior art by Ghamari et al. that renders obvious the claimed invention, wherein the prior art teaches compound 5 and that also renders obvious the subgenus of elected species having the structure of:
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. In light of this discovery, the search is expanded to the subject matter of the compound of formula (IV) to include compound 19 of Rapacz et al., compound 5 of Ghamari et al., and subgenus of compound having the structure of:
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in addition to the elected species of compound of formula (IV), such that it does not encompass the full scope of the claims.
Status of the Claims
Acknowledgement is made of the receipt and entry of the amendment to the claims filed on June 2, 2026, wherein claim 1 is amended; claims 2-3 are unchanged; and claims 24-28 are newly added.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Claims 1-3 and 24-28 are pending.
Claims 1-3 and 24-28 are under examination in accordance with the elected species along with the expanded compound species set forth in the Expansion of Election of Species Requirement section above.
Priority
The instant application 18/003,807 filed on December 29, 2022 is a 371 of PCT/US2021/040294 filed on July 2, 2021, which claims priority to, and the benefits of U.S. Provisional Application No.
63/047,364 filed on July 2, 2020.
Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged. Applicant has not complied with one or more conditions for receiving the benefit of an earlier filing date under 35 U.S.C. 119(e) as follows:
The later-filed application must be an application for a patent for an invention which is also disclosed in the prior application (the parent or original nonprovisional application or provisional application). The disclosure of the invention in the parent application and in the later-filed application must be sufficient to comply with the requirements of 35 U.S.C. 112(a) or the first paragraph of pre-AIA 35 U.S.C. 112, except for the best mode requirement. See Transco Products, Inc. v. Performance Contracting, Inc., 38 F.3d 551, 32 USPQ2d 1077 (Fed. Cir. 1994).
The disclosure of the prior-filed application, Application No. 63/047,364, fails to provide adequate support or enablement in the manner provided by 35 U.S.C. 112(a) or pre-AIA 35 U.S.C. 112, first paragraph for one or more claims of this application. Specifically, the disclosure of the prior-filed application fails to disclose the following compound species of formula (IV):
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,
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and a pharmaceutically acceptable salts thereof; Therefore, to the extent that claims 1-3 and 24-26 are drawn to the compound species of formula (IV) noted above, the claims are not entitled to the benefit of prior-filed application and will receive an effective filing date of July 2, 2021, which is the filing date of 371 of PCT/US2021/040294.
Response to Arguments
Applicant's arguments filed on June 2, 2026 with respect to the priority section have been fully considered and are persuasive.
In Summary, Applicant argues the claims should receive an effective filing date of 371 of PCT/US2021/040294, which is July 2, 2021, rather than the filing date of instant application.
In response, applicant’s argument is found persuasive that the Examiner has mistakenly inserted the filing date of instant application rather than the filing date of 371 of PCT/US2021/040294. Since the Examiner clearly indicate instant claims 1-3, to the extent that they are drawn to the compound species of formula (IV) indicated to the compound species noted above, will receive the effective filing date of 371 of PCT/US2021/040294. The priority section has been amended merely to correct the typographical error for the sake of clarity. In addition, since applicant has newly added claims 24-28, the priority section of record has been revisited and modified in light of the claim amendments.
Action Summary
Acknowledgement is made of the receipt and entry of the amendment to the specification filed on June 2, 2026, which is amended to update the cross-reference to related applications statement.
Claim 1 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 is withdrawn in light of the claim amendments, which specifically deletes the group “X” in the body of the claim.
Claims 1-2 rejected under 35 U.S.C. 102(a)(1) as being anticipated by Rapacz et al. (MedChemComm vol. 8, 1 220-238; cited in the IDS filed on June 25, 2024) are maintained.
Claims 1-2 rejected under 35 U.S.C. 103 as being unpatentable over Ghamari et al. (Chem Biol Drug Des, 2019. Vol. 93(5): 832-843) are withdrawn; however, upon further consideration, a new ground(s) of rejection is made in view of Ghamari et al. and Chen et al. shown below.
Claims 1-3 rejected under 35 U.S.C. 103 as being unpatentable over Ghamari et al. (Chem Biol Drug Des, 2019. Vol. 93(5): 832-843) as applied to claims 1-2 above, and further in view of Schwartz et al. (WO 00/06254) are withdrawn; however, upon further consideration, a new ground(s) of rejection is made in view of Ghamari et al. and Chen et al., and further in view of Schwartz et shown below.
New Claim Objections
Claim 26 is objected to under 37 CFR 1.75 as being a substantial duplicate of claim 24. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1-2 remain rejected under 35 U.S.C. 102(a)(1) as being anticipated by Rapacz et al. (MedChemComm, 2017. vol. 8, 1: 220-238; cited in the IDS filed on June 25, 2024).
Rapacz et al. teaches a compound 19, 1-{2-[2-(2,3-dimethylphenoxy)ethoxy]ethyl}piperidin-3-ol hydrochloride, having the structure of:
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is the most promising compound (see e.g., Fig. 10; Table 1, Compd. 19; abstract). Rapacz et al. further teaches in the maximal electroshock seizure threshold (MEST) test, two compounds, 19 and 27, caused a significantly elevated electroconvulsive threshold (ECT) in comparison to vehicle-treated mice shown below:
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, specifically, compound 19 at a dose of 30 mg kg−1 increased the ECT by 75% (p < 0.001) (see e.g., p. 226, left column, line 17-20; Table 3).
Please note the compound 19 of Rapacz et al. is a compound of instant formula (IV):
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or a pharmaceutically acceptable salt thereof, wherein R1 and R2 are each CH3; R3, R4 and R5 are each hydrogen; Ra and Rb are taken together with the nitrogen atom to which they are attached to form
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(an substituted heterocyclyl).
Rapacz et al. is silent regarding “promoting oligodendrocyte precursor cell differentiation”; However, “promoting oligodendrocyte precursor cell differentiation” will necessarily present by practicing the method of Rapacz et al. Since the same compound (compound 19 of Rapacz et al.) at an effective amount (30 mg/kg) is being administered to a subject (mice), it will necessarily deliver said compound at a cellular level, in this case, to one or more oligodendrocyte precursor cells in the subject even though the prior art was not aware of it.
MPEP 2112, I states: “[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer.” Atlas Powder Co. v. Ireco Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus, the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977).”
Therefore, the claimed invention is being anticipated by Rapacz et al.
Response to Arguments
Applicant's arguments filed on June 2, 2026 with respect to the rejection of claims 1-2 under 35 U.S.C. 102(a)(1) as being anticipated by Rapacz et al. (MedChemComm vol. 8, 1 220-238) have been fully considered but they are not persuasive.
In Summary, applicant argues the claimed invention is drawn to a method of use rather than a composition claim; therefore, a new use for an old structure based on unknown properties of the structure might be patentable to the discoverer as a process of using. Applicant further argues the term “effective amount” has a definition set forth in page 9, line 13-16, of instant specification to refer to an amount that is “effective to induce or promote differentiation of at least one oligodendrocyte precursor”; However, Rapacz et al. fails to teach the 30 mg/kg dose is an OPC-differentiation-effective amount. Applicant further argues the mere fact that a certain result or characteristic may occur or be present in the prior art is not sufficient to establish the inherency of that result or characteristic; and therefore, there is no factual basis in Rapacz et al. supporting that the administration of compound 19 in the seizure threshold testing will necessarily produce an OPC-differentiation-effective concentration at OPCs or necessarily caused such cells to differentiate.
In response, applicant’s arguments are not found persuasive for the reasons set forth below:
First, the anticipation-type rejection under 35 U.S.C. 102 is form on the basis that the compound 19 of Rapacz et al., which reads on the compound of formula (IV) instantly claimed, inherently possesses the biological activity of promoting oligodendrocyte precursor cell (OPC) differentiation; therefore, the administration of the identical compound would necessarily result in that property whenever the compound contacts with oligodendrocyte precursor cells under physiologic conditions. According to MPEP 2112, V, “[t]he PTO can require an applicant to prove that the prior art products do not necessarily or inherently possess the characteristics of his [or her] claimed product. Whether the rejection is based on ‘inherency’ under 35 U.S.C. 102, on ‘prima facie obviousness’ under 35 U.S.C. 103, jointly or alternatively, the burden of proof is the same.” In re Best, 562 F.2d 1252, 1255, 195 USPQ 430, 433-34 (CCPA 1977). If applicant contends the compound with identical chemical structure exhibits mutually exclusive properties when administer to a living subject, said objective evidence is respectfully requested.
In response to applicant's argument that the references fail to show certain features of the invention, it is noted that some of the features upon which applicant relies (i.e., Rapacz contains no disclosure of myelin, demyelination, remyelination or any demyelinating disease; see p. 9, line 9-10 of the reply) are not recited in the rejected claim(s). Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993). Specifically, instant claim is drawn to “[a] method of promoting oligodendrocyte precursor cell, comprising administering to one or more oligodendrocyte precursor cells an effective amount of a compound of formula (IV)…”, which requires the effective amount of the compound of formula (IV) to be in contact with one or more oligodendrocyte precursor cells; and that does not require the feature of myelin, demyelination, remyelination or any demyelinating disease.
Solely to rebut applicant’s arguments that the administration of 30 mg/kg of compound 19 to mice in the maximal electroshock seizure threshold test (MEST) does not necessarily promote oligodendrocyte precursor cells, according to Wang et al. (Brain research, 2018. Vol. 1679: 53-63), brain glutamic acid would increase after seizure, and studies have reported that glutamic acid may affect OPC proliferation, differentiation and migration through AMPA receptors; and blocking neural activity and AMPA receptors could promote OPC differentiation, which demonstrated glutamic acid could inhibit OPCs from differentiating into mature oligodendrocyte cells (see e.g., p. 60, left column, line 12-14; p. 60, right column, line 17-19 and 28-32). In other words, one skilled in the art would have known seizure and epilepsy can trigger an excessive release of glutamic acid, which directly impacts the differentiation of oligodendrocyte precursor cells; and therefore, by blocking the seizure activity, one would have reasonably expected that the differentiation of oligodendrocyte precursor cells in the central nervous system would naturally be promoted. In addition, it is respectfully noted that Rapacz et al. clearly teaches said MEST is a test employed to evaluate the anticonvulsant or anti-epileptic activity of the compound (see e.g., abstract). While Rapacz et al. teaches the use of compound 19 in seizure and epilepsy, these diseases clearly belongs to the field of central nervous system, where oligodendrocyte precursor cells are present. A person skilled in the art would have reasonably expected that the compound 19 of Rapacz et al., which exhibits anticonvulsant or anti-epileptic activity in the central nervous system, would naturally be in contact with oligodendrocyte precursor cells present in the central nervous system when treating seizure or epilepsy. If applicant contends this is not the case, said objective evidence is respectfully requested.
Solely to rebut applicant’s assertion that the 30 mg/kg dose taught by Rapacz et al. is not an OPC-differentiation-effective amount, it is respectfully noted that the instant application discloses “[p]harmaceutical compositions for use in the methods of the present invention preferably have a therapeutically effective amount of the compound or salts thereof in a dosage in the range 10 of .01 to 1,000 mg/kg of body weight of the subject, and more preferably in the range of from about 10 to 100 mg/kg of body weight of the patient” (see e.g., p. 35, line 8-11 of the specification). In other words, the administration of the identical compound at 30 mg/kg dose, which is an effective amount within the disclosed range, would necessarily result in that property. If applicant contends the 30mg/kg dose of compound 19 is not an amount effective to promote oligodendrocyte precursor cell differentiation, said objective evidence is respectfully requested.
Therefore, the arguments are not found persuasive for the same reasons of record and for the reasons set forth herein.
New Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1-2 are rejected under 35 U.S.C. 103 as being unpatentable over Ghamari et al. (Chem Biol Drug Des, 2019. Vol. 93(5): 832-843), in view of Chen et al. (PloS one, 2017. vol. 12,12: e0189380.)
Ghamari et al. teaches Compound 5 having the structure of:
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appears as a pitolisant counterpart and has affinity at human histamine H3 receptor (H3R) (see e.g., Table 1; Table 3; p. 840, right column, line 10-11). Please note the pitolisant taught by Ghamari et al. has the structure of
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(see e.g., Figure 1 (c)). Ghamari et al. further teaches said compound is one of the lead candidates that may serve as starting point for further medicinal chemistry optimization for development of novel CNS selective H3R antagonist to be used in neurodegenerative disease (see e.g., p. 840, right column, “5 | conclusion” section). Ghamari et al. further teaches candidate molecules have lead-likeness properties, and are predicted to be of desirable blood–brain barrier (BBB) permeability and of oral bioavailability, inferred from Abbott bioavailability score with potential synthetic accessibilities (see e.g., p. 837, right column, 2nd paragraph). Ghamari et al. further teaches on the basis of several recent investigations, H3R antagonists and inverse agonists would be effective in CNS-related diseases and neuronal abnormalities such as attention deficit hyperactivity disorder (ADHD), Alzheimer’s disease, schizophrenia, learning and memory disorders, sleep disorders epilepsy, and obesity (see e.g., p. 833, left column, line 20-25). Please note the compound 5 of Ghamari et al. is a compound of formula (IV)
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, wherein R4 is Cl [a halo]; R1, R2, R3 and R5 are each hydrogen; Ra and Rb are taken together with the nitrogen atom to which they are attached to form
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.
Ghamari et al. does not teach one or more oligodendrocyte precursor cells.
Chen et al. teaches histamine receptor-3 (H3R) may be a potential therapeutic target for promotion of remyelination in multiple sclerosis (MS) (see e.g., p. 16, “Discussion” section, last 2 lines). Chen et al. further teaches the presence of H3R alone negatively regulates OPC differentiation; H3R knockdown in this oligodendrocyte precursor cell (OPC) culture system promoted differentiation, as demonstrated by increased expression of differentiation markers MAG and MBP, and increased the number of mature oligodendrocytes with membrane-like morphology, while H3R overexpression had the converse effect (see e.g., p. 16, last paragraph and p. 18, line 1). Chen et al. further teaches to validate H3R as a target for promotion of OPC differentiation, five well-characterized H3R tool compounds with diverse structures were selected for use in the OPC differentiation assay; of these, three were inverse agonists, all of which promoted OPC differentiation in a dose-dependent manner with nanomolar potency (see e.g., p. 8, “Results”, “Phenotypic screening and investigation of OPC differentiation”, 2nd paragraph); Chen et al. further teaches the inverse agonists includes compound BF2649 shown below:
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(see e.g., Fig 2), which shows the percentage fold change from control in MBP staining in OPCs treated with BF2649 as the H3R inverse agonist.
It would have been prima facie obvious to one of ordinary skill in the art at the time the application was filed to administer the compound 5 of Ghamari et al. at an effective amount to a subject for treating CNS-related diseases and neuronal abnormalities to arrive at the claimed invention. One would have been motivated to do so, because Ghamari et al. teaches compound 5 is an anti-H3R agent predicted to have desirable blood–brain barrier permeability and oral bioavailability that can be used in the treatment of neurogenerative diseases. One would have a reasonable expectation of success to arrive at the claimed invention, because one would have reasonably expected that the administration of compound 5 of Ghamari et al. at an effective amount to a subject would have successfully treat neurodegenerative disease by binding to the histamine H3 receptor. In the present case, Ghamari et al. is silent about “promoting oligodendrocyte precursor cell differentiation”; However, Chen et al. teaches modulation of histamine receptor 3 (H3R) promotes oligodendrocyte precursor cell differentiation and remyelination, and specifically teaches Compound BF2649, H3R inverse agonist, successfully promotes oligodendrocyte precursor cells differentiation in a dose-dependent manner. One of ordinary skill in the art would have reasonably expected that the compound 5 of Ghamari et al., which is a counterpart of BF2649 (referred therein as “pitolisant”), would have exhibits the same or substantially similar antagonizing effect against histamine receptor-3 (H3R) for promoting oligodendrocyte precursor cell differentiation; therefore, by practicing the method of Ghamari et al. set forth above, one would also be “promoting oligodendrocyte precursor cell differentiation” by targeting H3R at a cellular level in the subject, and that renders obvious the limitation instantly claimed.
Therefore, the claimed invention would have been prima facie obvious to one of ordinary skill in the art at the time the application was filed, absent factual evidence to the contrary.
Response to Arguments
Applicant's arguments filed on June 2, 2026 with respect to the rejection of claims 1-2 under 35 U.S.C. 103 as being unpatentable over Ghamari et al. (Chem Biol Drug Des, 2019. Vol. 93(5): 832-843) have been fully considered. Upon further consideration, the previous rejection has been withdrawn and Ghamari et al. has been reapplied in view of Chen et al. (PloS one, 2017. vol. 12,12: e0189380) as shown above. The arguments specifically against Ghamari et al. are addressed below.
In Summary, Applicant argues while Ghamari et al. discussed the CNS indications, said prior art is silent regarding oligodendrocyte precursor cells, oligodendrocyte differentiation, myelin, demyelination, and remyelination; and therefore, there is no factual basis or technical reasoning supporting that the administration of an H3R antagonist in an amount effective for treating any CNS indications taught by Ghamari would necessarily promote oligodendrocyte precursor cell differentiation with a reasonable expectation of success.
In response, applicant’s arguments are not found persuasive for the reasons set forth below:
In response to applicant's argument that the Ghamari et al. fail to show certain features of the invention, it is noted that some of the features upon which applicant relies (i.e., Ghamari is silent regarding myelin, demyelination, and remyelination; see p. 10, last paragraph of the reply) are not recited in the rejected claim(s). Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993).
Specifically, instant claim is drawn to “[a] method of promoting oligodendrocyte precursor cell, comprising administering to one or more oligodendrocyte precursor cells an effective amount of a compound of formula (IV)…”, which requires the effective amount of the compound of formula (IV) to be in contact with one or more oligodendrocyte precursor cells; and that does not require the feature of myelin, demyelination and remyelination. It is respectfully noted that the obviousness-type rejection under 35 U.S.C. 103 is based on inherency rather than an express disclosure of “promoting oligodendrocyte precursor cell differentiation” in the prior art(s). In other words, the Compound 5 of Ghamari et al., which reads on the compound of formula (IV) instantly claimed, inherently possesses the biological activity of promoting oligodendrocyte precursor cell (OPC) differentiation; therefore, the fact that the method of administering the compound 5 of Ghamari et al. at an effective amount or dosage to a living subject for treating CNS-related disease and neuronal abnormalities would have been obvious to a person skilled in the art (see rejection above), the administration of identical compound at an effective dosage to a subject would naturally result in that property whenever the compound contacts with oligodendrocyte precursor cells under physiologic conditions. Where the prior-art method necessarily results in the claimed biological properties, discovery of that previously unrecognized properties of the same structure does not render the prior-art method patentably distinct.
According to MPEP 2112, I, “’[t]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer.’ Atlas Powder Co. v. IRECO Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus, the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977)”; and MPEP 2112.02, II. “[t]he discovery of a new use for an old structure based on unknown properties of the structure might be patentable to the discoverer as a process of using. In re Hack, 245 F.2d 246, 248, 114 USPQ 161, 163 (CCPA 1957). However, when the claim recites using an old composition or structure and the “use” is directed to a result or property of that composition or structure, then the claim is anticipated. In reMay, 574 F.2d 1082, 1090, 197 USPQ 601, 607 (CCPA 1978)”. In other word, the method claims drawn to the biological property of the structure does not make the method patentably distinct, because a compound with identical structure and its properties are inseparable. Further according to MPEP 2112, V, “[t]he PTO can require an applicant to prove that the prior art products do not necessarily or inherently possess the characteristics of his [or her] claimed product. Whether the rejection is based on ‘inherency’ under 35 U.S.C. 102, on ‘prima facie obviousness’ under 35 U.S.C. 103, jointly or alternatively, the burden of proof is the same.” In re Best, 562 F.2d 1252, 1255, 195 USPQ 430, 433-34 (CCPA 1977). In the present case, applicant does not present any evidence demonstrating the compound with identical chemical structure does not necessarily or inherently possess the biological properties claimed, said objective evidence is respectfully requested.
Solely to rebut Applicant's arguments that an effective amount useful for treating a CNS-related disease does not necessarily promote oligodendrocyte precursor cell differentiation. According to Chen et al. (PloS one, 2017. vol. 12,12: e0189380.), the presence of histamine receptor-3 (H3R) alone negatively regulates OPC differentiation (see e.g., p. 16, last paragraph and p. 18, line 1); and study demonstrates that anti-H3R agents, including inverse agonist BF2649, promote oligodendrocyte precursor cell differentiation in a dose-dependent manner (see e.g., p. 8, “Results”, “Phenotypic screening and investigation of OPC differentiation”, 2nd paragraph). Consistent with these findings, Chen et al. concludes that "H3R as a novel therapeutic target to promote remyelination in patients with multiple sclerosis"(see e.g., abstract, “conclusions”). Thus, the biological effect relied upon by Applicant is not unrelated to H3 receptor modulation, but rather is a recognized consequence of H3 receptor-targeted therapy.
Therefore, the arguments are not found persuasive for the same reasons of record and for the reasons set forth herein.
Claims 1-3 are rejected under 35 U.S.C. 103 as being unpatentable over Ghamari et al. (Chem Biol Drug Des, 2019. Vol. 93(5): 832-843) in view of Chen et al. (PloS one, 2017. vol. 12, 12: e0189380) as applied to claims 1-2 above, and further in view of Schwartz et al. (WO 00/06254).
The teachings of Ghamari et al. and Chen et al. are set forth above and applied as before.
Ghamari et al. and Chen et al. does not teach the expanded compound species of formula (IV), i.e.,
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Schwartz et al. teaches compound no. 117, 3-(4-chlorophenyl)propyl 3-piperidinopropyl ether, 7 mmol, having the structure of:
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(see e.g., p. 96, no. 117) is an exemplary compound having the following formula (IIa) and (IIb):
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(see e.g., claims 29 and 38; p. 19, line 7). Schwartz et al. further teaches a method comprising administering a therapeutically effective dose of the compound of formula (I) to (XVIII) (see e.g., p. 73, line 21-22). Schwartz et al. further teaches a medicament acting as an antagonist and/or agonist of the histamine H3-receptors, characterized in that it comprises as active ingredients, an effective amount of the compound no. 117 (see e.g., claim 80); and for the treatment of central nervous system disorders, in particular, inter alia, Alzheimer disease and mood and attention alterations (see e.g., claim 81). Schwartz et al. further teaches formula (IIa) and (IIb), wherein XII is preferably an oxygen atom (see e.g., claim 31); AII is a chain –(CH2)nII- with nII preferably from 1 to 4 (see e.g., claim 35; p. 15, line 22-24); chain BII represents unbranched, branched or unsaturated lower alkyl comprising from 1 to 8 carbon atoms, –(CH2)nII(hetero atom)-, where the hetero atom is preferably a sulphur or oxygen atom, nii is preferably an integer between 1 and 4 (see e.g., p. 15, line 31 to p. 16, line 3); YII represents a phenyl group, unsubstituted or mono- or polysubstituted with one or more identical or different substituents selected from, inter alia, halogen atoms (see e.g., p. 16, line 4-6). Schwartz et al. further teaches the term “halogen, as used herein refers to any of fluorine, chlorine, bromine and iodine (see e.g., p. 35, line 4-5). Schwartz et al. further teaches said compound is useful derivatives in human or veterinary medicine (see e.g., p. 66, line 6-7).
In the present case, the difference between the compound 5 of Ghamari et al. and the claimed compound is that the prior art compound contains a single chloro at the meta position on the phenyl group rather than the para position, and does not contain a bromine at the ortho position on the phenyl group shown below (see shaded):
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. Ghamari et al. teaches Compound 5, a pitolisant counterpart and an anti-H3R agent, may serve as lead candidate for development of novel CNS selective H3R antagonist; and Schwartz et al. teaches a compound genus, i.e., formula (IIa) and (IIb) that expressly encompasses the compound 5 of Ghamari et al. and compound no. 117 (Ghamari et al. refers to compound no. 117 as “pitolisant”) acting as antagonists and/or agonists of the histamine H3-receptors; and further teaches compounds of formula (IIa) and (IIb) can contains a phenyl group at YII, which can be substituted with one or more identical or different substituents selected from halogen atoms, such as chlorine and bromine. Accordingly, a person skilled in the art would have recognized that the Compound 5 disclosed by Ghamari et al. is one embodiment of the genus taught by Schwartz et al., because Schwartz et al. contemplates that species as part of its disclosed genus, a person of skilled in the art would have had a reason to employ the Compound 5 of Ghamari et al. as a representative embodiment of the teachings of Schwartz et al. It would have been prima facie obvious to one of ordinary skill in the art at the time the application was filed to arrive at the claimed invention by selectively choose to modify the compound 5 of Ghamari et al. in the method set forth above by modifying the position of chlorine substituent on the phenyl ring, and further substituted said phenyl ring with a bromine as taught by Schwartz et al. One would have been motivated to do so in order to obtain another pitolisant counterpart expect to be acting as an antagonist and/or agonist of the histamine H3-receptors. A person of ordinary skill in the art would have a reasonable expectation of success to arrive at the claimed invention, because Schwartz et al. teaches the phenyl group can be substituted with one or more identical or different halogen atoms, including chlorine and bromine, to arrive at a compound of (IIa) and (IIb) acting as an antagonist and/or agonist of the histamine H3-receptors. Accordingly, changing the position of chlorine substituent on the phenyl ring of Compound 5 of Ghamari et al., and substituting said phenyl ring of with a bromine as a different halogen atom would have presented the predictable modification to obtain an antagonist and/or agonist of the histamine H3-receptors that can be employed in the method of treating neurodegenerative disease by binding to the histamine H3-receptors.
It is noted that Ghamari et al. and Schwartz et al. is silent about “promoting oligodendrocyte precursor cell differentiation”; However, Chen et al. teaches modulation of histamine receptor 3 (H3R) promotes oligodendrocyte precursor cell differentiation and remyelination, and specifically teaches Compound BF2649 (Schwartz et al. refers to Compound BF2649 as a salt of “Compound no. 117”; and Ghamari et al. refers to the free base form of Compound BF2649 as “pitolisant”) is a H3R inverse agonist that promotes oligodendrocyte precursor cells differentiation in a dose-dependent manner. One of ordinary skill in the art would have reasonably expected that the modified compound 5 set forth above would have exhibits the same or substantially similar antagonizing effect against histamine receptor-3 (H3R) for promoting oligodendrocyte precursor cell differentiation; therefore, by practicing the method set forth above, one would also be “promoting oligodendrocyte precursor cell differentiation” by targeting H3R at a cellular level in the subject, and that renders obvious the limitation instantly claimed.
Therefore, the claimed invention would have been prima facie obvious to one of ordinary skill in the art at the time the application was filed, absent factual evidence to the contrary.
Response to Arguments
Applicant's arguments filed on June 2, 2026 have been fully considered.
Applicant's arguments filed on June 2, 2026 with respect to the rejection of claims 1-3 under 35 U.S.C. 103 as being unpatentable over Ghamari et al. (Chem Biol Drug Des, 2019. Vol. 93(5): 832-843) as applied to claims 1-2 above, and further in view of Schwartz et al. (WO 00/06254) have been fully considered. Upon further consideration, the previous rejection has been withdrawn, and Ghamari et al. and Schwartz et al. has been reapplied in view of Chen et al. (PloS one, 2017. vol. 12,12: e0189380) as shown above. The arguments specifically against Ghamari et al. and Schwartz et al. are addressed below.
In Summary, applicant argues the teachings of Schwartz et al. fails to remedy the deficiencies of Ghamari noted above, because Schwartz et al. does not teach “oligodendrocyte precursor cells, oligodendrocyte differentiation, myelin, demyelination, or remyelination”. Applicant further argues the compound 5 of Ghamari is less potent than pitolisant attributes to its reduced affinity to structural different from pitolisant; therefore, substituents changes to pitolisant-type compounds does not lead to predictable result for retaining the relevant biological activity. Applicant further argues the examiner’s conclusion of obviousness is based upon improper hindsight reasons, because the disclosure of Schwartz et al. is broad; the compound 117 of Schwartz et al. is not a compound 5 of Ghamari et al.; Schwartz et al. does not exemplify any compound species bearing two covalently bound halogen substituents on the aryl group; and therefore, the generic disclosure of Schwartz et al. would not have motivated a person to selectively choose to modify the compound 5 of Ghamari et al. to arrive at the claimed invention.
In response, applicant’s arguments are not found persuasive for the reasons set forth below:
First, Applicant’s arguments with respect to Ghamari et al. are addressed above and applied as before.
In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971). It is respectfully noted that the obviousness-type rejection under 35 U.S.C. 103 does not require that every claimed limitation be disclosed within a single reference. In the present case, the obviousness-type rejection of record is form using the combination of Ghamari et al. and Schwartz et al., rather than each of them individually. The Examiner does not rely on Schwartz et al. to teach compound 5 of Ghamari et al., a pitolisant counterpart (see e.g., p. 840, right column, line 10-11; Figure 1c), but rely on the fact that Schwartz et al. discloses a genus, i.e., compounds of formula (IIa) and (IIb), that expressly encompasses the compound 5 of Ghamari et al. (a pitolisant counterpart) and pitolisant (Ghamari et al. refers to compound no. 117 as “pitolisant”, see Fig 1c), that are antagonists and/or agonists of the histamine H3-receptors. It may well be true that compound 5 of Ghamari et al. and compound no. 117 of Schwartz et al. are not structurally identical; However, each of these compounds are taught to have modulating effect against histamine receptor 3 (H3R), and Ghamari et al. clearly recognized compound 5 as a “pitolisant counterpart” (see e.g., p. 840, right column, line 10-11; Figure 1c), which is compound no. 117 of Schwartz et al. A person of skilled in the art would have recognized that the species disclosed by Ghamari et al., i.e., pitolisant and compound 5, are embodiments of the genus taught by Schwartz et al., because Schwartz et al. contemplates that species as part of its disclosed genus, a person of skilled in the art would have had a reason to employ the species of Ghamari et al., i.e., compound 5, as a representative embodiment of the teachings of Schwartz et al. Accordingly, a person of skilled in the art would have reasonably expected to be successful in modifying the pitolisant counterpart, i.e., compound 5 of Ghamari et al. in accordance with the formulae (IIa) and (IIb) as taught by Schwartz et al. to arrive at the compounds with the same or substantially similar activity against histamine H3-receptors, because Schwartz et al. teaches the phenyl ring of pitolisant or formulae (IIa)-(IIb) can be modified to include one or more identical or different halogen atoms (see e.g., p. 16, line 4-6), including chlorine and bromine (see e.g., p. 35, line 4-5), to arrive at an antagonist and/or agonist of the histamine H3-receptors.
Applicant’s argument that the compound 5 of Ghamari et al. is less potent than pitolisant, thus, it fails to support substituent changes from pitolisant-type compounds could be predictably transplanted onto compound 5 while retaining the relevant biological activity are not found persuasive. The mere fact that the compound 5 of Ghamari et al. is reported to have H3R affinity constant values (Ki) at 1.2 μM rather than 0.0071 μM as reported by pitolisant (see Table 3), it does not mean said compound 5 cannot be select for modification. It is respectfully noted that Ghamari et al. clearly recognized “compound 5 appears as a pitolisant counterpart” (see e.g., p. 840, line 10-11), and concludes that “[i]n the present investigation, novel anti-H3R agents were introduced using ligand-and structure-based virtual screening approaches followed by in vitro binding assays. Biological evaluations revealed micromolar and submicromolar Ki values (i.e., 0.49–1.2 μM) for three of the identified molecules. The mode of interactions for the selected compounds was predicted using molecular modeling techniques. Taken together, the presented lead candidates may serve as starting points for further medicinal chemistry optimization for development of novel CNS selective H3R antagonists to be used in neurodegenerative diseases” (see e.g., p. 840, right column, “5 | Conclusion”). In summary, the compound 5 with a Ki value of 1.2 μM is clearly taught by Ghamari et al. to be a lead candidate that can be optimize for further medicinal chemistry optimization for development of novel CNS selective H3R antagonists to be used in neurodegenerative diseases. In other words, while compound 5 is not the best performing agent with the greatest binding affinity at human histamine H3 receptor, said compound 5 is still, in fact, an active anti-H3R agent capable of binding to human histamine H3 receptor and there is clearly a suggestion in the prior art to modify the compound 5 of Ghamari et al. for treating neurodegenerative diseases. Therefore, in view of the teachings of Ghamari et al. and Schwartz et al., one would have reasonably expected that the compound 5 of Ghamari et al., a counterpart of pitolisant, can be modified using the substitution taught by Schwartz et al. to arrive at compounds that bind to H3R. If applicant contends any substituent(s) added to the compound 5 of Ghamari et al. does not retain the relevant biological activity of binding to human histamine H3 receptor, said objective evidence is respectfully requested.
In response to applicant’s argument that the teachings of Schwartz et al. is broad and generic, according to MPEP 2141.02, VI, “‘the prior art’s mere disclosure of more than one alternative does not constitute a teaching away from any of these alternatives because such disclosure does not criticize, discredit, or otherwise discourage the solution claimed…’ In re Fulton, 391 F.3d 1195, 1201, 73 USPQ2d 1141, 1146 (Fed. Cir. 2004). See also MPEP § 2123”. ”. Same logic is applicable to instant case, the mere fact that the teachings of Schwartz et al. include other substituent(s) or species, the disclosure of more than one alternative does not mean the phenyl ring cannot be modified to include one or more identical or different halogen atoms, including chlorine and bromine, at the position claimed, because such disclosure does not criticize, discredit, or otherwise discourage the incorporation of more than one halogen substituents (including chlorine and bromine) to the phenyl ring or substituting one or more halogens at any position of the phenyl ring.
In response to applicant’s argument that Schwartz et al. fails to exemplify compound species bearing two covalently bound halogen substituents on the aryl group, according to MPEP 2141.02, VI, “[a] prior art reference must be considered in its entirety, i.e., as a whole, including portions that would lead away from the claimed invention. W.L. Gore & Assoc., Inc. v. Garlock, Inc., 721 F.2d 1540, 220 USPQ 303 (Fed. Cir. 1983), cert. denied, 469 U.S. 851 (1984)”. The mere fact that Schwartz et al. does not exemplify a compound species bearing two halogens substituted on the phenyl ring does not constitute a teachings away from a broader disclosure of incorporating one or more identical or different halogen substituent(s) to the phenyl ring, because a reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill in the art.
Therefore, the arguments are not found persuasive for the same reasons of record and for the reasons set forth herein.
Claims 1-3 and 24-28 are rejected under 35 U.S.C. 103 as being unpatentable over Ghamari et al. (Chem Biol Drug Des, 2019. Vol. 93(5): 832-843) in view of Chen et al. (PloS one, 2017. vol. 12, 12: e0189380) as applied to claims 1-2 above, and further in view of Schwartz et al. (WO 00/06254).
To the extent that the claims are drawn to the elected compound species, then the following rejection applies.
Ghamari et al. and Chen et al. does not teach the elected compound species of formula (IV), i.e.,
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.
Schwartz et al. teaches compound no. 117, 3-(4-chlorophenyl) propyl 3-piperidinopropyl ether, 7 mmol, having the structure of:
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(see e.g., p. 96, no. 117) is an exemplary compound having the following formula (IIa) and (IIb):
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(see e.g., claims 29 and 38; p. 19, line 7). Schwartz et al. further teaches a method comprising administering a therapeutically effective dose of the compound of formula (I) to (XVIII) (see e.g., p. 73, line 21-22). Schwartz et al. further teaches a medicament acting as an antagonist and/or agonist of the histamine H3-receptors, characterized in that it comprises as active ingredients, an effective amount of the compound no. 117 (see e.g., claim 80); and for the treatment of central nervous system disorders, in particular, inter alia, Alzheimer disease and mood and attention alterations (see e.g., claim 81). Schwartz et al. further teaches formula (IIa) and (IIb), in which R1 and R2 can be taken together with the nitrogen atom to which they are attached to be a saturated nitrogen-containing ring
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, with m ranging from 2 to 8, Ra-d being independently, inter alia, a hydrogen atom or a lower alkyl (see e.g., claims 1 and 30); XII is preferably an oxygen atom (see e.g., claim 31); AII is a chain –(CH2)nII- with nII preferably from 1 to 4 (see e.g., claim 35; p. 15, line 22-24); chain BII represents –(CH2)nII(hetero atom)-, where the hetero atom is preferably a sulphur or oxygen atom, nii is preferably an integer between 1 and 4 (see e.g., p. 15, line 31 to p. 16, line 3); YII represents a phenyl group, unsubstituted or mono- or polysubstituted with one or more identical or different substituents selected from, inter alia, halogen atoms (see e.g., p. 16, line 4-6). Schwartz et al. further teaches the term “halogen, as used herein refers to any of fluorine, chlorine, bromine and iodine (see e.g., p. 35, line 4-5). Schwartz et al. further teaches said compound is useful derivatives in human or veterinary medicine (see e.g., p. 66, line 6-7). Schwartz et al. further teaches typically examples of lower alkyl are methyl, ethyl, propyl, isopropyl and butyl groups (see e.g., p. 5, line 1-2). Schwartz et al. further teaches a suitable effective dose will be in general in the range of from 10 to 500 mg per day and of from 1 to 10 mg/day for particularly active compounds (see e.g., p. 73, line 25-27). Schwartz et al. further teaches Compound 149, 3-(4-chlorophenyl) propyl 3-(4-methylpiperidino) propyl ether, having the structure of:
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is an exemplary compound (see e.g., p. 102, Compound 149; p. 138, Example 149). In the present case, the difference between the compound 5 of Ghamari et al. and the claimed compound is that the prior art compound contains a single chloro- at the meta-position on the phenyl group rather than three chloro moieties, and does not contain a methyl substituted on the piperidine ring (see shaded):
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. Ghamari et al. teaches Compound 5, a pitolisant counterpart and an anti-H3R agent, may serve as lead candidate for development of novel CNS selective H3R antagonist; and Schwartz et al. teaches a compound genus, i.e., formula (IIa) and (IIb) that expressly encompasses the compound 5 of Ghamari et al. and compound no. 117 (Ghamari et al. refers to compound no. 117 as “pitolisant”) acting as antagonists and/or agonists of the histamine H3-receptors; and further teaches compounds of formula (IIa) and (IIb) can contains a phenyl group at YII, which can be substituted with one or more identical or different substituents selected from halogen atoms, such as chlorine and bromine; and the saturated nitrogen-containing ring joined together by R1 and R2 can be substituted with lower alkyl, such as methyl, as Ra or Rb group. Accordingly, a person skilled in the art would have recognized that the Compound 5 disclosed by Ghamari et al. is one embodiment of the genus taught by Schwartz et al., because Schwartz et al. contemplates that species as part of its disclosed genus, a person of skilled in the art would have had a reason to employ the Compound 5 of Ghamari et al. as a representative embodiment of the teachings of Schwartz et al. It would have been prima facie obvious to one of ordinary skill in the art at the time the application was filed to arrive at the claimed invention by selectively choose to modify the compound 5 of Ghamari et al. in the method set forth above by modifying the position of chlorine substituent on the phenyl ring, and further substituted said phenyl ring with two more identical halogen (i.e., chlorine), and then substitute the piperidine ring with methyl as taught by Schwartz et al. One would have been motivated to do so in order to obtain another pitolisant counterpart expect to be acting as an antagonist and/or agonist of the histamine H3-receptors. A person of ordinary skill in the art would have a reasonable expectation of success to arrive at the claimed invention, because Schwartz et al. teaches compound 149, which added a methyl substituent to the 4 position of pyridinyl ring when compared to compound 117, also act as antagonist and/or agonist at histamine H3-receptor; and further teaches the phenyl group can be substituted with one or more identical halogen atoms, including chlorine, to arrive at a compound of (IIa) and (IIb) acting as an antagonist and/or agonist of the histamine H3-receptors. Accordingly, changing the position of chlorine substituent on the phenyl ring of Compound 5 of Ghamari et al., substituting said phenyl ring of with one or more identical halogens, including 2 chlorine atoms, and substituted the piperidine ring with a methyl as the lower alkyl would have presented the predictable modification to obtain an antagonist and/or agonist of the histamine H3-receptors that can be employed in the method of treating neurodegenerative disease by binding to the histamine H3-receptors.
It is noted that Ghamari et al. and Schwartz et al. is silent about “promoting oligodendrocyte precursor cell differentiation”; However, Chen et al. teaches modulation of histamine receptor 3 (H3R) promotes oligodendrocyte precursor cell differentiation and remyelination, and specifically teaches Compound BF2649 (Schwartz et al. refers to Compound BF2649 as a salt of “Compound no. 117”; and Ghamari et al. refers to the free base form of Compound BF2649 as “pitolisant”) is a H3R inverse agonist that promotes oligodendrocyte precursor cells differentiation in a dose-dependent manner. One of ordinary skill in the art would have reasonably expected that the modified compound 5 set forth above would have exhibits the same or substantially similar antagonizing effect against histamine receptor-3 (H3R) for promoting oligodendrocyte precursor cell differentiation; therefore, by practicing the method set forth above, one would also be “promoting oligodendrocyte precursor cell differentiation” by targeting H3R at a cellular level in the subject, and that renders obvious the limitation instantly claimed.
Therefore, the claimed invention would have been prima facie obvious to one of ordinary skill in the art at the time the application was filed, absent factual evidence to the contrary.
Conclusion
No claims are allowed.
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/CHIHYI LEE/Examiner, Art Unit 1628 /JEAN P CORNET/Primary Examiner, Art Unit 1628
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