DETAILED ACTION
Notice of 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 with traverse of Group I in the reply filed on 11/25/2025 is acknowledged. Referring to M.P.E.P § 803, Applicant argues that “examining the claim groups together would not impose a serious burden on the Office” (Applicant Arguments, Page 3). Of course, as Applicant is no doubt aware, search burden is not a criterion for restriction in a U.S. National Stage Application submitted under 35 U.S.C. 371.
The requirement is still deemed proper and is therefore made FINAL.
Applicant’s election without further specifying traverse of a single method in the reply filed on 11/25/2025 is also acknowledged.
The elected species read upon claims 57-59, 61-63, 65-70 and 72-73. Claims 60, 64, 71 and 74-76 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected species, there being no allowable generic or linking claim.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of 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.
Claims 57-59, 61-63, 65-70 and 73 are rejected under 35 U.S.C. 112(a) because the specification, while being enabling for inhibiting or attenuating IL-6, TNF-α, and PGE-2 secretion from LPS-treated human primary monocytes comprising pre-treating human primary monocytes with HNK, does not reasonably provide enablement for inhibiting or attenuating proinflammatory agent secretion from immune cells in general. Nor does the specification reasonably provide enablement for treating or attenuating inflammation in a subject in need thereof. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
Enablement is considered in view of the Wands factors (MPEP 2164.01(A)). These include: nature of the invention, breadth of the claims, guidance of the specification, the existence of working examples, state of the art, predictability of the art and the amount of experimentation necessary. All of the Wands factors have been considered, with the most relevant factors discussed below.
Nature of the Invention and Broadness of the Claims: The instant claims are drawn to methods of treating or attenuating inflammation in a subject in need thereof and/or inhibiting or attenuating proinflammatory agent secretion from immune cells, the method comprising administering to the subject and contacting the immune cells with a composition comprising an effective amount of hydroxynorketamine (HNK).
There are dozens of inflammatory conditions encompassing a wide range of pathological conditions including inflammatory bowel disease, atherosclerosis, rheumatoid arthritis, multiple sclerosis, asthma, psoriasis, Alzheimer’s disease, lupus, and so on.
Similarly, there are numerous immune cells including, for example, granulocytes, mast cells, monocytes, neutrophils, dendritic cells, natural killer (NK) cells, B cells and T cells.
Lastly, there are several proinflammatory agents including cytokines such as interleukins IL-1, IL-6, IL-8, IL-11, IL-17 and IL-18, interferons IFN-α, IFN-β, and tumor necrosis factors TNF-α and TNF-β; chemokines such as CXC, CC, CX3C, X3; eicosanoids such as prostaglandin PGE2, thromboxane TXA2, and leukotrienes LTB4, LTC4, LTD4, LTE4; histamine; kinins; and so on.
The extreme broadness of the claims exacerbates the complexity of the invention. There is no known agent capable of treating all inflammation in all inflammatory conditions. And there is no known agent capable of inhibiting the release of all proinflammatory agents from all immune cells.
Guidance of the specification/The existence of working examples: The amount of direction provided by the Applicant is considered to be determined by the specification and the working examples. At the outset, the specification does not provide even a single example of administering HNK for the treatment of inflammation of any kind in a subject in need thereof. Similarly, the specification does not provide even a single example of inhibiting or attenuating proinflammatory agent secretion from immune cells in a subject in need thereof. Rather, the specification only describes the effect of 30-minute, 24-hour, and 48-hour (2R,6R)-HNK pre-treatment of human primary monocytes against LPS-induced IL-6, IL-8, TNF-α, and PGE2 release in vitro, further stating that “all ketamines had no effect on IL-8” (Page 32, Line 25).
State of the art/Predictability of the art: The level of predictability in the art is considered to be extremely low. As discussed above, there is no known agent capable of treating all inflammation in all inflammatory conditions. Moreover, there is no evidence that (2R,6R)-HNK, in particular, is capable of treating inflammation. Indeed, as demonstrated by Xiong et al (Behavioural Brain Research 368:111904, 2019), administration of (2R,6R)-HNK to “susceptible mice after chronic social defeat stress (CSDS)” had no effect on “plasma levels of inflammatory bone markers, which included osteoprotegerin (OPG), receptor activator of nuclear factor kB ligand (RANKL), and osteopontin” (Abstract). Similarly, as demonstrated by Yamaguchi et al (Neuropsychopharmacology 43:1900-1907, 2018), administration of (2R,6R)-HNK to a “lipopolysaccharide (LPS)-induced inflammation model of mice” had no effect on immobility times using the forced swimming test (Abstract).
Additionally, while the specification demonstrates that HNK pre-treatment of human primary monocytes attenuates LPS-induced IL-6, TNF-α, and PGE2 release in vitro, as discussed above, the specification also demonstrates that HNK pre-treatment “had no effect on IL-8” (Page 32, Line 25). Moreover, as demonstrated by Mattsson et al (JID 173:212-218, 1996), the protein tyrosine kinase inhibitor AG 126 suppresses peptidoglycan-induced TNF-α release from human monocytes but has no effect on LPS-induced TNF-α release from human monocytes (Abstract). As such, it is highly unpredictable whether an agent such as HNK which attenuates LPS-induced IL-6, TNF-α, and PGE2 release in human monocytes in vitro would similarly attenuate IL-6TNF-α, and PGE2 release in human monocytes subjected to different pro-inflammatory stimuli.
Amount of experimentation necessary: Given the complex nature of the invention, which is exacerbated by the breadth of the claims, and given the lack of working examples and the high degree of unpredictability in the art, it would require undue experimentation for a person of ordinary skill in the art to make and use the invention as claimed.
As such, claims 57-59, 61-63, 65-70 and 73 are rejected.
Claims 61, 69 and 72 are rejected under 35 U.S.C. 112(b) as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor regards as the invention.
Claim 61 is drawn to the method according to claim 57, wherein the concentration of HNK is at least about 0.1 mM, at least about 10 µM, or at least about 50 µM. And claim 69 is drawn to the method of claim 66, wherein the dosage of HNK within the composition “is within the range of from 0.01 mg to 5000 mg, from 1 mg to 5000 mg, from 1 mg to 1000 mg…” and so on.
A broad range or limitation together with a narrow range or limitation that falls within the broad range or limitation (in the same claim) may be considered indefinite if the resulting claim does not clearly set forth the metes and bounds of the patent protection desired. See MPEP § 2173.05(c). In the instant case, claims 61 and 69 are considered indefinite because there is a question or doubt as to whether the feature introduced by such narrower language is (a) merely exemplary of the remainder of the claim, and therefore not required, or (b) a required feature of the claims.
Claim 72 is drawn to the method of claim 66, “wherein said proinflammatory agent is…”. The recitation of “said proinflammatory agent” does not find antecedent basis in claim 66.
As such, claims 61, 69 and 72 are rejected as indefinite.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale or otherwise available to the public before the effective filing date of the claimed invention.
Claims 66-70 and 73 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Kroin et al (Reg Anesth Pain Med 44:111-117, published online 2018).
Claim 66 is drawn to a method of treating or attenuating inflammation (more specifically, inflammation caused by a trauma (claim 73)) in a subject in need thereof, the method comprising administering (more specifically, intraperitoneally (claim 68) and repeatedly (claim 70)) to the subject a pharmaceutical composition comprising:
a therapeutically effective amount of hydroxynorketamine (HNK) (more specifically, (2R,6R)-hydroxynorketamine (claim 67) wherein the dosage within the composition is within the range of from 0.01 mg to 5000 mg (claim 69)); and
a pharmaceutically acceptable carrier;
thereby treating inflammation in the subject.
Kroin et al teach administration of “(2R,6R)-hydroxynorketamine ((2R,6R)-HNK)” to a mouse model for “tibia fracture complex regional pain syndrome type-1 (CRPS1) pain” comprising “three (2R,6R)-HNK injections” (Abstract; see also Page 2, Column 1: “the mice received daily intraperitoneal injections of 10 mg/kg (2R,6R)-HNK… for three consecutive days”), wherein said (2R,6R)-HNK “was dissolved in normal saline, at 1.33 mg/mL” and administered at a dose of “0.2 mg, which in a 0.02 kg mouse is 10 mg/kg” (Page 1, Column 2), further noting that “the CRPS1 model… produce[s] intense peripheral inflammation” (Page 6, Column 1).
As such, Kroin et al teach a method of administering (2R,6R)-hydroxynorketamine to a subject recognized as suffering from inflammation and in need of treatment thereof. And it is necessarily the case that said administration treats inflammation in said subject. As stated in In re Papesch, 315 F.2d 381 (CCPA 1963), “[f]rom the standpoint of patent law, a compound and all its properties are inseparable”.
Applicant is reminded that a preamble is generally not accorded any patentable weight where it merely recites the purpose of a process or the intended use of a structure, and where the body of the claim does not depend on the preamble for completeness but, instead, the process steps or structural limitations are able to stand alone (see In re Hirao, 535 F.2d 67 (CCPA 1976) and Kropa v. Robie, 187 F.2d 150 (CCPA 1951)). Similarly, a “whereby clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited” (see Hoffer v. Microsoft Corp., 405 F.3d 1326 (Fed. Cir. 2005), quoting Minton v. Nat’l Ass’n of Securities Dealers, Inc., 336 F.3d 1373 (Fed. Cir. 2003)); see also Verdegaal Bros., Inc. v. Union Oil Co. of Calif., 814 F.2d 628 (Fed. Cir.), cert. Denied, 484 U.S. 827 (1987), noting that merely discovering and claiming a new benefit of an old process cannot render the process again patentable. As in Verdegaal Bros., Inc. v. Union Oil Co. of Calif., the burden of proof is limited to establishing that prior art discloses the same process).
In view of all of the foregoing, claims 66-70 and 73 are anticipated.
Claims 57-59, 61-63 and 65 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Kroin et al (Reg Anesth Pain Med 44:111-117, published online 2018) as applied to 66-70 and 73 above, as further evidenced by Highland et al (J Psychopharmacol 33:12-24, 2019).
Claim 57 is drawn to a method of inhibiting or attenuating proinflammatory agent secretion from immune cells, the method comprising contacting the immune cells with a composition comprising an effective amount (more specifically, at least about 10 µM (claim 61)) of HNK (more specifically, (2R,6R)-hydroxynorketamine (claim 59)). More specifically, the proinflammatory agents are IL-6 and TNF-α (claim 58) and secretion is reduced by least about 20% as compared to untreated immune cells (claim 65), and the immune cells comprise monocytes (claim 62) which are stimulated for enhanced proinflammatory agent secretion by a trauma (claim 63).
As discussed above, Kroin et al teach administration of “(2R,6R)-hydroxynorketamine ((2R,6R)-HNK)” to a mouse model for “tibia fracture complex regional pain syndrome type-1 (CRPS1) pain” comprising “three (2R,6R)-HNK injections” (Abstract; see also Page 2, Column 1: “the mice received daily intraperitoneal injections of 10 mg/kg (2R,6R)-HNK… for three consecutive days”), wherein said (2R,6R)-HNK “was dissolved in normal saline, at 1.33 mg/mL” and administered at a dose of “0.2 mg, which in a 0.02 kg mouse is 10 mg/kg” (Page 1, Column 2), further noting that “the CRPS1 model… produce[s] intense peripheral inflammation” (Page 6, Column 1).
And, as evidenced by Highland et al, intraperitoneal administration of (2R,6R)-HNK to mice delivers (2R,6R)-HNK to the plasma (Page 18, Figure 1).
Accordingly, it is evident that intraperitoneal administration of (2R,6R)-HNK to mice as taught by Kroin et al entails contacting monocytes with a composition comprising an effective amount of (2R,6R)-HNK as claimed and, as such, would necessarily attenuate proinflammatory agent secretion from said monocytes by at least about 20% compared to untreated monocytes as claimed. As stated in In re Papesch, 315 F.2d 381 (CCPA 1963), “[f]rom the standpoint of patent law, a compound and all its properties are inseparable”.
Applicant is reminded that a preamble is generally not accorded any patentable weight where it merely recites the purpose of a process or the intended use of a structure, and where the body of the claim does not depend on the preamble for completeness but, instead, the process steps or structural limitations are able to stand alone (see In re Hirao, 535 F.2d 67 (CCPA 1976) and Kropa v. Robie, 187 F.2d 150 (CCPA 1951)). Similarly, a “whereby clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited” (see Hoffer v. Microsoft Corp., 405 F.3d 1326 (Fed. Cir. 2005), quoting Minton v. Nat’l Ass’n of Securities Dealers, Inc., 336 F.3d 1373 (Fed. Cir. 2003)); see also Verdegaal Bros., Inc. v. Union Oil Co. of Calif., 814 F.2d 628 (Fed. Cir.), cert. Denied, 484 U.S. 827 (1987), noting that merely discovering and claiming a new benefit of an old process cannot render the process again patentable. As in Verdegaal Bros., Inc. v. Union Oil Co. of Calif., the burden of proof is limited to establishing that prior art discloses the same process).
In view of all of the foregoing, claims 57-59, 61-63 and 65 are also anticipated.
Claims 66-70 and 73 are ADDITIONALLY rejected under 35 U.S.C. 102(a)(1) as being anticipated by Wainer et al (US 9,650,352) as evidenced by Wen et al (J Pain Res 16:3061-3073, 2023).
Claim 66 is drawn to a method of treating or attenuating inflammation (more specifically, inflammation caused by a trauma (claim 73)) in a subject in need thereof, the method comprising administering to the subject a pharmaceutical composition comprising:
a therapeutically effective amount of hydroxynorketamine (HNK) (more specifically, (2R,6R)-hydroxynorketamine (claim 67)); and
a pharmaceutically acceptable carrier;
thereby treating inflammation in the subject.
Wainer et al teach “pharmaceutical preparations containing (2R,6R)-hydroxynorketamine” and “methods of treating bipolar depression, major depressive disorder, neuropathic and chronic pain, including complex regional pain disorder (CRPS)” (Abstract) comprising “administering an effective amount of… (2R,6R)-hydroxynorketamine… to a patient in need of such treatment” (Column 3, Lines 14-17), more specifically where said “[c]ompounds… are preferably administered as a pharmaceutical composition… together with at least one pharmaceutically acceptable carrier” (Column 13, Lines 56-61).
However, Wainer et al do not teach treating or attenuating inflammation as recited by the instant claims.
Yet, as evidenced by Wen et al, “[c]omplex regional pain syndrome (CRPS) is an excess and/or prolonged pain and inflammation condition that follows an injury to a limb” (Abstract) in which “concentrations of proinflammatory cytokines, including interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor (TNF)-α are elevated in the serum, cerebrospinal fluid, and skin blister fluid of patients with CRPS” (Page 3063).
As such, Wainer et al teach a method of administering (2R,6R)-hydroxynorketamine to a subject recognized as suffering from inflammation and in need of treatment thereof. And it is necessarily the case that said administration treats inflammation in said subject. As stated in In re Papesch, 315 F.2d 381 (CCPA 1963), “[f]rom the standpoint of patent law, a compound and all its properties are inseparable”.
Applicant is reminded that a preamble is generally not accorded any patentable weight where it merely recites the purpose of a process or the intended use of a structure, and where the body of the claim does not depend on the preamble for completeness but, instead, the process steps or structural limitations are able to stand alone (see In re Hirao, 535 F.2d 67 (CCPA 1976) and Kropa v. Robie, 187 F.2d 150 (CCPA 1951)). Similarly, a “whereby clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited” (see Hoffer v. Microsoft Corp., 405 F.3d 1326 (Fed. Cir. 2005), quoting Minton v. Nat’l Ass’n of Securities Dealers, Inc., 336 F.3d 1373 (Fed. Cir. 2003)); see also Verdegaal Bros., Inc. v. Union Oil Co. of Calif., 814 F.2d 628 (Fed. Cir.), cert. Denied, 484 U.S. 827 (1987), noting that merely discovering and claiming a new benefit of an old process cannot render the process again patentable. As in Verdegaal Bros., Inc. v. Union Oil Co. of Calif., the burden of proof is limited to establishing that prior art discloses the same process).
In view of all of the foregoing, claims 66-67 and 73 are anticipated.
Claim 68 is drawn to the method of claim 66, wherein the pharmaceutical composition is for oral administration.
As taught by Wainer et al, “‘[a]dministration’ means dispensing a compound or composition containing the compound for use via any appropriate route, for example, oral administration” (Column 7, Lines 17-19; see also Column 14, Lines 6: “[c]ompounds disclosed herein may be administered orally”).
Accordingly, claim 68 is also anticipated.
Claim 69 is drawn to the method of claim 66, wherein the dosage of HNK is within the range of from 0.01 mg to 5000 mg.
As taught by Wainer et al, “[i]n certain embodiments, the pharmaceutical composition is an oral dosage form that contains from about 0.1 to about 1000 mg… compound” (Column 13, Line 64 to Column 14, Line 1).
Accordingly, claim 69 is also anticipated.
Claim 70 is drawn to the method of claim 66, wherein the administration comprises a repeated administration.
As taught by Wainer et al, “[p]referred oral dosage forms are formulated for once a day or twice a day administration” (Column 14, Lines 41-42).
Accordingly, claim 70 is also anticipated.
Claims 57-59, 61-63 and 65 are ADDITIONALLY rejected under 35 U.S.C. 102(a)(1) as being anticipated by Wainer et al (US 9,650,352) as evidenced by Wen et al (J Pain Res 16:3061-3073, 2023) as applied to 66-70 and 73 above, as further evidenced by Highland et al (J Psychopharmacol 33:12-24, 2019).
Claim 57 is drawn to a method of inhibiting or attenuating proinflammatory agent secretion from immune cells, the method comprising contacting the immune cells with a composition comprising an effective amount (more specifically, at least about 10 µM (claim 61)) of HNK (more specifically, (2R,6R)-hydroxynorketamine (claim 59)). More specifically, the proinflammatory agents are IL-6 and TNF-α (claim 58) and secretion is reduced by least about 20% as compared to untreated immune cells (claim 65), and the immune cells comprise monocytes (claim 62) which are stimulated for enhanced proinflammatory agent secretion by a trauma (claim 63).
As discussed above, Wainer et al teach “pharmaceutical preparations containing (2R,6R)-hydroxynorketamine” and “methods of treating bipolar depression, major depressive disorder, neuropathic and chronic pain, including complex regional pain disorder (CRPS)” (Abstract) comprising “administering an effective amount of… (2R,6R)-hydroxynorketamine… to a patient in need of such treatment” (Column 3, Lines 14-17), more specifically where said “[c]ompounds… are preferably administered as a pharmaceutical composition… together with at least one pharmaceutically acceptable carrier” (Column 13, Lines 56-61).
And, as evidenced by Wen et al, “[c]omplex regional pain syndrome (CRPS) is an excess and/or prolonged pain and inflammation condition that follows an injury to a limb” (Abstract) in which “concentrations of proinflammatory cytokines, including interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor (TNF)-α are elevated in the serum, cerebrospinal fluid, and skin blister fluid of patients with CRPS” (Page 3063).
As such, Wainer et al teach a method of administering (2R,6R)-hydroxynorketamine to a subject recognized as suffering from inflammation and in need of treatment thereof. And it is necessarily the case that said administration treats inflammation in said subject.
And, as evidenced by Highland et al, oral administration of (2R,6R)-HNK to mice delivers (2R,6R)-HNK to the plasma (Page 18, Figure 1).
Accordingly, it is evident that oral administration of (2R,6R)-HNK as taught by Wainer et al entails contacting monocytes with a composition comprising an effective amount of (2R,6R)-HNK as claimed and, as such, would necessarily attenuate proinflammatory agent secretion from said monocytes by at least about 20% compared to untreated monocytes as claimed. As stated in In re Papesch, 315 F.2d 381 (CCPA 1963), “[f]rom the standpoint of patent law, a compound and all its properties are inseparable”.
Applicant is reminded that a preamble is generally not accorded any patentable weight where it merely recites the purpose of a process or the intended use of a structure, and where the body of the claim does not depend on the preamble for completeness but, instead, the process steps or structural limitations are able to stand alone (see In re Hirao, 535 F.2d 67 (CCPA 1976) and Kropa v. Robie, 187 F.2d 150 (CCPA 1951)). Similarly, a “whereby clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited” (see Hoffer v. Microsoft Corp., 405 F.3d 1326 (Fed. Cir. 2005), quoting Minton v. Nat’l Ass’n of Securities Dealers, Inc., 336 F.3d 1373 (Fed. Cir. 2003)); see also Verdegaal Bros., Inc. v. Union Oil Co. of Calif., 814 F.2d 628 (Fed. Cir.), cert. Denied, 484 U.S. 827 (1987), noting that merely discovering and claiming a new benefit of an old process cannot render the process again patentable. As in Verdegaal Bros., Inc. v. Union Oil Co. of Calif., the burden of proof is limited to establishing that prior art discloses the same process).
In view of all of the foregoing, claims 57-59, 61-63 and 65 are also anticipated.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP §§ 706.02(l)(1) - 706.02(l)(3) 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 USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The 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/process/file/efs/guidance/eTD-info-I.jsp.
Claims 57-59, 61-63, 65-70 and 72-73 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-22 of U.S. Patent No. 9,650,352 as evidenced by Wen et al (J Pain Res 16:3061-3073, 2023) and Highland et al (J Psychopharmacol 33:12-24, 2019).
Although the claims at issue are not identical, they are not patentably distinct from each other. Claim 19 of the ‘352 patent is drawn to methods of treating CRPS comprising administering a compound of claim 7 (which includes hydroxynorketamine) and which can be formulated as a composition comprising an excipient (claim 20) for oral administration (claim 21) in an amount of from 0.05 mg/ml to 0.5 mg/ml (claim 22).
For all the reasons discussed above, the administration of said composition to a subject suffering from CRPS entails (a) administering (2R,6R)-hydroxynorketamine to a subject recognized as suffering from inflammation and in need of treatment thereof, and (b) contacting monocytes with (2R,6R)-hydroxynorketamine, and necessarily treats said inflammation in said subject and attenuates proinflammatory agent secretion from said monocytes
Conclusion
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/CRAIG D RICCI/Primary Examiner, Art Unit 1611