DETAILED ACTION
Claims 1-18, submitted 05 October 2023, are pending in the application. Claim 17 has been withdrawn. Claims 1-16 and 18 are subject to examination in the instant Office 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 of the species of the NMDA receptor antagonist, ketamine, the KCNQ channel activator, retigabine, and the psychiatric disorder, treatment-resistant depression, in the reply filed on 02 June 2026 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)).
Claim 17 is withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected species, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 02 June 2026.
Specification
The disclosure is objected to because of the following informalities: Page 18 of the instant specification recites “(www(dot)dsm5(dot)org)”.
Appropriate correction is required.
Claim Objections
Claim 3 is objected to because of the following informalities: Claim 3 recites “…wherein the NMDA receptor antagonist is a ketamine or analogs or derivatives thereof.”. The claim should read “…wherein the NMDA receptor antagonist is ketamine or analogs or derivatives thereof.” Appropriate correction is required.
Claim 12 is objected to because of the following informalities: Claim 12 recites “…wherein the KCNQ channel activator is ketamine and the KCNQ channel activator is retigabine…”. The Examiner respectfully asks the Applicant to amend the claim to read “…wherein the NMDA receptor antagonist is ketamine…”. Appropriate correction is required.
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 the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1-16 and 18 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Claim 1 recites “an N-methyl-D-aspartate (NMDA) receptor antagonist” and “a KCNQ channel activator” for which the specification does not provide an adequate written description to convey that the inventors were in possession of the full scope of the claimed invention to include all combinations of known NMDA receptor antagonist and KCNQ channel activators. The Applicant has claimed the functional property of the aforementioned genera of compounds and that does not permit one to envisage which compounds would have the desired biological function.
The instant claim lacks written description because the claim is claiming
compounds based on the compounds function while the evidence found within the
specification is drawn to a very particular NMDA receptor antagonist and KCNQ channel activator. The Examiner would like to point the Applicant to MPEP 2163(II)(A)(3)(a) which recites “An applicant may also show that an invention is complete by disclosure of sufficiently detailed, relevant identifying characteristics which provide evidence that inventor was in possession of the claimed invention, i.e., complete or partial structure, other physical and/or chemical properties, functional characteristics when coupled with a known or disclosed correlation between function and structure, or some combination of such characteristics. Enzo Biochem, 323 F.3d at 964, 63 USPQ2d at 1613 (quoting the Written Description Guidelines, 66 Fed. Reg. at 1106, n. 49, stating that "if the art has established a strong correlation between structure and function, one skilled in the art would be able to predict with a reasonable degree of confidence the structure of the claimed invention from a recitation of its function".).
However, Serafini et al. ("NMDA receptor antagonists for depression: critical considerations." Annals of Clinical Psychiatry 27.3 (2015): 213-220.) states that “Ketamine, a moderate/low affinity noncompeti-tive NMDAR antagonist, is similar to memantine, a derivative of amantadine; however, unlike ketamine, memantine failed to improve depressive symptoms” (pg. 214, Section “Introduction”, Left Col., 5th paragraph) which would lead to uncertainty in the treatment of all claimed psychiatric disorders with all known NMDA receptor antagonists and KCNQ channel activators because ketamine and memantine are both derivatives of amantadine however only ketamine has exhibited improvements in depressive symptoms. Additionally, this bears more evidence to the assertation that the Applicant was not in possession of the full scope of the claimed invention.
MPEP 2164.05(a) states that “If a publication demonstrates that those of ordinary skill in the art would find that a particular invention was not enabled years after the filing date, the publication would be evidence that the claimed invention was not possible at the time of filing. See In re Wright, 999 F.2d 1557, 1562, 27 USPQ2d 1510, 1513-14 (Fed. Cir. 1993)”. As such, the Examiner would like to underscore the need for post-filed art, Johnston et al. ("Ketamine in neuropsychiatric disorders: an update." Neuropsychopharmacology 49.1 (2024): 23-40.), to demonstrate that not all NMDA receptor antagonist would be applicable in the treatment of depression.
Johnston teaches “Given that ketamine is a canonical NMDAR antagonist, preclinical and clinical research on various NMDAR antagonists quickly followed the discovery of ketamine’s rapid-acting therapeutic effects. Early work in this area, however, found that few NMDAR antagonists and modulators had clinical success, failing to replicate ketamine’s broad therapeutic profile and rapid onset of robust antidepressant effects. For example, non-specific NMDAR antagonists such as memantine had extremely varied results in clinical studies due to differences in patient population, dosing regimen, and concurrent antidepressant medications. Lanicemine (AZD6765) initially demonstrated rapid-acting anti-depressant effects in patients with TRD, but these findings were not replicated in a Phase 2 trial. Glycine site modulators such as GLYX-13, apimostinel, and 4-Chlorokynurenine (AV-101) experienced similar difficulties. Following the failure of more generalized NMDAR antagonists and modulators as clinically effective antidepressants, NR2B-specific subunit antagonists such as traxoprodil (CP-101,606), MK-0657 (CERC-301), and eliprodil (EVT-101) were developed but suffered similar failures. Broadly, these agents demonstrated no significant antidepressant efficacy and an adverse events profile that led to the early terminations of some clinical trials in indications such as MDD, TRD, and Parkinson’s disease” (pg. 33, Section “NMDAR modulators”, Left Col., 1st paragraph).
In Example 8, found on pages 84-85 of the specification, the Applicant teaches a specific combination of NMDA receptor antagonist, ketamine, and KCNQ channel activator, retigabine, in the modulation of antidepressant-like behaviors in mice within a semi-naturalistic living environment or “Social Box”. This is considered to be adequate written description to support the claims within the narrower scope of treating depression symptoms with an NMDA receptor antagonist, wherein the NMDA receptor antagonist is ketamine, and a KCNQ channel activator, wherein the KCNQ channel activator is retigabine. As claim 1 currently reads, the Examiner cannot conclude that the Applicant was in possession of the full scope of the claimed invention.
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1-16 and 18 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for the treatment of depression, does not reasonably provide enablement for the treatment of all psychiatric disorders. 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.
Breadth of the Claims
Claim 1 recites the limitation “A method for treating a psychiatric disorder in a subject in need thereof…”. Claim 1 is not drawn to any psychiatric disorder in particular and is thus interpreted to encompass all psychiatric disorders.
Nature of the Invention
The nature of the invention is within the pharmaceutical arts with regards to the treatment of psychiatric disorders through the administration of an NMDA receptor antagonist and a KCNQ channel activator.
State of the Prior Art
The state of the prior art is what one skilled in the art would have known, at the
time the application was filed, about the subject matter to which the claimed invention
pertains. The relative skill of those in the art refers to the skill of those in the art at the
time the application was filed. See MPEP 2164.05(b). See Pac. Bioscience of Cal., Inc.
v. Oxford Nanopore Techs., Inc., 996 F.3d 1342, 1352, 2021 USPQ2d 519 (Fed. Cir. 2021).
The state of the prior art provides evidence for the degree of predictability in the
art and is related to the amount of direction or guidance needed in the specification as
filed to meet the enablement requirement. The state of the prior art is also related to the
need for working examples in the specification. See MPEP 2165.05(a).
Serafini teaches “Major depressive disorder (MDD) is a disabling dis-order associated with significant psychosocial impair-ment and negative outcomes, including an increased risk of suicidal behaviors. Although many pharma-cological agents are currently available for treating MDD, approximately 10% to 20% or more patients treated with traditional antidepressants do not achieve complete recovery and thus are considered treatment-resistant.”(pg.214, Section “Introduction”, Left Col., 1st paragraph). The use of ketamine and other NMDA receptor antagonist in the treatment of depression is known in the prior art. For example, Serafini also teaches that “NMDAR antagonists such as ketamine repre-sent promising, rapid action pharmacological options to treat patients with major depression and treatment-resistant depression.” (pg. 218, Section “Discussion”, Left Col., 1st paragraph).
Feng et al. ("Reversal of a treatment-resistant, depression-related brain state with the Kv7 channel opener retigabine." Neuroscience 406 (2019): 109-125.) teaches “The biology of MDD remains poorly understood but is note-worthy for its enormous complexity (Thomas et al., 2013). Based on twin studies, approximately 40% of the variation in liability of MDD has been attributed to additive genetic factors (Rice et al., 2002; Viktorin et al., 2016), indicating that most of the vulnerability to MDD is determined environmentally. Among diverse environmental factors, chronic forms of stress have been widely recognized as key contributors (Duman, 2014). Consistent with stress as a causal factor, chronic stress-based animal models reproduce various aspects of the pathology of MDD, including reduced brain volumes of the hippocampus and medial prefrontal cortex (Delgado y Palacios et al., 2011), dysregulated HPA axis function (Checkley, 1996), reduced complexity of neural dendrites (Magarinos et al., 1999; Liu and Aghajanian, 2008), heightened anxiety and anhedonia, and reduced self-care (Surget et al., 2011), as well as limited cognitive deficits (Willner and Belzung, 2015). The detrimental effects of stress can be attenuated and reversed by both conventional monoaminergic antidepressants (Bessa et al., 2009)as well as ketamine (Donahue et al., 2014; Brachman et al., 2016; Hare et al., 2017). However, while these studies confirm that stress plays a key role in MDD, they also suggest that stress by itself does not play a distinctive role that is specific to treatment-resistant depression.” (pg. 109-110, Section “Introduction”, Bridging Right and Left Col., 2nd and 1st paragraphs). Feng also states “Neuroinflammation involves increased production and release of microglia and astrocyte-derived pro-inflammatory cytokines such as TNF-α, IL-6, Il-1β, which ultimately act to increase the ratio of glutamatergic to GABAergic synaptic transmission (Pribiag and Stellwagen, 2013a), which is predicted to increase neural excitability. Conversely, agents that enhance the function of K+ channels reduce neuronal excitability. In particular, the Kv7 channel opener and anticonvulsant retigabine (also known as ezogabine) is of interest as it has recently been shown to exhibit antidepressant activity in both patients (Tanetal.,2018) and animals (Friedman et al., 2016).” (pg. 110, Section “Introduction”, Right Col., 2nd paragraph).
Finally, there is uncertainty in the treatment of all psychiatric disorders through administration of a NMDA receptor antagonist and a KCNQ channel activator because Sanacora et al. ("A consensus statement on the use of ketamine in the treatment of mood disorders." JAMA psychiatry 74.4 (2017): 399-405.) teaches that “To date, the strongest data supporting ketamine’s clinical benefit in psychiatric disorders are in the treatment of major depressive episodes without psychotic features associated with major depressive disorder.”, followed by “Although some limited data on the use of ketamine in treating other psychiatric diagnoses exist we do not believe there are sufficient data to provide a meaningful review of the assessment of risks and benefits of ketamine use in these other disorders at present” (pg. E2, Section “Patient Selection”, Left Col., 1st paragraph).
Level of Skill in the Art
The person of ordinary skill in the art is a person who is presumed to have known
the relevant art at the relevant time. Factors that may be considered in determining the
level of ordinary skill in the art may include: (A) "type of problems encountered in the
art;" (B) "prior art solutions to those problems;" (C) "rapidity with which innovations are
made;" (D) "sophistication of the technology; and" (E) "educational level of active
workers in the field. In a given case, every factor may not be present, and one or more
factors may predominate." In re GPAC, 57 F.3d 1573, 1579, 35 USPQ2d 1116, 1121
(Fed. Cir. 1995); Custom Accessories, Inc. v. Jeffrey-Allan Indus., Inc., 807 F.2d 955,
962, 1 USPQ2d 1196, 1201 (Fed. Cir. 1986); Environmental Designs, Ltd. V. Union Oil
Co., 713 F.2d 693, 696, 218 USPQ 865, 868 (Fed. Cir. 1983). See MPEP 2141.03 (I).
The invention described pertains to the medical or pharmaceutical arts. One of
ordinary skill would be trained in pharmacology, biochemistry, medicine, or a related art
field with a Ph. D or other advanced degree in these or other related fields.
Level of Predictability in the Art
The amount of guidance or direction needed to enable the invention is inversely
related to the amount of knowledge in the state of the art as well as the predictability of
the art. In re Fisher, 427, F.2d 833, 839, 166 USPQ 18, 24 (CCPA 1970). The “amount of guidance or direction” refers to that information in the application, as originally filed,
that teaches exactly how to make or use the invention. The more that is known in the
prior art about the nature of the invention, how to make, and how to use the invention,
and the more predictable the art is, the less information needs to be explicitly stated in
the specification. In contrast, if little is known in the prior art about the nature of the
invention and the art in unpredictable, the specification would need more detail as to
how to make and use the invention in order to be enabling. The scope of the required
enablement varies inversely with the degree of predictability involved, but even in
unpredictable art, a disclosure of every operable species is not required. A single
embodiment may provide broad enablement in cases involving predictable factors, such
as mechanical or electrical elements. In re Vickers, 141 F.2d 522, 526-27, 61 USPQ
122, 127 (CCPA 1944); In re Cook, 439 F.2d 730, 734, 169 USPQ 298, 301 (CCPA
1971). However, in applications directed to inventions in arts where the results are
unpredictable, the disclosure of a single species usually does not provide an adequate
basis to support generic claims. In re Soll, 97 F.2d 623, 624, 38 USPQ 189, 191 (CCPA
1938). In cases involving unpredictable factors, such as most chemical reactions and
physiological activity, more may be required. In re Fisher, 427 F.2d 833, 839, 166
USPQ 18, 24 (CCPA 1970). See MPEP 2164.03. The applicant would need to provide
more objective evidence to support the enablement of the aforementioned claims to
contrast the unpredictability of the subject matter art.
There is unpredictability in the field of endeavor in regards to the currently claimed method of treating all psychiatric diseases with a combination of all known NMDA receptor antagonist and all known KCNQ channel activators. The unpredictability stems from the prior art teaching that certain NMDA receptor antagonist do not exhibit anti-depressant like properties and the fact that there is no support, either in the prior art or the provided disclosure, in the treatment of all psychiatric disorders.
Amount of Direction Provided by the Inventor
The amount of direction provided by the inventor is correlated by the nature of
the unpredictability of the art. Given the context and scope of the claims mentioned
above, the inventor failed to provide the necessary amount of direction for one skilled in
the art to adequately use the invention across all suggested utility in the broadly stated
disease and disorders disclosed above. (See: Section (A) Breadth of the Claims).
The Applicant has provided guidance, found in Example 3 on pages 78-79 of the specification, with regards to ketamine increasing KCNQ channel currents in a mouse model. In Example 7, found on pages 83-84 of the specification, the Applicant teaches that manipulation of the KCNQ channel modulates antidepressant-like behaviors in mice using the KCNQ channel activator, retigabine, when in combination with ketamine. Finally, the Applicant teaches the treatment of depression symptoms with the combination treatment of ketamine and retigabine in Example 8 on pages 84-85 of the specification.
Quantity of Experimentation Needed to Make or Use the Invention Based on the Content of the Disclosure
As previously stated, the amount of experimentation depends on the art, the
predictability of the art, and the direction provided by the inventor. For one skilled in the art to practice the invention as disclosed, the artisan trying to practice Applicant’s
claimed invention would be required to undertake unduly burdensome activities
including:
Experimentation to demonstrate the treatment of at least all claimed psychiatric disorders.
Experimentation to show the dosage and frequency required in the treatment of all claimed psychiatric disorders.
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.
Claims 1-16 and 18 are rejected under 35 U.S.C. 103 as being unpatentable over Davoudian et al. ("Clinical overview of NMDA-R antagonists and clinical practice." Advances in pharmacology 89 (2020): 103-129.) in view of Tan et al. ("Effects of the KCNQ channel opener ezogabine on functional connectivity of the ventral striatum and clinical symptoms in patients with major depressive disorder." Molecular psychiatry 25.6 (2020): 1323-1333.) and Shirawi et al. ("Oral ketamine in treatment-resistant depression: a clinical effectiveness case series." Journal of clinical psychopharmacology 37.4 (2017): 464-467.).
Davoudian teaches a method of treating depression, wherein the depression is treatment-resistant depression, in patients using NMDA receptor antagonist. Specifically, Davoudian teaches that the NMDA receptor antagonist, ketamine, is the first promising NMDA receptor antagonist for the treatment of depression (Abstract). This also reads on the limitations of instant claims 2 and 3 which further limit the NMDA receptor antagonist to the elected species of ketamine.
However, Davoudian does not teach the use of the KCNQ channel activator, retigabine, or any KCNQ channel activator in combination with ketamine. This deficiency is cured by Tan, which teaches the use of the KCNQ channel activator, retigabine (also known as ezogabine), in the treatment of Major Depressive Disorder (MDD) (Abstract). This also reads on the limitation of instant claims 9 and 10 which further limit the KCNQ channel activator to retigabine. Finally, Tan teaches “Ezogabine selectively binds to and activates KCNQ transmembrane K+ ion channels, thereby enhancing transmembrane potassium currents mediated by the KCNQ (Kv7.2–7.5; e.g., KCNQ2/3) family of ion channels” (pg. 1324, Section “Ezogabine’s pharmacology, brain exposure, safety, and tolerability”, Right Col., 1st paragraph) which indicates that the KCNQ channel activator comprises a Kv7.2 subunit which reads on the limitations of instant claim 8.
The prior art separately recognizes the use of NMDA receptor antagonist, specifically ketamine, and the use of KCNQ channel activators, specifically retigabine, as being useful for the treatment of depressive symptoms. Furthermore, “It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art." See eMPEP 2144.06. In the instant case, Davoudian (ketamine) and Tan (retigabine) separately disclose the use of two drugs for the treatment of depression, so their combined use for treating the same disorder would have been prima facie obvious. So, it would have been obvious to one having ordinary skill in the art to combine the teachings of Davoudian with the teachings of Tan to treat treatment-resistant depression symptoms in a subject in need thereof through the administration of an NMDA receptor antagonist and a KCNQ channel activator because Tan teaches that “this is the first study investigating the antidepressant effect of the KCNQ-selective channel potentiator ezogabine in subjects with MDD” (pg. 1332, Section “Discussion”, Left Col., 2nd paragraph) and Davoudian teaches that “only the S(+) enantiomer was recently approved in nasal spray form for treatment-resistant depression” (pg. 5, Section “Ketamine: History and emergence as antidepressant”, 1st paragraph). Thus, it would have been prima facie obvious to one skilled in the art to combine the aforementioned references, prior to the effective filing date of the instant application, to arrive at the instantly claimed invention. Consequently, this also reads on the limitations of instant claim 12 which understandably is meant to recite that the NMDA receptor antagonist is ketamine and the KCNQ channel activator is retigabine.
With respect to claim 4, Davoudian teaches a study that administered 0.5 mg/kg and 1.0 mg/kg through the intravenous route which exhibited significant decrease in 6-item-Hamilton Depression Rating Scale (HAM-D-6) while the weaker doses 0.1 mg/kg and 0.2 mg/kg did not show significant improvement. Thus, Davoudian teaches administration of ketamine within the 0.1-1.0 mg/kg range for intravenous administration. Additionally, according to the specification, page 31 lines 1-3, Davoudian teaches administration of ketamine that is lower than the “Gold standard” administered to psychiatric patients which also reads on instant claim 7. Davoudian also teaches a study which demonstrated the efficacy of the intranasal route of administration for ketamine for treatment-resistant depression at a dose ranging from 56-84 mg which falls within the range of 10-300 mg as taught by the Applicant which reads on the limitations of instant claim 5 and instant claim 13.
With respect to claim 6, Davoudian nor Tan teach the oral administration of ketamine at a dose ranging from 10-500 mg. However, Shirawi et al., which also teaches the use of ketamine in the treatment of treatment-resistant depression states that “data on 22 patients with treatment resistant depression, who failed at least 3 adequate antidepressant treatment trials and 1 adequate trial of repetitive transcranial magnetic stimulation; subsequently, they received open-label treatment with oral ketamine, commenced at a dose of 50 mg every 3 days, titrated up by 25 mg every 3 days, according to response and tolerability” (Abstract, Section “Methods”). Shirawi also states that the amount of ketamine administered was titrated up until improvement in depressed mood was achieved, the patient lacked tolerability to the dose, or the upper limit of 300 mg was reached. Shirawi states “The dose commenced at 50 mg and was titrated upward by 25 mg at each dose (i.e., every 3 days), until reaching 1 of the following 3 end points: (1) improvement in depressed mood on the day after the dose, (2) a lack of tolerability of the dose, without improvement in mood, or (3) no improvement in mood despite reaching a dose of 300 mg” (pg. 465, Section “Treatment Approach”, Right Col., 1st paragraph) which falls within the range taught by the Applicant.
Regarding claim 11, Tan teaches that retigabine (ezogabine) was administered orally in the treatment of MDD at a dose up to 900 mg per day over the course of 10 weeks (Abstract; pg. 1325, Section “Study participants and design”, Left Col., 2nd paragraph) which is within the range of 0.5-2000 mg/day. This also reads on the limitation of instant claim 14 which recites wherein the retigabine (ezogabine) is to be administered orally.
With respect to claim 15, as detailed above, Davoudian, Tan and Shirawi all teach wherein the psychiatric disorder is a depression-related disorder. Additionally, Davoudian teaches wherein the S(+) enantiomer of ketamine was approved in the nasal spray form for treatment-resistant depression (pg. 5, Section “Ketamine: History and emergence as antidepressant”, 1st paragraph), Shirawi teaches the use of ketamine as an antidepressant treatment in adults with treatment-resistant depression (Abstract, Section “Purpose”, 1st paragraph), and Tan teaches the use of retigabine in the treatment of Major Depressive Disorder (MDD). While Tan does not teach retigabine for the treatment of subjects with treatment-resistant depression, Shirawi teaches that “at least one third of patients with major depressive disorder (MDD) do not achieve remission with conventional, monoaminergic antidepressant medications” (pg. 464, Section “Introduction”, Left Col., 1st paragraph). Thus, it would have been prima facie obvious for a person having ordinary skill in the art to at least try to treat a patient with treatment-resistant depression with a combination of ketamine and retigabine because there is overlap in patient populations which suffer from treatment-resistant depression and MDD.
Finally, with respect to claim 18, Tan teaches the administration of retigabine in a human subject by teaching “Based on these findings, we conducted a 10-week open-label pilot of ezogabine with the aim of determining whether ezogabine significantly engages the reward system in human patients with MDD” (pg. 1324, Section “Introduction”, Left Col., 3rd paragraph). Shirawi also teaches administration of ketamine to human subjects by teaching “Here, we report on a case series of 22 patients with TRD who received rescue open-label treatment with a course of oral keta mine at Toronto Western Hospital, University Health Network, Toronto, Canada, between July 2013 and November 2015.” (pg. 465, Section “Case Series”, Left Col. and Right Col., 1st paragraph)
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to JUSTIN CHRISTOPHER SANCHEZ whose telephone number is (703)756-5336. The examiner can normally be reached Monday -Friday (0730-1700).
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, James H Alstrum-Acevedo can be reached at 571-272-5548. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
JUSTIN CHRISTOPHER SANCHEZ
Examiner
Art Unit 1622
/J.C.S./Examiner, Art Unit 1622
/JAMES H ALSTRUM-ACEVEDO/Supervisory Patent Examiner, Art Unit 1622
Prosecution Insights