DETAILED ACTION
Status of Claims
The amendment submitted August 7, 2026 has been entered.
Claims 1-20 are pending and under consideration.
Claims 8 and 18-20 are withdrawn in the instant office action as explained below in the Election/Restriction section.
Claims 1-7 and 9-17 are under consideration in the instant office action as explained below in the Election/Restriction section.
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, claims 1-17 drawn to a method of treating ischemic injury in a subject having an ischemic injury, the method comprising administering to the subject a composition comprising an effective amount of a Sigma receptor agonist to treat the ischemic injury in the subject, wherein the composition is administered at least about 6 hours after occurrence of the ischemic injury in the reply filed on August 7, 2026 is acknowledged.
Applicant’s election without traverse of oxeladin a species of the sigma receptor agonist and ischemic injury induced by cerebral ischemia as a species of ischemic injury in the reply filed on August 7, 2026 is likewise acknowledged.
Claims 1-7 and 9-17 read on the elected species.
For the purposes of compact prosecution, the search was expanded. Applicant should not construe this to indicate the full scope of the claims has been searched.
Claims 8 and 18-20 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on July 30, 2026
Claims 1-7 and 9-17 are under consideration and the subject of this Office Action.
Information Disclosure Statement
Two information disclosure statements (IDS) submitted on July 1, 2024 and September 29, 2025 are acknowledged. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements are being considered by the examiner.
Claim Rejections - 35 USC § 112(a)
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 1-7 and 9-17 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 enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
There are many factors to be considered when determining whether there is sufficient evidence to support a determination that a disclosure does not satisfy the enablement requirement and whether any necessary experimentation is "undue." These factors include, but are not limited to: (A) The breadth of the claims; (B) The nature of the invention; (C) The state of the prior art; (D) The level of one of ordinary skill; (E) The level of predictability in the art; (F) The amount of direction provided by the inventor; (G) The existence of working examples; and (H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure. See MPEP § 2164.01 (a).
Upon consideration of the factors discussed below, the examiner concludes that one skilled in the art would be unable to practice the invention as disclosed without being burdened with undue experimentation based on the information provided by the applicant.
A discussion of these factors in relation to the pending claims follows.
The breadth of the claims and nature of invention
Claim 1 is directed towards a method of treating ischemic injury in a subject having an ischemic injury, the method comprising administering to the subject a composition comprising an effective amount of a Sigma receptor agonist to treat the ischemic injury in the subject, wherein the composition is administered at least about 6 hours after occurrence of the ischemic injury.
Claims 2-4 are directed towards types of ischemic injury, specifically ischemic injury induced by cerebral ischemia, wherein the cerebral ischemia is thrombotic ischemia, embolic ischemia, hypoperfusion, or ischemic stroke.
Ischemic injury well-known to be heterogenous and vary based on severity, issue damage cell type and diversity, and patient population.
Cleveland Clinic outlines different types of ischemia which include myocardial ischemia, mesenteric ischemia, peripheral or limb ischemia, ischemic stroke and transient ischemic attack; consequently, there is high variability ranging from the heart to digestive system to arms or legs and brain (Cleveland Clinic, “Ischemia,” https://my.clevelandclinic.org/health/diseases/ischemia, Updated: Feburary 29, 2024).
By example only, pertaining ischemic stroke, Stamova describes that “ Stroke is a multifaceted disease with genetic and environmental components like diet and lifestyle. The central nervous and immune systems display complex interactions, with the peripheral immune response participating in brain injury and repair mechanisms following stroke. The bidirectional communication between the injured brain and peripheral blood presents an opportunity to investigate the molecular changes in the latter. There is substantial heterogeneity in stroke pathogenesis, pathophysiology, comorbidities, and response to treatment and outcome (Stamova B, Knepp B, Rodriguez F. Molecular heterogeneity in human stroke - What can we learn from the peripheral blood transcriptome? J Cereb Blood Flow Metab. 2026 Jun;46(6):1424-1446. doi: 10.1177/0271678X251322598. Epub 2025 Mar 13. PMID: 40079561; PMCID: PMC11907527).”
Stamova further explains “IS [ischemic stroke] has different etiologies including cardioembolic (CE), large-vessel atherosclerotic (LVA), lacunar (small vessel, SV), other causes, and undetermined (cryptogenic). Identifying the IS cause is essential for optimal treatment and prevention strategies. The heterogeneity in etiologies is also reflected in the composition of the thrombi, with CE stroke having less red blood cells and more fibrin/platelets than thrombi with non-CE origin.”
Consequently, Stamova demonstrates the diversity in etiologies and how that can effect optimal treatment and prevention.
Stamova further explains “Stroke comorbidities, such as age, diabetes, hypertension, hyperlipidemia, smoking, and sex (discussed in a separate section below) increase stroke risk and worsen outcome (reviewed in47,48). The experimental stroke field recognizes that a critical factor for improving the clinical translation of findings is to address the presence of comorbidities in human stroke which often have not been represented sufficiently in preclinical research (reviewed in18,49).”
Consequently, Stamova teaches challenges in translating from preclinical to clinical settings based on diversity in comorbidities that are often not represented.
Stamova further explains that “Though common pathways have been identified in different phenotypic subgroups, caution must be exercised since different genes may be modulated in the common pathways. For example, even though there were common pathways in the peripheral blood transcriptome of ICH patients with hemorrhage in Deep ICH and Lobar ICH as compared to controls, 44 we found many of the affected genes in the common pathways were ICH-location-specific…We also found heterogeneity in the differentially expressed genes in common biofunctions associated with the peripheral immune response to ischemic stroke in males and females….Overall, molecular heterogeneity in stroke subgroups can have significant repercussions when treatment and prevention strategies are developed and may warrant search for subgroup-specific treatments.”
Consequently, Stamova teaches the importance in patient population and molecular heterogeneity in developing treatment and prevention strategies.
Stamova further explains that “As noted throughout this review, significant and pervasive molecular heterogeneity in stroke subgroups exists….The peripheral immune and coagulation responses contribute to injury and repair mechanisms in the injured brain following stroke. This is underlined by molecular changes at many biological levels including the transcriptome. Transcriptomic studies in peripheral blood following human stroke have revealed considerable heterogeneity in the transcriptome architecture in subgroups related to etiology, comorbidities, biological sex, outcome, response to treatment, temporal evolution, cell-specific responses, and even common pathways. Additionally, we show that subject-level combinatorial heterogeneity exists with different stroke subjects having different combinations of pathways potentially altered. Differences in the individual’s response to stroke reveal molecular subgroups and emphasize the need for precision medicine in future treatments and therapeutics…The molecular heterogeneity may have significant repercussions for the development of treatment targets and prevention strategies, and sub-group specific approaches may be needed to advance towards personalized medicine.”
Consequently, Stamova illustrates the heterogeneity on various levels regarding ischemic stroke by example only, including the importance of patient populations amongst other factors.
Claims 5-7 and 9 are directed towards sigma receptor agonists, particularly wherein the sigma receptor agonist comprises an antitussive, an antipsychotic, an antidepressant, a neurosteroid, a neuroleptic, or a psychostimulant, or any combination thereof and more specifically where the sigma receptor agonist is oxeladin.
Each of these classes of drugs comprises a broad class of possible therapies that are diverse in activity, function, structure, pharmacokinetics, administration, etc.
It is therefore reasonable to conclude the claims are broad with respect towards what comprises a sigma receptor agonist.
Claim 9 recites a functional limitation wherein the sigma receptor agonist “crosses the subject’s blood-brain barrier.”
Claim 10 defines the ischemic injury as having “an acute phase and a chronic phase.”
Claims 11-14 define the dosing schedule for the composition.
Claim 15 and 17 define the dosage.
Claim 16 defines the administration mode.
On page 6, paragraph [0020], Applicant defines subject as “The term "subject," as used herein, can be any organism or animal subject that is an object of a method or material, including mammals, c.g., humans, laboratory animals (e.g.,primates, rats, mice, rabbits), livestock (e.g., cows, sheep, goats, pigs, turkeys, and chickens), household pets (e.g., dogs, cats, and rodents), horses, and transgenic non-human animals. The subject can be a patient, e.g., have or be suspected of having a disease (that may be referred to as a medical condition), such as ischemic injury. The subject may being undergoing or having undergone treatment. The subject may be asymptomatic. Subjects may be healthy individuals that are desirous of prevention of ischemic injury. The terms "patient" and "individual" may be used interchangeably with "subject," in at least some cases. An individual may comprise any age of a human or non-human animal and therefore includes both adult and juveniles.”
Consequently, it is reasonable to conclude the claims are broad with respect to subject which includes all organism, animals, and humans across all ages and patient populations.
On page 6, paragraph [0021], Applicant defines treating as “As used herein, the terms "treatment," "treat," or "treating" refers to intervention in an attempt to alter the natural course of the subject being treated. Treatment includes any beneficial or desirable effect on the symptoms or pathology of a disease or pathological condition, and may include even minimal reductions in one or more measurable markers of the discase or condition being treated, c.g., ischemic injury. Treatment may serve to accomplish one or more of various desired outcomes, including, for example, preventing occurrence or recurrence of disease, alleviation or reduction in severity of symptoms, and diminishment of any direct or indirect pathological consequences of the disease, preventing disease spread, delaying the rate of disease progression, amelioration or palliation of the disease state, and remission or improved prognosis. "Treatment" does not necessarily indicate complete eradication or cure of the disease or condition, or associated symptoms thereof.”
Consequently, Applicant’s definition of treating additionally included prophylaxis.
Consequently, it is reasonable to conclude that the claims are broad with respect to subject, therapeutic, disease, and aim of “treating,” which includes prophylaxis.
The 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 in relation to the subject matter to which the claimed invention pertains at the time the application was filed. See MPEP § 2164.05(b). See Pac. Biosciences 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 § 2164.05 (a).
There is no general treatment in the art known to treat all types of ischemic injury, including that any sigma receptor agonist would be effective in treating all types of ischemic injury.
In fact, there are contradicting examples in the prior art about whether sigma receptor agonist are effective in treating certain types of ischemic injury.
By example only Wiszniewska teaches that “Spinal cord ischemia or spinal cord infraction (SCI) is a relatively rare disease compared to cerebral stroke… It is diagnosed 100 times less often than cerebral stroke. SCI typically occurs between 50 and 70 years old on average [2]. It mainly presents as either anterior spinal artery syndrome or anterior spinal cord syndrome (ASCS) in up to 87.2% of cases [3-5]. Magnetic resonance imaging (MRI) with (diffusion-weighted contrast (DWI) should be considered for an initial diagnosis of spinal cord ischemia. A combination of DWI with ADC maps is recommended to distinguish SCI from other differential disorders. There are no established rules for the treatment of this condition (Wiszniewska M, Sankowska M. Spinal cord ischemia - from diagnosis to treatment. Postep Psychiatr Neurol. 2024 Jun;33(2):93-97. doi: 10.5114/ppn.2024.141367. Epub 2024 Jul 11. PMID: 39119546; PMCID: PMC11304228).
Additionally, Wiszniewska teaches that “Spinal cord ischemia is a condition in which accurate treatment in necessary to achieve a favorable functional outcome. Unlike cerebral stroke, in which guidelines for management are well-established, the management of acute SCI is still under discussion. If the cause is ischemic etiology, the assessment of risk factors such as diabetes mellitus, hypertension, and hyperlipidemia should be carried out and accurate treatment should be implemented.”
Consequently, Wiszniewska teaches that spinal cord ischemia is a rare disease that is hard to diagnosis, which there are still no developed guidelines to treat.
Lattard teaches that sigma-1 receptor agonist have a negative impact on spinal cord injury (Lattard et al. 2021. Negative impact of sigma-1 receptor agonist treatment on tissue integrity and motor function following spinal cord injury. Frontiers in pharmacology, 12, p.614949).
Specifically, Lattard teaches that “Traumatic spinal cord injury (SCI) results in 0.6–0.9 million annual new cases worldwide (Kumar et al., 2018). SCI symptoms include sensory, motor and autonomic deficits ranging from minimal dysfunctions to complete tetraplegia. Following the primary traumatic mechanical disruption of spinal cord tissues, a cascade of events including vascular impairment, mitochondrial dysfunction, excitotoxicity and calcium overload characterizes the secondary phase of injury and further exacerbates the lesion. There is currently no curative treatment to improve neurological recovery after SCI.”
Additionally, Lattard teaches that, “Here, we investigated whether sigma-1 receptor activation with PRE-084 is beneficial or detrimental following SCI in mice. First, we report that PRE-084 treatment after injury does not improve motor function recovery. Second, using ex vivo diffusion weighted magnetic resonance imaging completed by histological analysis, we highlight that σ1R agonist treatment after SCI does not limit lesion size. Finally, PRE-084 treatment following SCI decreases NeuN expression and increases astrocytic reactivity. Our findings suggest that activation of sigma-1 receptor after traumatic spinal cord injury is detrimental on tissue preservation and motor function recovery in mice.”
Furthermore, there have been noted issues in translating preclinical studies into the clinic.
Leonardo teaches that “Many pharmacological treatments for stroke have afforded protection in rodent models but failed to show efficacy in clinical trials. This discrepancy may be due to the lack of long-term functional studies….Despite short-term efficacy, DTG failed to improve behavioral outcomes or reduce infarct volumes after 96 h. While DTG may prove beneficial as a short-term therapy, these data highlight the importance of long-term functional recovery when evaluating novel therapies to treat stroke (Leonardo CC, Hall AA, Collier LA, Green SM, Willing AE, Pennypacker KR. Administration of a Sigma Receptor Agonist Delays MCAO-Induced Neurodegeneration and White Matter Injury. Transl Stroke Res. 2010 Jun;1(2):135-45. doi: 10.1007/s12975-009-0005-9. PMID: 20563232; PMCID: PMC2885737).”
Consequently, Leonardo emphasizes that timing is important, and that short-term efficacy does not suggest such compounds are effective long-term.
Leonardo further teaches that “Mounting evidence suggests that the lack of efficacy may be due, at least in part, to the complex immune response to ischemic insult. The initial wave of cell death resulting from ischemia initiates a local [6] and systemic immune response [7–10] that ultimately contributes to neural injury, encompassing both neuronal death and injury to cerebral white matter tracts [11]. Activation of resident microglia and extravasation of peripheral leukocytes into the brain facilitate pro-inflammatory signaling [12, 13]. Despite the purported deleterious role of microglia/macrophages, ablation of these cells increases infarct volume [14] and impairs remyelination following injury [15], indicating that these cells play a complex role in the post-stroke immune response.”
Leonardo further emphasizes that “Regardless of the precise mechanisms involved, data here clearly show that demonstrating short-term protection is not sufficient to deem a compound promising for the treatment of stroke. As novel therapies continue to fail clinical trials, the field of stroke research would likely benefit from instituting long-term behavioral recovery as the bench mark for efficacy.”
Finally, Schreihofer teaches that “Numerous pharmaceutical interventions for acute stroke in rodent models of cerebral ischemia have failed to be translated to clinical use, suggesting that interventions within the first few hours of stroke may not provide suitable targets for stroke therapy in the human population…This study examined the potential to repurpose the antitussive drug oxeladin for delayed treatment in focal cerebral ischemia…These data support the role of oxeladin as a S1R agonist with the ability to improve stroke outcomes when administered beginning 48 h after stroke, in agreement with other systemically administered S1R agonists (Schreihofer DA, Dalwadi D, Kim S, Metzger D, Oppong-Gyebi A, Das-Earl P, Schetz JA. Treatment of Stroke at a Delayed Timepoint with a Repurposed Drug Targeting Sigma 1 Receptors. Transl Stroke Res. 2024 Dec;15(6):1035-1049. doi: 10.1007/s12975-023-01193-x. Epub 2023 Sep 13. PMID: 37704905.”
Schreihofer teaches that “Repurposing of drugs for a new target or new indication raises multiple tractable questions. First, do any other actions of the drug lead to deleterious actions along with the beneficial actions targeted? The reported LD 50 of oxeladin citrate in mice injected subcutaneously is 244 mg/kg [55]. In this study we did not observe overt toxic effects at 135 mg/kg p.o. in rats. Similarly, we did not observe significant changes in thrombosis in vitro, and in rats euthanized 24 h after oxeladin treatment we so no increase in hemorrhagic transformation (data not shown). Second, do any of the original targets of the drug have the potential to interfere with recovery? Oxeladin was developed as an antitussive with reduced side effects of related compounds [55]. Unlike dextromethorphan, oxeladin does not cause drowsiness and is not reported to have significant side effects at therapeutic doses. Notably, oxeladin was withdrawn from the US, Canadian, and UK markets in 1976 after warnings of potential carcinogenicity were reported in Germany. However, primary sources for this warning or toxicity data were unavailable from the World Health Organization (author inquiry). France also briefly limited marketing of oxeladin, but it is still marketed in France and other countries where it was reintroduced in 1996 [56]. Whereas other repurposed drugs that activate S1R may influence serotonergic [39, 57], dopaminergic [38], or adrenergic systems [40] and have sedative properties [40, 42], no such effects have been reported for oxeladin. However, literature is sparce and specific examination of oxeladin binding to other membrane receptors in the CNS is not known…Additional studies are clearly needed to determine the mechanism(s) for oxeladin’s beneficial effects in stroke and to specifically link them to its activity at S1Rs.”
Consequently, Schreihofer teaches that there are still many unknowns regarding oxeladin.
Schreihofer also teaches limitations regarding oxeladin: “The present study supports our previous study that identified oxeladin as a potential drug repurposing candidate for the delayed treatment of cerebral ischemia due to its ability to bind S1R and stimulate BDNF release. Oxeladin showed good oral bioavailability and pharmacokinetics. Oxeladin is more potent that other antitussive drugs with S1R activity and has fewer undesirable side effects. Daily oral treatment was well tolerated and improved functional outcomes and reduced the final extent of ischemic injury. Initial examination of mechanisms of action do not support anti-inflammatory or proliferative actions, however, the end points for these measures was 15 days after stroke and may have missed critical actions in the first few days of treatment. Alternatively, other S1R actions may be more critical for the beneficial effects we observed, including those involving ER stress, the unfolded protein response, and autophagy. Future mechanistic studies will be necessary to determine the precise mechanisms and dosing requirements and long-term outcomes before advancing drugs like oxeladin into clinical settings.”
Furthermore, Schreihofer teaches that more experimentation is required for dosing, long-term outcomes and before oxeladin can be advanced into a clinical setting.
The level of one of ordinary skill
The person of ordinary skill in the art is a hypothetical 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 biomedical and pharmaceutical arts. One of ordinary skill would be a person with considerable training in medicine, veterinary medicine, pharmacology, oncology, medicinal chemistry, biochemistry or a related technical discipline.
The 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 in 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 is 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 arts, 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. See MPEP § 2164.03.
Consequently, technologies involving physiological activity as opposed to mechanical or electrical inventions are generally regarded as being unpredictable sciences.
As aforementioned, ischemic injury is high heterogenous in terms of etiology, patient population, response to treatment, cell-specific responses, etc. For such a broad class of compounds, there are also conflicting reports on if sigma receptor agonist are beneficial for all ischemic injury. Additionally, there are well-known challenges in translating preclinical data to the clinic in treating ischemic stroke and unknowns pertaining oxeladin, which is a repurposed antitussive.
Consequently, there are various facets contributing to high unpredictability.
In this context, based on assessing the fields of study, the predictability in art is low.
Consequently, the applicant would need to provide more details, working examples and guidance in order for the claimed invention to be enabling based on the scope and nature of the claimed invention.
The amount of direction provided by the inventor
As aforementioned, the amount of direction provided depends on the prior art and predictability of in the art. Based on the scope of protection sought by the applicant and the discussion aforementioned, the inventor has failed to provide sufficient direction for one ordinarily skilled in the art to practice the disclosed invention as claimed.
The existence of working examples
The applicants’ working examples are directed towards:
Effect of oxeladin on rats with focal cerebral ischemia (page 32, paragraph [0101]).
Sigma receptor binding by S1R ligands over S2R using Human MCF-7 cells (in vitro, Example 2, page 36, paragraph [0111]).
Determination of maximum tolerating dose and brain pharmacokinetics in rates (examples 4-5).
Effect of oral oxeladin on thrombosis and thrombotic activity and neurological function of sigma 1 compounds (example 6-7, rats).
However, Applicant’s data does not cover the full scope of invention and focuses only on focal cerebral ischemia. It is known in the art that ischemia injury is highly heterogenous across etiology, site of injury, patient population, etc.
There are also no working examples supporting the broad range of sigma receptor agonists as being effective in treating all types of ischemic injury across the broad class of subjects and patient populations claimed. It is well-known that patient population can play a critical role in dictating success of translating from preclinical to clinic setting. There is also no support for prophylactic treatment as claimed based on Applicant’s definition.
On this basis and the prior discussion, the working examples are both not commensurate with the scope of protection sought and are not enabling. One ordinarily skilled in the art would unable to simply translate the evidence provided by the applicant into methods encompassing the broad scope of subjects, diseases, compounds and aim of treatment as claimed without undue experimentation.
The quantity of experimentation needed to make or use the invention based on the content of the disclosure.
As aforementioned, the quantity of experimentation depends on the prior art, the predictability of the art, and the direction provided by the inventor, which are factors that were already discussed.
In order for one ordinarily skilled in the art to practice the invention as disclosed, some attributes one would require, but are not limited to:
Studies supporting translation from preclinical to clinical setting encompassing the diverse class of subjects listed (i.e.: organisms, humans, including juveniles, and other animals) and broad range of ischemic injury and sigma receptor agonists as claimed.
Support demonstrating prophylactic treatment as claimed.
Additional details on development of a treatment regime including how to determine effective dosage, timing, monitoring plan and administration method for the diverse class of subjects, diseases and disease progression, particularly account for the critical role of patient population and other comorbidities in effecting treatment outcomes.
Based on the evidence and rationale put forth, the examiner concludes that one ordinarily skilled in the art would require undue experimentation in order to practice invention based on the details provided and scope of invention defined in Claims 1-7 and 9-17
Consequently, Claims 1-7 and 9-17 are rejected for lacking enablement.
Conclusion
Claims 1-7 and 9-17 are under consideration and are rejected. No claims allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to CAROLYN L. LADD whose telephone number is (703)756-5313. The examiner can normally be reached M-Th, 7:00 am to 5:30 pm EST.
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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.
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/C.L.L./Examiner, Art Unit 1622
/JAMES H ALSTRUM-ACEVEDO/Supervisory Patent Examiner, Art Unit 1622
