An Expert Report on the Investigational Compound JNJ-69095897

1. Executive Summary

JNJ-69095897 was an investigational small molecule drug developed by Janssen Research & Development LLC. It was designed as a selective, reversible, and centrally active inhibitor of monoacylglycerol lipase (MAGL), an enzyme pivotal in the endocannabinoid system. The primary therapeutic rationale for JNJ-69095897 centered on its potential to treat central nervous system (CNS) disorders, with preclinical evidence specifically indicating efficacy in models of stress and anxiety.[1]

The compound advanced to Phase 1 clinical development with the initiation of trial NCT04920578 (also known as EudraCT 2021-000609-26). This study was a randomized, placebo-controlled, double-blind, single ascending dose trial in healthy participants, designed to assess the safety, tolerability, pharmacokinetics (PK), and pharmacodynamics (PD) of orally administered JNJ-69095897.[4] However, this clinical trial was subsequently terminated prior to its planned completion.[4]

The specific reasons for the termination of the Phase 1 trial and the discontinuation of JNJ-69095897's development have not been publicly disclosed in the available documentation. This absence of information precludes a definitive understanding of the factors leading to its cessation, which could range from safety or tolerability concerns, unfavorable pharmacokinetic properties, lack of target engagement, to strategic portfolio decisions by the developer. The trajectory of JNJ-69095897, from promising preclinical signals for a novel CNS mechanism to early clinical-phase termination, is characteristic of the significant translational challenges encountered in neuroscience drug development.

2. Introduction to JNJ-69095897

2.1. Overview and Originator

JNJ-69095897 is identified as an investigational small molecule drug candidate.[4] Its development was undertaken by Janssen Research & Development LLC, a pharmaceutical company of Johnson & Johnson, known for its extensive research programs in various therapeutic areas, including neuroscience.[4] The primary focus for JNJ-69095897 was within the domain of central nervous system (CNS) disorders. Preclinical investigations suggested potential utility in conditions related to stress and anxiety, driven by its mechanism of action as a monoacylglycerol lipase (MAGL) inhibitor.[1]

2.2. Chemical Nature and Development Codes

JNJ-69095897 was pursued under several development codes and identifiers, including 69095897EDI1001 and CR108935, which were associated with its clinical trial program.[5] Despite its progression into Phase 1 clinical studies, detailed information regarding the specific chemical structure and Chemical Abstracts Service (CAS) number for JNJ-69095897 is not explicitly available in the reviewed public domain documents. This lack of precise chemical identification is somewhat atypical for compounds that have entered human trials, where such information often becomes accessible through trial registries or initial scientific disclosures. The absence of these details may reflect limited public disclosure by the originator following the compound's discontinuation.

Table 1: JNJ-69095897 - Core Drug Characteristics

Characteristic	Details	Source(s)
Name	JNJ-69095897	4
Development Codes/Synonyms	69095897EDI1001, CR108935	5
Originator	Janssen Research & Development LLC	4
Chemical Type	Small molecule	4
Proposed Mechanism of Action	Selective, reversible, non-competitive Monoacylglycerol Lipase (MAGL) inhibitor	3
Primary Therapeutic Area Investigated	CNS disorders (e.g., stress, anxiety)	1
Highest Phase of Development	Phase 1	4
Current Status	Discontinued (Phase 1 trial terminated)	4

3. Pharmacological Profile: Monoacylglycerol Lipase (MAGL) Inhibition

3.1. The Endocannabinoid System and the Role of MAGL

The endocannabinoid system (eCB system) is a complex lipid signaling network that plays a crucial modulatory role in a wide array of physiological processes within the human body, particularly in the central nervous system. Key components of this system include cannabinoid receptors (primarily CB1 and CB2), endogenous cannabinoid ligands (endocannabinoids), and the enzymes responsible for their synthesis and degradation.[3]

One of the principal endocannabinoids is 2-arachidonoylglycerol (2-AG), which is present in high concentrations in the brain and acts as a full agonist at both CB1 and CB2 receptors.[3] Monoacylglycerol lipase (MAGL) is the primary serine hydrolase responsible for the catabolism of 2-AG, hydrolyzing it into arachidonic acid (AA) and glycerol.[3] This enzymatic action serves two main purposes: it terminates 2-AG signaling and concurrently liberates arachidonic acid, a key precursor for the biosynthesis of prostaglandins and other eicosanoids, many of which are pro-inflammatory mediators.[12]

3.2. JNJ-69095897: A Selective, Reversible MAGL Inhibitor

JNJ-69095897 was developed as a selective, reversible, and centrally active inhibitor of MAGL.[3] Some documentation also refers to it as a non-competitive inhibitor of MAGL.[3] The "reversible" nature of its inhibition is a particularly important characteristic. Earlier generations of MAGL inhibitors were often irreversible, leading to prolonged and profound elevation of 2-AG levels. This, in turn, was associated with desensitization and downregulation of CB1 receptors, potentially limiting their therapeutic efficacy and contributing to undesirable side effects, thereby hindering their clinical development.[13] The design of JNJ-69095897 as a reversible inhibitor likely represented a strategic effort by Janssen to achieve a more controlled and potentially transient modulation of MAGL activity. This approach could theoretically offer an improved therapeutic window by minimizing the risk of CB1 receptor desensitization and other target-related adverse events associated with sustained, high levels of 2-AG, thus addressing a key challenge faced by previous MAGL inhibitor programs.

3.3. Therapeutic Implications of MAGL Inhibition in CNS Disorders

The inhibition of MAGL is hypothesized to exert therapeutic effects by augmenting endocannabinoid signaling. By blocking the degradation of 2-AG, MAGL inhibitors lead to an increase in the concentration of this endocannabinoid in the brain and peripheral tissues.[3] Elevated 2-AG levels enhance the activation of cannabinoid receptors, particularly CB1 receptors which are densely expressed in CNS regions critical for mood, cognition, and stress responses.

The eCB system is known to play a critical modulatory role in synaptic plasticity, neuronal excitability, neuroinflammation, stress adaptation, learning, memory formation, and mood regulation.[3] Dysregulation of eCB signaling has been implicated in the pathophysiology of various neuropsychiatric conditions, including anxiety disorders, depression, and post-traumatic stress disorder.[3] Consequently, MAGL inhibitors have garnered significant interest as potential therapeutic agents for a range of conditions, including pain, anxiety, depression, neuroinflammatory disorders, and even neurodegenerative diseases and certain cancers.[12] The anxiolytic and mood-regulating potential derived from enhanced 2-AG signaling formed the core rationale for investigating JNJ-69095897 in CNS disorders.

4. Preclinical Research and Rationale

4.1. In Vitro Characterization

Specific quantitative data from in vitro characterization of JNJ-69095897, such as its half-maximal inhibitory concentration (IC50​) against MAGL, enzyme kinetics, or selectivity profiling against other hydrolases or receptors, are not detailed in the provided documents. While other MAGL inhibitors, including some from Janssen's research programs (e.g., JNJ-42226314), have published IC50​ values [11], such specific data for JNJ-69095897 itself are absent from the available materials. This represents an information gap regarding the fundamental biochemical potency and selectivity of the compound.

4.2. In Vivo Efficacy in CNS Models (Stress, Anxiety)

Despite the lack of detailed in vitro data in the provided sources, JNJ-69095897 was advanced into preclinical development, indicating that it likely demonstrated promising characteristics in earlier screening assays.[3] The key preclinical evidence supporting its progression to human trials comes from in vivo studies. JNJ-69095897 was reported to attenuate stress and anxiety in rodent models.[1] These findings provided direct preclinical validation for its potential therapeutic application in human anxiety and stress-related disorders. This aligns with the broader understanding of the endocannabinoid system's role in modulating pain perception, cognition, and mood, where dysregulation is linked to conditions such as anxiety and depression.[1]

4.3. Target Engagement and Biomarker Strategy (Planned)

A critical aspect of early CNS drug development is the demonstration of target engagement in humans. The Phase 1 clinical trial for JNJ-69095897 (NCT04920578) included objectives to investigate its pharmacodynamics (PD).[5] For a MAGL inhibitor, a primary PD effect would be the elevation of 2-AG levels in relevant biological matrices. The importance of PD biomarkers for guiding dose selection and confirming mechanism of action in first-in-human (FIH) studies of MAGL inhibitors was recognized.[3]

Significantly, a study identified as NL-OMON52349, which is associated with JNJ-69095897 [4], was described as "A methodology study to characterize 2-AG as a potential [biomarker]".[3] The execution of a dedicated biomarker methodology study in parallel with, or in support of, the Phase 1 trial for JNJ-69095897 indicates a sophisticated and integrated early development strategy by Janssen. This suggests a commitment to rigorously validating the tools necessary to measure the direct biological effect of JNJ-69095897. Such an approach is crucial for de-risking the development of drugs with novel mechanisms, particularly in the challenging field of CNS therapeutics, by ensuring that any observed clinical effects (or lack thereof) can be correctly interpreted in the context of verified target engagement.

5. Clinical Development: The NCT04920578 Phase 1 Study

5.1. Study Design, Objectives, and Participant Population

The clinical development of JNJ-69095897 commenced with a Phase 1 study, registered under multiple identifiers: NCT04920578 in the ClinicalTrials.gov database, EudraCT number 2021-000609-26 in the European Union Clinical Trials Register, and sponsor protocol numbers CR108935 and 69095897EDI1001.[5]

The official title of the study was "A 3-Part, Randomized, Placebo-controlled, Double-blind, Single Ascending Dose Study to Investigate Safety and Tolerability, Pharmacokinetics and Pharmacodynamics of JNJ-69095897 in Healthy Participants".[4] An associated study, NL-OMON52349, shared a similar focus on safety and pharmacokinetics of JNJ-69095897.[4] The trial was sponsored by Janssen Research & Development LLC.[4]

The primary purpose of this FIH study was to investigate the safety and tolerability of JNJ-69095897 compared to placebo following single or divided oral dose administration in healthy participants.[5] Secondary objectives included the characterization of the pharmacokinetic (PK) profile and pharmacodynamic (PD) effects of JNJ-69095897.[5]

The study intended to enroll a total of 48 healthy participants.[5] The eligibility criteria specified adults aged 18 to 75 years with a body mass index (BMI) between 18.0 and 30.0 kg/m2.[5] The study design was structured in three parts: Part 1 involved single ascending dose (SAD) cohorts with healthy male participants receiving JNJ-69095897 or placebo in a double-blind manner. Part 2 was an open-label, single-dose cohort in healthy male participants. Part 3 planned for a single or divided dose cohort including healthy male participants and women of non-childbearing potential (WONCBP), also in a double-blind fashion.[6] The investigational drug, JNJ-69095897, was administered orally, with a matching placebo as the comparator.[5]

5.2. Pharmacokinetic and Pharmacodynamic Assessments

A key component of the Phase 1 study was the detailed characterization of JNJ-69095897's pharmacokinetics. Assessments were planned in multiple biological matrices, including blood, plasma, cerebrospinal fluid (CSF), and urine.[5] The inclusion of CSF sampling is particularly noteworthy for a CNS-targeted drug, as it aims to directly measure the compound's ability to cross the blood-brain barrier and achieve potentially therapeutic concentrations in the target organ.

Pharmacodynamic assessments were also integral to the study, likely involving the measurement of 2-AG levels or other relevant biomarkers to confirm target engagement by MAGL inhibition, as discussed in the preclinical strategy (Section 4.3). Furthermore, the study protocol mandated participation in a pharmacogenomic component, suggesting an effort to identify potential genetic factors influencing the drug's PK, PD, safety, or tolerability.[5] This proactive inclusion of pharmacogenomics reflects a comprehensive approach to understanding inter-individual variability in drug response from an early stage of development.

5.3. Termination of the Clinical Trial and Reported Rationale

The Phase 1 clinical trial NCT04920578 was officially terminated before its planned completion.[4] The study commenced on June 16, 2021, and its anticipated or actual completion date was listed as February 27, 2023.[5] Reports from Larvol Delta indicate activity or reporting related to JNJ-69095897 between April 2022 and March 2024, consistent with the trial's operational period and subsequent discontinuation.[18] While the main trial (NCT04920578) is consistently reported as terminated, the status of the associated biomarker methodology study (NL-OMON52349) is variably listed as "Completed" [4] or "Recruitment stopped".[3]

Critically, the specific reason for the termination of the NCT04920578 trial is not provided within the scope of the available research documents. This lack of a publicly disclosed rationale is a significant information gap. Phase 1 SAD studies in healthy volunteers are primarily designed to establish initial safety, tolerability, and PK. Termination at this early stage typically suggests that the investigational compound did not meet predefined criteria for progression to higher doses or further cohorts. Common reasons for such terminations include unacceptable safety or tolerability signals, a highly unfavorable PK profile (such as poor bioavailability, excessively rapid metabolism preventing adequate exposure, inability to achieve target concentrations at safe doses, or the formation of problematic metabolites), or strategic decisions by the sponsoring company. Given the plan to assess CSF PK, any failure to demonstrate adequate CNS penetration could also have been a decisive factor for a drug intended for CNS disorders.

Table 2: Clinical Trial NCT04920578 - Summary Details

Detail	Information	Source(s)
Trial Identifier (NCT)	NCT04920578	5
EudraCT Number	2021-000609-26	5
Sponsor Protocol Number(s)	CR108935, 69095897EDI1001	5
Official Title	A 3-Part, Randomized, Placebo-controlled, Double-blind, Single Ascending Dose Study to Investigate Safety and Tolerability, Pharmacokinetics and Pharmacodynamics of JNJ-69095897 in Healthy Participants	4
Phase	1	4
Sponsor	Janssen Research & Development LLC	4
Study Purpose	Investigate safety, tolerability, PK, and PD of single/divided oral doses of JNJ-69095897.	5
Key Objectives	Assess safety and tolerability (primary); Characterize PK in blood, plasma, CSF, urine, and PD (secondary).	5
Study Population	Healthy adult male and female (WONCBP) volunteers, N=48.	5
Investigational Drug	JNJ-69095897 (oral)	5
Comparator	Placebo (oral)	5
Status	Terminated	4
Study Dates	Start June 16, 2021; Anticipated/Actual Completion February 27, 2023.	5
Stated Reason for Termination	Not provided in the available research material.	-

6. Safety and Tolerability Profile (from planned/conducted Phase 1)

6.1. Anticipated Safety Monitoring

The Phase 1 trial NCT04920578 incorporated a comprehensive safety monitoring plan, standard for FIH studies. This included regular physical examinations, monitoring of vital signs (including orthostatic blood pressure measurements), 12-lead electrocardiograms (ECGs) with specific attention to parameters such as the Fridericia-corrected QT interval (QTcF) and heart rate (with exclusion criteria for baseline QTcF prolongation or bradycardia), and routine clinical laboratory tests encompassing serum chemistry, hematology, and urinalysis.[5] The study's exclusion criteria were designed to minimize risks by excluding individuals with current significant medical illnesses (including cardiac, liver, or renal insufficiency), active sleep disorders, major or clinically relevant psychiatric disorders, or recent acute illnesses.[5]

6.2. Observed Safety and Tolerability

Despite the planned safety assessments, no specific adverse event data or detailed safety and tolerability outcomes for JNJ-69095897 from the terminated NCT04920578 trial are available in the provided documents. This information deficit is a direct consequence of the trial's early termination and the lack of subsequent public disclosure or publication of any interim findings. While Janssen has commented on the safety profile of other discontinued compounds (e.g., aticaprant was reported as safe and well-tolerated despite efficacy failure [19]), such statements are specific to those individual agents and cannot be extrapolated to JNJ-69095897. The absence of disclosed safety data from the terminated trial, combined with the unstated reason for termination, leaves a significant ambiguity. It cannot be definitively concluded whether safety or tolerability issues contributed to the discontinuation, or if other factors such as pharmacokinetics or strategic considerations were primary.

7. Intellectual Property Landscape

The provided information indicates an association of patent activity with JNJ-69095897, with general database listings referring to "100 Patents (Medical) associated with JNJ-69095897".[4] However, these listings do not offer specific details such as patent numbers, jurisdictions, claims related to composition of matter, method of use, or formulation for JNJ-69095897 itself.

Other documents describe patent applications from Janssen Pharmaceutica NV pertaining to different series of MAGL inhibitors. For instance, patent application WO2021191391A1 covers aminocyclobutane compounds as MGL modulators for diseases including neurodegenerative conditions, pain, and inflammation.[14] Similarly, application MX2024008337A relates to (1H-pyrazol-5-yl)-2-azaspiro[3.3]heptan-2-yl methanone compounds for inhibiting MAGL in the context of neurodegenerative diseases and pain.[15] These examples illustrate Janssen's broader engagement in securing intellectual property for MAGL inhibitors around the period of JNJ-69095897's active development. This is a standard practice in pharmaceutical research, aiming to protect novel chemical entities and their therapeutic applications. The discontinuation of a single compound like JNJ-69095897 would not necessarily invalidate a broader patent strategy if other distinct chemical scaffolds or backup compounds are covered by existing or pending patents. However, the specific intellectual property rights directly covering JNJ-69095897 remain unclarified in the available materials.

8. Discussion and Concluding Remarks

8.1. Contextualizing JNJ-69095897 in MAGL Inhibitor Development

Monoacylglycerol lipase (MAGL) inhibitors have represented an area of considerable therapeutic interest, primarily due to their capacity to modulate the endocannabinoid 2-arachidonoylglycerol (2-AG), a key signaling molecule in the CNS and periphery.[10] The therapeutic potential of MAGL inhibition has been explored for a variety of conditions, including CNS disorders (such as anxiety and depression), pain syndromes, and inflammatory conditions. The pharmaceutical industry showed notable interest in this target class, particularly around 2019, with several entities pursuing MAGL inhibitors.[22]

A significant challenge in the development of MAGL inhibitors has been achieving an optimal pharmacological profile. This includes attaining high selectivity for MAGL over other serine hydrolases (like FAAH or ABHD6/12), ensuring adequate CNS penetration for neurological targets, and, crucially, avoiding adverse effects associated with chronic elevation of 2-AG and subsequent CB1 receptor desensitization or downregulation. This latter issue was particularly problematic for early-generation irreversible MAGL inhibitors.[13] The development of JNJ-69095897 as a reversible inhibitor was likely a strategic attempt to overcome these limitations, aiming for a more controlled modulation of 2-AG levels and potentially a better safety and tolerability profile.

8.2. Potential Reasons for Discontinuation

The termination of JNJ-69095897's Phase 1 clinical trial in healthy volunteers, without a publicly disclosed reason, invites speculation based on common patterns in early-stage drug development. Such discontinuations can stem from several factors:

1. Safety or Tolerability Concerns: Unexpected or dose-limiting adverse events emerging at early doses.
2. Unfavorable Pharmacokinetics: Issues such as poor oral bioavailability, excessively rapid metabolism leading to insufficient drug exposure, inability to achieve target concentrations in the CNS (despite planned CSF measurements), or the formation of undesirable or toxic metabolites.
3. Negative Pharmacodynamic Findings: Lack of evidence of target engagement (e.g., insufficient elevation of 2-AG) at doses considered safe.
4. Strategic Portfolio Decisions: Pharmaceutical companies continuously evaluate their R&D pipelines. JNJ-69095897 might have been discontinued due to resource reallocation, a shift in therapeutic area focus, emerging data from competitor programs, or an internal assessment that its overall profile was less promising compared to other assets in Janssen's neuroscience portfolio. Janssen and its parent company Johnson & Johnson have made several adjustments to their neuroscience pipeline over recent years, including the discontinuation of other programs and strategic acquisitions to bolster this area.[19]

Without specific disclosure from the sponsor, these possibilities remain speculative.

8.3. Current Status and Future Perspectives for JNJ-69095897

The development of JNJ-69095897 has been definitively discontinued, as evidenced by the termination of its Phase 1 trial.[4] There are no indications from the available information that Janssen has plans to revive this specific compound or pursue it for alternative indications.

However, Janssen's commitment to neuroscience research and development remains substantial. The company continues to advance a broad pipeline of candidates for various CNS disorders and has actively engaged in mergers and acquisitions to strengthen its position in this therapeutic area, such as the planned acquisition of Intra-Cellular Therapies and its assets.[19] The decision to halt JNJ-69095897, an internally developed MAGL inhibitor, likely reflects a comprehensive assessment of its profile against the high bar for progression within a dynamic R&D environment, where resources are prioritized towards assets perceived to have the highest probability of success or the most compelling differentiation.

8.4. Concluding Thought

The development trajectory of JNJ-69095897, a selective and reversible MAGL inhibitor, highlights the profound difficulties inherent in translating promising preclinical concepts for central nervous system disorders into clinically viable therapeutics. Despite a strong scientific rationale for MAGL inhibition in conditions such as anxiety and stress, supported by preclinical efficacy in animal models, and a carefully designed early-phase clinical study that included CSF pharmacokinetic measurements and pharmacogenomic assessments, the compound's journey was cut short in Phase 1. The absence of a publicly disclosed reason for this termination prevents a definitive analysis of the specific hurdles encountered but underscores the high attrition rates that characterize CNS drug discovery and development. Future advancements in this challenging field will continue to rely on rigorous preclinical validation, innovative and adaptive clinical trial designs, robust biomarker strategies to confirm target engagement and patient stratification, and a deeper understanding of the complex neurobiology underlying CNS disorders.

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