Onvatilimab (JNJ-61610588): A Clinical Development Review of a Discontinued VISTA-Targeting Monoclonal Antibody

1. Executive Summary

JNJ-61610588, also known by the non-proprietary name Onvatilimab, is an investigational human IgG1κ monoclonal antibody.[1] It was developed by Janssen Research & Development, LLC, a pharmaceutical company of Johnson & Johnson, with the objective of targeting advanced solid tumors.[2] The antibody was designed to bind to V-domain Ig Suppressor of T-cell Activation (VISTA), a negative immune checkpoint protein.[1] As a VISTA antagonist, Onvatilimab's intended mechanism of action was to block VISTA-mediated immune suppression, thereby enhancing anti-tumor T-cell responses within the tumor microenvironment.[2]

The primary clinical investigation for Onvatilimab was a Phase 1 trial, registered under NCT02671955, which commenced in January 2016. This study aimed to evaluate the safety, pharmacokinetics, and pharmacodynamics of Onvatilimab in participants with various advanced solid tumors.[1] However, the clinical trial was terminated prematurely by the sponsor after enrolling only 12 participants.[2] Subsequent to this termination, JNJ-61610588 (Onvatilimab) has not appeared in Janssen's publicly disclosed active oncology development pipeline, signaling a discontinuation of its development program.[5]

The early cessation of a Phase 1 trial for an immune checkpoint inhibitor, particularly one targeting a novel pathway like VISTA and developed by a major pharmaceutical entity, is a significant event. VISTA has been regarded as a promising target due to its role in immune regulation and its homology to established checkpoint proteins like PD-1.[2] The discontinuation of Onvatilimab prompts a closer examination of the complexities associated with targeting the VISTA pathway, the specific circumstances of the NCT02671955 trial, and the broader implications for the development of VISTA-targeted therapies in oncology.

2. Introduction to JNJ-61610588 (Onvatilimab) and its Target VISTA

2.1. JNJ-61610588 (Onvatilimab): Identity and Properties

Onvatilimab (JNJ-61610588) is a fully human monoclonal antibody belonging to the IgG1κ isotype.[1] The IgG1 isotype is frequently utilized for therapeutic antibodies in oncology, offering a long half-life and the potential for antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC), although these effector functions can be modulated through Fc engineering. The molecular weight of Onvatilimab is reported as 144520.00 Daltons, and it was formulated as a liquid, typically colorless to light yellow in appearance.[1]

The development of Onvatilimab was undertaken by Janssen Research & Development, LLC, a subsidiary of Johnson & Johnson, a global corporation with extensive research and development programs in oncology.[2] The primary therapeutic area for Onvatilimab investigation was oncology, with a focus on treating patients with advanced solid tumors that were refractory to standard therapies.[2]

2.2. The VISTA Immune Checkpoint Pathway

V-domain Ig Suppressor of T-cell Activation (VISTA), also known by several other designations including PD-1H (Programmed Death-1 Homolog), C10orf54, DD1α, Gi24, Dies1, and SISP1, is a type I transmembrane protein. It is a member of the B7 family of immune regulatory proteins and shares structural homology with PD-1, a well-established immune checkpoint target.[2] VISTA is highly conserved across different species, suggesting a fundamental role in immune regulation.[2]

VISTA exhibits a distinct and broad expression profile, predominantly on cells of the hematopoietic lineage. It is constitutively expressed at high levels on myeloid cells, including macrophages, dendritic cells, and myeloid-derived suppressor cells (MDSCs). Its expression can also be found on T cells, particularly naive T cells and regulatory T cells (Tregs), and can be upregulated upon T-cell activation.[2] Uniquely among immune checkpoints, VISTA can function both as an inhibitory receptor when expressed on T cells and as an inhibitory ligand when expressed on antigen-presenting cells (APCs) and, in some cases, tumor cells.[2] This dual functionality contributes to its complex role in modulating immune responses.

The primary mechanism of VISTA-mediated immune suppression involves the maintenance of peripheral tolerance and T-cell quiescence.[2] As a ligand on APCs or tumor cells, VISTA can interact with putative receptors on T cells, leading to the suppression of T-cell activation, proliferation, and cytokine production. Conversely, when acting as a receptor on T cells, VISTA can directly transmit inhibitory signals. Its regulatory activity is particularly prominent during the early stages of T-cell activation, distinguishing its temporal influence from other checkpoints like CTLA-4 and PD-1, which act at T-cell priming and effector stages, respectively.[2] While VISTA’s role as an immune checkpoint is well-recognized, its specific counter-receptors or ligands, beyond its capacity for homotypic interactions or interactions with broadly expressed molecules, remain an area of active investigation. VSIG-3 has been proposed as one such binding partner, although this is not explicitly detailed in the provided source materials.

2.3. Rationale for Targeting VISTA in Cancer Therapy

The expression of VISTA within the tumor microenvironment (TME) by both tumor-infiltrating immune cells (such as MDSCs and Tregs) and, in some malignancies, by tumor cells themselves, contributes significantly to an immunosuppressive milieu. This environment curtails effective anti-tumor immune surveillance and promotes tumor progression.[2] Consequently, VISTA emerged as an attractive target for cancer immunotherapy.

The therapeutic hypothesis underpinning VISTA blockade centers on the premise that antagonizing its immunosuppressive signals can reinvigorate anti-tumor immunity. This is expected to be achieved by promoting the activation and proliferation of tumor-specific effector T cells, reducing the abundance and inhibitory function of MDSCs and Tregs within the TME, and enhancing the infiltration and cytotoxic capacity of TILs.[2]

Preclinical studies have provided validation for this approach. Genetic ablation of VISTA (VISTA knockout mice) or administration of anti-VISTA antibodies has demonstrated anti-tumor activity in a range of syngeneic tumor models. These effects were often correlated with enhanced T-cell responses and a shift in the TME towards a more pro-inflammatory state.[2] For instance, VISTA deficiency led to tumor resistance in glioma models, and anti-VISTA antibodies showed efficacy in murine models of melanoma, colon cancer, and bladder carcinoma.[2]

Furthermore, the VISTA pathway is considered to be largely non-redundant with the PD-1/PD-L1 axis.[2] This non-redundancy suggested that VISTA blockade could offer therapeutic benefits even in patients whose tumors are resistant or refractory to existing PD-1/PD-L1 inhibitors. It also opened the possibility of synergistic effects when combined with other immune checkpoint inhibitors or standard cancer therapies. The substantial investment by Janssen in the development of Onvatilimab indicates a strong belief in the scientific rationale for VISTA as a novel and druggable immune checkpoint target, with the potential to address unmet medical needs in patients with advanced cancers where existing immunotherapies had limited efficacy or had failed.

Table 1: Key Characteristics of JNJ-61610588 (Onvatilimab)

Attribute	Details	Source(s)
Alternative Name	Onvatilimab	1
Drug Class	Monoclonal Antibody	1
Isotype	Human IgG1κ	1
Target	VISTA (V-domain Ig Suppressor of T-cell Activation)	1
Mechanism of Action	VISTA antagonist / Immune checkpoint inhibitor	2
Developer	Janssen Research & Development, LLC	1
Investigated Indications	Advanced Solid Tumors	2
Highest Development Phase	Phase 1 (Terminated)	2
Key Clinical Trial Identifier	NCT02671955	1

This table provides a concise summary of Onvatilimab's fundamental properties and its developmental context, serving as a quick reference for understanding the drug's profile.

3. Preclinical Profile of JNJ-61610588 (Onvatilimab)

The preclinical development of Onvatilimab established its fundamental ability to interact with its designated target, VISTA. Bio-Layer Interferometry (BLI) assays confirmed that Onvatilimab binds to human VISTA/B7-H5 protein with a high affinity constant (Kd) of 2.039×10−10 M.[1] This picomolar affinity signifies a strong and specific interaction, a critical prerequisite for a therapeutic monoclonal antibody to effectively modulate its target's function.

As an anti-VISTA monoclonal antibody, Onvatilimab was anticipated to exert anti-tumor activity by disrupting the immunosuppressive signals mediated by VISTA. This blockade was expected to restore and enhance T-cell-mediated anti-cancer immune responses.[1] The general scientific understanding of VISTA's role as an immune checkpoint supports this expectation of anti-tumor potential upon its inhibition.[2]

While the high binding affinity is a positive indicator from its preclinical assessment, the publicly available information from the provided sources does not include detailed specific in vitro functional data for JNJ-61610588, such as its ability to reverse VISTA-mediated T-cell suppression or to modulate cytokine production by immune cells. Similarly, specific in vivo efficacy data from animal tumor models for Onvatilimab itself are not detailed. Although [2] references general preclinical findings supporting VISTA targeting, the absence of molecule-specific preclinical performance data for Onvatilimab represents an information gap. Such data would typically be crucial in assessing its unique therapeutic promise prior to clinical translation and in understanding the basis for its advancement into Phase 1 trials.

4. Clinical Development Program: The NCT02671955 Phase 1 Study

4.1. Study Rationale and Design

The sole clinical trial identified for Onvatilimab (JNJ-61610588) was a Phase 1, first-in-human (FIH) study registered under ClinicalTrials.gov identifier NCT02671955 and EudraCT number 2016-001903-22.[2] The official title of the study was "A Study of Safety, Pharmacokinetics, Pharmacodynamics of JNJ-61610588 in Participants With Advanced Cancer".[3] The primary purpose of this multicenter, open-label, non-randomized, single-group assignment study was to evaluate the safety and tolerability of JNJ-61610588 in participants with advanced cancer and to determine a Recommended Phase 2 Dose (RP2D) for subsequent investigation.[2]

The study was designed with up to four distinct parts [2]:

• Part 1 (Dose Escalation): This initial part involved participants with a variety of advanced solid tumors. They were to receive escalating intravenous doses of JNJ-61610588 to establish the MTD or RP2D.
• Part 2 (Biomarker Evaluation): This part was planned for participants with metastatic non-small cell lung cancer (NSCLC), who would be treated at or below the determined RP2D. The focus here was on assessing biomarkers to understand the drug's biological effects.
• Part 3 (Dose Expansion): Participants with metastatic NSCLC were to receive JNJ-61610588 at the RP2D to gather further safety and preliminary efficacy data in this specific tumor type.
• Part 4 (Dose Expansion): This part aimed to expand investigation at the RP2D into other specific advanced solid tumor types, including small cell lung cancer (SCLC), head and neck (H&N) cancer, pancreatic cancer, colorectal cancer, and cervical cancer.

This structured, multi-part design is a standard approach in early oncology drug development, facilitating an initial focus on safety and dose-finding, followed by more targeted exploration of activity and biomarker responses in selected patient populations.

4.2. Endpoints

The primary endpoints for a Phase 1 study of this nature would typically revolve around safety and tolerability. These would include the incidence and severity of adverse events (AEs), the identification of any dose-limiting toxicities (DLTs), and the determination of the MTD and/or RP2D of Onvatilimab.[2]

Secondary endpoints would likely have encompassed the characterization of Onvatilimab's pharmacokinetic (PK) profile (e.g., half-life, clearance, volume of distribution) and its pharmacodynamic (PD) effects. PD markers could include VISTA receptor occupancy on target cells, modulation of immune cell populations (e.g., T cells, MDSCs) in peripheral blood or tumor biopsies, and changes in relevant biomarkers (e.g., cytokines). Preliminary assessment of anti-tumor activity, such as Objective Response Rate (ORR) according to Response Evaluation Criteria in Solid Tumors (RECIST), Duration of Response (DOR), and Progression-Free Survival (PFS), would also be standard exploratory objectives.[3]

4.3. Patient Population and Investigated Tumor Types

General eligibility criteria for the NCT02671955 trial included adult participants with histologically or cytologically confirmed advanced solid tumors that had progressed following at least one prior standard therapy. Participants were required to have radiographically measurable disease (or evaluable disease for Part 1 only). Other common inclusion criteria for such trials typically include an adequate Eastern Cooperative Oncology Group (ECOG) performance status (e.g., 0 or 1, as implied by "able to carry out daily life activities without difficulty"), and sufficient organ and hematologic function.[2] Willingness to provide tumor tissue samples for biomarker analyses was also a requirement for Parts 2 and 3.[3]

The specific tumor types designated for the expansion cohorts (Parts 2, 3, and 4) included NSCLC, SCLC, H&N squamous cell carcinoma, pancreatic adenocarcinoma, colorectal cancer, and cervical cancer.[2] This range indicates Janssen's intent to explore Onvatilimab's potential across a spectrum of cancers where immune checkpoint inhibition might be relevant.

4.4. Dosing Regimen and Administration

Onvatilimab was administered via intravenous (IV) infusion.[2] The study design incorporated a dose-escalation strategy in Part 1 to identify the MTD/RP2D. Participants in the subsequent biomarker evaluation and dose expansion parts (Parts 2, 3, and 4) were to receive Onvatilimab at the established RP2D. Treatment was generally planned to continue until disease progression or the occurrence of unacceptable toxicity.[2] The precise dosing frequency (e.g., every two weeks, every three weeks) is not specified in the provided materials.

4.5. Enrollment and Study Status

The sponsor of the NCT02671955 trial was Janssen Research & Development, LLC.[1] The study was initiated in January 2016 [1] and was planned to be conducted at approximately 4 international locations.[3]

A critical aspect of this trial is its enrollment and ultimate status. A total of only 12 participants were enrolled in the study.[2] Subsequently, the trial was terminated by the sponsor.[2] While the provided snippets confirm the "Terminated" status on clinical trial registries, they do not specify the exact date of termination or provide an explicit reason from the sponsor for this decision. The low enrollment number, far short of what would be required to complete all planned parts of a multi-cohort Phase 1 study, strongly suggests that the termination occurred very early in the dose-escalation phase (Part 1).

Table 2: Summary of Phase 1 Clinical Trial NCT02671955 for JNJ-61610588 (Onvatilimab)

Parameter	Details	Source(s)
Official Title	A Study of Safety, Pharmacokinetics, Pharmacodynamics of JNJ-61610588 in Participants With Advanced Cancer	3
Phase	Phase 1	1
Status	Terminated	2
Sponsor	Janssen Research & Development, LLC	1
ClinicalTrials.gov ID	NCT02671955	1
EudraCT No.	2016-001903-22	3
Primary Purpose	Treatment; Evaluate safety and tolerability; Determine Recommended Phase 2 Dose (RP2D)	2
Key Endpoints	Safety (AEs, DLTs), MTD/RP2D, Pharmacokinetics, Pharmacodynamics, Preliminary Anti-tumor Activity	3 (explicitly PK/PD, safety); Others inferred
Patient Population	Adults with advanced solid tumors, progressed after prior standard therapy	2
Planned Parts	Part 1 (Dose Escalation), Part 2 (Biomarker NSCLC), Part 3 (Expansion NSCLC), Part 4 (Expansion other solid tumors)	2
Actual Enrollment	12 participants	2
Intervention	JNJ-61610588 (Onvatilimab) via intravenous infusion	2
Start Date	January 2016	1
Reason for Termination	Not explicitly stated in provided sources; terminated by sponsor	2

This table consolidates the critical details of the NCT02671955 trial, highlighting the significant discrepancy between its ambitious multi-part design and its early termination after minimal patient accrual.

5. Clinical Trial Findings (NCT02671955)

Despite the initiation of the NCT02671955 Phase 1 trial in 2016 and its subsequent termination, there is a notable absence of publicly available detailed clinical results from the 12 enrolled participants. The provided source materials, including literature reviews and database entries up to early 2020, indicated that results were "awaited".[2] However, no subsequent presentations at major oncology conferences such as ASCO or ESMO, nor publications in peer-reviewed journals detailing the safety, tolerability, pharmacokinetic, pharmacodynamic, or any preliminary efficacy signals from these 12 patients, are evident within the scope of the research provided.[8]

Consequently, specific data regarding:

• Safety and Tolerability: The nature, frequency, and severity of adverse events (AEs), any observed dose-limiting toxicities (DLTs), or whether a maximum tolerated dose (MTD) was reached, remain undisclosed.
• Pharmacokinetics and Pharmacodynamics: Information on the PK profile of Onvatilimab in humans (e.g., half-life, clearance) or PD effects (e.g., evidence of VISTA receptor occupancy, changes in immune cell subsets, or biomarker modulation) is not available.
• Anti-tumor Activity / Efficacy Signals: There is no information regarding any objective responses or other indicators of anti-tumor activity in the participants.

The trial was officially terminated by the sponsor, Janssen Research & Development, LLC.[2] The specific rationale for this termination has not been publicly detailed in the provided materials.

The lack of disseminated data from the NCT02671955 trial is significant. In drug development, particularly for novel targets or mechanisms, early-phase data, even from discontinued programs, often contribute valuable information to the scientific community. The absence of such disclosure for Onvatilimab could imply several possibilities: the findings from the 12 patients may have been clearly unfavorable (e.g., unacceptable toxicity with no discernible benefit), the data set may have been too small or inconclusive to draw meaningful conclusions, or a strategic decision to halt development was made so early that extensive analysis and public presentation were not pursued by the sponsor.

6. Overall Development Status and Future Outlook

The development of Onvatilimab (JNJ-61610588) by Janssen Research & Development, LLC appears to have been definitively discontinued. This conclusion is supported by its conspicuous absence from recent (2024) public disclosures of Johnson & Johnson's and Janssen's oncology development pipelines.[5] Pharmaceutical companies typically maintain and update such pipelines, and the removal of a compound is a strong indicator of cessation of active development.

This situation can be contrasted with other discontinued programs by Johnson & Johnson, such as aticaprant for major depressive disorder. In that instance, despite a Phase III trial failure, the company explicitly stated an intention to continue exploring the mechanism of action in other indications.[10] No similar statements regarding any future plans for Onvatilimab or further VISTA targeting by Janssen have been found in the provided materials, reinforcing the likelihood of a complete halt.

Furthermore, there is no information within the provided sources to suggest that Onvatilimab received any special regulatory designations from the U.S. Food and Drug Administration (FDA), such as Fast Track, Breakthrough Therapy, or Orphan Drug status, or from the European Medicines Agency (EMA), such as PRIME designation.[11] Such designations are often sought for investigational drugs that show early promise in treating serious conditions with significant unmet medical needs. Their absence for Onvatilimab might be attributable to its very early stage of termination or a lack of sufficiently compelling early data to support such applications.

Despite the discontinuation of Onvatilimab, the VISTA pathway remains a target of considerable interest within the immuno-oncology field. The termination of this specific monoclonal antibody program does not necessarily invalidate VISTA as a therapeutic target. Indeed, other companies are actively pursuing VISTA-targeting agents using different approaches. A notable example is CA-170, an orally bioavailable small-molecule dual inhibitor of VISTA and PD-L1, which has progressed into Phase II clinical trials for various solid tumors and Hodgkin lymphoma.[2] This suggests that alternative modalities (e.g., small molecules versus monoclonal antibodies) or strategies (e.g., dual checkpoint blockade) might offer more viable paths to therapeutically exploit the VISTA pathway.

The decision by a major pharmaceutical entity like Janssen to discontinue Onvatilimab is a significant event for the VISTA field. It may temper enthusiasm for VISTA-targeting monoclonal antibodies as monotherapy, particularly if the underlying reasons for termination were related to on-target toxicity or a lack of compelling monotherapy activity. However, the continued investigation of other VISTA modulators indicates that the scientific community is still actively exploring optimal strategies to harness this immune checkpoint for cancer therapy. The outcomes of these ongoing programs will be critical in shaping the future therapeutic landscape for VISTA.

7. Expert Analysis and Concluding Remarks

The development trajectory of Onvatilimab (JNJ-61610588), a human IgG1κ monoclonal antibody targeting the VISTA immune checkpoint, represents a case study in the challenges of translating novel immuno-oncology concepts into clinical reality. Developed by Janssen, Onvatilimab entered a Phase 1 clinical trial (NCT02671955) in 2016 with the aim of evaluating its potential in patients with advanced solid tumors. However, this trial was prematurely terminated after the enrollment of only 12 participants, and the compound is no longer part of Janssen's active development portfolio.

The specific reasons for Onvatilimab's discontinuation have not been publicly disclosed. In the absence of such information, potential contributing factors can be speculated based on common challenges in early-phase oncology drug development:

• Unacceptable Toxicity: The initial dose cohorts may have revealed dose-limiting toxicities (DLTs) at levels that were too low to achieve therapeutic drug exposure or target engagement.
• Unfavorable Pharmacokinetics/Pharmacodynamics: The drug might have exhibited a poor pharmacokinetic profile (e.g., rapid clearance, low bioavailability if target-mediated drug disposition was an issue) or failed to demonstrate adequate pharmacodynamic effects (e.g., insufficient VISTA receptor occupancy or lack of downstream immune modulation) in the initial patient group.
• Lack of Early Efficacy Signals: While Phase 1 trials primarily focus on safety, a complete absence of any biological activity or encouraging anti-tumor signals, even in a small cohort, can influence decisions regarding further investment, especially for a novel target.
• Strategic Reprioritization: Pharmaceutical companies continuously evaluate their pipelines based on evolving scientific understanding, competitive landscapes, and internal strategic priorities. Janssen may have made a portfolio decision to allocate resources to other, perceivedly more promising, assets within its extensive oncology pipeline.[5]

The Onvatilimab program underscores several important considerations for the development of VISTA-targeted therapies. Firstly, translating the preclinical promise of a novel immune checkpoint like VISTA into a clinically successful agent is a complex endeavor. The choice of antibody format, the specific epitope targeted on VISTA, and the patient selection strategy are all critical variables that can influence outcomes. Secondly, the development of robust biomarker strategies is paramount in immuno-oncology. Early demonstration of target engagement and identification of patient populations most likely to benefit are key to navigating early clinical development.

The VISTA pathway itself is intricate, with VISTA functioning as both a ligand and a receptor, and being expressed on multiple cell types within the TME.[2] This complexity might mean that a monoclonal antibody monotherapy approach, as pursued with Onvatilimab, may not be the optimal strategy for therapeutic modulation. Alternative approaches, such as small-molecule inhibitors (which may offer different biodistribution and target engagement profiles) or combination strategies (e.g., dual checkpoint blockade, as with CA-170 targeting VISTA and PD-L1 [2]), may hold greater promise.

In conclusion, JNJ-61610588 (Onvatilimab) is a discontinued investigational agent. Its early termination in Phase 1 development highlights the significant attrition rates and inherent risks associated with oncology drug discovery and development, even for targets within promising pathways like immune checkpoints. While this specific molecule did not advance, the VISTA pathway continues to be an area of active research and development. The experiences with Onvatilimab, though not fully transparent due to the lack of published clinical data, will invariably inform future efforts to therapeutically target VISTA, as the scientific community seeks to determine if and how this immune checkpoint can be effectively leveraged for the benefit of cancer patients. The progress of other VISTA-targeting agents, employing different modalities and strategies, will be closely watched.

Works cited

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