Golimumab (Simponi®, Simponi Aria®): A Comprehensive Pharmacological and Clinical Review

I. Introduction and Overview

1.1. Executive Summary

Golimumab is a fully human immunoglobulin G1 kappa (IgG1κ) monoclonal antibody that functions as a high-affinity antagonist of tumor necrosis factor-alpha (TNF-α), a pivotal cytokine in the pathophysiology of numerous inflammatory conditions.[1] Developed and marketed by Janssen Biotech, Inc., a subsidiary of Johnson & Johnson, golimumab represents a significant therapeutic advancement in the management of chronic, immune-mediated inflammatory diseases.[3] It is available under two distinct brand names corresponding to its route of administration: Simponi® for subcutaneous (SC) injection and Simponi Aria® for intravenous (IV) infusion.[3] The fundamental therapeutic principle of golimumab is the neutralization of excess TNF-α, which in turn interrupts the downstream inflammatory cascade responsible for tissue damage and clinical symptoms. This mechanism has demonstrated efficacy in reducing disease activity, improving physical function, and, in several key indications, inhibiting the progression of structural joint damage.[5]

1.2. Drug Identification

• [Generic Name:] Golimumab [2]
• [DrugBank ID:] DB06674 [2]
• [CAS Number:] 476181-74-5 [1]
• [Type:] Biotech, Monoclonal Antibody (mAb), Protein-Based Therapy [2]
• [Other Names:] CNTO-148 [3]
• [Chemical Formula & Weight:] The protein has a chemical formula of C6530​H10068​N1752​O2026​S44​ and an average molecular weight of 146,943.1937 Daltons.[2]

1.3. Place in Therapy

Golimumab is categorized as a TNF-blocker and a biologic Disease-Modifying Antirheumatic Drug (DMARD).[1] Its position in treatment algorithms is typically for patients with moderate to severe disease activity who have not achieved an adequate response to, or who are intolerant of, conventional synthetic DMARDs (csDMARDs), most notably methotrexate (MTX).[1] For several conditions, including rheumatoid arthritis (RA) and psoriatic arthritis (PsA), clinical practice guidelines support the use of TNF-blocking agents like golimumab as a first-line biologic therapy following the failure of csDMARDs.[7] The selection of golimumab among other biologics depends on various factors, including disease characteristics, prior therapies, comorbidities, and patient or physician preference regarding the route and frequency of administration.[7]

II. Molecular Profile and Mechanism of Action

2.1. Structure and Production

Golimumab is a fully human IgG1κ monoclonal antibody, a structural characteristic that distinguishes it from chimeric (e.g., infliximab) and humanized antibodies.[2] The "fully human" designation implies that the protein sequences are of human origin, which is intended to minimize the potential for immunogenicity and the formation of anti-drug antibodies that can compromise efficacy and safety.[6] The antibody is generated using recombinant DNA technology within a murine hybridoma cell line.[9] Specifically, it was isolated from a selected hybridoma clone that was produced by immunizing transgenic mice—genetically engineered to produce human antibodies—with human TNF-α.[2]

2.2. Primary Mechanism: TNF-α Neutralization

The core mechanism of action of golimumab is the specific and high-affinity binding to human TNF-α.[1] This binding is comprehensive, targeting both the soluble, circulating form of the cytokine and its transmembrane form expressed on the surface of cells.[1] In numerous autoimmune diseases, including RA, PsA, AS, and ulcerative colitis (UC), the overproduction of TNF-α in inflamed tissues such as the synovium, joints, and colonic mucosa is a central driver of pathology.[2] By forming a stable complex with TNF-α, golimumab effectively prevents the cytokine from binding to its cognate receptors, TNFR1 and TNFR2, which are present on a wide variety of cell types, including immune cells, endothelial cells, and fibroblasts.[1] This blockade at the apex of a key inflammatory pathway is the basis for its therapeutic effects.[5]

The ability to neutralize both soluble and transmembrane TNF-α is a critical feature that defines both the therapeutic power and the risk profile of golimumab. Soluble TNF-α is a primary mediator of systemic inflammation, propagating signals throughout the body. In contrast, transmembrane TNF-α functions not only as a ligand for adjacent cells but also as a receptor capable of "reverse signaling" back into the cell expressing it. This cell-to-cell contact is crucial for localized inflammatory responses and is fundamentally important for the formation and maintenance of granulomas—the organized cellular structures the immune system uses to contain certain intracellular pathogens, most notably Mycobacterium tuberculosis. By comprehensively blocking both forms, golimumab effectively shuts down a wide range of TNF-α-mediated pro-inflammatory activities. This comprehensive blockade, however, directly explains one of its most significant clinical risks. The inhibition of transmembrane TNF-α's role in maintaining granuloma integrity can lead to the breakdown of these structures, allowing for the reactivation of latent tuberculosis, a key risk highlighted in the drug's black box warning. This dual-target mechanism is thus a "double-edged sword," providing potent anti-inflammatory effects while simultaneously creating a specific vulnerability to certain opportunistic infections.

2.3. Downstream Pharmacodynamic Effects

The neutralization of TNF-α by golimumab initiates a cascade of downstream anti-inflammatory and immunomodulatory effects that manifest clinically. Evidence demonstrates that golimumab administration leads to a profound reduction in the levels of key inflammatory biomarkers and effector molecules.[2]

• [Reduction of Inflammatory Mediators:] Treatment results in a marked decrease in serum levels of C-reactive protein (CRP) and pro-inflammatory cytokines such as interleukin-6 (IL-6), interleukin-8 (IL-8), granulocyte-colony stimulating factor (G-CSF), and granulocyte-macrophage colony-stimulating factor (GM-CSF).[2]
• [Inhibition of Leukocyte Infiltration:] Golimumab mitigates the recruitment of immune cells to sites of inflammation. It achieves this by preventing the TNF-α-induced upregulation of endothelial adhesion molecules, including E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1), which are essential for leukocyte trafficking from the bloodstream into tissues.[2]
• [Modulation of Tissue Remodeling:] The drug influences the processes of tissue degradation and pathological angiogenesis. It has been shown to reduce serum levels of matrix metalloproteinase-3 (MMP-3), an enzyme that degrades cartilage and bone, and vascular endothelial growth factor (VEGF), a key promoter of new blood vessel formation in inflamed synovium.[3] This provides a direct mechanistic explanation for its ability to inhibit the radiographic progression of joint damage observed in clinical trials.[5]
• [Induction of Apoptosis:] Golimumab can alter the cellular balance in inflamed tissues by influencing apoptosis (programmed cell death). By neutralizing the survival signals that TNF-α provides to certain pathogenic immune cells, golimumab may promote their apoptosis, thereby reducing the inflammatory cell burden.[11]

III. Clinical Pharmacology and Pharmacokinetics (PK)

3.1. Absorption

Following subcutaneous (SC) administration, golimumab is absorbed relatively slowly, with the median time to reach maximum serum concentration (Tmax) ranging from 2 to 6 days.[1] The estimated absolute bioavailability for the SC formulation is approximately 53%, indicating that just over half of the administered dose reaches systemic circulation.[1] In a study involving healthy volunteers, a single SC dose led to a mean maximum concentration (Cmax) of 3.2 ± 1.4 μg/mL.[2]

3.2. Distribution

After intravenous (IV) administration, golimumab exhibits a mean volume of distribution (Vd) that ranges from 58 to 126 mL/kg.[1] This relatively small Vd suggests that the drug's distribution is largely confined to the circulatory system (intravascular space) with only limited penetration into extravascular tissues.[1] Plasma protein binding has not been specifically quantified.[2]

3.3. Metabolism and Elimination

The precise metabolic fate and route of elimination for golimumab have not been formally determined through dedicated studies.[1] However, as a large protein therapeutic, it is expected to undergo catabolism through general proteolytic pathways, where it is broken down into smaller peptides and constituent amino acids that are then recycled or eliminated by the body. This is the standard metabolic pathway for endogenous and therapeutic antibodies.

Systemic clearance of golimumab is low, estimated to be between 4.9 and 6.7 mL/kg/day.[1] A key feature of its pharmacokinetic profile is a long median terminal half-life of approximately 2 weeks (14 days).[1]

The pharmacokinetic profile of golimumab is a primary determinant of its clinical utility and dosing convenience. The combination of a long elimination half-life of approximately two weeks with the subcutaneous route of administration directly underpins the once-monthly dosing regimen that is a hallmark of the Simponi® formulation for rheumatologic indications.[1] This long half-life is not an accidental feature but a direct consequence of its molecular structure as a fully human IgG1 antibody. This structure allows it to engage with the neonatal Fc receptor (FcRn), a cellular mechanism present in endothelial and other cells that actively rescues IgG antibodies from lysosomal degradation and recycles them back into circulation. This FcRn-mediated protection from catabolism is what confers its extended presence in the body. This favorable pharmacokinetic property translates into a significant clinical and lifestyle advantage for patients, offering improved convenience and potentially better adherence compared to biologics requiring more frequent injections. This once-monthly schedule was a key differentiator upon its initial approval.[14] The same long half-life is leveraged by the intravenous Simponi Aria® formulation, enabling a maintenance dosing interval of every 8 weeks after loading doses, which is also a significant convenience factor for patients and healthcare systems compared to more frequently infused biologics.[1]

3.4. Special Populations

• [Pediatric Use:] Specific pharmacokinetic studies in children have been crucial for establishing appropriate dosing. In an open-label Phase 3 study of children with polyarticular juvenile idiopathic arthritis (pJIA), a body surface area (BSA)-based dosing regimen of 80 mg/m² for the IV formulation was shown to provide pharmacokinetic exposure (specifically, steady-state trough concentrations and area under the curve) comparable to that achieved in adults with RA receiving the standard 2 mg/kg dose.[15] This finding validated the BSA-based dosing approach to achieve target drug levels across different age and size groups.
• [Renal and Hepatic Impairment:] Specific clinical studies of golimumab in patients with renal or hepatic impairment have not been conducted. As such, there are no specific dosage adjustment recommendations for these populations.[16]

IV. Regulatory History and Global Approvals

The regulatory journey of golimumab illustrates a strategic, multi-year effort by its developer, Janssen, to establish its role across multiple inflammatory diseases, using two distinct formulations to capture different segments of the healthcare market.

4.1. U.S. Food and Drug Administration (FDA) Approval Pathway

The introduction of golimumab in the United States occurred in two phases, first with the subcutaneous formulation and later with the intravenous version.

• [Simponi® (Subcutaneous):]
• The process began on June 27, 2008, when Centocor, Inc. (now Janssen Biotech, Inc.) submitted a Biologics License Application (BLA) to the FDA for the treatment of RA, PsA, and AS.[14]
• On [April 24, 2009], Simponi® received its first FDA approval for three core rheumatologic indications: moderately to severely active RA (in combination with MTX), active PsA (as monotherapy or with MTX), and active AS. This approval was a landmark event, as it introduced the first once-monthly, self-injectable anti-TNF agent, offering a new level of convenience for patients.[3]
• On [May 15, 2013], the FDA expanded the label to include the treatment of moderately to severely active Ulcerative Colitis (UC). This made Simponi® the first subcutaneously administered anti-TNF therapy available for UC patients, providing an alternative to IV infusions.[14]
• [Simponi Aria® (Intravenous):]
• On [July 19, 2013], Simponi Aria® received its initial FDA approval for the treatment of moderately to severely active RA (in combination with MTX), providing an infused option for patients and physicians who prefer this route of administration.[6]
• On [October 20, 2017], the FDA approved two new indications for Simponi Aria®, for the treatment of active PsA and active AS in adults, aligning its rheumatology approvals more closely with the SC formulation.[6]
• On [September 30, 2020], the label was further expanded to pediatric populations, with approvals for active pJIA and active PsA in patients aged 2 years and older.[19]

4.2. European Medicines Agency (EMA) Approval Pathway

Golimumab also has a broad set of approvals in the European Union, where it is marketed by Janssen Biologics B.V..[22]

• On [October 1, 2009], Simponi® received its initial marketing authorization valid throughout the EU for the treatment of RA, PsA, and AS.[22]
• Over the following years, the EMA approved label expansions to include non-radiographic axial spondyloarthritis (nr-axSpA), UC, and polyarticular juvenile idiopathic arthritis (pJIA) in children aged 2 years and older.[3]

This regulatory history reveals a deliberate, staggered, dual-formulation strategy. Janssen first capitalized on the convenience of the once-monthly subcutaneous Simponi® to penetrate the large outpatient and self-injection market, establishing a strong competitive position against other available biologics.[14] The subsequent development and approval of the intravenous Simponi Aria® four years later was a calculated move to compete directly with established infused therapies like infliximab and to capture the market segment of patients and infusion centers that prefer or require IV administration.[20] The every-8-week maintenance interval for the IV formulation provided a further competitive advantage over more frequently infused treatments. This two-pronged approach allowed Janssen to maximize market penetration by catering to the full spectrum of patient needs, administration settings, and reimbursement models.

4.3. The Emerging Biosimilar Landscape

The period of market exclusivity for originator golimumab is ending, paving the way for the introduction of biosimilars, which is expected to increase competition and potentially lower costs.

• On [November 4, 2024], Alvotech and Advanz Pharma announced that the EMA had accepted their Marketing Authorization Application (MAA) for AVT05, a proposed biosimilar to Simponi®. This was reported as the first such filing for a golimumab biosimilar to be accepted by a major regulatory agency globally, with a decision anticipated in the fourth quarter of 2025.[23]
• Shortly thereafter, on [February 10, 2025], another company, Bio-Thera Solutions, announced that the EMA had also accepted its MAA for BAT2506, a second proposed biosimilar to Simponi®.[25]

These developments signal the beginning of a new competitive era for golimumab, where originator and biosimilar products will compete across both the subcutaneous and intravenous administration channels established by Janssen.

Date	Regulatory Body	Formulation	Milestone/Indication Approved	Source(s)
Jun 27, 2008	FDA	Simponi® (SC)	BLA Submitted for RA, PsA, AS	14
Apr 24, 2009	FDA	Simponi® (SC)	Initial Approval for RA, PsA, AS	14
Oct 1, 2009	EMA	Simponi® (SC)	Initial EU Marketing Authorization for RA, PsA, AS	22
May 15, 2013	FDA	Simponi® (SC)	Approval for Ulcerative Colitis	14
Jul 19, 2013	FDA	Simponi Aria® (IV)	Initial Approval for Rheumatoid Arthritis	19
Oct 20, 2017	FDA	Simponi Aria® (IV)	Approval for Psoriatic Arthritis & Ankylosing Spondylitis	19
Sep 30, 2020	FDA	Simponi Aria® (IV)	Approval for pJIA & Pediatric PsA (≥2 years)	19
Nov 4, 2024	EMA	Biosimilar (AVT05)	Marketing Authorization Application Accepted	23
Feb 10, 2025	EMA	Biosimilar (BAT2506)	Marketing Authorization Application Accepted	25

V. Approved Clinical Indications, Dosing, and Efficacy

Golimumab has demonstrated efficacy across a range of immune-mediated inflammatory diseases. The dosing regimens are specific to the indication, formulation, and patient population.

5.1. Rheumatoid Arthritis (RA)

• [Indication:] For the treatment of adult patients with moderately to severely active RA, to be used in combination with methotrexate (MTX).[1]
• [Dosing:]
• [Simponi® (SC):] 50 mg administered subcutaneously once a month.[1]
• [Simponi Aria® (IV):] 2 mg/kg administered as a 30-minute intravenous infusion at weeks 0 and 4, followed by maintenance infusions every 8 weeks.[1]
• [Pivotal Trial Evidence:] The clinical development program for RA included several key Phase 3 trials:
• [GO-FORWARD (MTX-experienced patients):] This trial enrolled patients with active RA despite stable MTX therapy. It demonstrated that golimumab (50 mg and 100 mg) plus MTX was significantly superior to placebo plus MTX in achieving American College of Rheumatology (ACR) 20, 50, and 70 responses and in improving physical function as measured by the Health Assessment Questionnaire Disability Index (HAQ-DI).[5] The final 5-year results of the study showed a high retention rate of 70.5% and durable maintenance of clinical efficacy.[31]
• [GO-BEFORE (MTX-naïve patients):] In patients not previously treated with MTX, golimumab plus MTX was more effective than MTX alone in improving clinical signs and symptoms. Importantly, this trial also showed that the combination therapy led to significantly less radiographic progression of joint damage compared to MTX monotherapy.[5]
• [GO-AFTER (Prior anti-TNF failure):] This trial was crucial as it evaluated golimumab in a difficult-to-treat population of patients who had previously discontinued at least one other TNF inhibitor. The results showed that golimumab was significantly more effective than placebo in achieving ACR responses, establishing its utility as a subsequent anti-TNF option.[5]

5.2. Psoriatic Arthritis (PsA)

• [Indication:] For the treatment of active PsA in adults (used alone or in combination with MTX) and for active PsA in pediatric patients 2 years of age and older (IV formulation only).[1]
• [Dosing:]
• [Adults (SC):] 50 mg administered subcutaneously once a month.[1]
• [Adults (IV):] 2 mg/kg administered as a 30-minute intravenous infusion at weeks 0 and 4, then every 8 weeks.[1]
• [Pediatrics (IV):] 80 mg/m² BSA administered as a 30-minute intravenous infusion at weeks 0 and 4, then every 8 weeks.[16]
• [Pivotal Trial Evidence:]
• [GO-REVEAL (SC formulation):] This study demonstrated that subcutaneous golimumab was significantly superior to placebo, with a much higher proportion of patients achieving an ACR20 response at week 14.[5]
• [GO-VIBRANT (IV formulation):] This trial established the efficacy of intravenous golimumab in adults with active PsA. Patients receiving golimumab IV had significantly greater improvement in ACR20 responses compared to placebo at week 14 and also showed less radiographic progression of joint damage at week 24.[6]

5.3. Ankylosing Spondylitis (AS)

• [Indication:] For the treatment of adult patients with active AS.[1]
• [Dosing:]
• [Simponi® (SC):] 50 mg administered subcutaneously once a month.[1]
• [Simponi Aria® (IV):] 2 mg/kg administered as a 30-minute intravenous infusion at weeks 0 and 4, then every 8 weeks.[1]
• [Pivotal Trial Evidence:]
• [GO-RAISE (SC formulation):] In this trial, golimumab was shown to be superior to placebo in improving the signs and symptoms of AS. A significantly greater proportion of golimumab-treated patients achieved at least a 20% improvement in the Assessment in Ankylosing Spondylitis (ASAS20) criteria at week 14 compared to placebo recipients.[5]
• [GO-ALIVE (IV formulation):] This trial confirmed the efficacy of the intravenous formulation in active AS, demonstrating significant improvements in disease signs and symptoms, physical function, and overall quality of life.[20]

5.4. Ulcerative Colitis (UC)

• [Indication:] For the treatment of adult patients with moderately to severely active UC who have had an inadequate response to, are intolerant to, or have demonstrated corticosteroid dependence on conventional therapies (e.g., aminosalicylates, corticosteroids, azathioprine, or 6-mercaptopurine). The goals of therapy include inducing and maintaining clinical response and remission, as well as improving the endoscopic appearance of the colonic mucosa.[1]
• [Dosing (SC):] The regimen involves an induction phase followed by maintenance.
• [Induction:] An initial dose of 200 mg subcutaneously at Week 0, followed by 100 mg at Week 2.
• [Maintenance:] 100 mg subcutaneously every 4 weeks thereafter.[1]
• [Pivotal Trial Evidence:]
• [PURSUIT Program (Induction and Maintenance):] These landmark trials established the efficacy of golimumab in UC. Compared to placebo, golimumab was effective for both inducing a clinical response and remission in the short term, and for maintaining that response and remission in the long term in patients who initially responded. This program led to its approval as the first subcutaneous anti-TNF therapy for UC.[18]

5.5. Polyarticular Juvenile Idiopathic Arthritis (pJIA)

• [Indication:] For the treatment of active pJIA in children 2 years of age and older who have had an inadequate response to previous therapy with MTX. This indication applies to the intravenous (Simponi Aria®) formulation.[1]
• [Dosing (IV):] Dosing is based on body surface area (BSA) to account for variations in patient size.
• 80 mg/m² BSA administered as a 30-minute intravenous infusion at weeks 0 and 4, followed by maintenance infusions every 8 weeks.[1]
• [Pivotal Trial Evidence:]
• [GO-VIVA (NCT02277444):] This was an open-label, Phase 3 study designed to evaluate the pharmacokinetics, safety, and efficacy of IV golimumab in children with active pJIA. The study confirmed that the BSA-based dosing regimen was well-tolerated and provided adequate drug exposure to achieve high rates of clinical response (JIA ACR 30/50/70/90), which were maintained through 52 weeks of treatment.[15]
• [GO-KIDS (NCT01230827):] This earlier study was designed to evaluate the subcutaneous formulation of golimumab in children with JIA.[37]

Indication	Patient Population	Formulation	Induction Dose	Maintenance Dose	Key Concomitant Therapy Notes
Rheumatoid Arthritis	Adults	Simponi® (SC)	N/A	50 mg every 4 weeks	Must be used with Methotrexate
	Adults	Simponi Aria® (IV)	2 mg/kg at Weeks 0 & 4	2 mg/kg every 8 weeks	Must be used with Methotrexate
Psoriatic Arthritis	Adults	Simponi® (SC)	N/A	50 mg every 4 weeks	May be used with or without MTX
	Adults	Simponi Aria® (IV)	2 mg/kg at Weeks 0 & 4	2 mg/kg every 8 weeks	May be used with or without MTX
	Pediatrics (≥2 yrs)	Simponi Aria® (IV)	80 mg/m² at Weeks 0 & 4	80 mg/m² every 8 weeks	N/A
Ankylosing Spondylitis	Adults	Simponi® (SC)	N/A	50 mg every 4 weeks	May be used with or without MTX
	Adults	Simponi Aria® (IV)	2 mg/kg at Weeks 0 & 4	2 mg/kg every 8 weeks	May be used with or without MTX
Ulcerative Colitis	Adults	Simponi® (SC)	200 mg at Wk 0, 100 mg at Wk 2	100 mg every 4 weeks	N/A
Polyarticular JIA	Pediatrics (≥2 yrs)	Simponi Aria® (IV)	80 mg/m² at Weeks 0 & 4	80 mg/m² every 8 weeks	Used in patients with inadequate response to MTX

VI. Long-Term Efficacy, Safety, and Treatment Persistence

The chronic nature of the diseases treated by golimumab necessitates an understanding of its performance over extended periods. Data from long-term extensions (LTEs) of the pivotal clinical trials provide critical information on its durable efficacy, safety profile, and treatment persistence.

6.1. Long-Term Efficacy

Follow-up data from the major Phase 3 trials, extending up to 5 years, have consistently shown that for patients who continue on therapy, the clinical benefits observed in the initial placebo-controlled periods are well-maintained. In RA, PsA, and AS, clinical response rates (as measured by ACR and ASAS criteria) and improvements in physical function (measured by HAQ-DI) remained stable over the long term.[31] Furthermore, a key long-term benefit is the sustained inhibition of structural damage. In both RA and PsA, patients treated with golimumab showed minimal radiographic progression over 5 years, indicating a durable effect on preventing irreversible joint destruction.[5]

6.2. Treatment Persistence (Retention Rates)

Treatment persistence, defined as the duration of time from initiation to discontinuation of a therapy, serves as a valuable real-world surrogate for overall drug effectiveness. It integrates not only sustained efficacy but also long-term tolerability, safety, and patient satisfaction.[39] Pooled analyses of the golimumab Phase 3 trial LTEs provide a robust dataset on this metric.

A pooled analysis of five pivotal trials (GO-BEFORE, GO-FORWARD, GO-AFTER, GO-REVEAL, GO-RAISE) provides a clear picture of long-term retention.[39]

• [First-Line Biologic Therapy:] In patients who were biologic-naïve (receiving golimumab as their first biologic), the treatment retention rates were high and durable. The probability of remaining on therapy was 87.8% at Year 1 and [69.8%] at Year 5. Notably, these high retention rates were consistent across the different diseases (RA, PsA, and AS).[39]
• [Second-Line Biologic Therapy:] The results were markedly different for patients with RA who had previously failed another anti-TNF agent (from the GO-AFTER trial). In this more treatment-refractory population, the retention rate was significantly lower, at 76.1% at Year 1 and dropping to [41.6%] at Year 5.[39]

In contrast to these clinical trial findings, real-world data from registries often show lower persistence rates. For instance, the BIOBADASER registry reported a 5-year golimumab retention rate of approximately 44% overall, and around 56% when used as a first-line biologic.[39] This discrepancy highlights the difference between the carefully selected, highly monitored populations in clinical trials and the more complex, comorbid patient populations seen in routine clinical practice.

Therapy Line	Pooled Studies	Year 1 Retention Rate (95% CI)	Year 5 Retention Rate (95% CI)	Key Patient Characteristic
1st-Line Therapy	GO-BEFORE, GO-FORWARD, GO-REVEAL, GO-RAISE	87.8% (86.2–89.2)	69.8% (67.6–71.9)	Median Disease Duration: 3.7 years
2nd-Line Therapy	GO-AFTER	76.1% (71.8–79.9)	41.6% (36.8–46.3)	Median Disease Duration: 9.2 years

The substantial difference in 5-year retention rates between first-line (~70%) and second-line (~42%) use provides a quantitative measure of the clinical challenge posed by the "treatment-refractory phenotype." Patients who fail their first TNF inhibitor are not simply starting over with a new drug; they represent a distinct population. The reasons for the initial treatment failure—such as the development of neutralizing anti-drug antibodies, a disease process not predominantly driven by TNF-α, or a more aggressive and entrenched disease biology—are likely to persist and limit the efficacy of a second agent within the same mechanistic class. The significantly longer disease duration in the second-line cohort (9.2 years vs. 3.7 years) is a marker for this chronicity, which is often associated with accumulated joint damage, central pain sensitization, and potentially altered inflammatory pathways that are less responsive to TNF blockade.[39] This data has profound implications for clinical practice, suggesting that for a patient failing a first TNF inhibitor, a more effective strategy might be to switch to a therapy with a different mechanism of action (e.g., an IL-17, IL-23, or JAK inhibitor) rather than cycling to another anti-TNF. This evidence is crucial for informing treatment sequencing guidelines and managing patient expectations.

6.3. Long-Term Safety Profile

The long-term safety profile of golimumab has been extensively evaluated through pooled analyses of the LTEs. These analyses, with follow-up extending to 5 years, have not identified any new or unexpected safety signals.[30] The overall safety profile remains consistent with that observed in the shorter, placebo-controlled periods of the trials and is in line with the known safety profile of the anti-TNF class as a whole.[40] When adjusted for the duration of exposure (patient-years), the incidence rates of key adverse events of interest, such as serious infections and malignancies, remained stable over time.[40]

A consistent finding across these long-term analyses is a numerically higher incidence of certain serious adverse events in patients receiving the 100 mg dose compared to the 50 mg dose. This dose-dependent trend was observed for serious infections, tuberculosis, opportunistic infections, lymphoma, and demyelinating events.[30] While the absolute event rates remain low, this observation is clinically relevant and supports the use of the lowest effective dose (typically 50 mg for rheumatologic indications) to optimize the risk-benefit balance.

VII. Comprehensive Safety Profile and Risk Management

The use of golimumab, like all TNF inhibitors, requires a thorough understanding of its potential risks and a proactive approach to risk management.

7.1. FDA Black Box Warning

Golimumab's prescribing information includes a prominent boxed warning highlighting its most significant risks, which are class-wide effects for TNF blockers.[2]

• [Serious Infections:]
• Patients treated with golimumab are at an increased risk for developing serious infections that may lead to hospitalization or death. These include bacterial sepsis, tuberculosis (TB), and invasive fungal infections such as histoplasmosis, coccidioidomycosis, candidiasis, and aspergillosis, as well as other opportunistic infections caused by pathogens like Legionella and Listeria.[1]
• The risk of infection is further elevated in patients taking concomitant immunosuppressive medications, such as methotrexate or corticosteroids.[41]
• [Risk Management Strategy:] Before initiating therapy, all patients must be evaluated for active infection and risk factors for TB. They must be tested for latent TB infection (LTBI). If LTBI is detected, treatment for TB should be started before initiating golimumab. Patients must be closely monitored for the signs and symptoms of infection during and after treatment.[13] If a patient develops a serious infection or sepsis, golimumab should be discontinued.[41]
• [Malignancy:]
• Lymphoma and other malignancies, some of which have been fatal, have been reported in children and adolescent patients treated with TNF blockers.[2]
• A specific, rare, and often fatal type of cancer called hepatosplenic T-cell lymphoma has been observed, primarily in adolescent and young adult males with inflammatory bowel disease (Crohn's disease or ulcerative colitis) who were being treated with a TNF blocker in combination with azathioprine or 6-mercaptopurine.[13]
• The background risk of lymphoma may already be elevated in adult patients with long-standing, active RA, independent of TNF blocker therapy.[41]

7.2. Other Key Warnings and Precautions

Beyond the boxed warnings, several other important risks require clinical attention:

• [Hepatitis B Virus (HBV) Reactivation:] In patients who are chronic carriers of HBV (i.e., hepatitis B surface antigen positive), treatment with TNF blockers can lead to reactivation of the virus. Some of these cases have resulted in fulminant hepatitis and have been fatal. All patients must be tested for HBV infection before starting golimumab.[1]
• [Congestive Heart Failure (CHF):] Cases of worsening pre-existing CHF and new-onset CHF have been reported with TNF blockers. Golimumab should be used with caution in patients with a history of heart failure, and it should be discontinued if new or worsening symptoms appear.[1]
• [Demyelinating Disorders:] Although rare, TNF blockers have been associated with the new onset or exacerbation of central nervous system (CNS) demyelinating disorders, such as multiple sclerosis, and peripheral demyelinating disorders, like Guillain-Barré syndrome. Caution is advised when considering golimumab in patients with these conditions.[1]
• [Hypersensitivity Reactions:] Serious systemic hypersensitivity reactions, including anaphylaxis, have been reported post-marketing. These can occur even after the first dose. The needle shield of the prefilled syringe and autoinjector for the Simponi® formulation is manufactured from dry natural rubber (a derivative of latex), which may cause allergic reactions in individuals with latex sensitivity.[1]
• [Hematologic Cytopenias:] There have been post-marketing reports of pancytopenia, leukopenia, neutropenia, and thrombocytopenia with TNF blockers. Caution should be exercised in patients with a history of significant cytopenias.[41]
• [Lupus-like Syndrome:] Treatment with TNF blockers can induce the formation of autoantibodies and, rarely, the development of a lupus-like syndrome, which typically resolves upon discontinuation of the drug.[1]

7.3. Common Adverse Reactions

The most frequently reported adverse reactions in clinical trials (with an incidence greater than 5%) are upper respiratory tract infections (such as nasopharyngitis, pharyngitis, and laryngitis) and injection site reactions.[3] Other common adverse events include abnormal liver function tests, elevated blood pressure, skin rash, and viral infections (such as influenza and herpes).[27] Injection site reactions are typically mild to moderate and may include redness, swelling, itching, pain, and bruising.[41]

7.4. Immunogenicity

As with all therapeutic proteins, there is a potential for immunogenicity. In clinical trials, a small percentage of patients developed antibodies to golimumab. The concurrent use of methotrexate was found to significantly lower the proportion of patients who developed anti-drug antibodies.[15] The presence of these antibodies can be clinically significant, as they have been associated with lower trough concentrations of the drug in the blood and, in some cases, a reduction in clinical efficacy. In some patients, these antibodies can also be neutralizing, meaning they directly block the drug's ability to bind to TNF-α.[15]

VIII. Significant Drug-Drug Interactions

The management of patients on golimumab requires careful consideration of potential drug-drug interactions, particularly with other immunomodulating agents and drugs metabolized by the cytochrome P450 system.

8.1. Biologic DMARDs and JAK Inhibitors

Concurrent administration of golimumab with other biologic DMARDs or targeted synthetic DMARDs is [not recommended] due to a significantly increased risk of serious infections without evidence of enhanced clinical benefit.[1] This includes:

• [Other TNF Blockers:] (e.g., infliximab, adalimumab, etanercept, certolizumab pegol).
• [Abatacept (T-cell inhibitor):] Clinical trials combining abatacept with a TNF blocker showed a higher rate of serious infections.[1]
• [Anakinra (IL-1 inhibitor):] Combination with a TNF blocker led to more serious infections and neutropenia with no added benefit.[1]
• [Rituximab (B-cell inhibitor):] A higher rate of serious infections has been noted in RA patients who received a TNF blocker after being treated with rituximab.[41]
• [Other Interleukin (IL) Inhibitors:] (e.g., ustekinumab, secukinumab).
• [Janus Kinase (JAK) Inhibitors:] (e.g., tofacitinib, baricitinib, upadacitinib).[1]

8.2. Live Vaccines

The administration of live vaccines to patients receiving golimumab is [not recommended]. Due to its immunosuppressive effects, golimumab may potentiate the replication of the vaccine organism, leading to a disseminated infection.[1] For infants who were exposed to golimumab in utero, it is recommended to wait for 6 months after the mother's last dose before administering any live vaccines, as the infant's immune system may be affected.[41]

8.3. Cytochrome P450 (CYP450) Substrates

Golimumab can have an indirect but clinically important effect on the metabolism of other drugs. The underlying mechanism is related to its primary pharmacologic action.

• [Mechanism:] Chronic inflammation, driven by elevated levels of cytokines like TNF-α, is known to suppress the expression and activity of cytochrome P450 (CYP450) enzymes.
• [Effect of Golimumab:] By effectively neutralizing TNF-α and reducing systemic inflammation, golimumab therapy can reverse this suppression, leading to the normalization or upregulation of CYP450 enzyme activity.
• [Clinical Implication:] This change can alter the metabolism of co-administered drugs that are substrates of CYP450 enzymes, particularly those with a narrow therapeutic index. For example, the clearance of drugs like [warfarin (CYP2C9), cyclosporine (CYP3A4), and theophylline (CYP1A2)] could increase, leading to lower drug levels and reduced efficacy. Therefore, close therapeutic monitoring (e.g., INR for warfarin, serum levels for cyclosporine/theophylline) and potential dose adjustments of these medications are necessary when a patient starts or stops golimumab therapy.[1]

IX. Use in Special Populations

9.1. Pregnancy and Lactation

• [Pregnancy:] As an IgG1 monoclonal antibody, golimumab is actively transported across the placenta, particularly during the second and third trimesters, and can be detected in the infant's serum for up to 6 months after birth.[44] This raises theoretical concerns about the potential impact on the developing fetal immune system. However, accumulating data suggest that the risks of uncontrolled maternal inflammatory disease to the pregnancy often outweigh the potential risks of the medication. A review of cumulative data from Janssen's global safety database, including 261 prospectively reported pregnancies with golimumab exposure, found that the rates of adverse pregnancy outcomes (e.g., spontaneous abortion) and major congenital anomalies were consistent with the expected background rates in the general population.[45] Major clinical guidelines generally recommend continuing TNF inhibitor therapy during pregnancy when it is necessary to control maternal disease activity, with a shared decision-making process between the patient and physician.[45] As a precaution, it is recommended that women of childbearing potential use adequate contraception during therapy and for at least 6 months after their final dose.[44]
• [Lactation:] Data on golimumab in breast milk indicate that it is transferred in only minimal, often undetectable, amounts.[1] As a large protein molecule, it is also likely to be degraded in the infant's gastrointestinal tract, leading to negligible systemic absorption by the nursing infant.[1] Data from the PIANO registry, a multicenter study of mothers with inflammatory bowel disease, showed no differences in growth, development, or infection rates among infants breastfed by mothers taking biologics (including one on golimumab) compared to controls.[46] Based on this evidence, most experts and clinical guidelines consider golimumab to be probably acceptable for use during breastfeeding.[46]

9.2. Pediatric Population

The use of golimumab in children has been formally studied and approved for specific indications.

• [Approvals:] The intravenous formulation, Simponi Aria®, is approved by the FDA and EMA for the treatment of active polyarticular juvenile idiopathic arthritis (pJIA) and active psoriatic arthritis (PsA) in children aged 2 years and older.[19]
• [Clinical Data:] The GO-VIVA trial was instrumental in establishing the efficacy and safety of a BSA-based dosing regimen for IV golimumab in pJIA, demonstrating that this approach achieves appropriate drug exposure and leads to significant clinical improvement.[15] Additionally, a Phase 3 clinical trial (NCT03596645) is currently underway to evaluate the efficacy and safety of the subcutaneous formulation of golimumab for pediatric patients with moderately to severely active ulcerative colitis.[47]

9.3. Geriatric Population

The use of TNF inhibitors in elderly patients requires careful consideration due to age-related physiological changes and the higher prevalence of comorbidities.

• [Safety Concerns:] Clinical trial data suggest that patients over the age of 65 may be at a higher risk for developing serious infections while on golimumab, a concern that applies to the entire anti-TNF class.[29]
• [Real-World Evidence:] While pivotal trials often underrepresent the very elderly, a Japanese post-hoc analysis of post-marketing surveillance data provided valuable information on patients aged 75 years and older with RA.[48] This study found that the clinical effectiveness (as measured by EULAR response criteria) and the overall rate of adverse events were comparable between the elderly (≥75 years) and younger (<75 years) patient groups.[48]

Despite this comparable efficacy, a noteworthy finding from the Japanese study was a significant difference in treatment persistence. The survival curve for golimumab was lower in the elderly group, and the most common reason for discontinuation was not lack of efficacy or adverse events, but rather "patient choice".[48] This suggests a potential mismatch between the drug's effect on inflammatory markers and the patient's perceived overall benefit. One clue may lie in the finding that while disease activity scores improved in the elderly, their physical function scores (HAQ-DI) did not.[50] For an elderly patient whose primary goal is to improve their ability to perform daily activities, a treatment that reduces inflammation but does not improve function—perhaps due to established joint damage, muscle deconditioning, or other comorbidities—may be perceived as not being "worth" the risk, cost, or burden of administration. This highlights the critical importance of aligning treatment goals with patient priorities through shared decision-making, especially in the geriatric population. Success in this group cannot be measured by inflammatory markers alone; functional outcomes and quality of life are paramount considerations that directly influence treatment persistence.[48]

X. Off-Label and Investigational Applications

While golimumab is approved for a specific set of indications, its potent anti-TNF mechanism has led to its investigation and off-label use in other refractory inflammatory conditions.

10.1. Refractory Uveitis

• [Rationale:] TNF-α is a well-established key cytokine in the pathogenesis of non-infectious uveitis, an inflammatory eye condition that can be vision-threatening.[51]
• [Evidence:] Golimumab is not formally approved for uveitis. However, a growing body of evidence from retrospective studies and case series suggests it can be a promising and effective therapeutic option for patients with severe, refractory immune-mediated uveitis who have failed other therapies.[51] It has shown particular promise in patients with HLA-B27-positive anterior uveitis, which is often associated with ankylosing spondylitis.[54] In several reports, patients who were resistant to multiple other immunosuppressive agents were able to achieve complete control of their ocular inflammation with golimumab.[54] While the manufacturer acknowledges these reports, it cannot recommend any use that deviates from the approved prescribing information.[53]

10.2. Refractory Crohn's Disease (CD)

• [Status:] Golimumab is [not] licensed or approved for the treatment of Crohn's Disease.[12] While other anti-TNF agents (infliximab, adalimumab, certolizumab pegol) are mainstays of CD therapy, golimumab has not undergone the same formal approval process for this indication, likely due to strategic decisions by the manufacturer or the results of early, unpublicized trials.[34]
• [Rationale for Interest:] Despite the lack of approval, golimumab's unique properties, such as its high affinity for TNF and conformational stability, have made it an agent of interest for CD, particularly in patients who have lost response to other anti-TNF drugs.[34]
• [Evidence from Off-Label Use:] Several retrospective studies have examined the off-label use of golimumab in highly treatment-refractory CD populations, often as a third- or fourth-line anti-TNF agent.
• A study of 45 refractory CD patients reported a clinical response rate of nearly 78% at 3 months, with 64% of initial responders maintaining their response at 36 months. This study noted that efficacy was often achieved with higher-than-standard doses.[34]
• A Swedish national registry study of 94 golimumab-treated CD patients, the vast majority of whom had failed at least one prior anti-TNF, concluded that despite this being a very difficult-to-treat group, more than one-third appeared to derive clinical benefit.[56]
• A small case series of 8 severe, refractory adult CD patients who had failed all three other approved anti-TNFs found that a considerable fraction responded to golimumab, suggesting it may have a niche role as a rescue therapy.[55]
• Data in pediatric CD is extremely limited but similarly suggests a potential role as a rescue therapy in refractory cases.[57]

XI. Conclusion and Future Directions

11.1. Synthesis of Risk-Benefit Profile

Golimumab is a potent and effective TNF-α inhibitor, firmly established as a valuable therapeutic option for a broad spectrum of chronic immune-mediated inflammatory diseases in rheumatology and gastroenterology. Its robust clinical trial program has demonstrated significant efficacy in reducing disease activity, improving physical function, and inhibiting structural damage. A key feature is its favorable pharmacokinetic profile, which allows for convenient and less frequent dosing regimens—once-monthly for the subcutaneous formulation and every eight weeks for the intravenous formulation—that can enhance patient adherence and quality of life.

The risk profile of golimumab is well-characterized and consistent with that of the anti-TNF class. The most significant risks are serious infections, particularly the reactivation of latent tuberculosis, and an increased risk of certain malignancies. These risks necessitate a rigorous approach to patient management, including comprehensive pre-treatment screening, vigilant monitoring during therapy, and patient education. Long-term data extending to five years have confirmed the durability of its efficacy and have not revealed new safety signals, though a dose-dependent increase in the incidence of some rare but serious adverse events with the 100 mg dose underscores the importance of using the lowest effective dose for each patient.

11.2. Future Outlook

The therapeutic landscape for golimumab is entering a period of significant evolution. The primary driver of change is the imminent arrival of biosimilars in major markets, with multiple applications already under review by the European Medicines Agency. This transition is expected to increase market competition, which will likely lead to price reductions and could expand patient access to this class of therapy.

Future research will likely focus on several key areas. First, there is a need to better understand and predict which patients are most likely to respond to golimumab, particularly in treatment-refractory populations. This includes identifying biomarkers that could guide therapy selection and help determine whether a patient failing a first anti-TNF agent should switch to another anti-TNF or to a drug with a different mechanism of action. Second, further defining its role and optimizing its use in pediatric inflammatory diseases, including the potential approval of the subcutaneous formulation for younger patients, will be important. Finally, long-term pharmacovigilance, encompassing both the originator product and its forthcoming biosimilars, will be crucial to confirm the continued stability of its safety profile and to ensure that the high standards of efficacy and safety are maintained across all versions of the molecule.

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