Golimumab — a new tool in the armoury against inflammatory arthritis

Abstract

The development of biological drugs blocking tumour necrosis factor-alpha (TNF-α) has had a dramatic impact on the treatment of inflammatory arthritis in recent years. Golimumab is a fully human monoclonal antibody which inhibits TNF-α. It is licensed for the treatment of rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. In this review we evaluate the results of phase III studies using golimumab and explore the place of golimumab in the treatment of these diseases.

Key words::

• Biological therapy
• golimumab
• monoclonal antibodies
• psoriatic arthritis
• rheumatoid arthritis
• safety
• treatment efficacy
• tumour necrosis factor-alpha

Abbreviations
ACR	=	American College of Rheumatology
AS	=	ankylosing spondylitis
ASAS	=	ASsessment in AS International Working Group
BASDAI	=	Bath Ankylosing Spondylitis Disease Activity
BASFI	=	Bath Ankylosing Spondylitis Functional Index
CRP	=	C-reactive protein
DAS28	=	Disease Activity Score using a 28 joint count
DMARD	=	disease-modifying anti-rheumatic drug
EULAR	=	European League Against Rheumatism
FDA	=	Food and Drug Administration
HAQ	=	Health Assessment Questionnaire
HAQ-DI	=	Health Assessment Questionnaire Disability Index
IgG	=	immunoglobulin G
IL-6	=	interleukin 6
MASES	=	Maastricht Ankylosing Spondylitis Enthesitis Score
NAPSI	=	Nail Psoriasis Severity Index
NSAID	=	non-steroidal anti-inflammatory drug
PASI	=	Psoriasis Area Severity Index
PsA	=	psoriatic arthritis
PsARC	=	Psoriatic Arthritis Response Criteria
RA	=	rheumatoid arthritis
RCT	=	randomized controlled trial
SF-36	=	Short Form 36 Health Survey
TNF-α	=	tumour necrosis factor-alpha
US	=	United States

Key messages

• Golimumab and other anti-TNF-α agents have demonstrated efficacy in the treatment of rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis.

• On-going data collection is required to determine the short- and long-term safety of golimumab.

Introduction

In the last 10 years, treatment options for the management of rheumatoid arthritis (RA) and other rheumatic diseases have evolved with the development of a new class of drugs which target tumour necrosis factor-alpha (TNF-α). The integral role of TNF-α in the pathogenesis of rheumatoid arthritis was first demonstrated in animal models and then in humans (1).

With the use of standard disease-modifying therapies such as methotrexate, a proportion of patients fail to respond to treatment, or have disease which continues to progress and cause damage (2).

The anti-TNF-α agents have demonstrated efficacy in controlling the clinical manifestations of disease, reducing radiographic progression (2–4), reducing work disability (5,6), and inducing remission, both clinical and drug-free remission (7). Clinical absence of disease does not equate to perfect control; even in clinical remission, patients may still demonstrate synovitis on imaging (8). There is also an on-going need to educate both patients and doctors to expect good control of arthritis; protocols requiring frequent monitoring, tight control, and therapy escalations for active disease have demonstrated significant benefits (9).

Currently approved anti-TNF-α agents include adalimumab, certolizumab, etanercept, and infliximab. These can be classified into fusion proteins and monoclonal antibodies. Etanercept is a fusion protein of two TNFR2 receptor extra-cellular domains and the Fc portion of human immunoglobulin G (IgG) and is given subcutaneously once or twice a week. Infliximab is a human/mouse chimeric monoclonal antibody and is given intravenously every 8 weeks after an initial loading period. Adalimumab is a fully human monoclonal antibody and is given subcutaneously once a fortnight. Certolizumab is a PEGylated Fab’ antibody fragment which is given subcutaneously once a fortnight.

Other currently licensed biological drugs include abatacept (a fusion protein which is a selective co-stimulation modulator inhibiting the co-stimulation of T cells), rituximab (a chimeric monoclonal antibody against CD20, which primarily targets B cells), and tocilizumab (a humanized monoclonal antibody against the interleukin 6 (IL-6) receptor).

What is golimumab?

Golimumab is a fully human anti-TNF-α monoclonal antibody which inhibits TNF-α by binding to soluble and transmembrane TNF-α. The approved dose is 50 mg given subcutaneously once a month. In a phase I study the mean peak serum concentrations occurred 4–6 days after a subcutaneous dose, with a half-life of 11–13 days (10). With intravenous dosing the median half-life is 7–20 days (11). A further phase I study demonstrated mean absolute bioavailability of 51% after a subcutaneous dose, with no difference in pharmacokinetic properties between different anatomical sites of subcutaneous administration (12). Golimumab is approved in Europe and the United States (US) for the treatment of active rheumatoid arthritis, psoriatic arthritis (PsA), and ankylosing spondylitis (AS) in adults.

Efficacy in RA

Five randomized controlled trials (RCTs) on the use of golimumab in rheumatoid arthritis have been published; one phase II study and four phase III studies (Table I). One of the phase III studies involved the intravenous use of golimumab, while all other RCTs used subcutaneous administration.

Table I. Phase III studies in rheumatoid arthritis.

Name of study	Ref.	Disease stage	Treatment	Number of patients	Primary outcome	Result for primary outcome, n (%)		Primary outcome met?	Radiographic results
	(15)	MTX IR	iv PBO + po MTX	129	ACR50 response at week 14	17 (13.2)		No	ND
			iv GLM 2 mg/kg + po MTX	129		16 (12.5)
			iv GLM 2 mg/kg + po PBO	128		25 (19.4)
			iv GLM 4 mg/kg + po MTX	128		28 (21.7)
			iv GLM 4 mg / kg + po PBO	129		27 (21.1)
			Combined golimumab groups	514		96 (18.7)
GO-BEFORE	(16,17)	MTX naive	PBO sc + MTX	160	ACR50 response at week 24	47 (29.4)		No	Significant reduction in radiographic progression with GLM
			GLM 100 mg sc + PBO	159		52 (32.7)
			GLM 50 mg sc + MTX	159		64 (40.3)
			GLM 100 mg sc + MTX	159		58 (36.5)
			Combined GLM + MTX groups	318		122 (38.4)
GO-FORWARD	(17–19)	MTX IR			ACR20 response at week 14 and improvement in HAQ-DI at week 24	ACR20	HAQ-DI	Yes	No significant difference
			PBO sc + MTX	133		44 (33.1)	−0.13
			GLM 100 mg sc + PBO	133		59 (44.4)	−0.13
			GLM 50 mg sc + MTX	89		49 (55.1)	−0.38
			GLM 100 mg sc + MTX	89		50 (56.2)	−0.50
			Combined GLM + MTX groups	178		99 (55.6)	−0.44
GO-AFTER	(20)	TNF IR	PBO	155	ACR20 response at week 14	28 (18%)		Yes	ND
			GLM 50 mg	153		54 (35%)
			GLM 100 mg	153		58 (38%)
			Combined GLM groups	306		112 (37%)

ACR response = American College of Rheumatology % improvement criteria; GLM = golimumab; HAQ-DI = health assessment questionnaire disability index; IR = inadequate response; iv = intravenous; MTX = methotrexate; ND = not done; PBO = placebo; po = oral; sc = subcutaneous; TNF = tumour necrosis factor.

The phase II study was a randomized, double-blind, placebo-controlled, dose-ranging study (13). Patients were randomized to placebo (n = 35), 50 mg golimumab every two weeks (n = 34), 50 mg golimumab every four weeks (n = 35), 100 mg golimumab every two weeks (n = 34), or 100 mg golimumab every four weeks (n = 34). Entry requirements included an inadequate response to methotrexate at a dose of ≥ 10 mg per week, given for ≥ 3 months. All patients continued methotrexate at a stable dose throughout the study. At week 20, patients in the placebo group switched to open-label infliximab treatment, and patients in the golimumab groups continued their assigned dose, but those receiving treatment every two weeks reduced frequency to every four weeks. The primary outcome was the percentage of patients meeting the American College of Rheumatology 20% improvement criteria (ACR20) at week 16.

The primary outcome was met. A total of 61.3% of the patients in the combined golimumab group achieved an ACR20 response compared to 37.1% in the placebo group (P = 0.01). Significantly more patients receiving golimumab achieved ACR50 and ACR70 responses at 16 weeks. There was no definite dose–response relationship between groups in efficacy outcomes. There was a trend to higher trough serum golimumab concentrations in patients receiving the higher dose. Reductions in biomarkers (such as serum amyloid A, E-selectin, and matrix metalloproteinase 9) at week 4 were shown to correlate with improvements in the swollen joint count at week 16, suggesting their potential use in predicting response to treatment (14).

Nausea was reported more frequently in the golimumab groups (16.8%) compared to the placebo group (2.9%) but did not lead to treatment discontinuation. Injection site reactions were reported more frequently in those receiving 100 mg golimumab (36.1%) compared to those receiving placebo (11.8%). The overall rate of infections did not differ significantly between groups. Four malignancies developed in patients treated with golimumab: one lung cancer, one squamous cell carcinoma, and two basal cell carcinomas. Antibodies to golimumab developed in 6.5% patients treated with golimumab.

A phase III randomized, double-blind, placebo-controlled study assessed the efficacy and safety of the intravenous use of golimumab given every 12 weeks (15). Patients were randomized to placebo plus methotrexate (n = 129), golimumab 2 mg/kg with methotrexate (n = 129), golimumab 2 mg/kg with oral placebo (n = 128), golimumab 4 mg/kg with methotrexate (n = 128), or golimumab 4 mg/kg with oral placebo (n = 129). Blinded early escape was possible at week 16 and week 24. Treatment continued to week 48. Patients were required to have had an inadequate response to methotrexate at base-line. The primary outcome was the proportion of patients meeting an ACR50 response at week 14.

The primary outcome was not met. Altogether 21.4% of the combined golimumab group and 13.2% of the placebo group achieved an ACR50 response at 14 weeks (P = 0.051). However, significantly more patients in the combined golimumab groups achieved an ACR50 response at week 24 compared to those receiving placebo. Significant results were also seen for the physical component of the Short Form 36 Health Survey (SF-36) and for a reduction in the Disease Activity Score using a 28 joint count (DAS28 score). The greatest improvements were seen in those receiving golimumab 4 mg/kg with methotrexate.

There was no significant increase in adverse events with either the higher dose of golimumab or the concomitant use of methotrexate. Serious infections occurred more frequently in patients treated with golimumab (3.7%) than placebo (1.6%). Malignancies occurred in 1.6% patients receiving placebo with methotrexate and in 1.3% of those receiving golimumab. Antibodies to golimumab developed in 5% patients receiving golimumab by week 24, with a higher prevalence among those receiving monotherapy golimumab (9% versus 3%).

The GO-BEFORE study was a phase III study performed to assess the efficacy of golimumab in patients with rheumatoid arthritis who are methotrexate-naive (16). This was a 52-week study with patients randomized to placebo plus methotrexate (n = 160), golimumab 100 mg plus placebo (n = 159), golimumab 50 mg plus methotrexate (n = 159), or golimumab 100 mg plus methotrexate (n = 159). Patients were not allowed to have prior exposure to anti-TNF-α agents, nor to have received more than three prior doses of methotrexate. The joint primary outcomes were an ACR50 response at week 24 and a change from base-line in the modified Sharp/van der Heijde score at 52 weeks.

The ACR50 primary outcome was not met. In the combined golimumab plus methotrexate groups, 38.4% patients achieved an ACR50 response, compared to 29.4% of those in the placebo plus methotrexate group. Post-hoc modified analyses did detect significant differences between groups when patients randomized but not treated were excluded. The failure to achieve the primary outcome may be related to sample size. Significant benefits were shown for DAS28 score, ACR70 and ACR90 responses, C-reactive protein (CRP), and Health Assessment Questionnaire (HAQ). There was a significant reduction in radiographic progression, assessed as change from base-line to week 52 in the modified Sharp/ van der Heijde score, when comparing the combined golimumab group to placebo (17).

Serious adverse events were not more frequent in the golimumab treatment groups, although serious infections occurred more frequently with golimumab 100 mg plus methotrexate (4.4%) than the other groups (1.3% to 1.9%). Two unrelated deaths occurred in the golimumab groups. One patient on golimumab developed tuberculosis, although this may have pre-dated the study treatment. Four patients developed malignancies: breast cancer and a lip squamous cell carcinoma in the placebo and methotrexate group, breast cancer and Hodgkin's lymphoma in the golimumab groups. Antibodies to golimumab developed in 6.3% of the patients receiving golimumab.

The GO-FORWARD study assessed the efficacy of golimumab in patients with rheumatoid arthritis who had inadequate response to methotrexate (18). This was a phase III study for 52 weeks followed by an open-label extension up to 5 years. Patients were required to have active arthritis despite being on a stable dose of methotrexate of at least 15 mg once a week. Previous use of anti-TNF-α agents was not permitted. Patients were randomized to placebo plus methotrexate (n = 133), golimumab 100 mg plus placebo (n = 133), golimumab 50 mg with methotrexate (n = 89), or golimumab 100 mg plus methotrexate (n = 89). Blinded escape occurred at week 14 in those with inadequate response to study treatment. The two co-primary outcomes were the proportion of patients achieving an ACR20 response at week 14 and the improvement from base-line in HAQ Disability Index (HAQ-DI) score at week 24.

The two co-primary outcomes were achieved. In the combined golimumab plus methotrexate group, 55.6% patients achieved an ACR20 response compared to 33% of those on placebo and methotrexate (P < 0.001). There was a significantly greater improvement in the HAQ-DI in the combined golimumab plus methotrexate group compared to the placebo plus methotrexate group (improvement from base-line −0.44 versus −0.13; P < 0.001). Sustained efficacy has been confirmed in the week 52 data from the study (19). Radiographic progression did not differ significantly between groups at 24 weeks, but progression was minimal in all groups (17). This may be related to the short duration of the study and a lack of power to assess radiographic outcomes.

There was a non-significant trend to the occurrence of more serious adverse events in patients receiving golimumab 100 mg plus methotrexate compared to those on placebo plus methotrexate. One death due to sepsis occurred in a patient on golimumab and oral placebo. Malignancies occurred in four patients: one basal cell carcinoma in a patient on placebo plus methotrexate, a basal cell carcinoma, squamous cell skin cancer, and breast cancer in patients on golimumab. Antibodies to golimumab occurred in 2.1% patients at week 24, all of whom were in the group on golimumab but no methotrexate.

A further phase III study has assessed the efficacy of golimumab in patients with rheumatoid arthritis with an inadequate response to anti-TNF-α agents (20). The GO-AFTER study randomized patients to placebo (n = 155), golimumab 50 mg (n = 153), or golimumab 100 mg (n = 153). Blinded early escape to active treatment or the higher-dose golimumab occurred at week 16. Eligibility criteria included active rheumatoid arthritis with discontinuation of prior anti-TNF-α agent (for any reason). Concomitant disease-modifying anti-rheumatic drug (DMARD) therapy was permitted but not required.

The primary outcome was an ACR20 response at week 14 and was achieved (37% in the combined golimumab group versus 18% placebo; P < 0.0001). Significant benefits were also noted in physical function and fatigue.

Up to week 16, patients receiving golimumab 100 mg reported the greatest number of adverse events but the lowest number of serious adverse events. Malignancies developed in three patients: one pancreatic cancer in a patient on placebo, one lymphoma and one squamous cell carcinoma of the skin. Antibodies to golimumab developed in 3% of the patients who received golimumab.

Efficacy in psoriatic arthritis

One phase III multicentre, randomized, double-blind, placebo-controlled study has been reported on the use of golimumab in adults with active PsA: GO-REVEAL (21) (Table II).

Table II. Phase III studies in the spondyloarthropathies.

Name of study	Ref.	Disease	Treatment	Number of patients	Primary outcome	Result for primary outcome, n (%)	Primary outcome met?	Radiographic results
GO-REVEAL	(21,22)	PsA	Placebo	113	ACR20 response at week 14	10 (9)	Yes	Significant reduction in radiographic progression with GLM
			GLM 50 mg	146		74 (51)
			GLM 100 mg	146		66 (45)
			Combined GLM group	292		140 (48)
GO-RAISE	(24,25)	AS	Placebo	78	ASAS20 response at week 14	(21.8)	Yes	ND
			GLM 50 mg	138		(59.4)
			GLM 100 mg	140		(60.0)

ACR20 response = American College of Rheumatology 20% improvement criteria; AS = ankylosing spondylitis; ASAS20 response = ASessment in AS International Working Group criteria; GLM = golimumab; ND = not done; PsA = psoriatic arthritis.

The study randomized patients to placebo (n = 113), golimumab 50 mg (n = 146), or golimumab 100 mg (n = 146) for 24 weeks. Early escape was possible at week 16 for patients with inadequate response. Active PsA was defined as at least three tender and three swollen joints, with a negative rheumatoid factor, and plaque psoriasis with a lesion at least 2 cm in diameter. Patients were required to have had inadequate response to non-steroidal anti-inflammatory drug (NSAID) or DMARD therapy. Patients with previous use of biological agents were excluded. The primary end-point was the proportion of patients meeting the ACR20 response at week 14. Responses of skin psoriasis and nail psoriasis (using the Psoriasis Area Severity Index (PASI) and the target nail Nail Psoriasis Severity Index (NAPSI)) were also recorded.

The primary end-point was met, with 48% of the patients in the combined golimumab group achieving an ACR20 response, compared to 9% patients in the placebo group (P < 0.001). Significant differences were observed in ACR20, 50, and 70 responses at all time points. Significant benefits were also demonstrated for physical function, quality of life, morning stiffness, and achievement of Psoriatic Arthritis Response Criteria (PsARC) and European League Against Rheumatism (EULAR) responses. The PsA modified Maastricht Ankylosing Spondylitis Enthesitis Score (MASES) reduced significantly at 14 and 24 weeks in both golimumab groups, as did the dactylitis score with 100 mg golimumab at both time points. Significant reductions in psoriasis as well as the target nail NAPSI were demonstrated in the golimumab treatment groups. Radiographic outcomes have been reported only in abstract form but show significantly less radiographic progression with golimumab compared to placebo at 24 weeks (22).

Infections were seen more frequently in the higher treatment dose (in 41% patients receiving golimumab 100 mg, compared to 33% of those on 50 mg and 24% of those on placebo), although serious adverse events including serious infections were seen more frequently in the placebo group. No cases of tuberculosis were reported. Three malignancies occurred up to week 24, all in the golimumab 100 mg group: two basal cell carcinomas and one prostate cancer. Antibodies to golimumab occurred in 4.6% patients.

This study confirms the efficacy of golimumab in treating the articular and skin manifestations of PsA, in keeping with the other anti-TNF-α agents. Similar results for arthritis efficacy were observed with both doses, although there may have been greater responses in psoriasis with the 100 mg dose. Enthesitis, dactylitis, and nail disease have not previously been well recorded in clinical trials, but this study does demonstrate some benefits in these manifestations. The patients remain under follow-up as part of the study, and longer-term data are awaited to be published, although results reported as an abstract do show efficacy up to 104 weeks (23).

Efficacy in ankylosing spondylitis

GO-RAISE is an international multicentre phase III randomized, double-blind, placebo-controlled trial of golimumab in the treatment of active AS (24) (Table II). A total of 356 patients were recruited into three arms: placebo (n = 78), golimumab 50 mg once a month (n = 138), and golimumab 100 mg once a month (n = 140). Entry criteria included adult patients with ankylosing spondylitis meeting the modified New York criteria for AS, with an inadequate response to NSAID or DMARD therapy. Patients previously treated with an anti-TNF-α agent were excluded. Blinded treatment continued to week 24, but patients with an inadequate response at 16 weeks could enter an early escape pathway with patients on placebo commencing golimumab 50 mg, those on golimumab 50 mg escalating to 100 mg, and those on 100 mg continuing the same dose. The primary outcome was the proportion of patients achieving at least a 20% improvement in the ASsessment in AS International Working Group criteria at week 14 (ASAS20).

The primary outcome was met. Significantly more patients in the golimumab groups (59.4% on 50 mg and 60% on 100 mg) achieved an ASAS20 response compared to 21.8% of the placebo group (P < 0.001). Significant differences were seen between treatment and placebo groups in Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and Bath Ankylosing Spondylitis Functional Index (BASFI) scores at both 14 and 24 weeks. No significant differences were noted in spinal mobility. Significant improvements were seen in the CRP level and in quality of life at week 14 and 24.

Nasopharyngitis, upper respiratory tract infections, fatigue, headache, diarrhoea, injection site reactions, and raised liver enzymes were seen more frequently in patients receiving golimumab. Rates of serious adverse events were similar between groups; 2.9% of the patients receiving golimumab and 1.3% of the patients on placebo discontinued the study due to an adverse event. There were no deaths, cases of tuberculosis, or opportunistic infections. Basal cell carcinomas were reported in one patient receiving placebo and one receiving golimumab by week 24. Antibodies to golimumab were seen in 4.1% of the patients originally randomized to golimumab.

GO-RAISE demonstrates the efficacy of golimumab in patients with established moderate to severe AS. No clear difference was seen between the two doses used. A sub-analysis has also reported significant benefits on sleep disturbance in the golimumab treatment groups (25). These results are largely in keeping with trials on other anti-TNF-α agents. Further data including long-term outcomes and radiographic outcomes are needed, although inhibition of radiographic progression has not yet been demonstrated with other anti-TNF-α agents.

Is there additional benefit from the concomitant use of a DMARD?

In line with experience from other anti-TNF-α agents, pharmacokinetic studies have shown lower steady-state golimumab concentrations in patients receiving monotherapy golimumab 50 mg compared to those also receiving methotrexate (26). This difference was not seen at the 100 mg dosage.

In both GO-FORWARD and GO-AFTER, efficacy was greater in patients on combination DMARD plus golimumab than in those on golimumab monotherapy (18,20). In PsA, in line with experience with other anti-TNF-α agents, no additional clinical benefit was seen with the co-prescription of methotrexate (21), although no patients on concomitant methotrexate developed antibodies to golimumab. The RCTs in RA found that no patients (18) or fewer patients (15) on concomitant methotrexate developed antibodies to golimumab. As the formation of antibodies can be associated with the loss of clinical efficacy, concomitant methotrexate may have long-term beneficial effects which were not seen in the duration of the trial.

Treatment of asthma

Golimumab has also been investigated for the treatment of asthma (27). The trial was halted at 24 weeks as the risk-benefit ratio was not favourable.

Golimumab and the risk of malignancy

Patients with RA and other inflammatory diseases are at higher risk of developing lymphoma, especially those with high disease activity (28). Following the introduction of anti-TNF-α agents, registries and observational studies worldwide have studied the long-term risks of these agents, with some showing an increased risk of lymphoma (29) and some studies not (30).

An analysis by the Food and Drug Administration (FDA) of the controlled sections of the phase II and phase III studies in RA, PsA, and AS has shown an incidence of lymphoma of 0.21 per 100 patient years of follow-up in the combined golimumab groups (95% CI 0.03–0.77) compared to an incidence of 0.00 (95% CI 0.00–0.96) in the placebo group (31). Reviewing both the controlled and uncontrolled sections of these trials, they found a 3.8-fold increased risk of lymphoma compared to the general US population. Teasing out the confounding factors to elucidate whether this is a real increased risk is difficult and will require further large-scale studies and long-term follow-up in registries.

Role in current management and treatment

Not all patients respond to their first anti-TNF-α agent, and clearly it is useful to have a range of effective drugs available to treat patients with severe disease. These drugs are expensive, and thus in many countries their use is restricted. Where golimumab fits into these algorithms is yet to be decided. The advantages of golimumab include monthly dosing and the subcutaneous form of delivery which many patients prefer and which reduces hospital infusion costs. Disadvantages include the current lack of long-term data and experience with large numbers of patients in comparison to other anti-TNF-α agents.

There is an increasing focus on the early treatment of inflammatory arthritis and the concept of the ‘window of opportunity’ (32), where early treatment may allow a switching off of the inflammatory pathway and the possibility of drug-free remission. Disappointingly the RCT looking at the use of golimumab in methotrexate-naive rheumatoid arthritis did not meet its clinical primary end-point (16), but further studies would be warranted given the efficacy at reducing radiographic progression and the good responses achieved with other anti-TNF-α agents in this patient group (33–38).

Traditionally, patients who have already failed treatment with one anti-TNF-α agent have been among the most difficult to treat. Golimumab has demonstrated efficacy in this group (20), but further studies are still needed to determine the optimal order of different treatment options and predictors of response to allow individualized targeted treatment. Golimumab may be of particular use in patients with secondary non-response to another monoclonal antibody.

Conclusion

Golimumab has demonstrated efficacy in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis, thus offering patients a new option. Results for efficacy and safety are in keeping with the other anti-TNF-α agents. Golimumab has also shown efficacy in patients who have previously failed an anti-TNF-α agent. Further research is needed to determine optimal treatment strategies and to monitor the long-term safety.

Declaration of interest: Z Ash has received an unrestricted educational grant from Merck Sharpe & Dohme. She has also received conference expenses from Abbott, Chugai, and Merck Sharpe & Dohme and honoraria from Pfizer. P Emery has undertaken clinical trials and provided expert advice for Merck, Pfizer, Abbott, UCB, Roche, and Bristol-Myers Squibb.