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etanercept

✓ Approved

Harvest Moon Pharmaceuticals · TNF · Recombinant Proteins

What is etanercept?

etanercept is a recombinant proteins developed by Harvest Moon Pharmaceuticals. It is approved for therapeutic indications via injectable (others) or intraarticular injection or intravenous (iv) or subcutaneous injection.

Drug Profile

CompanyHarvest Moon Pharmaceuticals
Drug ClassRecombinant Proteins
Molecular TargetTNF
RouteInjectable (Others), Intraarticular Injection, Intravenous (IV), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Harvest Moon Pharmaceuticals

Mechanism of Action

Molecular Targets

etanercept acts on 1 molecular target:

TNFtumor necrosis factor (TNFA, TNF-alpha)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

etanercept is developed for 5 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Musculoskeletal and connective tissue disordersRheumatoid arthritis✓ Approved
Musculoskeletal and connective tissue disordersAnkylosing spondylitisPreclinical
Skin and subcutaneous tissue disordersPsoriasisPreclinical
Musculoskeletal and connective tissue disordersPsoriatic arthropathyPreclinical
Musculoskeletal and connective tissue disordersJuvenile idiopathic arthritisPreclinical

Related Research Articles

PubMedLife (Basel, Switzerland)2026-08-27

Lamotrigine-Induced Toxic Epidermal Necrolysis with Multiorgan Failure, Pneumatosis Intestinalis and Chronic Ocular Complications.

Szrama Jakub J, Smuszkiewicz Piotr P, Woźniak Amadeusz A, Lohani Ashish A et al.

Toxic epidermal necrolysis (TEN) is a rare, life-threatening mucocutaneous adverse drug reaction associated with extensive epidermal necrosis and severe systemic complications. We report the case of a 25-year-old woman who developed severe lamotrigine-induced TEN four weeks after treatment initiation. The disease rapidly progressed to involve approximately 60% of the body surface area, requiring intensive care unit admission, mechanical ventilation, and multidisciplinary management. Treatment included high-dose intravenous methylprednisolone, intravenous immunoglobulins, etanercept, plasmapheresis, and comprehensive supportive care. During hospitalization, the patient developed gastrointestinal complications manifested by pneumatosis intestinalis and portal venous gas, raising suspicion of bowel ischemia and prompting exploratory laparotomy. Following treatment, gradual clinical improvement and complete resolution of the cutaneous lesions were achieved. However, persistent ocular sequelae developed, including meibomian gland dysfunction, punctate epithelial erosions, conjunctival scarring, trichiasis, tear film instability, and early corneal neovascularization, requiring long-term ophthalmological follow-up. To provide clinical context, a narrative review of the literature on the diagnosis, multidisciplinary management, gastrointestinal manifestations, ocular complications, and systemic treatment of TEN was performed. A comprehensive literature search was conducted to identify relevant articles focusing on the intensive care management and specific organ-related manifestations of Toxic Epidermal Necrolysis (TEN). The gathered literature was narratively synthesized to present a cohesive update on current clinical practices and management controversies. This case highlights the potentially devastating multiorgan course of TEN and emphasizes the importance of early recognition, specialized intensive care, and long-term multidisciplinary follow-up.

PMID 42652926
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PubMedCureus2026-08-22

Rapid Improvement in Cerebral Palsy Following Treatment With Perispinal Etanercept: A Case Report.

Ucci Danielle D, Asseraf Samantha S, Prieto Genavieve G, Tucker Alanna A et al.

Etanercept, a selective inhibitor of the cytokine tumor necrosis factor (TNF), delivered by perispinal administration, has been used clinically for 15 years to treat chronic, intractable, post-stroke and post-brain injury neurological dysfunction. We report the case of a 19-year-old patient with cerebral palsy (CP) who experienced rapid and sustained neurological improvement after treatment with perispinal etanercept (PSE). The patient was born at 25 weeks gestation following a twin pregnancy complicated by abruptio placentae and premature onset of labor. The initial head ultrasound, performed four weeks after birth, demonstrated grade four intraventricular hemorrhage (IVH) with acquired ventriculomegaly and the patient was subsequently diagnosed with CP, hydrocephalus, and retinopathy of prematurity. She presented at age 19 to our clinic with chronic right hemiparesis, bilateral upper limb fine motor dysfunction, painful spasticity and multiple, additional chronic neurological symptoms. The patient received an initial 25mg dose of PSE, followed by doses at weeks three, 24 and 49. The patient reported reduced painful spasticity and improved sensation within 30 minutes of each dose. Clinically meaningful improvements that persisted over the entire one-year period of observation were noted in painful spasticity, sensation, gait, mobility, balance, coordination, fine motor function, strength, fatigue, and headaches; some of the improvements were progressive. PSE was well tolerated. Further study of PSE for selected patients with CP in properly designed, randomized, controlled trials is warranted.

PMID 42631301
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PubMedHand surgery & rehabilitation2026-08-22

Disease-modifying antirheumatic drugs for hand osteoarthritis: A systematic review and network meta-analysis.

Dong Pei P, Zhao Qianle Q, Yang Bo B, Kang Wulin W et al.

To compare the symptomatic efficacy, safety, and exploratory structural evidence of disease-modifying antirheumatic drug therapies in patients with hand osteoarthritis, with particular attention to inflammatory and erosive phenotypes. We searched PubMed, Web of Science, Embase, the Cochrane Library, ClinicalTrials.gov, and the Chinese Clinical Trial Registry from inception to 12 March 2026 for randomized controlled trials evaluating disease-modifying antirheumatic drug therapies in hand osteoarthritis. Eligible trials included patients with general, inflammatory, erosive, or thumb-base hand osteoarthritis, while studies involving rheumatoid arthritis or other inflammatory arthritides were excluded. Interventions were classified as conventional synthetic or biologic disease-modifying antirheumatic drugs. Pain intensity and hand function were considered primary clinical outcomes. Inflammatory symptom-related outcomes, including swollen and painful joint counts and stiffness, were analysed separately. Treatment-emergent adverse events and serious adverse events were primary safety outcomes, while imaging and biomarker outcomes were treated as exploratory evidence related to potential structural disease modification. A frequentist network meta-analysis was performed. Continuous outcomes were summarized as standardized mean differences and dichotomous outcomes as odds ratios, both with 95% confidence intervals. Twelve randomized controlled trials involving 1317 participants and seven active disease-modifying antirheumatic drug therapies were included. Methotrexate and hydroxychloroquine were classified as conventional synthetic disease-modifying antirheumatic drugs, whereas adalimumab, etanercept, tocilizumab, lutikizumab, and otilimab were classified as biologic disease-modifying antirheumatic drugs. No eligible trial of a targeted synthetic disease-modifying antirheumatic drug was identified. For pain intensity outcomes, etanercept and tocilizumab were associated with lower long-term visual analogue scale pain than placebo, whereas no intervention showed consistent improvement in hand function. For inflammatory symptom-related outcomes, tocilizumab showed a short-term reduction in painful and swollen joint counts, and adalimumab reduced swollen joint counts in some analyses. However, these findings were outcome-specific, time-dependent, and largely based on sparse, placebo-centred networks. No clear differences were detected in overall treatment-emergent adverse events or serious adverse events, but safety evidence was limited by small sample sizes, short exposure durations, and inconsistent adverse-event reporting. Imaging and biomarker outcomes were heterogeneous and insufficient for quantitative synthesis across most endpoints. Current randomized evidence does not support the routine use of disease-modifying antirheumatic drugs for hand osteoarthritis. Selected biologic agents showed limited symptomatic signals, particularly in pain or inflammatory joint outcomes, but these findings should not be interpreted as evidence of disease modification. Structural and biomarker evidence remains exploratory and insufficient. Future trials should focus on phenotype-enriched hand osteoarthritis populations and use standardized clinical, imaging, biomarker, and safety outcomes. Level I, therapeutic studies. PROSPERO CRD420261353132.

PMID 42632595
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PubMedWorld journal of clinical pediatrics2026-08-21

Clinical and laboratory manifestations and treatment of children with TNFRSF1A gene variants.

Alexeeva Ekaterina I EI, Shingarova Meiri Sh MS, Dvoryakovskaya Tatyana M TM, Isaeva Ksenia B KB et al.

The TNFRSF1A gene encodes TNFR1, which regulates inflammation and apoptosis. Variants in this gene present with an autoinflammatory phenotype and are linked to tumor necrosis factor receptor associated periodic syndrome (TRAPS), an orphan monogenic autoinflammatory disease (AID) that can mimic systemic juvenile idiopathic arthritis (sJIA) and other rheumatic diseases. Despite known mechanisms and classification criteria, diagnosing and choosing therapy for patients with TNFRSF1A variants remains challenging. Assessing phenotypic characteristics and considering alternative therapies for these patients is important. To evaluate the clinical and laboratory features of sJIA associated with the TNFRSF1A gene and treatment outcomes. A single-center, retrospective, cross-sectional cohort study with longitudinal follow-up was performed. A total of 66 patients with fever and a referral diagnosis of sJIA were included: 33 (50%) had TNFRSF1A gene variants identified by molecular genetic testing, and 33 (50%) had no TNFRSF1A or other autoinflammatory gene variants. Demographic, clinical, laboratory, and treatment data were collected before and after verification of AID, and again at 3, 6, and 12 months. Molecular genetic testing identified several TNFRSF1A variants. Of 33 patients, 4 (12%) had likely pathogenic variants, 1 (3%) had a pathogenic variant, and 3 (9.1%) had variants of uncertain significance; all were heterozygous. The most common, identified in 27 (82%), was a variant of uncertain significance (c.362G>A, p.Arg121Gln) with incomplete penetrance. These patients had paroxysmal (48.5%) or continuous fever (48.5%), rash (66.7%), joint syndrome (78.8%), abdominal pain (33.3%), gastrointestinal symptoms (27.2%), eye involvement (24.2%), chest pain (12.1%), hearing loss (9.1%), periorbital edema (9.1%), arrested development (6.1%), aseptic meningitis (3%), hydrocephalus (3%), and amyloidosis (3%). Endoscopic signs of intestinal damage were found in 20 patients (60.6%): 11 showed upper gastrointestinal tract issues; 9 had intestinal pathology. All patients with TNFRSF1A variants received antirheumatic therapy before genetic testing. Treatments included intravenous glucocorticoids (GC) (45.5%), oral GC (45.5%), intravenous immunoglobulin (18.1%), methotrexate (48.5%), cyclosporine (18.1%), azathioprine (3%), mesalazine (3%), sulfasalazine (3%), and biological (b) disease-modifying antirheumatic drugs (bDMARDs) (72.7%). Of those on bDMARDs, 39.4% received tocilizumab, 9.1% abatacept, 6.1% canakinumab, 6.1% infliximab, 3% rituximab, 3% etanercept, 3% adalimumab, and 3% certolizumab pegol. Among 24 patients with three prior bDMARD switches before genetic diagnosis, 17 (70.8%) achieved remission: 7 on tocilizumab, 6 on canakinumab, 2 on adalimumab, 1 on infliximab, and 1 on rituximab. After confirming AID, all patients received biological therapy: 9 previously untreated patients started canakinumab (3), tocilizumab (3), or etanercept (3); 7 switched drugs after ineffective prior therapy. After all therapy adjustments, all patients achieved remission: 13 on tocilizumab, 11 on canakinumab, 3 on adalimumab, 2 on etanercept, 1 on golimumab, 1 on rituximab, and 1 with GC and colchicine followed by withdrawal. Patients started on bDMARDs after genetic testing required fewer drug switches than those treated empirically before diagnosis (0.23 ± 0.42 vs 0.9 ± 0.6, P = 0.001). Variants in the TNFRSF1A gene may cause a wide range of clinical symptoms, including eye and intestinal lesions that are not typical of sJIA. All patients with fever and unusual sJIA symptoms should have molecular genetic testing for TNFRSF1A variants to confirm or exclude AID early. Early diagnosis enables timely therapy and prevents complications. Tocilizumab (39.3%), canakinumab (33.3%), and TNF inhibitors (21.2%) achieved remission in children with TNFRSF1A variants. Some patients required multiple bDMARD switches to achieve remission, highlighting the complexity of treatment decisions in this group.

PMID 42626148
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PubMedModern rheumatology case reports2026-08-20

Chronic Nonbacterial Osteomyelitis/Chronic Recurrent Multifocal Osteomyelitis - A Case Report and Literature Review.

Persad Christophe C, Donaldson Niamh N, Huica Simona S

Chronic non-bacterial osteomyelitis/chronic recurrent multifocal osteomyelitis (CNO/CRMO) is an autoinflammatory, sterile bone disorder that predominantly affects children but can also occur in adults. The nonspecific nature of its presentation, as well as relative lack of awareness of the condition, often results in significant diagnostic delay. In this article, we present the case of a female patient who began experiencing sternal pain at the age of 14, initially thought to be due to costochondritis but ultimately discovered to be secondary to CNO/CRMO. We demonstrate her long and tortuous diagnostic journey including key imaging and bone biopsy findings. We also report good clinical and radiographic response to tumour necrosis factor-α (TNF-α) inhibitors, despite having to switch from adalimumab (ADA) to etanercept (ETN) and then to methotrexate (MTX) due to side effects and anti-drug antibody production.

PMID 42623272
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PubMedRMD open2026-08-20

Prevalence and clinical relevance of anti-drug antibodies in psoriatic arthritis: a systematic review.

Kimpton James J, Akpabio Akpabio A, Watts Andrew A, Tansley Sarah S et al.

To determine the prevalence of anti-drug antibodies (ADAs) in patients with psoriatic arthritis (PsA) treated with biological disease-modifying antirheumatic drugs (bDMARDs) and to evaluate associations with serum drug levels, clinical efficacy and safety. A Preferred Reporting Items for Systematic Reviews and Meta-Analyses-guided systematic review was conducted. MEDLINE, Embase and Cochrane CENTRAL were searched from inception to September 2025. Randomised controlled trials and observational studies reporting ADA measurement in adults with PsA receiving bDMARDs were included. The risk of bias was assessed using the Cochrane Risk of Bias Tool 2 and the Risk of Bias in Non-randomised Studies of Interventions. 28 studies (19 randomised controlled trials and 9 observational studies) were included. ADA prevalence varied widely between bDMARDs and across studies of the same drug and was not directly comparable due to immunoassay heterogeneity. The highest ADA prevalence was observed with adalimumab, infliximab and golimumab followed by ustekinumab, ixekizumab, certolizumab pegol and guselkumab, while secukinumab and etanercept demonstrated very low or absent immunogenicity. Across tumour necrosis factor (TNF) inhibitor studies, ADAs were consistently associated with lower serum drug levels and reduced clinical response, while concomitant methotrexate was associated with lower ADA prevalence. In contrast, serum drug level and clinical outcome data for interleukin (IL)-17, IL-12/23 and IL-23 inhibitors were limited or lacking. Immunogenicity-related adverse events were uncommon, and evidence was insufficient to establish an association with ADAs across bDMARDs. ADA prevalence in PsA varies widely between bDMARDs and across studies of the same bDMARD. ADAs appear most clinically relevant for TNF inhibitors, whereas evidence for other biological classes remains limited. Immunoassay heterogeneity limits comparability, highlighting the need for standardised prospective studies. CRD420251121662.

PMID 42618212
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