Drug Database
ET

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

PubMedFrontiers in pharmacology2026-10-15

Monoclonal antibodies associated IgA nephropathy or other nephropathies.

Miedziaszczyk Miłosz M, Kosiorowski Gracjan G, Kubasik Janusz J, Grabowski Tomasz T et al.

The use of monoclonal antibodies (mAbs) has revolutionized the treatment of autoimmune, inflammatory, and neoplastic diseases. However, accumulating evidence indicates that biologic therapies may be associated with renal adverse events, including various types of glomerulonephritis. The aim of this review was to summarize all reports available in the scientific literature regarding the occurrence of IgA nephropathy after monoclonal antibody treatment. Additionally, the risk of other glomerulonephritis after biologic therapy was discussed. IgA nephropathy (IgAN) is the most commonly reported glomerular lesion associated with monoclonal antibody therapy, particularly with TNF-α inhibitors such as infliximab, adalimumab, golimumab, and etanercept, as well as with immune checkpoint inhibitors targeting the PD-1 (pembrolizumab, nivolumab) and interleukin (ustekinumab) pathways. Proposed mechanisms include immune dysregulation with a shift toward Th2 and Th17-dependent responses, increased production of galactose-deficient IgA1, complement activation, formation of circulating immune complexes, and loss of immune tolerance. In some cases, drug discontinuation and glucocorticoid therapy have resulted in partial or complete disease remission, although progression to end-stage renal disease has also been reported. Due to the potential severity of these complications, initial and periodic monitoring of renal function and urinalysis are recommended in patients receiving monoclonal antibody therapy. Early recognition of renal involvement and prompt treatment modification can improve prognosis.

PMID 42876810
Read full article →
PubMedCompendium of continuing education in dentistry (Jamesburg, N.J. : 1995)2026-10-13

Tumor Necrosis Factor-Alpha Inhibitors: Oral Health and Orthodontic Considerations.

Mahjour Neda N, Hersh Elliot V EV, Jeon Hyeran Helen HH, France Katherine K et al.

Autoimmune diseases affect approximately 4.6% of the US population and are frequently managed with immunomodulatory therapies, including tumor necrosis factor-alpha (TNF-α) inhibitors. These biologic agents, such as infliximab, adalimumab, etanercept, golimumab, and certolizumab pegol, target TNF-α, a key cytokine involved in inflammatory signaling and bone remodeling. While TNF-α inhibitors have demonstrated efficacy in reducing disease activity across a range of autoimmune conditions, their impact on oral health and orthodontic treatment remains underexplored. Clinical studies suggest that TNF-α inhibitors can affect oral health, potentially altering risk of periodontitis, oral infections, and caries. TNF-α also plays a central role in orthodontic tooth movement (OTM), and animal studies suggest that TNF-α inhibition, whether local or systemic, can significantly reduce OTM and root resorption by suppressing osteoclast activity and altering cytokine signaling. This review synthesizes the clinical pharmacology of TNF-α inhibitors, current knowledge of their systemic and oral effects, and their potential influence on OTM.

PMID 42867887
Read full article →
PubMedCureus2026-10-11

Haemophagocytic Lymphohistiocytosis Triggered by Visceral Leishmaniasis Masquerading as Epstein-Barr Virus (EBV)-Associated Haemophagocytic Lymphohistiocytosis in Rheumatoid Arthritis: A Case Report and Literature Review.

Fleurinck Frederik F, Henckaerts Liesbet L, Beckers Mariëlle M, Vanerwegen Eef E et al.

Haemophagocytic lymphohistiocytosis (HLH) is a life-threatening hyperinflammatory syndrome caused by uncontrolled immune activation. In adults, it is usually secondary to an underlying condition, such as infection, malignancy, or autoimmune disease. Identifying this trigger is essential, as treatment depends on the cause. Visceral leishmaniasis (VL) is a systemic parasitic infection that may mimic or trigger HLH, particularly in immunosuppressed patients. We report a 59-year-old man with seropositive rheumatoid arthritis, for which he received immunosuppressive treatment with methotrexate and etanercept. For eosinophilic asthma, he was treated with benralizumab. Four months after travelling to the Valencia region in Spain, the patient presented with high fever, marked splenomegaly and pancytopenia. Further laboratory findings showed progressive hyperferritinaemia, hypofibrinogenaemia, and hypertriglyceridaemia, together with haemophagocytosis on bone marrow examination, which supported the diagnosis of secondary HLH. Because Epstein-Barr virus (EBV) DNA was detected in peripheral blood, EBV-associated HLH was initially suspected, and treatment was started with rituximab, targeting potentially EBV-infected B cells, and dexamethasone to suppress the hyperinflammatory response. Further infectious work-up, however, revealed a strongly positive Leishmania serology. Leishmania polymerase chain reaction on the original bone marrow sample subsequently confirmed VL, despite the absence of amastigotes on Giemsa-stained microscopy. Treatment was redirected to liposomal amphotericin B; further HLH-directed immunosuppressive therapy was withheld, and corticosteroids were tapered. The patient became afebrile and showed progressive recovery of cytopenias and inflammatory markers. Detectable EBV DNA should not preclude investigation for alternative infectious triggers of HLH. In immunosuppressed patients with compatible epidemiological exposure, VL should remain in the differential diagnosis even when bone marrow microscopy is negative, as serology and molecular testing may be required for diagnosis.

PMID 42859823
Read full article →
PubMedInflammopharmacology2026-10-06

Bone and growth safety profiles of biologic and conventional DMARDs in juvenile idiopathic arthritis: a 21-year FAERS disproportionality analysis.

Erdem Fatih F, Gürbüz Nida N

Juvenile idiopathic arthritis (JIA) treatment relies on biologic and conventional disease-modifying anti-rheumatic drugs (b/csDMARDs), but pediatric-specific bone and growth safety remains incompletely characterized. Standard FAERS disproportionality analyses in pediatric polypharmacy may overstate signals through co-medication coding. We aimed to identify drug-specific bone-toxicity (Composite A) and growth/developmental (Composite B) signals and to test whether they survive a Primary-Suspect (PS) restriction designed to isolate reporter-attributed reactions. Pre-specified disproportionality analysis of FAERS Individual Case Safety Reports (2004-2024); pediatric (≤ 17 years) JIA cohort, n = 13,459. Two parallel exposure definitions were applied: PS + SS (Primary or Secondary Suspect, broad) and PS-only (strict). Reporting odds ratios (ROR), proportional reporting ratios with χ2, IC025 and a fixed-prior Bayesian shrinkage estimate were computed; a robust signal required multi-criteria thresholds in both tracks. The PS + SS analysis was independently reproduced in Python and R, with 100% concordance in signal classification. Of 21 drug × composite signals under broad PS + SS analysis, only 5 met the robust-signal definition after PS-only restriction: methotrexate (both composites; bone ROR 2.4, growth ROR 3.7) and infliximab (4.3), tocilizumab (2.8), and abatacept (3.4) for bone toxicity. Etanercept and adalimumab-the two highest-exposure drugs-showed no PS-only signal despite PS + SS Composite A signals. PS + SS magnitudes attenuated by a median 87% under PS-only restriction. Methotrexate was the only drug with robust bone and growth signals, supporting skeletal and growth surveillance during chronic therapy; three biologics showed bone-toxicity signals. In this cohort, conventional PS + SS analysis substantially overstated signal magnitudes, supporting dual-track (PS + SS and PS-only) reporting for pediatric pharmacovigilance.

PMID 42837100
Read full article →
PubMedIndian journal of pediatrics2026-10-05

Clinico-Radiologic Spectrum and Outcomes of Chronic Non-Infectious Osteomyelitis: Experience from India.

Chandola Stuti S, Mallick Sunil Kumar SK, Singla Tanya T, Mridha Asit Ranjan AR et al.

To study the clinical characteristics, radiological features and outcome of children with chronic non-infectious osteomyelitis (CNO). Children diagnosed with CNO (as per the Bristol diagnostic criteria) in between October 2016 to September 2024 were enrolled for this retrospective study. De-identified data from medical records were analysed to study clinico-radiological characteristics, treatment and outcomes. Among 19 children (11 boys) with median (range) age of 11 y (5-13 y), 5 had clinically unifocal osseous disease, while 14 had multifocal involvement. 15 (79%) patients were initially treated as infectious osteomyelitis (bacterial: 9, tubercular: 6). Median (range) delay in diagnosis from symptom onset was 13.5 mo (3-72). Whole-body magnetic resonance imaging (WBMRI) revealed 85 additional lesions than those identified by clinical examination. Clavicle (n = 9) and tibia (n = 20) were most common sites in axial and appendicular skeleton, respectively. Of 66 lesions in long bones, epiphysis, metaphysis, and diaphysis were involved in 11 (16.6%), 28 (42.5%), and 27 (40.9%), respectively. 15 diaphyseal lesions (22.8%) had concomitant metaphyseal involvement (categorised as meta-diaphyseal), while 12 lesions (18.1%) were localised to diaphysis only. Seventeen children opted for treatment at the present centre. Two children were managed with NSAIDS alone, 15 received pamidronate, and one required pamidronate along with steroids and etanercept. Ten patients (66%) achieved clinical remission after the second course of pamidronate. Two children experienced vertebral collapse and one developed left foot valgus deformity. More than half of the patients were treated as presumed infectious osteomyelitis before the definitive diagnosis of CNO. In the present series, 65.3% CNO lesions involved the metaphysis (42.5%) or meta-diaphysis (22.8%) of long bones. 18.1% lesions were restricted to diaphysis in isolation.

PMID 42832130
Read full article →
PubMedOsteoarthritis and cartilage2026-09-30

Combined anti-inflammatory and anti-depressant treatment reduces pain and spinal cord nociceptive and inflammatory markers in a rat discogenic pain model.

Iliff Denise D, Singh Harsev H, Huang Jonathan J JJ, Heggli Irina I et al.

To determine whether a combination therapy targeting spinal inflammation and spinal cord nociceptive and neuroinflammatory processes can improve chronic discogenic pain in a rat model. Chronic discogenic pain was induced in male (n=47) and female (n=20) rats with intervertebral disc (IVD) puncture injury. Duloxetine (20 mg/kg, intraperitoneal daily), a serotonin-norepinephrine reuptake inhibitor (SNRI), Etanercept (5 mg/kg, subcutaneous every three days), a tumor necrosis factor-α (TNFα) inhibitor, their combination, or vehicle were delivered 4-weeks post-injury for 2-weeks. Outcomes included hindpaw mechanical hypersensitivity, voluntary locomotion, IVD height and degeneration and immunostaining in the spine and spinal cord (SC) for Substance P (SubP; nociception), glial fibrillary acidic protein (GFAP; neuronal plasticity), TNFα and ionized calcium-binding adapter molecule 1 (Iba1; neuroinflammation). Random-forest regression identified variables associated with pain. Injury induced persistent mechanical hypersensitivity, IVD degeneration, spinal inflammation, and increased SC markers. Females exhibited higher baseline SC marker expression than male but responded similarly to combination therapy with improved hindpaw withdrawal thresholds in both sexes (males: Δ=21.08 g, 95% CI: 17.75-24.41; females: Δ=20.33 g, 95% CI: 16.90-23.76 vs Vehicle). Duloxetine partially improved mechanical pain, and reduced SC markers, while Etanercept selectively reduced TNFα with minimal behavioral improvement. Machine learning analysis identified SC markers as strongly associated with mechanical hypersensitivity. No treatments improved IVD degeneration or spinal inflammation. Combined Etanercept and Duloxetine treatment improved pain and reduced spinal cord nociceptive and neuroinflammatory markers, suggesting dual-target pharmacotherapy may be a promising strategy for chronic discogenic pain.

PMID 42815615
Read full article →

+8488 more articles available with a free account

Sign up free to view all articles →

Ask about etanercept