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etanercept (Qiangke)

✓ Approved

Shanghai Celgen · TNF · Recombinant Proteins

What is etanercept?

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

Drug Profile

Brand NamesQiangke
CompanyShanghai Celgen
Drug ClassRecombinant Proteins
Molecular TargetTNF
RouteInjectable (Others), Intraarticular Injection, Intravenous (IV), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Shanghai Celgen

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 disordersAnkylosing spondylitis✓ Approved
Skin and subcutaneous tissue disordersPsoriasis✓ Approved
Musculoskeletal and connective tissue disordersPsoriatic arthropathy✓ Approved
Musculoskeletal and connective tissue disordersRheumatoid arthritis✓ Approved
Musculoskeletal and connective tissue disordersJuvenile idiopathic arthritis✓ Approved

Related Research Articles

PubMedScientific reports2026-05-24

Impact of JAK-inhibition on pain and biphasic P2X7R expression on CD4+ T cells in experimental arthritis.

Biton Jérôme J, Hervé Roxane R, Breckler Magali M, Lemeiter Delphine D et al.

Pain improvement is a major unmet need for patients with rheumatoid arthritis (RA). The purinergic receptor P2 X7R may play a central role in inflammatory pain. We aimed to assess the differential effect of Jak and TNF-α inhibition on pain in a collagen-induced arthritis (CIA) mouse model and to decipher mechanisms, focusing on P2X7R. Either a Jak-inhibitor (baricitinib, BARI) or an anti-TNF-α (etanercept, ETN) were administered to CIA mice in early or late phase of arthritis. Pain was evaluated with three independent tests. We assessed P2X7R on leucocytes and IFN-γ, IL-1β, TNF-α, IL-10, IL-6 and IL-17 A concentrations. BARI and ETN decreased joint inflammation and ameliorated histologic destruction and inflammation. When administered in the late phase, ETN and BARI exerted an analgesic effect. P2X7R expression on blood CD4+ T cells was increased in early phase BARI treated mice, and decreased in late phase. When treatments were administered early, percentage of P2 × 7R+ CD4+ T cells inversely correlated with clinical and histological scores, and with IL-6, IL-17 A and IL-1β levels. In conclusion, both BARI and ETN improved pain in a CIA model. The differential expression of P2X7R on CD4+ T cells according to the time of BARI administration may contribute to a better understanding of pain mechanisms in arthritis.

PMID 42177286
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PubMedClinical medicine insights. Arthritis and musculoskeletal disorders2026-05-22

Prescription Pattern and Safety of Biologics in Autoimmune Rheumatologic Diseases in Tertiary Care Hospital of Bihar.

Shakur Adil Ali AA, Kumar Raj R, Ranjan Raushan Kumar RK, Hameed Saajid S et al.

Biologics have revolutionized the treatment of autoimmune rheumatologic diseases, but data on their real-world use and safety in resource-limited settings like Bihar, India, are scarce. This study aimed to evaluate the prescription patterns and safety profile of biologic disease-modifying antirheumatic drugs (b-DMARDs) in patients with rheumatoid arthritis (RA) at a tertiary care hospital in Bihar. A prospective, observational cohort study conducted over 12 months. A total of 120 adult patients with RA prescribed b-DMARDs were enrolled. Data on demographic, clinical characteristics, and treatment details were collected. Disease activity (DAS-28-CRP) and functional status (HAQ-DI) were assessed at baseline and 6 months. Adverse events, particularly infections, were recorded and analysed using multivariable logistic regression to identify risk factors. Biologicals were prescribed in 14.93% patients with RA. Adalimumab (49.17%) was the most prescribed b-DMARD, followed by etanercept (28.33%). Methotrexate was the most common concomitant conventional DMARD (85.83%). All b-DMARDs significantly improved DAS-28-CRP and HAQ-DI scores (P < .0001), with adalimumab showing the greatest improvement. Infliximab had the highest infection rate (53.33%), whereas etanercept had the lowest (14.70%). Regression analysis identified infliximab use (adjusted odds ratio [aOR]: 3.27), concomitant corticosteroid use (aOR: 2.74), and the presence of comorbidities (aOR: 2.13) as significant independent risk factors for infection. Biologic disease-modifying antirheumatic drugs are effective in RA, but infection risks vary. Adalimumab and etanercept demonstrated favourable efficacy and safety profiles, respectively. Treatment decisions should be personalized, considering drug-specific risks, corticosteroid co-therapy, and patient comorbidities, especially in resource-constrained settings.

PMID 42169865
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PubMedKlinische Monatsblatter fur Augenheilkunde2026-05-20

Interface Between Ophthalmology and Rheumatology in Uveitis and Retinal Vasculitis in Adult Patients, When Does Who Need Whom?

Kötter Ina I, Stübiger Nicole N, Deuter Christoph C

BACKGROUND: There is a significant interface between ophthalmology and rheumatology, particularly in uveitis and retinal vasculitis. This will be described in detail here. RESULTS: Analyses of uveitis consultations from university centres in Austria and Germany show that approximately 30% of anterior uveitis cases, 17% of intermediate and posterior uveitis cases, 7% of panuveitis cases, and 20% of retinal vasculitis cases, are associated with an inflammatory rheumatic systemic disease. The most frequent association (30%) is between spondyloarthritis and psoriatic arthritis with anterior uveitis (AAU). In approximately 1.3% of cases of intermediate uveitis, sarcoidosis is present, while in posterior uveitis and panuveitis, Behcet's syndrome (BS) is the most likely cause (2.5% and 12.6%, respectively). Retinal vasculitis is associated with BS in 18% of cases. Easily detectable "red flags" for inflammatory rheumatic diseases and the influence of uveitis on systemic immunomodulatory therapy in rheumatology have been described. For example, in AAU during SPA, monoclonal tumour necrosis factor inhibitors (TNFi) are more effective than etanercept, a fusion protein of the TNF receptor and immunoglobulin Fc segment. IL-17 antagonists and Janus-Kinase (JAK) inhibitors are also able to reduce the risk of uveitis flares, but are less effective than monoclonal TNFi. SUMMARY: Close collaboration between rheumatologists and ophthalmologists is essential, particularly in the treatment of uveitis and retinal vasculitis. Assessment for certain warning signs and determination of specific laboratory parameters are helpful in detecting the association, present in approximately 20% of cases, between uveitis and retinal vasculitis and inflammatory rheumatic systemic diseases, and in referring patients specifically to rheumatology. Conversely, rheumatologists require precise ophthalmological findings and information on treatment response, in order to adjust therapy in a targeted manner or, in cases of ocular symptoms associated with an underlying inflammatory systemic disease, in order to appropriately adapt the therapy to the ocular involvement.

PMID 42155459
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PubMedAnnals of clinical epidemiology2026-05-19

Effect of a financial incentive scheme on promoting prescription of biosimilars: a interrupted time-series analyses.

Morita Takahito T, Sasabuchi Yusuke Y, Yasunaga Hideo H

In Japan, biosimilars have the potential to reduce drug expenditure because their official price is lower than the price of the original products. To promote biosimilars, the Japanese government introduced a new financial incentive scheme for medical institutions to prescribe biosimilars to outpatients in April 2020. However, the impact of the incentive remains unevaluated. Hence, in this study, we conducted an interrupted time-series analysis to evaluate the impact of the incentive scheme on biosimilar prescription. We used the DeSC database in Japan. From this database, we included 3,348 patients who required self-injection and were prescribed insulin, human growth hormone, or etanercept. Interrupted time-series analyses were conducted by fitting Prais-Winsten linear regression models to assess the association of the financial incentive with the outcomes, namely, monthly proportions of biosimilar prescriptions between April 2019 and March 2021. No significant changes were observed in the monthly proportion of biosimilar prescriptions immediately after the introduction of the incentive. The sustained effect, representing the effect of the intervention over time, was also not significant. Our study suggests that the financial incentive introduced in April 2020 in Japan was not associated with an increase in biosimilar prescriptions.

PMID 42153172
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PubMedClinical pharmacology and therapeutics2026-05-15

Ten-Year Public Expenditure Savings Associated with TNF Inhibitor Biosimilars under Australia's Pharmaceutical Benefits Scheme.

Yiu Chin Hang CH, Ianni Bella D BD, Day Richard O RO, Raubenheimer Jacques J et al.

Biologic therapies are a major and growing driver of pharmaceutical expenditure globally, with tumor necrosis factor (TNF) inhibitors among the most widely used and costly biologics. In Australia, these therapies are funded through the Pharmaceutical Benefits Scheme (PBS), where biosimilars offer lower cost alternatives; however, the long-term public expenditure impact of TNF inhibitor biosimilars under regulated pricing systems has not been comprehensively quantified. We conducted a retrospective, population-level expenditure analysis using publicly available PBS Item Reports data from 2015 to 2025 to estimate PBS cost savings associated with the listing of adalimumab, etanercept, and infliximab biosimilars for inflammatory arthritis. Counterfactual scenarios were constructed to estimate expected expenditure in the absence of biosimilar entry, explicitly accounting for key PBS pricing mechanisms, including mandatory price reductions and price-disclosure cycles. Biosimilar listing was associated with cumulative PBS savings of AU$562.3 million over the study period. Etanercept biosimilar generated the largest absolute savings (AU$341.5 million; 23.7% reduction), whereas adalimumab biosimilars generated smaller relative savings (AU$195.3 million; 9.4% reduction), reflecting delayed biosimilar entry despite high utilization. Most savings accrued in rheumatoid arthritis, followed by ankylosing spondylitis and psoriatic arthritis. In conclusion, TNF inhibitor biosimilars were associated with substantial and sustained reductions in public medicine expenditure in Australia. The magnitude of savings varied markedly by molecule and was jointly determined by the timing of biosimilar entry and statutory pricing mechanisms, illustrating how regulated reimbursement systems shape realized biosimilar value.

PMID 42138454
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PubMedTzu chi medical journal2026-05-14

Tumor necrosis factor-alpha-mediated inflammatory bone loss: Pathogenic mechanisms and therapeutic potential of its inhibitors.

Lin Wen-Ying WY, Pan Yu-Jen YJ, Yeh Kuang-Ting KT, Su Kuei-Ying KY et al.

Bone remodeling preserves skeletal integrity through the balanced actions of bone-resorbing osteoclasts and bone-forming osteoblasts, regulated by mechanical, endocrine, and immune signals. Tumor necrosis factor-alpha (TNF-α), a key pro-inflammatory cytokine, disrupts this balance by enhancing osteoclast differentiation and activation in synergy with receptor activator of nuclear factor κB ligand, leading to net bone loss, microarchitectural deterioration, and increased fracture risk. Epidemiological studies consistently demonstrate that TNF-α-mediated inflammatory diseases are associated with systemic reductions in bone mineral density (BMD) and heightened fracture risk. Patients with rheumatoid arthritis have approximately twice the prevalence of osteoporosis compared to the general population. Similarly, individuals with ankylosing spondylitis, psoriatic arthritis, psoriasis, or inflammatory bowel disease often present with generalized BMD loss affecting both axial and appendicular skeletons. Notably, these skeletal deficits are observed even in patients without overt joint destruction, underscoring the systemic nature of TNF-α-driven bone pathology. Biological TNF-α inhibitors - etanercept, infliximab, adalimumab, golimumab, and certolizumab pegol - were primarily developed to control inflammation but have also demonstrated potential skeletal benefits, such as preservation or modest improvement in BMD and favorable modulation of bone turnover markers. This review synthesizes mechanistic and clinical evidence on TNF-α-mediated bone loss across diverse inflammatory diseases, evaluates the bone-protective potential of TNF-α inhibitors, and highlights shared pathogenic mechanisms and therapeutic considerations to guide future research.

PMID 42131412
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