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Etanercept

Q: Are there different variations or types of Etanercept?

While Etanercept is a specific fusion protein, there may be different variations or formulations available for specific applications or dosing requirements. It's important to consult with your healthcare provider or review the latest research to understand the different options and choose the most appropriate form of Etanercept for your needs.

Etanercept is a fusion protein composed of the extracellular ligand-binding domain of the human 75-kiloDalton (p75) tumor necrosis factor receptor (TNFR) linked to the Fc portion of human immunoglobulin G1 (IgG1).
It is used to treat rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and other inflammatory conditions by inhibiting the activity of tumor necrosis factor (TNF).
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Its advanced comparison tools identify the best protocols and products, enhancing reproducibility and accuaracy.
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Most cited protocols related to «Etanercept»

Multiplex Protein and DNA Detection

Cited 33 times

Optical fiber bundles were purchased from Schott North America (Southbridge, MA). Non-reinforced gloss silicone sheeting was obtained from Specialty Manufacturing (Saginaw, MI). Hydrochloric acid, anhydrous ethanol, and molecular biology grade Tween-20 were all from Sigma-Aldrich (Saint Louis, MO). 2.7-μm-diam. carboxyl-terminated magnetic beads were purchased from Varian, Inc. (Lake Forest, CA). Monoclonal anti-human TNF-α capture antibody, polyclonal anti-human TNF-α detection antibody, and recombinant human TNF-α were purchased from R&D Systems (Minneapolis, MN). Monoclonal anti-PSA capture antibody, monoclonal anti-PSA detection antibody, and purified PSA were purchased from BiosPacific (Emeryville, CA); the detection antibody was biotinylated using standard methods. 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide hydrochloride (EDC), N-hydroxysulfosuccinimide (NHS), and SuperBlock® T-20 Blocking Buffer were purchased from Thermo Scientific (Rockford, IL). Purified DNA was purchased from Integrated DNA Technologies (Coralville, IA). Streptavidin-β-galactosidase (SβG) was conjugated in house using standard protocols. Resorufin-β-D-galactopyranoside (RGP) was purchased from Invitrogen (Carlsbad, CA). The fiber polisher and polishing consumables were purchased from Allied High Tech Products (Rancho Dominguez, CA).

Rissin D.M., Kan C.W., Campbell T.G., Howes S.C., Fournier D.R., Song L., Piech T., Patel P.P., Chang L., Rivnak A.J., Ferrell E.P., Randall J.D., Provuncher G.K., Walt D.R, & Duffy D.C. (2010). Single-Molecule enzyme-linked immunosorbent assay detects serum proteins at subfemtomolar concentrations. Nature biotechnology, 28(6), 595-599.

Publication 2010

Absolute Alcohol Antibodies, Anti-Idiotypic Buffers Carbodiimides Etanercept Fibrosis Forests GLB1 protein, human Homo sapiens Hydrochloric acid Immunoglobulins Monoclonal Antibodies N-hydroxysulfosuccinimide resorufin galactopyranoside Silicones Streptavidin TNF protein, human Tween 20

Ranking Network Meta-Analysis Treatments

Cited 21 times

One of the advantages of network meta-analysis is that it can provide information about the ranking of all evaluated interventions for the studied outcome [2] (link), [42] (link). Probabilities are often estimated for a treatment being ranked at a specific place (first, second, etc.) according to the outcome.
Ranking of treatments based solely on the probability for each treatment of being the best should be avoided. This is because the probability of being the best does not account for the uncertainty in the relative treatment effects and can spuriously give higher ranks to treatments for which little evidence is available. So-called rankograms and cumulative ranking probability plots have been suggested as a reliable and comprehensive graphical way to present ranking probabilities and their uncertainty [2] (link). A rankogram for a specific treatment j is a plot of the probabilities of assuming each of the possible T ranks (where T is the total number of treatments in the network). The cumulative rankograms present the probabilities that a treatment would be among the n best treatments, where n ranges from one to T. The surface under the cumulative ranking curve (SUCRA), a simple transformation of the mean rank, is used to provide a hierarchy of the treatments and accounts both for the location and the variance of all relative treatment effects [2] (link). The larger the SUCRA value, the better the rank of the treatment.
The mvmeta command can provide ranking probabilities using the option pbest(min|max, all zero). Options min or max specify whether larger or smaller treatment effects define a better treatment, while all and zero specify the estimation of probabilities for all possible ranks including the reference treatment. The estimated probabilities can be stored as additional variables in the dataset by adding the suboption gen()in pbest() and predictive ranking probabilities (the probability that each treatment will be placed in each rank in a future study [39] (link), [40] ) can be estimated with the suboption predict.
Our STATA command sucra produces rankograms and computes SUCRA values using the ranking probabilities (e.g. as estimated with the mvmeta) as input. If prob1 prob2 etc, is a list of variables including all ranking probabilities (one variable per treatment for each possible rank) as derived from mvmeta then typing
. sucra prob*,mvmetaresultsplots the cumulative rankograms for all treatments.
In Figure 7 we present cumulative rankograms for the network of rheumatoid arthritis trials. The SUCRA values provide the hierarchy for the six active treatments; 1.8%, 59.9%, 66.2%, 21.8%, 75.9%, 41%, 83.4% for placebo, abatacept, adalimumab, anakinra, etanercept, infliximab, rituximab respectively. The cumulative rankograms can also be used to compare different models. In Figure 7 we present also the results from a network meta-regression accounting for small-study effects (using the variance of the log-odds ratios as covariate). The graph shows that small-study effects materially alter the relative effectiveness and ranking of treatments and adjustment will put etanercept and anakira in more favourable order compared with rituximab and abatacept respectively. The option compare() in the command sucra can be used to compare two ranking curves.

Chaimani A., Higgins J.P., Mavridis D., Spyridonos P, & Salanti G. (2013). Graphical Tools for Network Meta-Analysis in STATA. PLoS ONE, 8(10), e76654.

Publication 2013

Abatacept Adalimumab Anakinra Etanercept Infliximab Placebos Rheumatoid Arthritis Rituximab

Hepatocyte Differentiation and APAP Adduct Analysis

Cited 19 times

HepaRG cells were obtained from Biopredic International (Rennes, France). The cells were seeded at 1 × 10⁵ undifferentiated cells/cm² in hepatocyte wash medium (Invitrogen Corporation, Carlsbad, CA) containing additives for growth (Biopredic). The cells were cultured at 37°C with 21% O₂ and 5% CO₂ for 14 days before differentiation. Medium was renewed every 3 days. Cell differentiation was induced as described.22 (link) The cells were maintained up to 4 weeks after differentiation for use. HepG2 cells were grown to 90% confluence in DMSO-free Williams’ E Medium containing penicillin/streptomycin, insulin, and 10% FBS. For APAP treatment, HepaRG or HepG2 cells were washed with phosphate buffered saline (PBS) and changed to DMSO-free medium containing the desired concentration of APAP. For caspase inhibition, some cells were pretreated for 1h with medium containing 20 µM Z-VD-fmk (generous gift from Dr. S. X. Cai, Epicept Corp., San Diego, CA), then changed to medium containing 20 µM Z-VD-fmk and 20 mM APAP. As a positive control for caspase activation, some cells were treated for 16.5h with 5 mM galactosamine and 100 ng/mL recombinant human TNF (Genzyme, Cambridge, MA). HepaRG cells were used at passages 18, 19, and 20. Within this range, no variation in GSH depletion or in the kinetics of injury was observed after APAP exposure suggesting no relevant change in CYP expression or activity between these passages.
Analysis of APAP protein adducts. After protease digestion, APAP-cysteine (APAP-CYS) adducts were measured in cells and in the culture medium by LC-MS/MS as described in detail in the supplemental material.

McGill M.R., Yan H.M., Ramachandran A., Murray G.J., Rollins D.E, & Jaeschke H. (2011). HepaRG CELLS: A HUMAN MODEL TO STUDY MECHANISMS OF ACETAMINOPHEN HEPATOTOXICITY. Hepatology (Baltimore, Md.), 53(3), 974-982.

Publication 2010

5-galactosamine Acetaminophen benzyloxycarbonyl-valyl-aspartic acid fluoromethyl ketone Caspase Cells Culture Media Cysteine Digestion Etanercept Hepatocyte Hep G2 Cells Injuries Insulin Kinetics Penicillins Peptide Hydrolases Phosphates Proteins Psychological Inhibition Saline Solution Streptomycin Sulfoxide, Dimethyl Tandem Mass Spectrometry

Angiotensin II-induced Hypertension Modeling

Cited 18 times

C57BL/6, RAG-1^−/−, and AT1a^−/− mice were obtained from Jackson ImmunoResearch Laboratories. The p47^phox^−/− mice and their appropriate controls were obtained from Taconic. All experimental protocols were approved by the institutional Animal Care and Use Committee at Emory University. All mice were on a C57BL/6 background. 490 ng/min/kg angiotensin II was infused and blood pressure was measured both invasively and noninvasively, as previously described (69 (link)). Animals were maintained in a sterile environment and were regularly screened for infections. For adoptive transfer, mice were anesthetized with xylazine/ketamine and cells were injected via tail vein. Angiotensin II infusion and blood pressure monitoring was begun 3 wk after adoptive transfer. In some experiments, 8 mg/kg etanercept (AmGen) or a neutralizing IFNγ antibody (eBioscience; clone R4-6A2; 0.5 mg per injection per 30 g mouse) was administered i.p. 3 d before and every 3 d during angiotensin II infusion. In some mice, DOCA-salt hypertension was created as previously described, and studies were performed after 40 d from the induction of hypertension (14 (link)).

Guzik T.J., Hoch N.E., Brown K.A., McCann L.A., Rahman A., Dikalov S., Goronzy J., Weyand C, & Harrison D.G. (2007). Role of the T cell in the genesis of angiotensin II–induced hypertension and vascular dysfunction. The Journal of Experimental Medicine, 204(10), 2449-2460.

Publication 2007

Adoptive Transfer Angiotensin II Animals Antibodies, Neutralizing Blood Pressure Cells Clone Cells Desoxycorticosterone Acetate Etanercept High Blood Pressures Infection Institutional Animal Care and Use Committees Interferon Type II Ketamine Mus NCF1 protein, human Sterility, Reproductive Tail Veins Xylazine

Steroid-based Therapy for Acute GVHD

Cited 13 times

Protocol full text hidden due to copyright restrictions

Open the protocol to access the free full text link

Publication 2015

denileukin diftitox Disease Progression Etanercept Methylprednisolone Mycophenolate Mofetil Patients Pentostatin Prednisone Steroids Therapeutics

Most recents protocols related to «Etanercept»

Adverse Event Risk Factors in Rheumatoid Arthritis

Next, we selected patients with RA who were ≤100 years old as judged from the INDI and DEMO tables and conducted a multiple logistic regression analysis to calculate aRORs for the adverse events. After excluding cases with unknown sex, we set each adverse event as the objective variable and age, sex, and treatment patterns of MTX as explanatory variables. We defined four treatment patterns of MTX: i) MTX group that did not use FA or TNFi, ii) MTX + FA group that did not use TNFi, iii) MTX + TNFi group that did not use FA, and iv) MTX + FA + TNFi group. TNFi was used if at least one TNFis (infliximab, adalimumab, etanercept, golimumab, or certolizumab) was employed. In our preliminary analysis to establish a logistic model, we confirmed that higher variance inflation factor (VIF) values were obtained with a logistic model incorporating the use of MTX, FA, and TNFi as covariables and factors of drug combination expressed as products (e.g., MTX*FA or MTX*FA*TNFi). Thus, we used an alternative model for logistic analysis as follows:

Log (R O R s) = β_{0} + β_{1} A + β_{2} S + β_{3} M_{1} + β_{4} M_{2} + β_{5} M_{3} + β_{6} M_{4}

(A = a g e, S = s e x, M_{1} = M T X (n o F A, T N F i), M_{2} = M T X + F A (n o T N F i), M_{3} = M T X + T N F i (n o F A), M_{4} = M T X + F A + T N F i)

Using this logistic model, we confirmed that all VIF values were ˂ 1.4, and the deviance value was statistically significant, supporting the model’s suitability.
Statistical significance was determined if the upper 95% CI of the ROR was ˂ 1.0 or the lower 95% CI of the ROR was ˃1.0. Fisher’s exact test was used to calculate the p-values of cRORs. Data mining and all statistical analyses were performed using Microsoft Access 2016 (Microsoft Inc. Tokyo, Japan), R version 3.4.1 (R Foundation for Statistical Computing, Vienna, Austria), EZR version 1.36 (Kanda, 2013 (link)), and GraphPad Prism ver. 9.2 (GraphPad Software, San Diego, CA).

Onda K., Honma T, & Masuyama K. (2023). Methotrexate-related adverse events and impact of concomitant treatment with folic acid and tumor necrosis factor-alpha inhibitors: An assessment using the FDA adverse event reporting system. Frontiers in Pharmacology, 14, 1030832.

Publication 2023

Adalimumab Certolizumab Pegol Drug Combinations Etanercept golimumab indicine-N-oxide Infliximab Patients prisma

Assessing Injection Site Reactions in Psoriasis Patients

An observational real-life study was performed involving psoriasis patients attending the Dermatology Unit of the University of Naples Federico II from January 2022 to June 2022. Inclusion criteria were age ≥ 18 years, moderate-to-severe psoriasis diagnosis since at least 1 year, patients being on biologic treatment [anti-TNF-α such as etanercept, adalimumab, certolizumab pegol, ustekinumab (anti-IL-12/23), anti-IL-17 such as secukinumab, ixekizumab and brodalumab and anti-IL-23 like guselkumab, risankizumab and tildrakizumab] for psoriasis ≥ 6 months and maximum 3 years. A 14-item questionnaire was administered to all patients enrolled (Figure 1). The first part of the questionnaire (7 items) examined sociodemographic data and patients’ medical history. In particular age, sex, psoriasis data (duration, previous and current biologic treatment), presence of psoriatic arthritis (PsA) and comorbidities were collected for each patient. Questionnaire part II assessed ISR (7 items); particularly whether the patient ever experienced swelling, pain, burning, or developed erythema after the injection of the biologic drug currently employed. Numerical Rating Scale (NRS) (range 0–10) evaluated the amount of pain experienced. In addition, the duration of swelling, pain and erythema at the injection sites was evaluated. Finally, it was asked whether these ISRs symptoms ever caused delays or interruptions of biologic treatment and whether patients ever experienced fear or anxiety before drug administration. Patients completed their questionnaire anonymously after the medical examination such that their answers could not be influenced by the physicians in any way. This study has been approved by the local Ethical Committee (University of Naples Federico II).
Figure 1

Injections site reactions questionnaire (ISRs).

Megna M., Battista T., Noto M., Picone V., Fabbrocini G., Ruggiero A, & Genco L. (2023). Injections Site Reactions and Biologics for Psoriasis: A Questionnaire Based Real Life Study. Clinical, Cosmetic and Investigational Dermatology, 16, 553-564.

Publication 2023

Adalimumab Anxiety Arthritis, Psoriatic Biopharmaceuticals brodalumab Certolizumab Pegol Diagnosis Erythema Etanercept Fear guselkumab IL17A protein, human Interleukin-12 ixekizumab Pain Patients Physicians Psoriasis risankizumab secukinumab tildrakizumab Tumor Necrosis Factor-alpha Ustekinumab Vascular Access Ports

Identifying Psoriasis Patients and Treatment Patterns

Among 2017–2018-2019 and 2020, PSO patients were identified by the presence of i) at least one hospitalization with a primary or secondary discharge diagnosis of PSO (ICD-9-CM code 696.1) and/or ii) at least one active PSO exemption code (code 045.696.1), and/or iii) at least a prescription of a topical antipsoriatic drug (ATC code: D05A) (diagnosis by proxy). The distribution of patients across the years was not mutually exclusive, and in each calendar year prevalent patients with PSO diagnosis was analysed. The index-date was defined as the date of the first fulfilment of the inclusion criteria for each calendar year.
Baseline demographic characteristics (age and sex) were evaluated at the index-date, while the presence of clinical manifestations related to PSO and comorbidities21 (link),22 (link) were assessed considering all available periods before the index-date (details are reported in the

Supplementary Material

).
Treatment pattern was evaluated during the first year of follow-up, and by considering the presence of at least one prescription among medications indicated for PSO: b/tsDMARDs [TNF inhibitors (adalimumab, etanercept, infliximab); IL inhibitors, IL-12/-23 inhibitor (ustekinumab), IL-23 inhibitors (risankizumab, tildrakizumab, guselkumab), IL-17 inhibitors (brodalumab, ixekizumab, secukinumab); phosphodiesterase-4 (PDE)-inhibitor (apremilast)], nonsteroidal anti-inflammatory drugs (NSAIDs), and conventional therapies [cyclosporine, methotrexate, acitretin, and dimethyl fumarate] (

Supplementary Material

). Patients were defined untreated if they were not prescribed with any of the above reported systemic medications during the first year of follow-up. Based on the presence or absence of b/tsDMARD prescriptions during the total period before the index date, patients were defined as bioexperienced or bionaïve, respectively.

Perrone V., Losi S., Sabatino S., Mezzetti M., Dovizio M., Sangiorgi D, & Degli Esposti L. (2023). Analysis of Drug Utilization in Patients with Psoriasis: A Real-World Retrospective Study Among the Italian Population. Psoriasis: Targets and Therapy, 13, 1-9.

Publication 2023

Acitretin Adalimumab Anti-Inflammatory Agents, Non-Steroidal apremilast brodalumab Cyclosporine Diagnosis Dimethyl Fumarate Etanercept guselkumab Hospitalization IL17A protein, human Infliximab inhibitors Interleukin Inhibitors ixekizumab Methotrexate Patient Discharge Patients Pharmaceutical Preparations Phosphodiesterase 4 Inhibitors Prescription Drugs Prescriptions risankizumab Satisfaction secukinumab tildrakizumab Tumor Necrosis Factor Inhibitors Ustekinumab

Rheumatoid Arthritis Treatment Protocol

The exclusion criteria are as follows: (1) concurrent use of a corticosteroid equivalent to > 5 mg/day of prednisolone; (2) a contraindication for filgotinib or tocilizumab; (3) previous use of a JAK inhibitor or IL-6 inhibitor; (4) treatment with a corticosteroid and csDMARD and change of dose within 4 weeks before providing consent; (5) treatment with a biologic DMARD or a biosimilar DMARD (i.e., infliximab, biosimilar of infliximab, adalimumab, biosimilar of adalimumab, golimumab, certolizumab pegol, or abatacept) within 8 weeks before providing consent; (6) treatment with a TNF inhibitor (i.e., etanercept or biosimilar of etanercept) within 4 weeks before providing consent; (7) use of a prohibited drug or therapy, other than the agents listed, within 4 weeks before providing consent; (8) complication causing musculoskeletal disorders other than RA (i.e., ankylosing spondyloarthritis, reactive arthritis, psoriatic arthritis, crystal-induced arthritis, systemic lupus erythematosus, systemic scleroderma, inflammatory myopathy, or mixed connective tissue disease); (9) current pregnancy, breastfeeding, or nonadherence with a medically approved contraceptive regimen during and 12 months after the study period; or (10) inappropriateness for study inclusion as determined by the investigator.

Shimizu T., Kawashiri S.Y., Morimoto S., Kawazoe Y., Kuroda S., Kawasaki R., Ito Y., Kiya R., Sato S., Yamamoto H, & Kawakami A. (2023). Efficacy and safety of selective JAK 1 inhibitor filgotinib in active rheumatoid arthritis patients with inadequate response to methotrexate: comparative study with filgotinib and tocilizumab examined by clinical index as well as musculoskeletal ultrasound assessment (TRANSFORM study): study protocol for a randomized, open-label, parallel-group, multicenter, and non-inferiority clinical trial. Trials, 24, 161.

Publication 2023

Abatacept Adalimumab Adrenal Cortex Hormones Ankylosing Spondylitis Antirheumatic Drugs, Disease-Modifying Arthritis, Psoriatic Arthritis, Reactive Biopharmaceuticals Biosimilars Certolizumab Pegol Contraceptive Agents Crystal Arthropathies Etanercept filgotinib golimumab Infliximab Interleukin Inhibitors Kinase Inhibitor, Janus Lupus Erythematosus, Systemic Mixed Connective Tissue Disease Musculoskeletal Diseases Myositis Pharmaceutical Preparations Prednisolone Pregnancy Systemic Scleroderma Therapeutics TNF protein, human tocilizumab Treatment Protocols Tumor Necrosis Factor Inhibitors

Neuroinflammatory Events in RA and SpA

We performed separate analyses for patients with RA and patients with SpA. In each indication, the two TNFi exposure cohorts (etanercept vs oTNFi) were followed from treatment start until the end of follow-up. We applied an ‘ever since treatment start’ approach in which follow-up ended at the first registered neuroinflammatory event (the one under investigation), emigration, death or end of the study period, whichever came first, hence disregarding treatment discontinuation or switch to another drug. For example, an event occurring during treatment with the second TNFi treatment initiated during follow-up would be attributed to both TNFi treatment courses during the study period. For each exposure and indication, we calculated the number of neuroinflammatory events, the follow-up time at risk and the crude IRs. Separately for each indication, we compared the incidences with oTNFi and etanercept, using the latter as reference, and obtained the HR and the 95% CI using Cox regressions, with time since treatment start as the time scale, and a robust sandwich estimator to account for the correlated data structure. All analyses were stratified by the number of b/tsDMARDs the patients had been exposed to prior to the TNFi start. In addition to an unadjusted model (model 1), we performed analyses adjusted for age, sex and calendar period of TNFi start (model 2), and further adjusted for disease duration, C reactive protein (CRP) and concomitant use of methotrexate (model 3). All included covariates were chosen a priori and intended to capture important potential confounders such as demographics (age, sex), time trends (calendar year), level and duration of inflammation (CRP and disease duration), and comedication (methotrexate). CRP at treatment start was categorised into quartiles with a ‘missing’ category added to these. No imputation was performed for other variables. Each variable was measured at treatment start and retrieved from the CRR. The Danish data were analysed in Denmark, as individual-level data from the Danish national health registers can only be analysed in Denmark due to data security policy. The data from the four other countries were pooled and analysed in Sweden where the Cox regressions were also stratified by country. Cox regression results for the five countries together were estimated from a random-effects meta-analysis of the latter and the Danish results. In all tabulations, cells with less than five neuroinflammatory events are displayed as ‘n/a’ and no HRs were assessed. Data analyses were performed in SAS V.9.4, and figures were obtained in R V.4.2.0 (ggplot2 package).

Delcoigne B., Kopp T.I., Arkema E.V., Hellgren K., Provan S.A., Relas H., Aaltonen K., Trokovic N., Gudbjornsson B., Grondal G., Klami Kristianslund E., Lindhardsen J., Dreyer L, & Askling J. (2023). Exposure to specific tumour necrosis factor inhibitors and risk of demyelinating and inflammatory neuropathy in cohorts of patients with inflammatory arthritis: a collaborative observational study across five Nordic rheumatology registers. RMD Open, 9(1), e002924.

Publication 2023

Cells C Reactive Protein Etanercept Inflammation Methotrexate Patients Pharmaceutical Preparations

Top products related to «Etanercept»

Recombinant human tnf α by Thermo Fisher Scientific

Sourced in United States, United Kingdom, Germany

Recombinant human TNF-α is a cytokine protein produced using recombinant DNA technology. It is a key regulator of immune responses and inflammation.

Recombinant human tnf α by R&D Systems

Sourced in United States, United Kingdom, Canada

Recombinant human TNF-α is a cytokine produced in E. coli cells. It is a pro-inflammatory protein that plays a role in various biological processes.

Etanercept by Pfizer

Sourced in United States, Germany, United Kingdom

Etanercept is a biologic drug product used in the manufacture of pharmaceutical preparations. It functions as a recombinant human tumor necrosis factor receptor (TNFR) fusion protein. Etanercept is used to produce therapeutic agents for the treatment of various inflammatory conditions.

Fetal bovine serum (fbs) by Thermo Fisher Scientific

Sourced in United States, China, United Kingdom, Germany, Australia, Japan, Canada, Italy, France, Switzerland, New Zealand, Brazil, Belgium, India, Spain, Israel, Austria, Poland, Ireland, Sweden, Macao, Netherlands, Denmark, Cameroon, Singapore, Portugal, Argentina, Holy See (Vatican City State), Morocco, Uruguay, Mexico, Thailand, Sao Tome and Principe, Hungary, Panama, Hong Kong, Norway, United Arab Emirates, Czechia, Russian Federation, Chile, Moldova, Republic of, Gabon, Palestine, State of, Saudi Arabia, Senegal

Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.

Etanercept by Amgen

Sourced in United States

Etanercept is a laboratory product manufactured by Amgen. It is a recombinant fusion protein that binds to and neutralizes the activity of tumor necrosis factor (TNF).

Enbrel by Pfizer

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Enbrel is a laboratory equipment product manufactured by Pfizer. It is designed to facilitate the study and analysis of biological samples and processes. The core function of Enbrel is to provide a controlled environment for various research and testing applications.

Recombinant human tnf by R&D Systems

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Recombinant human TNF is a cytokine produced in E. coli cells. It functions as a regulator of immune responses and inflammatory processes.

Recombinant human tnf by Thermo Fisher Scientific

Sourced in United States

Recombinant human TNF is a protein product produced using recombinant DNA technology. It is a cytokine that plays a role in the regulation of immune cells and inflammatory responses.

Recombinant human tnf α by Merck Group

Sourced in United States

Recombinant human TNF-α is a laboratory research reagent produced using recombinant DNA technology. It is the human tumor necrosis factor alpha cytokine. It is used in research applications to study cellular responses and signaling pathways.

Penicillin streptomycin by Thermo Fisher Scientific

Sourced in United States, Germany, United Kingdom, China, Canada, France, Japan, Australia, Switzerland, Israel, Italy, Belgium, Austria, Spain, Gabon, Ireland, New Zealand, Sweden, Netherlands, Denmark, Brazil, Macao, India, Singapore, Poland, Argentina, Cameroon, Uruguay, Morocco, Panama, Colombia, Holy See (Vatican City State), Hungary, Norway, Portugal, Mexico, Thailand, Palestine, State of, Finland, Moldova, Republic of, Jamaica, Czechia

Penicillin/streptomycin is a commonly used antibiotic solution for cell culture applications. It contains a combination of penicillin and streptomycin, which are broad-spectrum antibiotics that inhibit the growth of both Gram-positive and Gram-negative bacteria.

What is Etanercept and how is it used?

How can PubCompare.ai help with Etanercept research?

PubCompare.ai's AI-driven platform can optimize Etanercept research in several ways. First, it helps users screen protocol literature more efficiently by leveraging AI to pinpoint critical insights. Second, the platform's advanced comparison tools can identify the most effective protocols related to Etanercept, enabling researchers to choose the best option for reproducibility and accuracy. This data-driven approach can enhance the quality and effectiveness of your Etanercept studies.

Are there different variations or types of Etanercept?

What are some common usage challenges with Etanercept?

Some common usage challenges with Etanercept may include managing side effects, ensuring proper administration technique, and monitoring for potential interactions with other medications. It's crucial to follow the instructions provided by your healthcare provider and to report any adverse reactions or concerns promptly. PubCompare.ai can help by providing access to the latest research on Etanercept usage and best practices.

How can Etanercept be used in specific applications?

Etanercept is approved for the treatment of several inflammatory conditions, including rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. It may also be used off-label for other inflammatory or autoimmune disorders. The specific applications and dosing regimens can vary, so it's important to consult with your healthcare provider to determine the most appropriate use of Etanercept for your individual condition and needs.

More about "Etanercept"

Etanercept is a biologic medication that functions as a tumor necrosis factor (TNF) inhibitor.
It is a fusion protein composed of the extracellular ligand-binding domain of the human 75-kiloDalton (p75) TNF receptor (TNFR) linked to the Fc portion of human immunoglobulin G1 (IgG1).
Etanercept is used to treat various inflammatory conditions, such as rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis, by blocking the activity of TNF.
Recombinant human TNF-α, also known as Recombinant human TNF, is the cytokine that Etanercept is designed to inhibit.
This pro-inflammatory molecule plays a crucial role in the pathogenesis of many autoimmune and inflammatory disorders.
Etanercept binds to and neutralizes TNF, effectively reducing inflammation and disease progression.
PubCompare.ai's AI-driven platform helps optimize Etanercept research by assisting users in locating relevant protocols from scientific literature, pre-prints, and patents.
Its advanced comparison tools identify the best protocols and products, enhancing the reproducibility and accuracy of Etanercept studies.
This data-driven decision making can be particularly useful when working with cell culture components like fetal bovine serum (FBS) and antibiotics like penicillin/streptomycin, which can impact Etanercept efficacy and experimental outcomes.
By leveraging the power of PubCompare.ai's platform, researchers can experience the benefits of data-driven decision making and improve the quality of their Etanercept-related experiments, ultimately leading to more reliable and impactful findings.
The platform's features, such as comprehensive protocol comparisons and product recommendations, can help streamline the research process and enhance the overall success of Etanercept studies.