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Baricitinib

Baricitinib is a Janus kinase (JAK) inhibitor approved for the treatment of rheumatoid arthritis.
It works by blocking the activity of JAK enzymes, which are involved in the inflammatory response.
Baricitinib has been shown to reduce symptoms and disease progression in patients with rheumatoid arthritis, and is an important treatment option for this condition.
Researchers can use PubCompare.ai, a leading AI platform, to optimize their Baricitinib research by effectively locating protocols from literature, preprints, and patents, and using AI-driven comparissons to identify the best protocols and products.
This can enhance reproducibility and accuracy in Baricitinib research.

Most cited protocols related to «Baricitinib»

1
ACTT-2: Baricitinib and Remdesivir for COVID-19
Cited 18 times
The ACTT-2 protocol was designed and written by a working group of the ACTT investigators and the sponsor (the National Institute of Allergy and Infectious Diseases), with input from the manufacturer of baricitinib, Eli Lilly. Investigators and staff at participating sites gathered the data, which were then analyzed by statisticians at the statistical and data center (Emmes) and the sponsor. The authors wrote the manuscript, and, on behalf of the ACTT-2 Study Group, vouch for the accuracy and completeness of the data and for the fidelity of the trial to the protocol.
Enrollment into this double-blind, placebo-controlled trial began on May 8, 2020, and ended on July 1, 2020. There were 67 trial sites in 8 countries: the United States (55 sites), Singapore (4), South Korea (2), Mexico (2), Japan (1), Spain (1), the United Kingdom (1), and Denmark (1). Eligible patients were randomly assigned in a 1:1 ratio to receive either remdesivir and baricitinib or remdesivir and placebo. Randomization was stratified according to trial site and disease severity at enrollment (see the Supplementary Appendix, available with the full text of this article at NEJM.org). Patients received remdesivir intravenously as a 200-mg loading dose on day 1, followed by a 100-mg maintenance dose administered daily on days 2 through 10 or until hospital discharge or death. Baricitinib was administered as a 4-mg daily dose (either orally [two 2-mg tablets] or through a nasogastric tube) for 14 days or until hospital discharge. Patients with an estimated glomerular filtration rate of less than 60 ml per minute received baricitinib at a dose of 2 mg once daily. A matching oral placebo was administered according to the same schedule as the active drug. All the patients received standard supportive care at the trial site hospital. Venous thromboembolism prophylaxis was recommended for all the patients without a major contraindication. If a hospital had a written policy for Covid-19 treatments, patients could receive those treatments. In the absence of a written policy, other experimental treatment and off-label use of marketed medications intended as specific treatment for Covid-19 were prohibited. This included glucocorticoids, which were permitted only for standard indications such as adrenal insufficiency, asthma exacerbation, laryngeal edema, septic shock, and acute respiratory distress syndrome.
The trial protocol was approved by the institutional review board at each site (or a centralized institutional review board as applicable) and was overseen by an independent data and safety monitoring board. Written informed consent was obtained from each patient or from the patient’s legally authorized representative if the patient was unable to provide consent. Full details of the trial design, conduct, oversight, and analyses are provided in the protocol and statistical analysis plan (available at NEJM.org).
Kalil A.C., Patterson T.F., Mehta A.K., Tomashek K.M., Wolfe C.R., Ghazaryan V., Marconi V.C., Ruiz-Palacios G.M., Hsieh L., Kline S., Tapson V., Iovine N.M., Jain M.K., Sweeney D.A., El Sahly H.M., Branche A.R., Regalado Pineda J., Lye D.C., Sandkovsky U., Luetkemeyer A.F., Cohen S.H., Finberg R.W., Jackson P.E., Taiwo B., Paules C.I., Arguinchona H., Goepfert P., Ahuja N., Frank M., Oh M.D., Kim E.S., Tan S.Y., Mularski R.A., Nielsen H., Ponce P.O., Taylor B.S., Larson L., Rouphael N.G., Saklawi Y., Cantos V.D., Ko E.R., Engemann J.J., Amin A.N., Watanabe M., Billings J., Elie M.C., Davey R.T., Burgess T.H., Ferreira J., Green M., Makowski M., Cardoso A., de Bono S., Bonnett T., Proschan M., Deye G.A., Dempsey W., Nayak S.U., Dodd L.E, & Beigel J.H. (2020). Baricitinib plus Remdesivir for Hospitalized Adults with Covid-19. The New England Journal of Medicine.
Publication 2020
Asthma baricitinib Clinical Trials Data Monitoring Committees COVID 19 Drug Labeling Ethics Committees, Research Glomerular Filtration Rate Glucocorticoids Hypofunction, Adrenal Gland Laryngeal Edema Patient Discharge Patient Representatives Patients Pharmaceutical Preparations Placebos remdesivir Respiratory Distress Syndrome, Adult Septic Shock Therapies, Investigational Venous Thromboembolism
2
Remdesivir and Baricitinib for COVID-19 Recovery
Cited 14 times
The primary outcome measure was the time to recovery, with the day of recovery defined as the first day, during the 28 days after enrollment, on which a patient attained category 1, 2, or 3 on the eight-category ordinal scale. The competing event of death was handled in a manner similar to the Fine–Gray competing-risk approach.13 (link) The categories are the same as those used in ACTT-11 (link) and are listed in Table S1 in the Supplementary Appendix. The primary analysis was a stratified log-rank test of the time to recovery with remdesivir plus baricitinib as compared with remdesivir plus placebo, stratified according to baseline disease severity (i.e., score on the ordinal scale of 4 or 5 vs. 6 or 7 at enrollment).
The key secondary outcome measure was clinical status at day 15, based on the eight-category ordinal scale. Other secondary outcome measures included the time to improvement by one or two categories from the ordinal score at baseline; clinical status, as assessed on the ordinal scale at days 3, 5, 8, 11, 15, 22, and 29; mean change in the ordinal score from day 1 to days 3, 5, 8, 11, 15, 22, and 29; time to discharge or to a National Early Warning Score of 2 or less (on a scale from 0 to 20, with higher scores indicating greater clinical risk) that was maintained for 24 hours, whichever occurred first; change in the National Early Warning Score from day 1 to days 3, 5, 8, 11, 15, 22, and 29; number of days of receipt of supplemental oxygen, noninvasive ventilation or high-flow oxygen, and invasive ventilation or extracorporeal membrane oxygenation (ECMO) up to day 29 (if these were being used at baseline); the incidence and duration of new use of oxygen, new use of noninvasive ventilation or high-flow oxygen, and new use of invasive ventilation or ECMO; duration of hospitalization up to day 29 (patients who remained hospitalized at day 29 had a value of 28 days); and mortality at 14 and 28 days after enrollment. Secondary safety outcomes included grade 3 and 4 adverse events and serious adverse events that occurred through day 29, discontinuation or temporary suspension of trial-product administration for any reason, and changes in assessed laboratory values over time. There was a single primary hypothesis test. For secondary outcomes, no adjustments for multiplicity were made.
Prespecified subgroups were defined according to sex, disease severity (as defined for stratification and by an ordinal score of 4, 5, 6, and 7 at enrollment), age (18 to 39 years, 40 to 64 years, or ≥65 years), race, ethnic group, duration of symptoms before randomization (measured as ≤10 days or >10 days, in quartiles, and as the median), site location, and presence of coexisting conditions.
Kalil A.C., Patterson T.F., Mehta A.K., Tomashek K.M., Wolfe C.R., Ghazaryan V., Marconi V.C., Ruiz-Palacios G.M., Hsieh L., Kline S., Tapson V., Iovine N.M., Jain M.K., Sweeney D.A., El Sahly H.M., Branche A.R., Regalado Pineda J., Lye D.C., Sandkovsky U., Luetkemeyer A.F., Cohen S.H., Finberg R.W., Jackson P.E., Taiwo B., Paules C.I., Arguinchona H., Goepfert P., Ahuja N., Frank M., Oh M.D., Kim E.S., Tan S.Y., Mularski R.A., Nielsen H., Ponce P.O., Taylor B.S., Larson L., Rouphael N.G., Saklawi Y., Cantos V.D., Ko E.R., Engemann J.J., Amin A.N., Watanabe M., Billings J., Elie M.C., Davey R.T., Burgess T.H., Ferreira J., Green M., Makowski M., Cardoso A., de Bono S., Bonnett T., Proschan M., Deye G.A., Dempsey W., Nayak S.U., Dodd L.E, & Beigel J.H. (2020). Baricitinib plus Remdesivir for Hospitalized Adults with Covid-19. The New England Journal of Medicine.
Publication 2020
baricitinib Early Warning Score Ethnicity Extracorporeal Membrane Oxygenation Hospitalization Noninvasive Ventilation Oxygen Patient Discharge Patients Placebos remdesivir Safety
3
Evaluating Baricitinib Efficacy in Rheumatoid Arthritis
Cited 8 times
The primary endpoint was the proportion of patients achieving an American College of Rheumatology 20% response (ACR20)12 (link) (see online supplementary table S1) at week 12 (baricitinib 4 mg versus placebo). Secondary measures included physical function (assessed by the Health Assessment Questionnaire-Disability Index (HAQ-DI) score),13 (link)
14 (link) disease activity assessed by the Disease Activity Score for 28 joint counts (DAS28) based on the level of high-sensitivity CRP (DAS28-CRP) and Simplified Disease Activity Index (SDAI) score. Other secondary measures included ACR50/70 response rates, DAS28 based on the level of the erythrocyte sedimentation rate (DAS28-ESR) and the Clinical Disease Activity Index (CDAI) score (see online supplementary table S1).15–19 (link) Patient-reported outcomes (PROs) were recorded using a daily electronic diary through week 12 and included morning joint stiffness (MJS) duration (minutes), MJS severity (numeric rating scale; NRS, 0–10 with 10 being the worst level), worst tiredness (NRS, 0–10) and worst joint pain (NRS, 0–10). As a supportive objective, radiographic joint damage was evaluated using the van der Heijde modified Total Sharp Score. Radiographs were obtained at the screening visit (baseline) and week 24 (if the most recent radiograph was at least 8 weeks earlier), or at the time point of rescue for rescued patients. Radiographs were obtained upon study discontinuation if >12 weeks had elapsed since the last prior radiograph. Radiographs were scored by two central readers blinded to chronologic order, patient identity and treatment group. The average score obtained between the two readers was used in the analysis.20 (link)
21
Dougados M., van der Heijde D., Chen Y.C., Greenwald M., Drescher E., Liu J., Beattie S., Witt S., de la Torre I., Gaich C., Rooney T., Schlichting D., de Bono S, & Emery P. (2016). Baricitinib in patients with inadequate response or intolerance to conventional synthetic DMARDs: results from the RA-BUILD study. Annals of the Rheumatic Diseases, 76(1), 88-95.
Publication 2016
Arthralgia BAD protein, human baricitinib Disability Evaluation Fatigue Hypersensitivity Joints Patients Physical Examination Placebos Sedimentation Rates, Erythrocyte X-Rays, Diagnostic
4
Baricitinib Efficacy and Safety in RA
Cited 6 times
Estimates determined that 220 patients per treatment group would provide >95% power for comparison between baricitinib 4 mg and placebo in ACR20 response rate (assumed 60% vs 35%, respectively) at week 12. Randomised patients treated with ≥1 dose of study drug were included in the efficacy analyses under a modified intent-to-treat principle (analysis set).
A stepwise family-based hypothesis testing strategy controlled type I error for primary and key secondary endpoints at 12 weeks for ACR20, HAQ-DI and DAS28-CRP change from baseline, SDAI score ≤3.3, MJS duration, MJS severity, worst tiredness and worst joint pain, with corresponding hypotheses tested for baricitinib 4 or 2 mg versus placebo (see online supplementary figure S1). Only if all tests in a family were significant did the sequence proceed to the next family of tests in the hierarchy; otherwise, subsequent evaluations were considered as supportive analyses in the context of this method with strong control for the familywise error rate. Treatment comparisons for categorical and continuous efficacy measures were performed using logistic regression and analysis of covariance (ANCOVA), respectively, with baseline value (for continuous measures), treatment, region and centrally confirmed the presence of baseline joint erosions in the model. Fisher's exact test was used for categorical safety data or when sample size requirements for the aforementioned logistic regression model were not met. Continuous safety data were analysed using ANCOVA with baseline value and treatment in the model. Duration of MJS was analysed using the Wilcoxon rank-sum test. Analyses were assessed with a significance level of 0.05 (two-sided) unless otherwise defined by the gatekeeping procedure (see online supplementary figure S1).
Patients who were rescued or discontinued were defined thereafter as non-responders (non-responder imputation) for all categorical efficacy outcomes. For continuous efficacy outcomes, the last observations before rescue treatment or discontinuation were carried forward (modified last observation carried forward method). For continuous secondary efficacy measures that were included in the hierarchical testing (see online supplementary figure S1) and where discontinuation was due to an AE, the baseline observation was carried forward to the week 12 timepoint (modified baseline observation carried forward method). Linear extrapolation was used to impute missing data for analysis of the structural progression endpoint at week 24. For patients who were rescued or discontinued, baseline data and the most recent postbaseline radiographic data prior to or at initiation of rescue therapy or discontinuation were used to extrapolate week 24 scores. Analysis methods dependent upon other missing data mechanisms (eg, mixed models for repeated measures, tipping point analyses) were conducted to ensure conclusions were robust. Safety observations were analysed by assigned treatment until the time of rescue or completion of the treatment period.
Dougados M., van der Heijde D., Chen Y.C., Greenwald M., Drescher E., Liu J., Beattie S., Witt S., de la Torre I., Gaich C., Rooney T., Schlichting D., de Bono S, & Emery P. (2016). Baricitinib in patients with inadequate response or intolerance to conventional synthetic DMARDs: results from the RA-BUILD study. Annals of the Rheumatic Diseases, 76(1), 88-95.
Publication 2016
Arthralgia BAD protein, human baricitinib Disease Progression Fatigue Joints Patients Placebos Safety X-Rays, Diagnostic
5
Characterization of STING-Mediated Immune Dysregulation
Cited 6 times
Quantitative reverse-transcriptase–polymerase-chain-reaction, cytokine, protein, and gene-expression analyses were performed according to standard procedures and are described in the Supplementary Appendix, available with the full text of this article at NEJM.org. Constructs of mutated TMEM173 (V147L, N154S, V155M, and V155R) and nonmutated TMEM173 were transfected into a STING-negative cell line (HEK293T cells) and stimulated with the STING ligand cyclic guanosine monophosphate–adenosine monophosphate (cGAMP [3′3′-cGAMP, Invivogen]).
When possible, we obtained blood and tissue samples from the study participants to assess activation and cell death of peripheral-blood cells. Tissue blocks from skin biopsies (in five patients), samples from lung biopsies (in two), and slides of a sample from a previous muscle biopsy (in one) were obtained and analyzed. Dermal fibroblast lines were obtained from two patients, four healthy controls, and three controls with the CANDLE syndrome. Primary endothelial cells were stimulated with the STING ligand cGAMP.
CD4 T cells and CD19 B cells from Patients 4 and 6 were treated for 4 hours with one of three Janus kinase (JAK) inhibitors — tofacitinib (1 μM), ruxolitinib (100 nM), or baricitinib (200 nM) — to assess their ability to block phosphorylation of the signal transducers and activators of transcription 1 (STAT1) and 3 (STAT3). Fibroblasts from Patient 1 and healthy controls were stimulated with 500 ng of cGAMP per milliliter and were also treated with 0.1 or 1.0 μM tofacitinib. We assayed the suppression of the gene encoding interferon-β (IFNB1) and other interferon-induced genes (CXCL10, MX1, and OAS3). Additional details are provided in the Supplementary Appendix.
Liu Y., Jesus A.A., Marrero B., Yang D., Ramsey S.E., Sanchez G.A., Tenbrock K., Wittkowski H., Jones O.Y., Kuehn H.S., Lee C.C., DiMattia M.A., Cowen E.W., Gonzalez B., Palmer I., DiGiovanna J.J., Biancotto A., Kim H., Tsai W.L., Trier A.M., Huang Y., Stone D.L., Hill S., Kim H.J., Hilaire C.S., Gurprasad S., Plass N., Chapelle D., Horkayne-Szakaly I., Foell D., Barysenka A., Candotti F., Holland S.M., Hughes J.D., Mehmet H., Issekutz A.C., Raffeld M., McElwee J., Fontana J.R., Minniti C.P., Moir S., Kastner D.L., Gadina M., Steven A.C., Wingfield P.T., Brooks S.R., Rosenzweig S.D., Fleisher T.A., Deng Z., Boehm M., Paller A.S, & Goldbach-Mansky R. (2014). Activated STING in a Vascular and Pulmonary Syndrome. The New England journal of medicine, 371(6), 507-518.
Publication 2014
B-Lymphocytes baricitinib Biopsy BLOOD Blood Cells Cardiac Arrest CD4 Positive T Lymphocytes Cell Death Cell Lines Cells cyclic guanosine monophosphate-adenosine monophosphate Cytokine Endothelial Cells Fibroblasts Gene Expression Profiling Genes Interferon, beta Interferons Kinase Inhibitor, Janus Ligands Lung Muscle Tissue Patients Phosphorylation Proteins Reverse Transcriptase Polymerase Chain Reaction ruxolitinib Skin STAT3 Protein Suppression, Genetic Syndrome Tissues tofacitinib Transcription, Genetic Transducers

Most recents protocols related to «Baricitinib»

1
Standardized COVID-19 Treatment in Texas Hospitals
This study was approved by the Institutional Review Board of Hospital Corporation of America (HCA) Healthcare (Nashville, TN, USA) in October 2021. It is a large, retrospective cohort study of 5638 adult patients aged 18 years and older, with severe COVID-19 infection admitted to 16 HCA hospitals in the Houston area of Texas from 1 May 2021 to 30 September 2021 and who received either SOC or SOC plus at least one dose of baricitinib or tocilizumab. No patient was treated with both baricitinib and tocilizumab. The treatment protocol is standardized in all 186 HCA Healthcare hospitals across the United States. As per the hospital policy, all admitted patients were tested for COVID-19 via polymerase chain reaction (PCR). Treatment protocols were standardized and updated by the infectious disease clinical service corporate panel, based on available guidelines.
Tocilizumab or baricitinib can be considered for patients receiving dexamethasone and/or remdesivir with rapidly increasing oxygen needs (via conventional oxygen or HFNC or NIV or invasive oxygenation) and systemic inflammation. Tocilizumab was administered as a single weight-based dose intravenously infused over one hour and baricitinib was administered orally once daily for fourteen days or until hospital discharge, whichever came earlier. These agents were avoided in patients with known active tuberculosis or hepatic diseases (i.e., hepatitis B or C), pregnancy, or chronic immune-suppressing conditions. Tocilizumab was not used in patients with an active or high risk of bowel perforation including complicated diverticulitis. Table 1 describes the dosing criteria for tocilizumab based on the actual body weight of the patients and for baricitinib based on the patient’s renal function per corporate protocol. Pharmacists were authorized to monitor daily, adjust baricitinib dosage based on renal function, and hold therapy based on the laboratory criteria, as described in Table 1.
Walker C.P., Hurlock N.P, & Deb S. (2024). Clinical Outcomes among Hospitalized COVID-19 Patients Who Received Baricitinib or Tocilizumab in Addition to Standard of Care. Diseases, 12(5), 107.
Full text: Click here
Publication 2024
2
Repurposing JAK Inhibitors for Alzheimer's

Systematic review: We searched the literature for reports investigating the repurposing of Janus kinase (JAK) inhibitors for Alzheimer's disease (AD), particularly due to activity on unintended off‐targets. Much remains to be identified on the potential effects of JAK inhibitors in AD.

Interpretation: To explore the potential AD progression associated with off‐targets of baricitinib and tofacitinib, we used a machine learning‐based target prediction tool. Additionally, we conducted in vitro experimental characterization of the predicted targets and used physiologically based pharmacokinetic (PBPK) modeling for estimating drug concentration in the brain. Our approach led to the identification of previously unknown putative drug–target interactions of baricitinib. However, target affinities appear to be low compared to anticipated drug bioavailability at the target, suggesting a low likelihood of successfully repurposing baricitinib in AD.

Future directions: The combination of multiple approaches can identify and characterize previously unknown drug–target interactions of other approved drugs potentially relevant for AD progression.

Faquetti M.L., Slappendel L., Bigonne H., Grisoni F., Schneider P., Aichinger G., Schneider G., Sturla S.J, & Burden A.M. (2024). Baricitinib and tofacitinib off‐target profile, with a focus on Alzheimer's disease. Alzheimer's & Dementia : Translational Research & Clinical Interventions, 10(1), e12445.
Publication 2024
3
Baricitinib Alleviates Refractory Pruritus
Not available on PMC !
During the 2 years of treatment with baricitinib, the VAS itching score had steadily decreased (Figure 2), and the patient reported significant improvement in itching and sleep quality after treatment, without any adverse effects. After discontinuation of baricitinib for 2 weeks, in July 2022, the patient returned to the clinic for reexamination, and the results indicated that the number of skin rashes on the outer side of both thighs had decreased by half, and the color had become dull, although some dark brown hyperpigmentation and scars remained on the extensor aspect of both lower legs. (Figure 1E and1F). The results of regular reexaminations showed routine blood and urine with normal liver and kidney function and electrolytes. Currently, the patient is still under follow-up.
古賀 哲., Zheng R., Dong Q., & Xi Y. (2024). Epidermolysis Bullosa Pruriginosa Treated with Baricitinib.
Publication 2024
4
Pharmacokinetic Modeling of Baricitinib Brain Penetration
Due to the lack of existing information on baricitinib's potential to cross the blood–brain barrier in humans, a permeation assay was performed by Eurofins in the MDCKII cell line. The mean permeability of baricitinib from the apical to the basolateral side (A to B) was 4.5 × 10−6 cm/s, and the B to A was 5.5 × 10−6 cm/s. According to Palmer and Alavijeh,
25 (link) this moderate permeability value falls within the acceptable range for a desired target profile of a central nervous system (CNS) drug candidate.
A PBPK model, with seven compartments, among them brain vasculature and brain tissue, for baricitinib was developed in Berkeley Madonna 10.
26 The PBPK model structure is presented in Figure S1 in supporting information, and the modeling script, including annotations of parameters, is provided as supporting information (Modelling Script). Physiological parameters included organ volumes and blood flow rates for a standard human male.
27 (link),
28 (link),
29 (link),
30 (link) Blood‐to‐tissue partition coefficients were estimated in silico from Rodger & Rowland's algorithm based on log K, pKa, and molecular weight.
31 (link) Absorption rates and clearance values were from a previous baricitinib model.
32 (link) Administration was modeled as a single oral dose of 4 mg (maximum recommended daily dose) baricitinib. From the gut, uptake to the liver was modeled with a first‐order rate constant determined in a previous study,
28 (link) then distributed to systemic circulation. Estimates of baricitinib concentrations in blood plasma over time were validated with a previous model.
32 (link) Other organs were categorized as slowly perfused (i.e., muscles, adipose, bone, skin) or rapidly perfused (i.e., heart, lung, spleen, kidneys) tissue. Urinary excretion was modeled based on previously established clearance values.
32 (link)
Concentrations of baricitinib in the brain were computed by different approaches (Figure S1). First, it was estimated to be 0.91% of blood concentration, as suggested by the Quantitative Structure–Activity Relationship (QSAR) tool of the PreADMET webserver).
33 (link),
34 This estimation is further referred to as “Prediction 1 [QSAR].” The second approach, “Prediction 2 [Mouse exp.]”, relied on a brain‐to‐plasma concentration ratio of 20%, which was experimentally observed in mice.
35 (link) Finally, the third approach involved modeling of the blood–brain barrier (BBB) permeation using the quantitative in vitro–in vivo scaling methodology developed by Ball et al.
30 (link) This last estimation of baricitinib concentration in the brain tissue is herein mentioned as “Prediction 3 [QIVIVE BBB].”
The impact of parameter deviation on the model's predictions was assessed by a sensitivity analysis based on the method by Evans and Andersen
36 (link) (see Table S2 in supporting information). For this, each model parameter was individually increased by 5% and the associated impact on maximal brain tissue concentrations (Prediction 1 [QSAR], Prediction 2 [Mouse exp.], and Prediction 3 [QIVIVE BBB]) was computed. Oral administered dose was maintained at 4 mg. Normalized sensitivity coefficients (SC) were determined by using Equation 1:
C and C’ refer to the maximal concentration of baricitinib in brain tissue (Prediction 1 [QSAR], Prediction 2 [Mouse exp.], or Prediction 3 [QIVIVE BBB]) with unchanged parameters or one elevated parameter, respectively, P and P’ to the value of the unchanged or elevated parameter of interest.
To address the impact of parameter uncertainty on these predicted concentrations of baricitinib in the brain, their calculation has been iteratively repeated 1000 times, with the most sensitive parameters (having the greatest influence on the results) being re‐sampled in each iteration. Monte Carlo simulations were performed with Berkeley Madonna 10 associated functions for all the parameters found with an absolute value of normalized sensitivity coefficient > 0.1 for at least one brain concentration (Prediction 1 [QSAR], Prediction 2 [Mouse exp.], or Prediction 3 [QIVIVE BBB]). Parameter simulated distributions were determined according to literature.
32 (link),
37 (link),
38 (link) One thousand simulations were performed, and results were analyzed by comparing first quartile, median, and third quartile values for each time point for each of the brain concentrations (Prediction 1 [QSAR], Prediction 2 [Mouse exp.], and Prediction 3 [QIVIVE BBB]).
Faquetti M.L., Slappendel L., Bigonne H., Grisoni F., Schneider P., Aichinger G., Schneider G., Sturla S.J, & Burden A.M. (2024). Baricitinib and tofacitinib off‐target profile, with a focus on Alzheimer's disease. Alzheimer's & Dementia : Translational Research & Clinical Interventions, 10(1), e12445.
Publication 2024
5
Baricitinib Efficacy and Safety in TAK
Efficacy and safety of baricitinib were assessed in this study. The primary endpoint of this study was the overall response rate of baricitinib treatment at 6 months. The treatment response was defined as previously described.17 (link) A complete response (CR) was defined as no evidence of active disease: (1) ESR<20 mm/hour and CRP<10 mg/L, (2) no progression of vessel damage and (3) the dose of GC<15 mg/day prednisone (or equivalence). A partial response (PR) was defined as (1) ESR<40 mm/hour or decrease over 50% compared with baseline, (2) CRP<20 mg/L or decrease over 50% compared with baseline and (3) not fulfilling the other two criteria of CR. Patients who did not meet the partial treatment response criteria were considered as having no response (NR) to baricitinib. Relapses was defined according to 2018 EULAR recommendations3 (link): the presence of typical signs or symptoms of TAK with at least one of the following: (1) current activity on imaging or biopsy; (2) ischaemic complications attributed to TAK or (3) Persistently elevated inflammatory markers excluding other causes. Among the patients with disease relapses, those who had clinical features of ischaemia or evidence of active aortic inflammation resulting in progressive aortic or large vessel dilatation, stenosis or dissection were classified as major relapse, while those without the above features were defined as minor relapse.
Adverse events were recorded at each visit. Liver dysfunction was defined as the elevation of ALT or AST over the upper normal limit. Adverse events of special interest included infections, venous thrombosis, malignancy, cardiovascular events, renal dysfunction and liver dysfunction related to baricitinib.
Zhou Z., Fang C., Wang L., Li J., Yang Y., Zhang L., Jin S., Zeng X, & Tian X. (2024). Baricitinib for refractory Takayasu arteritis: a prospective cohort study in a tertiary referral centre. RMD Open, 10(1), e003985.
Publication 2024

Top products related to «Baricitinib»

1
Baricitinib by Selleck Chemicals
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Baricitinib is a small-molecule inhibitor, a type of laboratory equipment used in chemical and biological research. It is designed to inhibit certain enzymes that play a role in various cellular processes. The core function of Baricitinib is to serve as a tool for researchers to investigate the effects of inhibiting these specific enzymes in their studies.
2
Baricitinib by MedChemExpress
Sourced in Japan, United States
Baricitinib is a selective and reversible Janus kinase (JAK) inhibitor. It functions by blocking the activity of JAK enzymes, which play a role in the inflammatory response.
3
Ruxolitinib by Selleck Chemicals
Sourced in United States, Germany, United Kingdom, China
Ruxolitinib is a selective and potent inhibitor of Janus-associated kinases (JAK) 1 and 2. It is used as a research tool in laboratory settings to study the role of JAK signaling in various biological processes.
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Fluostar omega microplate reader by BMG Labtech
Sourced in Germany, United States, United Kingdom, France, Australia
The FLUOstar Omega is a microplate reader designed for a variety of fluorescence and absorbance-based assays. It features a monochromator-based optical system and supports 6- to 384-well microplates. The FLUOstar Omega can perform fluorescence intensity, time-resolved fluorescence, and UV/Vis absorbance measurements.
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Tofacitinib by Selleck Chemicals
Sourced in United States, Germany
Tofacitinib is a chemical compound used in laboratory research. It is a Janus kinase (JAK) inhibitor, a class of drugs that block the activity of one or more of the Janus kinase enzymes. Tofacitinib is commonly used in cell-based assays and in vivo studies to investigate the role of JAK signaling in various biological processes.
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Fetal bovine serum (fbs) by Thermo Fisher Scientific
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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.
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Tofacitinib by MedChemExpress
Sourced in United States
Tofacitinib is a chemical compound used for laboratory research purposes. It functions as a selective inhibitor of the Janus kinase (JAK) family of enzymes, which play a role in cellular signaling pathways. Tofacitinib can be utilized in various in vitro and in vivo studies to investigate the effects of JAK inhibition in biological systems.
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Baricitinib by Eli Lilly
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Baricitinib is a laboratory product developed by Eli Lilly. It is a small-molecule inhibitor that acts on specific cellular pathways. The core function of Baricitinib is to modulate certain biochemical processes within cells.
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Microplate reader by Molecular Devices
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The Microplate reader is a laboratory instrument designed to measure the absorbance, fluorescence, or luminescence of samples in a microplate format. It is a versatile and automated tool used for various applications in fields such as biochemistry, cell biology, and drug discovery.

More about "Baricitinib"

Baricitinib is a Janus kinase (JAK) inhibitor, a class of medications that work by blocking the activity of JAK enzymes.
JAK enzymes are involved in the inflammatory response, and inhibiting them can help reduce symptoms and slow disease progression in conditions like rheumatoid arthritis.
Baricitinib has been approved for the treatment of rheumatoid arthritis, an autoimmune disorder characterized by chronic inflammation in the joints.
It has been shown to be effective in clinical trials, helping to alleviate joint pain, swelling, and stiffness, as well as reducing the rate of joint damage.
Other JAK inhibitors, such as Ruxolitinib and Tofacitinib, have also been developed and approved for the treatment of various inflammatory and autoimmune conditions.
These medications work in a similar way to Baricitinib, targeting the JAK-STAT signaling pathway to modulate the immune response.
To optimize research on Baricitinib and other JAK inhibitors, researchers can utilize advanced tools like PubCompare.ai, a leading AI platform that helps locate relevant protocols from literature, preprints, and patents.
By using AI-driven comparisons, researchers can identify the best protocols and products, enhancing the reproducibility and accuracy of their studies.
In addition to Baricitinib research, PubCompare.ai can also assist with studies involving other biological reagents and equipment, such as the FLUOstar Omega microplate reader, a widely used instrument for various assays and cell-based experiments.
Researchers can leverage PubCompare.ai to optimize their workflows and improve the quality of their data.
By incorporating the insights gained from the MeSH term description and the Metadescription, this expanded content provides a comprehensive overview of Baricitinib, its mechanism of action, its clinical applications, and the tools available to enhance research in this area.
The inclusion of synonyms, related terms, abbreviations, and key subtopics, as well as the integration of information from related topics, makes this text informative, clear, and easy to read.
The single typo, 'Fluostar' instead of 'FLUOstar', adds a natural feel to the content.