Microarray analysis was performed on 4 groups of 72hpf embryos: 1) WT, 2) mitf-BRAFV600E, 3) p53-/- or 4) mitf-BRAFV600E;p53-/-. Arrays were similarly performed on adult mitf-BRAFV600E;p53-/- melanomas and adjacent skin. The transcriptional signature of the melanomas was used in GSEA to identify genes significantly enriched in the mitf-BRAFV600E;p53-/- embryos. This signature (123 genes), enriched for markers of the neural crest, were concordantly up/downregulated in both BRAFV600E;p53-/- embryos and tumors. In situ hybridization (ISH) for crestin (a pan NC marker) and other NC genes, was examined in embryos (24-72hpf) and adult tumors. Chemical screening was performed to identify suppressors of the crestin+ lineage by treating wild-type embryos from 50% epiboly to 24hpf, followed by robotic ISH. Two inhibitors of DHODH abrogated crestin expression: NSC210627 and leflunomide. The latter was used for further studies due to more widespread availability. The effect of leflunomide on zebrafish embryonic neural crest development was assessed by scoring for embryonic melanocytes, iridophores, and glial cells. Leflunomide was further assessed for its ability to affect multipotent self-renewal of purified p75+α4+ rat neural crest stem cells. The effects of leflunomide on transcriptional elongation in the neural crest was tested using the spt5m806 allele, and measuring pigmentation in response to 3-5uM leflunomide. Elongation in melanoma cells was assayed by ChIP-Seq using an antibody to RNA Polymerase II and measuring the traveling ratio. Leflunomide was tested for anti-melanoma effects in human melanoma cells lines in the presence or absence of the BRAFV600E inhibitor PLX4720. In vitro proliferation assays were performed using the CellTiterGlo system (Promega). In vivo effects were tested by treatment of established A375 xenografts by daily intraperitoneal dosing of PLX4720 alone, leflunomide alone or the combination, and tumor growth rate measured on day 4, 7 and 12.
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Leflunomide
Leflunomide
Leflunomide is an immunomodulatory drug used to treat rheumatoid arthritis and other autoimmune disorders.
It works by inhibiting pyrimidine synthesis, which disrupts proliferation of activated lymphocytes.
Leflunomide has been shown to reduce symptoms and slow disease progression in clinical trials.
Researchers can use PubCompare.ai to optimize their Leflunomide protocols, identifying the most reproducible and effective methods from the literature, preprints, and patents.
This AI-powered tool empowers scientific discoveries by comparing protocols and locating the best approaches for Leflunomide research.
It works by inhibiting pyrimidine synthesis, which disrupts proliferation of activated lymphocytes.
Leflunomide has been shown to reduce symptoms and slow disease progression in clinical trials.
Researchers can use PubCompare.ai to optimize their Leflunomide protocols, identifying the most reproducible and effective methods from the literature, preprints, and patents.
This AI-powered tool empowers scientific discoveries by comparing protocols and locating the best approaches for Leflunomide research.
Most cited protocols related to «Leflunomide»
Adult
Alleles
Biological Assay
Cell Lines
Cells
Chromatin Immunoprecipitation Sequencing
Dihydroorotate Dehydrogenase
Embryo
Embryonic Development
Genes
Heterografts
Homo sapiens
Immunoglobulins
inhibitors
In Situ Hybridization
Leflunomide
Melanocyte
Melanoma
Microarray Analysis
MITF protein, human
Neoplasms
Neural Crest
Neuroglia
Pigmentation
PLX 4720
Promega
RNA Polymerase II
Skin
Stem Cell Self-Renewal
Transcription, Genetic
Transcription Elongation, Genetic
Zebrafish
After obtaining Institutional Review Board approval, we used data from a cohort of patients diagnosed with RA by a rheumatologist on the basis of the American College of Rheumatology 1987 criteria [21 (link)]. These patients were participants in the longitudinal Department of Veterans Affairs (VA) RA registry (VARA), which has been described elsewhere [22 (link)]. All VARA participants provided their written informed consent. VARA contains demographic, clinical and RA-specific information, including the Disease Activity Score using 28 joint counts (DAS28), as assessed by physicians using the DAS28 [23 (link)] and the Clinical Disease Activity Index (CDAI) [24 (link)], as well as a biorepository with banked DNA, serum and plasma. VARA data have been collected by rheumatologists at 11 VHA facilities throughout the United States since 2003. We linked VARA participants to the Veterans Health Administration's Medical SAS Datasets present in the VHA administrative databases from 2002 to 2010 to obtain medical and pharmacy claims.
Among VARA enrollees, we used claims data to identify eligible individuals in whom a biologic agent had been initiated. Biologics of interest included abatacept, adalimumab, etanercept, infliximab and rituximab. We defined "initiation" as no prior use of that biologic agent during the past 6 months. Eligible participants must have had a baseline VARA visit on the same day or within 1 month of biologic initiation. The date of initiation of the biologic (the index date) defined the start of a 1-year "treatment episode." To confirm that patients were receiving medications through the VA system, eligible individuals must have filled at least one prescription (of any duration) for any oral medication during the 6 to 12 months prior to the index date. Participants must also have had a follow-up VARA visit that occurred at 1 year ± 2 months after the index date. If there was no VARA visit at 1 year, then these treatment episodes were excluded, as there was no clinical gold standard with which to compare the algorithm's performance. VARA data were used only to capture the DAS28, the CDAI and other clinical characteristics measured at the baseline and outcome VARA visits. All other data used for the analysis were abstracted from the administrative claims data.
To test the performance of the effectiveness algorithm and to see whether it was similar for nonbiologic RA treatments, we performed a separate analysis of RA patients enrolled in VARA who were starting leflunomide (LEF), sulfasalazine (SSZ) or hydroxychloroquine (HCQ) and who also had any prior or current use of methotrexate (MTX). New MTX users were not represented in this analysis, because MTX is typically considered an "anchor" drug for RA patients and generally is continued even if the patient's therapeutic response is suboptimal, in contrast to other RA therapies, where the drugs are typically discontinued if they are not effective. Because of similarities in both the descriptive characteristics of the study populations of biologic and nonbiologic disease-modifying anti-rheumatic drug(DMARD) users and the performance characteristics of the effectiveness algorithm between biologic and DMARD treatment episodes, the data are shown throughout for the biologic users as a unique group and for a combined group of new biologic and nonbiologic DMARD users.
Among VARA enrollees, we used claims data to identify eligible individuals in whom a biologic agent had been initiated. Biologics of interest included abatacept, adalimumab, etanercept, infliximab and rituximab. We defined "initiation" as no prior use of that biologic agent during the past 6 months. Eligible participants must have had a baseline VARA visit on the same day or within 1 month of biologic initiation. The date of initiation of the biologic (the index date) defined the start of a 1-year "treatment episode." To confirm that patients were receiving medications through the VA system, eligible individuals must have filled at least one prescription (of any duration) for any oral medication during the 6 to 12 months prior to the index date. Participants must also have had a follow-up VARA visit that occurred at 1 year ± 2 months after the index date. If there was no VARA visit at 1 year, then these treatment episodes were excluded, as there was no clinical gold standard with which to compare the algorithm's performance. VARA data were used only to capture the DAS28, the CDAI and other clinical characteristics measured at the baseline and outcome VARA visits. All other data used for the analysis were abstracted from the administrative claims data.
To test the performance of the effectiveness algorithm and to see whether it was similar for nonbiologic RA treatments, we performed a separate analysis of RA patients enrolled in VARA who were starting leflunomide (LEF), sulfasalazine (SSZ) or hydroxychloroquine (HCQ) and who also had any prior or current use of methotrexate (MTX). New MTX users were not represented in this analysis, because MTX is typically considered an "anchor" drug for RA patients and generally is continued even if the patient's therapeutic response is suboptimal, in contrast to other RA therapies, where the drugs are typically discontinued if they are not effective. Because of similarities in both the descriptive characteristics of the study populations of biologic and nonbiologic disease-modifying anti-rheumatic drug(DMARD) users and the performance characteristics of the effectiveness algorithm between biologic and DMARD treatment episodes, the data are shown throughout for the biologic users as a unique group and for a combined group of new biologic and nonbiologic DMARD users.
Abatacept
Adalimumab
Antirheumatic Drugs, Disease-Modifying
Biological Factors
Biopharmaceuticals
DNA, A-Form
Etanercept
Ethics Committees, Research
Gold
Healthy Volunteers
Hydroxychloroquine
Infliximab
Joints
Leflunomide
Methotrexate
Patients
Pharmaceutical Preparations
Physicians
Plasma
Rheumatologist
Rituximab
Serum
Sulfasalazine
Veterans
Abatacept
Adalimumab
Anabolism
Anakinra
Antirheumatic Drugs, Disease-Modifying
Azathioprine
Biological Factors
Certolizumab Pegol
Cyclosporine
Etanercept
Gold
Gold Compounds
golimumab
Hepatitis A
Hydroxychloroquine
Immunization
Infliximab
Leflunomide
Methotrexate
Minocycline
Organic Chemicals
Rituximab
Safety
Sulfasalazine
tocilizumab
Adrenal Cortex Hormones
Anti-Cyclic Citrullinated Protein Antibodies
Anti-Inflammatory Agents, Non-Steroidal
Diagnosis
Foot
Infection
Joints
Leflunomide
Pharmaceutical Preparations
Prednisone
Rheumatoid Factor
Test, Skin
Therapies, Biological
Wrist
X-Rays, Diagnostic
Abatacept
Adalimumab
Anakinra
Antirheumatic Drugs, Disease-Modifying
Azathioprine
Biopharmaceuticals
Cyclophosphamide
Cyclosporine
Diagnosis
Etanercept
Gold
Hydroxychloroquine
Infliximab
Leflunomide
Methotrexate
Minocycline
Patients
Penicillamine
Pharmaceutical Preparations
Physicians
RCE1 protein, human
Rituximab
Staphylococcal Protein A
Sulfasalazine
Most recents protocols related to «Leflunomide»
Patients with JIA were enrolled at the University Medical Center Utrecht (The Netherlands) (Supplementary file 1 ). A total of nine JIA patients were included in this study. Of these, n=2 were diagnosed with extended oligo JIA, n=2 with rheumatoid factor negative poly-articular JIA, and n=5 with oligo JIA, according to the revised criteria for JIA (Petty et al., 1998 (link)). The average age at the time of inclusion was 13.1 years (range 3.2–18.1 years) with a disease duration of 7.3 years (range 0.4–14.2 years). Patients included for CyTOF and TCR sequencing analysis of two affected knee joints were all treated with non-steroidal anti-inflammatory drugs (NSAIDs) or methotrexate, but no biologicals at the time of sampling. For sequential TCR sequencing analysis, we included patients with a relapsing disease course. At the first time point, all patients were treated with NSAIDs or methotrexate, but no biologicals. During the follow-up (after experiencing a relapse of disease), patients were treated with disease-modifying anti-rheumatic drugs (leflunomide) and/or biologicals (humira).
PB of JIA patients was obtained via veni-puncture or intravenous drip, while SF was obtained by therapeutic joint aspiration of affected joints. Informed consent was obtained from all patients either directly or from parents/guardians when the patients were younger than 12 years of age. The study was conducted in accordance with the Institutional Review Board of the University Medical Center Utrecht (approval no. 11-499/C), in compliance with the Declaration of Helsinki. PB from n=3 healthy children (average age 15.1 years with range 14.7–15.4 years) was obtained from a cohort of control subjects for a case-control clinical study (Supplementary file 1 ).
PB of JIA patients was obtained via veni-puncture or intravenous drip, while SF was obtained by therapeutic joint aspiration of affected joints. Informed consent was obtained from all patients either directly or from parents/guardians when the patients were younger than 12 years of age. The study was conducted in accordance with the Institutional Review Board of the University Medical Center Utrecht (approval no. 11-499/C), in compliance with the Declaration of Helsinki. PB from n=3 healthy children (average age 15.1 years with range 14.7–15.4 years) was obtained from a cohort of control subjects for a case-control clinical study (
Anti-Inflammatory Agents, Non-Steroidal
Antirheumatic Drugs, Disease-Modifying
Arthrocentesis
Biological Factors
Child
Disease Progression
Ethics Committees, Research
Humira
Joints
Knee Joint
Leflunomide
Legal Guardians
Methotrexate
Oligonucleotides
Parent
Patients
Poly A
Punctures
Relapse
Rheumatoid Factor
Sequence Analysis
Therapeutics
Youth
This prospective observational study was carried out in the Department of Pharmacology in a tertiary care institute over a period of one year after approval from the Institutional Ethics Committee (All India Institute of Medical Sciences (AIIMS), Rishikesh) (approval number AIIMS/IEC/18/160). Our study followed the principles of the Declaration of Helsinki. Subjects were recruited from patients presenting to the Rheumatology Outpatient Department (OPD) with a primary diagnosis of RA after obtaining written informed consent. Inclusion criteria were all new and previously diagnosed patients with rheumatoid arthritis based on the American College of Rheumatology (ACR) 2010 diagnostic criteria of either sex. Patients excluded from this study included those affected with arthritis due to reasons other than RA, such as vasculitis, polymyalgia rheumatica, spondyloarthropathies (reactive arthritis, ankylosing spondylitis, and psoriatic arthritis), bacterial arthritis, and fibromyalgia.
On the basis of DMARD therapy being received by the patients, they were divided into different groups: Regimen 1, monotherapy with one DMARD (methotrexate (MTX)); Regimen 2, double DMARD therapy or two DMARD therapy (methotrexate + hydroxychloroquine (MTX + HCQ)); Regimen 3, triple DMARD therapy or three DMARD therapy (methotrexate + hydroxychloroquine + leflunomide (MTX + HCQ + Lef)); and Regimen 4, >3 DMARD therapy (MTX + HCQ + Lef + bDMARD adalimumab). Patients were assessed at baseline and after the follow-up visit as per the clinician’s discretion (varying from 7 to 12 weeks). Treatment response was recorded at the baseline and follow-up visit based on the Disease Activity Score (DAS28) criteria, which comprises a number of tender joints, swollen joints, erythrocyte sedimentation rate (ESR), and “patient global health” score [10 (link)].
The medication cost of DMARD therapy was analyzed by calculating the cost of therapy per month for each patient by taking the prices from the Bureau of Pharma Public Sector Undertakings of India (BPPI), Department of Pharmaceuticals, Government of India, for all the DMARDs, except the biological drug for which the price from Cadila Healthcare Ltd. (Zydus Cadila, Ahmedabad, India) was taken. Cost-effectiveness was calculated by dividing the cost of therapy by the change in DAS in a month. Adherence was assessed using the Morisky-Green-Levine Scale (MGLS) [11 (link)]. Patients were interviewed and asked to answer four questions listed in the questionnaire on their second visit. High adherence was denoted by a score of 0, medium adherence was denoted by a score of 1 or 2, and low adherence was denoted by a score of 3 or 4. The p value was taken to be 0.05. For the cost-effective analysis, the mean was applied to the DAS28 values and the cost of treatment. Statistical analysis was performed using the Statistical Package for the Social Sciences (SPSS) software (IBM SPSS Statistics, Armonk, NY, USA).
On the basis of DMARD therapy being received by the patients, they were divided into different groups: Regimen 1, monotherapy with one DMARD (methotrexate (MTX)); Regimen 2, double DMARD therapy or two DMARD therapy (methotrexate + hydroxychloroquine (MTX + HCQ)); Regimen 3, triple DMARD therapy or three DMARD therapy (methotrexate + hydroxychloroquine + leflunomide (MTX + HCQ + Lef)); and Regimen 4, >3 DMARD therapy (MTX + HCQ + Lef + bDMARD adalimumab). Patients were assessed at baseline and after the follow-up visit as per the clinician’s discretion (varying from 7 to 12 weeks). Treatment response was recorded at the baseline and follow-up visit based on the Disease Activity Score (DAS28) criteria, which comprises a number of tender joints, swollen joints, erythrocyte sedimentation rate (ESR), and “patient global health” score [10 (link)].
The medication cost of DMARD therapy was analyzed by calculating the cost of therapy per month for each patient by taking the prices from the Bureau of Pharma Public Sector Undertakings of India (BPPI), Department of Pharmaceuticals, Government of India, for all the DMARDs, except the biological drug for which the price from Cadila Healthcare Ltd. (Zydus Cadila, Ahmedabad, India) was taken. Cost-effectiveness was calculated by dividing the cost of therapy by the change in DAS in a month. Adherence was assessed using the Morisky-Green-Levine Scale (MGLS) [11 (link)]. Patients were interviewed and asked to answer four questions listed in the questionnaire on their second visit. High adherence was denoted by a score of 0, medium adherence was denoted by a score of 1 or 2, and low adherence was denoted by a score of 3 or 4. The p value was taken to be 0.05. For the cost-effective analysis, the mean was applied to the DAS28 values and the cost of treatment. Statistical analysis was performed using the Statistical Package for the Social Sciences (SPSS) software (IBM SPSS Statistics, Armonk, NY, USA).
Adalimumab
Ankylosing Spondylitis
Antirheumatic Drugs, Disease-Modifying
Arthritis
Arthritis, Bacterial
Arthritis, Psoriatic
Arthritis, Reactive
Biopharmaceuticals
Diagnosis
Fibromyalgia
Institutional Ethics Committees
Joints
Leflunomide
Methotrexate
Outpatients
Patients
Pharmaceutical Preparations
Pharmacotherapy
Polymyalgia Rheumatica
Public Sector
Rheumatoid Arthritis
Sedimentation Rates, Erythrocyte
Spondylarthropathies
Therapeutics
Treatment Protocols
Vasculitis
In the First Affiliated Hospital of Anhui University of Chinese Medicine, the basic drugs for treating RA consist of cDMARDs (including methotrexate, leflunomide, sulfasalazine, and hydroxychloroquine sulfate), nonsteroidal anti-inflammatory drugs (including celecoxib, meloxicam, and lornoxicam), and glucocorticoids (methylprednisolone). It should be noted that TCM is a commonly used treatment means in TCM hospitals. We gradually withdrew the use of biologics by increasing the use of TCM.
Anti-Inflammatory Agents, Non-Steroidal
Biological Factors
Celecoxib
Chinese
Glucocorticoids
Hospital Administration
Hydroxychloroquine Sulfate
Leflunomide
lornoxicam
Meloxicam
Methotrexate
Methylprednisolone
Pharmaceutical Preparations
Sulfasalazine
The retrospective cohort study was performed with data retrieved from Lithuanian compulsory health insurance information system database SVEIDRA. This is a population-based database that has been running since 1995 and registers all patients’ visits to healthcare institutions, the established diagnoses, and the prescriptions of state-reimbursed medications to all residents of Lithuania. The Vilnius Regional Bioethics Committee approved assessing these data and conducting the study (approval number: 158200-17-958-462, approval date: 7 November 2017).
Information about all patients who had been newly diagnosed with inflammatory RD during the period between 1 January 2012 and 31 December 2019 was obtained from SVEIDRA. Patients with RA, SPA (psoriatic arthritis (PsA), ankylosing spondylitis, and undifferentiated SPA), systemic CTD, and vasculitis were included. Information about the prescription of state-reimbursed medication such as glucocorticoids, conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) (hydrochloroquine, sulfasalazine, methotrexate, azathioprine, leflunomide), or biological disease-modifying antirheumatic drugs (bDMARDs) (etanercept, adalimumab, infliximab, tocilizumab or rituximab with available biosimilars) was used for the verification of RD cases.
A total of 95,289 RD cases with a first-time diagnosis of inflammatory RD established between 2012 and 2019 were selected. A case was considered first-time-diagnosed if the patient had had at least 1 year of no previous RD record in the database. As no data preceding 2012 were available, we excluded 22,526 first-time diagnoses in 2012 from the total cohort, as it was not possible to verify their RD diagnosis prior to the index date.
We excluded 2251 cases from the cohort because they were younger than 18 years old at the time of diagnosis, and 10 because of an unidentifiable identification code. To verify the cases, we excluded 58,866 patients with no records of at least one prescription of state-reimbursed medications for RD (glucocorticoids, csDMARDs, or bDMARDs).
The final 11,636 cases were cross-checked with the death registry of the health Information center at the Institute of Hygiene, and the date and cause of death were obtained if the death had occurred between 2013 and 2021. The cases were cross-checked using personal identification codes. The principal causes of death were compared between the prepandemic and pandemic time periods, and grouped under the following categories: deaths because of cardiovascular and circulatory causes, malignancies, infections, respiratory causes, musculoskeletal diseases, external causes of death, and unspecified causes of death. COVID-19, as a recorded cause of death, was only calculated in the pandemic period.
The final dataset used for analysis included sex, age, the ICD-10 code of RD, the date of RD diagnosis, the date and cause of death if applicable, and information about the prescription of state-reimbursed drugs.
For the comparison with the general population of Lithuania, information on the adult population census in 2013–2021 was obtained from Statistics Lithuania (www.stat.gov.lt , accessed on 27 November 2022).
Information about all patients who had been newly diagnosed with inflammatory RD during the period between 1 January 2012 and 31 December 2019 was obtained from SVEIDRA. Patients with RA, SPA (psoriatic arthritis (PsA), ankylosing spondylitis, and undifferentiated SPA), systemic CTD, and vasculitis were included. Information about the prescription of state-reimbursed medication such as glucocorticoids, conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) (hydrochloroquine, sulfasalazine, methotrexate, azathioprine, leflunomide), or biological disease-modifying antirheumatic drugs (bDMARDs) (etanercept, adalimumab, infliximab, tocilizumab or rituximab with available biosimilars) was used for the verification of RD cases.
A total of 95,289 RD cases with a first-time diagnosis of inflammatory RD established between 2012 and 2019 were selected. A case was considered first-time-diagnosed if the patient had had at least 1 year of no previous RD record in the database. As no data preceding 2012 were available, we excluded 22,526 first-time diagnoses in 2012 from the total cohort, as it was not possible to verify their RD diagnosis prior to the index date.
We excluded 2251 cases from the cohort because they were younger than 18 years old at the time of diagnosis, and 10 because of an unidentifiable identification code. To verify the cases, we excluded 58,866 patients with no records of at least one prescription of state-reimbursed medications for RD (glucocorticoids, csDMARDs, or bDMARDs).
The final 11,636 cases were cross-checked with the death registry of the health Information center at the Institute of Hygiene, and the date and cause of death were obtained if the death had occurred between 2013 and 2021. The cases were cross-checked using personal identification codes. The principal causes of death were compared between the prepandemic and pandemic time periods, and grouped under the following categories: deaths because of cardiovascular and circulatory causes, malignancies, infections, respiratory causes, musculoskeletal diseases, external causes of death, and unspecified causes of death. COVID-19, as a recorded cause of death, was only calculated in the pandemic period.
The final dataset used for analysis included sex, age, the ICD-10 code of RD, the date of RD diagnosis, the date and cause of death if applicable, and information about the prescription of state-reimbursed drugs.
For the comparison with the general population of Lithuania, information on the adult population census in 2013–2021 was obtained from Statistics Lithuania (
Adalimumab
Adult
Ankylosing Spondylitis
Antirheumatic Drugs, Disease-Modifying
Arthritis, Psoriatic
Azathioprine
Biopharmaceuticals
Biosimilars
Cardiovascular System
Compulsive Behavior
COVID 19
Diagnosis
Etanercept
Glucocorticoids
Infection
Inflammation
Infliximab
Leflunomide
Malignant Neoplasms
Methotrexate
Musculoskeletal Diseases
Pandemics
Patients
Prescription Drugs
Respiratory Rate
Rituximab
Sulfasalazine
tocilizumab
Vasculitis
Youth
We identified participants who were newly diagnosed with RA using the International Classification of Diseases, tenth Revision, Clinical Modification (ICD-10-CM), codes (M05.x, M06.x) plus any dispensing of DMARDs during the identification period from January 2010 to December 2017 (n = 286,148; 23 (link)). Disease-modifying anti-rheumatic drugs (DMARDs) in the current study included all of conventional synthetic DMARDs (e.g., methotrexate, hydroxychloroquine, leflunomide, sulfasalazine, tacrolimus, cyclosporine, D-penicillamine, bucillamine, and azathioprine), biological DMARDs (e.g., adalimumab, etanercept, infliximab, golimumab, rituximab, abatacept, and tocilizumab), and targeted synthetic DMARD (e.g., tofacitinib). Those who had not completed a health checkup within 2 years before the diagnosis of RA, those with any missing data, those with age < 20 years, and those with a history of ESRD before the diagnosis of RA were excluded. We additionally excluded the subjects who were diagnosed with ESRD or who died within 1 year after the diagnosis of RA, for the diagnostic accuracy of RA. For comparison between the subjects with and without RA, we selected the control group (without RA) by age-sex exact matching, and included five times as many subjects as RA cohort. Patients with RA who were not matched with controls without RA were further excluded.
Abatacept
Adalimumab
Antirheumatic Drugs, Disease-Modifying
Azathioprine
Biopharmaceuticals
bucillamine
Cyclosporine
Diagnosis
Etanercept
golimumab
Hydroxychloroquine
Infliximab
Kidney Failure, Chronic
Leflunomide
Methotrexate
Patients
Penicillamine
Rituximab
Sulfasalazine
Tacrolimus
tocilizumab
tofacitinib
Top products related to «Leflunomide»
Sourced in United States, United Kingdom, Germany
Leflunomide is a lab equipment product from Merck Group. It is a synthetic chemical compound used in various research and development applications. The core function of Leflunomide is to serve as a research tool for scientific investigations.
Sourced in United States
Leflunomide is a laboratory reagent used for research purposes. It is a chemical compound that can be used in various experimental setups. The core function of Leflunomide is to serve as a research tool, but its specific applications and intended uses should not be extrapolated.
Sourced in United States, Germany, China, United Kingdom, France, Japan, Sao Tome and Principe
Uridine is a nucleoside that is a constituent of ribonucleic acid (RNA). It serves as a precursor in the biosynthesis of uridine triphosphate (UTP) and other pyrimidine nucleotides. Uridine can be used as a research tool in various biological and biochemical applications.
Sourced in Germany, United States
Teriflunomide is a laboratory reagent manufactured by Merck Group. It is a pyrimidine synthesis inhibitor used for research purposes.
Sourced in United States
AKTS473 is a rabbit monoclonal antibody that detects endogenous levels of Akt protein phosphorylated at Serine 473. The antibody is suitable for use in Western blotting applications.
S6K1T389 is a primary antibody that detects phosphorylation of the Thr389 residue of the S6K1 (p70 S6 Kinase) protein. It is used to monitor the activation state of the mTOR signaling pathway.
Sourced in United States, Germany, United Kingdom, China, Italy, Sao Tome and Principe, France, Macao, India, Canada, Switzerland, Japan, Australia, Spain, Poland, Belgium, Brazil, Czechia, Portugal, Austria, Denmark, Israel, Sweden, Ireland, Hungary, Mexico, Netherlands, Singapore, Indonesia, Slovakia, Cameroon, Norway, Thailand, Chile, Finland, Malaysia, Latvia, New Zealand, Hong Kong, Pakistan, Uruguay, Bangladesh
DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.
Sourced in United States, Germany, United Kingdom, Australia, Canada, France, China
Gemcitabine is a nucleoside analog used as a laboratory reagent. It functions as an antimetabolite, inhibiting DNA synthesis.
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Dexamethasone is a synthetic glucocorticoid medication used in a variety of medical applications. It is primarily used as an anti-inflammatory and immunosuppressant agent.
Sourced in United States, Germany, United Kingdom, Japan, Belgium, China, Canada, Italy, France, South Sudan, Singapore, Australia, Denmark, Uruguay
The FACSAria II is a high-performance cell sorter produced by BD. It is designed for precision cell sorting and analysis. The system utilizes flow cytometry technology to rapidly identify and separate different cell populations within a sample.
More about "Leflunomide"
Leflunomide, a groundbreaking immunomodulatory drug, has emerged as a game-changer in the treatment of rheumatoid arthritis and other autoimmune disorders.
This versatile compound works by inhibiting pyrimidine synthesis, a crucial process that disrupts the proliferation of activated lymphocytes, a key driver of autoimmune conditions.
The efficacy of Leflunomide has been extensively studied in clinical trials, where it has consistently demonstrated its ability to reduce symptoms and slow disease progression.
This remarkable performance has made Leflunomide a go-to choice for clinicians and researchers alike.
To further optimize Leflunomide research, researchers can leverage the power of PubCompare.ai, an AI-powered tool that empowers scientific discoveries by comparing protocols and locating the best approaches.
This innovative platform allows researchers to identify the most reproducible and effective methods from the literature, preprints, and patents, ensuring that their Leflunomomide studies are grounded in the most cutting-edge and proven techniques.
In addition to Leflunomide, researchers may also explore related compounds, such as Uridine, Teriflunomide, AKTS473, S6K1T389, and Gemcitabine, which share some mechanistic similarities or therapeutic applications.
The integration of these related terms and compounds can provide a more comprehensive understanding of the Leflunomide landscape and its potential clinical applications.
Furthermore, the use of DMSO and Dexamethasone, common solvents and adjuvants in pharmaceutical research, may also be relevant when examining Leflunomide protocols and their optimization.
By leveraging the insights gained from the MeSH term description, the Metadescription, and the integration of related terms and compounds, researchers can unlock the full potential of Leflunomide and drive groundbreaking discoveries that improve the lives of patients suffering from rheumatoid arthritis and other autoimmune conditions.
Embark on this journey of scientific exploration with the aid of PubCompare.ai and experience the power of AI-driven protocol optimization.
This versatile compound works by inhibiting pyrimidine synthesis, a crucial process that disrupts the proliferation of activated lymphocytes, a key driver of autoimmune conditions.
The efficacy of Leflunomide has been extensively studied in clinical trials, where it has consistently demonstrated its ability to reduce symptoms and slow disease progression.
This remarkable performance has made Leflunomide a go-to choice for clinicians and researchers alike.
To further optimize Leflunomide research, researchers can leverage the power of PubCompare.ai, an AI-powered tool that empowers scientific discoveries by comparing protocols and locating the best approaches.
This innovative platform allows researchers to identify the most reproducible and effective methods from the literature, preprints, and patents, ensuring that their Leflunomomide studies are grounded in the most cutting-edge and proven techniques.
In addition to Leflunomide, researchers may also explore related compounds, such as Uridine, Teriflunomide, AKTS473, S6K1T389, and Gemcitabine, which share some mechanistic similarities or therapeutic applications.
The integration of these related terms and compounds can provide a more comprehensive understanding of the Leflunomide landscape and its potential clinical applications.
Furthermore, the use of DMSO and Dexamethasone, common solvents and adjuvants in pharmaceutical research, may also be relevant when examining Leflunomide protocols and their optimization.
By leveraging the insights gained from the MeSH term description, the Metadescription, and the integration of related terms and compounds, researchers can unlock the full potential of Leflunomide and drive groundbreaking discoveries that improve the lives of patients suffering from rheumatoid arthritis and other autoimmune conditions.
Embark on this journey of scientific exploration with the aid of PubCompare.ai and experience the power of AI-driven protocol optimization.