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Kinase Inhibitor, Janus

Kinase Inhibitors, Janus: A class of small-molecule compounds that target and inhibit the activity of Janus kinases (JAKs), a family of receptor-associated tyrosine kinases involved in various cellular processes.
Janus kinase inhibitors have emerged as important therapeutic agents for the treatment of inflammatory and autoimmune disorders, as well as certain types of cancer.
These compounds work by blocking the JAK-STAT signaling pathway, which regulates gene expression and immune response.
Researching and optimizing Janus kinase inhibitors is a crucial area of study for developing effective treatments for a range of medical conditions.
PubCompare.ai's AI-driven platform can help streamline this research by identifying relevant protocols and maximizing productivity.

Most cited protocols related to «Kinase Inhibitor, Janus»

Derivation of Mouse Pluripotent Stem Cells

Cited 7 times

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Publication 2011

2-Mercaptoethanol Amino Acids, Essential Blastocyst Cells Edetic Acid Embryonic Stem Cells Extracellular Matrix Feeder Cell Layers Feeder Cells Fibroblast Growth Factor 2 Growth Factor Kinase Inhibitor, Janus LIF protein, human Mus Needles Pluripotent Stem Cells Psychological Inhibition Serum Trypsin

Rising Up Trial: Upadacitinib for Atopic Dermatitis

Cited 6 times

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Publication 2021

Administration, Topical Adolescent Adult Biopharmaceuticals Body Surface Area Conferences Dermatitis, Atopic, 3 dupilumab Eczema Ethics Committees, Research Herpes Simplex Human Herpesvirus 3 Kinase Inhibitor, Janus Legal Guardians Parent Parenteral Nutrition Patients Phototherapy Pruritus Safety Sepsis Skin Diseases upadacitinib

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

Hypoxia-Induced Neuroprotective Signaling

Cited 6 times

The generation of the GFAP-GFP mouse used in this study has been described previously (Zhou et al., 1997) and CD1 mice were obtained from Charles River Labs (Wilmington, MA). All mouse colonies were maintained in the animal facility of Children’s National Medical Center, and all animal procedures complied with the guidelines of the National Institute of Health, and with the Children’s Research Institute Institutional Animal Care and Use Committee (IACUC) guidelines. Male mice were placed in a chamber containing 10.5 ± 0.5% O2 from P3 to P11 as previously described (Ment et al., 1998 ; Fagel et al., 2006 (link)). Strain-matched and age-matched animals reared in normal oxygen levels were used as controls (normoxia). For studies examining proliferation, BrdU (Sigma; 50μg per gram body weight) was administered 2hr prior to sacrifice. Mice were sacrificed at the given time point after hypoxia and perfused transcardially with phosphate buffered saline followed by 4% paraformaldehyde (PFA) and post fixed overnight in PFA followed by 20% glycerol and stored at 4°C. Treatment of mice with the JAK/STAT inhibitor AG490 has been previously described (Zhou et al., 2011 (link); Xu et al., 2011 ). Briefly, CD1 mice were treated with AG490 (10 mg/kg i.p.) or DMSO (control) twice daily (injections were ~8–10 hours apart) from P6 to P11. At P11 the white matter was carefully dissected out and lysed as described below, followed by Western blot analysis.

Raymond M., Li P., Mangin J.M., Huntsman M, & Gallo V. (2011). Chronic Perinatal Hypoxia Reduces Glutamate–Aspartate Transporter Function in Astrocytes through the Janus Kinase/Signal Transducer and Activator of Transcription Pathway. The Journal of Neuroscience, 31(49), 17864-17871.

Publication 2011

AG-490 Animals Body Weight Bromodeoxyuridine Child Glial Fibrillary Acidic Protein Glycerin Hypoxia Institutional Animal Care and Use Committees Kinase Inhibitor, Janus Males Mice, House Oxygen paraform Phosphates Rivers Saline Solution Strains Sulfoxide, Dimethyl trestolone Western Blot White Matter

Rheumatoid Arthritis Protocol: Eligibility and Exclusions

Cited 5 times

Eligible patients were ≥18 years with RA per 2010 ACR/EULAR criteria,15 (link) limited (<3 doses ≤25 mg) or no prior MTX exposure, ≥6 swollen joint count of 66 joints (SJC66)), and ≥6 tender joints of 68 joints (TJC68)) at screening and day 1. At screening, eligible patients were required to have 1 of the following: seropositivity for rheumatoid factor and/or anticyclic citrullinated peptide or ≥1 radiographic erosion (centrally read); or serum C-reactive protein (CRP) ≥4 mg/L. Key exclusion criteria included previous use of JAK inhibitors or biological DMARDs. Prior or concomitant use of stably dosed hydroxychloroquine was allowed. Full inclusion/exclusion criteria are in online supplemental methods.

Westhovens R., Rigby W.F., van der Heijde D., Ching D.W., Stohl W., Kay J., Chopra A., Bartok B., Matzkies F., Yin Z., Guo Y., Tasset C., Sundy J.S., Jahreis A., Mozaffarian N., Messina O.D., Landewé R.B., Atsumi T, & Burmester G.R. (2021). Filgotinib in combination with methotrexate or as monotherapy versus methotrexate monotherapy in patients with active rheumatoid arthritis and limited or no prior exposure to methotrexate: the phase 3, randomised controlled FINCH 3 trial. Annals of the Rheumatic Diseases, 80(6), 727-738.

Publication 2021

Antirheumatic Drugs, Disease-Modifying Biopharmaceuticals C Reactive Protein Hydroxychloroquine Joints Kinase Inhibitor, Janus Patients Peptides Rheumatoid Factor Serum X-Rays, Diagnostic

Most recents protocols related to «Kinase Inhibitor, Janus»

Synthesis of N-(3-(imidazo[4,5-d]pyrrolo[2,3-b]pyridin-1(6H)-yl)bicyclo[1.1.1]pentan-1-yl)-N′-dimethyl-1-sulfonamide

Not available on PMC !

Example 24

[Figure (not displayed)]
N-(3-(imidazo[4,5-d]pyrrolo[2,3-b]pyridin-1(6H)-yl)bicyclo[1.1.1]pentan-1-yl)-N′-dimethyl-1-sulfonamide (24)

To a solution of compound 1j (60 mg, 0.25 mmol) and DIPEA (130 mg, 1.00 mmol) in THE (1.5 mL) and DMSO (0.5 mL) was dropwise added a solution of dimethylsulfamoyl chloride (36 mg, 0.25 mmol) in 0.5 mL THE at 0° C. The mixture was stirred at 25° C. for 14 hrs. The mixture was diluted with H₂O (15 mL) and extracted with DCM (20 mL*2). The combined organic layers were concentrated and the residue was purified by prep-HPLC (Method A) to afford the title product as a white solid (15 mg, 17% yield). LC-MS (Method 1): t_R=2.59 min, m/z (M+H)⁺=347.1. ¹H NMR (400 MHz, CD₃OD) δ 8.48 (s, 1H), 8.02 (s, 1H), 7.38 (d, J=3.6 Hz, 1H), 6.71 (d, J=3.2 Hz, 1H), 2.73 (s, 6H), 2.68 (s, 6H).

US11858933B2. Tricyclic Janus kinase 1 inhibitors, and compositions and methods thereof (2024-01-02). LYNK PHARMACEUTICALS CO. LTD. [CN]. Inventors: Zhaokui Wan [CN], Michael Lawrence Vazquez [CN].

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Patent 2024

1H NMR Chlorides DIPEA High-Performance Liquid Chromatographies Kinase Inhibitor, Janus Sulfonamides Sulfoxide, Dimethyl

Synthesis of Imidazo-Pyrrolo-Pyridine Sulfonamide

Not available on PMC !

Example 25

[Figure (not displayed)]
N-(3-(imidazo[4,5-d]pyrrolo[2,3-b]pyridin-1(6H)-yl)bicyclo[1.1.1]pentan-1-yl)-N′-methyl-N’-ethyl-1-sulfonamide (25)

To a mixture consisting of compound 1j (70 mg, 0.29 mmol), Et₃N (148 mg, 1.46 mmol), K₂CO₃(404 mg, 2.93 mmol) and ACN (3 mL) was dropwise added a solution of ethyl(methyl)sulfamoyl chloride (46.0 mg, 0.29 mmol) in 0.5 mL ACN at 0° C. The mixture was stirred at 30° C. for 14 hrs. The mixture was diluted with H₂O (20 mL) and extracted with DCM (40 mL*2). The combined organic layers were concentrated to dryness and the residue was purified by prep-HPLC (Method A) to afford the title product as a white solid (8.0 mg, 9% yield). LC-MS (Method 1): t_R=2.96 min, m/z (M+H)⁺=361.1. ¹H NMR (400 MHz, CD₃OD) δ 8.48 (s, 1H), 8.02 (s, 1H), 7.38 (d, J=3.6 Hz, 1H), 6.71 (d, J=3.6 Hz, 1H), 3.17 (q, J=7.2 Hz, 2H), 2.75 (s, 3H), 2.68 (s, 6H), 1.14 (t, J=7.2 Hz, 3H).

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Patent 2024

1H NMR Chlorides High-Performance Liquid Chromatographies Kinase Inhibitor, Janus potassium carbonate Sulfonamides

Patient-Centered Shared Decision-Making in Rheumatic Diseases

Patient information at the time of SDM implementation was retrospectively obtained from the medical records. The surveyed items were sex, age (years), age (<65 years/≥65 years), RA, multiple rheumatic diseases, disease duration (years), disease duration (<10/≥10 years), disease activity (active/inactive), number of drugs used (number), number of drugs used (<5/≥5), history of allergy or side effects, history of allergy or side effects due to biologics or Janus kinase inhibitor, biologics, or Janus kinase inhibitor usage history before SDM. Age was classified into two categories according to the World Health Organization (WHO). Disease duration was classified into two categories based on a previous report on RA (12 (link)). Disease activity was classified into two categories; patients with RA were categorized as inactive if they exhibited low disease activity or remission based on their DAS28-CRP value and as active if they exhibited moderate or high disease activity. Those with other rheumatic diseases were classified as inactive if clinically judged by a physician to be in remission or have low disease activity and as active if they were otherwise judged to have moderate or higher-intensity symptoms. The number of drugs used was classified into two categories based on a previous report on polypharmacy (13 (link)).
The influential values of patients regarding drug treatment were compiled from subjective data describing values chosen by patients during conversations between pharmacists and patients during SDM implementation. The values compiled were multiple selected and single selected from the five values: effectiveness, safety, economic, daily life (drug treatment burden on life), and others (such as route of administration, type of device).
The continuance rate of treatment 6 months after SDM and disease status (improvement, aggravation, and no change) were evaluated, with reasons including inadequate effectiveness, side effects, economic issues, daily life issues, and other issues among patients.
The details of the drug treatment changes selected after the implementation of SDM were tabulated. The results included changing the drugs, tight control, no change, drug use cessation, increased dosage, change in the route of administration, addition of an oral drug, oral drug cessation, reduced dosage, changes in oral drug, and shortening of the interval between doses.
Because SDM was performed in the usual clinical setting, the pharmacists were not blinded to the outcomes, such as the continuance rate of treatment.

Hirata I., Hanaoka S., Rokutanda R., Funakoshi R, & Hayashi H. (2023). Shared decision-making practices and patient values in pharmacist outpatient care for rheumatic disease: A multiple correspondence analysis. Journal of Pharmacy & Pharmaceutical Sciences, 26, 11135.

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Publication 2023

Biological Factors Hypersensitivity Kinase Inhibitor, Janus Medical Devices Patients Pharmaceutical Preparations Physicians Polypharmacy Rheumatism Safety

Patient Clustering Based on Rheumatic Disease Factors

Sex (female or male), age_group (<65/≥65 years), disease duration_group (<10/≥10 years), disease activity (active/inactive), number of drugs used_group (<5/≥5), history of allergy or side effects caused by drugs in general (yes/no), history of allergy or side effects caused by biologics or Janus kinase inhibitor (yes/no), biologics or Janus kinase inhibitor usage history_before SDM (yes/no).
The information described in each dimension was evaluated using the Greenacre inertia adjustment, and the categorical variables were plotted in two dimensions with the highest inertia (15 ). A K-means cluster analysis, a non-hierarchical cluster analysis identifying mutually exclusive clusters by calculating the quadratic Euclidean distance (coefficient of similarity) of the point categories (16 (link), 17 (link)), was necessary to objectively ascertain which values each of the patient background items related to or belonged to. The coordinates (object scores) of each of the dimensions 1 and 2 of each variable calculated by MCA were input to K-means cluster analysis and the categorical variables, including the values and the basic information of patient characteristics, were grouped (18 (link)). The cubic clustering criterion (CCC) was calculated with statistical software and used to determine the optimal number of clusters (19 , 20 (link)). After clustering each variable, density ellipses (α = 95%) for each cluster were shown to indicate the overlap between clusters and were overlaid with the MCA plot. Statistical analyses were performed using JMP Pro 16 software (SAS Institute Inc., Cary, NC, United States).

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Publication 2023

Age Groups Biological Factors Cuboid Bone Hypersensitivity Kinase Inhibitor, Janus Males Patients Pharmaceutical Preparations Woman

Filgotinib vs. Tocilizumab in Moderate Rheumatoid Arthritis

Patients will be randomized in a 1:1 ratio to the administration of filgotinib 200 mg/day or subcutaneous tocilizumab 162 mg/biweekly switched from MTX ± other csDMARDs throughout the study period. Patients with moderate renal dysfunction (estimated glomerular filtration rate 30–60 mL/min/1.73 m²) will be allowed to be administered filgotinib 100 mg/day.
All patients must continue to receive the same doses of corticosteroid that they were receiving before providing consent throughout the study period. During the study period, the following treatments are prohibited: administration of a bDMARD, except tocilizumab, or JAK inhibitor, except for filgotinib; concomitant use of an immunosuppressant (azathioprine, cyclophosphamide, cyclosporine), csDMARD, or oral corticosteroids equivalent to more than 5 mg/day of prednisolone, in addition to intra-articular corticosteroid injections at joints, and nonsteroidal anti-inflammatory drug suppositories. During the study period, the dose of any oral nonsteroidal anti-inflammatory drug can be modified within the range of its approved doses in Japan.

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.

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Publication 2023

Adrenal Cortex Hormones Anti-Inflammatory Agents, Non-Steroidal Azathioprine Cyclophosphamide Cyclosporine filgotinib Glomerular Filtration Rate Immunosuppressive Agents Intra-Articular Injections Kidney Failure Kinase Inhibitor, Janus Patients Prednisolone Suppositories tocilizumab

Top products related to «Kinase Inhibitor, Janus»

Jak inhibitor 1 by Merck Group

Sourced in United States, Germany

JAK Inhibitor I is a laboratory product manufactured by Merck Group. It is a selective inhibitor of the Janus Kinase (JAK) enzyme family, which play a crucial role in the signal transduction of various cytokines and growth factors. The core function of JAK Inhibitor I is to modulate JAK-mediated signaling pathways in cellular and biochemical research applications.

Ag490 by Merck Group

Sourced in United States, Germany, China, Italy, Switzerland, Canada

AG490 is a lab equipment product manufactured by Merck Group. It functions as a tyrosine kinase inhibitor.

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.

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.

Dimethyl sulfoxide (dmso) by Merck Group

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.

Ly294002 by Merck Group

Sourced in United States, Germany, United Kingdom, China, Sao Tome and Principe, Macao, Italy, Canada, Switzerland, Japan, France, Israel, Spain, Morocco

LY294002 is a chemical compound that functions as a specific inhibitor of phosphoinositide 3-kinase (PI3K). It is commonly used in laboratory research settings to investigate the role of PI3K signaling pathways.

Azd1480 by Selleck Chemicals

Sourced in United States

AZD1480 is a small molecule that functions as a tyrosine kinase inhibitor. It is used as a research tool to study cellular signaling pathways involving tyrosine kinases.

Dulbecco modified eagle medium (dmem) by Thermo Fisher Scientific

Sourced in United States, China, United Kingdom, Germany, France, Australia, Canada, Japan, Italy, Switzerland, Belgium, Austria, Spain, Israel, New Zealand, Ireland, Denmark, India, Poland, Sweden, Argentina, Netherlands, Brazil, Macao, Singapore, Sao Tome and Principe, Cameroon, Hong Kong, Portugal, Morocco, Hungary, Finland, Puerto Rico, Holy See (Vatican City State), Gabon, Bulgaria, Norway, Jamaica

DMEM (Dulbecco's Modified Eagle's Medium) is a cell culture medium formulated to support the growth and maintenance of a variety of cell types, including mammalian cells. It provides essential nutrients, amino acids, vitamins, and other components necessary for cell proliferation and survival in an in vitro environment.

U0126 by Cell Signaling Technology

Sourced in United States, Germany, United Kingdom, China, France, Japan, Canada

U0126 is a specific inhibitor of the mitogen-activated protein kinase kinase (MEK1 and MEK2). It functions by blocking the activation of MAPK/ERK pathway.

Rpmi 1640 by Thermo Fisher Scientific

Sourced in United States, China, United Kingdom, Germany, France, Canada, Japan, Australia, Italy, Switzerland, Belgium, New Zealand, Austria, Netherlands, Israel, Sweden, Denmark, India, Ireland, Spain, Brazil, Norway, Argentina, Macao, Poland, Holy See (Vatican City State), Mexico, Hong Kong, Portugal, Cameroon

RPMI 1640 is a common cell culture medium used for the in vitro cultivation of a variety of cells, including human and animal cells. It provides a balanced salt solution and a source of essential nutrients and growth factors to support cell growth and proliferation.

More about "Kinase Inhibitor, Janus"

Kinase inhibitors targeting the Janus kinase (JAK) family of enzymes have emerged as crucial therapeutic agents for the treatment of a range of medical conditions, including inflammatory disorders, autoimmune diseases, and certain types of cancer.
These small-molecule compounds, often referred to as JAK inhibitors or Janus kinase inhibitors, work by blocking the JAK-STAT signaling pathway, which plays a central role in regulating gene expression and immune response.
The JAK family consists of four receptor-associated tyrosine kinases (JAK1, JAK2, JAK3, and TYK2) that are involved in various cellular processes.
Inhibiting the activity of these kinases can have significant therapeutic benefits, making Janus kinase inhibitor research an area of intense focus for drug development.
Some key subtopics and related terms in this field include: - JAK Inhibitor I: A highly selective and potent JAK1/JAK2 inhibitor used in research. - AG490: An inhibitor of the JAK2 kinase, often employed in studies of JAK-STAT signaling. - Ruxolitinib (Jakafi): A JAK1/JAK2 inhibitor approved for the treatment of myelofibrosis and polycythemia vera. - DMSO: A common solvent used to dissolve and deliver Janus kinase inhibitors in cell culture and animal studies. - LY294002: A PI3K inhibitor that can interact with and modulate the JAK-STAT pathway. - AZD1480: A JAK2-selective inhibitor with potential applications in cancer research and treatment.
Researchers can leverage PubCompare.ai's AI-driven platform to streamline their work on Janus kinase inhibitors.
The platform can help identify relevant protocols from literature, preprints, and patents, allowing researchers to quickly locate the most pertinent information and optimize their experimental design.
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