JAK1-IN-22
JAK1-IN-22 is a JAK1-selective inhibitor with an IC50 of 1.84 μM. JAK1-IN-22 exerts no significant inhibitory effect on JAK2 and JAK3. JAK1-IN-22 can be used in the research of JAK1-related diseases such as asthma, alopecia areata, and type 1 diabetes.
For research use only. We do not sell to patients.
- CAS No.: 2241039-80-3
- Formula: C28H31F2N7O4S
- Molecular Weight:599.66
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
JAK1 1.84 μM (IC50) |
In Vitro
JAK1-IN-22 (Example 34) inhibits IL-13-induced STAT6 reporter gene activity in U937-STAT6-Luc cells with an IC50 > 4.20 μM; it exhibits an IC50 of 1.84 μM in recombinant JAK1 enzymatic assays, while the IC50 values against JAK2 and JAK3 are both > 30 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 2241039-80-3
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Molecular Weight 599.66
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Formula C28H31F2N7O4S
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SMILES
N(C([C@H](COC)N1CCN(C)CC1)=O)C2=C3C(C(=CN3)C4=NC(NC5=C(F)C(S(C)(=O)=O)=CC=C5)=NC=C4F)=CC=C2
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Keywords
- JAK1-IN-22
- 2241039-80-3
- JAK
- JAK1 inhibitor
- selective JAK1 inhibitor
- Janus kinase 1
- JAK2 sparing
- JAK3 sparing
- indolylpyrimidine
- pyrimidine derivative
- S-enantiomer
- U937 cells
- STAT6 reporter assay
- IL-13 signaling
- asthma
- alopecia areata
- type 1 diabetes
- rheumatoid arthritis
- psoriasis
- lupus
- multiple sclerosis
- atopic dermatitis
- ulcerative colitis
- Crohn's disease
- autoimmune disease
- inflammatory disease
- C3H/HeJ mice
- Brown Norway rats
- OVA lung inflammation model
- Inhibitor
- inhibitor
- inhibit