JAK2-IN-13
JAK2-IN-13 is a potent and orally active JAK2 inhibitor with an IC50 of 54.7 nM. JAK2-IN-13 downregulates the expressions of p-STAT3 and p-STAT5. JAK2-IN-13 exhibits good bioavailability and potent inhibition of rhEPO-induced extramedullary erythropoiesis and polycythemia vera. JAK2-IN-13 can be used for the study of myeloproliferative neoplasms.
For research use only. We do not sell to patients.
- Formula: C25H28ClN5O2
- Molecular Weight:465.98
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
JAK2 54.7 nM (IC50) |
STAT3 |
STAT5 |
In Vitro
JAK2-IN-13 (Compound 11) (0.011-25 μM, 72 h) shows potent inhibitory activity against HEL and SET-2 cells, with IC50 values of 0.57 μM and 1.07 μM, respectively[1].
JAK2-IN-13 (0-10 μM, 3 h) significantly inhibits downstream signal pathways of JAK2 and downregulates p-STAT3 and p-STAT5 expression in HEL cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:HEL cells
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Concentration:0, 0.3, 1, 5, 10 μM
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Incubation Time:3 h
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Result:Dose-dependent downregulated p-STAT3 and p-STAT5 expressions.
Significantly inhibited the phosphorylation of STAT3 and STAT5 at 10 μM for 4 h.
Parmacokinetics
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:rhEPO-induced polycythemia model established in female BALB/c mice (8−10 weeks, 17−20 g)[1]
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Dosage:50, 75 and 100 mg/kg
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Administration:Oral administration (p.o.), once daily for 4 days
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Result:Suppressed the increase in reticulocyte counts and hematocrit expansion induced by rhEPO and alleviated splenomegaly.
Inhibited the expansion of Ter119/CD71 erythroblasts in both the spleen and bone marrow.
Had no significant impact on white blood cell counts and body weight.
Chemical Information
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Molecular Weight 465.98
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Formula C25H28ClN5O2
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SMILES
CC1=CN=C(NC(C=C2)=CC3=C2OCCN4CCCC4)N=C1NC5=CC(Cl)=CC(COC3)=C5
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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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Protocol for Pharmacokinetic Study
Pharmacokinetic studies quantify how an organism handles a drug over time through absorption, distribution, metabolism, and excretion, and the core experimental readout is the concentration-time profile of parent drug and, when relevant, metabolites in biological matrices such as plasma, whole blood, urine, bile, or tissue. Pharmacokinetic analysis links dose, route, exposure, clearance, half-life, distribution, bioavailability, and systemic exposure to drug efficacy and toxicity hypotheses rather than measuring a signaling pathway directly. The literature links pharmacokinetics to drug-development phenotypes by showing that drug metabolism and pharmacokinetics influence compound progression, exposure-response interpretation, safety margins, dosing strategy, and failure risk during discovery and development. DMPK science contributes to compound optimization by integrating physicochemical properties, in vitro metabolism, transporter behavior, in vivo exposure, and pharmacodynamic contex
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)