JAK2-IN-24
JAK2-IN-24 is an orally active JAK2 inhibitor with an IC50 < 0.003 μM. JAK2-IN-24 blocks the JAK/STAT signaling pathway. JAK2-IN-24 inhibits JAK1 and JAK3 tyrosine kinases. JAK2-IN-24 inhibits pSTAT5 levels in mouse spleen in the TEL-JAK2 implantation model. JAK2-IN-24 inhibits tumor growth. JAK2-IN-24 can be used in research on myeloproliferative neoplasms.
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- CAS No.: 1220516-48-2
- 화학식: C16H16FN9
- 분자량:353.36
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
IC50 & Target
[1]|
JAK2 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| BaF3 | IC50 |
0.24 μM
|
Inhibition of pSTAT5 in BaF3 TEL-TYK2 cells by Western blot.
Inhibition of pSTAT5 in BaF3 TEL-TYK2 cells by Western blot.
|
24359159 |
| SET-2 | IC50 |
0.030 μM
|
Inhibition of pSTAT5 in SET-2 cells at 1 h by Western blot.
Inhibition of pSTAT5 in SET-2 cells at 1 h by Western blot.
|
24359159 |
| SET-2 | IC50 |
0.054 μM
|
Inhibition of pSTAT5 in SET-2 cells at 24 h by Western blot.
Inhibition of pSTAT5 in SET-2 cells at 24 h by Western blot.
|
24359159 |
In Vitro
JAK2-IN-24 (Compound 19a) inhibits the proliferation of BaF3 TEL-Jak2 cells (GI50 0.012 μM) as well as the V617F cell lines SET-2 (0.014 μM) and UKE-1 (0.055 μM)[1].
JAK2-IN-24 (0.001-3 μM; 1-24 h (UKE-1 and SET-2)) inhibits pSTAT5 in JAK2-dependent and V617F cell lines[1].
JAK2-IN-24 is a potent biochemical Jak2 inhibitor (IC50 <0.003 μM) with selectivity over Jak3 (IC50 0.22 μM)[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:BaF3 TEL-JAK2, BaF3 TEL-TYK2, UKE-1, and SET-2 cells
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Concentration:0.001, 0.003, 0.010, 0.030, 0.100, 0.300, 1, and 3 μM
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Incubation Time:1 h and 24 h (UKE-1 and SET-2)
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Result:Inhibited pSTAT5 in BaF3 TEL-JAK2 with IC50 0.012 μM.
Inhibited pSTAT5 in BaF3 TEL-TYK2 with IC50 0.24 μM.
Inhibited pSTAT5 in UKE-1 with IC50 0.002 μM at 1 h and 0.005 μM at 24 h.
Inhibited pSTAT5 in SET-2 with IC50 0.030 μM at 1 h and 0.054 μM at 24 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:SCID (female)[1]
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Dosage:3 or 10 mg/kg
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Administration:p.o.; BID; 14 days
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Result:We observed a significant dose-dependent tumor growth inhibition with 19a-treated animals.
At the end of the dosing phase, maximum tumor growth inhibition was 77% with 10 mg/kg twice daily and 50% with 3 mg/kg twice daily.
No significant body weight loss was observed; maximum weight loss/gain on day 31 was 3.1% for 10 mg/kg and 7.2% for 3 mg/kg.
Chemical Information
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CAS No. 1220516-48-2
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분자량 353.36
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화학식 C16H16FN9
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SMILES
CN1C=C(NC2=C3C(NC=C3)=NC(N[C@H](C4=NC=C(F)C=N4)C)=N2)N=C1
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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Trophoblast Invasion Assay
The trophoblast invasion assay is commonly based on the Matrigel-coated Transwell invasion system, in which invasive cells migrate through a reconstituted basement membrane matrix toward a chemoattractant gradient, thereby modeling extracellular matrix (ECM) penetration and invasive behavior in vitro. The readout is typically the number of cells that traverse the Matrigel barrier and attach to the lower surface of a porous membrane, reflecting invasive capacity through ECM-like substrates and basement membrane components. This system was originally developed to quantify invasive cell behavior using Matrigel as a basement membrane analog in a Boyden chamber format.
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Patient-Derived Xenograft (PDX)
Patient-derived xenograft (PDX) models are generated by engrafting primary human tumor tissue directly into immunodeficient mice, allowing in vivo propagation of patient tumor biology without initial in vitro adaptation. These models are used to preserve key histopathological and molecular characteristics of the original tumor and enable assessment of tumor growth dynamics and therapeutic response in a living organism. The biological readout is tumor engraftment and subsequent growth in the murine host, which reflects the ability of human tumor cells to survive, vascularize, and expand in an immunocompromised microenvironment.
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Patient-Derived Orthotopic Xenograft (PDOX)
Patient-derived orthotopic xenograft (PDOX) modeling implants fresh patient tumor tissue or patient-derived tumor cells into the anatomically corresponding organ or tissue site of immunodeficient mice, usually by surgical orthotopic implantation, to preserve patient tumor histology, local microenvironmental context, invasion, metastatic behavior, and treatment-response features better than subcutaneous implantation. PDOX readouts include tumor engraftment, orthotopic tumor growth, local invasion, metastasis, recurrence after resection, histologic similarity to the donor tumor, biomarker retention, molecular concordance, survival, and response or resistance to therapy. PDOX models are used for preclinical drug testing and individualized therapy evaluation, but engraftment success varies by tumor type and specimen quality.
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Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
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Orthotopic Cell-Line Xenograft
Orthotopic cell-line xenograft models involve implantation of human cancer cell lines into the anatomically corresponding organ of immunodeficient mice to reproduce tumor growth within a native microenvironment, enabling more clinically relevant tumor behavior compared with subcutaneous models. These models are widely used because orthotopic placement better recapitulates tumor progression, including invasion and metastatic spread, which are often underrepresented in heterotopic implantation systems. Compared with conventional xenografts, orthotopic implantation is described as more technically complex but provides improved simulation of tumor-microenvironment interactions and metastatic behavior, making it particularly valuable for translational oncology research. Surgical orthotopic implantation approaches have been emphasized as enabling faithful reproduction of clinical cancer features, including metastasis and disease progression patterns that align with the tumor’s organ of origi
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)