JAS239
JAS239 is a blood-brain barrier-permeable ChoK inhibitor. JAS239 inhibits phosphocholine synthesis and reduces the expression level of E2F1 protein. JAS239 exhibits near-infrared fluorescence properties. JAS239 exerts anti-tumor activity against glioblastoma. JAS239 can be used in studies related to glioblastoma.
For research use only. We do not sell to patients.
- Formula: C31H37ClN2O2
- Molecular Weight:505.09
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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ChoK |
E2F1 |
JAS239 (maximum 100 μM; 24 h) reduces the metabolic activity (a surrogate marker for cell viability) of glioblastoma (GBM) cells, and exhibits comparable potency against the F98, 9L, U-87 MG and U-251 MG cell lines under both normoxic and hypoxic conditions[2].
JAS239 (500 nM; 24-96 h) inhibits the proliferation of GBM cells by inducing cell cycle arrest and downregulating E2F-1 expression[2].
JAS239 (500 nM; 0-96 h) inhibits the proliferation of the 9L glioblastoma cell line under normoxic conditions[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:rat F98, human U-87 MG GBM cell lines (3D spheroid assay); rat F98, 9L, human U-251 MG GBM cell lines (integrin expression analysis)
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Concentration:500 nM
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Incubation Time:16 h (3D spheroid assay)
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Result:Significantly reduced track straightness (0.28 ± 0.11 vs.
0.32 ± 0.12, p < 0.0001), track length (84.0 ± 48.0 μm vs.
113.2 ± 86 μm, p < 0.0001), and average speed (0.005 ± 0.001 μm/s vs.
0.007 ± 0.004 μm/s, p < 0.0001), and induced super-diffusive cell motion in normoxic F98 spheroids.
Significantly reduced track straightness and length, and increased cell speed, with induced super-diffusive cell motion in DMOG-hypoxic F98 spheroids.
Significantly increased track length (133.0 ± 61.6 μm vs.
120.7 ± 57.7 μm, p < 0.001) and average speed (0.007 ± 0.001 μm/s vs.
0.006 ± 0.001 μm/s, p < 0.0001), with no change in track straightness, and induced super-diffusive cell motion in normoxic U-87 MG spheroids.
Resulted in track straightness and speed comparable to DMOG-only treatment, with induced super-diffusive cell motion in DMOG-hypoxic U-87 MG spheroids.
Reduced integrin α3β1 protein expression (a marker of cell mobility) in F98, 9L, and U-251 MG cells.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Fischer F344 (female, weight 100-120 g, intracranial injection of 50,000 F98 GBM cells)[1]
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Dosage:4 mg/kg
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Administration:intraperitoneal injection; once daily; 5 consecutive days
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Result:Significantly reduced tumor growth (p < 0.05) and percentage change of tumor volume (p = 0.033) compared to controls.
Detected a significant reduction (p = 0.02) in mI/tCr ratio in treated tumors.
Noted a 32% non-significant reduction in Glx/tCr ratio.
Observed a near-significant 97% increase (p = 0.052) in (Lip + Lac)/tCr ratio.
Measured a near-significant lower mitotic index (p = 0.06) in treated tumors.
Showed non-significant reduction in tCho/tCr ratio and non-significant trend of reduction in tCho/NAA ratio.
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Animal Model:Fischer F344 (female, weight 100-120 g, intracranial injection of 100,000 9L GBM cells)[1]
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Dosage:4 mg/kg
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Administration:intraperitoneal injection; once daily; 5 consecutive days
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Result:Observed non-significant tumor growth arrest compared to controls.
Measured the largest non-significant reduction in tCho/tCr ratio (-42%) across all models.
Detected a significant reduction (p = 0.047) in tCho/NAA ratio.
Showed non-significant trend of reduction in mI/tCr ratio and Glx/tCr ratio.
Observed a non-significant -20% change in (Lip + Lac)/tCr ratio.
Measured a lower mitotic index in treated tumors.
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Animal Model:C57BL/6 (male, age 8-10 weeks, weight 20-25 g, intracranial injection of 500,000 GL261 GBM cells)[1]
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Dosage:4 mg/kg
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Administration:intraperitoneal injection; once daily; 5 consecutive days
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Result:Observed non-significant tumor growth arrest compared to controls.
Showed non-significant reduction in tCho/tCr ratio and non-significant trend of reduction in tCho/NAA ratio.
Detected non-significant trend of reduction in mI/tCr ratio.
Noted no significant change in Glx/tCr ratio and (Lip + Lac)/tCr ratio.
Measured a lower mitotic index in treated tumors.
Chemical Information
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Molecular Weight 505.09
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Formula C31H37ClN2O2
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SMILES
OCCN1C2=C(C(C)(C)C1=C/C=C/C=C/C=C/C(C(C)(C3=C4C=CC=C3)C)=[N+]4CCO)C=CC=C2.[Cl-]
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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.
Purity & Documentation
References
[1]. Bhaduri S, et al. Metabolic changes in glioblastomas in response to choline kinase inhibition: In vivo MRS in rodent models. NMR Biomed. 2023;36(3):e4855. [Content Brief]
[2]. Kelly CL, et al. Hypoxia Dependent Inhibition of Glioblastoma Cell Proliferation, Invasion, and Metabolism by the Choline-Kinase Inhibitor JAS239. Metabolites. 2025;15(2):76. Published 2025 Jan 26. [Content Brief]
[3]. Louise Kelly C, et al. Inhibition of glioblastoma cell proliferation and invasion by the choline-kinase inhibitor JAS239 varies with cell type and hypoxia. bioRxiv [Preprint]. 2024 Jan 20:2024.01.17.576078. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
JAS239 Related Classifications
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