Nanatinostat TFA
Based on 4 publication(s) in Google Scholar
Nanatinostat (CHR-3996) TFA is a potent, class I selective and orally active HDAC inhibitor with IC50s of 3 nM, 4 nM, and 7 nM for HDAC1, HDAC2, and HDAC3, respectively. Nanatinostat TFA has low activity against HDAC5 (IC50 of 200 nM) and HDAC6 (IC50 of 2100 nM). Nanatinostat TFA induces apoptosis in myeloma cells. Nanatinostat TFA has potent anticancer effects, such as myeloma, advanced solid tumours and colorectal cancer.
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- CAS No.: 1256448-48-2
- Formule: C22H20F4N6O4
- Masse moléculaire:508.43
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Pureté et documentation
- Références
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Publications Citing Use of MedChemExpress (MCE) Nanatinostat TFA
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Activité biologique
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HDAC1 3 nM (IC50) |
HDAC2 4 nM (IC50) |
HDAC3 7 nM (IC50) |
HDAC 8 nM (IC50) |
HDAC5 200 nM (IC50) |
HDAC6 2100 nM (IC50) |
Nanatinostat (CHR-3996) (0.0001-1 μM; 48 hours) TFA inhibits the proliferation of myeloma cell lines, with LC50 values ranging from 30.3-97.6 nM in different cell lines[2].
Nanatinostat (250-100 nM; 8-48 hours)TFA induces apoptosis and increases the level of acetylated H3K9 in H929 and RPMI-8226 myeloma cell lines[2].
Nanatinostat (0-200 nM; 24 hours) TFA reduces the levels of IL-6 and VEGF secreted by bone marrow stromal cells in the co-culture system of bone marrow stromal cells and myeloma cells[2].
Nanatinostat (250 nM and 100 nM; 48 hours) TFA arrests the cell cycle at the G0/G1 phase in H929 and RPMI-8226 myeloma cell lines[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:H929, RPMI-8226, KMS11, LP-1, MM1-S cells
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Concentration:0.0001 μM, 0.001 μM, 0.01 μM, 0.1 μM, 1 μM
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Incubation Time:48 hours
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Result:The cell viability decreased.
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Cell Line:H929 and RPMI-8226 myeloma cell lines
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Concentration:100 nM (RPMI-8226 cells), 250 nM (H929 cells)
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Incubation Time:8 hours, 24 hours, 48 hours
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Result:The percentage of apoptotic cells increased, with an increase in both early and late apoptotic cells.
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Cell Line:H929 and RPMI-8226 myeloma cell lines
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Concentration:100 nM (RPMI-8226 cells), 250 nM (H929 cells)
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Incubation Time:48 hours
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Result:The cell cycle was arrested at the G0/G1 phase.
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Cell Line:H929 and RPMI-8226 myeloma cell lines
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Concentration:100 nM (RPMI-8226 cells), 250 nM (H929 cells)
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Incubation Time:8 hours, 24 hours, 48 hours
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Result:The pro-apoptotic DNase Endonuclease G and p53 downstream mediator Noxa were up-regulated, and caspase 9 was cleaved.
Nanatinostat (25-50 mg/kg; orally administered; once daily; for 19 days) TFA can significantly reduce tumor volume in a dose-dependent manner in the female BALB/c nude mouse LoVo human colon xenograft model[1].
Nanatinostat (30 mg/kg; orally administered; once daily; for 28 days) TFA can effectively inhibit tumor growth in the NOD/SCID IL2R gammanull mouse myeloma model[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Female CrTac:NCr-Fox1(nu) mice (6-8 weeks old; inoculated bilaterally sc with 2 million human HCT116 colon carcinoma cells)[1].
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Dosage:50 mg/kg
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Administration:Orally administered, once daily, for 14 days
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Result:Almost completely suppressed tumor growth, and the tumor concentration was high, with a tumor-to-plasma concentration ratio reflecting good distribution to the tumor.
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Animal Model:Female BALB/c nude mice (inoculated with LoVo human colorectal xenograft)[1].
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Dosage:25 mg/kg and 50 mg/kg
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Administration:Orally administered, once daily, for 19 days
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Result:Significantly reduced tumor volume, and the effect was dose-dependent.
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Animal Model:NOD/SCID IL2R gammanull mice (inoculated subcutaneously with 2×106 H929 myeloma cells)[2].
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Dosage:30 mg/kg
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Administration:Orally administered, once daily, for up to 28 days
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Result:Effectively inhibited tumor growth.
Chemical Information
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CAS No. 1256448-48-2
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Masse moléculaire 508.43
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Formule C22H20F4N6O4
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SMILES
OC(C(F)(F)F)=O.FC(C=C1)=CC(C=C2)=C1N=C2CN[C@H]3[C@@]4([H])[C@]3([H])CN(C5=NC=C(C(NO)=O)C=N5)C4
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Synonyms
CHR-3996 TFA
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (4)
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Journal Impact Factor
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Most Recent
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Cancer Res
HDAC5 Loss Enhances Phospholipid-Derived Arachidonic Acid Generation and Confers Sensitivity to cPLA2 Inhibition in Pancreatic Cancer. [Abstract]2022 Dec 16;82(24):4542-4554. PMID: 36102738 -
Cell Rep
Comprehensive mass spectrometry screening-derived atlas of HDAC inhibitors reveals histone-specific acetylation changes. [Abstract]2026 May 26;45(5):117289. PMID: 42030158 -
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Pureté et documentation
Références
[1]. Moffat D, et al. Discovery of 2-(6-{[(6-fluoroquinolin-2-yl)methyl]amino}bicyclo[3.1.0]hex-3-yl)-N-hydroxypyrimidine-5-carboxamide (CHR-3996), a class I selective orally active histone deacetylase inhibitor. J Med Chem. 2010 Dec 23;53(24):8663-78. [Content Brief]
[2]. Smith EM, et al. The combination of HDAC and aminopeptidase inhibitors is highly synergistic in myeloma and leads to disruption of the NFκB signalling pathway. Oncotarget. 2015 Jul 10;6(19):17314-27. [Content Brief]
[3]. Banerji U, et al. A phase I pharmacokinetic and pharmacodynamic study of CHR-3996, an oral class I selective histone deacetylase inhibitor in refractory solid tumors. Clin Cancer Res. 2012 May 1;18(9):2687-94. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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