HIT211504993
HIT211504993 is a selective histone deacetylase 6 (HDAC6) inhibitor with an IC50 of 0.070 μM. HIT211504993 suppresses cancer cell proliferation, cause G1 phase cell cycle arrest and induces apoptosis. HIT211504993 inhibits Myc-driven tumorigenesis via nucleocytoplasmic acetylation, p53 modulation, and Wnt/β-catenin signaling modulation. HIT211504993 inhibits tumor growth in a colon cancer xenograft mouse model. HIT211504993 can be used for the research of colon cancer.
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- Formule: C23H27ClN2O6S
- Masse moléculaire:494.99
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Stockage:
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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Activité biologique
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HDAC6 0.07 μM (IC50) |
HIT211504993 potently and selectively inhibits HDAC6, with an IC50 of 0.070 ± 0.002 μM, showing 89-fold higher potency against HDAC6 than HDAC2 and 486-fold higher potency than against HDAC4[1].
HIT211504993 ( 48 h) selectively inhibits the viability of colorectal cancer cells (HCT-8, HCT116) with IC50 of 12.483 and 18.840 μM and other tumor cell lines, with lower toxicity to normal NCM460 intestinal epithelial cells[1].
HIT211504993 (10-50 μM; 12-48 h) effectively enhances histone H3 and non-histone α-tubulin acetylation in HCT-8 and HCT116 colorectal cancer cells in both concentration- and time-dependent manners[1].
HIT211504993 (20 μM; 24 h) inhibits the long-term proliferative capacity of HCT-8 and HCT116 colorectal cancer cells, as measured by reduced colony formation[1].
HIT211504993 (20 μM; 12-48 h) induces G1 phase cell cycle arrest and downregulates Cyclin D expression in HCT-8 and HCT116 colorectal cancer cells, inhibiting cell proliferation[1].
HIT211504993 (20 μM; 12-48 h) induces time-dependent apoptosis in HCT-8 and HCT116 colorectal cancer cells via the intrinsic mitochondrial pathway, as shown by altered Bcl-2/Bax expression and increased Annexin V-positive cells[1].
HIT211504993 (60 μM; 6 h) directly binds to HDAC1 and HDAC2 in HCT-8 colorectal cancer cells, increasing their thermal stability[1].
HIT211504993 (20 μM; 4-24 h) modulates gene expression in HCT-8 colorectal cancer cells, downregulating MYC and Wnt/β-catenin pathway components while upregulating p53 and DUSP1, to suppress tumorigenesis[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HCT-8, HCT116, NCM460, A2780, A549, MDA-MB-231, HepG2, HeLa, A375 cells
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Concentration:0.5-100 μM
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Incubation Time:48 h
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Result:Exhibited an IC50 of 12.483 ± 0.92 μM in HCT-8 cells.
Exhibited an IC50 of 18.840 ± 0.88 μM in HCT116 cells.
Exhibited an IC50 of 46.043 ± 3.39 μM in NCM460 cells.
Exhibited an IC50 of 33.080 ± 3.98 μM in A2780 cells.
Exhibited an IC50 of 25.967 ± 5.45 μM in A549 cells.
Exhibited an IC50 of 10.782 ± 0.76 μM in MDA-MB-231 cells.
Exhibited an IC50 of 26.680 ± 1.75 μM in HepG2 cells.
Exhibited an IC50 of 56.557 ± 3.74 μM in HeLa cells.
Exhibited an IC50 of 20.983 ± 0.48 μM in A375 cells.
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Cell Line:HCT-8, HCT116 colorectal cancer cells
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Concentration:10, 20, 30, 40,50 μM
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Incubation Time:12, 24, 36, 48 h
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Result:Increased acetyl-H3 and acetyl-α-tubulin levels in both cell lines, with the most substantial enhancement at 20 μM.
Induced time-dependent increases in acetyl-H3 and acetyl-α-tubulin levels in both cell lines when incubated for 12-48 h at 20 μM.
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Cell Line:HCT-8, HCT116 colorectal cancer cells
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Concentration:20 μM
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Incubation Time:12, 24, 36, 48 h
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Result:Induced G1 phase cell cycle arrest in both HCT-8 and HCT116 cells.
Caused a significant decrease in Cyclin D protein expression in a time-dependent manner.
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Cell Line:HCT-8, HCT116 colorectal cancer cells
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Concentration:20 μM
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Incubation Time:12, 24, 36, 48 h
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Result:Induced apoptosis in a time-dependent manner, with progressive increases in apoptotic cell proportions over 12-48 h.
Downregulated anti-apoptotic Bcl-2 protein expression in both cell lines.
Upregulated pro-apoptotic Bax protein expression in both cell lines.
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Cell Line:HCT-8 colorectal cancer cells
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Concentration:20 μM
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Incubation Time:4, 12, 24 h
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Result:Altered the expression of 2692, 4788, and 5627 differentially expressed genes at 4, 12, and 24 h respectively, with enrichment in histone modification, cell cycle arrest, p53 signaling, and Wnt/β-catenin signaling pathways.
Induced time-dependent downregulation of MYC mRNA and protein expression.
Induced upregulation of DUSP1 and p53 mRNA and protein expression.
Downregulated mRNA levels of Wnt4, β-catenin, TCF4, and LEF1.
Reduced β-catenin protein expression in HCT-8 cells.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nude (4−6 weeks old, 16−20 g, subcutaneous xenograft via HCT-8 cell injection)[1]
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Dosage:25 mg/kg; 50 mg/kg; 100 mg/kg
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Administration:I.p.; daily; 15 days
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Result:Reduced tumor weight relative to vehicle control at 25 mg/kg.
Reduced tumor volume by 77% and tumor weight by 68% relative to vehicle control at 50 mg/kg.
Suppressed tumor growth to a greater extent than the 50 mg/kg dose at 100 mg/kg.
Caused no significant body weight changes or histological abnormalities in heart, liver, spleen, kidneys, or lungs across all treatment doses.
Chemical Information
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Masse moléculaire 494.99
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Formule C23H27ClN2O6S
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SMILES
O=C(C1CCC(CN(CC2=CC=CC(Cl)=C2)S(=O)(C3=CC=C4OCCOC4=C3)=O)CC1)NO
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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.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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