HDAC6-IN-79
HDAC6-IN-79 is a HDAC6 inhibitor with an IC50 of 98.40 nM, and it also exhibits inhibitory activity against other HDAC subtypes (HDAC1: 639.0 nM, HDAC2: 798.9 nM, HDAC8: 865.7 nM, HDAC4: 1187 nM). HDAC6-IN-79 induces acetylation of α-tubulin and histone H3, reduces the viability of cancer cells, activates the autophagy pathway and induces apoptosis. HDAC6-IN-79 can be used for research related to urothelial carcinoma (bladder cancer).
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- Formel: C22H25N3O3S
- Molecular Weight:411.52
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biologische Aktivität
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Chemical Information
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Help & FAQs
Biologische Aktivität
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HDAC6 98.4 nM (IC50) |
HDAC1 639 nM (IC50) |
HDAC2 789.9 nM (IC50) |
HDAC4 1187 nM (IC50) |
HDAC8 865.7 nM (IC50) |
HDAC6-IN-79 (Compound 21e) (0.2-3.2 μM; 16 h) induces robust acetylation of both HDAC6 (α-tubulin) and nuclear HDAC (histone H3) substrates in HeLa cells after 16 h treatment, indicating limited HDAC6 isoform selectivity in a cellular context[1].
HDAC6-IN-79 (72 h) inhibits HeLa cell proliferation with an IC50 of 1914 nM after 72 h treatment, consistent with its pan-HDAC inhibitory profile[1].
HDAC6-IN-79 (0.3-30 μM; 48-96 h) inhibits T24 human urothelial carcinoma cell proliferation with IC50 values ranging from 6 μM to 8.13 μM across 48 to 96 h of treatment, with significant viability reduction at 10 μM and 30 μM[1].
HDAC6-IN-79 (10 μM; 24 h) significantly upregulates expression of key autophagy-related genes (BECLIN1, BNIP3, LAMP1, VPS34) in T24 cells after 24 h treatment, indicating activation of autophagic pathways[1].
HDAC6-IN-79 (10 μM; 48 h) induces apoptosis (early and late) in ~20% of T24 human urothelial carcinoma cells after 48 h treatment[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HeLa cells
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Concentration:0.2 μM, 0.8 μM, 3.2 μM
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Incubation Time:16 h
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Result:Induced strong, concentration-dependent acetylation of α-tubulin, accompanied by marked induction of histone H3 acetylation.
Maintained a ratio of acetyl-α-tubulin to acetyl-histone H3 consistently >1, which did not increase in a concentration-dependent manner.
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Cell Line:T24 cells (human urothelial carcinoma)
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Concentration:0.3 μM, 1 μM, 3 μM, 10 μM, 30 μM
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Incubation Time:48 h, 72 h, 96 h
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Result:Reduced T24 cell viability in a concentration-dependent manner, with IC50 values of 7.60 μM (48 h), 8.13 μM (72 h), and 6 μM (96 h).
Reduced cell viability to 70.39% at 10 μM, and to 42.65% at 30 μM.
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Cell Line:T24 cells
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Concentration:10 μM
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Incubation Time:24 h
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Result:Significantly upregulated expression of autophagy-related genes: BECLIN1, BNIP3, LAMP1, and VPS34, relative to untreated controls.
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Cell Line:T24 cells
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Concentration:10 μM
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Incubation Time:48 h
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Result:Induced apoptosis in approximately 20% of T24 cells, with increases in both early and late apoptotic populations relative to untreated controls.
Chemical Information
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Molecular Weight 411.52
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Formel C22H25N3O3S
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SMILES
O=C(NO)C1=CC=C(CN2C(CSC23CCN(CC4=CC=CC=C4)CC3)=O)C=C1
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
HDAC6-IN-79 Related Classifications
HY-182747 Related Classifications
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