1. Cell Cycle/DNA Damage Epigenetics Autophagy Apoptosis
  2. HDAC Autophagy Apoptosis
  3. 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).

For research use only. We do not sell to patients.

HDAC6-IN-79

HDAC6-IN-79 Chemical Structure

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Description

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)[1].

IC50 & Target[1]

HDAC6

98.4 nM (IC50)

HDAC1

639 nM (IC50)

HDAC2

789.9 nM (IC50)

HDAC4

1187 nM (IC50)

HDAC8

865.7 nM (IC50)

In Vitro

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.

Western Blot Analysis[1]

Cell Line: HeLa cells
Concentration: 0.2 μM, 0.8 μM, 3.2 μM
Incubation Time: 16 h
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.

Cell Viability Assay[1]

Cell Line: T24 cells (human urothelial carcinoma)
Concentration: 0.3 μM, 1 μM, 3 μM, 10 μM, 30 μM
Incubation Time: 48 h, 72 h, 96 h
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.

Real Time qPCR[1]

Cell Line: T24 cells
Concentration: 10 μM
Incubation Time: 24 h
Result: Significantly upregulated expression of autophagy-related genes: BECLIN1, BNIP3, LAMP1, and VPS34, relative to untreated controls.

Apoptosis Analysis[1]

Cell Line: T24 cells
Concentration: 10 μM
Incubation Time: 48 h
Result: Induced apoptosis in approximately 20% of T24 cells, with increases in both early and late apoptotic populations relative to untreated controls.
Molecular Weight

411.52

Formula

C22H25N3O3S

SMILES

O=C(NO)C1=CC=C(CN2C(CSC23CCN(CC4=CC=CC=C4)CC3)=O)C=C1

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation
References
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HDAC6-IN-79
Cat. No.:
HY-182747
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