2. Cell Cycle/DNA Damage Epigenetics Autophagy Apoptosis
  3. HDAC Autophagy Apoptosis
  4. HDAC6-IN-79

HDAC6-IN-79 是一种 HDAC6 抑制剂，其 IC50 为 98.40 nM，对其他亚型 HDAC 也具有抑制活性 (HDAC1: 639.0 nM, HDAC2: 798.9 nM, HDAC8: 865.7 nM, HDAC4:1187 nM)。HDAC6-IN-79 可诱导 α-微管蛋白和组蛋白 H3 的乙酰化，降低癌细胞的存活率，激活自噬 (autograpy) 通路并诱导细胞凋亡 (apoptosis)。HDAC6-IN-79 可用于尿路上皮癌 (膀胱癌) 的相关研究。

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HDAC6-IN-79

HDAC6-IN-79 Chemical Structure

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HDAC6-IN-79 相关抗体

Top Publications Citing Use of Products

查看 HDAC 亚型特异性产品:

查看所有亚型
HDAC HDAC1 HDAC2 HDAC3 HDAC4 HDAC5 HDAC6 HDAC7 HDAC8 HDAC9 HDAC10 HDAC11 HD1 HD2

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

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)

体外研究
(In Vitro)

HDAC6-IN-79 (Compound 21e) (0.2-3.2 μM; 16 h) 处理 HeLa 细胞 16 h 后，可诱导 HDAC6 底物 (α-微管蛋白) 和核 HDAC 底物 (组蛋白 H3) 发生显著乙酰化，表明其在细胞环境中对 HDAC6 亚型的选择性有限[1]。
HDAC6-IN-79 (72 h) 可抑制 HeLa 细胞增殖，处理 72 h 后的 IC50 为 1914 nM，与其泛 HDAC 抑制活性特征一致[1]。
HDAC6-IN-79 (0.3-30 μM; 48-96 h) 可抑制 T24 人膀胱移行细胞癌细胞的增殖，在 48 至 96 h 处理时长下的 IC50 值为 6 μM 至 8.13 μM，在 10 μM 和 30 μM 浓度下细胞活力显著降低[1]。
HDAC6-IN-79 (10 μM; 24 h) 可显著上调 T24 细胞中关键自噬相关基因 (BECLIN1、BNIP3、LAMP1、VPS34) 的表达，提示自噬通路被激活[1]。
HDAC6-IN-79 (10 μM; 48 h) 处理 48 小时后，可诱导约 20%的人膀胱移行细胞癌 T24 细胞发生凋亡 (早期和晚期)[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

HDAC6-IN-79 相关抗体:

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.
分子量

411.52

Formula

C22H25N3O3S
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

HDAC6-IN-79 相关分类

  • 摩尔计算器

  • 稀释计算器

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

HDAC6-IN-79HDACAutophagyApoptosisHistone deacetylasesHeLa cellsHDAC1HDAC2α-tubulinHDAC4histone H3T24 human urothelial carcinoma cellsautophagy-related genesHDAC6HDAC8Inhibitorinhibitorinhibit

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