2. Cell Cycle/DNA Damage Epigenetics Apoptosis
  3. HDAC Apoptosis
  4. HDAC8-IN-16

HDAC8-IN-16 是一种选择性的组蛋白去乙酰化酶 8 (HDAC8) 抑制剂，IC50 为 0.16 μM。HDAC8-IN-16 可诱导细胞凋亡 (apoptosis)、引发 G2/M 期细胞周期阻滞，并可中度抑制癌细胞增殖。HDAC8-IN-16 可用于结直肠癌的相关研究。

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HDAC8-IN-16

HDAC8-IN-16 Chemical Structure

CAS No. : 2464465-06-1

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HDAC8-IN-16 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

HDAC8-IN-16 is a selective histone deacetylase 8 (HDAC8) inhibitor with an IC50 of 0.16 μM. HDAC8-IN-16 induces cell apoptosis, triggers G2/M phase cell cycle arrest, and moderately inhibits cancer cell proliferation. HDAC8-IN-16 is applicable to relevant research on colorectal cancer[1].

IC50 & Target[1]

HDAC8

0.16 μM (IC50)

体外研究
(In Vitro)

HDAC8-IN-16 (Compound 16) (48 h) 对 Jurkat、MOLT-4 和 HCT116 肿瘤细胞表现出中等水平的抗增殖活性，其中对 HCT116 细胞的活性最强 (IC50 = 16.12 μM)，而对 K562、HL-60 和 HeLa 细胞仅表现出弱活性或无活性[1]。
HDAC8-IN-16 (5-20 μM; 48 h) 显著提高 HCT116 细胞中 HDAC8 特异性底物 SMC3 的乙酰化水平，证实其可在细胞水平抑制 HDAC8[1]。
HDAC8-IN-16 (5-20 μM; 48 h) 于 HCT116 细胞中诱导剂量依赖性细胞凋亡[1]。
HDAC8-IN-16 (5-20 μM; 48 h) 以剂量依赖方式将 HCT116 细胞阻滞于细胞周期的 G2/M 期[1]。

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

HDAC8-IN-16 相关抗体:

Western Blot Analysis[1]

Cell Line: HCT116 cells
Concentration: 5 μM, 10 μM, 20 μM
Incubation Time: 48 h
Result: Had a marginal effect on Ac-SMC3 levels at 5 μM and 10 μM.
Induced a significant, noticeable accumulation of Ac-SMC3 at 20 μM.
Had no significant effect on Ac-α-tubulin or histone H3 acetylation levels.

Apoptosis Analysis[1]

Cell Line: HCT116 cells
Concentration: 5 μM, 10 μM, 20 μM
Incubation Time: 48 h (treatment); 15 min (staining incubation at room temperature)
Result: Increased early apoptosis from 1.87% to 2.81% and late apoptosis from 0.90% to 3.12% at 5 μM.
Increased early apoptosis to 17.37% and late apoptosis to 7.53% at 10 μM.
Increased early apoptosis to 17.37% and late apoptosis to 25.57% at 20 μM, showing a dose-dependent increase in apoptotic cells.

Cell Cycle Analysis[1]

Cell Line: HCT116 cells
Concentration: 5 μM, 10 μM, 20 μM
Incubation Time: 48 h (treatment); overnight (fixation at 4 °C); 30 min (staining incubation at room temperature)
Result: Decreased G0/G1 phase from 67.23% to 57.84%, increased S phase from 16.87% to 19.01%, and increased G2/M phase from 15.90% to 23.15% at 5 μM.
Decreased G0/G1 phase to 40.67%, increased S phase to 27.13%, and increased G2/M phase to 32.20% at 10 μM.
Decreased G0/G1 phase to 27.62%, increased S phase to 27.02%, and increased G2/M phase to 45.36% at 20 μM, showing a pronounced G2/M phase arrest.
分子量

380.44

Formula

C21H24N4O3
CAS 号
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

HDAC8-IN-16 相关分类

  • 摩尔计算器

  • 稀释计算器

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  • 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:

HDAC8-IN-162464465-06-1HDACApoptosisHistone deacetylasescolorectal cancerSMC3apoptosishistone deacetylase 8G2/M phase cell cycle arrestJurkatMOLT-4HDAC1HDAC8HCT116Inhibitorinhibitorinhibit

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