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Merck
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文件

SML0061

Sigma-Aldrich

SAHA

≥98% (HPLC)

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别名:
N-羟基-N′-苯基-辛烷二酰胺, 伏立诺他, 辛二酰苯胺异羟肟酸
经验公式（希尔记法）:
C14H20N2O3
CAS号:
149647-78-9
分子量:
264.32
MDL编号:
MFCD00945317
UNSPSC代码:
12352200
PubChem化学物质编号:
329825127
NACRES:
NA.77

质量水平

100

检测方案

≥98% (HPLC)

形式

powder

颜色

white to tan

溶解性

DMSO: ≥15 mg/mL

运输

wet ice

储存温度

−20°C

SMILES字符串

ONC(=O)CCCCCCC(=O)Nc1ccccc1

InChI

1S/C14H20N2O3/c17-13(15-12-8-4-3-5-9-12)10-6-1-2-7-11-14(18)16-19/h3-5,8-9,19H,1-2,6-7,10-11H2,(H,15,17)(H,16,18)

InChI key

WAEXFXRVDQXREF-UHFFFAOYSA-N

基因信息

human ... HDAC1(3065) , HDAC2(3066) , HDAC3(8841) , HDAC6(10013)

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应用

SAHA可用于研究基因调控、转录调控和细胞信号转导。

生化/生理作用

SAHA或Vorinostat可促进导致细胞凋亡、分化和生长停滞的基因的转录。其已在淋巴瘤中获得有益结果，但在实体瘤中没有。
伏立诺他或辛二酰苯胺异羟肟酸（SAHA）是一种有效的、可逆的泛组蛋白去乙酰化酶（HDAC）抑制剂。其可抑制I类和II类HDAC，从而改变基因转录并诱导多种转化细胞中的细胞周期停滞和/或凋亡。

特点和优势

该化合物是基因调控研究的推荐产品。点击此处，了解更多精选基因调控产品。了解更多有关用于其他研究领域的生物活性小分子的信息，请访问 sigma.com/discover-bsm。

象形图

Health hazard
GHS08

警示用语：

Danger

危险声明

H341,H360

危险分类

Muta. 2 - Repr. 1A

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

分析证书(COA)

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  1. Which document(s) contains shelf-life or expiration date information for a given product?

    If available for a given product, the recommended re-test date or the expiration date can be found on the Certificate of Analysis.

  2. How do I get lot-specific information or a Certificate of Analysis?

    The lot specific COA document can be found by entering the lot number above under the "Documents" section.

  3. How do I find price and availability?

    There are several ways to find pricing and availability for our products. Once you log onto our website, you will find the price and availability displayed on the product detail page. You can contact any of our Customer Sales and Service offices to receive a quote.  USA customers:  1-800-325-3010 or view local office numbers.

  4. What is the Department of Transportation shipping information for this product?

    Transportation information can be found in Section 14 of the product's (M)SDS.To access the shipping information for this material, use the link on the product detail page for the product. 

  5. What is the solution stability of product SML0061, SAHA?

    Product SML0061, SAHA, should not be stored in an aqueous solution for more than 1 day.

  6. My question is not addressed here, how can I contact Technical Service for assistance?

    Ask a Scientist here.

Robert W Robey et al.
Molecular pharmaceutics, 8(6), 2021-2031 (2011-09-09)
The histone deacetylase inhibitors (HDIs) have shown promise in the treatment of a number of hematologic malignancies, leading to the approval of vorinostat and romidepsin for the treatment of cutaneous T-cell lymphoma and romidepsin for the treatment of peripheral T-cell
Sarah W Gordon et al.
American journal of clinical oncology, 42(8), 649-654 (2019-07-16)
Preclinical data suggest histone deacetylase inhibitors improve the therapeutic index of sorafenib. A phase I study was initiated to establish the recommended phase 2 dose of sorafenib combined with vorinostat in patients with unresectable hepatocellular carcinoma. Patients received vorinostat (200
Weiwei Yu et al.
British journal of pharmacology, 174(20), 3608-3622 (2017-07-28)
Intrinsic and/or acquired resistance of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) commonly occurs in patients with non-small-cell lung cancer (NSCLC). Here, we developed a combined therapy of histone deacetylase inhibition by a novel HDAC inhibitor, YF454A, with
Gloria Manzotti et al.
Journal of experimental & clinical cancer research : CR, 38(1), 346-346 (2019-08-10)
RUNX2 is a Runt-related transcription factor required during embryogenesis for skeletal development and morphogenesis of other organs including thyroid and breast gland. Consistent evidence indicates that RUNX2 expression is aberrantly reactivated in cancer and supports tumor progression. The mechanisms leading
Sachith Mettananda et al.
Scientific reports, 9(1), 11649-11649 (2019-08-14)
β-Thalassaemia is one of the most common monogenic diseases with no effective cure in the majority of patients. Unbalanced production of α-globin in the presence of defective synthesis of β-globin is the primary mechanism for anaemia in β-thalassaemia. Clinical genetic
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