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Merck

SML0061

SAHA

≥98% (HPLC), powder, HDAC inhibitor

Synonyme(s) :

N-hydroxy-N′-phenyl-octanediamide, Suberoylanilide hydroxamic acid, Vorinostat

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A propos de cet article

Formule empirique (notation de Hill) :
C14H20N2O3
Numéro CAS:
149647-78-9
Poids moléculaire :
264.32
UNSPSC Code:
12352200
PubChem Substance ID:
329825127
NACRES:
NA.77
MDL number:
MFCD00945317
Assay:
≥98% (HPLC)
Form:
powder
Quality level:
100

Principaux documents

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Nom du produit

SAHA, ≥98% (HPLC)

SMILES string

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

assay

≥98% (HPLC)

form

powder

color

white to tan

solubility

DMSO: ≥15 mg/mL

shipped in

wet ice

storage temp.

−20°C

Quality Level

100

Gene Information

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

Catégories apparentées

Application

SAHA may be used to study gene regulation, transcription regulation and cell signaling.

Biochem/physiol Actions

Potent, reversible pan-histone deacetylase (HDAC) inhibitor.
SAHA or Vorinostat facilitates the transcription of genes that result in apoptosis, differentiation and growth arrest. It has been observed to give beneficial results in lymphoma but not in solid tumors.
Vorinostat or suberoylanilide hydroxamic acid (SAHA) is a potent, reversible pan-histone deacetylase (HDAC) inhibitor. It inhibits both class I and class II HDACs, altering gene transcription and inducing cell cycle arrest and/or apoptosis in a wide variety of transformed cells.

Features and Benefits

This compound is a featured product for Gene Regulation research. Click here to discover more featured Gene Regulation products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.

pictograms

Health hazard
GHS08

signalword

Danger

hcodes

H341,H360

Hazard Classifications

Muta. 2 - Repr. 1A

Classe de stockage

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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Certificats d'analyse (COA)

Lot/Batch Number
0000496696
0000496696
0000401045
0000145388
0000401045

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Consulter la Bibliothèque de documents

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
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
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
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