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SML1923

Sigma-Aldrich

A-395 hydrochloride

≥98% (HPLC)

Synonyme(s) :

(3R,4S)-1-(7-Fluoro-2,3-dihydro-1H-inden-1-yl)-4-{4-[4-(methanesulfonyl)piperazin-1-yl]phenyl}-N,N-dimethylpyrrolidin-3-amine hydrochloride

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About This Item

Formule empirique (notation de Hill):
C26H35FN4O2S · xHCl
Numéro CAS:
Poids moléculaire :
486.65 (free base basis)
Numéro MDL:
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.77

Niveau de qualité

Pureté

≥98% (HPLC)

Forme

powder

Conditions de stockage

desiccated

Couleur

white to light brown

Solubilité

H2O: 10 mg/mL, clear

Température de stockage

2-8°C

Chaîne SMILES 

FC1=CC=CC2=C1C(N3C[C@H](C(C=C4)=CC=C4N5CCN(S(C)(=O)=O)CC5)[C@@H](N(C)C)C3)CC2

Actions biochimiques/physiologiques

A-395 is a potent and selective chemical probe for the polycomb protein EED (embryonic ectoderm development), an essential component of Polycomb repressive complex 2 (PRC2), involved in transcriptional repression through methylation of histone H3K27. A-395 has been found to bind to EED in vitro with a Ki value of 0.4 nM, inhibit the PRC2 complex with an IC50 value 34 nM for methylation of H3K27, and have >100-fold selectivity over other histone methyltransferases and non-epigenetic targets. In RD rhabdoid tumor cell line A-395 inhibited the PRC2 complex with an IC50 value of 90 nM, inhibiting the formation of H3K27me3. For characterization details of A-395, please visit the A-395 probe summary on the Structural Genomics Consortium (SGC) website.

A-395N is the negative control for the active enantiomer, A-395. A-395N is available from Sigma. To learn more about and purchase A-395N, click here.

To learn about other SGC chemical probes for epigenetic targets, visit sigma.com/sgc

Caractéristiques et avantages

A-395 is an epigenetic chemical probe available through a partnership with the Structural Genomics Consortium (SGC). To learn more and view other SGC epigenetic probes, visit sigma.com/SGC.

Pictogrammes

Skull and crossbones

Mention d'avertissement

Danger

Mentions de danger

Classification des risques

Acute Tox. 3 Oral - Eye Irrit. 2 - Skin Irrit. 2

Code de la classe de stockage

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

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Consulter la Bibliothèque de documents

Hywel Dunn-Davies et al.
Molecular therapy. Nucleic acids, 35(2), 102173-102173 (2024-04-15)
Epigenetic processes involving long non-coding RNAs regulate endothelial gene expression. However, the underlying regulatory mechanisms causing endothelial dysfunction remain to be elucidated. Enhancer of zeste homolog 2 (EZH2) is an important rheostat of histone H3K27 trimethylation (H3K27me3) that represses endothelial
Jie Yang et al.
eLife, 12 (2023-09-12)
Human health is facing a host of new threats linked to unbalanced diets, including high-sugar diet (HSD), which contributes to the development of both metabolic and behavioral disorders. Studies have shown that diet-induced metabolic dysfunctions can be transmitted to multiple
Coral K Wille et al.
Science advances, 9(46), eadf3980-eadf3980 (2023-11-17)
Embryonic stem cells (ESCs) have transcriptionally permissive chromatin enriched for gene activation-associated histone modifications. A striking exception is DOT1L-mediated H3K79 dimethylation (H3K79me2) that is considered a positive regulator of transcription. We find that ESCs are depleted for H3K79me2 at shared
Anne-Marie W Turner et al.
ACS infectious diseases, 6(7), 1719-1733 (2020-04-30)
A hallmark of human immunodeficiency type-1 (HIV) infection is the integration of the viral genome into host chromatin, resulting in a latent reservoir that persists despite antiviral therapy or immune response. Thus, key priorities toward eradication of HIV infection are
Alastair Davies et al.
Nature cell biology, 23(9), 1023-1034 (2021-09-08)
Cancers adapt to increasingly potent targeted therapies by reprogramming their phenotype. Here we investigated such a phenomenon in prostate cancer, in which tumours can escape epithelial lineage confinement and transition to a high-plasticity state as an adaptive response to potent

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