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Key Documents

H8787

Sigma-Aldrich

HA 14-1

≥95% (CHN/NMR), powder

Synonym(s):

2-Amino-6-bromo-α-cyano-3-(ethoxycarbonyl)-4H-1-benzopyran-4-acetic acid ethyl ester, Ethyl [2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)]-4H-chromene-3-carboxylate

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About This Item

Empirical Formula (Hill Notation):
C17H17BrN2O5
CAS Number:
Molecular Weight:
409.23
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77

Assay

≥95% (CHN/NMR)

form

powder

solubility

DMSO: 26 mg/mL

shipped in

wet ice

storage temp.

−20°C

SMILES string

CCOC(=O)C(C#N)C1c2cc(Br)ccc2OC(N)=C1C(=O)OCC

InChI

1S/C17H17BrN2O5/c1-3-23-16(21)11(8-19)13-10-7-9(18)5-6-12(10)25-15(20)14(13)17(22)24-4-2/h5-7,11,13H,3-4,20H2,1-2H3

InChI key

SXJDCULZDFWMJC-UHFFFAOYSA-N

Gene Information

human ... BCL2(596)
mouse ... BCL2(12043)
rat ... BCL2(24224)

Biochem/physiol Actions

HA 14-1 is a nonpeptide apoptosis inducer; Bcl-2 antagonist.

Features and Benefits

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

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Hai-Dong Xu et al.
PloS one, 8(5), e63232-e63232 (2013-05-10)
Autophagy can be induced under nutrition stress conditions. Bcl-2 is a pro-survival protein which inhibits apoptosis and autophagy. However, the role of Bcl-2 in autophagy regulation and cell survival under nutrition deprivation has not been fully understood. This study sought
Sebastian S Gerety et al.
Developmental biology, 350(2), 279-289 (2010-12-15)
Morpholino antisense oligonucleotides (MOs) are widely used as a tool to achieve loss of gene function, but many have off-target effects mediated by activation of Tp53 and associated apoptosis. Here, we re-examine our previous MO-based loss-of-function studies that had suggested

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