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Merck
CN

H8787

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:
65673-63-4
Molecular Weight:
409.23
NACRES:
NA.77
PubChem Substance ID:
24724505
UNSPSC Code:
12352200
MDL number:
MFCD00218213

Key Documents

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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

SMILES string

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

InChI key

SXJDCULZDFWMJC-UHFFFAOYSA-N

assay

≥95% (CHN/NMR)

form

powder

solubility

DMSO: 26 mg/mL

shipped in

wet ice

storage temp.

−20°C

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

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)

Regulatory Information

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Certificates of Analysis (COA)

Lot/Batch Number
118K46081
118K4608
096K46183
096K46182
096K46181

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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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