All Photos(1)

B39607

Sigma-Aldrich

1,1-Dichloro-2,2-bis(4-chlorophenyl)ethane

technical grade

Synonym(s):
TDE, 4,4′-DDD
Linear Formula:
(ClC6H4)2CHCHCl2
CAS Number:
Molecular Weight:
320.04
Beilstein:
1914072
EC Number:
MDL number:
PubChem Substance ID:

grade

technical grade

mp

94-96 °C

SMILES string

ClC(Cl)C(c1ccc(Cl)cc1)c2ccc(Cl)cc2

InChI

1S/C14H10Cl4/c15-11-5-1-9(2-6-11)13(14(17)18)10-3-7-12(16)8-4-10/h1-8,13-14H

InChI key

AHJKRLASYNVKDZ-UHFFFAOYSA-N

Gene Information

mouse ... Esr1(13982)
rat ... Ar(24208)

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Certificate of Analysis

Certificate of Origin

A Lødrup et al.
Alimentary pharmacology & therapeutics, 42(1), 84-90 (2015-05-06)
Guidelines recommend that patients with gastro-oesophageal reflux disease are adequately treated with acid-suppressive therapy before undergoing anti-reflux surgery. Little is known of the use of acid-suppressive drugs before anti-reflux surgery. To determine the use of proton pump inhibitors and H2
Daniel A King et al.
Human molecular genetics, 24(10), 2733-2745 (2015-01-31)
Delineating the genetic causes of developmental disorders is an area of active investigation. Mosaic structural abnormalities, defined as copy number or loss of heterozygosity events that are large and present in only a subset of cells, have been detected in
Yudi Pawitan et al.
European journal of cancer (Oxford, England : 1990), 51(6), 751-757 (2015-03-03)
A previous study showed that regular use of low-dose aspirin was associated with smaller tumour size and fewer metastases for colorectal and lung cancer. We aim to explain these distinct effects in terms of the anti-inflammatory and anti-thrombotic properties of
Merel Klaassens et al.
European journal of human genetics : EJHG, 23(5), 610-615 (2014-08-15)
De novo monoallelic variants in NFIX cause two distinct syndromes. Whole gene deletions, nonsense variants and missense variants affecting the DNA-binding domain have been seen in association with a Sotos-like phenotype that we propose is referred to as Malan syndrome.
Dennis Mircsof et al.
Nature neuroscience, 18(12), 1731-1736 (2015-11-17)
The NONO protein has been characterized as an important transcriptional regulator in diverse cellular contexts. Here we show that loss of NONO function is a likely cause of human intellectual disability and that NONO-deficient mice have cognitive and affective deficits.

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