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Merck

SML1642

Sigma-Aldrich

DHED

≥98% (HPLC)

Sinónimos:

(17β)-10,17-Dihydroxy-estra-1,4-dien-3-one, 10β,17β-Dihydroxyestra-1,4-dien-3-one, 3,16-Dihydroxyandrost-5-ene-17,19-dione

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About This Item

Fórmula empírica (notación de Hill):
C18H24O3
Número de CAS:
Peso molecular:
288.38
UNSPSC Code:
51111800
PubChem Substance ID:
NACRES:
NA.77

Quality Level

assay

≥98% (HPLC)

form

powder

optical activity

[α]/D -20 to -30°, c = 1 in methanol

color

white to light brown

solubility

DMSO: 10 mg/mL, clear

storage temp.

2-8°C

SMILES string

O[C@@]12C(CC[C@]3([H])[C@]2([H])CC[C@@]4(C)[C@@]3([H])CC[C@@H]4O)=CC(C=C1)=O

InChI

1S/C18H24O3/c1-17-8-7-15-13(14(17)4-5-16(17)20)3-2-11-10-12(19)6-9-18(11,15)21/h6,9-10,13-16,20-21H,2-5,7-8H2,1H3/t13-,14-,15-,16-,17-,18+/m0/s1

InChI key

UIKDFTLKOKNUJP-UGDFAFBOSA-N

Application

DHED has been used to induce an increase of estrogen levels in 3K transgenic mice with Parkinson′s disease (PD)-like motor syndrome.

Biochem/physiol Actions

DHED (10β,17β-dihydroxyestra-1,4-dien-3-one) is an inactive prodrug that selectively produces estrogen solely in the brain. DHED is converted to 17β-estradiol in the brain by an enzyme only expressed in the CNS, but is inert in the rest of the body. DHED was found to provide neuroprotection in a rat stroke model and reversed neurological symptoms of estrogen deprivation such as memory problems in female rats lacking ovaries.
DHED is a substrate for nicotinamide adenine dinucleotide phosphate (NADPH)-dependent dehydrogenase/reductase. Its expression in the brain is correlated to neuroprotection functionality.

pictograms

Health hazard

signalword

Danger

hcodes

Hazard Classifications

Repr. 1B

Storage Class

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

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Molly M Rajsombath et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 39(38), 7628-7640 (2019-08-14)
Many studies report a higher risk for Parkinson's disease (PD) and younger age of onset in men. This, and the fact that the neuropathological process underlying PD symptoms may begin before menopause, suggests that estrogen-based hormone therapy could modify this
Laszlo Prokai et al.
Science translational medicine, 7(297), 297ra113-297ra113 (2015-07-24)
Many neurological and psychiatric maladies originate from the deprivation of the human brain from estrogens. However, current hormone therapies cannot be used safely to treat these conditions commonly associated with menopause because of detrimental side effects in the periphery. The

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