SML1642
DHED
≥98% (HPLC)
別名:
(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
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
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
Quality Level
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.
DHED is an inactive prodrug that selectively produces estrogen solely in the brain.
signalword
Warning
hcodes
Hazard Classifications
Repr. 2
保管分類
11 - Combustible Solids
flash_point_f
Not applicable
flash_point_c
Not applicable
適用法令
試験研究用途を考慮した関連法令を主に挙げております。化学物質以外については、一部の情報のみ提供しています。 製品を安全かつ合法的に使用することは、使用者の義務です。最新情報により修正される場合があります。WEBの反映には時間を要することがあるため、適宜SDSをご参照ください。
SML1642INT1-BULK: + SML1642-VAR: + SML1642-BULK: + SML1642-5MG: + SML1642-25MG:
jan
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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