CAS 56-53-1 Diethylstilbestrol - Analytical Products / Alfa Chemistry

CAT	APS56531
CAS	56-53-1
Synonyms	Palestrol, trans-alpha,alpha'-Diethyl-4,4'-dihydroxystilbene, Rumestrol 1, Iscovesco, Stilboefral, Stil-Rol, Oestromensyl, Estrosyn, Bertrol, Syntofolin, Sibol, Phenol, 4,4'-(1,2-diethyl-1,2-ethenediyl)bis-, (E)-, DES, Synthofolin, DEB, Distilbene, Milestrol, DES (synthetic estrogen), DiBestrol 2 Premix,Diethylstilbestrol, Estromenin, Dawe's destrol, Sexocretin, Stilboestrol, Serral, 4,4'-Dihydroxy-alpha,beta-diethylstilbene, Cyren, Oestromon, trans-alpha,alpha'-Diethyl-4,4'-stilbenediol, Microest, NSC 3070, Estrobene, Grafestrol, (E)-4,4'-(1,2-diethylethene-1,2-diyl)diphenol, Di-Estryl, Fonatol, Hi-Bestrol, Menostilbeen, Antigestil, 4,4'-Stilbenediol, alpha,alpha'-diethyl-, (E)-, (E)-Diethylstilbestrol, 4,4'-Dihydroxydiethylstilbene, trans-Diethylstilbestrol, Stilbetin, Bio-des, (E)-3,4-Bis(4-hydroxyphenyl)-3-hexene, Neo-Oestranol I, Synestrin, Agostilben, Synthoestrin, Oestromenin, Estilbin MCO, Stilbestrol, trans-4,4'-Dihydroxy-alpha,beta-diethylstilbene, Cyren A, Domestrol, (E)-4,4'-(1,2-Diethyl-1,2-ethenediyl)bisphenol, Bufon, Oestrogenine, Stilboestroform, alpha,alpha'-Diethyl-4,4'-stilbenediol, Vagestrol, Rumestrol 2, 4,4'-Stilbenediol, alpha,alpha'-diethyl-, trans-, alpha,alpha'-Diethylstilbenediol, Comestrol, Stil, Pabestrol, Stilkap
IUPAC Name	4-[(E)-4-(4-hydroxyphenyl)hex-3-en-3-yl]phenol
Molecular Weight	268.35
Molecular Formula	C18H20O2
Canonical SMILES	CC\C(=C(\CC)/c1ccc(O)cc1)\c2ccc(O)cc2
InChI	InChI=1S/C18H20O2/c1-3-17(13-5-9-15(19)10-6-13)18(4-2)14-7-11-16(20)12-8-14/h5-12,19-20H,3-4H2,1-2H3/b18-17+

Accurate Mass	268.1463
Format	Neat

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CAT	Size	Shipping	Storage Conditions	Description	Price
APS56531-1	100MG	Room Temperature	2-8°C Fridge/Coldroom	Product Type: API; Subcategory: British Pharmacopoeia	Inquiry
APS56531-2	100MG	Room Temperature	+20°C	Subcategory: EU Methods, Pharmaceutical and veterinary compounds and metabolites	Inquiry
APS56531-3	100MG	Room Temperature	2-8°C Fridge/Coldroom	API Family: Matrix - API Family See respective official monograph(s); Product Type: API; Subcategory: European Pharmacopoeia (Ph. Eur.)	Inquiry
APS56531-4	250MG	Room Temperature	+5°C	API Family: Matrix - API Family Diethylstilbestrol; Product Type: API; Subcategory: Hormones, API standards, Mikromol	Inquiry

Case Study

Diethylstilbestrol as a Scaffold for the Synthesis of Selective Pregnane X Receptor Modulators

Hodnik, Žiga, et al. European Journal of Medicinal Chemistry 103 (2015): 551-562.

Diethylstilbestrol (DES), a synthetic nonsteroidal estrogen, has emerged as a promising scaffold for the development of novel modulators targeting the pregnane X receptor (PXR), a nuclear receptor central to drug metabolism regulation. In a recent study, a series of DES-based derivatives were synthesized by integrating structural motifs from marine-derived PXR agonists, solomonsterols A and B, and from bazedoxifene-based PXR antagonists.
The experimental evaluation in HepG2 cells revealed that methylated derivative 1 functions as a potent PXR agonist (EC₅₀ = 10.5 μM), effectively inducing CYP3A4 expression-a key enzyme in xenobiotic metabolism. In contrast, diethylstilbestrol itself (2, IC₅₀ = 14.6 μM), along with derivatives 3, 4, and 6 (IC₅₀ for 6 = 27.4 μM), displayed dose-dependent antagonistic activity by inhibiting rifaximin-induced CYP3A4 upregulation. These findings were substantiated through gene expression analysis.
Interestingly, structural modifications such as the loss of hydrogen-bond donors/acceptors reduced activity, suggesting that hydroxylation of the phenyl rings may enhance PXR interaction. Notably, both compounds 1 and 6 exhibited reduced off-target effects on estrogen receptor α and estrogen-related receptor β, highlighting the DES scaffold as a viable starting point for designing selective PXR modulators with minimal estrogenic interference.
This study positions diethylstilbestrol as a versatile molecular platform for developing next-generation PXR-targeted therapeutics.

Diethylstilbestrol Is Used to Investigate UGT-Mediated Estradiol Glucuronidation and Its Toxicological Mechanisms

Zhu, Liangliang, et al. Toxicology and Applied Pharmacology 283.2 (2015): 109-116.

Diethylstilbestrol (DES), a synthetic estrogen, has been extensively studied for its toxicological impact on estrogen metabolism. This in vitro study focuses on the modulatory role of DES in estradiol-3- and 17-O-glucuronidation by human liver microsomes (HLMs) and recombinant UDP-glucuronosyltransferases (UGTs).
DES was co-incubated with estradiol (E2) in HLMs or recombinant UGTs. Enzyme kinetic analyses revealed that DES competitively inhibits E2-3-O-glucuronidation, a reaction catalyzed by UGT1A1, with a Ki value of 2.1 ± 0.3 μM-suggesting significant in vivo inhibition potential. In contrast, DES markedly activates E2-17-O-glucuronidation, mediated by UGT1A4, leading to increased formation of cholestatic E2-17-glucuronide. The presence of DES (2 μM) elevated Vmax from 0.016 to 0.81 nmol/min/mg, with only a modest increase in Km, supporting an allosteric activation mechanism.
A two-site binding model fitted the activation kinetics well, yielding KA = 0.077 ± 0.18 μM, α = 3.3 ± 1.1, and β = 104 ± 56. Interestingly, such dual regulatory effects were not replicated in liver microsomes from common experimental animals, highlighting species-specific differences.
These findings provide novel insights into DES's dual role in modulating estrogen glucuronidation-simultaneously inhibiting detoxification (UGT1A1) and promoting cholestatic metabolite formation (UGT1A4), contributing to its endocrine-disrupting toxicity profile.

Diethylstilbestrol Used for the Promotion of Melanogenesis in B16 Melanoma Cells via the cAMP-PKA Pathway

Jian, Dan, et al. Steroids 76.12 (2011): 1297-1304.

Diethylstilbestrol (DES), a synthetic nonsteroidal estrogen, was employed in this study to explore its effect on melanogenesis in mouse B16 melanoma cells. The experimental approach focused on evaluating the modulation of melanin biosynthesis and its regulatory mechanisms under DES treatment.
B16 cells were treated with varying concentrations of DES, followed by assessments of cell viability, intracellular melanin content, tyrosinase activity, and cAMP levels. The expression levels of melanogenic enzymes (tyrosinase, TRP-1, TRP-2) and the transcription factor MITF were determined using quantitative PCR and Western blotting. Additionally, the involvement of estrogen receptors (ER) and the cAMP-dependent protein kinase A (PKA) pathway was evaluated through pharmacological inhibition using ICI182,780 (a selective ER antagonist) and H89 (a PKA inhibitor), respectively.
DES treatment resulted in enhanced proliferation, increased melanin content, elevated tyrosinase activity, and upregulated expression of tyrosinase family genes and MITF. Importantly, DES-induced melanogenesis was significantly attenuated by both ER and PKA inhibition, suggesting a dual role of ER activation and cAMP-PKA signaling in mediating this process. Elevated cAMP levels confirmed the activation of PKA downstream targets.
These findings demonstrate that diethylstilbestrol promotes melanogenesis in melanoma cells through estrogen receptor-mediated activation of the cAMP-PKA-MITF-tyrosinase axis. This highlights DES as a valuable chemical tool for mechanistic studies in pigment biology and melanoma research.