Estradiol (E2) is a natural estrogen and the primary female sex hormone. E2 and its esters, including estradiol cypionate and estradiol valerate, are used in combined oral contraceptives alongside progestins and as components of hormone replacement therapy.
DrugBank Accession Number
KEGG Entry Number
Wikipedia Entry Name
178.5° C (ChemIDPlus, Toxnet)
151-152° C (DrugBank)
3.9 mg/L water at 27° C. Freely soluble in alcohol,;soluble in acetone, dioxane, other organic solvents; sparingly soluble in vegetable oils.
Specific Optical Rotation
+76 - +83° at 25 °C for D (sodium) line (dioxane)
UV Max Absorption
225, 280 nm
Store between 15 and 30 °C.
GHS Hazard Code(s)
|Carcinogenicity||2||H351||Suspected of causing cancer if inhaled|
|Reproductive Toxicity||1A||H360||May damage fertility or the unborn child|
|Reproductive Toxicity, Effects On or Via Lactation||H362||May cause harm to breast-fed children|
|Reproductive Toxicity||1B||H360||May damage fertility or the unborn child|
|Specific Target Organ Toxicity, Repeated Exposure||1||H372||Causes damage to organs through prolonged or repeated exposure|
|Specific Target Organ Toxicity, Repeated Exposure||2||H373||Causes damage to organs through prolonged or repeated exposure|
Respiratory tract infection, localized exfoliation, headache, endometrial disorder, vulvovaginal mucotic infection, vulvovaginal pruritus, application site reaction, breast tenderness
"There is sufficient evidence in humans for the carcinogenicity of post-menopausal estrogen therapy. There is sufficient evidence in experimental animals for the carcinogenicity of estradiol and estrone."
Not found to be mutagenic in the Ames Salmonella/microsome direct plate incorporation protocol.
LD, rat subcutaneous: > 300 mg/kg
Estrogen Receptor Activity
Elimination Half-Life (t1/2)
Oral: 13-30 h (Stanczyk)
36 h (DrugBank)
20.1 h from oral administration (Toxnet)
Serum Protein Binding
60% to albumin, 38% to SHBG.
Hepatic, if oral administration.
54% in urine, 6% in feces.
For the treatment of urogenital symptoms associated with post-menopausal atrophy of the vagina (such as dryness, burning, pruritus and dyspareunia) and/or the lower urinary tract (urinary urgency and dysuria).
Formed by CYP1B1 in the liver. Minor pathway in liver but is formed in larger amount in extrahepatic tissues. Thought to be the most carcinogenic of all estradiol metabolites. Can bind to estrogen receptors.
Formed in liver by CYP1A2, CYP3A4, and CYP2C9. Major metabolic pathway of estradiol in liver. Has about 7% and 11% the affinity of estradiol to ERα and ERβ, respectively. Weakly estrogenic, with some antagonistic effects. Can be further metabolized to 2-methoxyestradiol by catechol O-methyltransferase (COMT) in the liver. Can also be metabolized to free radicals that cause DNA damage.
A number of other hydroxylated metabolites are also formed (6α-, 6β-, 7α-, 12β-, 15α-, 15β-, 16α, and 16β-hydroxyestradiol). Estradiol may also be metabolized to hydroxyestrones, such as 2-, 4-, and 16α-hydroxyestrone.
Major urinary metabolite. Formed from the estradiol metabolite estrone. 80 times less potent estrogen agonist than estradiol.
Formed in the liver by CYP2C9, CYP2C19, and CYP2C8. Undergoes further conversion to estriol, the major urinary metabolite. 10 times less potent estrogen agonist that estradiol.