Mestranol

310.43

310.43

200-777-8

B2V233XGE7

DTXSID0020814

C636

Crystals from methanol or acetone

29372900

29.5

4

Solid

1.2±0.1 g/cm3

150-151 °C

464.1°C at 760 mmHg

190.8±23.0 °C

1.591

3.77e-03 g/L

-20°C Freezer

9.75x10-9

LD50 oral in rat: > 10gm/kg

Henry's Law constant = 4.51X10-9 atm-cu m/mol at 25 °C (est)

Ⅲ

2811

3

36/37/38-40-48-68

22-26-36/37/39-45-36/37

RC8960000

Xn

The shelf life of Norinyl-1 tablets is 5 years.

P280-P305 + P351 + P338

H315-H319-H351

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.|SRP: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including mestranol, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

|Danger|H302 (19.28%): Harmful if swallowed [Warning Acute toxicity, oral]|P201, P202, P260, P261, P263, P264, P270, P271, P280, P281, P301+P312, P302+P352, P304+P312, P304+P340, P305+P351+P338, P308+P313, P312, P321, P322, P330, P332+P313, P337+P313, P362, P363, P405, and P501|Aggregated GHS information provided by 83 companies from 5 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

For mestranol, a concentration range of 0.50 to 1.94 ug/L was reported as a result of analysis of raw sewage entering 14 representative sewage plants within a 50-mile radius of Cincinnati, OH; the average concentration was 1.21 ug/L. The treated effluent concentration range was 0.40 to 1.90 ug/L, average 1.05 ug/L(1). Mestranol was detected in 3 of 38 German municipal sewage treatment plant effluents from below the limit of quantification to a maximum of 0.004 ug/L(2). Detected in 3 of 18 sewage treatment plant effluents in Baden-Wuerttemberg, southeastern Germany with a maximum concentration of 2.7 ng/L reported; sampling took place between August 1998 and December 1999 and the detection limit was 0.6 ng/L(3). Mestranol was detected, not quantified in influent samples to the Piera and Igualada sewage treatment plants, respectively, on the Anoia tributary in the vicinity of Barcelona, Spain, sampled from April to June, 1999; detected (method detection limits = 50-100 ng/L)(4). The compound was detected at concentrations of <2.0 (July 2003), <2.0 (Sept 2003, and <2.0 ng/L (Feb 2004) in effluent from the Eysines Sewage Treatment Plant (northern suburbs, Bordeaux, France) and runs through agricultural and residential areas(5).

Groups of 24 virgin female C57L mice (MTV-) received 7 or 70 ug of a mixture of mestranol:norethynodrel (1:50) in oil by gavage, 5 times per week, commencing when the animals were 13 weeks of age. Pituitary tumors were found at autopsy in 7/7 mice given the higher dose that lived 84-89 weeks and in 6/11 mice given the lower dose, compared with 2/15 controls that lived 90 weeks. In this, and in a concurrent experiment with norethisterone:ethinyloestradiol (50:1), hepatomas were found in 10/96 treated mice, but the distribution within the different treatment groups was not reported. No hepatomas occurred among 48 control mice.|Intact male (C3H x RIII)Fl mice (MTV+) given 3 mg/kg (ppm) Ovulen (90% ethynodiol diacetate and 10% mestranol) mixed into the diet (intake, 7.5-10.0 ug/mouse per day) showed an increased incidence of mammary tumors, from 0/76 to 14/25; in castrated males, the incidence was increased from 10/61 to 21/28. The high spontaneous incidence (161/167) and short latent period of tumor induction (30-33 weeks) in intact females were not altered (37/38). In ovariectomized females the tumor incidence was not altered by Ovulen (28/34 in controls as compared with 20/26), but the latent period was reduced in both ovariectomized females (from 49 to 26 weeks) and castrated males (from 82 to 43 weeks).

LD50 Mouse ip 3500 mg/kg|LD50 Mouse subcutaneous 2500 mg/kg

Oral contraceptives have been reported to produce harmful ocular effects in myopic women. In women who developed myopia at or near puberty and in whom myopia became stable in adulthood, the drugs have reportedly increased the refractive error 2- to 3-fold, usually after 6 months of use. In women who are myopic and have considerable astigmatism, oral contraceptives may produce marked changes in the astigmatic error, possibly leading to frank keratoconus. In addition, oral contraceptives may produce a rapid advancement of the ocular disorder in patients with a family history of marked myopic astigmatism or keratoconus. Contact lens wearers receiving estrogen-progestin contraceptives may have more difficulties with their contact lenses than do nonusers who wear contact lenses. Contact lens wearers who develop visual disturbances or changes in lens tolerance during estrogen-progestin contraceptive use should be assessed by an ophthalmologist; temporary or permanent cessation of contact lens wear should be considered. /Estrogen-Progestin Combination/|Mental depression may occur in women receiving oral contraceptives. In a few cases, mental depression has been severe and has led to suicidal behavior. Mental depression appears to occur most frequently in patients with a history of depression, including premenstrual depression; however, relief of premenstrual tension occurs in some women. Patients with a history of mental depression should be observed carefully and the estrogen-progestin contraceptive discontinued if severe depression recurs during use. /Estrogen-Progestin Combination/

Mestranol's production and use in combination with progestogen as an oral contraceptive(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 2.2X10+4(SRC), determined from a structure estimation method(2), indicates that mestranol is expected to be immobile in soil(SRC). Volatilization of mestranol from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 4.5X10-9 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Mestranol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 9.7X10-9 mm Hg at 25 °C(SRC), determined from a fragment constant method(4). Mestranol was greater than 90% removed in the sewage treatment process; however, 99.80% attributed to sludge adsorbance(5) indicating that biodegradation is not an important environmental fate process in soil(SRC).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 2.2X10+4(SRC), determined from a structure estimation method(2), indicates that mestranol is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 4.5X10-9 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 500(SRC), from a log Kow of 4.61(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is high, provided the compound is not metabolized by the organism(SRC). Mestranol was greater than 90% removed in the sewage treatment process; however, 99.80% attributed to sludge adsorbance(6), indicating that biodegradation is not an important environmental fate process in water(SRC).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), mestranol, which has an estimated vapor pressure of 9.7X10-9 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase mestranol may be removed from the air by wet or dry deposition(SRC). Mestranol absorbs at wavelengths of 287.5 nm(4), and therefore may be susceptible to direct photolysis by sunlight(SRC).

Mestranol is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(1). Mestranol absorbs at wavelengths of 287.5 nm(2), and therefore may be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 500 was calculated in fish for mestranol(SRC), using a log Kow of 4.61(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is high(SRC), provided the compound is not metabolized by the organism(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of mestranol can be estimated to be 2.2X10+4(SRC). According to a classification scheme(2), this estimated Koc value suggests that mestranol is expected to be immobile in soil. Mestranol exhibited a sorption coefficient (log Kd) of 2.26 using Blackwater estuary sediments and Thames River sediments, UK(3). The compound was not detected in the effluent of a 23-day column drainage study using Mahall-Laveen sandy loam soil from an area northwest of Phoenix, AZ and 200 L of treated effluent from a municipal waste treatment facility; reporting limit = 0.005 ug/L(4), suggesting adsorption to soil in the column(SRC). A log Koc of 5.85 was measured in a sewage treatment process, corresponding to a Koc of 707,397. Mestranol was greater than 90% removed in the sewage treatment process, with 99.80% attributed to sludge adsorbance(5).

The Henry's Law constant for mestranol is estimated as 4.5X10-9 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that mestranol is expected to be essentially nonvolatile from water and moist soil surfaces(2). Mestranol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 9.7X10-9 mm Hg(SRC), determined from a fragment constant method(3).

SURFACE WATER: Mestranol concentrations were reported at a 10% frequency with a maximum concentration of 0.407 ug/L and median 0.074 ug/L, in 70 of 139 U.S. streams sampled from 1999-2000 as part of the USGS National Reconnaissance Study(1). Mestranol was tested for but not detected in river water samples from the Jalle d'Eysines which receives effluent from the Eysines Sewage Treatment Plant (northern suburbs, Bordeaux, France) and runs through agricultural and residential areas; detection limit 0.7-3.0 ng/L(2). Mestradiol was not detected in 5 samples of unspecified surface waters from the Great Lakes Basin; minimum detection is <0.005 ug/L(3).

Patients who are fully breast-feeding should not take Norinyl-1 tablets since, in common with other combined oral contraceptives, the estrogen component may reduce the amount of milk produced. In addition, active ingredients or their metabolites have been detected in the milk of mothers taking oral contraceptives.

Occupational exposure to mestranol may occur through inhalation and dermal contact with this compound at workplaces where mestranol is produced or used. Exposure to mestranol via ingestion will occur when administered drugs containing this compound. Monitoring data indicate that the general population may be exposed to mestranol at well below the therapeutic dose via ingestion of drinking water. (SRC)

Mestranol was used as one of the first oral contraceptives.

Estrogens|Mestranol /is indicated in combination with an oral progestin/ for the prevention of pregnancy in women who elect to use this product as a method of contraception. /Included in US product label/

Cigarette smoking increases the risk of serious cardiovascular side effects from oral contraceptive use. This risk increases with age and with heavy smoking (15 or more cigarettes per day) and is quite marked in women over 35 years of age. Women who use oral contraceptives are strongly advised not to smoke.|Patients who are fully breast-feeding should not take Norinyl-1 tablets since, in common with other combined oral contraceptives, the estrogen component may reduce the amount of milk produced. In addition, active ingredients or their metabolites have been detected in the milk of mothers taking oral contraceptives.|Oral contraceptives should not be used in women who have the following conditions: thrombophlebitis or thromboembolic disorders; a past history of deep vein thrombophlebitis or thromboembolic disorders; cerebral vascular or coronary artery disease; known or suspected carcinoma of the breast; carcinoma of the endometrium or other known or suspected estrogen-dependent neoplasia; undiagnosed abnormal genital bleeding; cholestatic jaundice of pregnancy or jaundice with prior pill use; hepatic adenomas, carcinomas or benign liver tumors.|FDA Pregnancy Risk Category: X /CONTRAINDICATED IN PREGNANCY. Studies in animals and or humans, or investigational or post-marketing reports, have demonstrated positive evidence of fetal abnormalities or risk which clearly outweighs any possible benefit to the patient.|For more Drug Warnings (Complete) data for MESTRANOL (37 total), please visit the HSDB record page.

Compounds that interact with ESTROGEN RECEPTORS in target tissues to bring about the effects similar to those of ESTRADIOL. Estrogens stimulate the female reproductive organs, and the development of secondary female SEX CHARACTERISTICS. Estrogenic chemicals include natural, synthetic, steroidal, or non-steroidal compounds. (See all compounds classified as Estrogens.)|Oral contraceptives which owe their effectiveness to hormonal preparations. (See all compounds classified as Contraceptives, Oral, Hormonal.)

Mestranol binds poorly to the estrogen receptor and its estrogenic effect is due to its rapid demethylation in the liver to form ethinylestradiol; however, demethylation is not complete and more mestranol must be administered than ethinylestradiol to achieve similar effects.|The excretion of metabolites in urine ranged from 10-27%; that of ethinyloestradiol metabolites ranges from 36-54%. When position 2 or 4 of the mestranol molecule is tritiated or marked with (14)C, between 14-45% of the radioactivity is released into the body water.

Mestranol is rapidly absorbed and extensively metabolised to ethinylestradiol. Ethinylestradiol is rapidly and well absorbed from the gastro-intestinal tract but is subject to some first-pass metabolism in the gut-wall. Compared to many other estrogens it is only slowly metabolized in the liver. Excretion is via the kidneys with some appearing also in the feces.|In the body it undergoes rapid hepatic demethylation to ethinyl estradiol, which is its active form. /Estrogens/|Mestranol, the 3-methyl ether of ethinyloestradiol, is more lipophilic than ethinyloestradiol and has a greater affinity for adipose tissues, as shown by experiments in rats. Mestranol itself does not bind significantly to estrogen receptors at the sites of their antifertility action; its hormonal effectiveness relies on transformation to ethinyloestradiol. About 35% of a mestranol dose is transformed into ethinyloestradiol in rats, 61% in mice, 56% in rabbits and 54% in man. The demethylated portion then follows the pathways for ethinyloestradiol that are typical for the particular species, e.g., 2-hydroxylation in rats and D-homoannulation in rabbits and guinea-pigs. Mestranol is also demethylated to ethinylestradiol in non-human primates.|The metabolism of mestranol in humans is closely related to that of ethinyloestradiol. Mestranol is transformed to ethinyloestradiol by demethylation: after i.v. administration of (14)C-mestranol to human volunteers, about 50% of the dose is demethylated to ethinylestradiol. The main compound found in plasma is ethinyloestradiol-3-sulfate.|For more Metabolism/Metabolites (Complete) data for MESTRANOL (6 total), please visit the HSDB record page.|Mestranol has known human metabolites that include ethinylestradiol.

Mestranol is the 3-methyl ether of ethinylestradiol. Ethinylestradiol, is a synthetic derivative of estradiol. Ethinylestradiol is orally bio-active and the estrogen used in almost all modern formulations of combined oral contraceptive pills. It binds to (and activates) the estrogen receptor. Mestranol is a biologically inactive prodrug of ethinylestradiol to which it is demethylated in the liver with a conversion efficiency of 70%. Estrogens diffuse into their target cells and interact with a protein receptor. Target cells include the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary. The combination of an estrogen with a progestin suppresses the hypothalamic-pituitary system, decreasing the secretion of gonadotropin-releasing hormone (GnRH).|The mode of action of Norinyl-1 is similar to that of other progestogen/estrogen oral contraceptives and includes the inhibition of ovulation, the thickening of cervical mucus so as to constitute a barrier to sperm and the rendering of the endometrium unreceptive to implantation. Such activity is exerted through a combined effect on one or more of the following: hypothalamus, anterior pituitary, ovary, endometrium and cervical mucus.|Estrogens have an important role in the reproductive, skeletal, cardiovascular, and central nervous systems in women, and act principally by regulating gene expression. Biologic response is initiated when estrogen binds to a ligand-binding domain of the estrogen receptor resulting in a conformational change that leads to gene transcription through specific estrogen response elements (ERE) of target gene promoters; subsequent activation or repression of the target gene is mediated through 2 distinct transactivation domains (ie, AF-1 and AF-2) of the receptor. The estrogen receptor also mediates gene transcription using different response elements (ie, AP-1) and other signal pathways. Recent advances in the molecular pharmacology of estrogen and estrogen receptors have resulted in the development of selective estrogen receptor modulators (eg, clomiphene, raloxifene, tamoxifen, toremifene), agents that bind and activate the estrogen receptor but that exhibit tissue-specific effects distinct from estrogen. Tissue-specific estrogen-agonist or -antagonist activity of these drugs appears to be related to structural differences in their estrogen receptor complex (eg, specifically the surface topography of AF-2 for raloxifene) compared with the estrogen (estradiol)-estrogen receptor complex. A second estrogen receptor also has been identified, and existence of at least 2 estrogen receptors (ER-alpha, ER-beta) may contribute to the tissue-specific activity of selective modulators. While the role of the estrogen receptor in bone, cardiovascular tissue, and the CNS continues to be studied, emerging evidence indicates that the mechanism of action of estrogen receptors in these tissues differs from the manner in which estrogen receptors function in reproductive tissue. /Estrogen General Statement/|Intracellular cytosol-binding proteins for estrogens have been identified in estrogen-responsive tissues including the female genital organs, breasts, pituitary, and hypothalamus. The estrogen-binding protein complex (ie, cytosol-binding protein and estrogen) distributes into the cell nucleus where it stimulates DNA, RNA, and protein synthesis. The presence of these receptor proteins is responsible for the palliative response to estrogen therapy in women with metastatic carcinoma of the breast. /Estrogen General Statement/|Estrogens have generally favorable effects on blood cholesterol and phospholipid concentrations. Estrogens reduce LDL-cholesterol and increase HDL-cholesterol concentrations in a dose-related manner. The decrease in LDL-cholesterol concentrations associated with estrogen therapy appears to result from increased LDL catabolism, while the increase in triglyceride concentrations is caused by increased production of large, triglyceride-rich, very-low-density lipoproteins (VLDLs); changes in serum HDL-cholesterol concentrations appear to result principally from an increase in the cholesterol and apolipoprotein A-1 content of HDL2- and a slight increase in HDL3-cholesterol. /Estrogen General Statement/|For more Mechanism of Action (Complete) data for MESTRANOL (7 total), please visit the HSDB record page.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/SIGNS AND SYMPTOMS/ Overdosage may be manifested by nausea, vomiting, breast enlargement and vaginal bleeding. There is no specific antidote and treatment should be symptomatic...|/EPIDEMIOLOGY STUDIES/ There is some evidence from epidemiologic studies that use of oral contraceptives may be associated with an increased risk of cervical carcinoma. In one study, the incidence of biopsy-proven cervical neoplasia (ie, dysplasia, carcinoma in situ, or invasive carcinoma) was increased in long-term oral contraceptive users compared with women who used an intrauterine contraceptive device (IUD)...|/EPIDEMIOLOGY STUDIES/ Although a causal relationship to the drugs could not be excluded, data from a population-based (Costa Rican women), case-control study suggest that the increased risk of carcinoma in situ associated with oral contraceptive use may have resulted from a detection bias secondary to more frequent use of Papanicolaou tests in oral contraceptive users. These data revealed no evidence of increased risk of invasive cervical cancer in users compared with nonusers.|/EPIDEMIOLOGY STUDIES/ Several retrospective case-controlled studies have shown an increased relative risk of endometrial carcinoma in postmenopausal women who received prolonged estrogen replacement therapy for relief of menopausal symptoms. Although an increased risk of adenocarcinoma of the endometrium has been associated with sequential oral contraceptive use (sequential oral contraceptives are no longer available in the US), no association between increased risk of endometrial cancer and use of currently available estrogen-progestin combination preparations or progestin-only preparations has been shown, although individual cases have been reported. The Cancer and Steroid Hormone Study of the US Centers for Disease Control and Prevention (CDC) and the National Institute of Child Health and Human Development (NICHHD) showed that women who used estrogen-progestin oral contraceptives had decreased relative risk of epithelial endometrial cancer (ie, adenocarcinoma, adenoacanthoma, and adenosquamous cancers) compared with nonusers; the protective effect occurred in women who had used combination oral contraceptives for at least 12 months, and it persisted for at least 15 years after discontinuance of oral contraceptives. This decreased risk of endometrial cancer was not evident in women who had used oral contraceptives for less than 12 months.|For more Human Toxicity Excerpts (Complete) data for MESTRANOL (24 total), please visit the HSDB record page.

19-Norpregna-1,3,5(10)-trien-20-yn-17-ol, 3-methoxy-, (17alpha)-

Mestranol is commercially available as a component of combination tablets with chlormadinone acetate, ethynodiol diacetate, levonorgestrel, lynestrenol or norethisterone and formerly with norethynodrel.|ENOVID 5 MG CONTAINS 5 MG NORETHYNODREL & 0.075 MG MESTRANOL; ENOVID-E CONTAINS 2.5 MG NORETHYNODREL & 0.10 MG MESTRANOL.

Also used in combination with chlormadinone acetate, ethynodiol, kynestranol, norethindrone or norethynodrel, q.q.v.; has been used in combination with megestrol acetate, q.v.

Method: AOAC 971.42; Procedure: spectrophotometric method (Applicable in presence of norethindrone and norethynodrel; not applicable in presence of ethynodiol diacetate or chlormadinone acetate); Analyte: mestranol; Matrix: drugs; Detection Limit: not provided.|Method: AOAC 975.59; Procedure: spectrophotometric method; Analyte: mestranol with ethynodiol diacetate; Matrix: drugs; Detection Limit: not provided.|Analyte: mestranol; matrix: chemical identification; procedure: infrared absorption spectrophotometry with comparison to standards|Analyte: mestranol; matrix: chemical identification; procedure: ultraviolet absorption spectrophotometry with comparison to standards|For more Analytic Laboratory Methods (Complete) data for MESTRANOL (6 total), please visit the HSDB record page.

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Pharmaceuticals