Medroxyprogesterone

344.49

344.49

208-298-6

HSU1C9YRES

27408

DTXSID0036508

C629

Crystals from chloroform

G03AC06|G - Genito urinary system and sex hormones|L - Antineoplastic and immunomodulating agents

29372390

54.4

3.50 (est)

Solid

1.1±0.1 g/cm3

220-223.5 °C

488.0±45.0 °C at 760 mmHg

263.0±25.2 °C

1.554

In water, 2.95 mg/L at 25 deg C (est)

Refrigerator

1.93X10-10 mm Hg at 25 deg C (est)

D25 +75° (in chloroform)

Henry's Law constant = 1.34X10-8 atm-cu m/mol at 25 °C (est)

White to off-white, crystalline powder, odorless. Melting range 200-208 °C. Stable in air. Freely soluble in chlorform. /Medroxyprogesterone acetate/

NONH for all modes of transport

3

48-63-68

22-24/25

TU5300000

Xn

Stable in air. /Acetate/

P280

H361

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.|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.

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

Medroxyprogesterone was reported in 14% of 95-144 samples of central California municipal waste water treatment plant effluent with a maximum concentration of 14.9 ng/L(1). It was not detected in a typical dairy waste disposal system for 2000 dairy cows in San Jacinto, CA; samples include fresh manure less than 2 hrs old, piled manure at 2 weeks, and 3 lagoon dams at 3 months(2).

Sequential conversion of estradiol (E) to 2/4-hydroxyestradiols and 2-/4-methoxyestradiols (MEs) by CYP450s and catechol-O-methyltransferase, respectively, contributes to the inhibitory effects of E on smooth muscle cells (SMCs) via estrogen receptor-independent mechanisms. Because medroxyprogesterone (MPA) is a substrate for CYP450s, /investigators/ hypothesized that MPA may abrogate the inhibitory effects of E by competing for CYP450s and inhibiting the formation of 2/4-hydroxyestradiols and MEs. To test this hypothesis, /the authors/ investigated the effects of E on SMC number, DNA and collagen synthesis, and migration in the presence and absence of MPA. The inhibitory effects of E on cell number, DNA synthesis, collagen synthesis, and SMC migration were significantly abrogated by MPA. For example, E (0.1micromol/L) reduced cell number to 51+/-3.6% of control, and this inhibitory effect was attenuated to 87.5+/-2.9% by MPA (10 nmol/L). Treatment with MPA alone did not alter any SMC parameters, and the abrogatory effects of MPA were not blocked by RU486 (progesterone-receptor antagonist), nor did treatment of SMCs with MPA influence the expression of estrogen receptor-alpha or estrogen receptor-beta. In SMCs and microsomal preparations, MPA inhibited the sequential conversion of E to 2-2/4-hydroxyestradiol and 2-ME. Moreover, as compared with microsomes treated with E alone, 2-ME formation was inhibited when SMCs were incubated with microsomal extracts incubated with E plus MPA. /These/ findings suggest that the inhibitory actions of MPA on the metabolism of E to 2/4-hydroxyestradiols and MEs may negate the cardiovascular protective actions of estradiol in postmenopausal women receiving estradiol therapy combined with administration of MPA.|Medroxyprogesterone acetate (MPA) ... is extensively metabolized in the intestinal mucosa and in the liver. Cytochrome P450s (CYPs) involved in the metabolism of MPA were identified by using human liver microsomes and recombinant human CYPs. In this study, the overall metabolism of MPA was determined as the disappearance of the parent drug from an incubation mixture. The disappearance of MPA in human liver microsomes varied 2.6-fold among the 18 samples studied. The disappearance of MPA in the same panel of 18 human liver microsomes was significantly correlated with triazolam alpha-hydroxylase activity, a marker activity of CYP3A (r = 0.764; P < 0.001). Ketoconazole, an inhibitor of CYP3A4, potently inhibited the disappearance of MPA in 18 human liver microsomes. Anti-CYP3A antibody also inhibited 86% of the disappearance of MPA in human liver microsomes. Although sulfaphenazole (an inhibitor of CYP2C9) and S-mephenytoin (an inhibitor of CYP2C19) partially inhibited the disappearance of MPA, no effect of the anti-CYP2C antibody was observed. The disappearance of MPA did not correlate with either the activity metabolized via CYP2C9 (diclofenac 4'-hydroxylase activity) or the activity metabolized via CYP2C19 (S-mephenytoin 4'-hydroxylase activity). Among the 12 recombinant human CYPs (CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C18, CYP2C19, CYP2D6, CYP2E1, CYP3A4, and CYP3A5) studied, only CYP3A4 showed metabolic activity of MPA. These results suggest that CYP3A4 is mainly involved in the overall metabolism of MPA in human liver microsomes.|This report describes a fatal pneumonitis occurring in a breast cancer patient while on adjuvant treatment with radiotherapy and medroxyprogesterone acetate. The clinical and radiologic features, as well as the timing of this pneumonitis, make a radiation pneumonitis more than probable. A radiation pneumonitis was also observed in other patients treated in the same way. Medroxyprogesterone acetate thus seems to act as a radiosensitizer since no such effects were seen in patients treated with radiotherapy alone. The radioenhancing effect is not limited to the lungs, since radioesofagitis was also encountered in similarly treated patients.

Medroxyprogesterone's production and use as a progestogen, injectable contraceptive, and hormonal antineoplastic in humans and also as an estrus regulator in veterinary medicine(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 1,200(SRC), determined from a structure estimation method(2), indicates that medroxyprogesterone is expected to have low mobility in soil(SRC). Volatilization of medroxyprogesterone from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.3X10-8 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Medroxyprogesterone is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.9X10-10 mm Hg at 25 °C(SRC), determined from a fragment constant method(4). Biodegradation data in soil were not available(SRC, 2011).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1,200(SRC), determined from a structure estimation method(2), indicates that medroxyprogesterone 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 1.3X10-8 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 94(SRC), from an estimated log Kow of 3.50(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is moderate(SRC). Biodegradation data in water were not available(SRC, 2011).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), medroxyprogesterone, which has an estimated vapor pressure of 1.9X10-10 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 medroxyprogesterone may be removed from the air by wet or dry deposition(SRC). Medroxyprogesterone contains chromophores that absorb at wavelengths >290 nm(3), and therefore may be susceptible to direct photolysis by sunlight(SRC).

Medroxyprogesterone is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(1). Medroxyprogesterone contains chromophores that absorb at wavelengths >290 nm(1), and therefore may be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 94 was calculated in fish for medroxyprogesterone(SRC), using an estimated log Kow of 3.50(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is moderate(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of medroxyprogesterone can be estimated to be 1,200(SRC). According to a classification scheme(2), this estimated Koc value suggests that medroxyprogesterone is expected to have low mobility in soil.

The Henry's Law constant for medroxyprogesterone is estimated as 1.3X10-8 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that medroxyprogesterone is expected to be essentially nonvolatile from water surfaces(2). Medroxyprogesterone's Henry's Law constant indicates that volatilization from moist soil surfaces may not occur(SRC). Medroxyprogesterone is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.9X10-10 mm Hg(SRC), determined from a fragment constant method(3).

SURFACE WATER: Medroxyprogesterone was detected at a maximum concentration of 0.4 ng/L in 1% of 89 water samples from 30 rangeland grazing areas in Stanislaus, Marin, and Sonoma counties in central California, between April 2005 and March 2006. It was detected in 12% of 32 samples collected near dairy farms, with a maximum concentration of 1.0 ng/L(1).

Radioimmunoassay methods were used estimating contraceptive levels in breast milk and plasma samples in 7 lactating women after injection of 150 mg medroxyprogesterone acetate. Levels in breast milk were similar to plasma; ratio being almost 1:1 up to 87 days.

NIOSH (NOES Survey 1981-1983) has statistically estimated that 339 workers (170 of these were female) were potentially exposed to medroxyprogesterone in the US(1). Occupational exposure to medroxyprogesterone may occur through inhalation and dermal contact with this compound at workplaces where medroxyprogesterone is produced or used. Exposure to medroxyprogesterone via ingestion will occur when administered drugs containing this compound. Monitoring data indicate that the general population may be exposed to medroxyprogesterone at well below the therapeutic dose via ingestion of drinking water(SRC).

Contraceptives, Oral, Synthetic; Progestational Hormones, Synthetic|Medroxyprogesterone Acetate Tablets USP are a progestin indicated for the treatment of secondary amenorrhea and abnormal uterine bleeding due to hormonal imbalance in the absence of organic pathology, such as fibroids or uterine cancer. /Included in US product label/|Medroxyprogesterone Acetate Tablets USP are indicated to reduce the incidence of endometrial hyperplasia in nonhysterectomized postmenopausal women receiving daily oral conjugated estrogens tablets. /Included in US product lable/|Adjunctive therapy and palliative treatment of inoperable, recurrent, and metastatic endometrial or renal carcinoma. /Included in US Product label/|For more Therapeutic Uses (Complete) data for MEDROXYPROGESTERONE (11 total), please visit the HSDB record page.

In women receiving parenteral medroxyprogesterone for contraception (alone or in fixed combination with estradiol cypionate) or the management of pain associated with endometriosis, the most common adverse effects are menstrual abnormalities. Irregular and unpredictable menstrual bleeding pattern, including spotting, occurs frequently during the first months of therapy with the drug. In women receiving IM medroxyprogesterone acetate in fixed combination with estradiol cypionate, about 59% experienced alterations in menstrual bleeding pattern (eg, amenorrhea; frequent, irregular, prolonged, or infrequent bleeding) after 1 year of use; the incidence of irregular bleeding remained relatively constant at approximately 30% throughout the first year of use. If abnormal bleeding persists or is severe, appropriate steps to investigate the possibility of organic pathology should be undertaken, and appropriate therapy instituted as necessary.|Amenorrhea also occurs frequently in women receiving the drug for contraception or the management of pain associated with endometriosis, and as the duration of therapy increases the likelihood of intermenstrual bleeding decreases and that of amenorrhea increases; up to about 60 and 70% of women reportedly have amenorrhea after 1 and 2 years, respectively, of contraceptive therapy with medroxyprogesterone.|Although concomitant use of low doses of estrogens has been suggested to treat medroxyprogesterone-induced menstrual disturbances, the evidence for efficacy of this therapy is equivocal. Contraceptive use of the drug should be discontinued in women who do not tolerate irregular and unpredictable bleeding or amenorrhea.|Heavy or continuous vaginal bleeding may occur in some women receiving medroxyprogesterone, but rarely requires estrogen therapy. Impaired fertility persists long after discontinuance of the drug.|For more Drug Warnings (Complete) data for MEDROXYPROGESTERONE (38 total), please visit the HSDB record page.

Oral contraceptives which owe their effectiveness to hormonal preparations. (See all compounds classified as Contraceptives, Oral, Hormonal.)|Oral contraceptives which owe their effectiveness to synthetic preparations. (See all compounds classified as Contraceptives, Oral, Synthetic.)

No specific investigation on the absolute bioavailability of medroxyprogesterone (MPA) in humans has been conducted. MPA is rapidly absorbed from the gastrointestinal tract, and maximum MPA concentrations are obtained between 2 to 4 hours after oral administration.|Administration of medroxyprogesterone acetate with food increases the bioavailability of MPA. A 10 mg dose of medroxyprogesterone acetate, taken immediately before or after a meal, increased MPA Cmax (50 to 70%) and AUC (18 to 33%). The half-life of MPA was not changed with food.|Medroxyprogesterone is approximately 90% protein bound, primarily to albumin; no MPA binding occurs with sex hormone binding globulin.|Most MPA metabolites are excreted in the urine as glucuronide conjugates with only minor amounts excreted as sulfates.|For more Absorption, Distribution and Excretion (Complete) data for MEDROXYPROGESTERONE (10 total), please visit the HSDB record page.

Following oral dosing, MPA is extensively metabolized in the liver via hydroxylation, with subsequent conjugation and elimination in the urine. ...MPA is almost exclusively eliminated via hepatic metabolism. In 14 patients with advanced liver disease, MPA disposition was significantly altered (reduced elimination). In patients with fatty liver, the mean percent dose excreted in the 24-hour urine as intact MPA after a 10 mg or 100 mg dose was 7.3% and 6.4%, respectively.

Elimination half-life of oral preparation is 32 to 44 hr. /Acetate/

Medroxyprogesterone shares the pharmacologic actions of the progestins. In women with adequate endogenous estrogen, medroxyprogesterone transforms a proliferative endometrium into a secretory one. Medroxyprogesterone has been shown to have slight androgenic activity in animals. Anabolic effects have also been reported, but the drug apparently lacks appreciable estrogenic activity in humans. In animals, the drug exhibits pronounced adrenocorticoid activity, but a clinically important effect has not been observed in humans. Medroxyprogesterone inhibits the secretion of pituitary gonadotropins following usual IM or subcutaneous dosages (eg, 150 or 104 mg every 3 months), thus preventing follicular maturation and ovulation and resulting in endometrial thinning; these effects result in contraceptive activity. Available evidence indicates that these effects do not occur following oral administration of usual dosages (ie, 5-10 mg daily as single daily doses) of the drug. High doses of medroxyprogesterone inhibit pituitary secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and will prevent cyclic gonadotropin surges that occur during the normal menstrual cycle. It has been suggested that the drug acts at the hypothalamus since it does not suppress the release of LH and FSH following administration of gonadotropin-releasing hormone and since basal concentrations of LH and FSH remain within the low normal range when the drug is used as a contraceptive. Although the mechanism of action has not been determined, medroxyprogesterone has antineoplastic activity against some cancers (eg, endometrial carcinoma, renal carcinoma).|Progestins elicit, to varying degrees, all the pharmacologic responses usually produced by progesterone: induction of secretory changes in the endometrium, increase in basal body temperature (thermogenic action), production of histologic changes in vaginal epithelium, relaxation of uterine smooth muscle, stimulation of mammary alveolar tissue growth, pituitary inhibition, and production of withdrawal bleeding in the presence of estrogen. /Progestins/|Following binding to cytoplasmic receptor protein, steroid is transported to nucleus, and complex is bound there in reactions analogous to those described... for estrogens. However, there is no apparent need for receptor alteration, as with estrogen receptor. /Progesterone/|Although medroxyprogesterone acetate (MPA) is used as an injectable contraceptive, in hormone replacement therapy (HRT) and in treatment of certain cancers, the steroid receptors and their target genes involved in the actions of MPA are not well understood. /Investigators/ show that MPA, like dexamethasone (dex), significantly represses tumour necrosis factor (TNF)-stimulated interleukin-6 (IL-6) protein production in mouse fibroblast (L929sA) cells. In addition, MPA repressed IL-6 and IL-8 promoter-reporter constructs at the transcriptional level, via interference with nuclear factor kappaB (NFkappaB) and activator protein-1 (AP-1). Furthermore, like dex, MPA does not affect NFkappaB DNA-binding activity. /The authors/ also observed significant transactivation by MPA of a glucocorticoid response element (GRE)-driven promoter-reporter construct in both L929sA and COS-1 cells. The MPA-induced nuclear translocation of the glucocorticoid receptor (GR), as well as the antagonistic effects of RU486, strongly suggest that the actions of MPA in these cells are mediated at least in part via the GR.|/Investigators/ assessed the transcriptional effects of MPA as compared with those of progesterone and dihydrotestosterone (DHT) in human breast cancer cells. A new progesterone receptor-negative, androgen receptor-positive human breast cancer cell line, designated Y-AR, was engineered and characterized. Transcription assays using a synthetic promoter/reporter construct, as well as endogenous gene expression profiling comparing progesterone, MPA and DHT, were performed in cells either lacking or containing progesterone receptor and/or androgen receptor. In progesterone receptor-positive cells, MPA was found to be an effective progestin through both progesterone receptor isoforms in transient transcription assays. Interestingly, DHT signaled through progesterone receptor type B. Expression profiling of endogenous progesterone receptor-regulated genes comparing progesterone and MPA suggested that although MPA may be a somewhat more potent progestin than progesterone, it is qualitatively similar to progesterone. To address effects of MPA through androgen receptor, expression profiling was performed comparing progesterone, MPA and DHT using Y-AR cells. These studies showed extensive gene regulatory overlap between DHT and MPA through androgen receptor and none with progesterone. Interestingly, there was no difference between pharmacological MPA and physiological MPA, suggesting that high-dose therapeutic MPA may be superfluous. /This/ comparison of the gene regulatory profiles of MPA and progesterone suggests that, for physiologic hormone replacement therapy, the actions of MPA do not mimic those of endogenous progesterone alone. ... It is possible that the increased breast cancer risk and/or the therapeutic efficacy of MPA in cancer treatment is in part mediated by androgen receptor.

Reported impurities include: 6alpha,17a-dimethyl-3,17-dioxo-D-homoandrost-4-en-17aalpha- yl acetate, 6beta-hydroxy-6-methyl-3,20-dioxopregn-4-en-17-yl acetate (6beta-hydroxymedroxyprogesterone acetate), 17-hydroxy-6alpha-methylpregn-4-ene-3,20-dione (medroxyprogesterone), 6-methyl-3,20-dioxopregna-4,6-dien-17-yl acetate, 6alpha-methyl-3,20-dioxo-5beta-pregnan-17-yl acetate (4,5beta-dihydromedroxyprogesterone acetate), 6beta-methyl-3,20-dioxopregn- 4-en-17-yl acetate (6-epimedroxyprogesterone acetate) and 6-methylene-3,20-dioxopregn- 4-en-17-yl acetate. /Medroxyprogesterone acetate/

/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/

/HUMAN EXPOSURE STUDIES/ When medroxyprogesterone is used as a contraceptive, unintended pregnancies that occur within 1-2 months after IM injection of the drug may be characterized by impaired fetal growth as evidenced by low birthweights, which theoretically could result in an increased risk of neonatal death. However, the attributable risk of this adverse effect is low because such pregnancies are unlikely. The risk of low birthweight was particularly evident when conception was estimated to occur within 4 weeks of medroxyprogesterone injection. ... An increase in polysyndactyly particularly among offspring of women younger than 30 years of age, and chromosomal anomalies also have been observed in neonates born to women who received IM medroxyprogesterone contraception.|/HUMAN EXPOSURE STUDIES/ Milk quality and quantity was studied in 6 breast feeding women admin 150 mg depomedroxyprogesterone acetate im every 3 months. The drug was associated with a decrease in concentration of protein in milk.|/HUMAN EXPOSURE STUDIES/ ...The purpose of this study was to determine the acute effects of MPA when used in combination with estradiol on markers of cardiovascular risk in young women. /The authors/ suppressed endogenous estrogens and progesterone in 10 premenopausal women using a gonadotropin-releasing hormone antagonist (GnRHa) for 10 days. On day 4 of GnRHa subjects received 0.1 mg of estradiol (GnRHa+E(2)), and on day 7 5 mg of MPA was added (GnRHa+E(2)+MPA). Endothelium-dependent vasodilation and endothelium-independent vasodilation of the brachial artery, lipids, homocysteine, high-sensitivity C-reactive protein, and endothelin-1 were assessed during treatment with GnRHa, GnRHa+E(2), and GnRHa+E(2)+MPA. Four additional subjects were tested to validate the efficacy of the GnRHa model and confirm the findings. Endothelium-dependent vasodilation was greater during GnRHa+E(2) than during GnRHa or GnRHa+E(2)+MPA (P = 0.006). Endothelin-1 was lower during GnRHa+E(2) than GnRHa alone (P = 0.039). Endothelin-1 increased with the addition of MPA and was not significantly different from GnRHa alone. There were no differences in the other markers of cardiovascular risk between hormone treatment days. These data suggest that acute MPA administration negates the beneficial effects of estradiol on endothelium-dependent vasodilation in young women. In addition, these data suggest that estradiol decreases endothelin-1 concentrations and the addition of MPA may counteract the effect of estradiol on endothelin-1.|/SIGNS AND SYMPTOMS/ Overdosage of estrogen plus progestin therapy may cause nausea and vomiting, breast tenderness, dizziness, abdominal pain, drowsiness/fatigue and withdrawal bleeding may occur in women. Treatment of overdose consists of discontinuation of CE/MPA together with institution of appropriate symptomatic care.|For more Human Toxicity Excerpts (Complete) data for MEDROXYPROGESTERONE (26 total), please visit the HSDB record page.

(6 alpha)-17-Hydroxy-6-methylpregn-4-ene-3,20-dione

Medroxyprogesterone acetate is available commercially as single-ingredient tablets, as combination tablets with conjugated estrogens, estradiol or estradiol cypionate and as sterile suspensions. /Medroxyprogesterone acetate/

...Used in human medicine in US for treatment of endometriosis, habitual abortion and threatened abortion. ...in Oct 1973 US Food & Drug Administration announced plans to withdraw approval for certain strengths and vial sizes ... destined for these applications ... /Medroxyprogesterone acetate/|...In Oct 1973 US Food & Drug Administration proposed to restrict approved uses of medroxyprogesterone acetate tablets to treatment of endometriosis, secondary amenorrhea and abnormal uterine bleeding due to hormonal imbalance, in absence of organ pathology such as submucous fibroids or uterine cancer... /Medroxyprogesterone acetate/|From 1964 until late 1970...product was withdrawn from US market, medroxyprogesterone acetate was used in us as component of oral contraceptives. ... Product was removed...because studies showed that breast nodules developed in beagles given high doses of medroxyprogesterone acetate. /Medroxyprogesterone acetate/

Method: AOAC 971.43; Procedure: spectrophotometric method; Analyte: medroxyprogesterone acetate; Matrix: drugs; Detection Limit: not provided. /Medroxyprogesterone acetate/|Analyte: medroxyprogesterone; matrix: chemical identification; procedure: infrared absorption spectrophotometry with comparison to standards /Medroxyprogesterone acetate/|Analyte: medroxyprogesterone; matrix: chemical identification; procedure: ultraviolet absorption spectrophotometry with comparison to standards /Medroxyprogesterone acetate/|Analyte: medroxyprogesterone; matrix: chemical purity; procedure: liquid chromatography with ultraviolet detection at 254 nm and comparison to standards /Medroxyprogesterone acetate/|For more Analytic Laboratory Methods (Complete) data for MEDROXYPROGESTERONE (6 total), please visit the HSDB record page.

Quantification of the intact drug in plasma was made via GLC using an electron capture detector. The assay is quantitative above 1 ng/mL and overall precision approx 10% in the range of 5-20 ng/mL.|Radioimmunoassay methods were used estimating contraceptive levels in breast milk and plasma samples in 7 lactating women after injection of 150 mg medroxyprogesterone acetate. Levels in breast milk were similar to plasma; ratio being almost 1:1 up to 87 days.

Lipids -> Sterol Lipids [ST] -> Steroids [ST02] -> C21 steroids (gluco/mineralocorticoids, progestogins) and derivatives [ST0203]|Pharmaceuticals -> Animal Drugs -> Approved in Taiwan