Cyproterone acetate

416.94

416.94

207-048-3

4KM2BN5JHF

81430

DTXSID5020366

C1059

Crystals from diisopropyl ether|White crystalline powder

2937290090

60.4

3.6

Odour

1.3±0.1 g/cm3

200-201 °C

525.9°C at 760 mmHg

177.6±29.1 °C

1.582

Practically insoluble in water, very soluble in methylene chloride, freely soluble in acetone, soluble in methanol, sparingly soluble in anhydrous ethanol.

2-8°C

4.27X10-7 mm Hg at 25 deg C (est)

Specific rotation = +152 deg to +157 deg at 20 °C

Henry's Law constant = 4.25X10-90 atm-cu m/mol at 25 °C (est)

199.4 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]

Crystals from acetate, mp 237.5-240 °C /Cyproterone/|Hydroxyl radical reaction rate constant = 1.87X10-10 cu cm/molec-sec at 25 °C (est)|Ozone radical reaction rate constant = 5.2X10-17 cu cm/molec-sec at 25 °C (est)

NONH for all modes of transport

3

20/21/22-40-36/37/38

22-36-26

GZ2230000

Xn,Xi

Stable under recommended storage conditions.

P261-P280

H312 + H332-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.

Hand protection: For prolonged or repeated contact use protective gloves. Eye protection: Safety glasses with side-shields conforming to EN166. Skin and body protection: Choose body protection according to the amount and concentration of the dangerous substance at the work place.|Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. ... Wear self contained breathing apparatus for fire fighting if necessary.

Personal precautions: Use personal protective equipment. Avoid dust formation. Avoid breathing dust. Ensure adequate ventilation. Environmental precautions: Do not let product enter drains. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Keep in suitable, closed containers for disposal.

Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Provide appropriate exhaust ventilation at places where dust is formed. Normal measures for preventive fire protection.|Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.|SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

At high therapeutic cyproterone acetate doses of three times 100 mg per day, cyproterone acetate may inhibit CYP2C8. Thiazolidinediones (ie the anti-diabetics pioglitazone and rosiglitazone) are substrates or CYP2C8 (increased blood levels of these anti-diabetics may require dose adjustment).|Alcohol appears to reduce the effect of /cyproterone/ which is of no value in chronic alcoholics.|The risk of statin-associated myopathy or rhabdomyolysis may be increased when those HMG-CoA inhibitors (statins) which are primarily metabolised by CYP3A4 are co-administered with high cyproterone acetate doses, since they share the same metabolic pathway.|Drugs acting on androgen receptors modify opioid transmission in the central nervous system. To investigate a direct interaction, /investigators/ studied whether the binding of [3H]diprenorphine to mouse brain membranes was modified by cyproterone acetate (progesterone derivative with antiandrogen activity), flutamide (non-steroidal antiandrogen), 5alpha-dihydrotestosterone and progesterone. Only cyproterone acetate inhibited [3H]diprenorphine binding (IC50 = (1.62 +/- 0.33) x 10(-6) M) without modifying its association rate. These results suggest that cyproterone acetate binds to opiate receptors independently of its classical androgenic intracellular receptor effect.

LD50 Rat intraperitoneal 565 mg/kg|LD50 Mouse intraperitoneal 3300 mg/kg

/BIRDS and MAMMALS/ To gauge the relative regulative roles of adrenal, gonadal, and thyroid hormones on uropygial gland of male adult pigeons, morphometric, histological, and histochemical observations have been made on a seasonal basis in normal as well as experimentally manipulated birds. Normal birds showed a parallel adrenal-gonadal-uropygial relationship and inverse adrenal-thyroid, thyroid-gonadal, and thyroid-uropygial relationships. Induced hypocorticalism by dexamethasone in the breeding season and hypercorticalism by ACTH or corticosterone treatment in the nonbreeding season were marked by inhibitory and stimulatory changes respectively in the uropygial gland and testis and by inverse thyroid activity. Further, cyproterone acetate treatment in the breeding season completely suppressed testicular functions and increased thyroid activity without affecting either adrenal or uropygial weight, structure, and functions. Based on the observations it is concluded that adrenal steroids are principally involved in regulating the uropygial gland while the gonadal steroids are involved in qualitative aspects of secretion during the breeding phase and thyroid hormones in maintaining the general metabolic profile.|/AQUATIC SPECIES/ A short-term gonadal recrudescence bioassay using the mummichog (Fundulus heteroclitus) was employed to examine the consequences of environmentally relevant and pharmacological exposures (1-1000 ng/L) of the androgen, 17alpha-methyl testosterone, and the anti-androgen, cyproterone acetate, on reproductive endocrine endpoints. Recrudescing male (GSI = approx. 2%) and female (GSI = approx. 10%) fish were exposed to graded concentrations of 17alpha-methyl testosterone and cyproterone acetate for 7 or 14 days. In the first experiment (7-day exposure), 17alpha-methyl testosterone concentrations of 250 or 1000 ng/L decreased circulating testosterone and estradiol in female fish, and 11-ketotestosterone in male fish. Plasma T, 11-ketotestosterone and estradiol were decreased following cyproterone acetate exposure (250 and 1000 ng/l). Gonadal steroid biosynthetic capacity was also inhibited in both sexes after exposure to 17alpha-methyl testosterone or cyproterone acetate, as evidenced by decreased in vitro production of testosterone and estradiol. In experiment 2 (14-day exposure), exposures to lower 17alpha-methyl testosterone and cyproterone acetate concentrations (1, 10 and 100 ng/L) resulted in decreased plasma testosterone, with females showing greater sensitivity than males. Both 11-ketotestosterone and estradiol were significantly reduced beginning at 10 ng/L 17alpha-methyl testosterone. In vitro gonadal testosterone production was impaired at 100 ng/L 17alpha-methyl testosterone in both males and females while 1 ng/L cyproterone acetate caused a significant decrease in female fish. In experiment 2, in vitro estradiol production was decreased in females at all concentrations of 17alpha-methyl testosterone and cyproterone acetate, while only 100 ng/L reduced 11-ketotestosterone synthesis in males. Plasma vitellogenin was reduced in females exposed to 1000 ng/L (experiment 1) and 100 ng/L (experiment 2) 17alpha-methyl testosterone, while cyproterone acetate did not alter plasma vitellogenin at any concentration.|/AQUATIC SPECIES/ This study was focused on determining the effects of exposure to antiandrogens on the gonadal development of Japanese medaka (Oryzias latipes). Test compounds included the fungicide, vinclozolin and the clinical antiandrogen, cyproterone acetate. Newly hatched medaka were exposed to aqueous solutions of vinclozolin (2500 ug/L) and the vinclozolin fungicide formulation, Ronilan (1000 and 5000 ug/L) and cyproterone acetate (1 and 10 ug/L), for 3 months. Histological evaluation of the gonadal tissues of exposed fish indicated that the 5000 ug/L concentration of the vinclozolin formulation (Ronilan) induced a low incidence of intersex (ie testis-ova) and the 2500 ug/L concentration of vinclozolin-affected spermatogenesis in males. Also, the vinclozolin treatments induced moderate ovarian atresia. Cyproterone acetate also induced a low incidence of testis-ova, but in contrast to the vinclozolin treatment the amount of ovarian tissue in the testis-ova was equal to or greater than the amount of testicular tissue. In the cyproterone acetate treatments, both oogenesis and spermatogenesis were moderately inhibited at all test concentrations. ...|/AQUATIC SPECIES/ The objective of this study was to identify specific physiologic parameters in crustaceans that are targeted by chemicals known to be antiandrogenic in vertebrates. /It was/ hypothesized that chemicals capable of binding to the vertebrate androgen receptor would also elicit toxicity to crustaceans by binding to specific steroid hormone receptors in an antagonistic manner. This hypothesis was tested by evaluating the effects of the antiandrogen cyproterone acetate on growth, molting, sexual differentiation, and reproduction of Daphnia magna. Exposure of daphnids to concentrations of cyproterone acetate appreciably below those that elicited mortality reduced growth but had no effect on molting. These concentrations of cyproterone acetate had no effect on various developmental and maturation parameters. Cyproterone acetate also reduced the number of offspring produced by parthenogenetically reproducing daphnids, but this effect appeared to be a consequence of the reduced size of the daphnids and their inability to accommodate a brood of more than approximately 10 eggs. These results indicate that the antiandrogen cyproterone acetate specifically targets a process critical to growth of daphnids that is independent of molting. Additional studies are warranted to established whether this is an endocrine-related toxicity to crustaceans that is associated with environmental antiandrogens such as some pesticide metabolites.|/AQUATIC SPECIES/ The effects of suspected endocrine disrupting chemicals on freshwater and marine prosobranch species were analysed in laboratory experiments. ... The responses of the fresh water snail Marisa cornuarietis and of two marine prosobranchs (Nucella lapillus, Nassarius (Hinia) reticulatus) to the antiandrogenic model compounds cyproterone acetate and vinclozolin (VZ) are presented. The snails were exposed to nominal cyproterone acetate concentrations of 1.25 mg/L alone and simultaneously to a potent synthetic estrogen (ethinylestradiol), androgen (methyltestosterone) or an indirectly acting xeno-androgen (tributyltin) in experiments with adult specimens and in a life cycle test for 12 months. Marisa and Nucella were furthermore exposed to nominal concentrations of 0.03-1.0 microgram vinclozolin/L for up to 5 months. The antiandrogens induced a number of biological responses in all three species. The length of the penis and of accessory male sex organs (e.g., penis sheath, prostate) were significantly reduced. For Marisa, this effect occurred only in sexually immature specimens and was reversible as the males attained puberty. Typical androgen-mediated responses (imposex development, delayed spermatogenesis, tubulus necrosis of the testis with orchitis and Leydig cell hyperplasia) were partially or totally suppressed by a simultaneous administration of cyproterone acetate. In the two marine species even adult, sexually mature males responded to antiandrogens with a reduction of the male sex organs and an advancement of the sexual repose phase. The results for cyproterone acetate and vinclozolin are compared with the effects of an exposure to xeno-estrogens (bisphenol A, octylphenol) and xeno-androgens (triphenyltin, tributyltin) in the same species. Each group of endocrine disruptors induces a characteristic set of toxicological effects in prosobranch snails which can be used as endpoints in an organismic invertebrate test for the identification of endocrine mimetic test compounds. Estrogens cause primarily an induction of superfemales resulting in an increased female mortality by the enhancement of spawning mass and egg production. The main effects of androgens are a virilization of females by imposex development and a marked decrease of the fecundity. Compared with estrogens and androgens, the antiandrogen responses seem to be less drastic and might have--in contrast to the two other disruptor classes--no biologically significant effects at the population level.

In patients with a history of thromboembolic processes or suffering from sickle-cell anemia or severe diabetes with vascular changes, the risk: benefit ratio must be considered carefully in each individual case before Cyprostat is prescribed.|Cyprostat must not be used in patients with: Meningioma or a history of meningioma; Liver diseases (including Dubin-Johnson syndrome and Rotor syndrome); Malignant tumors (except for carcinoma of the prostate); Previous or existing liver tumors (only if these are not due to metastases from carcinoma of the prostate); Wasting diseases (with the exception of inoperable carcinoma of the prostate); Existing thromboembolic processes; Hypersensitivity to the active substance or any of the excipients.

For the palliative treatment of patients with advanced prostatic carcinoma.

Androgen Antagonists; Antineoplastic Agents; Contraceptive Agents, Male; Progestational Hormones, Synthetic|/Cyproterone is indicated for the/ control of libido in severe hypersexuality and/or sexual deviation in the adult male.|/Cyproterone is indicated for the/ management of patients with prostatic cancer (1) to suppress "flare" with initial LHRH analogue therapy,(2) in long-term palliative treatment where LHRH analogues or surgery are contraindicated, not tolerated, or where oral therapy is preferred, and (3) in the treatment of hot flushes in patients under treatment with LHRH analogues or who have had orchidectomy.|Dianette (cyproterone acetate/ethinylestradiol) is recommended for use in women only for the treatment of (a) severe acne, refractory to prolonged oral antibiotic therapy; (b) moderately severe hirsutism.|Although Dianette also acts as an oral contraceptive, it should not be used in women solely for contraception, but should be reserved for those women requiring treatment for the androgen-dependent conditions.

Direct hepatic toxicity, including jaundice, hepatitis and hepatic failure, has been observed in patients treated with Cyprostat. At dosages of 100 mg and above cases with fatal outcome have also been reported. Most reported fatal cases were in men with advanced prostatic cancer. Toxicity is dose-related and develops, usually, several months after treatment has begun. Liver function tests should be performed pre-treatment, regularly during treatment and whenever any symptoms or signs suggestive of hepatotoxicity occur. If hepatotoxicity is confirmed, Cyprostat should be withdrawn, unless the hepatotoxicity can be explained by another cause, eg metastatic disease, in which case Cyprostat should be continued only if the perceived benefit outweighs the risk.|In very rare cases benign and malignant liver tumors, which may lead to life-threatening intra-abdominal hemorrhage, have been observed after the use of Cyprostat. If severe upper abdominal complaints, liver enlargement or signs of intra-abdominal hemorrhage occur, a liver tumor should be considered in the differential diagnosis.|The occurrence of thromboembolic events has been reported in patients using Cyprostat, although a causal relationship has not been established. Patients with previous arterial or venous thrombotic/thromboembolic events (eg deep vein thrombosis, pulmonary embolism, myocardial infarction), with a history of cerebrovascular accidents or with advanced malignancies are at increased risk of further thromboembolic events, and may be at risk of recurrence of the disease during Cyprostat therapy.|In patients with a history of thromboembolic processes or suffering from sickle-cell anemia or severe diabetes with vascular changes, the risk: benefit ratio must be considered carefully in each individual case before Cyprostat is prescribed.|For more Drug Warnings (Complete) data for CYPROTERONE ACETATE (17 total), please visit the HSDB record page.

Cyproterone is an antiandrogen. It suppresses the actions of testosterone (and its metabolite dihydrotestosterone) on tissues. It acts by blocking androgen receptors which prevents androgens from binding to them and suppresses luteinizing hormone (which in turn reduces testosterone levels).

Chemical substances or agents with contraceptive activity in males. Use for male contraceptive agents in general or for which there is no specific heading. (See all compounds classified as Contraceptive Agents, Male.)|Substances that inhibit or prevent the proliferation of NEOPLASMS. (See all compounds classified as Antineoplastic Agents.)|Compounds which inhibit or antagonize the biosynthesis or actions of androgens. (See all compounds classified as Androgen Antagonists.)

Completely absorbed following oral administration.|It is excreted approximately 60% in the bile and 33% through the kidneys.|Following oral administration, cyproterone acetate is completely absorbed over a wide dose range. The ingestion of two cyproterone acetate 50 mg tablets gives maximum serum levels of about 285 ng/mL at about 3 hours. Thereafter, drug serum levels declined during a time interval of typically 24 to 120 hr, with a terminal half-life of 43.9 +/- 12.8 hr. The total clearance of cyproterone acetate from serum is 3.5 +/- 1.5 mL/min/kg.|The absolute bioavailability of cyproterone acetate is almost complete (88% of dose).|Some drug is excreted unchanged with bile fluid. Most of the dose is excreted in the form of metabolites at a urinary to biliary ratio of 3:7.|Cyproterone acetate is almost exclusively bound to plasma albumin. About 3.5 - 4% of total drug levels are present unbound. Because protein binding is non-specific, changes in SHBG (sex hormone binding globulin) levels do not affect the pharmacokinetics of cyproterone acetate.|For more Absorption, Distribution and Excretion (Complete) data for CYPROTERONE ACETATE (6 total), please visit the HSDB record page.

Primarily hepatic. Cyproterone acetate is metabolized by the CYP3A4 enzyme, forming the active metabolite 15beta-hydroxycyproterone acetate, which retains its antiandrogen activity, but has reduced progestational activity.|Cyproterone acetate is metabolized by various pathways, including hydroxylations and conjugations. The main metabolite in human plasma is the 15beta-hydroxy derivative.

Elimination Following oral or intramuscular administration, the plasma half-life is 38 and 96 hours, respectively.|The renal and biliary excretion proceeds with a half-life of 1.9 days. Metabolites from plasma are eliminated at a similar rate (half-life of 1.7 days).|Terminal half-life of 43.9 +/- 12.8 hr.

The direct antiandrogenic effect of cyproterone is blockage of the binding of dihydrotestosterone to the specific receptors in the prostatic carcinoma cell. In addition, cyproterone exerts a negative feed-back on the hypothalamo-pituitary axis, by inhibiting the secretion of luteinizing hormone resulting in diminished production of testicular testosterone.|Prostatic carcinoma and its metastases are in general androgen-dependent. Cyproterone acetate exerts a direct anti-androgen action on the tumor and its metastases. It also has progestogenic activity, which exerts a negative feedback effect on the hypothalamic receptors, so leading to a reduction in gonadotrophin release, and hence to diminished production of testicular androgens. Sexual drive and potency are reduced and gonadal function is inhibited.|Cell proliferation and cell death appear in several systems as mutually exclusive, which raises the assumption that a same factor or secondary signal(s) might exert opposite control on the two processes. To test this assumption we investigated the time-course evolution of the S phase and apoptotic indices in rat liver during cyproterone acetate (CPA) induced hyperplasia and during the recovery of normal liver mass provoked, respectively, by cyproterone acetate (CPA) treatment and withdrawal. The levels of c-myc and c-ras transcripts were also followed in view of the indications of a positive role of these oncogenes in proliferation. The data showed that proliferation and cell death are not always mutually exclusive and that a high rate of cell death was indifferently associated with high or low c-ras expression. Our data are consistent with a role of this gene in proliferation but exclude that it plays an opposite role in controlling cell death.|The antigonadotropic effect of cyproterone acetate is also exerted when administered with LHRH analogues. The initial increase of testosterone caused by this class of substances is reduced by cyproterone acetate. An occasional tendency for the prolactin levels to increase slightly has been observed under higher doses of cyproterone acetate.|Dianette blocks androgen-receptors. It also reduces androgen synthesis both by negative feedback effect on the hypothalamo-pituitiary-ovarian systems and by the inhibition of androgen-synthesising enzymes.|For more Mechanism of Action (Complete) data for CYPROTERONE ACETATE (8 total), please visit the HSDB record page.

Reported impurities include: 3,20-dioxo-1beta,2beta-dihydro-3'H-cyclopropa[1,2]pregna-1,4,6-trien-17-yl acetate and 6-methoxy-3,20-dioxo-1beta,2beta-dihydro-3'H-cyclopropa[1,2]-pregna-1,4,6-trien-17-yl 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/ One daily dose of either 5 mg or 10 mg cyproterone acetate (CA) was administered to 2 groups of 4 fertile men for 6 months. The medication was preceded by a 3 months placebo period and followed by a recovery phase of 5 to 8 months. During CA-treatment the sperm count/mL decreased and the percentage of abnormal spermatozoa increased slightly (0.991 less than P less than 0.05). Sperm penetration assessed by the Kremer test did not show any decrease during treatment. Serum levels of testosterone and FSH decreased, but those of LH remained unchanged during treatment. Two pregnancies occurred after 13/4 and 51/2 months of CA-treatment. The serum-CA concentration in these 2 volunteers did not differ from that of the remainder. Three subjects who began the study were withdrawn because of depressive mood changes (2) and weakness combined with dizziness (1). Data from these subjects were not included. The results indicate that daily doses of 5 mg and 10 mg of cyproterone acetate are not effective as a male contraceptive.|/SIGNS AND SYMPTOMS/ Overdose may cause nausea, vomiting and, in females, withdrawal bleeding. There are no specific antidotes and further treatment should be symptomatic.|/CASE REPORTS/ The multiplicity of meningiomas or abrupt lesion growth in patients treated with cyproterone acetate suggests that this progestative treatment may promote lesion growth. /The authors/ report the rapid regression of an incidental meningioma after discontinuation of a 10-year cyproterone acetate treatment. This unique observation suggests that conservative management of meningiomas may be the best option among users of high doses of cyproterone acetate, given that spontaneous regression may occur after hormonal treatment discontinuation.|/CASE REPORTS/ ... Three male patients aged 78-83 years are presented, in whom severe hepatotoxic reactions emerged after cyproterone acetate (CPA) administration. Patients were treated with CPA at the doses of 200-300 mg/day for malignant prostate disease for 3-12 months prior to the acute manifestation of the hepatic disease. Clinical features compatible with mixed hepatocellular and cholestatic liver disease including jaundice, white stools and dark urine, manifested in all three cases whereas encephalopathy and ascites were present in two of the patients. Other primary causes of hepatotoxicity (alcohol consumption and viral hepatitis) were also verified in two cases, and in those patients biopsy findings revealed the presence of cirrhotic lesions in liver parenchyma. Discontinuation of the therapeutic agent led to the amelioration of the clinical profile in all the patients whereas a patient died 40 d after hospital admission due to sepsis, despite acute liver disease improvement. ...|For more Human Toxicity Excerpts (Complete) data for CYPROTERONE ACETATE (20 total), please visit the HSDB record page.

Androcur

Mixture of acetate with ethinyl estradiol|... Commercially available as tablets and as an injectable solution.|Oral: Tablet: 50, 100 mg cyproterone acetate, Cyprostat (Bayer plc).|Oral: Tablet: 2 mg cyproterone acetate 35 ug ethinylestradiol, Dianette (Bayer plc)|Oral: Tablet: 50 mg cyproterone acetate, Androcur (Bayer plc).

... Infra-red absorption spectrophotometry and thin-layer chromatography ... /are/ methods for identifying cyproterone acetate; liquid chromatography and ultra-violet absorption spectrophotometry are used to assay its purity.