Stanozolol

Anticoagulant effect may be increased during concurrent use with anabolic steroids, especially 17-alpha-alkylated compounds, because of decreased procoagulant factor concentration caused by alteration of procoagulant factor synthesis or catabolism and increased receptor affinity for the anticoagulant; anticoagulant dosage adjustment based on prothrombin time determinations may be required during and following concurrent use. /Anabolic steroids/

Anabolic steroids may decrease blood glucose concentrations; diabetic patients should be closely monitored for signs of hypoglycemia and dosage of hypoglycemic agent adjusted as necessary. /Anabolic steroids/

Concurrent use /of glucocorticoid corticosteroids, especially with significant mineralocorticoid activity; mineralocorticoid corticosteroids; corticotropin, especially prolonged therapeutic use; or sodium-containing medications or foods/ with anabolic steroids may increase the possibility of edema; in addition, concurrent use of glucocorticoids or corticotropin with anabolic steroids may promote development of severe acne. /Anabolic steroids/

Concurrent use of anabolic steroids with somatrem or somatropin may accelerate epiphyseal maturation. /Anabolic steroids/

Concurrent use /of other hepatotoxic medications/ with anabolic steroids may result in an increased incidence of hepatotoxicity; patients, especially those on prolonged administration or those with a history of liver disease, should be carefully monitored. /Anabolic steroids/

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 15,000(SRC), determined from a structure estimation method(2), indicates that stanozolol is expected to be immobile in soil(SRC). Volatilization of stanozolol from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.1X10-8 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Stanozolol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.3X10-9 mm Hg(SRC), determined from a fragment constant method(4). No biodegradation data were available(SRC, 2005).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 15,000(SRC), determined from a structure estimation method(2), indicates that stanozolol 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 1.1X10-8 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 an estimated log Kow of 4.4(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is high(SRC). No biodegradation data were available(SRC, 2005).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), stanozolol, which has an estimated vapor pressure of 3.3X10-9 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 stanozolol may be removed from the air by wet and dry deposition(SRC). Stanozolol does not absorb light at wavelengths >290 nm(3), and therefore should not be susceptible to direct photolysis.

IDENTIFICATION: Stanozolol is an anabolic steroid used for systemic use. Origin of the substance: Naturally occurring anabolic steroids are synthesised in the testis, ovary and adrenal gland from cholesterol via pregnenolone. Synthetic anabolic steroids are based on the principal male hormone testosterone, modified in one of three ways: alkylation of the 17-carbon; esterification of the 17-OH group and modification of the steroid nucleus Stanozolol is a white or almost white solid crystals and it is odorless. It is practically insoluble in water; soluble alcohol, chloroform and ether. It is soluble in dimethylformamide; slightly soluble in acetone and ethyl acetate. Description: The only legitimate therapeutic indications for anabolic steroids are: (A) replacement of male sex steroids in men who have androgen deficiency, for example as a result of loss of both testes. (B) the treatment of certain rare forms of aplastic anaemia which are or may be responsive to anabolic androgens. (C) the drugs have been used in certain countries to counteract catabolic states, for example after major trauma. HUMAN EXPOSURE: Main risks and target organs: The main risks are those of excessive androgens: menstrual irregularities and virilization in women and impotence, premature cardiovascular disease and prostatic hypertrophy in men. Both men and women can suffer liver damage with oral anabolic steroids containing a substituted 17-alpha-carbon. Psychiatric changes can occur during use or after cessation of these agents. Summary of clinical effects: Acute over-dosage can produce nausea and gastrointestinal upset. Chronic usage is thought to cause an increase in muscle bulk, and can cause an exaggeration of male characteristics and effects related to male hormones. Anabolic steroids can influence sexual function. They can also cause cardiovascular and hepatic damage. Acne and male-pattern baldness occur in both sexes; irregular menses, atrophy of the breasts, and clitoromegaly in women; and testicular atrophy and prostatic hypertrophy in men. Diagnosis: The diagnosis depends on a history of use of oral or injected anabolic steroids, together with signs of increased muscle bulk, commonly seen in body builders. Biochemical tests of liver function are often abnormal in patients who take excessive doses of oral anabolic steroids. Laboratory analyses of urinary anabolic steroids and their metabolites can be helpful in detecting covert use of these drugs. First aid measures and management principles: Supportive care is the only treatment necessary or appropriate for acute intoxication. Chronic abusers can be very reluctant to cease abuse, and may require professional help as with other drug misuse. Parenteral: Intramuscular or deep subcutaneous injection is the principal route of administration of all the anabolic steroids except the 17-alpha-substituted steroids which are active orally. Contraindications: Known or suspected cancer of the prostate or (in men) breast. Pregnancy or breast-feeding and known cardiovascular disease is a relative contraindication. Routes of exposure: Oral: Anabolic steroids can be absorbed from the gastrointestinal tract, but many compounds undergo such extensive first-pass metabolism in the liver that they are inactive. Those compounds in which substitution of the 17-carbon protects the compound from the rapid hepatic metabolism are active orally. There are preparations of testosterone that can be taken sublingually. Absorption by route of exposure: The absorption after oral dosing is rapid for testosterone and probably for other anabolic steroids, but there is extensive first-pass hepatic metabolism for all anabolic steroids except those that are substituted at the 17-alpha position. The rate of absorption from subcutaneous or intramuscular depots depends on the product and its formulation. Absorption is slow for the lipid-soluble esters such as the cypionate or enanthate, and for oily suspensions. Distribution by route of exposure: The anabolic steroids are highly protein bound, and is carried in plasma by a specific protein called sex-hormone binding globulin. Biological half-life by route of exposure: The metabolism of absorbed drug is rapid, and the elimination half-life from plasma is very short. The duration of the biological effects is therefore determined almost entirely by the rate of absorption from subcutaneous or intramuscular depots, and on the de-esterification which precedes it. Metabolism: Free (de-esterified) anabolic androgens are metabolized by hepatic mixed function oxidases. Elimination by route of exposure: After administration of radiolabelled testosterone, about 90% of the radioactivity appears in the urine, and 6% in the feces; there is some enterohepatic recirculation. Pharmacology and toxicology: Mode of action: Toxicodynamics: The toxic effects are an exaggeration of the normal pharmacological effects. Pharmacodynamics: Anabolic steroids bind to specific receptors present especially in reproductive tissue, muscle and fat. The anabolic steroids reduce nitrogen excretion from tissue breakdown in androgen deficient men. They are also responsible for normal male sexual differentiation. The ratio of anabolic body-building effects to androgenic (virilizing) effects may differ among the members of the class, but in practice all agents possess both properties to some degree. There is no clear evidence that anabolic steroids enhance overall athletic performance. Carcinogenicity: Precocious prostatic cancer has been described after long term anabolic steroid abuse. Cases where hepatic cancers have been associated with anabolic steroid abuse have been reported. Teratogenicity: Androgen ingestion by a pregnant mother can cause virilization of a female fetus. Main adverse effects: The adverse effects of anabolic steroids include weight gain, fluid retention, and abnormal liver function as measured by biochemical tests. Administration to children can cause premature closure of the epiphyses. Men can develop impotence and azoospermia. Women are at risk of virilization. Clinical effects: Acute poisoning: Ingestion: Nausea and vomiting can occur. Parenteral exposure: Patients are expected to recover rapidly after acute over-dosage, but there are few data. Body builders use doses many times the standard therapeutic doses for these compounds but do not suffer acute toxic effects. Chronic poisoning: Ingestion: Hepatic damage, manifest as derangement of biochemical tests of liver function and sometimes severe enough to cause jaundice; virilization in women; prostatic hypertrophy, impotence and azoospermia in men; acne, abnormal lipids, premature cardiovascular disease (including stroke and myocardial infarction), abnormal glucose tolerance, and muscular hypertrophy in both sexes; psychiatric disturbances can occur during or after prolonged treatment. Parenteral exposure: Virilization in women; prostatic hypertrophy, impotence and azoospermia in men; acne, abnormal lipids, premature cardiovascular disease (including stroke and myocardial infarction), abnormal glucose tolerance, and muscular hypertrophy in both sexes. Psychiatric disturbances can occur during or after prolonged treatment. Hepatic damage is not expected from parenteral preparations. Course, prognosis, cause of death: Patients with symptoms of acute poisoning are expected to recover rapidly. Patients who persistently abuse high doses of anabolic steroids are at risk of death from premature heart disease or cancer, especially prostatic cancer. Non-fatal but long-lasting effects include voice changes in women and fusion of the epiphyses in children. Other effects are reversible over weeks or months. Systematic description of clinical effects: Cardiovascular: Chronic ingestion of high doses of anabolic steroids can cause elevations in blood pressure, left ventricular hypertrophy and premature coronary artery disease. Neurological: Central nervous system: Stroke has been described in a young anabolic steroid abuser. Mania and psychotic symptoms of hallucination and delusion in anabolic steroid abusers has been described. Depression after withdrawal from anabolic steroids has been described. There is also considerable debate about the effects of anabolic steroids on aggressive behavior and on criminal behavior. Mood swings were significantly more common in normal volunteers during the active phase of a trial comparing methyltestosterone with placebo. Gastrointestinal: Acute ingestion of large doses can cause nausea and gastrointestinal upset. Hepatic: Orally active (17-alpha substituted) anabolic steroids can cause abnormalities of hepatic function, manifest as abnormally elevated hepatic enzyme activity in biochemical tests of liver function, and sometimes as overt jaundice. The histological abnormality of peliosis hepatis has been associated with anabolic steroid use. Angiosarcoma and a case of hepatocellular carcinoma in an anabolic steroid user has been reported. Urinary: Other: Men who take large doses of anabolic steroids can develop prostatic hypertrophy. Prostatic carcinoma has been described in young men who have abused anabolic steroids. Endocrine and reproductive systems: Small doses of anabolic steroids are said to increase libido, but larger doses lead to azoospermia and impotence. Testicular atrophy is a common clinical feature of long-term abuse of anabolic steroids, and gynaecomastia can occur. Women develop signs of virilism, with increased facial hair, male pattern baldness, acne, deepening of the voice, irregular menses and clitoral enlargement. Dermatological: Acne occurs in both male and female anabolic steroids abusers. Women can develop signs of virilism, with increased facial hair and male pattern baldness. Eye, ear, nose, throat: local effects: Changes in the larynx in women caused by anabolic steroids can result in a hoarse, deep voice. The changes are irreversible. Hematological: Anabolic androgens stimulate erythropoiesis. Metabolic: Fluid and electrolyte disturbances: Sodium and water retention can occur, and result in edema; hypercalcemia is also reported. Others: Insulin resistance with a fall in glucose tolerance, and hypercholesterolemia with a fall in high density lipoprotein cholesterol, have been reported.

Using a structure estimation method based on molecular connectivity indices(1), the Koc for stanozolol can be estimated to be 15,000(SRC). According to a classification scheme(2), this estimated Koc value suggests that stanozolol is expected to be immobile in soil.

/CASE REPORTS/ Anabolic steroids are frequently abused, thus increasing the risk of cardiovascular disease, despite the known unfavorable influence on lipid profiles. We report on a young bodybuilder who presented with ventricular tachycardia as the first manifestation of severe underlying coronary heart disease. Coronary angiogram revealed severe stenotic lesions in the right coronary artery and the left descending coronary artery, and hypokinetic regions corresponded to posterolateral and anterior myocardial infarctions. This young patient had a history without any coronary risk factors, but with a 2-year abuse of the anabolic steroid stanazolol.

/CASE REPORTS/ A 28-year-old body builder was admitted because of jaundice. For 80 days, until 3 weeks before hospitalization, he had been taking moderately high doses of anabolic steroids: metandienone (methandienone), 10-50 mg daily by mouth, and stanozolol, 50 mg intramuscularly every other day. Physical examination was unremarkable except for yellow discoloration of the skin and sclerae. Bilirubin concentration was raised to 4.5 mg/dl, cholestasis enzymes were normal, while transaminase activities were raised. Liver biopsy was compatible with cholestasis induced by anabolic steroids. Although the steroids had been discontinued, the patient's general condition deteriorated over 7 weeks. Serum bilirubin rose up to a maximum of 77.9 mg/dl. In addition renal failure developed with a creatinine concentration of 4.2 mg/dl. The patient's state improved simultaneously with the administration of ursodeoxycholic acid and the biochemical values gradually reached normal levels after several weeks. Anabolic steroids can cause severe cholestasis and acute renal failure. In this case there was a notable temporal coincidence between the administration of ursodeoxycholic acid and the marked clinical improvement.

Drug-Induced Liver Injury Severity and Toxicity (DILIst)

STANOZOLOL

DILI Positive

DOI:10.1016/j.drudis.2019.09.022

An estimated BCF of 500 was calculated for stanozolol(SRC), using an estimated log Kow of 4.4(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).

The Henry's Law constant for stanozolol is estimated as 1.1X10-8 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that stanozolol is expected to be essentially nonvolatile from moist soil(SRC) and water surfaces(2). Stanozolol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.3X10-9 mm Hg(SRC), determined from a fragment constant method(3).

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ The aim of this study was to analyze the cardiovascular effects of chronic stanozolol administration in male rats. The rats were randomly assigned to one of three groups: (1) control (n=12), (2) chronic treatment with low dose of stanozolol (LD, n=18, 5 mg/kg week) and; (3) treatment with high dose of stanozolol (HD, n=28, 20 mg/kg week). Mean arterial pressure (MAP) was higher in both HD (128 + or - 2.2 mm Hg) and LD (126 + or - 2.5 mm Hg) than control (116 or - 2 mm Hg). The LD group showed an increase in cardiac output (control 121 + or - 2.5, LD 154 + or - 5.9 mL/min), whereas in the HD group total peripheral resistance increased (control 1.03 + or - 0.07, HD 1.26 + or - 0.07 mm Hg/mL/min). Acute sympathetic blockade caused a similar decrease in MAP in all groups. In conscious rats, the baroreflex index for bradycardia (control -3.7 + or - 0.4, LD -2.0 + or - 0.1 beat/mm Hg) and tachycardia (control -3.6 + or - 0.3, LD -4.7 + or - 0.2 beat/mm Hg) responses changed only in the LD group. Cardiac hypertrophy was observed in both treated groups (P<0.05). In conclusion, hypertension with differential hemodynamic changes and alterations in the reflex control in heart rate is seen at different stanozolol doses, which may be important variables in the cardiovascular effects of anabolic steroids.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ The continuous infusion of an anabolic steroid, stanozolol was investigated to determine if it would alter skeletal muscle size and performance in sedentary male mice. The study was performed as a preliminary to an investigation on the effect of anabolic steroids on skeletal muscle regeneration in the mdx mouse, an animal model used for the study of Duchenne muscular dystrophy. Skeletal muscle structure and contractile behavior, and heart, liver, kidney, and testis wet weights were assessed after 3 or 6 wk of continuous exposure to one of two concentrations of stanozolol. Continuous release pellets containing either a high (1.5 mg) or low (0.5 mg) concentration of stanozolol were implanted into 8 wk old C57BL/6J male mice. Control mice were implanted with pellets containing the drug vehicle. Stanozolol infusion had no significant effect on the contractile strength or mass of either fast twitch extensor digitorum longus or slow twitch soleus muscle. The resistance to fatigue of both muscles, assessed in vitro, was unaffected by stanozolol; however, postfatigue recovery of soleus twitch and tetanic tension after 3 wk of treatment was significantly (p< 0.05) increased in high dose mice compared with control and low dose mice. Androgen sensitive muscles, bulbocavernosus and levator ani, were significantly (p< 0.05) increased in wet weight after 3 wk of stanozolol treatment, but were not significantly different from control muscles after 6 wk, suggesting that continuous infusion produced a tolerance to the drug. Similarly, heart wet weight was significantly (p< 0.05) increased in stanozolol treated mice compared with control after 3 wk, but not after 6 wk. Testis wet weight was significantly (p< 0.05) decreased in low dose mice compared with control mice at 3 wk, but not at 6 wk. Plasma testosterone concentration was not significantly different between any of the groups after 3 or 6 wk of treatment. This study suggests that in the absence of other factors (eg, high-intensity exercise or other degenerative changes in muscle fibers), continuous infusion of an anabolic steroid produces no significant effect on the growth, contractile strength, or endurance of hindlimb skeletal muscles.

Anabolic steroids are not recommended for use during pregnancy, since studies in animals have shown that anabolic steroids cause masculinization of the fetus. Risk-benefit must be carefully considered. /Anabolic steroids/

Anabolic steroids should be used with caution in children and adolescents and only by specialists who are aware of their effects on bone maturation because of possible premature epiphyseal closure, precocious sexual development in males, and virilization in females. The epiphyseal maturation may be accelerated more rapidly than linear growth in children, and the effect may continue for 6 months after the medication has been discontinued. /Anabolic Steroids/

Anabolic steroids may decrease blood glucose concentrations; diabetic patients should be closely monitored for signs of hypoglycemia and dosage of hypoglycemic agent adjusted as necessary. /Anabolic steroids/

Stanozolol is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups(1). Stanozolol does not absorb light at wavelengths >290 nm(2), and therefore should not be susceptible to direct photolysis.

Schedules of controlled substances are established by section 202 of the Controlled Substances Act (21 U.S.C. 812). Schedule III shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Unless specifically excepted or unless listed in another schedule, any material, compound, mixture, or preparation containing any quantity of the following substances, including its salts, isomers, and salts of isomers whenever the existence of such salts of isomers is possible within the specific chemical designation. DEA Code #: 4000; Drug class: anabolic steroids.

Implantation or injectable dosage form new animal drugs. Stanozolol sterile suspension. ... Used as a anabolic steroid treatment in dogs, cats, and horses.

Oral dosage form new animal drugs. Stanozolol tablets. ... Conditions of use: Used as an anabolic steroid treatment in dogs and cats.

Oral dosage form new animal drugs. Stanozolol chewable tablets. ... Conditions of use: Used as an anabolic steroid treatment in dogs.

MEDICATION (VET)

MEDICATION

Treatment of hereditary angioedema /Former/

Manson, US 3030358 (1962 to Sterling Drug).

17-Methyl-5alpha-androstan-17beta-ol-3-one is converted into its 2-formyl derivative which is then condensed with hydrazine hydrate.

...Introduced primarily for use as anabolic agents with expectation that they would be relatively less androgenic than testosterone & its close relatives. None is free of androgenic activity in man, & in many instances androgenicity is much greater than results of animal tests had predicted. /Anabolic Steroids/

Bioassay for anabolic potency. /Androgens & Anabolic steroids/

Sanofi ... production suspended in October, 2002

Discontinued

For more General Manufacturing Information (Complete) data for STANOZOLOL (7 total), please visit the HSDB record page.