Stanozolol☆

BL Furman, Strathclyde Institute of Pharmacy & Biomedical Sciences, Glasgow, United Kingdom
ã 2017 Elsevier Inc. All rights reserved.

Introduction 1
Basic Chemistry 1
Human Pharmacokinetics 2
Targets-Pharmacodynamics 2
Therapeutics 2
Indications 2
Contraindications 2
Adverse Effects 2
Agent-Agent Interactions 2
References 3

Name of the clinical form Stanazolol

Related names source: 17alpha methylandrostano[3,2 c]pyrazol 17beta ol; 17alpha methyl 17beta hydroxyandrostano[3,2 c]pyrazole; anabol;
EMTREE androstanasol; androstanazole; androstanopyrazole; 17 beta hydroxy 17 alphamethylandrostano [3,2 c] pyrazole;
17beta hydroxy 17alphamethylandrostano(3,2 c)pyrazole; 17beta hydroxy 17alpha methylandrostano[3,2 c]pyrazole;
methylandrostanopyrazole; methylstanazole; nsc 43193; stanazolol; stanozol; stanozole; stromba; strombaject; win
14833; winstrol; Stanozolol; 2’H-Androst-2-eno(3,2-c)-pyrazol-17-ol, 17-methyl-, (5alpha,17beta); Winstrol (trade);
17 beta hydroxy 17 alpha methylandrostano [3,2 c] pyrazole; 17beta hydroxy 17alpha methylandrostano(3,2 c)pyrazole;
nsc43193; win14833
Chemical names
CAS number 10418-03-8

Introduction

Stanazolol is an orally active, anabolic steroid, the main uses of which are in vascular manifestations of Behcet’s disease and in
hereditary angioedema (see Anabolic steroids). As with other anabolic steroids, it has been used in anemias and osteoporosis.
It appears to have reduced androgenic properties relative to its anabolic actions, although androgenic adverse effects are seen in
clinical use. In common with other 17-alpha-alkylated steroids, it may produce hepatotoxicity, including peliosis hepatitis and
hepatic tumors.

Basic Chemistry

Chemical structure
Structure

Chemical formula C21 H32 N2 O

Properties
Physical properties White, odorless, crystalline powder. There are two forms: needles melting 155 C and prisms melting 235 C Parfitt (1999).
Molecular weight 328.497
Solubility Insoluble in water; soluble in dimethylformamide, ethanol (1:41), chloroform (1:71), and ether (1:370) Parfitt (1999).

☆
Change History: January 2016. BL Furman added keywords and updated abstract.

Reference Module in Biomedical Sciences http://dx.doi.org/10.1016/B978-0-12-801238-3.98039-5 1

2 Stanozolol

Human Pharmacokinetics

Stanozolol is absorbed from the gastrointestinal tract and its metabolites excreted in the urine. Both it and its metabolites are largely
excreted in a conjugated form. It is hydroxylated on the pyrazole ring and at several places on the steroid nucleus Schanzer
et al (1990).

Targets-Pharmacodynamics

It acts at the androgen receptor. However, its effects on the liver are unlikely to be mediated by androgen receptors, because they are
not mimicked by testosterone. In both rat and human liver microsomes, stanozolol binds to a low-affinity glucocorticoid binding
site, which binds neither natural estrogens nor androgens Luzardo et al (2000).

Therapeutics

Stanozolol has been used for postmenopausal osteoporosis, hereditary angioedema, anemias, and vascular manifestations of
Behcet’s disease. In the United Kingdom, its only recommended uses are for Behcet’s disease and hereditary angioedema.

Indications

Prep.and
route of
Value Units admin. Reference Comments

Hereditary angioneurotic edema

Dosage 2.5- mg Tablets; oral Parfitt Stanozolol is an effective prophylactic agent Sheffer et al. (1987). It increases serum
10 daily (1999) levels of C1-esterase inhibitor activity Curd et al (1981), but this may not be the only
mechanism of 17-alpha-alkylated steroids Warin et al (1980).
Vascular manifestations of Behcet’s disease
Dosage 10 mg Tablets; oral Parfitt Although recommended for this condition, there is very little published literature and
daily (1999) no controlled trials Parfitt (1999)

Contraindications

Pregnancy; established liver disease; carcinoma of the prostate.

Adverse Effects

Adverse effects are those expected of an androgen (hirsutism, hoarseness, acne, clitoral hypertrophy, amenorrhea; inhibition of
spermatogenesis; premature epiphyseal closure; virilisation of a female fetus) Matsumoto (2001). Stanozolol may also produce
hepatitis, hepatic tumors, and peliosis hepatitis Matsumoto (2001). However, long-term treatment (15–47 months) of 13 angioe-
dema patients with low doses did not reveal any significant hepatic damage as revealed by laboratory tests or liver biopsy Cicardi
et al (1983). High concentrations of stanozolol produce toxic effects in primary rat hepatic cell cultures Welder et al (1995).

Agent-Agent Interactions

Agent Mode of interaction

name
Warfarin Stanozolol may increase bleeding in patients receiving warfarin because stanozolol increases antithrombin III Sue-Ling et al (1985). The
dose of warfarin may require reducing by 50%.
 Stanozolol 3

References
Journal Citations

Cicardi M, Bergamaschini L, Tucci A, Agostoni A, Tornaghi G, Coggi G, Colombi R, and Viale G (1983) Morphologic evaluation of the liver in hereditary angioedema patients on long-
term treatment with androgen derivatives. J. Allergy Clin. Immunol. 72(3): 294–298.
Curd JG, Yelvington M, Ziccardi RJ, Mathison DA, and Griffin JH (1981) Purification and characterization of two functionally distinct forms of C1 inhibitor from a patient with
angioedema. Clin. Exp. Immunol. 45(2): 261–270.
Luzardo OP, Machin RP, Diaz-Chico BN, and Fernandez L (2000) Photoaffinity labelling identification of a specific binding protein for the anabolic steroids stanozolol and danazol:
An oligomeric protein regulated by age, pituitary hormones and ethinyl estradiol. Endocrinology 141(9): 3377–3387.
Schanzer W, Opfermann G, and Donike M (1990) Metabolites of stanozolol: identification and synthesis of urinary metabolites. J. Steroid Biochem. 36: 153–174.
Sheffer AL, Fearon DT, and Austen KF (1987) Hereditary angioedema: a decade of management with stanozolol. J. Allergy Clin. Immunol. 80(6): 855–860.
Sue-Ling HM, Davies JA, Prentice CR, Verheijen JH, and Kluft C (1985) Effect of oral stanozolol used in the prevention of postoperative deep vein thrombosis on fibrinolytic activity.
Thromb. Haemost. 53(1): 141–142.
Warin AP, Greaves MW, Gatecliff M, Williamson DM, and Warin RP (1980) Treatment of hereditary angio-oedema by low-dose attenuated androgens:disassociation of clinical
response from levels of C1 esterase inhibitor and C4. Br. J. Dermatol. 103(4): 405–409.
Welder AA, Roberson JW, and Melchert RB (1995) Toxic effects of anabolic-androgenic steroids in primary rat hepatic cell cultures. J. Pharmacol. Toxicol. Methods 33(4): 187–195.

Book Citations
Matsumoto AM (2001) Clinical use and abuse of androgens and antiandrogens. In: Becker KL (ed.) Principles and Practice of Endocrinology and Metabolism, 3rd ed., pp. 1181–1200,
USA: Lippincott, Williams &Wilkins.
Parfitt K (1999) Martindale: The complete drug reference, 32nd ed. London: Pharmaceutical Press.