February 6, 2024
Testosterone Cyclopionate Injection, for intramuscular injection, contains Testosterone cyclopionate, the oil-soluble 17 (beta)—cyclopentyl propionate ester of the androgenic hormone testosterone.
It is a white or creamy white crystalline powder, odorless or nearly so, and stable in air. It is insoluble in water, freely soluble in alcohol, chloroform, dioxane, ether, and soluble in vegetable oils.
The chemical name for Testosterone Cypionate is androst-4-en-3-one,17-(3-cyclopentyl-1- oxopropoxy)-, (17β)-. Its molecular formula is C27H40O3, and its molecular weight 412.61.
The structural formula is represented below:
Testosterone Clopionate Injection is available at 200 mg/mL. Each solution contains 200 mg/mL Testosterone Clopionate, 200 mg benzoate, 0.2 mL cottonseed oil, 560 mg benzyl alcohol (as a preservative), and 9.45 mg.
Endogenous androgens are responsible for the average growth and development of the male sex organs and the maintenance of secondary sex characteristics.
These effects include growth and maturation of the prostate, seminal vesicles, penis, and scrotum; development of male hair distribution, such as beard, pubic, chest, and axillary hair; laryngeal enlargement, vocal cord thickening, and alterations in body musculature and fat distribution.
Drugs in this class also cause retention of nitrogen, sodium, potassium, and phosphorous, lowering urinary excretion of calcium. Androgens increase protein anabolism and decrease protein catabolism. Nitrogen balance is better only when sufficient calories and protein intake are used.
Androgens are responsible for the growth spurt of adolescence and the eventual termination of linear growth brought about by the fusion of the epiphyseal growth centers. In children, exogenous androgens accelerate linear growth rates but may cause disproportionate advancement in bone maturation.
Use over long periods may result in fusion of the epiphyseal growth centers and termination of the growth process. Androgens stimulate the production of red blood cells by enhancing the production of erythropoietic stimulation factor.
Exogenous administration of androgens inhibits the release of endogenous testosterone by feedback inhibition of pituitary luteinizing hormone (LH). At high doses of exogenous androgens, feedback inhibition of pituitary follicle stimulating hormone (FSH) may also suppress spermatogenesis.
There is a lack of substantial evidence that androgens are effective in fractures, surgery, healing, and functional uterine bleeding.
Testosterone esters are less polar than free testosterone. When specialists inject oil intramuscularly, testosterone esters absorb slowly from the lipid phase; thus, specialists can administer testosterone cypionate at two to four-week intervals.
Plasma testosterone levels are 98 percent when it binds to a specific testosterone-estradiol binding globulin, and about 2 percent remains unbound. The amount of sex-hormone-binding globulin in the plasma generally determines the distribution of testosterone between its free and bound forms, and the concentration of free testosterone influences its half-life.
Testosterone excretes about 90 percent of its dose in the urine as glucuronic and sulfuric acid conjugates along with its metabolites. Approximately 6 percent of the dose is excreted in the feces, mostly in the unconjugated form. The liver primarily deactivates testosterone.
Testosterone is metabolized into various 17-keto steroids through two different pathways. When injected intramuscularly, Testosterone Cyclopionate has a half-life of approximately eight days.
Many tissues show that testosterone's activity relies on reducing it to dihydrotestosterone, which then binds to cytosol receptor proteins. The steroid-receptor complex gets transported to the nucleus, which initiates transcription events and brings about cellular changes related to androgen action.
Indications for Testosterone cypionate injection include replacement therapy in males with conditions linked to symptoms of deficient or absent endogenous testosterone.
Primary hypogonadism results from testicular failure due to various factors such as cryptorchidism, bilateral torsion, orchitis, or vanishing testis syndrome, or it can occur due to orchidectomy.
Hypogonadotropic hypogonadism, on the other hand, is caused by either congenital or acquired conditions like idiopathic gonadotropin or LHRH deficiency or pituitary-hypothalamic injury resulting from tumors, trauma, or radiation.
Patients should be instructed to report any of the following: nausea, vomiting, changes in skin color, ankle swelling, too frequent erections of the penis.
Hemoglobin and hematocrit levels (to detect polycythemia) should be checked periodically in long-term androgen administration patients. Serum cholesterol may increase during androgen therapy.
Androgens may increase sensitivity to oral anticoagulants. Consequently, the anticoagulant dosage may require reduction to maintain satisfactory therapeutic hypoprothrombinemia. When specialists administer oxyphenbutazone and androgens concurrently, higher serum levels of oxyphenbutazone may result. In diabetic patients, the metabolic effects of androgens may lead to a decrease in blood glucose levels, thus reducing insulin requirements.
Androgens may decrease levels of thyroxine-binding globulin, resulting in decreased total T4 serum levels and increased resin uptake of T3 and T4. However, free thyroid hormone levels remain unchanged, and there is no clinical evidence of thyroid dysfunction.
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