Its safety in andropause (late-onset hypogonadism in men) has not yet been established. It is currently used off-label for breast cancer, breast disorders, delayed puberty in boys, oligospermia (low sperm count), hormone replacement therapy in transgender men, and osteoporosis. Side effects
Side effects of testosterone cypionate include virilization among others. It can also create conditions for heart attack, enlargement of prostate gland, liver malfunction, issues related to coagulation, pulmonary embolism, and polycythemia. Pharmacology
Pharmacodynamics
Testosterone cypionate is a prodrug of testosterone and is an androgen and anabolic–androgenic steroid (AAS). That is, it is an agonist of the androgen receptor (AR). Pharmacokinetics
The pharmacokinetics of testosterone cypionate via depot intramuscular injection, including its elimination half-life and duration of action, are said to be extremely comparable to and hence essentially the same as those of testosterone enanthate. As such, testosterone cypionate and testosterone enanthate are considered to be "functionally interchangeable" as medications. For reference, testosterone enanthate has an elimination half-life of 4.5 days and a mean residence time of 8.5 days and requires frequent administration of approximately once per week. Large fluctuations in testosterone levels result with it, with levels initially being elevated and supraphysiological. The pharmacokinetics of testosterone cypionate have been studied and reported. Chemistry
Testosterone cypionate, or testosterone 17β-cyclopentylpropionate, is a synthetic androstane steroid and a derivative of testosterone. It is an androgen ester; specifically, it is the C17β cyclopentylpropionate (cypionate) ester of testosterone. History
Testosterone cypionate was first synthesized in 1951 and was introduced for medical use in the United States the same year under the brand name Depo-Testosterone.
Recent reports have shown that these stress distributions have been shown to correlate to the overall geometry of the AAA rather than solely to the maximum diameter. It is also known that wall stress alone does not completely govern failure as an AAA will usually rupture when the wall stress exceeds the wall strength. In light of this, rupture assessment may be more accurate if both the patient-specific wall stress is coupled together with patient-specific wall strength. A noninvasive method of determining patient-dependent wall strength was recently reported, with more traditional approaches to strength determination via tensile testing performed by other researchers in the field. Some of the more recently proposed AAA rupture-risk assessment methods include: AAA wall stress; AAA expansion rate; degree of asymmetry; presence of intraluminal thrombus (ILT); a rupture potential index (RPI); a finite element analysis rupture index (FEARI); biomechanical factors coupled with computer analysis; growth of ILT; geometrical parameters of the AAA; and also a method of determining AAA growth and rupture based on mathematical models.The postoperative mortality for an already ruptured AAA has slowly decreased over several decades but remains higher than 40%. However, if the AAA is surgically repaired before rupture, the postoperative mortality rate is substantially lower, approximately 1-6%. Epidemiology
The occurrence of AAA varies by ethnicity. In the United Kingdom, the rate of AAA in Caucasian men older than 65 years is about 4.7%, while in Asian men it is 0.45%. It is also less common in individuals of African, and Hispanic heritage.