<style>body { margin: 0px; padding: 10px; height: auto; width: 100%; float: left; word-wrap: break-word; box-sizing: border-box; direction : rtl; -webkit-touch-callout: none; -webkit-user-select: none; -khtml-user-select: none; -moz-user-select: none; -ms-user-select: none; user-select: none; }h1 { float: left; width: 100%; height: auto; color: #1666AA; font-size: 20px }h2 { float: left; width: 100%; height: auto; font-size: 18px; }h3 { float: left; width: 100%; height: auto; font-size: 16px; }p { float: left; width: 100%; height: auto; font-size: 18px; }img{ float: left; width: 100%; height: auto; border-radius: 2px; }#imgblock { float: left; width: 100%; height: auto; padding: 10px; margin-bottom: 10px; box-sizing: border-box; background-color: #EEEEEE; border-radius: 2px; box-shadow: 1px 2px 5px #D4D4D4; }table{ width: 100%; float: left; }table tr td{ text-align: center; border: 1px solid #000000; }</style> <body> <h1>Testoviron® (testosterone propionate/enanthate blend) </h1> <h2>Description: </h2> <div id=’imgblock’><img data-pointer=’7816’/></div><div id=’imgblock’><img data-pointer=’7817’/></div><p>Testoviron® is a mixed testosterone injectable, containing varying amounts of testosterone propionate and testosterone enanthate. The faster-acting propionate ester is included to support testosterone release during the early days of therapy, while the longer-acting ester is included to support the latter part of the therapeutic window. Together, the two are supposed to result in a rapid increase in testosterone level, followed by a sustained hormone elevation for approximately 2 weeks. The design of this steroid is therefore very similar to Sustanon®, although lacking the decanoate ester Testoviron® will remain active in the body for a shorter duration. Testoviron® was originally marketed as an improvement over single-ester preparations like testosterone enanthate, said to provide a much more balanced release of hormone in comparison. </p> <p>Upon close analysis, the pharmacokinetic properties of Testoviron® are not as ideal as initially described. The problem lies in the fact that testosterone enanthate is not a delayed-onset drug, but actually provides a sharp spike in testosterone levels 2448 hours after administration. Adding a fast-acting ester like testosterone propionate to a formulation of testosterone enanthate only compounds the initial testosterone spike. See the provided computer simulation of the release pattern. It shows an even sharper early testosterone peak compared to the use of testosterone enanthate alone, providing the user with a greater imbalance between the early and latter days of the administration window. A study administering a blend of 115.7mg of testosterone enanthate and 20 mg of testosterone propionate confirms this tendency; demonstrating maximal increases in serum testosterone the first day following injection.1 </p> <h2>History: </h2> <p>Testoviron® was developed by international pharmaceutical giant Schering in Germany (now Bayer), and marketed at one time in many of the European markets including Germany, Austria, Italy, Spain, Ireland, Greece, Switzerland, Netherlands, Denmark, and Sweden. </p> <p>This product is, likewise, usually identified as a European item, although it was produced scarcely in Eastern Europe and the Caribbean as well. Schering has also used the Testoviron® brand for its pure testosterone enanthate products, which are generally used for the same medical applications (generally male androgen replacement therapy), and have always been much more widely distributed. </p> <p>The Schering Testoviron® products first surfaced in Europe during the early 1950’s, and have since been duplicated in one form or another by numerous different drug manufacturers in many different parts of the world. Although scarcely remembered, blended enanthate and propionate products were once even available commercially in the U.S. Most notable was the brand Testoject E.P. from Mayrand, which contained 200 mg of testosterone enanthate and 25 mg of testosterone propionate in a 1 mL vial. Today, however, no such commercial product exists. At this time, blended testosterone enanthate/propionate products remain in extremely limited production globally. </p> <h2>How Supplied: </h2> <p>Testosterone propionate and testosterone enanthate blends are available in various human and veterinary drug markets. Composition and dosage may vary by country and manufacturer. Schering Testoviron® products contained a blend of 20 mg/55 mg, 25 mg/110 mg, or 50 mg/200 mg of testosterone propionate and enanthate (respectively) per milliliter; packaged in 1 mL ampules. </p> <h2>Structural Characteristics: </h2> <p>Testoviron® contains a mixture of two testosterone compounds, which weere modified with the addition of carboxylic acid esters (propionic and enanthoic acids) at the 17-beta hydroxyl group. </p> <p>Esterified forms of testosterone are less polar than free testosterone, and are absorbed more slowly from the area of injection. Once in the bloodstream, the ester is removed to yield free (active) testosterone. Esterified forms of testosterone are designed to prolong the window of therapeutic effect following administration, allowing for a less frequent injection schedule compared to injections of free (unesterified) steroid. Testoviron® is designed to provide a rapid peak in testosterone levels (24-48 hours after injection), and maintain physiological concentrations for approximately 14 days. </p><div id=’imgblock’><img data-pointer=’7818’/></div> <h2>Side Effects (Estrogenic): </h2> <p>Testosterone is readily aromatized in the body to estradiol (estrogen). The aromatase (estrogen synthetase) enzyme is responsible for this metabolism of testosterone. Elevated estrogen levels can cause side effects such as increased water retention, body fat gain, and gynecomastia. Testosterone is considered a moderately estrogenic steroid. An anti-estrogen such as clomiphene citrate or tamoxifen citrate may be necessary to prevent estrogenic side effects. One may alternately use an aromatase inhibitor like Arimidex® (anastrozole), which more efficiently controls estrogen by preventing its synthesis. Aromatase inhibitors can be quite expensive in comparison to antiestrogens, however, and may also have negative effects on blood lipids. </p> <p>Estrogenic side effects will occur in a dose-dependant manner, with higher doses (above normal therapeutic levels) of testosterone more likely to require the concurrent use of an antiestrogen or aromatase inhibitor. </p> <p>Since water retention and loss of muscle definition are common with higher doses of testosterone, this drug is usually considered a poor choice for dieting or cutting phases of training. Its moderate estrogenicity makes it more ideal for bulking phases, where the added water retention will support raw strength and muscle size, and help foster a stronger anabolic environment. </p> <h2>Side Effects (Androgenic): </h2> <p>Testosterone is the primary male androgen, responsible for maintaining secondary male sexual characteristics. Elevated levels of testosterone are likely to produce androgenic side effects including oily skin, acne, and body/facial hair growth. Men with a genetic predisposition for hair loss (androgenetic alopecia) may notice accelerated male pattern balding. Those concerned about hair loss may find a more comfortable option in nandrolone decanoate, which is a comparably less androgenic steroid. Women are warned of the potential virilizing effects of anabolic/androgenic steroids, especially with a strong androgen such as testosterone. These may include deepening of the voice, menstrual irregularities, changes in skin texture, facial hair growth, and clitoral enlargement. </p> <p>In androgen-responsive target tissues such as the skin, scalp, and prostate, the high relative androgenicity of testosterone is dependant on its reduction to dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor such as finasteride or dutasteride will interfere with site-specific potentiation of testosterone action, lowering the tendency of testosterone drugs to produce androgenic side effects. It is important to remember that anabolic and androgenic effects are both mediated via the cytosolic androgen receptor. Complete separation of testosterone’s anabolic and androgenic properties is not possible, even with total 5-alpha reductase inhibition. </p> <h2>Side Effects (Hepatotoxicity): </h2> <p>Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One study examined the potential for hepatotoxicity with high doses of testosterone by administering 400 mg of the hormone per day (2,800 mg per week) to a group of male subjects. The steroid was taken orally so that higher peak concentrations would be reached in hepatic tissues compared to intramuscular injections. The hormone was given daily for 20 days, and produced no significant changes in liver enzyme values including serum albumin, bilirubin, alanineaminotransferase, and alkaline phosphatases.2 </p> <h2>Testosterone (nmol/l)</h2> <h2>Side Effects (Cardiovascular): </h2> <p>Anabolic/androgenic steroids can have deleterious effects on serum cholesterol. This includes a tendency to reduce HDL (good) cholesterol values and increase LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a direction that favors greater risk of arteriosclerosis. The relative impact of an anabolic/androgenic steroid on serum lipids is dependant on the dose, route of administration (oral vs. injectable), type of steroid (aromatizable or non-aromatizable), and level of resistance to hepatic metabolism. Anabolic/androgenic steroids may also adversely affect blood pressure and triglycerides, reduce endothelial relaxation, and support left ventricular hypertrophy, all potentially increasing the risk of cardiovascular disease and myocardial infarction. </p> <p>Testosterone tends to have a much less dramatic impact on cardiovascular risk factors than synthetic steroids. This is due in part to its openness to metabolism by the liver, which allows it to have less effect on the hepatic management of cholesterol. The aromatization of testosterone to estradiol also helps to mitigate the negative effects of androgens on serum lipids. In one study, 280 mg per week of testosterone ester (enanthate) had a slight but not statistically significant effect on HDL cholesterol after 12 weeks, but when taken with an aromatase inhibitor a strong (25%) decrease was seen.3 Studies using 300 mg of testosterone ester (enanthate) per week for 20 weeks without an aromatase inhibitor demonstrated only a 13% decrease in HDL cholesterol, while at 600 mg the reduction reached 21%.4 The negative impact of aromatase inhibition should be taken into consideration before such drug is added to testosterone therapy. </p> <p>Due to the positive influence of estrogen on serum lipids, tamoxifen citrate or clomiphene citrate are preferred to aromatase inhibitors for those concerned with cardiovascular health, as they offer a partial estrogenic effect in the liver. This allows them to potentially improve lipid profiles and offset some of the negative effects of androgens. With doses of 600 mg or less per week, the impact on lipid profile tends to be noticeable but not dramatic, making an anti-estrogen (for cardioprotective purposes) perhaps unnecessary. Doses of 600 mg or less per week have also failed to produce statistically significant changes in LDL/VLDL cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive protein, and insulin sensitivity, all indicating a relatively weak impact on cardiovascular risk factors.5 When used in moderate doses, injectable testosterone esters are usually considered to be the safest of all anabolic/androgenic steroids. </p> <p>To help reduce cardiovascular strain it is advised to maintain an active cardiovascular exercise program and minimize the intake of saturated fats, cholesterol, and simple carbohydrates at all times during active AAS administration. Supplementing with fish oils (4 grams per day) and a natural cholesterol/antioxidant formula such as Lipid Stabil or a product with comparable ingredients is also recommended. </p> <h2>Side Effects (Testosterone Suppression): </h2> <p>All anabolic/androgenic steroids when taken in doses sufficient to promote muscle gain are expected to suppress endogenous testosterone production. Testosterone is the primary male androgen, and offers strong negative feedback on endogenous testosterone production. Testosterone-based drugs will, likewise, have a strong effect on the hypothalamic regulation of natural steroid hormones. Without the intervention of testosterone-stimulating substances, testosterone levels should return to normal within 1-4 months of drug secession. Note that prolonged hypogonadotrophic hypogonadism can develop secondary to steroid abuse, necessitating medical intervention. </p> <p>The above side effects are not inclusive. For more detailed discussion of potential side effects, see the Steroid Side Effects section of this book. </p> <h2>Administration (General): </h2> <p>Testosterone propionate is often regarded as a painful injection. This is due to the very short carbon chain of the propionic acid ester, which can be irritating to tissues at the site of injection. Many sensitive individuals choose to stay away from this steroid completely, their bodies reacting with a pronounced soreness and low-grade fever that may last for a few days after each injection. </p> <h2>Administration (Men): </h2> <p>For the treatment of low androgen levels, prescribing guidelines for Testoviron® call for a dosage of 250 mg once every 3-6 weeks. For bodybuilding purposes, this drug is usually injected on a weekly basis, in a dosage of 250-500 mg. Cycles are generally between 6 and 12 weeks in length. This level is sufficient to provide excellent gains in muscle size and strength. Given the poor pharmacokinetics and higher price of Testoviron® and related products, testosterone enanthate or cypionate are often given preference. Testosterone drugs are ultimately very versatile, and can be combined with many other anabolic/androgenic steroids depending on the desired effect. </p> <h2>Administration (Women): </h2> <p>Testoviron® is not commonly prescribed to women in clinical medicine. It is occasionally used to treat a declining sex drive with age, in which case a low dose (50 mg) may be given every 5-6 weeks. It is also sometimes used to treat advanced inoperable breast cancer, at a dose of 250 mg every 2-4 weeks (virilizing effects are expected at such dosing). This drug is not recommended for women for physique- or performanceenhancing purposes due to its strong androgenic nature, tendency to produce virilizing side effects, and slow-acting characteristics (making blood levels difficult to control). </p> <h2>Availability: </h2> <p>Schering (now Bayer) has discontinued manufacture of its blended Testoviron product in most parts of the world. </p> <p>Testoprim-D from Mexico is still in production. This item comes in a light resistant ampule that is packaged in a bright red box. </p> <p>Aratest from Aranda (Mexico) appears to still be in circulation. This product comes in a 10 mL multi-dose vial, and was recently updated to a red/white label. The library reflects the previous look. </p> <p>1 The effects of depot testosterone therapy on serum levels of luteinizing hormone and follicle-stimulating hormone in patients with Klinedelter’s syndrome and hypogonadotrophic eunuchoidism.Fukutani K, Isurugi K et al. J Clin Endocrinol Metab 39:856-64. </p> <p>2 Enzyme induction by oral testosterone. Johnsen SG, Kampmann JP, Bennet EP, Jorgensen F. 1976 Clin Pharmacol Ther 20:233-237. </p> <p>3 High-density lipoprotein cholesterol is not decreased if an aromatizable androgen is administered. Friedl K, Hannan C et al. Metabolism 39(1) 1990:69-74 </p> <p>4 Testosterone dose-response relationships in healthy young men. Bhasin S, Woodhouse L et al. Am J Physiol Endocrinol Metab 281:E117281,2001. </p> <p>5 The effects of varying doses of T on insulin sensitivity, plasma lipids, apolipoproteins, and C-reactive protein in healthy young men. Singh A, Hsia S, et al. J Clin Endocrinol Metab 87:136-43, 2002. </p> </body>
