<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>Neotest 250 (testosterone decanoate) </h1> <h2>Description: </h2> <p>Testosterone decanoate is a slow-acting injectable form of the primary male androgen testosterone. This steroid is mostly commonly identified as part of the four-ester blend in Sustanon® 250, but here is described as a standalone agent. The long decanoate ester used to make testosterone decanoate creates a drug with pharmacokinetic properties similar to nandrolone decanoate, providing a sustained release of hormone (in this case testosterone) for approximately three weeks following injection. Testosterone decanoate is slightly slower-acting than the commercially available esters cypionate and enanthate, and could provide a slightly less frequent injection schedule in comparison. </p> <h2>History: </h2> <p>Testosterone decanoate was developed decades ago, and offers favorable pharmacokinetics of testosterone release (arguably more balanced than Sustanon® 250). In spite of this, testosterone decanoate was never a commercial success as a single-agent steroid product. The only modern preparation to contain this testosterone ester exclusively has been Neotest 250, a veterinary steroid produced by Loeffler in Mexico. This drug was favored by a small audience of loyal consumers because it offered less frequent injections than testosterone enanthate, and more user comfort than Sustanon® 250 (notorious for pain and soreness at the injection site). Neotest was only sold on the Mexican veterinary market for a short while, however. Political pressures against steroid sales and a U.S. indictment of the company (Operation Gear Grinder) have apparently resulted in Loeffler eliminating Neotest from their product line, as well as many other ‘controversial’ products. No other commercial product using testosterone decanoate as the only active agent is known to exist at this time. </p> <h2>How Supplied: </h2> <p>Testosterone decanoate is no longer available as a standalone commercial drug product. When produced, the Neotest 250 brand contained 250 mg/ml of testosterone decanoate in oil, packaged in a 10 mL multi-dose vial. </p> <h2>Structural Characteristics: </h2> <p>Testosterone decanoate is a modified form of testosterone, where a carboxylic acid ester (decanoic acid) has been attached to the 17-beta hydroxyl group. 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. </p> <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 anti-estrogen 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 a 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 5alpha 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, alanine-aminotransferase, and alkaline phosphatases.1 </p> <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 nonaromatizable), 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.2 Studies using 300 mg of testosterone ester (enanthate) per week for twenty weeks without an aromatase inhibitor demonstrated only a 13% decrease in HDL cholesterol, while at 600 mg the reduction reached 21%.3 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/LDL cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive protein, and insulin sensitivity, all indicating a relatively weak impact on cardiovascular risk factors.4 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 (Men): </h2> <p>Although active in the body for longer, testosterone decanoate is usually injected once every 7 to 10 days for bodybuilding purposes. The total weekly dosage is typically 200-600 mg, which is sufficient to provide excellent gains in muscle size and strength. Testosterone drugs are ultimately very versatile, and can be combined with many other anabolic/androgenic steroids depending on the desired effect. Administration (Women): Testosterone decanoate is not recommended for women for physique- or performance-enhancing 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>Neotest 250 is no longer available. No other testosterone decanoate product is known to be in circulation. </p> <p>1 Enzyme induction by oral testosterone. Johnsen SG, Kampmann JP, Bennet EP, Jorgensen F 1976 Clin Pharmacol Ther 20:233-237. </p> <p>2 High-density lipoprotein cholesterol is not decreased if an aromatizable androgen is administered. Karl Friedl, Charles Hannan et al. Metabolism 39(1) 1990:69-74. </p> <p>3 Testosterone dose-response relationships in healthy young men. Bhasin S, Woodhouse L et al. Am J Physiol Endocrinol Metab 281:E117281, 2001. </p> <p>4 The effects of varying doses of T on insulin sensitivity, plasma lipids, apolipoproteins, and C-reactive protein in healthy young men. Atam Singh, Stanley Hsia, et al. J Clin Endocrinol Metab 87: 136-43, 2002. </p> </body>
