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The alkyl group cannot be removed metabolically, and therefore inhibits reduction of the steroid to its inactive 17-ketosteroid form by occupying one of the necessary carbon bonds. Before long, pharmaceutical companies had utilized this advance (and others) to manufacture an array of effective oral steroids including methyltestosterone, Dianabol, Winstrol’, Anadrol 50′, Halotestin’, Nilevar, Orabolin, and Anavar. The principle drawback to these compounds is that they place a notable amount of stress on the liver, which in some instances can lead to actual damage to this organ. Because the alkyl group cannot be removed, it mediates the action of the steroid in the body. Methyltestosterone, for example, is not simply an oral equivalent of testosterone, as the added alkylation changes the activity of this steroid considerably. One major change we see is an increased tendency for the steroid to produce estrogenic side effects, despite the fact that it actually lowers the ability of the hormone to interact with aromatase. These estrogens are more biologically active than estradiol due to their longer half-life and weaker tendency to bind with serum proteins, buy rexobol 10 mg oral steroids oral winstrol. In some instances, 17alpha-alkylation will also enhance the ability of the initial steroid compound to bind with and activate the estrogen or progesterone receptor. Dianabol is clearly more estrogenic than Equipoise’, a drug not noted for producing strong side. The same holds true for the comparison of Nilevar to Deca-Durabolin, a compound that we also know to be extremely mild in this regard. C17 alpha alkylation also typically lowers the affinity in which the steroid binds to the androgen receptor, as is noted with the weak relative binding affinity of such popular agents as Dianabol and Winstrol (stanozolol). However, since this alteration also greatly prolongs the half-life of a steroid, as well as increases the tendency for it to exist in an unbound state, it creates a more potent anabolic/androgenic agent in both cases. This explains why Dianabol and stanozolol are notably effective in relatively lower weekly doses (often 140 mg weekly will produce notable growth) compared to injectables such as testosterone and nandrolone, which often need to reach doses of 300-400 mg weekly for a similar level of effect. In an attempt to solve the mentioned problems with liver toxicity we see with c17-alpha alkylated compounds, a number of other orals with different chemical alterations (such as Primobolan’, Proviron’, AndriolE, and Anabolicum Vister) were created. Primobolan’ and Proviron’ are alkylated at the one position (methyl), a trait which also slows ketosteroid reduction. Andriol’ uses a 17beta carboxylic acid ester (used with injectable compounds, discussed below), however, here the oil-dissolved steroid is sealed in a capsule and is intended for oral administration. This is supposed to promote steroid absorption through intestinal lymphatic ducts, bypassing the first pass through the liver. In addition to 1 methylation, Primobolan’ also utilizes a 17 beta ester (acetate) to further protect against reduction to inactive form (here there is no lymphatic system absorption). Anabolicum Vister uses 17beta enol ether linkage to protect the steroid, which is very similar to esterification as the ether breaks off to release a steroid base (boldenone in this case). 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