This is the scenario: a guy, say age 21, becomes serious about gaining muscle. He’s 5′ 10″, 7″ wrists, 9″ ankles, average genetics for muscle size-and-proportioned. He’s played sports, but never done more than an occasional resistance workout. Now, he begins a good training-eating-and-resting program. With his genetics, he has the potential for naturally gaining 45 pounds of lean mass if he stays consistent with progressive training/proper eating for a continuous 3 to 4 years.
But, about three months after beginning his training, he starts taking steroids. He does three steroid cycles in the following 18 months, and includes proper post-cycle therapy. That entire time, he’s continuing to consistently train and eat properly. Before the end of two years, he’s gained 45 pounds of lean mass (which with steroids, by the way, is not necessarily typical but neither improbable). At that point, he permanently quits using steroids, but he does continue properly training and eating for another two years. At the end of four years, he carries the same 45 pounds of lean mass.
Generally it is accepted that due to the toxicity issues of Stanozolol, its use should be limited to 6 weeks & as with anything though, many people have run it for up to 12 weeks with no problems. As previously stated, this compound is unique, as it is available in both an oral form as well as an injectable form. Both forms contain the exact same compound, but injecting this compound (and yes, you can drink the injectable version, and no you shouldn’t) is superior to ingesting it orally in terms of nitrogen retention (6), and thus one would also imagine, for overall anabolism. Injecting it also has the advantage of avoiding the “first pass” through your liver, and thus places your liver under less stress.
Bortezomib, a boronic acid dipeptide, is a highly selective, reversible inhibitor of the 26S proteasome which primarily functions in the degradation of mis-folded proteins and is essential for the regulation of the cell cycle. Exposure to Bortezomib has been shown to stabilize p21, p27, and p53, as well as the proapoptotic Bid and Bax proteins, caveolin-1, and inhibitor κB-α, which prevents activation of nuclear factor κB-induced cell survival pathways. Bortezomib also promotes the activation of the proapoptotic c-Jun-NH2 terminal kinase, as well as the endoplasmic reticulum stress response. Alteration of the levels of these cellular proteins leads to inhibition of proliferation, migration, and promotion of apoptosis of cancer cells.  Bortezomib is shown to penetrate into cells and inhibit proteasome-mediated intracellular proteolysis of long-lived proteins with a concentration that inhibits 50% of the proteolysis of ∼ μM. The average growth inhibition of 50% value for Bortezomib across the entire panel of 60 cancer cell lines derived from multiple human tumors from the US National Cancer Institute (NCI) is 7 nM. Treatment of PC-3 cells with Bortezomib (100 nM) for 8 h results in the accumulation of cells in G2-M, with a corresponding decrease in the number of cells in G1. Bortezomib kills PC-3 cells at 24 and 48 hr with IC50 of 100 and 20 nM, respectively. Bortezomib induces nuclear condensation at 16–24 hr after treatment. Bortezomib treatment leads to PARP cleavage in a time-dependent manner with concentrations as low as 100 nM being effective at 24 hr.