Superdrol, Sdrol, Prohormone confusion

The confusion surrounding superdrol is the result of an ill-conceived name, given to this substance, probably for marketing purposes. Which ever idiot came up with the name or first starting suggesting that superdrol has anything in common with oxymetholone (Anadrol) has thoroughly demonstrated that he/she lacks any and all insight in biochemistry. Other than the fact that both are 5alpha-reduced anabolic androgenic steroids, they have very little if anything in common.

Superdrol is a compound that was known for some time prior to it being known as such. I for one came in contact with the drug following the debate surrounding IP’s equally ill-named product called ‘oral Masteron’, which ended up being nothing more than mestanolone (17alpha-methyl-DHT). Mestanolone is actually oral DHT (if for arguments sake we suggest that the addition of 17alpha-methyl group indicates the compound as being the oral of the parent steroid, which is not strictly true). I commented that to be oral masteron it would have to be 2alpha-methyl-mestanolone, or more aptly 17alpha-methyl-drostanolone (drostanolone being Masteron). That is what we called the product back then, 17alpha-methyl-drostanolone. That was only a few years ago. But it seems somehow inconceivable that this compound hadn’t been investigated decades before. So it probably has an even longer history.

From this you can also already deduce that ‘superdrol’ is in actuality a cross between drostanolone and mestanolone, since it has the 2alpha-methyl group of drostanolone and the 17alpha-methyl-group of mestanolone. Oxymetholone is an entirely different compound, which differs from superdrol by substitution of the 2-methyl group with a 2-hydroxymethylene group. A methyl group is completely inert, since it is apolar. It confers no special biochemical properties upon the group, it is merely steric bulk. Which is exactly its purpose. It provides steric hindrance for 3alpha- and 3beta-hydroxysteroid dehydrogenase enzymes, so that in contrast to mestanolone, the product is not deactivated in muscle tissue so fast. Mestanolone is nearly inactive as an anabolic substance, because it is rapidly deactivated to 3-hydroxy metabolites. Because the 2-methyl group reduces binding of the enzymes that catalyze this, it reduces the rate of deactivation and superdrol, in contrast to mestanolone, has some anabolic activity.

Oxymetholone on the other hand has a hydroxylated carbon attached to the 2nd carbon, a polar group that is chemically reactive. That carbon is also double-bonded tot the steran nucleus, which further increases reactivity of the oxygen atom. By what mechanisms is not exactly clear yet, but this gives oxymetholone some rather unique properties, likely due to interaction with other structures that most AAS do not, or barely interact with. To illustrate I uploaded the following drawing. It shows superdrol as the cross of mestanolone and drostanolone, and underneath mestanolone is oxymetholone, since oxymetholone is also a derivative of mestanolone.


Anabolic activity : Because of the added 17alpha-methyl group, superdrol is less succeptible to metabolic deactivation. It cannot form 17-keto-steroids, and the likelihood of 16-hydroxylations is considerably reduced as well, due to this addition. This means it probably stays active longer than does drostanolone and is excreted at a lower rate. Unfortunately, the 2-methyl-group already reduces binding to the androgen receptor (1) and the 17alpha-methyl group further reduces it (1). This seems to even out the odds for superdrol, giving it roughly the same amount of anabolic activity as drostanolone. That means superdrol is by no means a serious muscle builder, except perhaps to those smaller in stature or as of yet unexperienced with other anabolic androgenic steroids. This puts its anabolic activity in the neighbourhood of other non-aromatizing, weak oral androgens, such as Anavar (oxandrolone), Winstrol (Stanozolol) and Halotestin (Fluoxymesterone).

Androgenic activity : Comparing it to these other weak, oral, non-aromatizing androgens, the androgenic activity is considerably less than for halotestin, but considerably higher than for winstrol and anavar. The reason being that despite increased activity in muscle compared to mestanolone, deactivation is still stronger in muscle (the 2-methyl group reduces but does not eliminate reduction of the 3-keto function (2)). And contrary to popular belief, a non-deactivated DHT does still not have the same level of activity in muscle as it does in androgenic target tissues. Androgenic side-effects rarely occur in healthy young men, but if you have reason to fear such effects, than superdrol is probably the poorer choice when compared to anavar or winstrol. A lot of athletes however seem to suggest that using stronger androgens seems to increase muscle density when body-fat is low. And while this is a rather subjective trait, this does seem to hold true for superdrol as well. In which case it would then probably be a better choice than the other mentioned oral steroids.

Estrogenic/Progestagenic activity : Like most 5-alpha-reduced steroids, this product has no estrogenic activity. Neither mestanolone nor drostanolone are capable of aromatization either. Whoever is producing this stuff now seems to want to convey that it is a major plus that this does not have estrogenic effects like oxymetholone, but first off, remember that this steroid has NOTHING in common with oxymetholone and secondly, the perceived estrogenic effects of oxymetholone have never been established as being estrogenic, because despite massive bloating, the prevalence of estrogenic side-effects with oxymetholone remains low when used with other AAS to non-existent when used alone. Whether or not this drug still has anti-estrogenic activity like drostanolone is questionable. I certainly wouldn’t count on it.

Liver-toxicity : The hepatoxicity of this compound is rather high. That may have been one of the reasons no one has marketed or researched such a compound for pharmaceutical use before. In all instances I observed personally (which were admittedly only 4 instances of use of 40 mg/day for 6 weeks), liver values were elevated above acceptable levels, and considerably elevated above the values seen for the same duration of time with equal (dbol) or higher (Anavar, Anadrol, Winstrol) doses of other commonly (ab)used oral steroids. Use should therefore definitely be restricted to 30-40 mg/day for 6 weeks. If higher doses are used, or compound is used for a longer period of time, liver values should be checked at regular intervals.

Stacking and use : It should be quite obvious that the use of this compound (at least to the experienced steroid user) will be limited to cutting purposes. For the same amount of money there are simply far more suitable compounds for gaining muscle mass. As with most oral steroids (with notable exception of Halotestin) I would advise against using it alone, in conjunction with other oral steroids, or in the last week of a cycle. This because most 17alpha-alkylated androgens are known to increase glucocorticoid receptor density (3) and result in increased loss of muscle mass post-cycle. An added reason for not using it with other oral steroids is the increased risk for hepatoxic side-effects.

References

(1) Ojasoo T, Raynaud JP.Unique steroid congeners for receptor studies.Cancer Res. 1978 Nov;38(11 Pt 2):4186-98

(2) de Boer D, de Jong EG, Maes RA, van Rossum JM.The methyl-5 alpha-dihydrotestosterones mesterolone and drostanolone; gas chromatographic/mass spectrometric characterization of the urinary metabolites.J Steroid Biochem Mol Biol. 1992 May;42(3-4):411-9.

(3) Fernandez L, Boada LD, Luzardo OP, Zumbado M, Lopez A, Diaz-Chico BN, Chirino R.[3H]dexamethasone binding activity in liver microsomes is modulated differently by 17 alpha-alkylated androgens and testosterone in vivo.Pharmacol Toxicol. 1995 Oct;77(4):264-9.