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Fluoxymesterone (Halotestin) by Big Cat



Friends Remembered
Oct 11, 2010


To people who are familiar with the compound, fluoxymesterone is probably better known as Halotestin, its brand name as produced by the pharmaceutical company Upjohn. Fluoxymesterone was and is immensely popular among power- and weightlifting athletes and for a while among endurance athletes as well. Although well known in the bodybuilding community, it was not a much sought after substance in that sport. That is likely because fluoxymesterone has a reputation of being a harsh steroid that produces relatively mild results. While this statement is not entirely untrue, it does deserve some nuance. Fluoxymesterone is definitely a unique and possibly useful compound.

The main problem with the compound is its relatively high toxicity. Some toxicity is logically expected, since fluoxymesterone is a 17α-alkylated compound, generally consumed orally, but it should be considered one of the harsher products among this class of steroids as well, something that warrants some care on the part of the user. Because of this it can also not be used for prolonged periods of time. The limit is usually a good 6 weeks at 40 mg per day, which is a relatively low dose for a compound with such low affinity for the androgen receptor. Because of this and the low rate of actual muscle gained when using fluoxymesterone alone, usually causes potential users, especially beginners (and that is probably a good thing) to opt for less toxic and more effective drugs.

Fluoxymesterone is derived from methyltestosterone (and not a precursor of said compound, as was once reported in the now defunct World Anabolic Review) and differs from this product by the addition of an 11β-hydroxyl group and a halogenation with fluorine at the 9th carbon atom, both alterations commonly seen with corticosteroids, and not androgens. Both the 11β-hydroxyl1 group and the 9α-fluoro2 group are known to increase binding to the glucocorticoid receptor. This imparts on fluoxymesterone a strong affinity for the glucocorticoid (cortisol) receptor3, without activating it4, thus consistent with a model of competitive inhibition. As we will see throughout this profile, a lot of the actions that are unique to fluoxymesterone are to a large extent the direct result of this interaction. The increased affinity for the glucocorticoid receptor in mind seems to be the only logical explanation for the addition of these two specific groups, although 11β-hydroxy-testosterone has been tentatively identified as a very potent inhibitor of the 11β-hydroxysteroid dehydrogenase Type 1 enzyme22, which converts cortisone to its more active metabolite cortisol. The addition of the 9-fluoro group would likely increase its affinity for that enzyme as well, since it bends the A-ring of the steroid to the α-side2, resulting in a more glucocorticoid like structure. As such a large part of the anti-glucocorticoid action of fluoxymesterone may also be the result of a reduction of metabolism of cortisone to the more potent glucocorticoid cortisol. In support of the latter, a study conducted by Mayer and Rosen3 seem to indicate that while fluoxymesterone is more potent than testosterone in the glucocorticoid receptor inhibiting department, long term, it is not that much more potent in that regard to explain the enormous effect of fluoxymesterone on in vivo glucocortiocid activity. Also in support of this, Ojasoo and Raynaud23 report that C-1 Double bond is more potent than either of the substituents of fluoxymesterone at increasing glucocorticoid receptor affinity, yet fluoxymesterone is considerably more potent as an anti-glucocorticoid than boldenone, though both drugs share similar traits (Increase in appetite, increased stamina and endurance). This would suggest that 11β-HSD1 inhibition is a major pathway in the effect of fluoxymesterone, likely due to its 11β-hydroxy group. In short, many of the potent effects of fluoxymesterone should be seen in light of its anti-glucocorticoid properties, more than its (admittedly weak) androgenic-anabolic properties.


Anabolic Characteristics : As was alluded to previously, fluoxymesterone will rarely be called a potent anabolic, which doesn’t mean you should underestimate its quality as a muscle building agent. The history of figure sports has taught us that there are many way to successfully incorporate weak anabolic drugs into a successful pharmacological regimen. The anabolic effect of fluoxymesterone is, milligram for milligram, definitely not much weaker than that of popular anabolic androgenic steroids like oxandrolone or stanozolol. But where we can easily dose those drugs at 50-100 mg per day for several weeks, with monitoring of blood for hepatoxicity of course, this approach is unlikely with fluoxymesterone, since it is more androgenic and considerably more hepatoxic than the aforementioned products. As such, fluoxymesterone is definitely not a drug used often in cycles to accrue a maximum amount of muscle. It’s low anabolic activity seems to be in line with its low relative binding affinity for the androgen receptor5. And while it does seem to convert to a number of more potent metabolites via 5α-reduction6, their A-ring is not protected against metabolism by 3α-hydroxysteroid dehydrogenase in muscle, and they are therefore not active anabolic agents in skeletal muscle tissue.

Androgenic Characteristics : Although the androgenic effect of fluoxymesterone is often exaggerated, it is a fairly androgenic steroid. The parent compound is a very weak androgen receptor agonist, and that means the same holds true for metabolites with similar structural differences, including its 5α-reduced metabolites6. So, in total, one can still state that fluoxymesterone is less potent androgenically speaking, than testosterone. But as a whole, for an anabolic steroid, it’s a very potent androgen and should be treated as such. This does of course make the compound off limits for individuals with reasons to avoid strong androgens, such as women, elderly men with prostate problems and men with a genetic tendency to male pattern hair loss, since the androgenic effect mostly outweighs the anabolic benefits. Older research using the comparison between the weight increase in seminal vesicles or ventral prostate and the levator ani muscle in castrated rats indicates that the actions of fluoxymesterone favour anabolism, but any person who has actually used the compound will testify against that. As stated, commonly the androgenic strength of this drug is wildly exaggerated, but at best it has an anabolic:androgenic dissociation close to that of testosterone (which indicates no real dissociation since testosterone is the reference drug).

Estrogenic/Progestagenic Characteristics : Fluoxymesterone does not aromatize in any way. This is likely due to the addition of the 11β-hydroxyl group. Fluoxymesterone also has no appreciable binding to the estrogen receptor. Progestagenic activity of this steroid seems somewhat unlikely as well, since the same 11β-hydroxyl group reduces progesterone binding1.

If anything fluoxymesterone has a unique estrogen lowering effect, especially when used in combination with steroids that normally aromatize. This is the result of its potent anti-glucocorticoid effects. Glucocorticoid receptor activation in tissue that produce aromatase, usually results in an increased production of aromatase. Inhibition of glucocorticoid action7 or reduction of glucocorticoid potency8 leads to reduced expression of aromatase. This provides a cumulative role for the use of fluoxymesterone with competitive inhibitors of aromatase or the estrogen receptor in reducing circulating estrogen.

Fluoxymesterone and aggression : Fluoxymesterone is a drug that is often used because it seems to increase the level of aggression in an athlete notably, and short term. This effect is often desired by power- and weightlifters, where a sudden burst of energy/aggression, seems to increase self-confidence and performance. In bodybuilders too, this effect is sometimes desirable to survive the hard, final weeks of a cutting phase, to maintain work-out intensity when energy and caloric intake are low. Some people have mistakenly attributed this characteristic to be androgenic in nature. A grave mistake, since fluoxymesterone is often used as an example of a product that causes roid rage. But the resulting aggression, of this all in all mild androgen receptor binding steroid, stem, you guessed it, from its anti-glucocorticoid action. Glucocorticoid deprivation can notably increase aggression9. Since we know aggression to be a very relative understanding, this basically means that if you already have aggressive tendencies or a short temper, using fluoxymesterone may cause you to lash out quicker, but should be less of an issue if you are not usually quick to fly off the handle. Be aware that the use of strong androgens, estrogens11 or progestins10 can augment aggressive behaviour when using fluoxymesterone.

Fluoxymesterone increases endurance : Several anabolic androgenic steroids are known for their effect on increasing hematocrit and red blood cell mass. For this reason a lot of them have been used in the past to treat various forms of anemia. Increased hematocrit, however, also increases the oxygen content of blood and oxygen delivery to tissues. This in turn increases performance. Before the appearance of synthetic erythropoietin (rhuEPO, Epogen) and its derivatives, various brands of fluoxymesterone were much sought after by professional and semi-professional cyclists and long-distance runners, because it is very potent in this regard12,13. This is of course in part to its androgen mediated effect on erythropoietin release, but it is also noted that fluoxymesterone also seemed to distinguish itself from the other steroids in that it seemed to mediate increased responsiveness to erythropoietin in cells of the erythrocyte (red blood cell) lineage14. I found this to be very interesting and set out to see if there was a link between this phenomenon and the anti-glucocorticoid activity of fluoxymesterone, and indeed there was. Glucocorticoids seem to reduce the effect of erythropoietin on these cells, most likely due to anti-inflammatory effects15 (the reduction of prostaglandin formation, since prostaglandin E2 has a stimulatory effect on erythropoietin action). In this regard, by the way, it is still a very useful compound, since this indicates a synergistic effect with the use of erythropoietin (rhuEPO, Epogen) or its derivatives. Of course in light of the mechanism behind this effect, it could easily be substituted with other anti-glucocorticoid agents that are more difficult to detect (cycling especially is a sport where thorough drug testing is prevalent) and less toxic. It also seems to plead against the common practice of using corticosteroids for endurance athletes.

Fluoxymesterone is not very suppressive of HPTA : Although suppressive of endogenous testosterone production, just like any androgen, it can be duly noted that fluoxymesterone is all in all much less suppressive than most androgens16. Again, this is likely a result of the anti-glucocorticoid action of fluoxymesterone, since the GnRH gene (which encodes for GnRH, the hypothalamic hormone that initiates the cascade to testosterone synthesis) contains a glucocorticoid response element17. Indeed, Chandran et al.18 demonstrated that dexamethasone had a direct supressive effect on GnRH release. This also means that incorporating fluoxymesterone in a stack, especially at the end of a stack, can take the edge off recovery a bit, especially if post-cycle a non-HPTA-inhibitory glucocorticoid reducing agent is used, such as arginine19,20 for example.

Pharmacokinetic information

Fluoxymesterone is readily metabolized in a number of ways6. This probably causes a rapid reduction in active metabolites, despite the protection of the 17α-alkyl group. Given that none of the additional synthetic groups adds any major protection against metabolism (except aromatisation), its deactivation can probably likened to that of methyltestosterone. Like methyltestosterone it is therefore not active quite as long as many other steroids that are far more resistant to metabolism after oral ingestion, but still, a single daily dose should suffice for fluoxymesterone as well. Given the low dose normally used (10-40 mg/day), splitting up your doses would likely offer no real benefit. Although I’m not aware of injectable preparations of fluoxymesterone circulating, such a preparation would likely be more suited since it would reduce hepatoxicity somewhat, as well as metabolism of the parent compound.

There are some sublingual compounds circulating, but I’ve never seen an anlysis of such tablets, so that I could not say whether they posses a pharmacologically suitable mechanism to deliver a fatty compound like a steroid across the mucous membranes in the mouth, which usually absorb more hydrophilic substances, like sugars. If such a preparation does work with sufficient delivery of fluoxymesterone, its pharmacokinetic properties would likely be less than favourable, since it would be in and out of the body very quickly. Such method of delivery is however conducive of the increase in aggressiveness seen with fluoxymesterone, and it is conceivable that such a sublingual product was made with just that purpose in mind, by analogy with cheque drops (mibolerone), which also increased aggressiveness drastically and rapidly, and was immensely popular among boxers and weightlifters.


After reading this profile, two things should be obvious. The first is that fluoxymesterone is a much more useful compound than originally believed, and the second is that this is probably not a compound to be used by beginners. Because of dosage and duration-of-use restrictions, fluoxymesterone is likely not a good candidate for incorporotian of mass stacks. During such periods you are likely not going to be in a catabolic state, and a lot of steroids that you would use in such a situation, like testosterone and trenbolone, possess at least some degree of anti-glucocorticoid activity, that should be more than sufficient given the situation.

So it should be obvious that if we are going to incorporate the use of fluoxymesterone in a stack it will be most useful during periods of caloric deprivation, when maintenance of muscle mass is required. In this respect it should show a great degree of synergy with numerous compounds, including potent anabolic androgens like trenbolone, beta-2 adrenoreceptor agonists like ephedrine and clenbuterol, and will offer an added value to your dual goal of maintaining as much muscle as possible while losing fat. Fluoxymesterone may in fact directly contribute to fat loss by increasing oxidation of fatty acids and triglyceride secretion21, although this is an effect shared by many androgens. More importantly, in contrast to many 17α-alkylated steroids, which can increase glucocorticoid receptor density in certain tissues22, fluoxymesterone appears to reduce glucocorticoid receptor density. Combined with its inhibitory effect on glucocorticoid binding to the glucocorticoid receptor, this makes it a good candidate to be used at the end of a cycle. The common problem with other drugs with similar characteristics in regards to cutting, like stanozolol and oxandrolone, was the rapid loss of gained mass after discontinuation. Fluoxymesterone likely does not suffer this drawback and on top of that will ease transition into the post-cycle, due to blocking the inhibitory effect of glucocorticoids on GnRH release, making it rather perfect for such use.

It is also worth mentioning that the added aggression and energy is useful (when harnessed by a responsible person) to help one through the difficult last weeks of a diet, when caloric restriction is usually high enough to cause lethargy, depression and one tends to lose sight of his goals. Fluoxymesterone can help fuel workouts again and keep your eye on the prize.

Because of dose restrictions a user will likely add about 30 or 40 mg/day for a period of 5-6 weeks, preferably the last 6 weeks, of a cutting cycle. Even with this dose it is advisable to get a check-up of liver values at 4 and 6 weeks, and it shouldn’t have to be mentioned, but if higher doses are used, or the drug is administered for longer periods of time, such monitoring of liver values is absolutely necessary. The use of ancillary drugs should not be required during use of the compound. For those with reason to be concerned over the androgenic effect, finasteride does help in such cases, since the principle cause of its androgenic potency is 5-alpha-reduction.

For endurance athletes, use of the compound 1 or 2 hours prior to competition or training may suffice, but here too, longer protocols are advised. 20-30 mg per day for 4 weeks is a good place to start. The drug will prove especially useful to people using erythropoietin or analogues of that drug, or individuals following altitude training in preparation for competition. Use of the drug during competition is usually not an option for tested athletes as the drug is detectable up to 2 months after use if screened for. Which is of course a pity as the increased aggression usually benefits performance. Since it isn’t very likely to show that far after last use, the combination of erythropoietin, altitude training and fluoxymesterone up to 3-4 weeks before competition may pay off big time.


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

2) Duax WL, Griffin JF, Weeks CM, Wawrzak Z. The mechanism of action of steroid antagonists: insights from crystallographic studies. J Steroid Biochem. 1988 Oct;31(4B):481-92.

3) Mayer M, Rosen F. Interaction of anabolic steroids with glucocorticoid receptor sites in rat muscle cytosol. Am J Physiol. 1975 Nov;229(5):1381-6.

4) Donald F. Haggerty, Elaine B. Spector, Maureen Lynch, Rita Kern, Laura B. Frank, and
Stephen D. Cederbaum. Regulation by Glucocorticoids of Arginase and Argininosuccinate Synthetase in Cultured Rat Hepatoma Cells. J Biol Chem 257, (5). 2246-2253, 1982

5) Saartok T, Dahlberg E, Gustafsson JA. Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin. Endocrinology. 1984 Jun;114(6):2100-6

6) Kammerer RC, Merdink JL, Jagels M, Catlin DH, Hui KK. Testing for fluoxymesterone (Halotestin) administration to man: identification of urinary metabolites by gas chromatography-mass spectrometry. J Steroid Biochem. 1990 Aug 28;36(6):659-66.

7) Nawata H, Ono K, Ohashi M, Kato K, Ibayashi H. RU486 inhibits induction of aromatase by dexamethasone via glucocorticoid receptor in cultured human skin fibroblasts. J Steroid Biochem. 1988 Jan;29(1):63-8.

8) Yang K, Khalil MW, Strutt BJ, Killinger DW. 11 beta-Hydroxysteroid dehydrogenase 1 activity and gene expression in human adipose stromal cells: effect on aromatase activity. J Steroid Biochem Mol Biol. 1997 Feb;60(3-4):247-53.

9) Haller J, Halasz J, Mikics E, Kruk MR. Chronic glucocorticoid deficiency-induced abnormal aggression, autonomic hypoarousal, and social deficit in rats. J Neuroendocrinol. 2004 Jun;16(6):550-7.

10) Johanna S. Schneider, Marielle K. Stone, Katherine E. Wynne-Edwards,† Teresa H. Horton, John Lydon, Bert O'Malley, Jon E. Levine. Progesterone receptors mediate male aggression toward infants. Proc Natl Acad Sci U S A. 2003 March 4; 100(5): 2951–2956.

11) Sonoko Ogawa, April E. Chester, Sylvia Curtis Hewitt, Vickie R. Walker, Jan-Ake Gustafsson, Oliver Smithies, Kenneth S. Korach, and Donald W. Pfaff. Abolition of male sexual behaviors in mice lacking estrogen receptors α and β (αβERKO). Proc Natl Acad Sci U S A. 2000 December 19; 97(26): 14737–14741.

12) Bai GZ, Hara H, Nagai K. Influence of fluoxymesterone on in vitro erythropoiesis affected by leukemic cells. Exp Hematol. 1984 Mar;12(3):171-6.

13) Schulz E, Dickmans HA, Heesen D. [Erythropoietin in serum and urine in healthy persons and patients with chronic renal disease upon hypoxic stimulation and hypoxic stimulation after pretreatment with fluoxymesterone (author's transl)]. Klin Wochenschr. 1978 Oct 15;56(20):1019-27.

14) Singer JW, Adamson JW. Steroids and hematopoiesis. II. The effect of steroids on in vitro erythroid colony growth: evidence for different target cells for different classes of steroids. J Cell Physiol. 1976 Jun;88(2):135-43.

15) Mayeux P, Billat C, Felix JM, Jacquot R. Mode of action of erythropoietin and glucocorticoids on the hepatic erythroid precursor cells: role of prostaglandins. Cell Differ. 1986 Jan;18(1):17-26.

16) Hopwood NJ, Kelch RP, Zipf WB, Hernandez RJ. The effect of synthetic androgens on the hypothalamic-pituitary-gonadal axis in boys with constitutionally delayed growth. J Pediatr. 1979 Apr;94(4):657-62.

17) Radovick S, Wondisford FE, Nakayama Y, Yamada M, Cutler GB Jr, Weintraub BD.Isolation and characterization of the human gonadotropin-releasing hormone gene in the hypothalamus and placenta.Mol Endocrinol. 1990 Mar;4(3):476-80.

18) Chandran UR, Attardi B, Friedman R, Zheng Z, Roberts JL, DeFranco DB.Glucocorticoid repression of the mouse gonadotropin-releasing hormone gene is mediated by promoter elements that are recognized by heteromeric complexes containing glucocorticoid receptor.J Biol Chem. 1996 Aug 23;271(34):20412-20.

19) Duma D, Silva-Santos JE, Assreuy J.Inhibition of glucocorticoid receptor binding by nitric oxide in endotoxemic rats.Crit Care Med. 2004 Nov;32(11):2304-10.

20) Pennisi P, D'Alcamo MA, Leonetti C, Clementi A, Cutuli VM, Riccobene S, Parisi N, Fiore CE.Supplementation of L-arginine prevents glucocorticoid-induced reduction of bone growth and bone turnover abnormalities in a growing rat model.J Bone Miner Metab. 2005;23(2):134-9.

21) Bagdade JD, Livingston R, Yee E. Effects of synthetic androgen fluoxymesterone on triglyceride secretion rates in the rat. Proc Soc Exp Biol Med. 1975 Jun;149(2):452-4.

22) Latif SA, Pardo HA, Hardy MP, Morris DJ. Endogenous selective inhibitors of 11beta-hydroxysteroid dehydrogenase isoforms 1 and 2 of adrenal origin. Mol Cell Endocrinol. 2005 Sep 23

23) Ojasoo T, Raynaud JP, Dore JC. Correspondence factor analysis of steroid libraries. Steroids. 1995 Jun;60(6):458-69.



VIP Member
Nov 4, 2010
Halotestin, the good old days when getting ready for a show, never have a female around while on Halo's...


Senior Moderators
Staff Member
Dec 25, 2010
I've only tried halo once, and it was from a compounding pharmacy, so I think it was legit. However, I was underwhelmed. I ran 20mg/day for about 2 weeks and didn't notice much. I know some people swear by the stuff...


Bigger Than MAYO - VIP
Sep 9, 2010
I think you have to take about 40-50mg to get an overwhelming response... I was never a fan either...
porky little keg

porky little keg

May 21, 2011
Super excited to try halo for my recent powerlifting meet...... only to get scammed.

$2 a tab, 50mg halo tabs turned out to be MAYBE dbol or something cheaper, but definitely not halo. I didn't get a headache so maybe not even dbol..... suck!


Jun 13, 2012
I remember back in the 90s we use to get hg Halo from Greece in little glass bottles with a tube inside to keep the pills against the glass, my first 10mg dose was so good I had to have my buddy try it and the first thing he said was I can feel it, we were both red skinned and tight ready to attack the weights, damn I miss those days.


VIP Member
Oct 30, 2011
I remember back in the 90s we use to get hg Halo from Greece in little glass bottles with a tube inside to keep the pills against the glass, my first 10mg dose was so good I had to have my buddy try it and the first thing he said was I can feel it, we were both red skinned and tight ready to attack the weights, damn I miss those days.
That was before my time but that must have been nice.


Jun 11, 2014
This is about to come into my prep. So it was a great read!


New Member
Oct 21, 2014
Been thinking about using this for a while. However I am always caution of liver toxicity for oral form


Senior Moderators
Staff Member
Aug 13, 2013
I don't cycle it any more, but I do love taking 20mg about an hour pre-workout on Leg & Back days. You can absolutely feel the aggression.
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