- Mechanstically they are very similar(Aromasin and ATD), there is no data on cholesterol. However it is likely the impact is very similar as they are both steroidal AI's (as opposed to dex and femara which are not)

- The main ingredient is ATD;
1,4,6 androstatriene-3,17-dione a steroidal aromatase inhibitor

- Aromasin is;
6-methylenandrosta-1,4-diene-3,17-dione (better oral bioavailability)

- ATD has relatively poor oral bioavailability hence why the need for a "topical".

- Read the feedback, it’s VERY effective. Why is it not sold as a drug... not patentable- for 2 reasons 1. it was widely studied as an aromatase inhibitor before a treatment value had been assigned to aromatase inhibition and it exists in nature.

- tested clinically ATD, clinically tested in numerous animal and cell models, is as effective as exemestane (aromasin) and formestane (lentaron), it like formestane (lentaron is an injectable) is not particularly well suited for oral adminstration.

- ATD is a PROVEN aromatase inhibitor, a steroidal aromatase inhibitor.

- In truth its quite like saying testosterone is not effective, only dianabol. exemestane(aromasin) is really a methylated derivative of ATD making it orally "active".

- It is rediculous to compare ATD to chrysin. Chrysin is a flavanoid. ATD is a naturally occuring steroid, but because its not an androgen its not an anabolic steroid (governments definition), thus is legal.

- There are a number of steroidal and non steroidal AI's that were not marketed, not because they were not effective, but because either they were not patentable or not suitable for the treatment of WOMENS breast cancer... ie. some had direct androgenic effects, some elevated testosterone too much, etc....

- because the most "interesting" area in animals is sexual differentiation, much of the research is done using silastic capsules which release ATD directly into the brain (great for studying very specific effects of aromatase deprivation on the brain.... but not of too much value in this discussion other than to establish that it is a potent aromatase inhibitor). however feel free to do a search on pubmed for ATD or 1,4,6-androstatriene-3,17-dione. there are nearly 100 studies.

- ADT is 1,4,6-androstatriene-17beta-ol-3-one acetate or ANDROSTERONE
perhaps that is why he is confused about efficacy

- ATD is an effective AI, in fact. IMHO based on both the studies and initial testing its as or more effective than aromasin in MEN (sample size is small, though over the male population response is likely to be similar).

Now since AI's have been developed to treat women its not surprising that many of the earlier and potent steroidal AI's were "passed" over.

Basically ATD is an effective AI, how effective compared directly to the three main commercial AI's remains to be seen. Based on the results of our trials it is just as effective as the most popular AI’s being used.

Some studies:

Cancer Res. 1982 Aug;42(8 Suppl):3327s-3333s.


A new hypothesis based on suicide substrate inhibitor studies for the mechanism of action of aromatase.

Covey DF, Hood WF.

Recently, it was discovered that 4-hydroxy-4-androstene-3,17-dione, 4-androstene-3,6,17-trione, and 1,4,6-androstatriene-3,17-dione, compounds previously reported to be competitive inhibitors of aromatase, cause a time-dependent loss of aromatase activity in human placental microsomes. We report here that 1,4-androstadiene 3,17-dione (Ki 0.32 microM; kinact 0.91 X 10(-3)/sec) and testolactone (Ki 35 microM; kinact 0.36 X 10(-3)/sec) also cause a similar loss of aromatase activity.
Physiol Behav. 1987;39(1):141-5.


The aromatase inhibitor, 1,4,6-androstatriene-3,17-dione (ATD), blocks testosterone-induced olfactory behaviour in the hamster.

Steel E, Hutchison JB.

The effect of ATD on olfactory investigation in intact and in castrated, testosterone-treated male hamsters was studied using subcutaneous silastic implants. In intact males, there was a dose-dependent action of ATD in reducing sniffing towards novel females and in eliminating the discrimination between females after pre-exposure to vaginal odour. Both sniffing and olfactory discrimination reappeared after removal of ATD implants. Neither the weight nor the general behavioural activity of treated males was affected, indicating a specific behavioural affect. Testosterone (T) maintained olfactory behaviour in castrated males. Untreated castrates and castrates with ATD + T implants showed reduced sniffing and showed no discrimination between females after exposure to female odour. We conclude that conversion of T to oestrogen plays an essential role in the control of male olfactory behaviour.


1: Brain Res Dev Brain Res. 1995 Apr 18;85(2):273-9. Related Articles, Links


Increased number of vasopressin neurons in the suprachiasmatic nucleus (SCN) of 'bisexual' adult male rats following perinatal treatment with the aromatase blocker ATD.

Swaab DF, Slob AK, Houtsmuller EJ, Brand T, Zhou JN.

Netherlands Institute for Brain Research, Graduate School Neurosciences Amsterdam.

In an earlier article an enlarged subpopulation of vasopressin containing neurons was found in the suprachiasmatic nucleus (SCN) of homosexual men as compared to heterosexuals. The present study investigates the possibility that the number of vasopressin neurons in the SCN and sexual partner preference behavior in male rats are both influenced by sex hormones during brain development. For this purpose, we studied groups of adult male rats that had been treated either prenatally or pre- and postnatally with the aromatase inhibitor ATD (1,4,6-androstatriene-3,17-dione) which blocks the aromatization of testosterone to estradiol. Rats treated with ATD in both pre- and postnatal periods showed 'bisexual' partner preference behavior and appeared to have 59% more vasopressin-expressing neurons in the SCN than the controls. The prenatally treated rats did not differ from the controls. This observation supports the hypothesis that the increased number of vasopressin neurons found earlier in the SCN of adult homosexual men might reflect differences that took place in the interaction between sex hormones and the brain early in development




This study is not ideal though it is reflective of the comparative delivery

J Endocrinol. 1996 Sep;150 Suppl:S107-18. Related Articles, Links


High bioavailability of dehydroepiandrosterone administered percutaneously in the rat.

Labrie C, Flamand M, Belanger A, Labrie F.

Laboratory of Molecular Endocrinology CHUL Research Center, Quebec, Canada.

Dehydroepiandrosterone (DHEA) administered percutaneously by twice daily application for 7 days to the dorsal skin of the rat stimulates an increase in ventral prostate weight with approximately one third the potency of the compound given by subcutaneous injection. The doses required to achieve a 50% reversal of the inhibitory effect of orchiectomy are approximately 3 and 1 mg respectively. By the oral route, on the other hand. DHEA has only 10-15% of the activity of the compound given percutaneously. Taking the bioavailability obtained by the subcutaneous route as 100%, it is estimated that the potencies of DHEA by the percutaneous and oral routes are approximately 33 and 3% respectively. Similar ratios of activity were obtained when dorsal prostate and seminal vesicle weight were used as parameters of androgenic activity. When examined on an estrogen-sensitive parameter, namely uterine weight in ovariectomized rats, the stimulatory effect of DHEA was much less potent than its androgenic activity measured in the male animal, a 50% reversal of the inhibitory effect of ovariectomy on uterine weight being observed at the 3 and 30 mg doses of DHEA administered by the subcutaneous and percutaneous routes respectively. When measured on uterine weight, percutaneous DHEA thus shows a 10% potency compared with the subcutaneous route. The sulfate of DHEA (DHEA-S), on the other hand, was approximately 50% as potent as DHEA at increasing ventral prostate weight after subcutaneous or percutaneous administration. When the effect was measured on dorsal prostate and seminal vesicle weight, percutaneous DHEA-S had 10-25% of the activity of DHEA. DHEA decreased serum LH levels in ovariectomized animals, an effect which was completely reversed by treatment with the antiandrogen flutamide. On the other hand, flutamide had no significant effect on the increase in uterine weight caused by DHEA, thus suggesting a predominant estrogenic effect of DHEA at the level of the uterus and an estrogenic effect on the feedback control of LH secretion. The present data show a relatively high bioavailability of percutaneous DHEA as measured by its androgenic and/or estrogenic biological activity in well-characterized peripheral target intracrime tissues in the rat.

Thanks for posting your results bro.