Please Scroll Down to See Forums Below
How to install the app on iOS

Follow along with the video below to see how to install our site as a web app on your home screen.

Note: This feature may not be available in some browsers.

napsgear
genezapharmateuticals
domestic-supply
puritysourcelabs
UGL OZ
UGFREAK
napsgeargenezapharmateuticals domestic-supplypuritysourcelabsUGL OZUGFREAK

Trans dermal info for everyone

Trenbolone Acetate structure
E3171 4,9,11-ESTRATRIEN-17-OL-3-ONE ACETATE
Formula C18 H24 O3

Molecular Weight 312.4 Rotation +36.8° MeOH
Melting Point 96-97°C
 
I'm willing to see what happens if i use SUST 250 transdermal. Do you guys think that it can go through?

LORD_REGULATOR - YOU'VE GOT MAIL.:alien:
 
the ester is what gives an INJECTABLE drug its half-life. It modifies the drug's potential to remain in it's vehicle (oil or water), or to exit the vehicle and enter the tissues/blood

on a side a note: the longer the side chain on the 17a the lower the androgenic activity

it's not the 1-beta alkylation that protects it, but the double bond that is transferred from the 4 position to the 1 position that allows it to survive first pass in the liver. instead of bypassing the enzyme that deactivates AS like 17-aa steroid primo works on this enzyme to reverse the reaction equilibrium to favor the active state instead of the inactive state. this doesn't do jack though.


no flame intended but what did you reference in order you come up with that MOA.

As a general rule, the metabolism of steroid hormones involves sequential additions of oxygen or hydrogen atoms, followed by conjugation to form water-soluble derivatives. Reduction of the 4,5 double bond occurs at both hepatic and extrahepatic sites, yielding inactive compounds. Subsequent reduction of the 3-ketone substituent to the 3-hydroxyl derivative, occuring only in the liver. Most of these A ring-reduced steroids are conjugated through the 3-hydroxyl group with sulfate or glucuronide by enzymatic reactions that take place in the liver and, to a lesser extent, in the kidney. The resultant sulfate esters and glucuronides form water-soluble derivatives and are the predominant forms excreted in the urine. Neither biliary nor fecal excretion is of quantitative importance in human beings.
 
Last edited:
I would like to see ANY facts on transdermals absorbtion rate.. Whether it is 20, 30 or 80 percent, everything you guys has stated is hypothetic. Personally, I would rate transdermal at near 80%.
 
Interesting structure as compared to test........

anex_a3.gif



A6950.gif




"these compounds resist metabolic deactivation by profoundly shifting what is known as the “17-keto redox potential” towards the formation of active 17beta-hydroxyl steroids.[ii],[iii] What does this mean? It means that when you take 1-AD, the liver serves primarily to activate the compound, rather than break it down and excrete it as it does with other prohormones and testosterone. It means that 1-AD is “orally active,” yet it does not impart the liver toxicity that 17alpha-alkylation does."
 
"I would like to see ANY facts on transdermals absorbtion rate.. Whether it is 20, 30 or 80 percent, everything you guys has stated is hypothetic. Personally, I would rate transdermal at near 80%."

Here you go, BSMOOTH:

J Clin Endocrinol Metab 2000 Dec;85(12):4500-10

"Long-term pharmacokinetics of transdermal testosterone gel in hypogonadal men."

Swerdloff RS, Wang C, Cunningham G, Dobs A, Iranmanesh A, Matsumoto AM, Snyder PJ, Weber T, Longstreth J, Berman N.

Divisions of Endocrinology, Departments of Medicine/Pediatrics, Harbor-University of California-Los Angeles Medical Center, Torrance, California 90509, USA.

Transdermal delivery of testosterone (T) represents an effective alternative to injectable androgens. Transdermal T patches normalize serum T levels and reverse the symptoms of androgen deficiency in hypogonadal men. However, the acceptance of the closed system T patches has been limited by skin irritation and/or lack of adherence. T gels have been proposed as delivery modes that minimize these problems. In this study we examined the pharmacokinetic profiles after 1, 30, 90, and 180 days of daily application of 2 doses of T gel (50 and 100 mg T in 5 and 10 g gel, delivering 5 and 10 mg T/day, respectively) and a permeation-enhanced T patch (2 patches delivering 5 mg T/day) in 227 hypogonadal men. This new 1% hydroalcoholic T gel formulation when applied to the upper arms, shoulders, and abdomen dried within a few minutes, and about 9-14% of the T applied was bioavailable. After 90 days of T gel treatment, the dose was titrated up (50 mg to 75 mg) or down (100 mg to 75 mg) if the preapplication serum T levels were outside the normal adult male range. Serum T rose rapidly into the normal adult male range on day 1 with the first T gel or patch application. Our previous study showed that steady state T levels were achieved 48-72 h after first application of the gel. The pharmacokinetic parameters for serum total and free T were very similar on days 30, 90, and 180 in all treatment groups. After repeated daily application of the T formulations for 180 days, the average serum T level over the 24-h sampling period (C(avg)) was highest in the 100 mg T gel group (1.4- and 1.9-fold higher than the C(avg) in the 50 mg T gel and T patch groups, respectively). Mean serum steady state T levels remained stable over the 180 days of T gel application. Upward dose adjustment from T gel 50 to 75 mg/day did not significantly increase the C(avg), whereas downward dose adjustment from 100 to 75 mg/day reduced serum T levels to the normal range for most patients. Serum free T levels paralleled those of serum total T, and the percent free T was not changed with transdermal T preparations. The serum dihydrotestosterone C(avg) rose 1.3-fold above baseline after T patch application, but was more significantly increased by 3.6- and 4.6-fold with T gel 50 and 100 mg/day, respectively, resulting in a small, but significant, increase in the serum dihydrotestosterone/T ratios in the two T gel groups. Serum estradiol rose, and serum LH and FSH levels were suppressed proportionately with serum T in all study groups; serum sex hormone-binding globulin showed small decreases that were significant only in the 100 mg T gel group. We conclude that transdermal T gel application can efficiently and rapidly increase serum T and free T levels in hypogonadal men to within the normal range. Transdermal T gel provided flexibility in dosing with little skin irritation and a low discontinuation rate.


The gel only showed bioavailability of 9-14%, and the patch around 10% (5-10mg T/day from 50-100mg patches).
 
It all depends on the type of transdermal used in the process IE DMSO, Phlojel, and some others. Some people say you get anywere from 20-80percent absorbtion. Well the only way to know for sure is to do both and i can persoanlly say i have done test propinate injection before did 150mg Monday Wednesday & Friday. Stacked with injection of Primo at 300mg Per Week. Receptors were fresh from a 6 month lay off and put on the average about 16 pounds and about a 8 pound fat loss. over 6 weeks. had a real strict diet to. Did the same amounts all the same amounts of both drug about 1 year later fresh recopters clean diet and gained about 10 pounds and lost about 14 fat. Gained less muscle but lost more fat.

I will be over the next 6 months experimenting using transdermal with various drugs and posting resluts and pictures just for scientific reasons. I guess i will be the scientific guine pig for all :angel:
 
I take injectable primo. I was wondering if you could mix something like Phlojel with the primo i already have or if I would need to get oral primo and crush it up. The post was not clear on that. Also, How much phlojel or DMSO would I have to mix with whichever form of primo? is it mg for mg? does it make a difference which steroid I use...would the formula still be the same?
 
trenbolone orally?

Can i take trenbolone orally, and if i can, how much should i take to get the same effekt as injecting 75mg?
 
Top Bottom