Primobolan Enathate

Status
Not open for further replies.

PHD

IFBB Pro -Coach - sponsored athlete
Staff member
IFBB Pro
Hey fan wanted to share some insight on primoE. I know a lot of people here love primo so wanted to share this. Hope this helps you understand this amazing anabolic @Omegaman

Remember with gear guys less is more not more is more lol

Description

Primobolan Depot is an injectable version of the steroid methenolone. This is the same constituent in Primobolan orals (methenolone acetate), although here an enanthate ester is used to slow the steroid’s release from a site of injection. Methenolone enanthate offers a similar pattern of steroid release as testosterone enanthate, with blood hormone levels remaining markedly elevated for approximately two weeks. Methenolone itself is a moderately strong anabolic steroid with very low androgenic properties. Its anabolic effect is considered to be slightly less than Deca-Durabolin (nandrolone decanoate) on a milligram-for-milligram basis. Methenolone enanthate is most commonly used during cutting cycles, when lean mass gain, not a raw mass increase, is the main objective.

How Supplied

Methenolone enanthate is usually supplied in the form of 1 ml ampules and 10 ml vials containing 100 mg/ml of steroid in oil.

Effective Dosages

When used for physique- or performance-enhancing purposes, the usual administration protocols among male athletes call for a 200-400 mg per week dosage, which is taken for six to 12 weeks. It is not unusual, however, to see the drug taken in doses as high as 600 mg per week or more, although such amounts are likely to highlight a more androgenic side of methenolone, as well as exacerbate its negative effects on serum lipids. Female athletes generally respond well to a dosage of 50-100 mg per week. If both oral and injectable versions are available, the oral is often given preference, as it allows for greater control over blood hormone levels. As with all anabolic-androgenic steroids (AAS), even though this is regarded as a milder anabolic agent, virilizing side effects cannot be excluded.

Side Effects

Estrogenic:
Methenolone is not aromatized by the body,and is not measurably estrogenic. Estrogen-linked side effects should not be seen when administering this steroid. Sensitive individuals need not worry about developing gynecomastia, nor should they be noticing any appreciable water retention with this drug.

Androgenic: Although classified as an anabolic steroid, androgenic side effects are still possible with this substance. This may include bouts of oily skin, acne and body/facial hair growth. Anabolic-androgenic steroids may also aggravate male pattern hair loss. Women are warned of the potential virilizing effects of AAS. These may include a deepening of the voice, menstrual irregularities, changes in skin texture, facial hair growth and clitoral enlargement. Methenolone is still a very mild steroid, however, and strong androgenic side effects are typically related to higher doses. Women often find this preparation an acceptable choice, observing it to be a very comfortable and effective anabolic.

Liver Toxicity: Methenolone is not considered a hepatotoxic steroid; liver toxicity is unlikely. Studies have failed to produce appreciable changes in markers of hepatic stress when the drug was given in therapeutic levels.

Cardiovascular: Anabolic-androgenic steroids can have deleterious effects on serum cholesterol, increasing the risk of arteriosclerosis. They may also adversely affect blood pressure and triglycerides, reduce endothelial relaxation and support left ventricular hypertrophy, all potentially increasing the risk of cardiovascular disease and myocardial infarction. People with high cholesterol or a familial history of heart disease should be especially careful when considering AAS abuse. To help reduce cardiovascular strain, it is advised to maintain an active cardiovascular exercise program and minimize the intake of saturated fats, cholesterol and simple carbohydrates at all times during active AAS administration. It is of note that methenolone should have a stronger negative effect on the hepatic management of cholesterol than testosterone or nandrolone due to its non-aromatizable nature, yet a weaker impact than c-17 alpha alkylated steroids.

Testosterone Suppression: All AAS, when taken in doses sufficient to promote muscle gain, are expected to suppress endogenous testosterone production. At a moderate dosage of 100-200 mg weekly, methenolone should offer measurably less testosterone suppression than an equal dose of nandrolone or testosterone, due to its non-aromatizable nature. This may result in a shorter recovery time with moderate use.

The above side effects are not inclusive.

Availability

Pharmaceutical preparations containing methenolone enanthate remain scarce. The bulk of the supply for this compound comes from underground steroid manufacturers.

References:

Wiechert R, et al. Chem Ber 93 (1960):1710.

Methenolone enanthate, summary of information for clinical investigators. New Brunswick, NJ. The Squibb Institute for Medical Research, April 15, 1962.

Anabolic effects of methenolone enanthate and methenolone acetate in underweight, premature infants and children. New York State Journal of Medicine, March 1, 1965, 645-8.

Proc Intern Congr Hormonal Steroids, Milan, 1962. Excerpta Med Intern Congr. Ser No. 51, p. 209. Excerpta Med Found, Amsterdam, 1962.

Failure of non-17-alkylated anabolic steroids to produce abnormal liver function tests. J Clin Endocrinol Metab 1964 Dec;24:1334-6.
 
Last edited:
I honestly don’t know the answer to that. I just had blood work done last week. When I get them back I’ll see if they tested that. @NeuroRN do you know the answer to this. I think it wouldn’t affect it but im not really sure.
 
So a brief look into pubmed I find no actual studies including primo and it’s effect on SHBG, but there’s some threads on other forums with corresponding bloodwork over several months of primo use. Ranging from 200-600mg of primo, and those show anecdotal evidence/correlational evidence of decreased SHBG over the course of their cycle.

I’ll definitely look into it more. For now @Aude_Aliquid_Dignu I would say it’s probably not your best option until I can find more substantial evidence either way.
 
SHBG acts as a natural buffer to keep your test/estrogen ratio in check. When one is too high it binds to SHBG rendering it unavailable to perform its function.

So if SHBG is low … that would theoretically mean more bioavailable test for the body to use… but also more estrogen available in its active and free form.

So all the symptoms of high estrogen is what is typically seen in men, but also out of proportion to test which is a problem.

I’m not sure about his specific symptoms.

A low production is a different problem than low unbound SHBG. Typically low bound SHBG isn’t a problem as it’s just doing its job, and we can take proviron or mast to bind to SHBG and keep our test and estro ratio high and pleasant. If the body is simply not producing enough SHBG you will most often see an imbalance in hormones.

This is off the top of my head so it’s probably not as thorough as I’d like.

@Louisianastrength
 
Last edited:
After digging through pubmed with every combo of words I can only find one study that says proviron has the strongest binding affinity to SHBG then it lists comparisons of other AAS binding to AR in skeletal muscle.

Not helpful.

LOTS of conflicting bro science out there. Some say it’s week binding to SHBG. Some say it’s a wonder drug for binding to SHBG making all your other juice better. :roll_eyes:

I would still say as a dht derivative it’s going to have some sort of affinity for SHBG receptors. But that’s ultimately more assumption…

However, I did find more lab results of people claiming to only be running test and primo and there does appear to be consistency in the fact that SHBG does decrease throughout their cycle. Unfortunately this is the best I have to offer.
 
I’ve combed the interweb for this answer for months. And have found the same conflicting information.

I think I will actually be my own “science project” and test this out. I am only running test right now and a SARM who’s run will be done. So it should be a pretty clean causal relationship potentially.

After my next blood, if all looks good, I will run primo at a 1:1 ration to my TRT and see if there is a statistically significant difference in the numbers.

I know for me, Primo is like a bottomless pit of storied energy I can tap into during my hardest workouts. Like surprisingly so. And thats during a partial run b/c my bloods came back concerning. Or maybe its just a psychosomatic effect…who knows.
 
Last edited:
  1. SHBG still seems to be a bit of mystery in how and why it does it magic. But with all things, we want to keep it as balanced as possible with our other levels. I did once here a talking head refer to SHBG as Testosterone’s Postman which I thought was a clever analogue.
What we do know is that it is as important as fuck. Here are a couple links for a deeper dive…

  1. Wiki has it rated as 3% affinity on this chart.
  1. I posted this last year from a Reddit guy who claims to have researched SHBG for ten years:
"Low SHBG increases Free Test (FT)%, not T output. The hypothalamus responds by seeing it as an excess and lowering LH pulses to maintain homeostasis and get back to the FT target it wanted. This decreases total testosterone.

Check out the studies that show that SHBG and TT are positively correlated. So, the higher SHBG, the higher the TT, and the lower the SHBG, the lower the TT (in men without deficiency.)

This is the mechanism by which hypothyroidism or insulin resistance (which cause very low SHBG) lead to hypogonadism (low T.) "

also…

There is no such thing as waste with SHBG. The broscience is that SHBG “stealz ur T”, but the exact opposite is true. SHBG does not metabolize or destroy testosterone. SHBG does not “steal” T and then perform some biochemical magic to make the T vanish from the universe, either.

SHBG prevents the metabolism of testosterone and slows down your overall MCR (metabolic clearance rate) by preventing the liver from destroying testosterone and also prolonging the action of T within cells (SHBG passes into the cell via endocytosis instead of free diffusion.)

SHBG+T has an approximate half-life of 2 hours in serum. Then, the complex dissociates. The T is returned to the bloodstream — intact.

Do you know what wastes your testosterone/other compound? The liver. Get rid of the liver and you’ll enjoy all the benefits of your pinning. Also, stop cellular glucuronidation and you’re “GTG”, as they say.

Decreasing SHBG is the fastest and most guaranteed way ensure free androgens are removed from your body as rapidly as possible.

In healthy men with naturally high testosterone levels, SHBG correlates positively with TT.

When steroids are used, SHBG becomes nearly irrelevant because androgen levels grossly outweigh the binding capacity of SHBG. In a normal, healthy male, there are more SHBG glycoproteins than there are molecules of androgen. In a steroid user, SHBG becomes oversaturated and the liver attempts to address the androgen excess by reducing SHBG concentration to speed up the clearance (removal) of androgens from the body. However, due to the relentless exogenous supply of androgen, the liver’s effort is futile. MCR is maximized and overridden.

Excessive SHBG can interfere with passive diffusion through cellular membranes by limiting the concentration of T in its free moiety. Aromatization slows and both DHT and E2 become excessively bound to SHBG, limiting the immediate action of all major steroid hormones before they are degraded.

Normal SHBG slows MCR, prevents over-metabolization and also enhances cellular uptake and retention by reducing the glucuronidation and efflux of FT from cells and excites the SHBG-R receptor to increase cellular cAMP. SHBG at adequate level preserves testosterone and enhances the action of two pathways: the endocytic pathway and the extracellular (SHBG-R) pathway. (Androgens bind to SHBG which has already bound to extracellular megalin.)

Insufficient SHBG increases MCR (your liver destroys T rapidly), allows for excessive metabolization to DHT and E2, and speeds up (per study!) the breakdown of testosterone in cells. Secondary pathways are starved. This is situation is either genetic, the result of excessive inflammation (or other disease state) or due to an excess of androgen in the body."

Credit: Reddit user Vestpocket
 
Status
Not open for further replies.
Back
Top