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MassFX 25R-diol Write-Up?

Point taken. If you were in our situation you would see the other factors that play in much heavier. Companies that like to steal or copy formulas are the reason that things are this way. All too often lot's of effort and money is put into a supplement only to have it copied and whored out weeks later. The consumer does not care because they get the product for much less. The company that copies the formula just has to make a call to china and nothing else. We in the end lose out. Because of this our synth on 25R-diol and any documentation relating to it will remain company private.

So once again points have been taken but at this moment the AX partners do not want to release the study docs.
 
It is great that some in the medical field want to learn, but really, how many of our consumers are going to go to pubmed, and research compounds?

Is it a wonder that LabCoats are not part of marketing, nor sales, they just get the compounds and get stuff that works. They have no knwledge about consumer base, and from the looks of it I see a couple of lab coats trying to find info, (which is Great) but asking what exactly what it is no good for business...
 
Apowerz6 said:
It is great that some in the medical field want to learn, but really, how many of our consumers are going to go to pubmed, and research compounds?

Is it a wonder that LabCoats are not part of marketing, nor sales, they just get the compounds and get stuff that works. They have no knwledge about consumer base, and from the looks of it I see a couple of lab coats trying to find info, (which is Great) but asking what exactly what it is no good for business...

Hey! There are some kind of brains behind those lab coats :-)

Now you put a hot supermodel under those lab coats wearing nothing but AX logos pasted on - then we've got some marketing potential!!

Cheers!
 
so an AI is or isn't needed?

If the only test increasing substance in Mass FX is DVTHF, and the 25R--diol doesn't increase test, an AI really isn't necessary. ActivaTe uses more DVTHF and you don't need rebound with it.
 
25R-Diol will increase test it is just not the main mode of action. Give the write-up a read. Until we are informed by Dr.D otherwise yes an AI is recommended.
 
The write-up seems to say that it is a pretty weak androgen. I guess its androgenic enough to need an AI when combined w/ DVTHF
 
TeamSavage said:
... You are essentially saying "Trust us" with your promotion of the product. You are making claims, but the customer has to take a leap-of-faith to believe these claims and buy the product. Quality supplements are not the results of sloppiness. Did the company check out the raw material supplier? Did the company have the raw material independently analyzed? Is the company using a GMP-certified, Drug Licensed manufacturing facility? Did the company thoroughly review the supporting research, or did they just glance at a few abstracts? When a write-up is riddled with simple spelling and grammar errors, it signals sloppiness. If a company is sloppy with something like a write-up, this suggests they may also be sloppy in other, more complex (and more important) areas of the process.

Frankly, I don't give a sh!t about the spelling and grammar errors. But since you want to focus on that comment, there's the reason why it matters and isn't trivial.

Savage! What the hell are you really up to man? I answered your question specifically in PMs so don't act like you don't know, please. As far as the write-up, blame me for the spelling and grammar errors. It was a bit rushed and I'm not an English major.

Let me put this to rest right here and now. I formulated Activate a long time ago for a different company. I have released a ton of articles and advice and bloodwork that is directly applicable to MFX and it's mechanisms. You don't need a leap of faith, nettles benefits are well established and if you look, I referenced dozens of articles about the anti-inflammatory, anti-microbial, pro-prostate, pro-cardio, etc.. benefits of nettle already.

As far as suppliers, yes, it took years to find good suppliers but I know who they are and have half a dozen trusted sources at this point. Still, I test batch samples before we ever buy a lot from even those good sources.

Is the material independently analyzed? Damn straight! Don't ever take a manufacturer's CofA at face value. I have been a raw material analyst in the Quality Control division of a major pharmaceutical company for the last 9 years. So yeah, to say I know exactly what I'm doing is an understatement. I know the USP like the back of my hand and QC is my passion! There is no corner cutting when I'm in charge, I do have a rep to uphold. :) My products are always solid, unless you can name one that isn't?

Yes, out compounding modules are approved by me alone and our cappers follow current GMP and CRF protocols. Not only that, the finished goods are tested again by a third lab to insure that they are consistent so AX is totally confident not only in the raws that go in but the product that comes out.

Like I said, about research, I've researched and developed this technology for the last 2.5 years so I've looked at more that "a few abstracts" bud. The formula works and works well and the ref's and logs are out there if you look. I will not elaborate since I was told not too but as I said, this is already well established info that's out there anyway if you look and has been posted everywhere when I first made this type of product for another company.

MFX is just the pinnacle of that original concept. AX has gone a step further from my original formula. The DVTHF in the product increases free test levels no doubt. Why does nettle also increase total test and lower estrogen at the same time? Because of the sterols present, mainly b-sito's (diosgenin).

Do you need an AI to make this happen? Nope! The recommended HD stack only amplifies steroidogenisis though a cAMP path while the AI boost test even higher, but estro sides are controlled alone by MFX, regardless if it's stacked or not. The bloodwork abounds so it's pointless to argue that.

Does the sterol component elevate LH levels? Probably, at least indirectly though proven reductase lowering activity and possible SERM like activity too on FSH levels but that's not it's primary mode of benefit.

What is the main mode of action? 25R has a direct anabolic effect on ARs (high receptor affinity with low intrinsic androgenic activity). And yes, there are articles to show this.

Why do we fortify with a sterol? Because the extraction process that isolates the high concentration of lignan removes the sterols. This mean that using NRX alone is only doing half the job it should be.

Why do we use a specialty sterol to fortify the extract? Because diosgenin itself is great, but the form we use is more anabolic based on the Russian studies showing it's anabolic character and also far more resistant to metabolic breakdown thus greatly improving effectiveness. Efficacy is further enhanced by the addition of a well established absorption enhancer and well proved CYP enzyme inhibitor, thus the free test generated as well as the sterol have an even greater half-life and are less likely to undergo adverse metabolism. This lowers estro potential even more!

It all makes perfect sense when you see the bloodwork and the logs that it works just like it was designed to. The product is not only effective, it goes beyond safe to the point it is actually healthy! If anti-arteriosclerosis, anti-prostate cancer, lower cholesterol, and lower BP are side effects, then I admit, it has them! Gimme a break. :rolleyes:

You can not win this battle Savage, so think real hard about what you're trying to accomplish with this attack before you continue bro.
 
Thank you for the reference.

Dr. D - Let me be clear: I am not trying to attack you. I am not trying to attack AX. I am not even trying to attack MassFX. My questions about raw materials, analysis, manufacturing, etc. were just to illustrate the many complexities of supplement development, in the context of explaining why sloppiness in promotion (i.e. an un-proofread write-up) could raise questions of sloppiness in other, more important areas. I was NOT saying that this is the case with AX. (I have used 5 AX products in the past, seen good results, and have recommended them to others... not an AX hater!) All that said, thank you for taking the time to explicitly address these points.

I agree that nettle benefits are well established. As I said before, even if 25R-diol is completely inactive, MassFX would still be an effective product due to the DVTHM. I was specifically looking for more info on 25R-diol.

Now, regarding the compound itself. You state in the write-up and the PM that it has high affinity to AR receptors but low intrinsic activity at those receptors, and thus does not cause shutdown. What exactly do you mean by "intrinsic activity"? The high affinity for AR receptors but low intrinsic activity at those same receptors seems to be contradictory. Unless I'm missing something, the only way this makes sense is if it binds to AR in muscle tissue but not in the pituitary. An MD I talked to mentioned that the moiety that binds to the androgen receptors is also the moiety that lets the pituitary recognize the amounts of androgen in the circulation, in which case this would not possible. Can you please clarify this and explain how this is working? (I am NOT saying you are wrong. I freely admit that you know more about this than I do, which is why I'm asking questions... that's how this whole thread started, a question for specifics on how 25R-diol works.) If you can't explain exactly how it works, can you explain how these conclusions were drawn from the research?

Regarding research, I understand AX wants to keep it tight. Fine. But without giving us the reference keys to the kingdom, could you give us some basic outline of the research that was conducted on this compound, regarding the AR-affinity and low suppression as well as the LH increase, libido increase, and 5AR activity? What was measured and how? What were the results? In vitro or in vivo? Humans or rats? etc. Just a summary, so those of us who care about research (as you do) know what we are dealing with.

Finally, let me just say that if 25R-diol was being promoting by a company that usually produced sh!t and was designed by somebody who I know was full of sh!t then I wouldn't be asking all these questions, because I would assume that it's all hype with little behind it. The reason I am so interested in 25R-diol and how it works is because (a) AX has a history of producing quality products, and (b) you, Dr. D, generally have valid, accurate opinions and know what you're talking about. My interest in this is a reflection of my positive view of both parties, not a negative view. All that said, it's still important to review support for claims rather than accepting them without seeing the evidence, regardless of the source.
 
TeamSavage said:
Thank you for the reference.

Dr. D - Let me be clear: I am not trying to attack you. I am not trying to attack AX. I am not even trying to attack MassFX. My questions about raw materials, analysis, manufacturing, etc. were just to illustrate the many complexities of supplement development, in the context of explaining why sloppiness in promotion (i.e. an un-proofread write-up) could raise questions of sloppiness in other, more important areas. I was NOT saying that this is the case with AX. (I have used 5 AX products in the past, seen good results, and have recommended them to others... not an AX hater!) All that said, thank you for taking the time to explicitly address these points.

I agree that nettle benefits are well established. As I said before, even if 25R-diol is completely inactive, MassFX would still be an effective product due to the DVTHM. I was specifically looking for more info on 25R-diol.

Now, regarding the compound itself. You state in the write-up and the PM that it has high affinity to AR receptors but low intrinsic activity at those receptors, and thus does not cause shutdown. What exactly do you mean by "intrinsic activity"? The high affinity for AR receptors but low intrinsic activity at those same receptors seems to be contradictory. Unless I'm missing something, the only way this makes sense is if it binds to AR in muscle tissue but not in the pituitary. An MD I talked to mentioned that the moiety that binds to the androgen receptors is also the moiety that lets the pituitary recognize the amounts of androgen in the circulation, in which case this would not possible. Can you please clarify this and explain how this is working? (I am NOT saying you are wrong. I freely admit that you know more about this than I do, which is why I'm asking questions... that's how this whole thread started, a question for specifics on how 25R-diol works.) If you can't explain exactly how it works, can you explain how these conclusions were drawn from the research?

Regarding research, I understand AX wants to keep it tight. Fine. But without giving us the reference keys to the kingdom, could you give us some basic outline of the research that was conducted on this compound, regarding the AR-affinity and low suppression as well as the LH increase, libido increase, and 5AR activity? What was measured and how? What were the results? In vitro or in vivo? Humans or rats? etc. Just a summary, so those of us who care about research (as you do) know what we are dealing with.

Finally, let me just say that if 25R-diol was being promoting by a company that usually produced sh!t and was designed by somebody who I know was full of sh!t then I wouldn't be asking all these questions, because I would assume that it's all hype with little behind it. The reason I am so interested in 25R-diol and how it works is because (a) AX has a history of producing quality products, and (b) you, Dr. D, generally have valid, accurate opinions and know what you're talking about. My interest in this is a reflection of my positive view of both parties, not a negative view. All that said, it's still important to review support for claims rather than accepting them without seeing the evidence, regardless of the source.
Savage now that was a well stated set of questions. I bet you get those questions answered if you stay respectful :)

Give Dr.D some time though. He is a busy man. We have a lot of things going on and you have a lot of questions that are going to take some time to compile solid answers for. Okay? I am sure he will answer what he can based on the research that we do have. Dr.D did ask me to post the Russian study for you and I did above his post.
 
BigSmith said:
Savage now that was a well stated set of questions. I bet you get those questions answered if you stay respectful :)

I better get my ******* answers after 62 posts and about 10,000 words! :D
 
TeamSavage said:
I better get my ******* answers after 62 posts and about 10,000 words! :D
:icon_lol: Now go find us a few gold members or board supporters to participate in our testing spree. :)
 
well there was that spelling error in your last post........

:icon_lol:

Just tell me when your log starts, Savage!
 
macedaddy said:
Just tell me when your log starts, Savage!

Like I said, I'll be happy to log it in April or May, once the "confounding variables" of January and February have cleared my system. ;)

Or, here's an idea... How about a log of straight 25R-diol? No Hyperdrol. No DVTHM.

I could take it in the same dose found in MassFX to see how it performs alone. Or better yet I could mega-dose it to find out just how anabolic it can get. Pre, during, and post bloodwork could evaluate (a) its effects on LH, and (b) how much, if any, endogenous suppression occurs. (Albeit this "study" would be n=1, so not exactly conclusive... But hey, if I gain 15 lbs on 25R-diol alone with no suppression, those results could be pretty darn interesting. Or even if my nuts shrivel and my LH and natty test plummet, still interesting.)
 
TeamSavage said:
Or, here's an idea... How about a log of straight 25R-diol? No Hyperdrol. No DVTHM.
We could do that. Pretty much what the beta testers did minus the HD. Of course it would be best to run the straight 25R-diol with the DHB and Bioperine for absorption. But yeah, we could work that out. Just let us know when you are ready in the spring.
 
TeamSavage said:
... All that said, it's still important to review support for claims rather than accepting them without seeing the evidence, regardless of the source.

Ok, I can understand that. I also appreciate you pointing out the sloppiness of the write up. You are correct saying that it reflects poorly on a good product. I take the blame. I admit, I am probably the only one that can read the chicken scratch in my lab notebooks too and can't type to save my a** so blame that on me. I am far more concerned with putting out a safe and effective product that polishing the write up and marketing it with all the right flash. I'm a chemist and not a PR or business man so what can I say? I am a meticulous analyst though and you can rest assured I am responsible enough to research, test and try everything before I ever give it a thumbs up to release to you guys.

I do not have time to dig up and repost all the refs right now, plus I have been gagged on posting some of them, but 90% of it is already out there as I said earlier. You could search and consolidate in a few hours probably if you took the time. I simple don't have the time. I work for 3 different companies all designing 3-6 products each at the moment, plus I get 30-50 PMs a day plus regular emails too and have 2 special forums I have to answer questions in now not to mention the threads I'm subscribed to already with 3 kids and a pissed off wife that threatens to hide my modem every night because I'm on the computer so damn much! I hope you can understand and do the homework for yourself. Nonetheless, you will find everything I've stated to be true and I challenge you to show otherwise. I know what I know and I stand by what I have said. That's the best I can do for you my friend. If you just try the product, I'm sure you won't have any more questions though. The results speak for themselves!

I will say about intrinsic activity: Take nandrolone for example. It has higher "receptor affinity" that testosterone meaning it binds to the AR more tightly than test. However, it only has a fraction of the androgenic potency of test so it has lower "intrinsic activity". The net effect is something 90% as anabolic as test with only 10% the androgeny. That equals out in the real world to a good anabolic with few sides when used at the proper dose. That's the way 25R works. The more androgenic a compound, the more shutdown and sides, but the greater the affinity the more anabolism and the less sides, provided the compound is not inherently androgenic. This must be the case with 25R or else total test levels would not continue to rise week after week.

Also, in my trials I have tested this compound on women that no longer have ovaries. They have reported oily skin and increased acne sometimes with mild mood alterations similar to that which would be expected of an androgen. That means that it's likely acting directly or ARs because LH boosting would have no affect on these individuals.
 
DR.D said:
The more androgenic a compound, the more shutdown and sides, but the greater the affinity the more anabolism and the less sides, provided the compound is not inherently androgenic.


This is what I have been trying to grapple with. So if, for instance, a compound could bind to the AR with ZERO androgenic sides, there would be no shutdown? Androgenic activity is the signal for negative feedback, not anabolic activity?

So you are saying that 25R-diol is SARM-like?
 
Enigma76 said:
This is what I have been trying to grapple with. So if, for instance, a compound could bind to the AR with ZERO androgenic sides, there would be no shutdown? Androgenic activity is the signal for negative feedback, not anabolic activity?

So you are saying that 25R-diol is SARM-like?

Yes, theoretically a pure anabolic would cause no shutdown, but no researcher has ever been able to completely divorce anabolic and androgenic activity. Teslac is the closest I've seen, but it was never further developed to make a really useful anabolic with. Winni and SD have excellent separation of these two qualities, but still are not totally pure anabolics. You have the right idea though.

Androgeny is nothing more than local anabolism. Try to picture it that way. If something is very anabolic to the prostate, they just call it an androgen, that's the distinction. Estrogen shuts down FSH first and foremost (contrary to popular belief that is shuts down LH) and DHT shuts down LH with greatest priority. So, the more androgenic a compound is, the greater the odds of shutdown and the faster it occurs proportional to the dose being used. That's why SD or Var may not even cause your boys to shrink on a 3-4 wk cycle at 20mg but 10mg of M1T will practically do it overnight and test can do it in just a week or two! Also remember that over a certain stochastic threshold, both DHT and estrogen will shut down both FSH and LH equally, so if you are taking a gram of test a wk with 50mg winni/d you are shutting down the whole axis regardless. With something like 25R, SARM-like would be a reasonable way to state it alright because it obviously can't bind at the most important location on the AR site (where the C-17 hydroxyl usually occupies) but still must bind at the 3 or 6 because it clearly demonstrates direct action. In the pituitary, binding at the 17 position may be essential for true recognition and thus shut down to occur or it may be androgenically weak enough not to cause a major androgenic response but plant sterols are well know for being excellent prostate protectors so with 25R we probably ran across a natural SARM that just so happens to favor anabolism. That what the research, clinical data and bloodwork suggest so far.
 
DR.D said:
Yes, theoretically a pure anabolic would cause no shutdown, but no researcher has ever been able to completely divorce anabolic and androgenic activity. Teslac is the closest I've seen, but it was never further developed to make a really useful anabolic with. Winni and superdrol have excellent separation of these two qualities, but still are not totally pure anabolics. You have the right idea though.

Androgeny is nothing more than local anabolism. Try to picture it that way. If something is very anabolic to the prostate, they just call it an androgen, that's the distinction. Estrogen shuts down FSH first and foremost (contrary to popular belief that is shuts down LH) and DHT shuts down LH with greatest priority. So, the more androgenic a compound is, the greater the odds of shutdown and the faster it occurs proportional to the dose being used. That's why SD or Var may not even cause your boys to shrink on a 3-4 wk cycle at 20mg but 10mg of M1T will practically do it overnight and test can do it in just a week or two! Also remember that over a certain stochastic threshold, both DHT and estrogen will shut down both FSH and LH equally, so if you are taking a gram of test a wk with 50mg winni/d you are shutting down the whole axis regardless. With something like 25R, SARM-like would be a reasonable way to state it alright because it obviously can't bind at the most important location on the AR site (where the C-17 hydroxyl usually occupies) but still must bind at the 3 or 6 because it clearly demonstrates direct action. In the pituitary, binding at the 17 position may be essential for true recognition and thus shut down to occur or it may be androgenically weak enough not to cause a major androgenic response but plant sterols are well know for being excellent prostate protectors so with 25R we probably ran across a natural SARM that just so happens to favor anabolism. That what the research, clinical data and bloodwork suggest so far.

Thank you Dr. D! So with androgenicity being nothing more than local anabolism, for a compound to lack shutdown effects it would have to have very little "anabolic" action in the pituitary? This makes sense, as I've been reading up on SARMs lately, and they all stress the importance of tissue specificity; they never explain why, however. Basically, if the anabolic action of a compound in negative-feedback tissues (pituitary, hypothalamus?) is small, shutdown will be small (or delayed)?

Another quick question; I'm fairly certain there are two (or more?) estrogen receptor subtypes in the body. I was under the assumption that Tamoxifen exerted its action by binding at one of the subtypes but not the other (its alpha and beta subtypes, right?).

Do androgen receptors have the same subtype classifications as estrogen receptors? Or is there just one androgen receptor that is populated all over the body?

Regarding bloodwork, has it been released?

Thank you for your time.
 
Jayhawkk said:
Hmmm, what's the coefficient of the average check out line at best buy on black friday?
:rofl:
That is the Jay I know and miss !!! Bring him back, bring him BACK!!!
 
Enigma76 said:
Thank you Dr. D! So with androgenicity being nothing more than local anabolism, for a compound to lack shutdown effects it would have to have very little "anabolic" action in the pituitary? This makes sense, as I've been reading up on SARMs lately, and they all stress the importance of tissue specificity; they never explain why, however. Basically, if the anabolic action of a compound in negative-feedback tissues (pituitary, hypothalamus?) is small, shutdown will be small (or delayed)?

Another quick question; I'm fairly certain there are two (or more?) estrogen receptor subtypes in the body. I was under the assumption that Tamoxifen exerted its action by binding at one of the subtypes but not the other (its alpha and beta subtypes, right?).

Do androgen receptors have the same subtype classifications as estrogen receptors? Or is there just one androgen receptor that is populated all over the body?

Regarding bloodwork, has it been released?

Thank you for your time.

Yes, an "androgen" just means that it's possesses tissue specific anabolism in sex tissues like the prostate, so specificity means everything when it comes to SARMs and good anabolics (as we normally think of them).

There are several distinct estrogen receptors as you mention that have higher populations in certain tissues than others. There are probably at least 2 androgen receptors (and I suspect even sub-receptors within both groups) though the animals most used in testing (rats) show the presence of no ARs at all but often still respond predictably as if they had them! So I have never seen conclusive enough evidence to say, but I'd be surprised if it were not found to be true one day that multiple ARs and sub-sets of ARs exist in various ratios within different human tissues.
 
DR.D said:
Yes, an "androgen" just means that it's possesses tissue specific anabolism in sex tissues like the prostate, so specificity means everything when it comes to SARMs and good anabolics (as we normally think of them).

There are several distinct estrogen receptors as you mention that have higher populations in certain tissues than others. There are probably at least 2 androgen receptors (and I suspect even sub-receptors within both groups) though the animals most used in testing (rats) show the presence of no ARs at all but often still respond predictably as if they had them! So I have never seen conclusive enough evidence to say, but I'd be surprised if it were not found to be true one day that multiple ARs and sub-sets of ARs exist in various ratios within different human tissues.


Thank you for your insight.

I figured there might be more androgen receptor subtypes as well; my thinking was that because of breast cancer, SERM research has really outpaced SARM research, and SERM research elucidated the various estrogen receptors and subtypes.

Looking foward to the first couple logs/bloodwork on this compound.
 
Well there will be a BUNCH of logs up real soon :) !!
 
Dr. D i was doing some research and discovered that the 25-R compound used in mass fx was basically diosgenin altered at C-5 and C-6 where the double bond was broken and an alcohol group was added at the C-6. Is this correct? Because I know that the person who first discorverd how to extract diosgenin and convert it to testosterone, Russell Marker, a maverick biochemist in 1940, did so in vitro as apposed to in vivo, is the body equipped with the right enzymes to make the conversion?
 
Strong first post. This kind if thing is over my head. BUT if the first question related to our synth, he won't be answering it. For you second question here is the mechanism of action from Dr.D.........

So how does it work? 25R-diol™ has direct anabolic effects on androgen receptors however is causes no endogenous shutdown of testosterone biosynthesis. This is because 25R-diol™ has minimal intrinsic androgenic activity at those receptors. It is important to remember that androgenecy and anabolism are related. Since the compound has high receptor affinity, it will bind securely to Androgen Receptors. But because of it’s low intrinsic activity it's not very stimulating (like deca for example) thus you get a good anabolic but a weak androgen. This is the key to 25R-diol™. Regardless, although it is a weak androgen, 25R-diol™ is an excellent libido enhancer. This very positive side effect is a result of enzyme activity which causes smooth muscle relaxation from enhanced nitric oxide formation. 25R-diol™ will boosts LH activity slightly and acts as a mild reductase inhibitor to counter androgenic effects. This is based on the anti-androgenic effect of a reductase inhibitor on the hypothalamus which in turn signals the pituitary to start cranking out more LH. This explains why this compound is so clean with none of the typical androgenic side effects.
 
Thanks bigsmith, but i was actually more concerned with the chemical mechanism by which it works, because like i said diosgenin is inert in vivo and it would not convert to DHEA much less testosterone, I know biological processes are extremely specific (active sites, polar/nonpolar solvents etc.) but I can't see how the elimination of a double bond and the addition of an alcohol group (most likely via an anti-markovnikov bromination with HBr and an Sn1 reaction with MeOH?) could make THAT much of a difference?

The product as a whole sounds promising, but from here I can't see what this compound (25R-diol) could do, the DVTHM is another story that looks good.
 
3PeteNC said:
Thanks bigsmith, but i was actually more concerned with the chemical mechanism by which it works, because like i said diosgenin is inert in vivo and it would not convert to DHEA much less testosterone, I know biological processes are extremely specific (active sites, polar/nonpolar solvents etc.) but I can't see how the elimination of a double bond and the addition of an alcohol group (most likely via an anti-markovnikov bromination with HBr and an Sn1 reaction with MeOH?) could make THAT much of a difference?

The product as a whole sounds promising, but from here I can't see what this compound (25R-diol) could do, the DVTHM is another story that looks good.

You can have your question personally reviewed by Dr.D at our forum at anabolicx.com in the DR.D section :D

Hope that will help!
 
3PeteNC said:
Dr. D i was doing some research and discovered that the 25-R compound used in mass fx was basically diosgenin altered at C-5 and C-6 where the double bond was broken and an alcohol group was added at the C-6. Is this correct? Because I know that the person who first discorverd how to extract diosgenin and convert it to testosterone, Russell Marker, a maverick biochemist in 1940, did so in vitro as apposed to in vivo, is the body equipped with the right enzymes to make the conversion?

Have you seen the Russian study of the 6-keto version, the most abundant metabolite of 25R? Twice as strong as Dbol! It's kind of a pro-form of that. It was never claimed to convert to test. None of the spiros metabolize on the lactone rings.
 
I am not sure what more can or will be explained about it's chemistry. We have released its mechanism of action. And the product is EXTREMELY popular due to the end results people are getting. We and every major distributor are out of stock. I have yet to see a single person have anything bad to say about it.

The tough part is not getting ripped off yet still releasing enough info. The supplier that creates the 25R ingredient via Dr.D’s synth charges us an arm and a leg (over $600kg) and we have a VERY large monthly order commitment. If we do not hit the numbers they can sell it to anyone. If we do hit the numbers we are told our secret is safe. So until we are completely sold out by our suppliers we are not going to be handing out too many details that have not been passed out already. This is one product that we spent a good deal of time and money on and I want as much time as possible before we are copied.

All of the good formulas and companies are copied sooner than later. AX, Gaspari :) , etc

I have a hunch that this synth or version we call 25R-diol is going to be very popular in this industry. The amount of queries our factory gets and passes on to us proves this to me every day. But the feedback is huge. We get about 5-6 testimonials a day. Here is one received about 6 hours ago.

I have tried many supplements in the 16 years I have been lifting. I have tried almost everything under the sun and got little to no gains from it. I came across Anabolic Xtreme and started to read up on their products, most notably Superdrol.

I was very impressed with the feedback this company has gotten. To me, reputation means the most in a company. So, I decided to try MassFX, man, I was expecting "some" results but this stuff just took off! My strength has increased as well as my size.

I am sold on Anabolic Xtreme. Their products are second to none, there representatives are very professional and always very helpful. I am an Anabolic Aholic!

Keep up the great work AX, you guys are the best!

 
I'd defer to Dr.D to explain how this stuff works but anecdotally, I'm enjoying a nice run on it (about 2 weeks now at 4 a day).
 
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