USPlabs Conducts Study with Indigo Biosciences: Penn State Researchers - AnabolicMinds.com

USPlabs Conducts Study with Indigo Biosciences: Penn State Researchers

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    USPlabs Conducts Study with Indigo Biosciences: Penn State Researchers


    The following was a study conducted at Indigo Biosciences, by Penn State University researchers, written by BA Sherf, Ph.D and approved by J. Vanden Heuvel, Ph.D to validate one of the major claims [and benefits] surrounding PRIME?s efficacy: A lack of suppressive hormonal action. While "hormonal suppression" is almost exclusively represented as sex-steroidal, suppressive can refer to other endocrine functions such as GR [glucocorticoid receptor] antagonism. GR expression is ubiquitous: Appearing in almost every cell-type in the human body, the agonism and antagonism [and resultant effects on gene regulation] of the GR has a wide array of physiological consequences; ranging from sex-function to the immune system. As a result, this particular endeavor was undertaken to determine whether or not GR antagonism was occurring, and to what degree, to ensure that no hormonal action was occurring.

    Fortunately for the consumer, this Penn State Study is the first step in a thorough legitimization process that USPlabs is embarking on with PRIME; it (the Penn State study) will be accompanied by an objective trial of sorts (The Staley Report), where trainees were selected away from mainstream boards (and the associated biases ? positive or negative) and thoroughly recorded their progress under Charles Staley; it will also be accompanied by the release of the Beta Tester's blood abstracts which, along with this particular study, will display no cyto-toxicity and no suppression of endogenous hormones.

    Simply, we are objectively validating what we know to be subjectively successful, through unaffiliated, and independent means. While detractors will no doubt detract - merely on a new tangent - upon seeing this study, we feel it important to communicate the uniqueness of the actions we are currently undertaking. The expense and bureaucracy involved in securing studies such as this one from respectable and recognized Universities is enormous; and this is exactly why we [as an industry and consumer] seldom see them surface. While University studies such as this one are often utilized as objective research, they are very seldom conducted for the company itself; however, in the case of PRIME, realizing a lack of objective data to validate consumer feedback, we thought it was only necessary. Fortunately for the consumer, that process has only begun, and not ended, here: The results in respects to GR Antagonism came back negative, as we had hoped;however, as a company we are diligent in our desire to positively illuminate the exact MoA [method of action] of USPlabs PRIME.

    However, in that light, we must remember that many products we commonly use today do not have validated MOAs; much in the fashion we have done here, simply their safety and efficacy need be validated for them to be produced en masse. For example, Minoxidil (Rogaine), one of the most effective and the widest-selling hair treatment products available, does not have a proven MOA. Much like PRIME, there are several postulates (one being the mediation of the NO pathway, despite the fact no cGMP-specific action has been proven) but none proven. Does this in any way invalidate the massive body of anecdotal feedback surrounding Minoxidil? Of course not: Despite the lack of MOA for Minoxidil, it is still regarded as the ?first-line-of-defense? for uncomplicated hair loss.

    Even Acetaminophen - a compound so engrained in popular culture and medicine, your spell-checker recognizes it - has no verified specific MoA. While it has been elucidated that Acetaminophen lowers levels of Prostaglandin E2, the exact mechanism [Mechanism of Action] through which this is accomplished has not been elucidated. As PGE is a product of the commonly inhibited COX [cyclo-oxygenase, in forms I and II] pathway, Acetaminophen?s exact effect on COX [if any is occurring] is unknown and debatable. This point, then, cannot be stressed enough in regards to the actions USPlabs is currently undertaking: We are seeking to provide for PRIME what has not been provided for the widest-selling analgesic available. Why USPlabs is being subjected to a standard not subjected to a compound each person reading this has ingested remains a mystery ? this being said, we do intend to live up to even the most veracious of detractors in regards to our attempts to validate and legitimize PRIME.

    In conclusion, we realize two things: a) that PRIME is a contemptuous topic as of late and; b) that this product, as efficacious as it may be, needs some external validation to dissuade some of the negativity surrounding it. We are going through these great lengths ? funding University Studies, in-depth trials and blood tests and expending massive amounts of capital and energy to do so? to address both of these things at the same time. Simply put, a ?scam company? would not do anything of this scope or magnitude for an ineffective product; we know PRIME works, we simply want to know how, and want YOU to know how.
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    Strag's thoughts.

    Quote Originally Posted by Strategicmove
    Following up on Mulletsoldier's post, I would like to add further perspective to the motivation behind the Penn Study. Initial beta-tester feedback on an earlier (beta) version of PRIME was overwhelmingly positive and consistent in the elucidation of the results (cumulative dramatic improvement in strength and endurance, favourable body recomposition, increased libido, truncated post-exercise recovery, and so on) from PRIME beta. A combination of these consistent beta reviews coupled with subsequent favourable reviews of PRIME further fuelled our excitement and led us to investigate various possible mechanisms of action (MoAs) that PRIME may act through. After blood tests showed neither an up-regulation nor a suppression of endogenous hormone production, we decided to investigate whether or not PRIME may act via a glucocorticoid-receptor mechanism. Our a priori expectation was that it does not, implying the absence of a hormonal action by PRIME. The Penn State study showed that PRIME does not act via glucocorticoid antagonism, in line with our a priori postulate. So, what are the implications of the outcome of the Penn State Study? In order to answer this question fairly and completely, we may want to take a step back and consider the background. First of all, sponsoring a study of this type, not only reflects a deep confidence and commitment on the part of a supplement company to a particular product or compound that it considers novel, but also requires significant commitment of resources to the project. Many readers may agree that no company would make this move, if it lacked confidence in its innovation. Second, it was necessary to commit resources to understanding PRIME's mechanism of action (MoA), to not only validate the favourable reviews that countless users have reported, but also to respond to the legitimate inquiry of others with respect to the specific or approximate mechanisms through which PRIME exerts its effects. Our conviction that the positive results reported by many users were not delusional, coupled with the fact that we also have an interest in understanding the full potential of our novel compound, via understanding its biosynthesis, provided further motivation to expose PRIME to rigorous scientific scrutiny. As it turned out, professional laboratory analysis confirmed that PRIME's pathway is non-hormonal, matching our expectations.

    So, what now? By showing that PRIME acts other than via a glucocorticoid-receptor antagonism, the Penn State Study does not suggest in any manner that PRIME is ineffective; rather, it implies that the mechanism of action lies elsewhere.

    As is well-known the absence of a well-described and known mechanism of action relating to any particular agent, is neither a necessary nor a sufficient condition for its efficacy. On the contrary. Drug-discovery or drug-development programmes are known to be littered with cases of powerful compounds with unknown mechanisms of action. In a related fashion, it is not uncommon in those programmes to identify a mismatch between an agent?s postulated in vivo MoA and its in vitro MoA. A couple of examples may suffice. Take the antibacterial compound, hexachlorophene, whose in vivo MoA turned out to diverge from its expected MoA from in vitro biochemical data. Furthermore, in HIV-research, there are various compounds that are known to have bioactivity against HIV, but with unknown MoAs. These compounds are the subject of promising drug-development programmes. For perspective, typically, inhibition of the HIV virus occurs via the well-known MoA, reverse transcriptase (the HIV virus relies on the so-called transfer RNA for its replication. Inhibiting the virus? affinity for tRNA is a preferred anti-viral pathway). As it turns out, certain novel agents have shown promise in the inhibition of the HIV virus while plotting an unknown MoA. Furthermore, (natural) lignans are known to include compounds with antiviral and antineoplastic properties. These include podophyllotoxin, and etoposide and teniposide, two of podophyllotoxin?s semi-synthetic derivatives. Podophyllotoxin?s antiviral MoA is known to be via its inhibition of microtubule assembly in the mitotic apparatus, leading to a blockage of cell division. However, although etoposide and teniposide are included in many cancer chemotherapy protocols, they are known to have a completely different MoA (inhibition of DNA topoisomerase II); while other podophyllotoxin analogues (weak topoisomerase II inhibitors), also used in chemotherapy protocols, do not have a known MoA! Another example: Tyloindices, isolated from a plant from India, were known to be one of the most potent anti-tumor compounds ever screened at the National Institute of Cancer. Yet, their MoA was unknown! To continue, Chagas? disease is a well-known social and health challenge in Latin America. Caused by epimastigotes cultures of Trypanosoma cruzi, it afflicts millions in Latin America. A novel compound, 5-nitro-2-thienyl-malononitrile, was accidentally derived in the process of an unsuccessful attempt to obtain new 3,5-diamino-4-(5'-nitroarylidene)-4H-thiadiazine 1,1-dioxide derivatives. Although, the MoA of 5-nitro-2-thienyl-malononitrile was unknown, it still demonstrated significant anti-Trypanosoma cruzi activity. And so on. Examples abound of compounds without a known MoA, yet demonstrate significantly favourable pharmacological activity. So, is PRIME necessarily ineffective because its MoA has not been uniquely determined? Are users delusional when they report tangible results from PRIME supplementation, just because PRIME's MoA is still undetermined? My response would be a resounding "NO"! Most would admit that agents possessing a potent bioactivity, but with an unknown mechanism of action, are in fact highly sought-after in drug-development circles, as they may embed considerable potential in the activation of key pharmacological pathways.

    We would like you to consider the commissioning of this Penn State Study as a demonstration of our confidence in our product. Beyond this, we would also like you to consider this Penn State Study as a validation of our original postulate about PRIME's non-hormonal action, further advancing our confidence in, and passion for, PRIME.

    Thank you very much for supporting USPLabs!
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    Thanks! Looking over it now.

    Coles notes: MoA still unknown, further confirmation non-hormonal.
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    Quote Originally Posted by Mulletsoldier View Post
    Strag's thoughts.
    Thanks, Mullet!
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    So in short...........study found no evidence to support the glucocorticoid receptor theory? THAT SUCKS!

    What's next for you guys? Is there even anything more you can do?

    PS- I thought this was a Penn State study? I saw no mention of Penn State in the PDF but rather a private business? Not that it matters...
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    Quote Originally Posted by Rugger View Post
    So in short...........study found no evidence to support the glucocorticoid receptor theory? THAT SUCKS!...
    I see it differently. The study confirmed the absence of glucocorticoid-receptor antagonism, in line with our a priori expectations.

    Quote Originally Posted by Rugger View Post

    What's next for you guys? Is there even anything more you can do?
    We will test for other mechanisms of action.

    Quote Originally Posted by Rugger View Post
    PS- I thought this was a Penn State study? I saw no mention of Penn State in the PDF but rather a private business? Not that it matters...
    Indigo Biosciences was founded by Penn State professors and is located on the Penn State premises.


    Indigo Biosciences was cofounded in 2004 by Blake R. Peterson, Ph.D., and Jack Vanden Heuvel, Ph.D. Dr. Peterson is an Associate Professor in the Department of Chemistry at Penn State University. Dr. Vanden Heuvel is a Professor in the Department of Veterinary & Biomedical Sciences at Penn State University. Indigo leverages their combined knowledge to provide cutting-edge scientific services and products.
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    Quote Originally Posted by strategicmove View Post
    I see it differently. The study confirmed the absence of glucocorticoid-receptor antagonism, in line with our a priori expectations.



    We will test for other mechanisms of action.



    Indigo Biosciences was founded by Penn State professors and is located on the Penn State premises.
    Could not have said anything better than Ike here.
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    Can't say I'm not disappointed. Although, I was under the impression that the trials were going to find an MOA, not merely test a theory, if that makes sense

    Either way, still can't wait to try it but I gotta turn some more tricks first.
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    Quote Originally Posted by Rugger View Post
    Can't say I'm not disappointed. Although, I was under the impression that the trials were going to find an MOA, not merely test a theory, if that makes sense

    Either way, still can't wait to try it but I gotta turn some more tricks first.
    You can't find the MOA without testing theories
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    Quote Originally Posted by Steveoph View Post
    You can't find the MOA without testing theories
    Of course, but I was thinking that the lab had been employed to find an MOA not test a single theory, and be done with it.
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    Quote Originally Posted by Rugger View Post
    Of course, but I was thinking that the lab had been employed to find an MOA not test a single theory, and be done with it.
    Oh this is by no means it! This was simply to ensure that no hormonal action, of whatever kind, was occurring.

    Now it is on to identifying a particular MoA with these Penn State researchers.
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    Quote Originally Posted by Mulletsoldier View Post
    Oh this is by no means it! This was simply to ensure that no hormonal action, of whatever kind, was occurring.

    Now it is on to identifying a particular MoA with these Penn State researchers.
    Well then that explains it. I hope you guys end up finding something
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    thanks for posting the study's findings Mullet

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    Great post, and very intreresting...
    Gause institute member

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    Nice read, I'm like 10 minutes away from the university. Most interesting indeed.
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    Any ETA on when you will release the beta-testers blood abstracts?
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    Frak, I had this typed out and then they decided to do upgrades when I submitted.

    Not trying to "stir up sh!t" or anything, just wondering about the methods which they tested.

    Why do they test antagonist properties in a mixture with an agonist? Why not test it by itself? Since people taking Prime would most likely not be taking a glucocorticoid receptor agonist. Is dexamethasone a strong agonist, possibly being strong enough to overpower the antagonist properties of the 2 supplied compounds?

    Since the conclusions state that they found "statistically significant" GR activity reduction even in the presence of dex but not enough to say that it was the MoA. But I wonder what it would have been if they did not include dex in the mixture.
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    Quote Originally Posted by eatingisfun View Post
    Frak, I had this typed out and then they decided to do upgrades when I submitted.

    Not trying to "stir up sh!t" or anything, just wondering about the methods which they tested...
    You do not stir up anything by seeking objective clarification.

    Quote Originally Posted by eatingisfun View Post
    Why do they test antagonist properties in a mixture with an agonist? Why not test it by itself? Since people taking Prime would most likely not be taking a glucocorticoid receptor agonist....
    Let me try to explain this in as simple terms as possible. What the researchers did was standard practice. If you want to test whether a compound has any glucocorticoid-receptor activity, you need a base. If it were a trial with human (or murine/rodent) subjects, pre- and post-administration glucocorticoid-receptor activity would be measured and tested for statistical significance of the administered compounds. In the absence of murine or human subjects, as in the study here, a classical glucocorticoid-receptor agonist, namely, dexamethasone, is used.

    Quote Originally Posted by eatingisfun View Post
    Is dexamethasone a strong agonist, possibly being strong enough to overpower the antagonist properties of the 2 supplied compounds?
    Yes, and yes. It is one of the most standard agents used in such analyses.

    Quote Originally Posted by eatingisfun View Post
    Since the conclusions state that they found "statistically significant" GR activity reduction even in the presence of dex but not enough to say that it was the MoA. But I wonder what it would have been if they did not include dex in the mixture.
    Without dexamethasone in the mixture, there would have been nothing to test against!
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    Thanks. I understand what you are saying.

    I guess my thinking is that if you test the supplied compounds without the agonist, given their baseline numbers of 0.569 for compound 1 where there isn't any external compounds added, *if* Prime was a GR antagonist, the numbers they would get would be negative compared to the baseline of no external compounds(the Media Control). For example, if testing an appetite suppressant(assuming you could somehow measure the results in a cell culture), would you add a mixture of a known appetite stimulant to see how much the compound being tested reduced appetite or would you use the baseline of no external compounds as the comparator.

    Obviously they must use this method for a reason but it is different than what I would have thought. Can't wait to read more from the other test results.
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    Quote Originally Posted by strategicmove View Post
    I see it differently. The study confirmed the absence of glucocorticoid-receptor antagonism, in line with our a priori expectations.
    Then why was it postulated in the writeup?

    Also, what direction are you guys thinking now, as far as potential moa? Calpain inhibition? cAMP elevation?

    Just throwing this out there, but perhaps prime could affect ACh, its receptors, or act an acetylcholinesterase antagonist? I didn't notice much in terms of recomp from Prime, but I noticed the neural benefits in regards to lifting heavier weights.
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    Quote Originally Posted by papagunz View Post
    Also, what direction are you guys thinking now, as far as potential moa? Calpain inhibition? cAMP elevation?

    Just throwing this out there, but perhaps prime could affect ACh, its receptors, or act an acetylcholinesterase antagonist? I didn't notice much in terms of recomp from Prime, but I noticed the neural benefits in regards to lifting heavier weights.
    cAMP and acetylcholine elevation are both possibilities, particularly the latter due to, as you said, the strength increases mostly seen with PRIME. cAMP is the first MoA on the docket.
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    Quote Originally Posted by Mulletsoldier View Post
    cAMP and acetylcholine elevation are both possibilities, particularly the latter due to, as you said, the strength increases mostly seen with PRIME. cAMP is the first MoA on the docket.
    it would have to be a huge increase in cAMP i'd think. I'll put a dollar on acetylcholine
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    You should definitely remove the Penn State from the portion of the study. Penn State did not run the testing of the product, I do not think that this i fair to them at all.

    Just because the Lab is close to the school and some guy founded it went to Penn State, doesn't mean anything. Just doesn't make sense to me.
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    Hooray!
    Last edited by Rugger; 01-19-2009 at 12:41 PM.
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    yeah not for nothing, but this place is just a CRO founded by two guys that teach/research at Penn.

    This is very misleading........
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    Quote Originally Posted by Rugger View Post
    x2. If the lab itself doesn't associate itself with Penn State then neither should you. Their lab is also not on the Penn State campus.
    I must admit when I opened that PDF the first time labeled Penn State and didn't see any reference to the university, I was a bit
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    You should have used an arial font too.


    How could you.
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    Yes, these are things we addressed on this thread at BB.com. Just a simple mistake.

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    Quote Originally Posted by JOakman View Post
    You should definitely remove the Penn State from the portion of the study. Penn State did not run the testing of the product, I do not think that this i fair to them at all.

    Just because the Lab is close to the school and some guy founded it went to Penn State, doesn't mean anything. Just doesn't make sense to me.
    Quote Originally Posted by Rugger View Post
    x2. If the lab itself doesn't associate itself with Penn State then neither should you. Their lab is also not on the Penn State campus.
    This is very misleading........
    As I say, it was a mistake rectified several days ago 'over there'. This thread did not receive nearly the attention and therefore was not rectified as promptly!

    B, could you please change the title of this thread to: USPlabs Conducts Study with Indigo Biosciences: Penn State Researchers

    Quote Originally Posted by Cosmo Kramer View Post
    You should have used an arial font too.


    How could you.
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    Quote Originally Posted by Rugger View Post
    x2. If the lab itself doesn't associate itself with Penn State then neither should you. Their lab is also not on the Penn State campus.

    The title is being changed...

    This still does not change the fact that these researchers Teach at Penn State, Graducated from Penn Sate, the lab is surrounding the Penn State campus with other Penn State associated labs and charge Penn State money....

    So we can look beyond this miscommunication and speak about the research or we can attack the title..

    If it was purposely done to decieve, we would blanked out the name of the research group which is plastered all over the study on the PDF and replaced with Penn Sate..

    either way it will change...
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    Thank you B! You are damn fast, lol! I had to wait about 8 hours 'over there'!
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    ..for a 2 second edit.
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    Yes, exactly, haha. I was a bit surprised, lol.
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    Quote Originally Posted by Mulletsoldier View Post
    cAMP and acetylcholine elevation are both possibilities, particularly the latter due to, as you said, the strength increases mostly seen with PRIME. cAMP is the first MoA on the docket.
    Quote Originally Posted by EasyEJL View Post
    it would have to be a huge increase in cAMP i'd think. I'll put a dollar on acetylcholine
    come on, nobody willing to take my bet?
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    Quote Originally Posted by EasyEJL View Post
    come on, nobody willing to take my bet?
    Would you even have a bet to offer if I didn't offer the suggestion first?

    Just messin'.
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    Why just one?


    Quote Originally Posted by EasyEJL View Post
    come on, nobody willing to take my bet?
    Why does is only have to be ONE single MOA. Couldn't it have 2 or more MOA like acetylcholine, cAMP, Nitric Oxide enhancement working all together to produce results seen?
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    Why just one?


    Quote Originally Posted by EasyEJL View Post
    come on, nobody willing to take my bet?
    Why does is only have to be ONE single MOA. Couldn't it have 2 or more MOA like acetylcholine, cAMP, Nitric Oxide enhancement working all together to produce results seen?
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    Quote Originally Posted by saludable24 View Post
    Why does is only have to be ONE single MOA. Couldn't it have 2 or more MOA like acetylcholine, cAMP, Nitric Oxide enhancement working all together to produce results seen?
    Good point! Some agents certainly have more than one MoA.
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    u guys are talking over my head but this is how one learns. Im glad to see a company out there doing a study on their products. doesnt happen alot
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    Quote Originally Posted by freezito View Post
    u guys are talking over my head but this is how one learns. Im glad to see a company out there doing a study on their products. doesnt happen alot
    Thanks. We would be pleased to answer any questions you may have.
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