Originally Posted by StrategicmoveFollowing 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.
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