Melanotan II is a non-selective melanocortin agonist, which is why its effects are not confined to pigmentation. The non-selectivity is the mechanism and not a side issue.
Revisiting: Melanocortin agonists: mechanism and the documented adverse profile posts 61–90
This is a continuation of a long topic, addressed by post number rather than by page. Start at post 1 · go to the accepted answer.
I had written a reply contradicting post #60 and deleted it. Here is what survived.
Thymosin alpha-1 has a regulatory history in several jurisdictions and a real clinical literature, which puts it in a different evidential category from most of its neighbours here.
Worth one more sentence than it usually gets.
Picking up post #62: that is the part I would want checked first.
Where I have landed on Melanocortin agonists, having got it wrong once in public: the direction is clear, the magnitude is not, and anyone quoting a precise magnitude has borrowed it from somewhere that did not measure it.
Worth separating Melanocortin agonists as a question about the compound from Melanocortin agonists as a question about the documentation. They get answered by different people and only one of them is answerable here.
Appreciated. The plain phrasing does more work here than a longer post would.
Where I part company with post #64, and it is a narrow parting.
Storage guidance for the less common material is usually copied from the incretin guidance and may not apply. Where the supplier has its own stability statement, that is the one to use.
If that reads as pedantic, it is, and it has saved me twice.
PT-141 was developed from the same family with a different receptor profile, and it has a considerably better documented human evidence base than most compounds discussed in this subcategory.
The interesting part of this is the exception, and I do not understand the exception.
Before the thread moves on from Melanocortin agonists — what is the sample size behind the claim? I am not being difficult; I have seen the same figure quoted from an n of four and from an n of four hundred.
Collapsed as off-topic by two members at trust level 3 or above
Dose conversions between related compounds in this subcategory are made far too casually. Structural similarity does not imply potency similarity and frequently does not imply the same receptor profile.
It is the sort of thing that seems obvious in retrospect and was not at the time.
I disagree with the framing of Melanocortin agonists above, and I think it is a substantive disagreement rather than a terminological one. Setting out why, so it can be checked.
The reasoning depends on an assumption that is doing a lot of work and is never stated. If the assumption holds, the conclusion follows. I do not think it holds generally.
Melanocortin agonists looks different depending on whether you are reading the primary literature or the summaries of it, and the difference is not in our favour.
Thymosin alpha-1 has a regulatory history in several jurisdictions and a real clinical literature, which puts it in a different evidential category from most of its neighbours here.
The honest summary for most of this subcategory: a plausible mechanism, animal data, and first-hand accounts. Saying so is more useful than assembling the accounts into something that reads like evidence.
Collapsed as off-topic by two members at trust level 3 or above
Adding thanks rather than a view. I do not have a view worth the space.
Coming back to post #71, because the follow-up matters more than the original answer.
Melanotan II is a non-selective melanocortin agonist, which is why its effects are not confined to pigmentation. The non-selectivity is the mechanism and not a side issue.
For what it is worth, the same held on the two occasions I checked.
Melanocortin agonists: I have looked for the primary source twice and failed twice. Either it does not exist or it is somewhere I do not know to look, and I would like to know which.
Melanocortin agonists: mechanism involves the melanocortin-4 receptor pathway that regulates appetite. The documented adverse profile includes blood pressure elevation and erections of sustained duration, the second of which is specific enough that it is the first thing worth mentioning.
The thing about Melanocortin agonists that took me longest to accept is that a plausible mechanism is not evidence of an effect. It is a reason to look, not a result.
The arithmetic in post #79 is right; the assumption feeding it is the part to check.
PT-141 was developed from the same family with a different receptor profile, and it has a considerably better documented human evidence base than most compounds discussed in this subcategory.
Reading it back, the second half matters more than the first.
Narrowing post #80, because the general version has more than one answer.
AOD-9604 is a fragment of human growth hormone and has been discussed as a potential weight-loss agent based on theoretical mechanism. The fragment hypothesis — that the fragment retains a specific property of the intact hormone — is not settled for this compound.
Where I would look next, rather than where I would stop.
I have been on both sides of the Melanocortin agonists argument in this category within eighteen months, which should tell you how strong the evidence for either side is.
Bookmarking this. I will come back when I have something worth adding.
I read post #82 twice before replying, because I had assumed the opposite.
One caution on Melanocortin agonists: everything above assumes the underlying documentation is what it claims to be. That assumption is doing real work and is rarely stated.
Solubility varies far more across this subcategory than within the incretins. A compound that needs a specific diluent or a specific pH is not being difficult; it has a solubility profile and the supplier should state it.
The number people quote for Melanocortin agonists is a central estimate presented without its interval, and the interval is wide enough that the estimate is nearly uninformative on its own.