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.
Post #89 describes the usual case. This is about the unusual one.
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.
Someone should write this up properly, and it should probably not be me.
Adding the measurement that post #89 says would settle it.
Answering the Melanocortin agonists question as asked, then the question I think is meant. As asked: yes, with the qualification below. As meant: it depends on how the first measurement was taken.
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.
Reading a supplier's product description as a marketing document: that is exactly what it is. The hyperbole, the mechanism written as fact, the theoretical benefits stated as established benefits — all of that is marketing. Treat it as such and separate it from evidence where evidence exists.
Picking up post #93: that is the part I would want checked first.
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.
It took me longer than it should have to see that.
Agreed on all of that, and I have nothing to add to it.
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.
Noting that I have skin in this question and have tried to discount for it.
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.
Speaking for myself and not for anyone else who has posted 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.
Post #101 is right about the mechanism and I think understates the practical bit.
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.
That matches what I was told, which is not the same as knowing it.
The failure mode on Melanocortin agonists is boring rather than dramatic. It is almost always the step everyone assumes was done correctly because it is too simple to get wrong.
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.
Post #105 answers the question as asked. The question underneath it is different.
Melanocortin agonists is a question about a distribution, not about a value, and treating it as a value is what produces the confident wrong answers.
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.
Reading a supplier's product description as a marketing document: that is exactly what it is. The hyperbole, the mechanism written as fact, the theoretical benefits stated as established benefits — all of that is marketing. Treat it as such and separate it from evidence where evidence exists.
Genuinely open to being wrong about this one.
Worth stating the null on Melanocortin agonists before we explain it: the observation may be nothing. That possibility deserves a sentence and usually does not get one.
Confirming post #112 from a second method, which matters more than confirming it from a second person.
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 arithmetic on Melanocortin agonists is the easy part and it is where the errors are, which is an uncomfortable combination. Show your working and someone will catch it.
Where the Melanocortin agonists discussion usually stalls is that nobody wants to say "I do not know" and everyone is willing to say "it varies". Those are the same sentence with different clothes on.
Thank you — that answers what I came here to find out.
Compounds this community declines to help with, and why: there are specifics in the guidelines and they are not arbitrary. They exist because of failure modes that have happened in real people, not because of prudishness.
The number is defensible. The precision I gave it is not.
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.
Flagging that the sources on this are thinner than the confidence in the thread suggests.
This follows post #118 rather than contradicting it.
The most useful reply I ever got about Melanocortin agonists was a request to state my units. It sounds like pedantry and it has saved me twice.