Why plausible mechanism is not evidence of effect

Asking directly, because I could not find a straight answer: Why plausible mechanism is not evidence of effect

What changes if the standard account of plausible mechanism is wrong? I ask because I have been treating it as settled and I noticed this week that I could not say why.

Working through the consequences rather than the evidence, since others here are better placed on the evidence.

BPC-157's published evidence is overwhelmingly preclinical and mostly rodent. That is not a dismissal — it is the state of the literature, and any discussion that starts elsewhere is starting from something that is not there.

On the opening post — agreed on the reasoning, with one qualification.

Why plausible mechanism is not evidence of effect: a mechanism that is chemically or biologically plausible can fail in practice for dozens of reasons — bioavailability, off-target effects, metabolism, clearance, or simply that the mechanism does not do what the theory predicts in a living system. Plausibility is necessary for hope but not sufficient for evidence.

Anyone who has looked at this more carefully, please correct the record.

Reframing plausible mechanism slightly, because I think the disagreement is about the question rather than the answer. If the question is "does it happen", yes. If it is "how often", nobody here knows.

The documentation on plausible mechanism is better than this thread and I say that as someone who has posted in the thread.

This follows post #6 rather than contradicting it.

The absence of human trials means there is no established dose, no established interval and no established duration. Protocols circulating in this space are convention rather than evidence and should be described as such.

That is the version I use. It may not be the version that is correct.

Anecdote is the whole of the human evidence base here, and this community's convention is to say so rather than to aggregate anecdotes into something that sounds like data.

I am not the right person to answer the follow-up to this.

Building on post #6 rather than restating it.

A useful discipline for this family: write down what you would accept as evidence that it did not work, before starting. Most of the accounts here have no such criterion in them.

Post #8 put the caveat in the right place and I want to underline it.

My understanding of plausible mechanism is a few years old and may have been superseded. If it has been, I would genuinely like to know rather than keep repeating it.

TB-500 is usually the 7-residue actin-binding fragment of thymosin beta-4, not the full 43-residue protein. The two are routinely conflated in supplier documentation and in the literature. Evidence about the full protein does not automatically apply to the fragment.

I have seen it go both ways, which is why I hedge.

BPC-157: the preclinical literature is extensive, mostly from a small number of research groups, and reports effects across a wide range of injury models. The breadth of reported effects is itself worth noting — a compound that improves outcomes in tendon, muscle, gut, nerve and bone through a single mechanism would be remarkable, and remarkable claims deserve proportionate scrutiny.

The short answer was in the first line; everything after is the working.

On post #11 — agreed on the reasoning, with one qualification.

Plausible mechanism came up in a thread eighteen months ago and was answered well. I cannot find it, which is itself the problem, so here is the reconstruction.

Picking up post #11: that is the part I would want checked first.

Oral versus injected administration claims for BPC-157: the preclinical work studied injection. Oral claims are common in supplier marketing and poorly supported by published evidence. If you are comparing orality between compounds, that is a distinction worth noting.