None of them are so far as I can tell, really, nor should they be expected to be. Here's my copy/pasted speculative explanation from a previous post as to why:
IIRC the reason NBOMes are so much more potent than their 2C-X counterparts is because the portion of the 2C-X molecule within the NBOMe structure that actually docks with receptors ("functional group," I believe) on neurons juts out into space more than it does in the 2C-X structure, making it more accessible. This alteration in how the molecule interacts with receptors is pretty dramatic it terms of potency increase, and so I'd think it would also dramatically change other properties of the molecule that relate to producing qualitative effects. This qualitative change with 25-Xs could partially owe, for example, to a change in the pattern of "
spreading activation" of neural networks, perhaps by causing individual neurons to fire at a higher or lower frequency than their less potent 2C-X counterparts. Even a slight change at the local neuronal level could snowball into dramatically different network activity patterns, and so there goes any consistency we might expect to find between the actions of 25-Xs and 2C-Xs in the brain.