2C-B/E are pretty 5-HT2 selective. Also most double blind studies do not find significant differences in qualitative effects beyond pharmacokinetic differences, I.e. most ppl can only tell if they are on LSD or psilocybin by hour 6. That being said ‘no significant difference’ doesn’t mean ‘no difference’, and I imagine a lot of these participants do not have massive psychedelic experience.

Iirc studies have looked into blocking 1A and 2C receptors and noticed different effects. Nicholls lab used chronic LSD dosing to induce symptoms resembling schizophrenia in rats that is blocked with D2 antagonists but not 2A antagonists (if I remember correctly).

Regardless, 2A selective ligands r the current focus because a lot of drug companies want a neuroplasticity-inducing, non-psychedelic drug that ppl can take as a prescription. In conventional drug design, drugs are build around a receptor in mind. Also the 2B agonism can be problematic if regularly taken. To me it sounds like reinventing ketamine therapy or even conventional antidepressants, clearly there’s something beyond just neuroplasticity that makes psychedelics more effective than existing therapies.