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I know that generally, evolution tends to evolve towards having some wiggle room in respect to effect of polymorphisms on binding of endogenous ligands, but with synthetic ligands, especially modern structurally-unrelated molecules, does the same continue to hold true?

I've been particularly wondering about this in respect to biased agonists with selective functionality for some pathways activated by a receptor over others - wouldn't activity of that degree of selectivity be particularly vulnerable to disruptions by SNPs?

Hypothetically, would a ligand preferentially activating therapeutic pathway A but not a highly hazardous pathway B of an ABC receptor be a viable drug at all? Or would it be prime "expect it to kill somebody sooner or later" material?

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    $\begingroup$ Can you please define what you mean by "effector"? It's not standard terminology. At first I thought you meant receptors, but you mention receptors in your last paragraph, so I have no idea what you're talking about. $\endgroup$
    – MattDMo
    Commented Oct 13, 2020 at 16:22
  • $\begingroup$ @MattDMo Sorry, I'm still catching up to speed on biology - I'm thinking about the components of the signaling cascade that are responsible for activating the different separate effects that a receptor's activation induces with e.g. functionally selective ligands. I must have misinterpreted something along the way, as I thought the component was called an effector. $\endgroup$ Commented Oct 14, 2020 at 15:52
  • $\begingroup$ So basically, effector == signaling pathway? $\endgroup$
    – MattDMo
    Commented Oct 14, 2020 at 17:59
  • $\begingroup$ @MattDMo Is that the proper term, then? If so then yes. $\endgroup$ Commented Oct 14, 2020 at 18:11

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