Ah, thanks. I assumed tapinarof was an inhibitor, as the papers on its mechanism describe it as downregulating cytokines. It appears the exact mechanism isn't quite clear. Bissonette et al 2021 [1]:

  Tapinarof was found to bind directly to AhR, resulting in 
  downregulation of inflammatory cytokines, regulation of
  skin barrier protein expression, and antioxidant activity
  ... In a T-cell polarization assay, tapinarof markedly
  inhibited T-cell expansion and Th17-cell differentiation 
  and reduced the production of IL-17, while also reducing
  IL-17A and IL17F levels in a CD4 T-cell assay.

It looks like tapinarof modulates the signaling behaviour of AhR, but so far the precise mechanisms are educated guesses.

The story of tapinarof's discovery is fascinating. It's produced by a bioluminescent (!) bacillus P. luminescens that (quoting from the paper) "lives symbiotically within parasitic, soil-living entomopathogenic nematodes." It was observed in the 1950s that "the nematode did not putrefy once dead, in contrast to the rapid decay seen in the absence of the nematode," leading to the idea that the bacillus' metabolites had antimicrobial activity — which turned out to include what is now synthesized as tapinarof.

Coal tar is another semi-natural substance that is thought to act on AhR.

[1] https://www.jaad.org/action/showPdf?pii=S0190-9622%2820%2932...

This open-access paper is pretty interesting with respect to mechanisms of action and how tapinarof differs from other stilbenes and AhR agonists: https://www.jidonline.org/article/S0022-202X(17)31543-9/full...

And, yeah, good point re coal tar. AhR was once thought to be a toxin or junk receptor that activated liver enzymes for clearance of environmental waste and other chemical byproducts. The constitutive androstane receptor (CAR) and pregnane X receptor (PXR) were, at one time, thought to be very similar. That might still be the case with respect to PXR and CAR, but I'm thinking that the way to bet is that there's more to them than was once thought...

I don’t have any particular point to this post, just tossing out that resveratrol itself seems to be an antagonist of AhR, as it seems to compete with and block agonists.

https://onlinelibrary.wiley.com/doi/10.1155/2019/5847040

Also of note for those curious since I haven’t seen it mentioned yet, Dioxins are potent agonists of AhR.

My own interest in AhR is that it seems to play a role in metabolism. Lower levels of exposure to AhR activators seems to kick off a complicated series of effects that seem to ultimately lower metabolism, potentially being a factor in obesity. Higher levels of exposure to dioxins however results in wasting. AhR is poster child for hideously complicated biochemical relationships, so do be careful of simple summaries of exposure/response relationships.

I would be cautious of AhR agonists though, I recall coming across a number of potential negative associations in regards to cardiovascular health.