It appears DMT has little affinity for TAAR receptors (see table 2).

Normalization

The raw Ki values are distributed over several orders of magnitude, thus a log transformation is a good first step in the analysis. In addition, higher affinities produce lower Ki values, thus it is valuable to calculate: pKi = −log10(Ki). Higher affinities have higher pKi values, and each unit of pKi value corresponds to one order of magnitude of Ki value. Table S4 presents the raw data transformed into pKi values. Generally, the highest Ki value generated by NIMH-PDSP is 10,000, which produces a pKi value of −4 (although a value of 10,450 was reported for 5-MeO-TMT). For non-PDSP data gathered from the literature, some Ki values greater than 10,000 are reported (i.e. 12,500, 14,142, 22,486, 39,409 and 70,000 for ibogaine).

When the primary assay did not produce >50% inhibition, the Ki value is treated as >10,000. When the primary assay hit, but the secondary assay was not performed, the Ki value is also treated as >10,000. If a secondary assay produced a Ki value significantly greater than 10,000, it is usually also reported as >10,000. The lowest Ki value in the data set of this study is 0.3 (lisuride at 5-HT1A) and the highest value is 70,000 (ibogaine at D3), thus collectively, the data in this study cover nearly six orders of magnitude of Ki values. However, ignoring values reported as >10,000, the Ki values for a single drug in this study never exceed four orders of magnitude in range.

The goal of the normalization used in this study is to factor out potency, in order to allow easy comparison of the multi-receptor affinity profiles of different drugs. The normalization will adjust the highest pKi value for each drug to a value of 4, and set all Ki values reported as >10,000 to a value of zero. Ki values actually measured as greater than 10,000 are not set to zero (i.e. 5-MeO-TMT and ibogaine). We will call this normalized value npKi. Let the maximum pKi value for each drug be called pKiMax. For each individual drug:

If Ki treated as >10,000, then npKi = 0
npKi = 4+pKi−pKiMax
With this normalization:

higher affinities have higher values
affinities too low to be measured will be reported as zero
for each drug, the highest affinity will be set to a value of 4
each unit of npKi value represents one order of magnitude of Ki value
potency is factored out so that drugs of different potencies can be directly compared
This normalization effectively factors out the absolute potency of each drug, and allows us to focus on the relative affinities of each drug at each receptor.

forty-two sites at which most compounds were assayed and at least one “hit” (Ki <10,000 nm)

it is unclear whether TAARs mediate the psychedelic effect of trace amines, including DMT, because TAAR antagonists have not been tested in humans in this regard."

The inhibitory constant (Ki)

I will link to this educational piece again. Like I said before, it's been a looong time since any formal education in this realm.
But from what I can tell, Ki applies only to inhibition (antagonism). If I'm wrong here, someone please tell me how and why. This is a key (bad pun) part of research I'm doing not only into psychedelics, so it would be good to know if I'm making such a mistake.

I know there is a strong desire to take DMT off the chopping block for nausea, but the evidence is not being kind to it. I have no vested interest in it either way. I just want to know what exactly the mechanism is so that I can combat it.

If you cannot see the motion your body's feeling, or conversely, if you cannot feel the motion your eyes see, then it is likely that the brain will get mixed signals and the person will develop some aspect or symptom of motion sickness.

I'm sorry, but this explains nothing about Ki. And isn't the "i" for inhibitor?

So, if I'm understanding correctly: DMT does not do well in competing with antagonists for the 5HT3 receptor. ??

This still says nothing about whether it is a 5HT3 agonist or if it is, it's efficacy in agonising the receptor in the absence of an antagonist.
Essentially, if it is a 5HT3 agonist, a small dose of Ondansetron would probably be very effective in negating it's nauseating effects.

I have a fair amount of experience with DPT. It's definitely a powerful substance that I have a lot of respect for. I find it much easier to leave reality with DPT. What I'm taking note of is it's lacking of the raw anxiety that often accompanies a DMT trip. This is at least true for me.

[...]what we don't know about the 5HT3 receptors. Apparently, there are 5 different types of them, 5-HT3-A,B,C,D,&E. Most testing is done on 5-HT3A. But... ... apparently, they bind together to form many different combinations that have very different profiles. Different individuals have different combinations in differing amounts. Some of these combinations are possibly responsible for things like IBS and anxiety disorders and possibly even schizophrenia.