EQ still available at decent prices (for domestic vendors), I just stocked up on some from OEP Labs here. I'm sure Axle will have it too when he reopens... I have my wish list ready!
So I have run primo a few times now, and haven't been too impressed with it re: muscle accrual or estrogen control, and I've used vials from several good sources, all bought more than a year ago before the raw shortage. I have not had any tested myself, but have no reason to think they were not primo - all had good Jano testing from seller (including 808 Labs = Axle), oil was thick despite MCT, and most caused some PIP if not warmed and/or diluted. And I didn't really 'feel anything' from them, unlike say tren which I most definitely feel.
I think primobolan may be more heavily degraded in skeletal muscle by 3⍺-HSD than other DHT 'derivatives' - most of which are specifically modified at C2 (methylation or other) to prevent this; the metabolites of predominant 3⍺ metabolites of primobolan would seem to support this, although there are multiple isoforms of that enzyme expressed in different tissues. In comparison, masteron (and other C2 modified AAS ie oxandrolone, oxymetholone, winstrol, stenbolone, etc) do not have significant 3⍺ metabolites.
As far as estrogen control, the best and most consistent androgen for that is exemestane. I don't think most people use it correctly, but that is another topic. All DHT 'derivates' seems to modify estrogen response to some degree, but I don't think any of them (or their metabolites) can actually act as a true non-competitive AI, based on their A-ring structure; while not a DHT 'derivative' boldenone is one possible exception. Others at best could act as a weak competitive AI. But DHT and all 'derivatives' can do and do modify translational activity of the ER in a tissue specific manner, hence why several were developed for and some still used for metastatic breast cancer. DHB and its c1-methylated doppelgänger primobolan could also inhibit 17β-HSD1, which will shift balance of estradiol towards the much less active estrone, which effectively becomes a competitive inhibitor of estradiol at the ER.
Just finished my open primo vial and decided to trying a seemingly unconventional mix of 210mg EQ + 105mg DHB instead (10mg + 15mg per day ea)... the cyp of DHB and enanthate of primo have fairly similar half lives so should be a smooth transition, less mg of DHB but it is considerably more potent, 2-3x maybe more. Obviously the EQ will take a long time to build up, which is fine; if it were a shorter ester I might have front loaded it but that seems pointless with undecylenate, and complicates resolution of problems should any develop. Unlikely though at the dose I'm using.
I've avoided EQ until now because of purported Hct issues, but my current supplement regimen of silymarin, taxifolin, and naringin seems to have that very well controlled - last HgB was 15.8 after nearly two years w/o donation, even with primo in the mix most of that time. My base of low dose test, MENT, and tren plus mast seem to not affect it very much. And single most important thing in managing hematocrit is hydration... it can increase > 5 points if volume depleted. Substantially increasing my sodium intake has helped a lot with that, ironically, perhaps because I take a sodium wasting drug (empoglaflozin).