HA-966 + 2F-DCk (Fail; and here's why)

[negrogesic]

(+/-)-HA-966 is an NMDA antagonist/weak partial agonist as well as a mysterious GBL like sedative (it is of course molecularly an analog of a rolled up ball of gaba -- its a cyclized gaba analog). The (R)-(+)-enantiomer is the glycine/NMDA receptor antagonist, which moderates its anticonvulsant (and ostensibly antidepressant and analgesic properties). The (S)-(-)-enantiomer is a very weak NMDA-receptor antagonist, but is somehow a potent sedative despite looking alot like GBL but having no GABA-B or GHB affinity. Pretty mysterious in that regard.

It is worth noting that in even giant doses it doesn't fully antagonize NMDA, which has some reachers thinking that a giant dose could replicate near death experience (NDE) with the subject remaining awake.

With that primer on this weird but useful compound (i find it a good fast acting anxiolytic with some antidepressant properties at moderate doses and at high doses an ok sleep aid).

Doses about 70mg start to bring out faint nitrous oxide like closed eye visuals (vague, grey and colorless in nature) which can be annoying. Sleep dose is 50-60mg

But to introduce HA-966 isnt the point for me posting this.

Two hours and 15 minutes ago i consumed 100mg of 2-fdck (i have no dissociative tolerance and don't like them much) along with 61mg HA-966. The HA-966 was added to reduce the anxiety (100mg 2fdck is relatively strong for me, and oral is as strong and almost as fast as intranasal -- though less than rectal).

So i sit on my chair and set a timer. I feel a little comeup and then it abruptly stops 10 minutes into it. I though id be more wonked from the 2fdck since ha-966 is also NMDA-antagonist but it would at the same time make me more relaxed as 2fdck can cause some anxiety in me.

I was wrong. Instead of the normal 2fdck energy/hypomania and racing thoughts after the 15 min comeup, i instead felt strongly sedated, way more than 61mg of HA-966 makes me feel (i have a tolerance to it now, 50mg causes little sedation).

It killed the 2fdck trip entirely. Slight visual changes, zero 2fdck headspace, zero mania and some minor dissociation. Main thing was extreme tiredness, my left eye is closed as i write this only 2+ hours after. Normally id be pretty wonky from 100mg at this point.

Turns out this is why:

The glycine/NMDA receptor antagonist, R-(+)-HA-966, blocks activation of the mesolimbic dopaminergic system induced by phencyclidine and dizocilpine (MK-801) in rodents - PubMed

1. The effects of the glycine/N-methyl-D-aspartate (NMDA) receptor antagonist, R-(+)-HA-966 on the neurochemical and behavioural responses to phencyclidine (PCP) and dizocilpine (MK-801) have been determined in rodents. 2. In rats, pretreatment with PCP (5 and 10 mg kg-1) or MK-801 (0.25 and 0.5...

pubmed.ncbi.nlm.nih.gov

On a side note it might be a good tool for a while 3-meo-pcp freakout. Also FYI i once killed a high dose 2fdck (intentionally, it was taking a negative turn) with 1000mg of theanine (which happens to be an NMDA-agonist).

 

[dopamimetic]

Interesting, thanks for sharing!

Yet do I suspect that with based on you experienced, there will be more going on than just an abolished dopaminergic activation. This explains the lack of mania and accelerated thoughts but not less dissociation or heavy sedation but without more data it is just wild guessing of course..

Maybe there is some sort of interaction at the NMDA receptor, as to my understanding its activation is mediated by Ca influx and the typical disso is a channel blocker; such one can't have agonistic properties, even if it's just very weak partial agonism and thus these two chems will bind to different sites of NMDAr, leading to very different kinetics (amplified blockade and less preservation of natural function).

Indeed Wikipedia confirms:

R-(+)-HA-966 did not induce drug-appropriate responding in animals trained to discriminate phencyclidine (PCP) from saline, suggesting that the glycine receptor ligand R-(+)-HA-966 has a significantly different behavioral profile than drugs affecting the ion channel of the NMDA receptor complex.[6]

This could explain the strong sedation, less glutamatergic activation very roughly equates to an increase in GABA, and the lack of dopaminergic response(?)

Other possibility is about autoreceptors but need to read up how the feedback works about glutamate. Dissociatives usually increase the release of many transmitters incl. glutamate which might be reduced by ha-966.

Or it directly hits some GABA receptors. Does it come with any benzodiazepine like feelings?

Strange that you all require so high amounts of 2F. I have acquired sort of semi-permatolerance to dissos but still felt like 15mg if it (nowhere full dissociation but would have said that 100mg were, and that it's at least 2x as potent than K, probably more 3 times)