I’ve been experimenting over the past 6 months or so with d9THC homologs such as THCP and dimethylheptyl THC (800 times the potency as normal d9). I think there’s a lot of potential with these in the medical industry, specifically because of their greatly increased metabolic half-life. A friend of mine uses cannabis every day for medical reasons, but has to consume several times a day, and often has dramatic highs and lows. I’ve been giving him small doses of DMH-THC recently, and he has had nothing but great things to say about it. According to him, the effects are identical except for an elimination half life about an order of magnitude greater, meaning that he can go much longer between doses, and experiences significantly reduced fluctuations in effects.
But that being said, I would definitely not recommend that anyone without extensive knowledge in chemistry and pharmacology attempt THC homologue syntheses, as these compounds can be fatal at high doses, as well as the multitude of unknowns formed in the alkyl-resorcinol condensation.
Just thought I’d put that out there. Some cool stuff yet to explore. Stay safe!
They are similar. What I think he was talking about is a compound called HU-210. The only difference in what I’m doing here and normal cannabis is the length of the carbon chain, which generally doesn’t affect anything except receptor binding affinity.
Very interesting. I suppose the difference is a controlled setting. Even methamphetamine and fentanyl are beneficial in controlled medical environments.
I am not sure this is an appropriate answer.
THC is a partial agonist of the CB1 receptor.
Is THCP a partial agonist or a full agonist (like synthetics).
The enhanced binding charateristics reported by binding studies does not really answer this question.
If it is a full agonist, one tote of pure THCP
should put you on the floor for a while…perhaps quite a while…
We need a report from someone who has done spice or other full agonist synthetics to give us a 'first hand " report…
we need an experienced cannabinoid abuser.
This question needs to be answered : is it more intoxicating than THC?
Benzene3…if you are feeding synthetic analogues to your “patients”, do you really want to advertise that on a public
forum.
I read the paper months ago…and looked closely at the data.
increased binding affinity…does not
denote full agonist activity.
If you have a paper referencing or describing D9 THC as a
full agonist of the CB1 receptor please inform.
To my knowledge, D9 is catagorized as a partial agonist of the CB1 receptor.
I am not quite sure you full understand the concepts expressed here?
Moreover, there would be caveats even in a discussion amongst pharmacologists e.g., (specific GPCR multiple pathways of action are difficult to describe without defacto
definitions of what we are actually talking about and attempting to measure)
…but here we are simply talking about being intoxicated or more easily understood as “how fucked up can you get” concept. three categories subjective:
1.) shit, 2.) THC-Fucked up, and 3.) way beyond anything like THC. max dose concepts.
We need THCP bioassay report from an experienced cannabinoid abuser.
I wrote the head author of the paper a letter concerning this exact subject. I did not get a reply. But the xray studies comparing the side chain interactions with receptor binding site of THCP and synthetic agonist AM11542; and, the in vivo work with mice: (Δ9-THCP at 2.5 mg/kg markedly reduced the spontaneous activity of mice in the open field, while at 5 and 10 mg/kg it induced catalepsy on the ring with the immobility as compared to the vehicle treated mice) certainly suggest full agonist activity…emphasis “induced catalepsy…with immobility”.
Kush, you need to take a sufficient dose of a synthetic full agonist drug that gives you the full effect:
1( Paranoia, anxiety, panic attacks, hallucinations, and giddiness) but not a dose this high:
2( * Increase in heart rate and blood pressure* Convulsions, organ damage, or death).
the partial agonist THC does not effect the latter (2).
If you have ever been on the ground (immobility) hallucinating with a 100mg dose of pure THC …then you have only experienced the “CB1- Partial Agonist effect” inducing intoxication and immobility.
edit: 8 mon later…if you look closely at the mice locomotion data in the original paper…the mice “don’t” move after thcp treatment…this is very similar to DOD experiments with dimethylheptyl analogues on humans…
out of commission for 30 plus hours…or so…
So the evidence suggests “full agonist” …certainly
I mean all you have to do is Google it and you’ll find a ton of papers on the subject…
Hu-210 will put you out with just a single hit according to my friend who’s tried it
Him and his dad tried some and they both got addicted and had to go to synthetic cannabinoids clinics in the EU to get help
They were literally addicted physically to it
Couldn’t eat or sleep unless they smoked it, they were irritable when they didn’t have it
I wish my old IG didn’t get deleted I’d show you exactly what the dude said. I was talking about trying some and he was like nooooo bro don’t fuck your life up…
He said it was like smoking H
One hit, you black out and come back 4 hours later like wtf happened
with respect to the 2010 reference: Concentration-response curves revealed that the maximal effects of Delta(9)-THC and WIN55,212-2 were similar, indicating that Delta(9)-THC is a full agonist at CB1Rs on GABA axon terminals. These results suggest that Delta(9)-THC inhibits GABA release, but does not directly alter GABA(A) receptors or GABA uptake in the hippocampus. Furthermore, full agonist effects of Delta(9)-THC on IPSCs likely result from a much higher expression of CB1Rs on GABA versus glutamate axon terminals in the hippocampus.
“similar”
so you understand why I was restricting my comments:
“Moreover, there would be caveats even in a discussion amongst pharmacologists e.g., (specific GPCR multiple pathways of action are difficult to describe without defacto
definitions of what we are actually talking about and attempting to measure)”
You understand that all this cannabinoid physiology and binding studies are done in detergent…and what we are looking at is "detergent solubilized’ cannabinoid dose response curves.
Especially at the higher concentrations…micromolar…where one would begin to expect problems…
I guess we will have to restrict our definitions of delta 9/ CB1 interactions to specific preparations with caveat.
thanks again for that specific reference …
And…from your descriptions of others indulging in Hu-210!
“way beyond” category
So now I am really interested in the THCP report!
The proper grouping would be “classical cannabinoids” or more specifically benzopyrans (or even more specifically dibenzopyran). That is the structural class that THC and it’s analogs such as HU-210 refer to. But most will want to refer to them as “classical cannabinoids” which groups structural classes benzopyrans like THC and hydrodiphenyls like CBD together, or to keep it simple, actual structural analogs of THC and CBD/related. These compounds like HU-210 have little to do with other synthetic cannabinoids structural classes that are dangerous besides the receptor they hit.
The synthetic “cannabinoids” that people have died from, have major seizures and issues are of a completely different structure than THC/HU-210 but are grouped together only because they all hit the CB1 receptor and that’s it. Things like Naphthoylindoles which is the structural class that related to substances like JWH-018 are simply unrelated drugs that happen to hit the CB1 receptor and so they wrongfully get grouped with actual analogs of THC or CBD itself which is exactly what the government wanted i’m sure. People have who have memories of good times on "1st gen compounds: like JWH-018 were likely smoking a blend with HU-210 or one of the CP-series which is more closely related structurally to classical cannabinoids than other structural series of drugs but cannot be considered one. Most manufactures did not opt for classical cannabinoids because they were direct analogs of THC which added extra legality issues most did not want to take, they were harder to source, much more expensive (like 10x-100x) to make than others and back then people actually sought after crazy intense trippy shit indole based effects and they became popular instead.
Officially HU-210 was never made a federally controlled substance under the CSA (or the FDA 2012 synthetic act) but because it’s an analog of THC in both structure and/or action it’s considered an illegal under the federal analog act but in addition to that most states have made HU-210 specifically illegal in blanket bans, some states even have wording which makes any CB1 agonist illegal. However, if your opinion is that Delta-8-THC is legal because its an isomer of CBD/cannabinoids in hemp, and you think the FAA does not apply to that for some reason then technically HU-210 would be the same legality but as the kingofthekush420 knows we have differing opinions on D8 legality but yeah if you think D8 is federally legal so would HU-210 as long as you don’t sell either for consumption but doing either would be a bad idea in my opinion.
bottom line:
does HU-210 get a two thumbs up for “full agonist”?
i.e., using the ad hoc definition of “way beyond THC”
level of intoxication at max dose?
Back on topic, 1.)has anyone out there taken a hit of THCP?
2.) has anyone ever seen a hit of strawberry-banana (or similar) drop someone? …with a prolonged recovery time??
sporadic THCP production may be an explanation.
off topic,
It does seem quite a mystery how these “other synthetics”
can produce seizures simply by CB1 agonism. There is more to that story.
I have tried it. I am not a heavy smoker but it knocked me on my ass. I took 2 long draws and after a half an hour the psychoactive effects were extremely strong. It would be great for someone who really desires that “stoned” effect. I much prefer and inbibe daily cbdp. There is not much of a psychoactive effect, you can still function but I feel a euphoric rush, my pain is not as noticeable and it appears to help (me at least) with sleep and anxiety.
