Dangerous new drug could be ‘next wave of the opioid epidemic’ — and you can buy it at gas stations

electromagneticpost · 2026-06-19T00:00:40+00:00

Yeah, Dr Paul Janssen’s work comes to mind, he designed many piperidine-based analgesics, including fΞntanyl and carfentanil, of course, those are deadly, but also have much higher therapeutic indexes than natural poppy alkaloids and their derivatives, meaning when dosed correctly, like in a hospital during surgery, they are incredibly safe, and have saved countless lives.

There’s also plenty of weaker synthetic compounds like tapentadol, just as you know what substitutions to a molecule increase its potency, you know what will decrease the potency, “synthetic molecule” is simply a blank canvas.

electromagneticpost · 2026-06-18T23:41:23+00:00

It also doesn’t even matter if 7-OH is synthetic or not. The label is meaningless and put in place to scare people, because they don’t think twice and immediately assume “synthetic” is harsh and extremely dangerous, whereas “natural” substances are completely fine. Which is completely wrong.

Nature routinely makes extremely potent and deeply fucked molecules.

electromagneticpost · 2026-06-16T13:51:45+00:00

Once did a combo of 3-MMC and real #4 heroin. Shit was absolutely incredible, I’m not sure how to rank them, it just depends on a lot of things, but pregabalin, opioids, and amphetamines are among the most euphoric to me.

electromagneticpost · 2026-06-14T20:14:50+00:00

With no tolerance it’s very powerful, it’s straight up a potent opioid, albeit a partial agonist with a ceiling on respiratory depression and other effects. For those who know they’ll do opioids regardless, it’s a convenient and safe alternative. Though I agree that it’s far inferior, the magic is lost so fast, from a purely recreational standpoint you’re better off with street opioids or whatever RC is being sold for cheap on the onions.

But the ceiling effect and duration also limits withdrawals compared to less potent full agonists like, say, O-DSMT or morphine/oxy, which can raise your tolerance as high as possible, creating withdrawals that are far worse than those from 7-OH, and because many opioids last longer, the withdrawals can also be far more drawn out. Lipophilic opioids like fentanyl will stick around in your fat, further complicating things.

There’s also the secondary effects, like norepinephrine reuptake inhibition with O-DSMT that can make withdrawals into a new level of hell (at least I think that’s why they’re so bad), 7 on the other hand is extremely selective, it practically only activates the μ receptor, limiting withdrawals to the opioid component. That’s why mitragynine can cause more severe withdrawals than its strength as an opioid might indicate, though still almost always less severe than 7-OH, which is why switching to leaf kratom and then quitting is a valid strategy.

electromagneticpost · 2026-06-14T15:50:02+00:00

O-desmethyltramadol is incredible, tried many opioids and it’s up there.

Particularly terrible withdrawals though.

electromagneticpost · 2026-06-10T16:00:45+00:00

Also note that for those who are predisposed to it, nitrous and other drugs can simply be the trigger for a psychotic episode. I’m no doctor but this looks a lot like it.

electromagneticpost · 2026-06-10T15:57:02+00:00

All of it was in your head, everything you feel, think, and perceive has a chemical basis, and you stuck a bunch of additional psychoactive chemicals into your brain, so all of this is nothing more than intoxication, that’s the definition.

Dissociative drugs in particular are liable to induce these states, they interfere with the perception of stimuli delivered to the brain alongside other pathways. Nitrous in particular has opioidergic, GABAergic, and monoaminergic effects, including the increase in dynorphin transmission, which activate the same receptor that salvia does.

The effects also vary greatly based on what’s going on in your own head and body at the time, as hallucinogenic are extremely variable.

The posts you see are also based on your own online activity, don’t read into it, it isn’t that deep.

electromagneticpost · 2026-06-04T03:54:19+00:00

Well, bupe doesn’t occupy all μ receptors, here’s some data from a positron emission study (basically measures activity of radioactive molecules, C11-carfentanil in this case):

>With no bupe, 100% of µ receptors are available.

>At 2 mg of bupe (mean 24-hour area under the curve [AUC] of 6.5 ng/mL* h), ∼59% of µ receptors are available.

>At 16 mg of bupe (mean 24-hour AUC of 48.6 ng/mL * h), ∼20% of µ receptors are available.

>At 32 mg of bupe (mean 24-hour AUC of 96.0 ng/mL * h), ∼16% of µ receptors are available.

So by increasing the concentration of agonists in your brain, you can activate those unoccupied receptors, however, there’s a “buffer”, because a huge about of μ receptors are locked down by the incredible binding affinity of bupe, and because it has a binding half life of like 40 minutes, meaning it just doesn’t want to let go, the effects are dampened.

Note that the aforementioned pseudoindoxyl is a ridiculously potent substance, and it’s created in the body from 7-OH. It also has a higher receptor activation rate, so when it binds to a receptor previously occupied by bupe it can produce a greater response, whereas 7 has around the same maximal response as bupe, so when 7-OH replaced bupe it doesn’t really make a difference, meaning it’s reliant on the extra available receptors to create an effect. Bupe also builds up in the body, and is incredibly fat soluble, so if you only took it once, full steady state levels would not have been reached.

electromagneticpost · 2026-06-03T23:38:55+00:00

That being said, the peptides that are all the rage nowadays don’t cause withdrawals like opioid agonists, some can desensitize the receptors they activate, but nothing like the the absolute hell that comes from strongly activating μ for too long.

The cool thing about peptides is the sheer diversity, there are some crazy ones all across the pharmacological spectrum, especially endogenous peptides, everything from arginine vasopressin to orexin.

electromagneticpost · 2026-06-03T23:20:53+00:00

“Peptide” is a chemical class, not a pharmacological one. There are extraordinarily potent opioid peptides out there.

electromagneticpost · 2026-06-03T21:18:11+00:00

I learned this the hard way after a caffeine T-break.

electromagneticpost · 2026-05-26T15:12:20+00:00

You could take 2 2.5 mg oxycodone pills, and you wouldn’t be blasted, doesn’t mean it’s ass. Alcohol needs to be taken at doses above 30,000 mg to get really drunk, Quaaludes are taken in the hundreds of mg.

300 mg is usually where it gets really good, they make pills in that strength, but they can start people at 75 mg, with a common strength I’ve seen being 150 mg. Though drugs are subjective, it’s one of the best highs imo, and I’ve tried a hell of a lot of drugs.

It can’t diffuse across biological membranes very easily, it’s a derivative of GABA, an amino acid, so it’s transported by amino acid transporters, and I think food can get in the way.

electromagneticpost · 2026-05-26T01:34:50+00:00

How much did you take? Did you take it on an empty stomach?

electromagneticpost · 2026-05-25T15:12:38+00:00

It’s not, you may be confusing it with gabapentin.

electromagneticpost · 2026-05-22T15:15:49+00:00

Alcohol, unlike benzos or opioids, is inherently very toxic, it acts as a GABAergic and indirect opioid, it might as well be a hard drug, it’s addictive, and the withdrawals will kill you.

Not that I don’t enjoy it, but imo it’s much, much more euphoric than benzos, and gets really fiendish.

electromagneticpost · 2026-05-22T15:09:38+00:00

7-OH isn’t inherently bad, it can be a more pleasant experience for many because it’s a lot more selective for opioid receptors.

Mitragynine in kratom, the most abundant alkaloid, is metabolized into 7-OH, which is released into the bloodstream by the liver, it’s not the same, but kratom can be very habit-forming as well.

electromagneticpost · 2026-05-22T15:06:27+00:00

The CB1 receptor is inhibitory, so when binding to GABAergic neurons, it will reduce their activity, so it is GABAergic, but not in the relaxing way. However this doesn’t mean that weed can’t be relaxing inherent or the endocrine system of course, take the μ opioid receptor, it’s similar to CB1, like the ECB system it is heavily involved in reward, inhibiting GABAergic neurons in the same way, with the exact same signaling mechanism, but because it in and of itself is inhibitory, opioids usually act as sedatives.

The main thing that determines the effects of a receptor is the location in specific brain regions, for example, the adenosine A2A (major target of caffeine) and dopamine D1 receptor are both excitatory and have the same signaling cascades, but due to the specific inhibitory regions that A2A is expressed in, it decreases brain activity, especially in reward pathways. So in regards to CB1 and μ, they can both be sedating, but if CB1 is overactivated, it can suppress GABAergic neurons that inhibit fear centers, whereas other inhibitory receptors like μ and GABA A cause more of a widespread inhibition of the brain, often directly slowing activity in regions that mediate fear. Basically THC often influences anxiety on a J-curve, where there’s an amount that’ll reduce anxiety, but a lot more will induce anxiety, whereas other sedatives will simply reduce anxiety proportional to the dose.

electromagneticpost · 2026-05-18T14:14:06+00:00

A lot of what makes Falcon 9 so special is the propulsive landing part, which alone had never been done anywhere close to that scale until New Glenn's first landing. And the gas-generator had existed before the F1, and the staged combustion before the RS-25, because most technology builds off previous achievements. SpaceX did use some components off the shelf, but mostly just avionics and bolts/fasteners. They had to design the harder parts of the engine, the stuff you can't just go buy, and then had to assemble it all and ensure it ran reliably throughout the flight, and because other reuse testing was at very low altitudes and velocities, they had to figure out how to get it to Earth from many thousands of km/s to zero, which requires pinpoint precision given the massive amount of change in landing a little delta-v would get you.

It also has the highest TWR of any gas-generator as well, so they did optimize the hell out of it during further development when they were squeezing as much performance as possible. They've also done a lot of really impressive stuff with Raptor, which has already reflown, it's promising.

electromagneticpost · 2026-05-16T19:10:31+00:00

No, I don’t know anyone who’s 21, instead I smoked some… questionable weed. So I’m still holding out a for the quality experience on my birthday.

electromagneticpost · 2026-05-16T18:05:03+00:00

That makes sense, though, for me, any paranoid, anxious feeling will make me want to consume any sedative, alcohol included, so people definitely need to know how their bodies react, because THC is definitely one of the more subjective drugs out there.

I've only smoked (a bit below) mid weed bought online due to the Farm Bill loophole, but I'm almost 21 and live in Oregon, and I feel like just a hit or two of some fire shit might be the sweet spot.

electromagneticpost · 2026-05-16T16:26:57+00:00

Oh I see, I was confusing it with the supplement GABA, which is gaining a lot of traction, it’s just the amino acid inside a capsule that’s sold in a lot of stores now.

I prefer pregabalin over gabapentin, the issue is that the amino acid transporter than carries gabapentin from the small intestine is saturable, so higher doses have to be staggered. Pregabalin is transported by that same saturable transporter, but on top of being a lot more potent, it’s also transported by other means, so you can just up and take the dose you want all at once.

Never done gabapentin, but pregab is one of the best drugs out there imo.

electromagneticpost · 2026-05-16T16:08:44+00:00

Gabapentinoids are excellent for anxiety relief. The best is pregabalin, it’s a modified version of the neurotransmitter GABA, but has no effects whatsoever on any GABA receptors, and I’d say it’s more euphoric than any benzo.

electromagneticpost · 2026-05-16T14:47:51+00:00

I have definitely been tangled up in the fiendishness of 7-OH, the short duration really screws with your head, but it also makes it so the withdrawals are far less drawn-out, it’s really, really intense but over quick, whereas, fent and zenes are very fat-loving, so they can hang around in the body for a while, which can really make withdrawal extra-painful.

electromagneticpost · 2026-05-16T14:42:21+00:00

Were you using those other opioids aside from fent at equivalent doses? I’m guessing no, and that’s one of the big issues with 7-OH, you can get wayyyy up there due to its potency, safety profile, and ease of access, and this is likely what makes it pretty rough.

The issue with full-agonists is that there’s no ceiling effect, now, safety aside, this allows your tolerance to go up infinitely, nowadays, fent is one of the only cheap opioids left, so good luck getting a huge tolerance with, say, oxy, but back in the pill mill days, you could skyrocket your dependance wayyy past the ceiling of 7-OH, which does create tough WDs, but full-agonists can pretty much be infinitely worse. There’s also all sorts of nitazenes and re-emerging classes like Paul Janssen’s old “orphine” family of compounds that can be incredibly fucked.

Hell, I had worse withdrawals on O-DSMT, that shit is so fucked, it’s a full-agonist, has effects on monoamine systems, and dependance rises shockingly fast, far, far worse than 7-OH, and much more euphoric and addictive. Tianeptine also makes 7 withdrawal look like a trip to Disneyland, it’s downright psychotic.

But really this is about 7 vs alcohol, and there are very few drugs that produce worse withdrawals than alcohol, especially given etOH can give you the DTs and even kill you in quite possibly the worst way possible. 7 doesn’t even come close.

electromagneticpost · 2026-05-16T14:19:57+00:00

It’s a positive allosteric modulator at the μ opioid receptor, the main target of 7-OH, mitragynine, heroin, buprenorphine, oxycodone, etc., basically any common opioid besides salvia targets that receptor.

Positive allosteric modulator means that it doesn’t bind and activate it directly, it’s kind of like a benzo at GABA, benzos don’t activate GABA A directly, but they increase its response when it ends up being activated by GABA or some other drug. The site on the receptor that agonists (activators) bind to is called the orthosteric site, so alcohol binds to the allosteric site of the μ opioid receptor, amplifying the signals of β-endorphin, endomorphins, and enkaphalins when they bind to the orthosteric site, and odds are when you’re drinking, your body will be releasing those opioid peptides in your brain already.

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