Felt very similar to me personally. I've used cocaine on at least 300 days of my life, amphetamine on an estimated 800 and dabbled with countless other stimulants via all ROAs (preferably IV). This new compound felt like cocaine. The girlfriend who also loves speed but hates cocaine agreed. It apparently blocks sodium channels as well, which is another very striking similarity if you ask me. I would not be surprised if it shared other pharmacomechanisms with cocaine. It felt just as shitty as cocaine. No other stimulant ever makes me feel comparably shitty. Not even MDPV which I have also abused excessively. God I hate cocaine.
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N&PD Moderators: Skorpio | someguyontheinternet
Novel cathinone ethyl-hexedrone
- Thread starter dopamimetic
- Start date
adder
Bluelighter
- Joined
- Mar 28, 2006
- Messages
- 2,851
I don't really know cocaine in and out like I have no idea what cravings or very bad comedown for cocaine feels, moreover, my experience with cathinones is very limited and stimulants are definitely not my thing although I've had my share of amphetamine use, but out of all stimulants I always tolerated those with serotonergic action much better, so I can't speak from experience.
Has it been confirmed or is it just speculation at this point?
Has it been confirmed or is it just speculation at this point?
NoArtFlav
Bluelighter
So this is NOT for cke lol
Well, it acts as a local anaesthetic. That is as sure as eggs is eggs, but just as much speculation as calling it a stimulant is.
How it prevents those nerves from firing however is pure speculation on my part, yes. I might have went ahead of myself there.
So let me rephrase my original statement from
"It apparently blocks sodium channels as well, which is another very striking similarity if you ask me."
to
"It is a local anaesthetic as well, which is another very striking similarity if you ask me."
Limpet_Chicken
Bluelighter
In fairness, it wasn't an altogether implausible or unlikely mechanism to assume of a local anaesthetic, that is would be a sodium channel blocker. Most are. Come to think of it, what if any are not? The other mechanism I can think of are is affecting TRPV receptors of the kind sensitive to capsicin, or to menthol. I know at least some NMDA antagonist drugs produce a similar numbing, but is it entirely centrally mediated via NMDARs, or do the likes of ket, MXE, PCP and its relatives also block Na+ channels?
Adder-with regards to naltrexone and opioid receptors, endorphins etc:
The mechanism of action of ULD naltrexone is mediated by blocking a high-affinity subpopulation of Mu-ORs, that are excitatory in nature. Weather Mu1ORs behave as typical, rewarding, pleasant opioid type drugs is dependent upon the state of MOR
G protein coupling. Typical bog standard MOR1 (technical term there
I mean the Mu opioid receptor types we all know...and usually love
, that are when stimulated by agonist ligands, inhibitory in their signal transduction, rewarding, relaxing, sedating you get the idea..) are coupled to Gi/o and form the majority of, but the lower binding affinity population of MOR1 and their Mu1/DOR heterodimers. Agonists (most of them, the common opioidergic drugs of medicine and of recreational use and ab-use) result in a delta-OR mediated recruitment of beta-arrestin2 and desensitization of the receptors (upregulation of DOR sensitivity within the heterodimers? not sure on that but it seems as though it would make sense to me), and with continued use of the agonist another change occurs, a switch in G protein coupling from inhibitory Gi/o binding to a higher affinity state in which MORs are coupled to excitatory, Gs and also excitatory effects mediated via Gβγ.
The excitatory population being higher affinity makes it possible to selectively block these altered receptor types using naltrexone in doses insufficient to induce blockade of inhibitory Gi and Go coupled MORs, and it also appears to directly increase
the density of these inhibitory populations. Naltrexone (and naloxone) was relatively recently also found to bind to filamin-a, which results in prevention of the switch in effector coupling from Gi/o to Gs, as supported by this paper:
http://paintrials.com/publications/pone208.pdf
Weather or not it also does so via this particular route to Gβγ I'm not sure. Still reading the paper.
I'd bet that a ligand acting as a dual MOR1 agonist/delta antagonist, inverse agonist or possibly partial agonist, not sure which subtype of delta-ORs is responsible for the beta-arrestin2 recruitment when in the guise of
MOR/delta heterodimeric receptors, and coadministration of ULD-naltrexone would make a mighty fine way to reverse and prevent the further development of tolerance to the MOR agonist.
Adder-with regards to naltrexone and opioid receptors, endorphins etc:
The mechanism of action of ULD naltrexone is mediated by blocking a high-affinity subpopulation of Mu-ORs, that are excitatory in nature. Weather Mu1ORs behave as typical, rewarding, pleasant opioid type drugs is dependent upon the state of MOR
G protein coupling. Typical bog standard MOR1 (technical term there
I mean the Mu opioid receptor types we all know...and usually love, that are when stimulated by agonist ligands, inhibitory in their signal transduction, rewarding, relaxing, sedating you get the idea..) are coupled to Gi/o and form the majority of, but the lower binding affinity population of MOR1 and their Mu1/DOR heterodimers. Agonists (most of them, the common opioidergic drugs of medicine and of recreational use and ab-use) result in a delta-OR mediated recruitment of beta-arrestin2 and desensitization of the receptors (upregulation of DOR sensitivity within the heterodimers? not sure on that but it seems as though it would make sense to me), and with continued use of the agonist another change occurs, a switch in G protein coupling from inhibitory Gi/o binding to a higher affinity state in which MORs are coupled to excitatory, Gs and also excitatory effects mediated via Gβγ.The excitatory population being higher affinity makes it possible to selectively block these altered receptor types using naltrexone in doses insufficient to induce blockade of inhibitory Gi and Go coupled MORs, and it also appears to directly increase
the density of these inhibitory populations. Naltrexone (and naloxone) was relatively recently also found to bind to filamin-a, which results in prevention of the switch in effector coupling from Gi/o to Gs, as supported by this paper:
http://paintrials.com/publications/pone208.pdf
Weather or not it also does so via this particular route to Gβγ I'm not sure. Still reading the paper.
I'd bet that a ligand acting as a dual MOR1 agonist/delta antagonist, inverse agonist or possibly partial agonist, not sure which subtype of delta-ORs is responsible for the beta-arrestin2 recruitment when in the guise of
MOR/delta heterodimeric receptors, and coadministration of ULD-naltrexone would make a mighty fine way to reverse and prevent the further development of tolerance to the MOR agonist.
http://www.ncbi.nlm.nih.gov/pubmed/11748399
"Ketamine interacts with sodium channels in a local anesthetic-like fashion, including sharing a binding site with commonly used clinical local anesthetics."
In my experience the superficial numbing sensations caused by menthol and capsaicin analogues feels distinctly different from cocaine, lidocaine and the like. What if this does act through yet another different mechanism? That may make it a drug worth researching, eventhough it probably carries the same vasodilatory and vasoconstrictive side effects that known local anaesthetics carry.
Another problem is that the latter don't work very well when there is an acute infection in the area. However my money is on this one sharing affinity for the same binding pockets as cocaine or at least some other type of avidity for the respective receptor proteins. The drugs just feel strikingly similar and the local anaesthetic effects can hardly be denied. That is a pretty rare sight when it comes to psychostimulants.
Nagelfar
Bluelight Crew
Menthol activates surface/topical TRPM8 "sensory" receptors that mimic low temperature, i.e.feeling cold, a chill, freeze etc. Whereas sodium channel blockers inhibit the movement of salt in conjunction to the nerve firing of action potentials and effectively cut out sensation altogether; the other way 'round is why 'rubbing salt into a wound' greatly increases its pain/discomfort when it gets into the body.
Capsaicin relates to a topical heat sensation and is used even as a weapon (pepper-spray) not what I'd call a correlative to subjective numbing feeling; more like the adding of salt to an open sore is.
Limpet_Chicken
Bluelighter
Capsaicin at least works by, as I understand it, overstimulating TRPV1 receptors (transient receptor potential vanilloid-1), these are the targets responsible for the burning of chili peppers (yum! I LOVE chili pepper in/on food. I like to fry my steaks in tabasco with some worcestershire sauce, or to use tabasco to help my fly agaric/peppery boletus/black/pink/szechuan pepper and cubeb steak spice powder stick to the meat properly.
Capsaicin stimulates until the receptors desensitize, resulting in a long-term analgesic and iirc, locally operative antihyperalgesic/antiallodynic effect. Of course that means one has to first endure the burn, and its obviously most unsuitable for use on skin with cuts or worse, raw, skinned areas, the idea is to induce a longterm inability of the nerves to fire. It does indeed have direct (as opposed to simply from its counterirritant, rubefacient effects when used to treat pain of musculoskeletal origin) analgesic effects on nerves, as its used to treat neuralgia, such as of the post-herpetic variety. I could be wrong here but I THINK it also has longterm effects on substance P. As far as its use as a weapon, sure, you don't generally want irritants sprayed in your face
Some southamerican tribes used to use the forced inhalation of smoke from burning chilli peppers as a method of punishing unruly kids (along with Datura species...jesus...lovely parenting skills there, although I bet it was effective!).
HOW unruly one had to be, I don't know, but lets not forget these are some of the same lot (aztec, etc) who had a taste for ripping hearts out, burying the wives of dead emperors alive with the body, and arranged-by-consent wars in order to provide sufficient numbers of victims for their human sacrifices. So I bet the kids were on their best behaviour when they could be caught
Capsaicin stimulates until the receptors desensitize, resulting in a long-term analgesic and iirc, locally operative antihyperalgesic/antiallodynic effect. Of course that means one has to first endure the burn, and its obviously most unsuitable for use on skin with cuts or worse, raw, skinned areas, the idea is to induce a longterm inability of the nerves to fire. It does indeed have direct (as opposed to simply from its counterirritant, rubefacient effects when used to treat pain of musculoskeletal origin) analgesic effects on nerves, as its used to treat neuralgia, such as of the post-herpetic variety. I could be wrong here but I THINK it also has longterm effects on substance P. As far as its use as a weapon, sure, you don't generally want irritants sprayed in your face
Some southamerican tribes used to use the forced inhalation of smoke from burning chilli peppers as a method of punishing unruly kids (along with Datura species...jesus...lovely parenting skills there, although I bet it was effective!).HOW unruly one had to be, I don't know, but lets not forget these are some of the same lot (aztec, etc) who had a taste for ripping hearts out, burying the wives of dead emperors alive with the body, and arranged-by-consent wars in order to provide sufficient numbers of victims for their human sacrifices. So I bet the kids were on their best behaviour when they could be caught
Blu-Shad0w
Bluelighter
- Joined
- Oct 22, 2014
- Messages
- 58
hmmmm
It seems repeate capsaicin exposure causes inhibition of heat-shock protein in turn decreasing some transcription factors' activity which are responsible for expressing the vanilloid receptor and a number of other proteins, similar to how cells react to high temperature. Most of us know that the more often you burn your fingers, e.g. during cooking, the more resistant you seem to becoming to heat induced pain. I can pull noodles from boiling water without pain. Pretty sure TVRP1 activation can also cause cell death.Capsaicin at least works by, as I understand it, overstimulating TRPV1 receptors (transient receptor potential vanilloid-1), these are the targets responsible for the burning of chili peppers (yum! I LOVE chili pepper in/on food. I like to fry my steaks in tabasco with some worcestershire sauce, or to use tabasco to help my fly agaric/peppery boletus/black/pink/szechuan pepper and cubeb steak spice powder stick to the meat properly.
Capsaicin stimulates until the receptors desensitize, resulting in a long-term analgesic and iirc, locally operative antihyperalgesic/antiallodynic effect. Of course that means one has to first endure the burn, and its obviously most unsuitable for use on skin with cuts or worse, raw, skinned areas, the idea is to induce a longterm inability of the nerves to fire. It does indeed have direct (as opposed to simply from its counterirritant, rubefacient effects when used to treat pain of musculoskeletal origin) analgesic effects on nerves, as its used to treat neuralgia, such as of the post-herpetic variety. I could be wrong here but I THINK it also has longterm effects on substance P. As far as its use as a weapon, sure, you don't generally want irritants sprayed in your face
HOW unruly one had to be, I don't know, but lets not forget these are some of the same lot (aztec, etc) who had a taste for ripping hearts out, burying the wives of dead emperors alive with the body, and arranged-by-consent wars in order to provide sufficient numbers of victims for their human sacrifices. So I bet the kids were on their best behaviour when they could be caught
Don't take my word on the mentioned mechanisms (!), I can't quite remember the details, but it's all easily accessible information. There is a lot that is yet to be cleared up. What is established though is that capsaicin and it's analogues have much more profound effects than once assumed.'
Oh and btw I've applied menthol, capsaicin and lidocaine to my body more than once, even injected them into my urethra in hopes to maintain an erection on very high stimulant doses due to their vasodilatory effects (lidocaine for combating the pain though). Worked btw, but the misses did not appreciate it. :D This felt very different from capsaicin or menthol, indistinguishable to the sensation I get from lidocaine and other local anesthetics.
http://link.springer.com/article/10.1007/s12576-015-0427-y
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Limpet_Chicken
Bluelighter
Regardless of whether or not that works, the only way the least picomolar or lower, trace concentrations of capsaicinoids are going anywhere NEAR my jap's eye is after I've eaten chilli in something and I need to have a piss. I'm surprised the other half let you live after doing that!
Limpet_Chicken
Bluelighter
Not if the burning is due to the wife going off to grab some acid... (and no I don't mean derivatives of the lysergic kind)
Limpet_Chicken
Bluelighter
Seems like its not mutual
Got 5g that will be within the week, does anyone know why vaping it on tinfoil will degrade it more than an oil burning pipe, I read that. I plan on vaping it BEFORE I snort, so I can report my research. Might get a pipe, I smoked a PvP and a php but I'm going to use cocaine as my benchmark. Peace
Limpet_Chicken
Bluelighter
If nothing else, the wall of the pipe provides a means to expose to less heat than does the very thin, and being aluminium, foil has very good thermal transfer properties, and is also easy to burn through. Take smoking heroin for example, its really easy to overheat and fuck it up good and proper on foil, and its wasteful as hell. Far more can be vaped and less put to the torch by the means of a long, narrow-bore (mine is around 3-3.5mm internal diameter, although flared a little at the tip to allow for loading)
A good way, if you need a pipe is to use a borosilicate test tube, heated first in the flame of a propane or oxypropane flame, evenly rolling the closed end around so as to distribute the heat and avoid thermal shock cracking (even borosilicate, whilst having a low coefficient of thermal expansion can crack or break if really, really abused although they can be relied upon to take anything a normal or jet flame lighter will throw at them), and using a narrow, heated nail, like a panel pin, held in pliers, slightly wider is a bit better than the narrowest gauge tacks, about as wide as a pencil lead (which can be coopted for making these pipes in one other respect, although not sufficiently strong to drive the hole into the semi-molten glass) through the side wall just behind the tip.
The trick with the pencil lead that I came up with involves using a wide gauge guitar bottom E string, or light bass string, covered in powdered graphite, with the free end tucked through that which wraps round the brass loop, like a noose, because graphite serves as a nonstick, to lubricate the string and avoid adhering to the glass, and cinch it carefully, round the test tube neck about an inch to three quarters round the far (closed) end, preferably after driving in the hole, this provides a wasp-waist kind of partial neck to the new pipe, that serves to prevent you accidentally getting molten meth, skag or whatever else your using it to smoke backwashing all over the thing once you start using it, and least of all, wanting it dripping out on you or in your mouth.. If your careful, then its possibly to slice the end off a glass pippete (I used a burette I broke IIRC once, the glass tubing being more or less disposable or would just have sat waiting to be recycled to some other purpose until required otherwise) to the inside wall, at the other end, CAREFULLY done, to provide a long stem that helps avoid breathing searing hot air from a sub-red-hot short pipe like that made from a ttest tube alone, fuse it with a micro torch, if necessary using supplementary oxygenation through a blowpipe connected to a welding gas bottle to direct a portion of the flame into an intense pinpoint, via an axial orientation to the length of the flame to rapidly weld the two together, with the end going down to just before the waist at the business end. Also having a long, narrower bore stem close to the drug being vaporised lowers the effective vapor pressure of it somewhat, albeit at a very low level compared to the effect it mimics, vacuum distillation. The operating principle is not dissimilar in operation however, and it helps at least to lower the temperature the drug needs to be exposed to and get it fuming quicker and harder.
I've been contemplating building one with a couple of V-shaped bipods to allow standing the pipe on surfaces without either burning them, or dropping the temperature down during a session whilst its heated. Maybe even electrical heating of the sucking tube, hell why not of the glass vape chamber section itself, that way warming the mouthpiece tube would help avoid rapid recrystallization of the drug vapor on its cool surface.
A good way, if you need a pipe is to use a borosilicate test tube, heated first in the flame of a propane or oxypropane flame, evenly rolling the closed end around so as to distribute the heat and avoid thermal shock cracking (even borosilicate, whilst having a low coefficient of thermal expansion can crack or break if really, really abused although they can be relied upon to take anything a normal or jet flame lighter will throw at them), and using a narrow, heated nail, like a panel pin, held in pliers, slightly wider is a bit better than the narrowest gauge tacks, about as wide as a pencil lead (which can be coopted for making these pipes in one other respect, although not sufficiently strong to drive the hole into the semi-molten glass) through the side wall just behind the tip.
The trick with the pencil lead that I came up with involves using a wide gauge guitar bottom E string, or light bass string, covered in powdered graphite, with the free end tucked through that which wraps round the brass loop, like a noose, because graphite serves as a nonstick, to lubricate the string and avoid adhering to the glass, and cinch it carefully, round the test tube neck about an inch to three quarters round the far (closed) end, preferably after driving in the hole, this provides a wasp-waist kind of partial neck to the new pipe, that serves to prevent you accidentally getting molten meth, skag or whatever else your using it to smoke backwashing all over the thing once you start using it, and least of all, wanting it dripping out on you or in your mouth.. If your careful, then its possibly to slice the end off a glass pippete (I used a burette I broke IIRC once, the glass tubing being more or less disposable or would just have sat waiting to be recycled to some other purpose until required otherwise) to the inside wall, at the other end, CAREFULLY done, to provide a long stem that helps avoid breathing searing hot air from a sub-red-hot short pipe like that made from a ttest tube alone, fuse it with a micro torch, if necessary using supplementary oxygenation through a blowpipe connected to a welding gas bottle to direct a portion of the flame into an intense pinpoint, via an axial orientation to the length of the flame to rapidly weld the two together, with the end going down to just before the waist at the business end. Also having a long, narrower bore stem close to the drug being vaporised lowers the effective vapor pressure of it somewhat, albeit at a very low level compared to the effect it mimics, vacuum distillation. The operating principle is not dissimilar in operation however, and it helps at least to lower the temperature the drug needs to be exposed to and get it fuming quicker and harder.
I've been contemplating building one with a couple of V-shaped bipods to allow standing the pipe on surfaces without either burning them, or dropping the temperature down during a session whilst its heated. Maybe even electrical heating of the sucking tube, hell why not of the glass vape chamber section itself, that way warming the mouthpiece tube would help avoid rapid recrystallization of the drug vapor on its cool surface.
sturdychinfilms
Bluelighter
- Joined
- Aug 7, 2010
- Messages
- 83
I've found it to be very water soluble. May be just a crummy batch maybe?