Does a legal alternative to etizolam (or general research chemical benzo analogues) exist in the state of Ohio? They banned eizolam here some years ago. I was wondering if there was a similarly sedating benzo-like drug that easily-ordered researh chemical prefereably in pill or tablet form that I could use as a substitute for etizolam. Sorry I am new so my research chemicals knowledge is limlited. Thank you in advance.
Alternative to Eitzolam?
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LargeAppetite
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I can't believe this made it 30 minutes.
Viva La Bluelight
This is clearly an attempt at sourcing which is prohibited in the guidelines of this informative and enlightening website. Despite the fact the mods are either vacant, nodding or having divine visions of the past and future simultaneously, they request that you reformat/remove your post and or give up your position with the feds.com/remove your post still.
Viva La Bluelight
This is clearly an attempt at sourcing which is prohibited in the guidelines of this informative and enlightening website. Despite the fact the mods are either vacant, nodding or having divine visions of the past and future simultaneously, they request that you reformat/remove your post and or give up your position with the feds.com/remove your post still.
kongoman
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If you dont like BL. Feel free to not read it. Mods have their lifes and they do a very good work. Stop critisizing them.
Have you been on reddit? probably you will like More than BL.
I think you shouldnt write anything if you are not adding.
Have a good day
brokedownpalace10
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He didn't ask where to get it.
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I'm moving this thread to Drug Culture where it is better suited as a topic.
That said, yes there are alternatives to etizolam that are still legal in the US, but we can't really give you legal advice like this, and we also can't give you sources or vendors directly, as these things are against our rules.
The laws change quickly and vary so much state to state, that it would be irresponsible to just give you a name to search for and say it's legal, because ultimately we might not be correct.
All that said, definitely the most popular rc benzo after etizolam was scheduled, would be bromazolam. That went around a lot the past several years. I believe that is scheduled now too at this point, so I'm really not sure what other alternatives there are at the moment, as I personally am out of the game.
Also, it should be said for anyone, please be careful about talking to people about these things and trying to find sources on this website. 1) it's completely against our rules, but more importantly, you never know who could be on the other side of the screen or what their motives are.
That said, yes there are alternatives to etizolam that are still legal in the US, but we can't really give you legal advice like this, and we also can't give you sources or vendors directly, as these things are against our rules.
The laws change quickly and vary so much state to state, that it would be irresponsible to just give you a name to search for and say it's legal, because ultimately we might not be correct.
All that said, definitely the most popular rc benzo after etizolam was scheduled, would be bromazolam. That went around a lot the past several years. I believe that is scheduled now too at this point, so I'm really not sure what other alternatives there are at the moment, as I personally am out of the game.
Also, it should be said for anyone, please be careful about talking to people about these things and trying to find sources on this website. 1) it's completely against our rules, but more importantly, you never know who could be on the other side of the screen or what their motives are.
How about kava? There are kavalactone extracts available and these are GABAergic
Yeah I was just wondering where
Yeah I was just wondering if such a thing exists as I've been out of the loop for a while, I can find vendors or whatever on my own if I were so inclined.
Thank you for the info in your replies, everyone.
Yeah I was just wondering if such a thing exists as I've been out of the loop for a while, I can find vendors or whatever on my own if I were so inclined.
Thank you for the info in your replies, everyone.
Conky
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Kava smells and tastes like shit and causes nausea and vomiting
One man's shit is another man's sunshine. Never did any of those things to me and with extracts you can just throw it in a capsule
Unless you like the taste but hey whatever floats your boat
Unless you like the taste but hey whatever floats your boat
Kava is NOT GABA-active in a meaningful way, if at all.
I think you may be referring to the fact that flumanezil doesn't appear to block the anxiolytic effects of kava exctracts as was shown in this paper:
Extracts of kava (Piper methysticum) induce acute anxiolytic-like behavioral changes in mice - PubMed
Kava extracts produce significant murine anxiolytic-like behavioral changes and sedation that are not mediated through the benzodiazepine binding site on the GABA(A) receptor complex.
pubmed.ncbi.nlm.nih.gov
So there are a few different binding sites for the GABAa receptor and GABA, benzodiazepines, and barbiturates all bind at different sites. Flumazenil specifically competitively blocks the benzo site but only in a neutralizing manner, it doesn't appear to decrease the efficacy of endogenous GABA binding
There was a recent paper where experiments were performed on a variety of human GABAa receptors expressed in oocytes, they found that kavain has a modulatory effect similar to barbiturates and that it may bind at a site similar to some anesthetics.
"We demonstrate that the modulatory effect of kavain at GABAARs occurs in a subtype non-selective and flumazenil-insensitive manner. We also present evidence, for the first time, that kavain action at GABAARs is attenuated by the anaesthetic-impairing β3N265M point mutation."
"We investigated the effect of combining benzodiazepine site ligands with kavain at α1β2γ2L GABAARs (n = 5; Fig 4). In concordance with the literature, diazepam (1 μM) enhanced current responses elicited by 10 μM GABA in a flumazenil-sensitive manner, and flumazenil alone did not alter GABA responses, consistent with its neutralising modulator profile [33]. Unlike diazepam, the GABA-enhancing action of 300 μM kavain was unaffected in the presence of flumazenil. We also found that the co-application of kavain and diazepam resulted in significantly greater enhancement of GABA current (350 ± 10%) compared to their actions alone (GABA + diazepam: 260 ± 4.2%, p < 0.001; GABA + kavain: 260 ± 11%, p < 0.0001; paired t test; Fig 4B). However, this degree of potentiation was less than additive (expected additive value = 420%). The same experiment was repeated with 100 nM diazepam, and a less-than-additive interaction was detected again with the kava and diazepam combination (n = 3; data not shown)."
"Next, we assessed the possibility of kavain interacting with the transmembrane β+α‒ anaesthetic binding sites. To this end, we introduced the α1M236W, β2M286W and β3N265M point mutations which perturb etomidate and propofol actions, and investigated the impact of these mutations on kavain activity at GABAARs."
"Similar differential enhancement effects that arise from the distinct GABA efficacies at synaptic αβγ and extrasynaptic αβδ receptors have been described for other allosteric ligands such as etomidate [38], propofol [39], pentobarbital [40], and neurosteroids [41]. While our findings do not conclusively prove that GABAARs are the in vivo substrate for kavain, it is tempting to speculate that kavain may have a larger physiological impact on extrasynaptic than synaptic GABAARs."
"The low affinity of kavain detected in our study is in agreement with most studies conducted in the past using kava extracts or pure kavalactones [21, 22, 46]. The high-micromolar concentrations required to observe the pharmacological actions of kavalactones in vitro raise the critical question of whether the concentrations used in these studies are physiologically relevant. Studies conducted in mice showed that 100 mg/kg of kavain alone caused a rapid surge in brain concentration (up to 100 μM) within minutes after i.p. injection [22, 47]. A higher brain concentration of kavain was found (120 μM) in the presence of other kavalactones (44 mg kavain in 120 mg/kg kavalactone mixture; i.p.), clearly demonstrating pharmacokinetic synergism [22, 47]. Davies et al. (1992) predicted higher brain concentrations (300 μM) with the administration of larger doses (300 mg/kg) of kavain [22]. Thus, kavain concentrations used in our study appear to correlate well with the concentrations needed to induce anxiolysis and hypnosis in mice [27, 48]. Unfortunately, the relevance of this concentration range in humans cannot be established as no data is currently available [49]."
Kavain, the Major Constituent of the Anxiolytic Kava Extract, Potentiates GABAA Receptors: Functional Characteristics and Molecular Mechanism
Extracts of the pepper plant kava (Piper methysticum) are effective in alleviating anxiety in clinical trials. Despite the long-standing therapeutic interest in kava, the molecular target(s) of the pharmacologically active constituents, kavalactones have not been established. γ-Aminobutyric acid...
It is still relatively unknown if the primary anxiolytic effects are due to the specific GABAa modulation investigated in this paper and there are other studies which investigate inhibitory modulation through sodium and calcium channels as well. Like other phytochemicals, kavalactones are quite promiscuous and bind at a variety of receptors but GABAa interactions may very well play a role.
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