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The Big and Bangin' Pseudo-Advanced Drug Chemistry, Pharmacology and More Thread, V.2

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might want to avoid the heat though

"cold water extractions" are a standard method to remove aceteminophen from opiate pills. same method might apply with naproxen and carisoprodol.

look up the temperatures that they dissolve at perhaps
 
Thanks :)

I'll give it a try

Edit. Okay, here's an update.

I measured the contents of one capsule to be 500 mg, on the bottle it's says theres supposed to be 250 mg naproxen and 200 mg carisoprodol in each. Something doesn't add up.

Anyway, I dissolved the powder in some luke warm water, in a glass, which was then placed in a small dish with some boiling water. Visually it looked as expected. Some of the powder seemed to be dissolving and some seemed fall to the bottom as solid.
I filtered it through a coffee filter, and let it evaporate off from a plate.

Yield was a measly 100 mg.

I figured this is because carisoprodol only has slight solubility in water.

My second attempt was doing the same, but just using 40% vodka (and using a smaller amount of liquid too) as carisposprodol has total solubility in alcohol, and I'm hoping that naproxen hasn´t.

Again yield came out as precisely 100 mg?! WTF, maybe my experiment was succesfull and the capsules only contain 100 mg of carisoprodol?
 
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If I were you I would dissolve in hot water, allow the solution to cool fully and then filter it. I would definitely not use vodka.
 
Transform said:
If I were you I would dissolve in hot water, allow the solution to cool fully and then filter it. I would definitely not use vodka.
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How hot? luke warm or just below boiling?

Thanks a lot for responding, it's appreciated.
 
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okay, so I keep meeting people who take absurd amounts of MDMA. I've been trying to weigh the ethics of doing MDMA and the regularity in which you should do it because I pretty much lost the magic after doing it like 8 times over the course of like 5 months I think. So I haven't taken it since october. However, I just met a person that has taken like three and a half grams of it over the course of a weekend then takes psychedelics all week and is planning to go to ULTRA this weekend and do even more. Like wtf, shouldn't she have like a massive tolerance and an insane comedown right now? and the other night I was at someones house and found out there was a person there who was on over a gram and a half of MDA. I can't believe these people, like do they even roll at all? I'm assuming that they're doing some pretty heavy damage.

so my question to you is what magnitude of damage is occuring in these people's brains and is there any possible way that they haven't lost the magic yet? they roll like every weekend.
 
MDMA is actually pretty benign if you don't do truly absurd doses. Sure it loses efficacy with regular usage, but going through 3-7 grams on a weekend is not going to leave you crippled. It will, however, leave you pretty drained for a couple weeks.

People who go hard on MDMA usually recover fully in about a year's time, if not a little more. It's definitely not smart, but your brain won't just suddenly turn into chalk dust with regular usage.
 
Idk theres just a lot of research that needs to be done. I took MDMA maybe 7 times last year. I took a lot of psyches too but it made me totally depressed and crazy. Also, I used lots of vitamins too which none of these people are doing. What types of cells are being destroyed and do we know anything about how long it takes for them to be repaired/ regrown?
 
Everybody is different. I use MDMA maybe three times a year, 130mg in a single dose, usually at a party or festival with some 2C-B or ketamine. In the week that follows, if I don't get a severe cold then I am quite down and generally much less able to cope with life. Clearly other people don't suffer in the same way.
 
What types of cells are being destroyed and do we know anything about how long it takes for them to be repaired/ regrown?
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As far as we know, MDMA doesn't cause cell death unless you overheat yourself. It does cause temprary reduction in serotonin synthesis that rebounds after about 2 weeks.

The myth that "ecstacy puts holes in your brain" or "kills serotonin cells" is unfounded. Don't abuse your body, get plenty of rest and food, and you'll be fine.
 
http://www.erowid.org/chemicals/mdma/mdma_article3.shtml

Summary

MDMA causes a sharp increase in oxidative hydroxyl radicals shortly after administration. It is now believed that this rise in oxidative stress is likely involved in MDMA's neurotoxicity, and may be involved in some of its negative side effects. Very high doses of injected antioxidants have been shown in rats to dramatically reduce or block MDMA neurotoxicity as well as reduce tolerance to MDMA's effects between neurotoxic doses. Based on these findings, it is possible that common vitamin antioxidants may be effective at reducing risks of MDMA neurotoxicity, hangover effect, tolerance, and general body stress.

The practical implications of rat-based laboratory research are difficult to reliably assess. However, well-tolerated, common antioxidant supplements such as vitamins C, E, alpha lipoic acid, and others certainly warrant further investigation as a simple means to reduce the negative impact of ecstasy use on the body. For MDMA users who already take antioxidants occasionally, there seem to be few downsides to making sure to take reasonable doses of antioxidants in the days before, during, and after their ecstasy use. The risks are low and the benefits may be immediately apparent.

A potential side-benefit to suggesting ecstasy users take vitamin supplements may be to increase awareness that MDMA is hard on the body. Taking antioxidants before, during, and after experiences could help foster more intention around ingestion, act as a reminder that ecstasy is physically stressful, and could offer an additional way experienced users and harm reduction workers can communicate to new users about risks and precautions. Harm reduction groups could engage users in the issue of toxicity by discussing proper nutrition as a way to maintain the enjoyable effects and recover more quickly.

The primary downside to suggesting antioxidants may be neuroprotective is the chance that some ecstasy users will misunderstand the information and believe that taking vitamin C will protect them from harm or that some will assume that taking antioxidants will allow them to increase their use of MDMA. Increasing MDMA dosage or frequency of use is likely to significantly increase risk of neurotoxicity. The simplest and most effective way to reduce risk of neurotoxicity is to reduce dosage, refrain from re-dosing during an experience, and reduce frequency of use.
 
http://www.erowid.org/chemicals/mdma/mdma_neurotoxicity1.shtml#damage

is this really dated? because this seems to cite a lot of examples of how and why MDMA causes damage.

and also there's that one extreme example of this guy
http://www.guardian.co.uk/society/2006/apr/04/drugsandalcohol.drugs1

also I heard saw person claimed that using ecstacy too often is doing worse for your brain than doing meth or crack occasionally. would anyone like to discuss this?

thanks for your educated responses you guys are always very helpful here in ADD.

one more question, there aren't any major side effects from combining ritalin and cocaine right?
 
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^yea I know but that being said how relevant is the information in it? how many studies have taken place since? you guys have already swayed me that MDMA isn't so bad. I'm doing research on it now and while the thought of alpha-methyl-dopamine is not a good one I have no idea what portions it is made in comparison to the dose of MDMA or how much of that actually reacts with glutathione to produce the evidently neurotoxic effects.
 
no long-term serotonergic changes occurred after 2.5 mg/kg MDMA was given orally every two weeks for four months to squirrel monkeys (Ricaurte, unpublished, cited in Vollenweider, 1999). [Editor's note: a therapeutic dose of 125 mg in a 150 pound person would translate to 1.66 mg/kg]

Another commonly studied nonhuman primate species is the rhesus monkey. Determining the threshold dose for 5-HT depletions in this species is difficult since all published studies using rhesus monkeys have employed multiple dose neurotoxic regimens. In one study, 1.25 mg/kg oral MDMA did not produce any long-term serotonergic changes when given twice daily for 4 consecutive days. Similarly repeated doses of 2.5 mg/kg MDMA lowered hippocampal 5-HT (to about 80% of controls) but did not affect levels in 6 other brain regions at post one month (Ali, 1993). In another experiment, Insel (1989) found that 2.5 mg/kg MDMA given intramuscularly twice daily for 4 days to rhesus monkeys produced extensive (possibly short term) 5-HT depletions but did not alter SERT density at 16 to 18 hours after the last drug exposure. Since SERT was unaffected, the researchers concluded that axonal loss had not occurred, despite the 5-HT depletions.

In a study that raises interesting questions about possible tolerance to MDMA neurotoxicity, Frederick (1995) investigated the long-term effects of escalating doses of MDMA. Intramuscular MDMA (0.1-20 mg/kg) was given twice daily for 14 consecutive days at each dose level and followed by three dose-response regimens using single MDMA doses up to 5.6 mg/kg. One month after the final dose-response determination and 21 months after the initial escalating dose regimen, animals were sacrificed. Few significant serotonergic effects were found. MDMA exposure did not produce significant 5-HT depletions in any brain region and decreased SERT to about 60% of control levels only in the hippocampus (and not two other brain regions). Thus, data on rhesus monkeys are complex and perhaps all that can be said with certainty is that the threshold dose for long-term 5-HT depletions appears to be above 1.25 mg/kg oral MDMA in this species.
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from the erowid page

The boldest of the brain blood flow experiments was done by researchers from UCLA's Neurology, Radiology, and Psychiatry departments. They studied the amount of blood flow in current and former 'ecstasy' user's brains and found that recent users (within the past few weeks) had slightly lower blood flow to parts of the brain, but people who hadn't used for four weeks had perfectly normal levels of total and regional blood flow within their brains.[8] That wasn't the bold part, however: Not content simply to test volunteers who had used 'ecstasy' on their own, they gave recreational doses of MDMA to a number of the volunteers after their initial scan, then re-scanned their brains afterwards. As expected, there was a decrease in blood flow immediately after MDMA use, but it returned to normal within 3-4 weeks. In their final report, the researchers concluded that "Low-dose recreational MDMA use does not cause detectable persistent rCBF (regional cerebral blood flow) changes in humans."

Further research has only confirmed their findings, so the answer is...yes and no. Yes, there is a modest change to your brain after using MDMA that seems to last for about three to four weeks, give or take. It's not permanent, and there's no reason to believe it involves damage; rather, it appears to be a sort of 'hangover' effect caused by your brain's reaction to being exposed to a drug.
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thedea.org - neurotoxicity page
 
http://www.mdpi.com/1424-8247/4/7/992
Methylenedioxymethamphetamine (MDMA, 'Ecstasy'): Neurodegeneration versus Neuromodulation
Puerta E, Aguirre N

Abstract: The amphetamine analogue 3,4-methylenedioxymethamphetamine (MDMA, ‘ecstasy’) is widely abused as a recreational drug due to its unique psychological effects. Of interest, MDMA causes long-lasting deficits in neurochemical and histological markers of the serotonergic neurons in the brain of different animal species. Such deficits include the decline in the activity of tryptophan hydroxylase in parallel with the loss of 5-HT and its main metabolite 5-hydoxyindoleacetic acid (5-HIAA) along with a lower binding of specific ligands to the 5-HT transporters (SERT). Of concern, reduced 5-HIAA levels in the CSF and SERT density have also been reported in human ecstasy users, what has been interpreted to reflect the loss of serotonergic fibers and terminals. The neurotoxic potential of MDMA has been questioned in recent years based on studies that failed to show the loss of the SERT protein by western blot or the lack of reactive astrogliosis after MDMA exposure. In addition, MDMA produces a long-lasting down-regulation of SERT gene expression; which, on the whole, has been used to invoke neuromodulatory mechanisms as an explanation to MDMA-induced 5-HT deficits. While decreased protein levels do not necessarily reflect neurodegeneration, the opposite is also true, that is, neuroregulatory mechanisms do not preclude the existence of 5-HT terminal degeneration.
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Additive stimulant effects, but there aren't massive contradictions as far as I know. Don't go overboard on them and you should be as ok as someone doing cocaine and methylphenidate can be.
 
Help Me ID Chemical Structure

Hi - I bought two things which arrived unlabelled except for images of the chemical structure. I've forgotten what I ordered and the vendor keeps no purchasing history, nor do they detail your purchase in the email. Google image search is getting me nothing but IKEA instructions LOL

How do I upload images here or direct them to an outside link? I need help id-ing these chemical structures.

Cheers!
 
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