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

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Cachetol, aka pyrocachetol = 1,2 dihydroxy benzene.

So a cachetolamine is a 3,4-dihydroxy-phenethylamine. Dopamine and norepinephrine are the two Big Names.
 
How comes the 2c-x and especially nbomes can bind to the 5-HT receptor?

Because they interact with the protien in the right way, similar to 5HT. I believe they do bind to the same site that 5ht does.
It just so happens that the non-intelligently-designed receptors in your brain are more permissive than you'd expect.
 
I haven't been able to get a reasonable answer to this question. I searched, but either I didn't find answers for some reason, or maybe it's common knowledge for most people. (Mods if this question is off topic, out of place, or dumb, do as you will.)

Do amphetamines cause menstrual flooding and the passing of enormous blood clots that could almost be mistaken for a liver or something?
 
Do amphetamines cause menstrual flooding and the passing of enormous blood clots that could almost be mistaken for a liver or something?

that doesn't sound normal at all. i'd probably talk to a doctor if i were you if you think there is a problem. if you think the amphetamines are responsible then you probably should seriously consider quitting them.
 
I have experienced this on occasion but one of my friends (who, in my opinion, would use the stuff 24/7 if she could) has had symptoms like I described.

Well, lately she's got a sweet sugar daddy and I am pretty sure she's using a scary amount of speed. She says most women clot on speed and she doesn't see it as an issue.

I don't know where she "learned" that a nonstop issue of blood is a normal side effect. She's convinced all females have that response to the drug. I don't agree with her and I don't have any solid documentation to try to show her that it is NOT normal for blood clots big as man hole covers to drop out of her body.

I'm hoping to find an article or something that I could use to have a discussion with her about this. A basically unlimited amount of spendable dollars she has access to might be killing her. I really don't know, though. I saw her yesterday after about three months of not seeing her. She's looking unhealthy. Really unhealthy. One of her eyeballs has become just a red orb in her eye socket. She's lost a lot of weight, which she's never done before and she's used ever since we became friends 5 or 6 years ago. Her hair seems to be thinning also, in my estimation.

But blood clots that are so big she risks blocking up her toilet when she flushes??? Why would she think that's just part of the side effects??
 
Drug Half-life and Drugs detection time ?

So hello folks,
Im a little unwitting about this half-life calculation on drugs detection in urine. Would like to know for real.
Lets take one example with Phenergan(Promethzine) a antihistamine.
It has a half-life of 16-19 hours(wiki)
So it will go something like this
1 dose of Phenergan 25mg eaten,
19h later you have 12,5mg
And then it goes:
(19h) 6,25
(19h) 3,125
(19h) 1,5625
(19h) 0,78125
(19h) 0,390625

How many "cycles" does it takes for a drug to be undetectable on a drugscreening analysis methadon?

Thanks!
 
But blood clots that are so big she risks blocking up her toilet when she flushes??? Why would she think that's just part of the side effects??

That sounds like it might be unrelated to the speed and whether it is or not, it's worthy of seeing a doctor ASAP
 
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It doesn't work like that because you have left body metabolism out of the equation completely. THC has a half life of 20 hours yet it is detectable up to 30 days after cessation. I don't think this calculation is possible.
 
Merging this with the big and dandy thread.
Well DeLee is correct that half life is directly related to detectable limits (not going into drug testing specifics), however some drugs can be detected by metabolites or are stored in various tissues/hair. For example THC's ridiculously long half-life metabolite is what's tested for rather than THC itself. Detectable limits are the level at which the concentration of a drug in the body is below threshold X for a test.

Some drugs are even crazier with those half lifes, for example fluoxetine (Prozac) has a metabolite with a half life of ~31 days! Now that's pretty nuts. The only thing I know of with a longer half life is cadmium with a half life of ~20-30 years after the body has sequestered it.
 
I was wondering if it's possible in general to cleave a molecule at an amide bond, for example:


2-(2,6-dichloroanilino)phenol
2-26-dichloroanilinophenol_zps2282491a.png


Into:

1,3-dichlorobenzene and phenol
13-dichlorobenzene_phenol_zpsbdc2553e.png
 
Nope, not easily.

Usually atoms don't just disappear when compounds split. A more likely pattern would be metabolism to 2,6-dichloro-aniline, and 1,2-dihydroxy-benzene.
 
Also worth noting that that bond is an amine linkage, not an amide.

Amides can be hydrolysed with water, heat and a weak acid.
 
Anaphylaxsis and Morphine

Hey, I hope this is the right place to post. Now say someone is on a dose of opiates (a high recreational dose) and happens to eat something he or she is allergic to and receives a full allergic anaphylaxsis shock that only the epipen (nor-adrenaline) can fix. Will the morphine prevent the epipen from working?

Thanks, this info is very important.
 
Sorry, I can't answer your question.. I don't thin opioids will block (nor)adrenaline though.

BTW, isn't it adrenaline in an epipen? I imagine "epi" standing for epinephrine(andrenaline)
 
You might be best asking a pharmacist, just say you have a relative coming over after surgery with severe allergies of you get any questions.
 
Morphine should not stop epinephrine from working, but do realise that epinephrine is only a stopgap until you can have the anaphylaxis treated properly with e.g. corticosteroids. (Epi has a very short half life)

And yes, epinephrine is the same thing as adrenaline, and is found in Epi-Pens.
 
Has anyone experience with extracting and isolating pure nicotine from natural tobacco?
I tried once to extract it by cooking the leafs, filtering the boiled down next to black "soup" and drying it.
But usual tobacco does not only contain nicotine but many more other alkaloids which are seemingly causing much more undesirable side effects than nicotine itself does. I know this since the isolated nicotine containing fluid for electronic cigarettes for example is much better tolerable compared to inhaling vaporized (or smoked of course) tobacco...

Actually pharmaceutical grade pure nicotine(-HCl?) is rather cheap, but all the local pharmacy stores in my area are simply to scared of it to sell it - although it was absolutely legal in my country even without any kind of prescription.

I need it pure, since I wanna make a potent and tobacco free "white" alternative for "brown" powdered tobacco leaf snuff alternative - without all those unwanted other alkaloids and especially without all that other leaf-powder that can nastily mess up your nose after a while of intense nasal tobacco consume...

Sniffing tobacco can be nearly as addicting as smoking. (if not even more, since getting cancer from it is quite unlikely compared to inhaling all those smoke toxins...) Last but not least it is much more enjoyable to me - anywhere!
 
Actually snuff is usually smoke treated so it still contains the carcinogenic nitrosamines. The "unwanted other alkaloids" include cabolines which have an MAOI effect which is thought to greatly contribute to the addiction potential of tobacco and some of the enjoyment too. Nicotine is regulated as a poison in most countries rather than an illegal drug.
 
Schema for formation of the mystery compound. The URB ring opens up to a diphenyl urea type thing and a carboxylate group, the carboxylate forms an amide I guess?

PfNPhAx.png


URB754 was originally reported to be a potent, noncompetitive inhibitor of monoacylglycerol lipase.[1] However, recent studies have shown that URB754 failed to inhibit recombinant MGL, and brain FAAH activity was also resistant to URB754.[2] In a later study by Piomelli at al showed that the MGL-inhibitory activity attributed to URB754 is in fact due to a chemical impurity present in the commercial sample, identified as bis(methylthio)mercurane.

So the only reason there was any activity anyway, was organomercury contamination. I don't know why there is even methylthio mercury.

(Mercurane is the IUPAC systemic name for a compound of mercury and hydrogen. A google search misled me to think it's 1-mercurocyclohexane (pyran with oxygen replaced with mercury) but it is likely not)

This is plenty more evidence that nobody should touch "legal highs"... there really could be anything as an active ingredient unil there is independent confirmation.
 
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