• Neuroscience & Pharmacology Discussion Welcome Guest
    Posting Rules Bluelight Rules
    Recent Journal Articles Chemistry Mega-Thread
    FREE Chemistry Databases! Self-Education Guide

  • N&PD Moderators: Skorpio

5-(2-aminopropyl)-2,3-dihydrobenzofuran as a sedative (aka 5-apdb aka 3-desoxy-mda)

dread said:
What's that thing sticking from the O?
Click to expand...

appears to be an entirely heterosexual representation of a lone pair should be 2 on the O but it might not be visible from the angle.

it ain't hydrogen gay despite Jamshyds wishfull thinking,
 
The program used (Chem3D) displays electron pairs not as orbitals but uses ball-and-stick-models as if these were 'normal' substituents. FnB is right concerning the real shape...

And of course are electron pairs ALWAYS pink!
 
Electron pairs... two electrons getting it off with each other, while the protons are watching? Definitely gay exhibitionism.
 
sounds like this compound could be improved by mixing it with a dopamine releasing stimulant...
 
after a few months i collected a few more experiences from me and a bunch of friends:

like most of the entactogens 125 - 150 mg seems to be the magic range.

also good news : 20-40 mg as a slight anti-depressant seems to work also.
(not taken more then every other day for a week.)

more experiments to follow soon(ish) .

your ex.
 
so a few people have tried it, yet there is very little written about the quality of the effects besides that it is sedating in a way. is it empathogenic/entactogenic? euphoric? hallucingenic? come on, please describe its effects in some more detail!
 
ungelesene_bettlek said:
so a few people have tried it, yet there is very little written about the quality of the effects besides that it is sedating in a way. is it empathogenic/entactogenic? euphoric? hallucingenic? come on, please describe its effects in some more detail!
Click to expand...

yes ,
at a dose of 150 mg there is a defenit urge to touch everything (including non-persons) around you, you are also more prone to tell the truth , the half truth , spill about the mixed up feelings you have for your nieces dog.

The euphoria lasts about 5 hours total , tempers off for a few hours more.
it's mostly a heady hallucinogenic (more interaction between your conscience and your subconscious).
but i've Seen moving paintings on the wall and people faces look different but in a nicer way.


Your ex.

(p.s. can't wait to try MMDA next month)
 
On 200 mg you are not very capable of doing much else than rolling around and touching things and people - and moaning. On 120 mg + 110 mg at T+5, the effects got pretty visual and more psychedelic than earlier trials. Considerable visual breathing - very little headfuck. Mind though, that a small amount of 2-DPMP had been ingested on the morning the day before this evening. BTW the days after a 3D experience one can be emotionally unstable. I have very little experience with MDMA, so I can't compare the magnitude of these side effects. But it can be pretty bad on 3D.

What I am considering now is combos to increase euphoria - since IMO 3D lacks on mental euphoria even though the physical euphoria is through the roof. 3D just whacks you over the head and leaves you there moaning with closed eyes. So adding some edge and wakefulnes could be interesting. First and foremost, I'm thinking about combining with either 4-FA or bk-MBDB. Did anyone try one of those combos and can tell me about their experience? Does anyone see a significant danger in these combos? (Other than frying axon terminals a'la MDMA)

One monkey tried 3D after taking some speed earlier during the day. The effects of the speed wasn't very pronounced and the 3D just mashed it down. Perhaps if you take both compounds at the same time, the effects may be different.
 
^ Well it's not going to resu;lt in the dodgy, misery inducing metabolite of MDA/MDMA ie alphamethyldopamine, so the emotional unstability in the days following is a bit of a surprise (never had anything like the capacity of MDA/MDMA to reduce me to abject misery a couple of days afterwards - which is the main reason I no longer consume any MDA derivative that potentially can end up as alphamethyldopamine; the misery is just too much to handle).

Can't see how any serotonogic compound is going to help much seeing how the compound in question is as active as MDA re 5HT activity. Where it fails miserably, compared with MDA etc is that it has piss poor dopaminergic activity, either release or reuptake inhibition. To fix that you'd really need a drug that acts on dopamine release/reuptake, preferably with very little 5HT activity. The best candidate (of the top of my head) would be amphetamine, but it's already been mentioned that such a combination has a big toxic potential (as well as raising possible neurotoxic effects)
 
MDMA and 4-FA: DA/5HT/NE

(The -X is in power of ten, i.e. 10^-X)


EC50

MDMA 2.0-7 / 5.8-8 / 8.6-8
4-FA 2.0-7 / 7.3-7 / 3.7-8

IC50

MDMA 1.4-6 / 7.2-7 / 6.6-7
4-FA 7.7-7 / 6.8-6 / 4.2-7

So I was thinking that 3D has a similar profile as MDMA, but higher values on DA and NE - i.e. more selective for 5HT. 4-FA likely has significantly lower values on DA and NE, but higher on 5HT. Suppose that they have similar bioavailability, and that someone takes roughly equal amount of both drugs. Then 4-FA should dominate DA and NE release, while 3D dominates 5HT release.

Or is my reasoning off?
 
would a mix of 3D & ghb or gbl suffice for the missing dopamine component?

Gamma-hydroxybutyrate (GHB), a four-carbon fatty acid and anaesthetic, is widely considered to be a relatively specific inhibitor of central dopamine (DA) release. The inhibitory effect of GHB on the latter is thought to occur as a consequence of its diminution of impulse flow in central dopaminergic neurons. However, a number of studies have recently reported that GHB primarily stimulates rather than inhibits central DA release, with any inhibitory effect produced of a modest and transitory nature. GHB has been and continues to be widely used as an important research tool largely because it is one of only a few drugs available that acts primarily on DA release. Consequently, it is important to determine whether GHB inhibits DA release as previously thought, or stimulates DA release, as more recently suggested. Following a critical review of the literature, the present report suggests that GHB does inhibit rather than stimulate presynaptic DA release in consonance with its behavioral and pharmacological activity. Recent in vivo studies indicating that GHB stimulates DA release were done under anaesthesia or in the presence of a high concentration of calcium. Both conditions have been found to spuriously enhance striatal DA release in vivo, which may account for the failure of some studies to observe an inhibitory effect of GHB on DA release in vivo. http://biopsychiatry.com/ghbdop.htm
Click to expand...
 
Definately not.

Also, it's not "missing" - depends on what you're after. I have a feeling it could become pretty trippy with more dopamine released. I'm also thinking is that some stimulation could alter the experience in a positive way - but, of course, I'm not sure. Also, we know very little about 3D and pharmacological data on it. It's mere speculation.
 
I never understood why a super euphoric drug was thought to inhibit DA release. Nice to see that it does actually cause increased release.
 
Hammilton said:
I never understood why a super euphoric drug was thought to inhibit DA release. Nice to see that it does actually cause increased release.
Click to expand...

I read the abstract in post 39 as saying GHB _did _inhibit release, except where there was high ca2+ or anaesthetic agents present which cause release themselves...
though I tend to think that meta analyses are not really a substitute for a well designed experiment, as they become only as strong as the worst experiment.

I got the impression whether oxybate enhances or inhibits da release would seem to depend more on the dose low doses seeming to enhance higher doses seeming to inhibit
 
You must log in or register to reply here.
Top