New ingredient in Stimulant X.
Discuss.
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12-09-2010, 12:17 PM #1
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12-09-2010, 03:51 PM #2
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12-09-2010, 04:02 PM #3
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12-09-2010, 04:06 PM #4
Its something they were working on the last year I was with AX. Its really good. Before applying for a patent it went through a rigorous DSHEA compliance review.
Basically its medium on energy, but great on focus and mood. From my understanding this compound is what PEA converts into in the brain. It's also a pretty powerful neuro-protectant. They were trying to research what they could use in replacement of 1,3 Dymethl (geranium), and this was the one ingredient across the board testers loved over 1,3, as it is super clean, no crash and puts you in the zone.SmashBrand Marketing & Design
www.SmashBrand.com
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12-09-2010, 05:47 PM #5
Very interesting!
Would love to see some articles on it if anyone has any. If it's as awesome as you claim it to be then this would most certainly replace many 1,3 D products as it's a highly debated ingredient right now. Banned by the NCAA I believe. It specifically is not but it's chemically related and would cause a false positive, however, still a positive and something you don't want to go through to get fixed.NSCA CSCS
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12-09-2010, 06:40 PM #6
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12-09-2010, 07:06 PM #7
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12-09-2010, 08:11 PM #8
PEA doesn't "turn into" tetrahydroisoquinolines in the brain. Is "Dr.D" still your formulator? I'm surprised people can just take things without even reading up on them...1-Methyl-1,2,3,4-tetrahydroisoquinoline crosses the blood brain barrier and easily increases the brain's concentration of it's endogenous form by 4x. 1,2,3,4-tetrahydroisoqulnolin is the "bad" thing that people consider when discussing parkinson's, and there is the possibility that isoquinoline can be reduced back into 1,2,3,4-tetrahydroisoqulnoline. Not only that, but 1-Methyl-1,2,3,4-tetrahydroisoquinoline isn't easily metabolized either...the funny thing is, a metabolite of it is methyl-3,4-dihydroisoquinoline, a precursor to isoquinoline...the metabolite of the "bad" thing.
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12-09-2010, 08:16 PM #9
I don't have a formulator.
Maybe I used the wrong word, "convert." 1-Methyl-1,2,3,4-tetrahydroisoquinoline (1MeTIQ), an endogenous parkinsonism-preventing substance, is enzymatically synthesized from 2-phenylethylamine (PEA) in the brain. "Institute of Pharmaceutical Sciences"SmashBrand Marketing & Design
www.SmashBrand.com
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12-09-2010, 08:31 PM #10
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12-09-2010, 08:37 PM #11
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12-09-2010, 08:37 PM #12
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12-09-2010, 08:40 PM #13
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12-09-2010, 08:43 PM #14
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member since 2006
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it seems you've been very helpful in your stint here
heres another former AX tard doing the samething:
http://forum.bodybuilding.com/showpo...3&postcount=34
people here arent stupid
no ones forgotten about you or that crap company
or shall we bump all of Dr P's threads?Sponsored MAN Nolvadren XT Log: http://forum.bodybuilding.com/showthread.php?t=148109363
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12-09-2010, 08:48 PM #15
Guy, it no secret that 1,3 Dymethyl is in the hot seat. Nutritional orgs are talking about it, WADA is talking about it (banned it), FDA is talking about it. Its been in the news. So...there has been plenty of talk of it being banned. I am pretty sure that is Aaron asking about it. I don't see him bashing the ingredient. I like 1,3Dymethl, but I don't think its going to be around for that long. The only thing I don't like about it is the crash. I think its safe and effective and should be able to be sold, however I know the government and other organizations do not feel that way.
Maybe its around for another two years, or maybe OCI comes in three months and shuts it for being adulterated (eg they believe it is not DSHEA)...SmashBrand Marketing & Design
www.SmashBrand.com
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12-09-2010, 09:00 PM #16
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12-09-2010, 09:05 PM #17
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12-09-2010, 09:41 PM #18
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i was simply asking for peoples opinion on when its going to be banned, i think its a great ingredient and have nothing bad to say about it, i just wanted to know how much longer it will be around, i even pmed jacob, dan and matt asking them the same thing(you can ask them if u want to verify) edit- ooo your a USPlabs rep huh, well ask jacob we had a good convo on it
If any section deserves to be void of any drama its the sceince section.
im looking forward to Nuerons opinion on the ingredient, but while were here, what do yyou think PTB, your usually pretty insightful.Last edited by Adawg4929; 12-09-2010 at 10:02 PM.
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12-09-2010, 09:59 PM #19
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12-09-2010, 11:43 PM #20
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12-10-2010, 05:43 AM #21
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12-10-2010, 08:42 AM #22
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There are a few purported mechanisms here and they're mostly indirect through enzyme interaction and direct through receptor occupation. These effects are tissue specific as shown by its co-administrative synergistic effect with MK-801, a direct central dopamine releasing agent, on dopamine release in the rat prefrontal cortex. [1, 2] However, it has also been shown to inhibit agonist-induced excitation in the frontal lobe. [3] In vivo, it would be mildly dopaminergic through its direct mechanisms and broadly sympathomimetic through its facilitated exchange activity and through its COMT and MOAB inhibitory action. (Fig. 1) It also has been shown to be a potentially mild analgesic on its own in rats.
1-MeTIQ and N-MeTIQ given at doses of 50 mg=kg, in the first phase of their
action, produced a slight and not significant decrease of nociceptive threshold
but 90 min after the injection both compounds produced an analgesic effect,
which lasted for at least 150 min. However, the significance of the effect of
N-MeTIQ was borderline (P < 0.1)
The neuroprotective effects are direct through NMDA receptor antagonism and this is demonstrated through its ability to attenuate agonist-induced locomotion. [1] The direct central effects would be significant due to its ability to cross the blood-brain barrier, while the peripheral effects would be potentiated by psychoactive/peripherally active MAOB substrates (e.g. phenethylamine, tyramine).
Its structural limitations also affect its ability to interact with 5-HT receptors. Specific group and location substitutions facilitate all effective binding potentials of TIQ derivatives. [5] Substitutions are necessary to change the ligand's orientation in the binding pocket and unsubstituted 1Me-TIQ's action in vivo indicates that it either has antagonistic activity at 5-HT2a, alpha-1 (adrenergic), or both. [1]
Fig. 1. 1MeTIQ, at a 50mg/kg dose, significantly affects dopamine to HVA metabolism in vivo (in rats). This is suggestive of both MAOB and COMT inhibition.
Homovanillic acid (HVA)
1. http://www.springerlink.com/content/...3/fulltext.pdf
2. http://www.ncbi.nlm.nih.gov/pubmed/16897599
3. http://lib.bioinfo.pl/pmid:16515537
4. http://www.springerlink.com/content/...l/fulltext.pdf
5. http://dissertations.ub.rug.nl/FILES...rmeulen/c3.pdf
7. http://www.freepatentsonline.com/6596734.htmlLast edited by PinchTheBear; 12-11-2010 at 07:44 AM.
Driven Sports
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12-10-2010, 11:59 AM #23
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12-10-2010, 12:13 PM #24
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12-10-2010, 01:13 PM #25
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12-10-2010, 05:34 PM #26
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12-11-2010, 04:56 PM #27
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12-11-2010, 05:30 PM #28
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Strong post PinchTheBear~
Originally Posted by http://www.ncbi.nlm.nih.gov/pubmed/16897599
Would this be the cause of the 10/10 focus that BigSmith was speaking of?Personal Journal
http://forum.bodybuilding.com/showthread.php?t=155545753
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12-11-2010, 05:51 PM #29
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Thanks, man.
The inhibition is likely due to extra-neuronal 5-HT and NE respectively, not selective enzyme inhibition. So, in other words, the inhibition of NE metabolism is due to *******'s effect on re-uptake and the possibility that 1Me-TIQ occupies the transporter without causing an inhibitory conformational change. The changes in 5-HT metabolism are indicative of 1Me-TIQ's direct effects on 5-HT2a. That's source 2 in my post (forgive my ignorance if that's where you got it anyway).
The effects on NE are likely only relevant with *******, but the 5-HT2a effects would be independent.Driven Sports
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12-11-2010, 05:57 PM #30
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