I'm trying to purchase a compound from a lab and am hitting road blocks where I need more info.
The compound I'm looking to acquire is Vorinostat. There are many threads over the years here where people have experimented with it as an HDAC inhibitor and used it for fear extincition to great success. Very interesting stuff if you read up on on the existing threads.
I attempted to purchase from one lab using my own personal info. email address, and residential shipping and they asked me my intended purpose for the substance. I replied vaguely "research purposes" and they replied that they didn't recognize me as valid biomed institute and that I need to supply further evidence.
My question, is anyone familiar with the requirement to purchase from a lab? Is there a biomed institute database labs reference?
I have a couple options to move forward:
I have a start up in Plastic Engineering I could use to purchase through so it looks more official, with website, real address, etc. But this is not a "biomed institution". Will this be a problem? How deep do labs vet their purchasers? Will I need to provide some type of intended experimental documentation.
Or, I could also set up a shell website and company for bio medical research to move forward. But if there is an index of biomed institutions that labs reference, I wouldn't pass, so I have the same questions as above.
Please advise. Also if anyone is interested in a group buy of Vorinostat let me know.
Requirement to Purchase from a Lab; Vorinostat.
Started by
TeaCupGuineaPig
, Jun 23 2020 06:45 PM
vorinostat research chemicals lab
4 replies to this topic
#1
Posted 23 June 2020 - 06:45 PM
#2
Posted 24 June 2020 - 04:59 AM
Or you could try out Valproate which is much easier to get and does exactly the same thing with more nasty side effects.
#3
Posted 25 June 2020 - 01:18 AM
I'm also interested in a source.
#4
Posted 25 June 2020 - 08:18 PM
Tributyrin is available on amazon now. (Butycaps or Healus)
https://www.nature.c...1279?proof=true
"Efforts have also been directed toward developing drugs that can easily cross the blood–brain barrier and that exhibit good biological activity and oral bioavailability for use in humans. Butyrates in particular readily cross the blood–brain barrier "
"ROLE OF THE AMYGDALA IN PERSISTING PTSD SYMPTOMS
The biological basis for the development of PTSD is not yet known, but studies of Pavlovian fear conditioning suggest that persistent traumatic memories are likely established through multiple phases that involve a transition from recent to remote memories. Although PTSD has been associated with molecular changes in the hippocampus and the prefrontal cortex, the persistent symptoms of PTSD are most closely associated with alterations in the amygdala (Johnson et al, 2012), a region that has been implicated in the storage of remote memories for cued fear (Dudai, 2004; Gale et al, 2004; Medina et al, 2008). The transition of memories to a stable form is important for the persistence of PTSD and it is thus critical to understand the molecular mechanisms that underlie such memory stability in order to identify potential targets for pharmacological treatment. A variety of recent studies have used fear conditioning to explore the hypothesis that changes in the amygdala support long-lasting memories (Debiec et al, 2011; Gale et al, 2004; Monsey et al, 2011). These findings imply that a tangible persisting molecular mark in the amygdala must underlie the preservation of remote fear memory. There is now evidence for epigenetic changes in the amygdala during consolidation and reconsolidation of cued fear (Maddox and Schafe, 2011; Monsey et al, 2011), but no studies have examined the maintenance phase of cued fear memory. The potential involvement of DNA methylation in the maintenance of remote memory in the amygdala is an important directive for future research.
The advent of sophisticated molecular, genetic, and cellular techniques has lent itself to a relatively deep understanding of how memories are initially formed. By stark contrast, however, is our limited understanding of how these same memories are maintained by the brain (Dudai, 2004; Medina et al, 2008; Sacktor, 2008). While epigenetic blockade can lead to changes in fear learning, future studies need to focus on the mechanisms through which already learned fear responses are stored in order to understand the basis for the persistent fear observed in PTSD. We need to shift toward an understanding of the mechanisms involved in maintaining the pathological fear memory over time."
https://www.nature.c...1279?proof=true
"Efforts have also been directed toward developing drugs that can easily cross the blood–brain barrier and that exhibit good biological activity and oral bioavailability for use in humans. Butyrates in particular readily cross the blood–brain barrier "
"ROLE OF THE AMYGDALA IN PERSISTING PTSD SYMPTOMS
The biological basis for the development of PTSD is not yet known, but studies of Pavlovian fear conditioning suggest that persistent traumatic memories are likely established through multiple phases that involve a transition from recent to remote memories. Although PTSD has been associated with molecular changes in the hippocampus and the prefrontal cortex, the persistent symptoms of PTSD are most closely associated with alterations in the amygdala (Johnson et al, 2012), a region that has been implicated in the storage of remote memories for cued fear (Dudai, 2004; Gale et al, 2004; Medina et al, 2008). The transition of memories to a stable form is important for the persistence of PTSD and it is thus critical to understand the molecular mechanisms that underlie such memory stability in order to identify potential targets for pharmacological treatment. A variety of recent studies have used fear conditioning to explore the hypothesis that changes in the amygdala support long-lasting memories (Debiec et al, 2011; Gale et al, 2004; Monsey et al, 2011). These findings imply that a tangible persisting molecular mark in the amygdala must underlie the preservation of remote fear memory. There is now evidence for epigenetic changes in the amygdala during consolidation and reconsolidation of cued fear (Maddox and Schafe, 2011; Monsey et al, 2011), but no studies have examined the maintenance phase of cued fear memory. The potential involvement of DNA methylation in the maintenance of remote memory in the amygdala is an important directive for future research.
The advent of sophisticated molecular, genetic, and cellular techniques has lent itself to a relatively deep understanding of how memories are initially formed. By stark contrast, however, is our limited understanding of how these same memories are maintained by the brain (Dudai, 2004; Medina et al, 2008; Sacktor, 2008). While epigenetic blockade can lead to changes in fear learning, future studies need to focus on the mechanisms through which already learned fear responses are stored in order to understand the basis for the persistent fear observed in PTSD. We need to shift toward an understanding of the mechanisms involved in maintaining the pathological fear memory over time."
#5
Posted 06 December 2020 - 05:11 AM
Does anyone have more information on acquiring Vorinostat? I want to use it to reverse damage from sedative use. I would like to participate in a group buy.
Also tagged with one or more of these keywords: vorinostat, research chemicals, lab
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