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Merge discussion[edit]

The case for the merge is very simple. Any discussion of the properties of a mixture of enantiomers is made simpler if the similarities and differences of the individual enantiomers are also discussed. The stuctures of the two isomers are already shown in the section Amphetamine#Physical and chemical properties! Stereochemistry is important, even in articles on dugs, c.f. thalidomide.

Regarding the comments below, there is an argument for maintaining Dextroamphetamine as a separate article, but it is weak, as the separation results in a lot of unneccesary duplication. If the separation is retained the reason for retaining it needs to be explained in this article. The article on Levoamphetamine is short enough to make the merge easy.

If something is controversial, a Wikipedia article should present the cases for all sides of the controversy. Hopefully at some time in the future new experimental evidence will provide the basis for a resolution. Petergans (talk) 10:35, 5 April 2015 (UTC)

Oppose – The two enantiomers of amphetamine, Dextroamphetamine and Levoamphetamine have somewhat different rates of metabolism and pharmacological effects. Hence these two articles need to be kept separate from each other. Furthermore optically pure Dextroamphetamine and Adderall (75% dextroamphetamine salts and 25% levoamphetamine salts) both are prescribed pharmaceutical products and each deserves its own article. Finally the racemic mixture as well as the optically pure enantiomers have different registration numbers and external database entries hence merging of the infoboxes in each of these articles becomes impractical. Boghog (talk) 09:04, 5 April 2015 (UTC)
  • Note: This issue has come up in the past on this and related pages (i.e., d-amph and Adderall). To summarize all the discussions, these pages haven't been merged mainly because there's a ton of distinct coverage of enantiopure d-amph vs a mixture of both isomers (Adderall) in medical literature and the lack of consensus regarding a merge of any of these articles. A lot of material from this page is transcluded to D-amph and Adderall simply because reviews generally conclude that there isn't much of a pharmacological or clinical difference between the two mixtures, resulting in analogous side effect profiles. Levoamphetamine exists partly because it would be odd to redirect it here while D-amph exists as a separate article and partly because there's distinct coverage of the racemate and L-amph in chemistry DBs.
    In a nutshell, this article is the primary parent article of levoamphetamine, dextroamphetamine, Adderall, and (for now) lisdexamfetamine, so the current relationship follows what is required in WP:SUMMARY STYLE. Most of the content on these pages (except levoamph) is either a slightly modified section transclusion from this page (via {{if pagename}} templates in this article) or a summary of this article and relevant parts of history and culture of substituted amphetamines. Levoamphetamine is sort of just off on its own because enantiopure L-amph hasn't been used as a pharmacotherapy in any country for anything for a while (i.e., it's not really a drug article so much as it is a chemistry article). Seppi333 (Insert  | Maintained) 09:31, 5 April 2015 (UTC)
Unfortunately there doesn't seem to be a clean way to organize these related articles. Drugs that differ by stereochemical composition unless they rapidly interconvert are distinct. (Note that the regulatory position is that different stereochemical compositions of drugs are assumed to be different unless they are proven equivalent.) There are two distinct stereochemical drug compositions of amphetamine represented by Adderall and Dextroamphetamine (Dexedrine/Dextrostat). Hence separate articles should be devoted to each. At the same time, much of the material in this article is duplicated in Adderall and Dextroamphetamine which I think is unfortunately. However I do not see a better solution. Boghog (talk) 10:33, 5 April 2015 (UTC)

I see that the merge tags have been removed. I am an inorganic chemist and don't feel qualified to do something about merging articles that are primarily pharmaceutical and biochemical. Nevertheless, the current situation is most unsatisfactory: there is considerable triplication in the three articles Levoamphetamine, Dextroamphetamine and adderall. I make these suggestions

  • This article becomes the "main" article of two
  • Merge Levoamphetamine with this article. This will be quite easy as the levo article is very short.
  • Merge Dextroamphetamine and adderall. These are essentially about the same substance. Aderall is just a trade name for a commercial pharmaceutical product containing the active ingredient..
  • Set up links so that the currently triplicated tables, diagrams and related text will be shown once, preferably in this article. The links could simply use the "main" template.

Petergans (talk) 09:09, 14 April 2015 (UTC)

There is no consensus for this merger. In fact, taking into account both the present and past discussions, the consensus is clearly against it. Contrary to what you have stated above, the argument against the merger is strong. Because different stereochemical isomers of a drug can have markedly different pharmacological effects, half-lives, toxicities, etc. drug regulatory agencies treat different drug stereoisomers as different. So should we. Boghog (talk) 09:38, 14 April 2015 (UTC)
"So should we" Not so. There is a world of difference between a regulatory agency and Wikipedia. The audience for WP is universal and herein lies the dilemma. Conventions in the fields of pharmacy and chemistry have diverged. Chemistry students will be surprised to see enantiomers given separate articles. In fact, functional differences between enantiomers only appear in a biochemical context. Stereoisomers, on the other hand, can have quite different chemical properties, e.g. maleic acid and fumaric acid.
It is disappointing to see responses to my proposal from two editors only. As a chemistry person, I would not have been part of the "consensus", had I known of the discussion. Where can a vote on the previous merge discussion be found?. Petergans (talk) 09:15, 18 April 2015 (UTC)
Chemistry ≠ Universe. The universe also includes pharmacology. Since the main interest in amphetamine is as a drug, pharmacological arguments trump chemical ones. The universe also includes regulatory authorities and Wikipedia drug articles must take into account the views of these authorities. The regulatory view is enantiomers of drugs are assumed to be different unless proven equivalent (e.g., the enantiomers rapidly epimerize). The enantiomers of amphetamine do not interconvert and have documented differences in pharmacology. It is also important to note that both enantiomers of amphetamine have pharmacological activity and that activity is similar but not identical. Hence merging Adderall (enantiomerically enriched dextroamphetamine that also contains pharmacologically active levoamphetamine) into dextroamphetamine doesn't make any sense. Levoamphetamine also contributes to the pharmacological activity of Adderall.
Functional differences between enantiomers only appear in a biochemical context – exactly. The main interest in the amphetamine article is its biological context, not its chemistry. Boghog (talk) 11:07, 18 April 2015 (UTC)
Going through all the archives, I can see that the suggestion of a merge of L-amph, D-amph, and amphetamine only ever came up once on the dextroamphetamine talk page; it never gained any traction though. This merge proposal was never mentioned anywhere else. Frankly, I'm extremely disinclined to go through with a merge because of the amount of work it would require on my part to rewrite certain sections (e.g., medical uses) to tailor it to a specific page. I also have no clue what to title a page that combines both D-amph and Adderall, as they're distinct pharmaceutical products with different licence data. Both of those pages should exist anyway, as they're distinct pharmaceutical entities.
The normal venue for discussing a merge like this would be WP:Proposed mergers, but WT:PHARM+WT:CHEMICALS would likely be a better place to discuss this issue. Seppi333 (Insert ) 11:19, 18 April 2015 (UTC)

Fair enough. I won't press this any further. Just two last (rhetorical) questions. i) Is the effect of a mixture of D- and L- isomers equal to the sum of the parts? ii) Is the D-isomer R- or S-? Petergans (talk) 19:35, 18 April 2015 (UTC)

In answer to your questions: (i) To a first approximation, yes. (ii) Levo is R and Dextro is S. Boghog (talk) 20:06, 18 April 2015 (UTC)

Reference notes[edit]

Why are the references grouped into "Reference notes" rather than linking to the citation directly? --Nbauman (talk) 11:27, 10 April 2015 (UTC)

It is done when there are four or more references that need to be cited. Using the citations directly results in an excessively long number of citations. You would have to ask Seppi333 why all these citations are needed however. Sizeofint (talk) 15:06, 10 April 2015 (UTC)
The first 4 refnotes cite entire paragraphs in the lead while the remainder group 4 or more references together for brevity, as Sizeofint stated. This was done because one individual complained incessantly about it during the FA nomination. Sentences which are cited by 4+ references are generally extremely broad statements which require multiple references to fully support the statement. Seppi333 (Insert ) 19:37, 10 April 2015 (UTC)

Epigenetic mechanisms reviews[edit]

  • Review[1]
  • Review[2]
  • Review - already cited in the article[3]
  • Review[4]
  • 1st paper on psychostimulant HDACi (class I) efficacy[5]
  • 1st paper on alcoholism HDACi (class I) efficacy[6]
  • 1st paper on nicotine HDACi (class I) efficacy[7]


  1. ^ McCowan TJ, Dhasarathy A, Carvelli L (February 2015). "The Epigenetic Mechanisms of Amphetamine" (PDF). J. Addict. Prev. (Avens Publishing Group) (S1): 1–7. ISSN 2330-2178. Retrieved 30 April 2015. Epigenetic modifications caused by addictive drugs play an important role in neuronal plasticity and in drug-induced behavioral responses. Although few studies have investigated the effects of AMPH on gene regulation (Table 1), current data suggest that AMPH acts at multiple levels to alter histone/DNA interaction and to recruit transcription factors which ultimately cause repression of some genes and activation of other genes. Importantly, some studies have also correlated the epigenetic regulation induced by AMPH with the behavioral outcomes caused by this drug, suggesting therefore that epigenetics remodeling underlies the behavioral changes induced by AMPH. If this proves to be true, the use of specific drugs that inhibit histone acetylation, methylation or DNA methylation might be an important therapeutic alternative to prevent and/or reverse AMPH addiction and mitigate the side effects generate by AMPH when used to treat ADHD. 
  2. ^ Walker DM, Cates HM, Heller EA, Nestler EJ (February 2015). "Regulation of chromatin states by drugs of abuse". Curr. Opin. Neurobiol. 30: 112–121. doi:10.1016/j.conb.2014.11.002. PMID 25486626. Studies investigating general HDAC inhibition on behavioral outcomes have produced varying results but it seems that the effects are specific to the timing of exposure (either before, during or after exposure to drugs of abuse) as well as the length of exposure 
  3. ^ Nestler EJ (January 2014). "Epigenetic mechanisms of drug addiction". Neuropharmacology. 76 Pt B: 259–268. doi:10.1016/j.neuropharm.2013.04.004. PMC 3766384. PMID 23643695. Short-term increases in histone acetylation generally promote behavioral responses to the drugs, while sustained increases oppose cocaine’s effects, based on the actions of systemic or intra-NAc administration of HDAC inhibitors. ... Genetic or pharmacological blockade of G9a in the NAc potentiates behavioral responses to cocaine and opiates, whereas increasing G9a function exerts the opposite effect (Maze et al., 2010; Sun et al., 2012a). Such drug-induced downregulation of G9a and H3K9me2 also sensitizes animals to the deleterious effects of subsequent chronic stress (Covington et al., 2011). Downregulation of G9a increases the dendritic arborization of NAc neurons, and is associated with increased expression of numerous proteins implicated in synaptic function, which directly connects altered G9a/H3K9me2 in the synaptic plasticity associated with addiction (Maze et al., 2010).
    G9a appears to be a critical control point for epigenetic regulation in NAc, as we know it functions in two negative feedback loops. It opposes the induction of ΔFosB, a long-lasting transcription factor important for drug addiction (Robison and Nestler, 2011), while ΔFosB in turn suppresses G9a expression (Maze et al., 2010; Sun et al., 2012a). ... Also, G9a is induced in NAc upon prolonged HDAC inhibition, which explains the paradoxical attenuation of cocaine’s behavioral effects seen under these conditions, as noted above (Kennedy et al., 2013). GABAA receptor subunit genes are among those that are controlled by this feedback loop. Thus, chronic cocaine, or prolonged HDAC inhibition, induces several GABAA receptor subunits in NAc, which is associated with increased frequency of inhibitory postsynaptic currents (IPSCs). In striking contrast, combined exposure to cocaine and HDAC inhibition, which triggers the induction of G9a and increased global levels of H3K9me2, leads to blockade of GABAA receptor and IPSC regulation.
  4. ^ Biliński P, Wojtyła A, Kapka-Skrzypczak L, Chwedorowicz R, Cyranka M, Studziński T (2012). "Epigenetic regulation in drug addiction". Ann. Agric. Environ. Med. 19 (3): 491–496. PMID 23020045. For these reasons, ΔFosB is considered a primary and causative transcription factor in creating new neural connections in the reward centre, prefrontal cortex, and other regions of the limbic system. This is reflected in the increased, stable and long-lasting level of sensitivity to cocaine and other drugs, and tendency to relapse even after long periods of abstinence. These newly constructed networks function very efficiently via new pathways as soon as drugs of abuse are further taken ... In this way, the induction of CDK5 gene expression occurs together with suppression of the G9A gene coding for dimethyltransferase acting on the histone H3. A feedback mechanism can be observed in the regulation of these 2 crucial factors that determine the adaptive epigenetic response to cocaine. This depends on ΔFosB inhibiting G9a gene expression, i.e. H3K9me2 synthesis which in turn inhibits transcription factors for ΔFosB. For this reason, the observed hyper-expression of G9a, which ensures high levels of the dimethylated form of histone H3, eliminates the neuronal structural and plasticity effects caused by cocaine by means of this feedback which blocks ΔFosB transcription 
  5. ^ Kennedy PJ, Feng J, Robison AJ, Maze I, Badimon A, Mouzon E et al. (April 2013). "Class I HDAC inhibition blocks cocaine-induced plasticity by targeted changes in histone methylation". Nat. Neurosci. 16 (4): 434–440. doi:10.1038/nn.3354. PMC 3609040. PMID 23475113. While acute HDAC inhibition enhances the behavioral effects of cocaine or amphetamine1,3,4,13,14, studies suggest that more chronic regimens block psychostimulant-induced plasticity3,5,11,12. ... The effects of pharmacological inhibition of HDACs on psychostimulant-induced plasticity appear to depend on the timecourse of HDAC inhibition. Studies employing co-administration procedures in which inhibitors are given acutely, just prior to psychostimulant administration, report heightened behavioral responses to the drug1,3,4,13,14. In contrast, experimental paradigms like the one employed here, in which HDAC inhibitors are administered more chronically, for several days prior to psychostimulant exposure, show inhibited expression3 or decreased acquisition of behavioral adaptations to drug5,11,12. The clustering of seemingly discrepant results based on experimental methodologies is interesting in light of our present findings. Both HDAC inhibitors and psychostimulants increase global levels of histone acetylation in NAc. Thus, when co-administered acutely, these drugs may have synergistic effects, leading to heightened transcriptional activation of psychostimulant-regulated target genes. In contrast, when a psychostimulant is given in the context of prolonged, HDAC inhibitor-induced hyperacetylation, homeostatic processes may direct AcH3 binding to the promoters of genes (e.g., G9a) responsible for inducing chromatin condensation and gene repression (e.g., via H3K9me2) in order to dampen already heightened transcriptional activation. Our present findings thus demonstrate clear cross talk among histone PTMs and suggest that decreased behavioral sensitivity to psychostimulants following prolonged HDAC inhibition might be mediated through decreased activity of HDAC1 at H3K9 KMT promoters and subsequent increases in H3K9me2 and gene repression. 
  6. ^ Simon-O'Brien E, Alaux-Cantin S, Warnault V, Buttolo R, Naassila M, Vilpoux C (July 2015). "The histone deacetylase inhibitor sodium butyrate decreases excessive ethanol intake in dependent animals". Addict Biol 20 (4): 676–689. doi:10.1111/adb.12161. PMID 25041570. Altogether, our results clearly demonstrated the efficacy of NaB in preventing excessive ethanol intake and relapse and support the hypothesis that HDACi may have a potential use in alcohol addiction treatment. 
  7. ^ Castino MR, Cornish JL, Clemens KJ (April 2015). "Inhibition of histone deacetylases facilitates extinction and attenuates reinstatement of nicotine self-administration in rats". PLoS ONE 10 (4): e0124796. doi:10.1371/journal.pone.0124796. PMC 4399837. PMID 25880762. treatment with NaB significantly attenuated nicotine and nicotine + cue reinstatement when administered immediately ... These results provide the first demonstration that HDAC inhibition facilitates the extinction of responding for an intravenously self-administered drug of abuse and further highlight the potential of HDAC inhibitors in the treatment of drug addiction. 

@Boghog: This journal isn't pubmed indexed, so I can't use your cite tool to autoformat this citation; should the journal title be converted to sentence case? I'm also not really sure what to do about the issue parameter, since S(1) is used in the journal and (S1) is as much as I can get in the template output. Seppi333 (Insert ) 07:16, 30 April 2015 (UTC)

Hi Seppi. Looks fine as is. I assume "S1" is short for "Supplement 1". Either will work as the |issue= value. Ideally the journal title should in title case. I know that tool presently does not do this. I will see if I can tweak it to do this. Boghog (talk) 09:15, 30 April 2015 (UTC)
I feel stupid for not typo checking what I wrote... what I meant to ask was should the article title – |title=The Epigenetic Mechanisms of Amphetamine – be converted to sentence case? So far as I can tell, all the current cite journal templates in the amphetamine article have the title parameter in sentence case. Seppi333 (Insert ) 14:13, 30 April 2015 (UTC)

These reviews + primary research papers actually suggest that chronic pretreatment (not concurrent use) with HDAC class I inhibitors (e.g., butyric acid/sodium butyrate) would be an effective drug treatment for stimulant (cocaine/amphetamine) all addictions by promoting NAcc G9a expression... Face-surprise.svg Seppi333 (Insert ) 23:17, 7 May 2015 (UTC)


Article states "Cochrane reviews on the use of amphetamine following a stroke or acute traumatic brain injury indicated that it may improve recovery, but further research is needed to confirm this"

  • But the Cochrane reviews conclusions is "At present, too few patients have been studied to draw any definite conclusions about the effects of amphetamine treatment on recovery from stroke" [1]
  • The second review found just animal evidence [2]
  • And the third ref states "On the basis of current findings amphetamine after brain injury cannot be recommended" [3]

First of all this is research and not clinical use and thus should go at the end in a research section. Second we have misrepresented the sources. Doc James (talk · contribs · email) 12:37, 4 June 2015 (UTC)

Then delete the sentence. Seppi333 (Insert ) 12:38, 4 June 2015 (UTC)
Those were good sources. The content just needs to be reworded to acurate reflect the sources and placed in a second on research. Doc James (talk · contribs · email) 12:41, 4 June 2015 (UTC)

This is also research "A review of clinical trials that used lisdexamfetamine as an adjunct therapy with a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) for treatment-resistant depression indicated that this adjunct therapy is no more effective than the use of an SSRI or SNRI alone.[1] This observation is consistent with previous findings that serotonin–norepinephrine–dopamine reuptake inhibitors (SNDRIs) demonstrate no additional efficacy over SSRIs and SNRIs for the treatment of major depressive disorder.[1]" Doc James (talk · contribs · email) 12:41, 4 June 2015 (UTC)

What's your concern with that content? Seppi333 (Insert ) 12:44, 4 June 2015 (UTC)
It should go under research. It is not a medical use. As should a proper summary of the previous sources. It is important that their is not good human evidence for use in stroke and that it is not recommended in brain trauma. It is interesting that their is some tentative animal data. Doc James (talk · contribs · email) 12:52, 4 June 2015 (UTC)
If I had added a preclinical research section, it would be enormous to comply with the FA comprehensiveness criteria (e.g., the medications in the reviews in the above section), which is why I never included one when writing this article. I'm okay with putting the SSRI statements in a research section though. Seppi333 (Insert ) 13:03, 4 June 2015 (UTC)
It just needs to be the highlights. A comprehensive list here would be undue weight. One could have a subpage if people are interested. Doc James (talk · contribs · email) 19:22, 4 June 2015 (UTC)

concur with DocJames, logic indicates it should go under research section --Ozzie10aaaa (talk) 13:09, 4 June 2015 (UTC)

I've deleted the remaining content from this page. It's now only in the LDX article. Seppi333 (Insert ) 17:55, 4 June 2015 (UTC)


  1. ^ a b Dale E, Bang-Andersen B, Sánchez C (May 2015). "Emerging mechanisms and treatments for depression beyond SSRIs and SNRIs". Biochem. Pharmacol. 95 (2): 81–97. doi:10.1016/j.bcp.2015.03.011. PMID 25813654. 

Add table of potency of marketed amphetamines / "substituted amphetamine" term[edit]

There seems to be confusion about the comparative potency of marketed amphetamines. I seek comments on the following table that I created. I would add citations to the molecular weights (though they seem self evident from the formulas). The remainder is simple arithmetic and needs no citations. Do the formulas need citations?

I believe this table fits here and on the dextroamphetamine page. Forgive me if the addition is inappropriate to an FA class article.

Amphetamine base in marketed amphetamine medications
drug / drug component formula molecular weight amphetamine base amphetamine base
(g/mol) (percent) (30 mg dose)
total base total dextro- levo- dextro- levo-
dextroamphetamine sulfate (Dexedrine®) (C9H13N)2•H2SO4
22.0 mg
mixed amphetamine salts (Adderall®)
14.2 mg
4.5 mg
25% dextroamphetamine sulfate (C9H13N)2•H2SO4
25% amphetamine sulfate (C9H13N)2•H2SO4
25% dextroamphetamine saccharate (C9H13N)2•C6H10O8
25% amphetamine aspartate monohydrate (C9H13N)•C4H7NO4•H2O
lisdexamfetamine dimesylate (Vyvanse®) C15H25N3O•(CH4O3S)2
8.9 mg
Mixed amphetamine salts base percentage = sum of component values / 4.

Approximate equivalency: 30 mg dextroamphetamine ≈ 35 mg Adderall* ≈ 75 mg lisdexamfetamine (Vyvanse).

* assuming levoamphetamine and dextroamphetamine are equipotent.

Box73 (talk) 02:37, 18 August 2015 (UTC)


May be worth combining the tables, but otherwise the info looks good. Thanks. Seppi333 (Insert ) 04:29, 20 August 2015 (UTC)
Box73, the table above is ok. The text beneath it is not. The use of the pronoun "I" is not encyclopedic and shouldn't be in a note. This also shouldn't be transcluded in, as there's no reason for a template to exist solely to transclude a table to 2 articles. I've substituted the table with the MOS fixes; please do not re-add that content. Seppi333 (Insert ) 12:46, 30 August 2015 (UTC)
Small world Seppi. Hey thanks for your insightful comments. I find the one about the personal pronoun OK and have revised it. Regarding the template, I am not clear on the minimum number of pages required for a transcluded template. Could you offer a link? My sense is that even 2 articles are reasonable.
I reverted your modifications before reading your warning. My read of MOS is different than yours and let's discuss the matter here before making further changes.
I think you're reading too much into the MOS. You were OK with presenting relative potency. I'm using equivalent doses to represent relative potency because it is easier to understand. I'm not offering advice, instruction or "how to"s. Potency is relevant to such articles. Look at the opioid comparison table at opioid or better yet the morphine centric table at equianalgesic. You are of course familiar with the benzodiazepines page, since you've weeded out all references to dosing there, but the remaining table gives onset and half life just like you would find in the Merck Manual and other medical references and textbooks. Seems to me the MOS says, "Wikipedia is not a ... textbook".
There's another way. Loosen up a bit. Remember MOS also says: "Use common sense in applying it" and "If a rule prevents you from improving or maintaining Wikipedia, ignore it." WP:IAR There's a forest hidden amongst all these trees.
I'm considering the substituted amphetamines issue and will respond to that soon.Box73 (talk) 16:14, 30 August 2015 (UTC)

──────────────────────────────────────────────────────────────────────────────────────────────────── A unitless relative potency comparison is fine and this is made in this article when comparing the CNS/peripheral effects of the enantiomers; adding the mass makes it dosing information. The list of benzodiazepines deletions occurred as a result of 2 dialogues at WT:MED (now archived) and WT:PHARM. As a side issue, the potency of the two enantiomers differ by up to a factor of 4; they're not equivalent. Seppi333 (Insert ) 16:59, 30 August 2015 (UTC)

So what? It isn't offering advice, instruction or "how to"s. Look it, I'm not listing FDA approved doses, doses recommended by Joseph Biederman, controversy over absolute vs symptom based vs weight based dosing, issues of underdosing adults, issues of asymmetrical dosing, comparing recommended doses in ADHD vs narcolepsy vs weight reduction vs off label. I could simply show the percentage of base in each marketed formulation but this is a little abstract for the average reader. Translating this into equivalent doses makes the relative potency tangible without getting into actual dosing instruction or guidelines. WP:IAR How is this not improving the articles?
You may be both right and wrong about the potency of the enantiomers. In some types of ADHD, levoamphetamine is reported to be as effacious as dextroamphetamine. Further there is evidence that the levoamphetamine in Adderall improves the effects of the dextroamphetamine portion. This is beyond the obvious. Finally, practice guidelines tend to equate dextroamphetamine and Adderall. Being the fraction of levoamphetamine is ~25% I opted to show it as equipotent and note this. Would you suggest a better factor to use? Better wording of the note?
I want to compliment you on the graphics you created of the axon terminals.
I am open to discussing changes such as rationale for substs and MOS issues.Box73 (talk) 00:14, 31 August 2015 (UTC)
I'm not going to discuss this any longer. I told you that your recent edits are providing dosing info, pointed you to a guideline, and pointed you to an identical precedent for providing data on this (i.e., the WT:MED thread and WT:PHARM thread mentioned above). That entire column is uncited and the Adderall entry is based on your incorrect assumption - the latter point is WP:Original research. I've asked for a wider input here in this thread at WT:MED. Also, IAR isn't a policy you use to re-add content (special:diff/678603025/678686571) during a content dispute. Seppi333 (Insert ) 03:46, 31 August 2015 (UTC)
as Seppi333 has indicated dosing information (of any kind)should not be provided--Ozzie10aaaa (talk) 10:06, 31 August 2015 (UTC)

WikiProject Chemicals quality rating[edit]

Why does the banner for the Chemicals WikiProject show this article as A-class when it is FA-class? The parameter is FA in the template. Sizeofint (talk) 03:21, 18 August 2015 (UTC)

WP:CHEM doesn't use FA ratings - don't know why. Other FA chem articles have the same rating; e.g., see Talk:Acetic acid. Seppi333 (Insert ) 04:30, 20 August 2015 (UTC)