Talk:Guanfacine

Why not state what the cited reference states?

Just my take maybe but when an editor makes claims, (especially in a science article, especially in one about a drug) then cites an acceptable reference BUT the claim isn't substantiated by that reference, then that claim should be edited out. The 'claim' I'm referring to in this article on guanfacine is: "Its side-effects are dose dependent, with frequency and severity almost disappearing at doses of 2 mg and less." The cited reference DOES NOT make this claim. The reference cited (British Journal of Clinical Pharmacology (1980) 10 (Suppl 1): 157S–164S) states, in part:

"The overall frequencies of dryness of the mouth and sedation were 60 and 33%, respectively. At the end of one year of treatment these figures dropped to 15 and 5.7%. Further untoward reactions in the first and second year, respectively, were orthostatic disturbances (15 and 6.5%), constipation (14 and 4.1%), male sexual dysfunction (4.6 and 0.6%), insomnia (5.5 and 2.2%), and sweating (5.3 and 1.7%).

The frequency and severity of side-effects were dose dependent and related to increases in dosage. Doses of 2 mg and lower caused practically no dryness of the mouth."

So we see where his wording came from, but what is the value of exaggerating? — Preceding unsigned comment added by 69.127.76.38 (talk) 20:41, 19 November 2011 (UTC)

The sentence "Guanfacine can offer a synergistic enhancement of stimulants such as amphetamines and methylphenidate for treating ADHD, and in many cases can also help control the side effect profile of stimulant medications" is also not supported by the cited reference Aaiqbal (talk) 16:11, 28 September 2023 (UTC)

Mixed rhesus monkey results

http://www.ncbi.nlm.nih.gov/pubmed/21883531

Although the alpha-2 agonist guanfacine has been reported to improve working memory in aged primates, it has been difficult to assess the extent to which these improvements may be related to drug effects on attention and/or memory processes involved in task performance. The present study investigated effects of guanfacine on specific attention and memory tasks in aged monkeys. Four Rhesus monkeys...performed a sustained attention (continuous performance) task and spatial working memory task (self-ordered spatial search) that has minimal demands on attention. Effects of a low (0.0015 mg/kg) and high (0.5 mg/kg) dose of gunafacine were examined. Low-dose guanfacine improved performance on the attention task [i.e. decreased omission errors by 50.8 ± 4.3% (P = 0.001) without an effect on commission errors] but failed to improve performance on the spatial working memory task. The high dose of guanfacine had no effects on either task.

So it's dose-dependent with a U-curve, and only affects attention? --Gwern (contribs) 16:17 6 September 2011 (GMT)

Two studies present evidence that guanfacine does not improve PTSD symptoms

Though this Wikipedia article claims that guanfacine can help treat PTSD, only one study is cited to support that statement, which seems to be in some dispute. The following studies found no effect of guanfacine on PTSD symptoms, and in one study it also produced unwanted side effects.

Nevlan et al. 2006, Am. J. Psychiatry "No improvement of posttraumatic stress disorder symptoms with guanfacine treatment" http://www.ncbi.nlm.nih.gov/pubmed/17151174

Davis et al. 2008, Psychopharmacol Bull. "A placebo-controlled trial of guanfacine for the treatment of posttraumatic stress disorder in veterans" http://www.ncbi.nlm.nih.gov/pubmed/18362867 — Preceding unsigned comment added by 129.74.118.198 (talk) 22:24, 9 February 2012 (UTC)

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The two pictures depict two different substances

Look where the three nitrogen atoms are. On the ball and stick model, it looks like

C=N-C(-NH2)(-NH2)

Wheras the skeletal model shows

C-NH-C(-NH2)(=NH)

These are two different substances 13:32, 29 May 2018 (UTC) — Preceding unsigned comment added by Beautron7 (talk • contribs) PS. The Person Who Is Editing This Also Has A Guanfacine Prescription.

Here is the AHFS ref

https://web.archive.org/web/20180115071707/https://www.drugs.com/monograph/guanfacine.html

Ref says "Produces a moderate reduction in symptoms of ADHD†; stimulants (e.g., methylphenidate, amphetamines) remain the drugs of choice for the management of ADHD because of their greater efficacy compared with that of other drugs (e.g., guanfacine).9" Doc James (talk · contribs · email) 14:41, 7 April 2020 (UTC)

Possible errors in 'Drug Synthesis' section image.

I've spotted at least one definite error in the image showing two different synthesis methods for guanfacine HCl. The image is here: [[1]] The name of the starting compound in the lower left corner is shown as '2,6-dichlorophenylbenzyl cyanide,' this should be '2,6-dichlorobenzyl cyanide.'

I also believe this synthesis method may not result in the supposed end product, guanfacine HCl. As far as I can tell, the method is from a Chinese patent: https://patents.google.com/patent/CN103058890A/en The relevant text describing the synthesis method is: 'Method four: 2,6-dichloro benzyl cyanide is dissolved in ethanol, adds sodium ethylate, stirring at room 30min, then add ethyl formate, stirring at room 4h gets α-aldehyde radical-2, the 6-dichloro benzyl cyanide, be dissolved in ethanol, after the adding sodium ethylate stirs 30min, add Guanidinium hydrochloride, stirring at room 4h, vacuum filtration is removed inorganic salt, gets α-guanidine methylene radical-2,6-dichloro benzyl cyanide solution adds concentrated hydrochloric acid in solution, 80 ℃ of heated and stirred 4h, concentrated, naturally cool to the room temperature crystallization, vacuum filtration gets Guanfacine Hydrochloride.'

I tried to do a quick arrow-pushing sketch of the reaction to discern the mechanism, the image is attached.

After hydrolysis with aqueous HCl, the 'α-guanidine methylene radical-2,6-dichloro benzyl cyanide' should undergo decarboxylation, yielding a product with the wrong oxidation state on the carbon to which the guanidine residue is attached. This may be a typo or error in the patent text, as diethyl carbonate might give the appropriate product. I can't see any way the described reaction conditions would achieve a final transformation to guanfacine HCl.

Dreymond (talk) 16:11, 20 September 2021 (UTC)

I agree that there is something not right (or at the very least, something unusual that needs explanation to be useful) about this image. So I have removed it for now. Reba16 (talk) 15:17, 11 December 2021 (UTC)

Use of guanfacine as treatment in cases of hyperadrenergic PoTS

Guanfacine works to control postural tachycardia caused by excess levels of norepinephrine by activating alpha-2 adrenergic receptors in the brain thereby suppressing the production of norepinephrine and depressing the sympathetic nervous system as a result 199.59.86.127 (talk) 22:00, 4 June 2022 (UTC)

TAAR1 activity

Guanfacine is a TAAR1 agonist with roughly the same affinity for it as the α_2A-adrenoceptor but it should be known that it lacks any monoamine releasing properties as it has not been shown to compete with monoamines for reuptake at their respective electrochemical transporters. TAAR1 receptors can become extracellular and co-localized with α_2A-adrenergic receptors as the TAAR1-α_2A heterodimer which evidence in academia points toward. BoeingbusB380 (talk) 12:04, 21 November 2024 (UTC)