Talk:Clonidine

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I've been on a lot of medications used to treat my anxiety. The only drug that seemed to help me was Lorazapan, but over time it doesnt have nearly the same effect compared to when I first used it. Clonidine, however, has helped me and many others that are having high anxiety type issues. I just think this page needs a touch about how it can help anxiety, and also the long term effects of this specific medication. —Preceding unsigned comment added by 66.30.235.251 (talk) 06:19, 13 September 2007 (UTC)

Contrary to the article as written, I do not think Clonidine is generally used to "treat" ADHD, although many ADHD children receive it, off label at bedtime, to induce sleep. I suspect same is true with Tourette's although I am less certain of that. Although I am not qualified to prescribe, I deal with many children with both diagnoses and I only see it prescribed for use at bedtime. It is a sleep medication of choice because it does not have addictive potential and it does get the kids to slow down physically at bedtime. But I do not think any clinician would want children taking it because of ADHD during the active part of their day. Also note that clonidine and Klonopin are BOTH used to induce sleep (although not likely at the same time for the same person).

I looked at the study cited where the citation suggests otherwise. However that is not what the actual article says. It refers to a test of Ritalin and Clonidine used in combination. While I have not encountered this with children I have worked with (unless the Clonidine was administered only at bedtime) the COMBINATION makes sense. But I still doubt that Clonidine, by itself, is an appropriate treatment for either disorder. 70.90.220.214 22:04, 27 March 2007 (UTC)

There is a lot of info on this page[] --Clawed 05:07, 16 Jul 2004 (UTC)

Unless I got the wrong drug, Clonidine is also used off-label to treat insomnia. I once took it when I was young in really small doses. --User:Arm

You're probably thinking of clonazepam (Klonopin). - Nunh-huh 05:43, 3 Mar 2005 (UTC)

I was recently (yesterday) perscribed Clonidine by my psychiatrist for dealing with panic attacks and additionally to help with insomnia -- Anonymous 19:44, 3 February 2006 (UTC)

clonidine can be used for ADHD treatment and tics treatment in children(Dr Hussein Abdeldayem , Alex, Egypt)

I was prescribed clonidine specifically for my mild Tourette's syndrome, and it works very well. VCUchem 03:28, 10 April 2007 (UTC)

My son, 4.5 years old, has been on clonidine for two week to treat ADD, his prescription is 0.05mg. It is working well, but worried about longterm negative effects. Any articles? (user:woodmac)(December 18 2008)

Clonidine Transdermal "patch" .3 Is currently being used to treat my daughter's Cycling Vomiting Syndrome. see ref: http://digestive.niddk.nih.gov/ddiseases/pubs/cvs/#6 —Preceding unsigned comment added by Morrisindustries (talk • contribs) 12:11, 15 January 2008 (UTC)

Quitting smoking

The Surgeon General suggests that Clonidine can be used to aid in quitting smoking after nicotine replacement methods have failed. A potential source is http://surgeongeneral.gov/tobacco/treating_tobacco_use.pdf

Side-effects?

Did anyone ever hear of very bad chest and back pain with this medicine? Taking it four times a day, and my upper back and chest is killing me

Your side effect was probably a rare reaction. The only side effect I experienced was being extremely tired at first.

The most popular understated side effect of this medication is, for lack any milder way to put it, catastrophic loss of consciousness. Not so much "put them out like a light", but more like drop them like a punch from Mike Tyson, where they stand. — Preceding unsigned comment added by 208.127.80.59 (talk) 11:57, 27 September 2011 (UTC)

VCUchem 03:24, 10 April 2007 (UTC)

Cleanup

This page is a candidate for cleanup. I propose that all of the benzodiazepines be wikified at once. The benzodiazepines are a significant family of drugs, and better information should be available here on Wikipedia, due to their widespread use.

Clonidine is not a benzodiazepine.

You must be thinking of Klonopin (clonazepam).

[Speaking of which, does clonodine actually treat restless leg syndrome? or is that another klonopin accident? On the Restless legs syndrome wiki, clonidine is not mentioned...] — Preceding unsigned comment added by 212.179.160.18 (talk) 08:05, 5 June 2018 (UTC)

I agree that a lot of people do not understand that Klonopin is a completely different medication than clonadine!

Clonidine can indeed be used in the treatment of RLS. I've cited this statement in the article to clarify the point. Thank you for the notification! ―Biochemistry🙴❤ 23:37, 3 October 2018 (UTC)

Creditation

Clonidine is often used to treat tics, specifically Tourettes Disorder, due to research by Dr. Richard Ferre, M.D. of University of Utah. I do not have a link to the specific paper, but you can find it on a Google search "Richard Ferre"

Yea, i have Tourettes and i take this. EvilHom3r 18:49, 6 August 2007 (UTC)

I have used the patch form of this medicine before to treat parts/symptoms of Attention Deficit Hyperactivity Disorder, and it seems to work pretty well. User: mansharker8 —Preceding unsigned comment added by 207.157.138.39 (talk) 01:35, 30 October 2007 (UTC)

Clean-Up (again?)

The muddle with clonazepam (Klonopin) here remains - for a start, one of the most common side effects of clonidine is insomnia (see the British National Formulary entry - probably same info listing in the Physicians Desk Ref too...) and I can hardly see it being rx'd for such. Indeed, its one of the drawbacks of using it for opiate withdrawal as the resultant insomnia can be severe and prolonged even after the acute symptons are over. In the UK, it is usually therefore prescribed for this purpose along with strong benzos such as Rohypnol or with benzo/chlorpromazine combinations to overcome this lack of efficacy. Anyway, someone ought to clear this up some more. If no-one better qualied tries, 'll come back and have a go. Plutonium27 (talk) 02:47, 5 June 2008 (UTC)

Adrenergic Agonist AND NE antagonist?

How is this drug a "α2 adrenergic agonist" AND "inhibits the release of norepinephrine (NE)". Can someone explain? —Preceding unsigned comment added by 144.126.53.164 (talk) 11:51, 20 October 2009 (UTC)

In response to "Adrenergic Agonist AND NE antagonist?" I was wondering the same thing, as I'm at work researching Clonidine. I found this on a website: "Clonidine is an agonist, an alpha-2 agonist to be precise. But it acts primarily on noradrenergic autoreceptors thereby decreasing norepinephrine release. Thus clonidine is a direct-acting a2-noradrenergic agonist with indirect-acting antagonist action at other noradrenergic targets. (It has the physiological/behavioral effect of an antagonist at most doses, but it's still technically an agonist!) " —Preceding unsigned comment added by 216.63.110.9 (talk) 07:33, 15 January 2010 (UTC)

Clonodine

Clonodine is not Klonopin (clonazepam), it is not a benzodiazepine like (Valium, diazepam, Xanax, alprazolam, Ativan, lorazepam). etc... Clonidine is used alone or in combination with other medications to treat high blood pressure. Clonidine is in a class of medications called centrally acting alpha-agonist hypotensive agents. It works by decreasing your heart rate and relaxing the blood vessels so that blood can flow more easily through the body. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0000623 —Preceding unsigned comment added by Jodiah (talk • contribs) 20:47, 29 June 2010 (UTC)

bu ilacı hangi ülkeden ve hangi eczaneden temin edebiliriz reçetemiz var ilaç bulamıyoruz catapresan 78.190.150.221 (talk) 18:32, 28 September 2024 (UTC)

Structure

Resolved

 – The offending 3D structure was deleted here. I see no difference between the two models in the current article.―Biochemistry🙴❤ 05:29, 11 July 2018 (UTC)

The following discussion is closed. Please do not modify it. Subsequent comments should be made on the appropriate discussion page. No further edits should be made to this discussion.

---

I'm no expert, but do the two structure models agree? The 3D model shows both N atoms of the imidazoline ring with H's (implying imidazolidine), whereas the planar model shows N at position 2 with no H (imizazoline). The 3D model shows the N of the amine with no H and the planar model shows it with one. —Preceding unsigned comment added by 220.244.145.200 (talk) 00:38, 8 December 2010 (UTC)

You are absolutely right. It is a mistake and should be corrected. The 3D model is missing one H atom.— Preceding unsigned comment added by 209.175.69.2 (talk • contribs) 19:04, 28 April 2011 (UTC)

The discussion above is closed. Please do not modify it. Subsequent comments should be made on the appropriate discussion page. No further edits should be made to this discussion.

Uses

There are two "Uses" paragraphs in the article. Should be restructured. — Preceding unsigned comment added by Vbond (talk • contribs) 06:25, 3 February 2011 (UTC)

Other uses: I deleted everything but RLS, as the others were all mentioned in the "Uses" section. I propose that "Uses" should be for approved uses and "other uses" for off-label uses, as this is often how drug articles are structured. — Preceding unsigned comment added by 74.76.210.124 (talk) 04:49, 6 February 2012 (UTC)

Clonidine in combination with Methedone or Suboxone

Clonidine is also given in conjuction with methedone/suboxone to combat excessive persperation. It is rarely given alone to combat the affects of opioid withdrawls. When combined with methedone/suboxone it has shown evidence of improving comfort levels when it comes to exessive persperation. The typical does when combine with methedone is 0.1-0.2 micrograms twice daily. — Preceding unsigned comment added by 174.115.132.133 (talk) 20:07, 12 October 2011 (UTC)

I don't believe that the article claims that clonidine is used as monotherapy for opioid withdrawal, so I don't really see the point of your comment. However, it is not unusual for clonidine to be used alone; opioid substitution therapy isn't necessarily always employed. ―Biochemistry🙴❤ 23:32, 3 October 2018 (UTC)

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Citation update

Does there exist any more-recent paper that supports the citation no.2 - Lowenthal, DT; Matzek, KM; MacGregor, TR (May 1988). "Clinical pharmacokinetics of clonidine.". Clinical Pharmacokinetics. 14 (5): 287–310. PMID 3293868. doi:10.2165/00003088-198814050-00002 ? Thanks! : ) --It's gonna be awesome!✎Talk♬ 16:32, 8 September 2017 (UTC)

slow pulse

Other sources say that clonidine makes pulse get slower because of more action by the vagus nerve. This article says the idea that clonidine slows the heart because of tightening of the arteries but there is no reference. Which is right? — Preceding unsigned comment added by 152.133.8.193 (talk) 16:18, 15 July 2018 (UTC)

Very observant. It's my understanding that this isn't all too-well understood; it may indeed be a combination of multiple mechanisms, including those. A paper from 1995 notes the following:

The exact mechanism responsible for this clonidine-associated bradycardia is not well understood. The most plausible mechanisms are: (a) reduced sympathetic tone from central mediators, (b) increased vagal activity, (c) stimulation of presynaptic alpha-2 receptors in the heart which have a blocking effect on heart rate, (d) decreased automaticity of the bundles of His, and (e) atrioventricular nodal block. It is probable that the mechanisms vary from patient to patient.

— Lawrence L. Golusinski, Jr. and B. Wayne Blount, "Clonidine-induced bradycardia", source

If anyone can find a more recent source to confirm this speculation, it would be greatly appreciated. ―Biochemistry🙴❤ 18:53, 15 July 2018 (UTC)

Which receptor?

User:Sbelknap what are your thoughts on this diff? Jytdog (talk) 13:42, 8 August 2018 (UTC)

Fixed. Interesting, as there seems to be an error in this low-quality article, so I've removed the citation. The best citation is the Goodman and Gilman one on page 202 of the 13th edition. Its post-synaptic alpha 2 agonism in vascular smooth muscle that gives the transient rise in blood pressure. I notice that John Reid mentions both mechanisms in his article, citing Doxey et al for the alpha 1 mechanism and citing Drew and Whiting for the post-synaptic alpha 2 mechanism. I'll ask Tom Westfall, who wrote the Goodman and Gilman chapter, what he thinks. Sbelknap (talk) 18:12, 11 August 2018 (UTC)

Semantic Scholar

Afernand74 The Semantic Scholar PDF is not the article. It is just the abstract. It is misleading and confusing to click on the link and end up on a random unrelated site that doesn't provide the article. --Whywhenwhohow (talk) 20:05, 12 September 2020 (UTC)

The Citation bot added the s2cid and reports that the Semantic Scholar URL is not licensed. I am removing the unlicensed URL. --Whywhenwhohow (talk) 20:51, 12 September 2020 (UTC)

+ Adding s2cid: 40756251
 ! Should probably remove un-licensed Semantic Scholar URL that was converted to S2CID parameter

Conflicting structural formulae

Stick and ball strucutural formula shows the bridging Nitrogen without a Hydrogen. It shows both ring Nitrogens with a Hydrogen.

Letter structural formula shows bridge Nitrogen with a Hydrogen and one of the ring Nitrogens without a Hydrogen.

The following, currently reference 1, puts the Hydrogen on the bridging Nitrogen.

https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=d7f569dc-6bed-42dc-9bec-940a9e6b090d

2600:387:B:9A2:0:0:0:9 (talk) 08:46, 3 August 2021 (UTC) Drive By Editor

Selectivity

Димитрий Улянов Иванов, you keep changing the "alpha-2 agonist" to "alpha-2a agonist". The issue is the body doesn't support the selectivity for 2a (as it does in the guanfacine article). If you want to keep changing it to alpha-2a, please provide a source that supports clonidine being more selective for alpha-2a than the others. Kimen8 (talk) 13:33, 22 November 2023 (UTC)

My apologies, it does indicate alpha-2a selectivity. Kimen8 (talk) 15:24, 24 November 2023 (UTC)

Depression

In Germany a depression is considered a contraindication to clonidine. This seems plausible because of the old-school depression theory of a cerebral lack of sympathetic neuro-transmitters. Interestingly dexmedetomidine, having the same or similar pharmacodynamics, is now a candidate for treatment of otherwise non-treatable depression. Could someone elaborate on that? Elmar Hagemeyer (talk) 12:52, 23 June 2024 (UTC)

Article rewrite

Over the next couple days week or so, I'm going to be in the process of updating and rewriting content for this article. This will start with the medical uses section, the adverse effects section, and then the pharmacology section. Because of the way I'm rewriting the medical uses section, I'm thinking of rewriting the pharmacology section in a way that replaces "mechanism of action" for specific disease or condition subtypes with a broad pharmacodynamics section that is analogous to the featured article amphetamine.

I'm almost certainly going to be removing the borderline personality disorder section because based on the evidence presented in the article and current textbooks/medical reviews on the clinical utility of alpha-2 adrenoreceptor agonists, the use of clonidine in BPD does not meet WP:DUE in order to have its own subsection alongside ADHD, hypertension et al. Its use in the post-anaesthesia care unit in hospitals does meet WP:DUE, so I will be replacing BPD with a section on that. I wouldn't be opposed to having it placed in the "other uses" subsection if more MEDRS compliant evidence can be located. Professional Crastination (talk) 03:44, 12 December 2025 (UTC)

I will be hopefully making large revisions to the medical uses and pharmacology sections once I finish the latter; I plan on describing how Clonidine's mechanism of action treats the medical conditions it's used for in the medical uses section, whilst the "mechanism of action" section will be replaced with a "pharmacodynamics" section that describes its pharmacodynamic targets and effects across the nervous system, regardless who takes the drug. I think this change is beneficial because the drug effects that are described in patients who meet guidelines for hypertension that are treated for hypertension also occur in normotensive individuals (i.e., bradycardia and hypotension are common side effects in normotensive individuals at relatively lower doses via the same pharmacodynamic actions that treat hypertension). This is how the pharmacodynamics section is done on amphetamine and bupropion, which are both featured articles covering a drug with medical uses. Professional Crastination (talk) 00:29, 19 December 2025 (UTC)

Kapvay trade name repeated exclusions

@Whywhenwhohow Why do you keep removing the Kapvay trade name from the infobox? This started when I made the following edit:

"Kapvay is unique because it is an extended-release formulation (NB: catapres is IR) and unlike other trade names/formulations, it is USFDA-approved for ADHD; its inclusion into the infobox is representive of that whilst maintaining a non-exhaustive list"

Kapvay is one of only two oral dosage formulations (the other being Catapres) that's mentioned in Stahl's 2024 prescriber guide, which I used to write the Clonidine#Attention deficit hyperactivity disorder section and is cited in the article.

You reverted Kapvay's inclusion twice and your most recent edit note reads as follows: "the tradename field is for trade names by the originator."

Your edit note does not contradict my edit note. Why? Because Kapvay is the trade name originator for marketing of that oral dosage formulation of clonidine. You'll have to enlighten me when a Catapres oral extended-release formulation was approved for marketing in the United States.

Moreover, I noticed you had no issue with keeping Concerta - the controlled release formulation of methylphenidate - listed under trade names in the associated article last time you revised their infobox. The justification for placing Kapvay under the trade names is identical to Concerta; they're both the first marketed trade names of original oral extended release formulations. Just to be clear - there are no marketed oral extended-release formulations of Catapres. I stated as much in my very first edit note on the subject that was reverted hours later (i.e., "NB: catapres is IR").

Also, I've read the Template:Infobox drug guide. The only requirements listed for trade names are:

tradename – comma separated list of trade names by the originator (no generics, not more than three names).

So, I would like to know (1) why you believe that my inclusion rationale contradicts the template guideline and (2) since when has there been an oral extended-release dosage formulation of Catapres that's been approved for the treatment of ADHD? (i.e., when did Catapres assume USFDA-approved marketing claims of Kapvay?)

Thanks, Professional Crastination (talk) 08:29, 28 December 2025 (UTC)

Catapres was approved in 1974. Kapvay is the marketing name being used for a new indication from a new manufacturer. --Whywhenwhohow (talk) 06:17, 1 January 2026 (UTC)

Re: "Kapvay is the marketing name being used for a new indication from a new manufacturer."

At face value, this seems like a logical reply that supports your reversion of my edit. However, the only problem is that it doesn't add anything that I hadn't already addressed 3 interactions ago, does not respond to either question I asked, and it omits the central distinction that I'm now raising for a fourth time (NB: the 2nd occasion was here); Kapvay is not an immediate release drug and Catapres has never been an oral extended release drug. Funny that.

Why have I needed to refer to this fact several times throughout four interactions now? It seems straightforward to me. Here's a list of things I've stated in past replies over the last week.

Kapvay is unique because it is an extended release formulation (NB: catapres is IR)

Kapvay is the trade name originator for marketing of that oral dosage formulation of clonidine.

You'll have to enlighten me when a Catapres oral extended-release formulation was approved

Just to be clear - there are no marketed oral extended-release formulations of Catapres.

since when has there been an oral extended-release dosage formulation of Catapres?

Moreover, we have MEDRS-evidence cited in the article that supports Kapvay and Catapres as unique medications (Stahl states why Kapvay is different beyond what I included from the chapter in the reftemplate). You are not MEDRS-evidence.

In any event, I'd wager that the reason you omitted the persistently pointed out and easily verifiable fact that Catapres is not an extended-release drug and Kapvay is not an immediate-release drug (i.e., they're not the same drug despite sharing an active ingredient) is because absence of that context is needed to justify your reverts under Template:infobox drug.

That said, it just so happens that omitting the context about Catapres versus Kapvay helps you not look like a massive hypocrite given that I have multiple examples of you leaving trade name originators of extended-release formulations alongside their immediate release tradename counterparts in other articles (e.g., Concerta [not just Ritalin], Adderall XR [not just Adderall], OxyContin [not just Roxicodone]).

Seriously, what gives? Professional Crastination (talk) 08:08, 1 January 2026 (UTC)

By that logic, we wouldn't ever use brand names like Adderall (first was Obetrol), Adderall XR (ditto), Concerta (first was Ritalin), Sarafem (first was Prozac), Zyban (first was Wellbutrin), Zenzedi (first was Dexedrine), or any one of countless other cases where secondary trade names are listed in the drugbox. This is not a formal policy and I have never seen it applied in this way to any other pharm article throughout the last decade of editing med/pharm articles (I was even in the top 300 medical editors of the year for two years). Can you find any evidence to back up this 'policy' being anything more than something you invented out of thin air just now? Because without you producing some robust evidence to support your claims, I am inclined to go ahead and edit the secondary brand name of Kapvay back into the infobox, as I see no reason why it should be excluded and plenty of reason why it should be included. Garzfoth (talk) 15:16, 2 January 2026 (UTC)