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Guanfacine for ADHD


Guanfacine for ADHD

Guanfacine in sustained release form was approved in 2015 and entered the market in 2016 with an indication for ADHD in children and adolescents.1
Guanfacine has been approved in the United States since 2009, where it is also used for adult ADHD.
Guafacine is a selective postsynaptic α-2A-adrenoreceptor agonist in frontal pyramidal neurons.2
In addition, guanfacine is an imidazoline receptor agonist.
It is not subject to narcotics regulation.

Earlier designation: BS 100-141 (in the 1970s)
Trade name: Intuniv

ADHD efficacy likely due to increased α-2A-adrenergic signaling, postsynaptic in the PFC.3

A selective α-2A-adrenoreceptorantagonist significantly increased norepinephrine, serotonin, and dopamine levels in rats, which correlated with decreased monoamine turnover.4

Alpha-2 adrenoreceptors (also: adrenoceptors) are activated by the neurotransmitters adrenaline and noradrenaline. They are thus responsible for the effects mediated by adrenaline and noradrenaline.
Agonists enhance the action of the receptors.
Guanfacine thus has a noradrenergic effect.

Maximum blood plasma values after 5 hours.
Elimination half-life 18 hours, therefore suitable for once daily use.
Increased absorption of active ingredient when taken with a high-fat meal; should therefore be taken on an empty stomach
Guanfacine should not be taken with grapefruit juice.5
Do not chew or crush the tablets.
Metabolism also via CYP450 3A, therefore potential for drug interactions with drugs such as ketoconazole and rifampicin.5
Metabolized via CYP3A4/5.
Inhibitor of these CYP subtypes.

1. Efficacy, application

  • Several studies have confirmed the effectiveness of guanfacine in ADHD.56
  • In children and adolescents who do not respond optimally to stimulants, guanfacine is effective.78 Guanfacine is also approved for this purpose in Europe.9
  • According to one study, an alpha agonist (such as guanfacine) was primarily used in children with ADHD, conduct disorder (DBD), or autism spectrum disorder between the ages of 2 and 5 years in an academic medical treatment center (probably in the United States). In children without autism spectrum disorder, stimulants were primarily used.10
  • With regard to adult ADHD sufferers who do not respond optimally to stimulants, there is no clear evidence of efficacy. One study found improvements with guanfacine and with placebo over previous medication.11

1.1. Effect of guanfacine on symptoms

It is argued that guanfacine acts more selectively on the PFC and the inattention and organizational problems it harbors, whereas stimulants act more broadly, affecting not only the PFC but also the striatum, which is primarily responsible for hyperactivity and impulsivity.12

  • Working memory improved3
  • Attention improved313
  • Reduction of ADHD RS-IV total score by guanfacine by 8.9, atomoxetine by only 3.8.14
  • Rejection Sensitivity and/or Dysphoria in ADHD: A combination of clonidine and guanfacine is reported to be helpful.15
  • Hyperactivity161713
  • Impulsivity16313
  • Comorbid disorders in children and adolescents with ADHD1819
    • Autism symptoms
    • Oppositional defiant behavior17
    • Emotional and behavioral dysregulation due to traumatic stressful experiences.19
    • Possibly on tics
    • No effect on anxiety symptoms
    • Effects on depression is open
    • The side effects of guanfacine are similar in comorbid conditions and in pure ADHD
  • Effect comparable well in ADHD-I and ADHD-C.13
  • Guanfacine has long been used as an antihypertensive agent. In ADHD, it has particular advantages in the treatment of comorbid tic disorders.20
  • While stimulants primarily increase dopamine action levels and secondarily increase norepinephrine levels, guanfacine, as an alpha2 receptor agonist, improves signaling in the frontal lobe by making the signal clearer and more distinct.20

1.2. Effect size of guanfacine

  • The mean effect size of guanfacine is reported to be 0.76. In contrast, stimulants range from 0.9 to 1.1 (in responders).1 Further studies come to comparable results.21
  • Reduction of ADHD RS-IV total score by guanfacine by 8.9, atomoxetine by only 3.814
  • A combination medication of methylphenidate and guanfacine achieves a higher responder rate than guanfacine or methylphenidate alone. In one study, guanfacine alone was found to be inferior to methylphenidate alone (81% of subjects symptom reduction by at least 50%) in 68% of subjects with at least 50% symptom reduction. However, a combination medication of MPH and guanfacine was most successful (91% of sufferers with at least 50% symptom reduction).22
  • The effect on ADHD symptoms is somewhat worse than that of stimulants when the latter respond well. The effect is better in children than in adolescents.19

1.3. Mechanisms of action of guanfacine

  • As an alpha-2-adrenoceptor agonist, guanfacine (like clonidine) significantly reduces dopamine release in the nucleus accumbens in the laboratory.23
  • Methylphenidate and amphetamine drugs increase the power of alpha (in rats), whereas atomoxetine and guanfacine do not.24
  • Guanfacine appears to have multiple pathways of action:
    • Decreases direct noradrenergic transmission between locus coeruleus and orbitofrontal cortex (OFC) at rest2
    • Reduces noradrenaline release in the locus coeruleus, orbitofrontal cortex and reticular thalamic nucleus2
    • Enhances direct catecholaminergic transmission from the locus coeruleus to the orbitofrontal cortex (OFC)2
    • Enhanced catecholamine release by inhibiting GABA in the intermediate pathway locus coeruleus - reticular thalamic nucleus - mediodorsal thalamic nucleus - orbitofrontal cortex (OFC)2
    • Reduced GABA release in the mediodorsal thalamic nucleus2
    • Enhanced AMPA-induced release of L-glutamate, norepinephrine, and dopamine in the orbitofrontal cortex (OFC) by subchronic administration2
    • Guanfacing administration directly into the OFC did not alter catecholamine release in the OFC2
  • Acute local administration into locus coeruleus at therapeutic dosage causes25
    • Decreased noradrenaline release in OFC, VTA and nucleus reticularis (of the thalamus)
    • Unchanged dopamine release in the OFC
  • Chronic administration (14 days) in therapeutic dosage causes25
    • Downregulation of the α2A-adrenoceptor in locus coeruleus, OFC, and VTA, thereby
      • Increased basal noradrenaline release in OFC, VTA, nucleus reticularis (of thalamus)
      • Increased dopamine release in the OFC
    • Unaltered GABAergic transmission within the thalamus
    • Phasic increased glutamatergic transmission between thalamus and cortex.
  • Alpha-2A receptor agonists such as guanfacine and clonidine are thought to improve phasic norepinephrine release in the nucleus coeruleus, which improves attention as well as working memory and visuomotor-associated learning (in contrast to long-term tonic NE release, which worsens performance.26
    In view of the fact that high noradrenal stress responses cause the PFC to be switched off too frequently in ADHD-I, we think it might be questionable whether guanfacine also has a positive effect in ADHD-I or whether the positive effect is not rather limited to ADHD-HI. We do not have any empirical data on this.

1.4. Guanfacin reponding

One study addressed characteristics that predicted good responding of guanfacine or MPH monotherapy and MPH/guanfacine combination medication:

  • Higher hyperactivity-impulsivity and oppositional symptoms before treatment27
    • Predictor of good outcomes with MPH monotherapy, guanfacine monotherapy, and MPH/guanfacine combination medication
  • Reduced anxiety before treatment27
    • Predictor of good outcomes with MPH monotherapy, guanfacine monotherapy, and MPH/guanfacine combination medication
  • High event-related midfrontal beta power before treatment27
    • EEG activity from cortical sources localized in the regions of the middle frontal bone and the middle occipital bone
    • Stronger modulations during encoding and retrieval predictor of good outcomes with MPH monotherapy and guanfacine monotherapy
  • Weak event-related midfrontal beta power before treatment27
    • EEG activity from cortical sources localized in the regions of the middle frontal bone and the middle occipital bone
    • Predictor of good outcomes with MPH/guanfacine combination medication

2. Side effects

  • Higher side effects than methylphenidate and atomoxetine3
  • The side effects of guanfacine are similar in comorbid conditions and in pure ADHD18
  • Fewer side effects than clonidine (less antihypertensive and less sedating)28
  • Because of its antihypertensive effect, guanfacine should not be discontinued abruptly.5

There is no known liver damage or elevated enzyme levels in blood serum due to guanfacine.29

Guanfacine is particularly worth considering in cases where stimulants have a strong blood pressure-increasing effect.

3. Guanfacine degradation

Guanfacine is degraded via cytochrome P450 3A4, or CYP3A4.

In women, this cytochrome is more active than in men,30 so women may need a higher dose than men.
Further, there are interactions that increase (inducers) or inhibit (inhibitors) the enzyme activity of CYP3A4.

In vitro, the 3-OH guanfacine signaling pathway accounted for at least 2.6% of guanfacine metabolism in cryopreserved plated human hepatocytes and 71% in pooled human liver microsomes.31

4. Guanfacine interactions

4.1. CYP3A4 inducers

  • Phenobarbital (strong)3233
  • Rifampin / Rifampicin (strong)3233
  • Quinolone32
  • Anticonvulsants
    • Phenytoin (strong)3233
    • Carbamazepine (strong)3233
    • Oxcarbazepine (weak)3233
  • Modafinil (weak)3233
  • Armodafnil (weak)33
  • Topiramate (weak)33
  • Dexamethasone32
    • Not: Prednisone32
  • St. John’s wort (weak)3233
  • Ginger32
  • Garlic32
  • Licorice32

4.1.1. CYP3A4 inducers and guanfacine

Strong CYP3A4 inducers decrease blood levels of guanfacine within 2 to 3 weeks after initiation, whereas weak and moderate CYP3A4 inducers can c cause this.33 Conversely, guanfacine levels increase again 2 to 3 weeks after discontinuation of CYP3A4 inducers.

While the package insert recommends doubling the guanfacine dose with concomitant administration of CYP3A4 inducers, augmenting phenobarbital in a single case required a 5-fold dose.33 Avoidance of potent CYP3A4 inducers seems advisable when guanfacine is taken concomitantly.

4.2. CYP3A4 inhibitors

  • Antibiotics.
    • Macrolides
      • Erythromycin (strong)3332
      • Clarithromycin (strong)3332
      • Telithromycin32
    • Chloramphenicol32
  • Antifungals:
    • Fluconazole32
    • Ketoconazole (strong)3332
    • Itraconazole32
  • Diltiazem (strong)33
  • Grapefruit juice (strong)3332
  • Fluoxetine (weak to moderate)33
  • Fluvoxamine (weak to moderate)33
  • Protease inhibitors:
    • Ritonavir32
    • Indinavir32
    • Nelfinavir32
  • Verapamil32
  • Aprepitant32
  • Nefazodon32
  • Amiodarone32
  • Cimetidine32
  • Valerian32
  • Turmeric32
  • Ginseng32

4.2.1. CYP3A4 inhibitors and guanfacine

Strong CYP3A4 inhibitors increase blood levels of guanfacine after initiation; weak and moderate CYP3A4 inhibitors may do so if appropriate.33

While the package insert recommends halving the guanfacine dose when CYP3A4 inhibitors are administered concomitantly, halving does not appear to be sufficient when antipsychotics are taken augmentatively.33 Avoidance of CYP3A4 inhibitors appears to be recommended when guanfacine is taken concomitantly.

Grapefruit juice should always be avoided when taking psychiatric medications.33

4.3. Other interactions of Guanfacin

Valproate is reported to show increased plasma levels when taken concomitantly with guanfacine.34

Guanfacine and clonidine are thought to be antagonized by tricyclic antidepressants and phenothiazines.35

Concomitant use of beta-blockers or sudden discontinuation of guanfacine may result in a hypertensive response.35

5. Long-term effect: No habituation effects of guanfacine

A meta-analysis of 87 randomized placebo-controlled double-blind trials found no evidence of diminishing effects of methylphenidate, amphetamine medications, atomoxetine, or α2-antagonists with prolonged use.36

6. Theoretical considerations of guanfacine: only in ADHD-HI, not in ADHD-I / SCT?

A large increase in norepinephrine / dopamine shuts down the PFC. This deactivation of the PFC occurs through alpha 1-adrenoceptors, which have lower norepinephrine and cortisol affinity than alpha 2-adrenoceptors and are therefore only addressed at very high norepinephrine and cortisol levels. 3738394041

Therefore, a particularly large increase in DA and NE during severe stress could lead to (frequent) underactivation of the PFC, which is typical in ADHD-I.
This background could explain Raynaud’s and hypertension problems in some ADHD-I sufferers, which are also mediated by alpha-1-adrenoceptors.

The question is whether alpha-1-adrenoceptor antagonists, which have been used successfully against Raynaud’s disease and hypertension, might not also be helpful against the PFC blockades in ADHD-I.

Agonization of the more affine alpha-2 receptors is opposite in effect to antagonization of the alpha-1 receptors. As with the cortisol receptors, the less affine receptor (there: glucocorticoid receptor, here: alpha-1 adrenergic receptor) is responsible for shutting down the system and is only addressed at very high levels of messenger. If the more affine receptors (there: mineralocorticoid receptor, here: alpha-2 receptor) are too strong, the less affine shut-off receptors are not reached. Alpha-2 agonists occupy the free capacities of the more affine receptors, leaving more neurotransmitter free to now address the alpha-1 adrenoceptors. In ADHD-I, guanfacine and yohimbine would therefore need to enhance PFC cutoff.

Guanfacine is an alpha-2-A and alpha-2-D adrenoceptor agonist, and yohimbine is an alpha-2-B adrenoceptor agonist.

This connection opens the question of whether-at least in theory-guanfacine and yohimbine should be avoided in ADHD-I and might have a particularly useful use in ADHD-HI to shut down an overloaded PFC

7. Affected Person Report

An ADHD sufferer reports on guanfacine:

“I take 1 mg of guanfacine about 5 to 6 hours before bedtime.
When I take it in the morning, I get a little tired and don’t feel like it helps that much. When I take it so that the theoretical peak is at bedtime, I sleep much better.
My sleep is somehow deeper and more restful and my brain feels somehow… more alive? better supplied with blood? When I first started taking it, I felt a weird crackling sensation in my neck/under my ears after 5-6 hours, then a kind of wet-feeling pressure wave came through my head that briefly caused me dizziness, but immediately went away when I moved my head. Since then, I can feel more clearly when my neck is tense. Relaxation exercises now also reduce the pressure at the top, front and sides of the head, not just the neck.

It also helps me with an extremely strong stress response that paralyzes my brain at times.
I used to have blackouts in exams when I was starting out in college. It feels like a kind of “stress squeeze” in my stomach that gets squeezed out and causes a “stress wave” in the abdomen, which then crawls up and wants to tense the chest, and the brain above the eyes and “on top” feels “turned off”. I then can’t think straight. This is extremely mitigated with the guanfacine.“

The is the most vivid description of the shutdown of the PFC by alpha-1 adrenoceptors that we have found so far.

Caution: individual reports of drug effects must not be generalized!
Medication must always be discussed with the doctor!


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  32. CYP3A4 bei DocCheck Flexikon, abgerufen am 23.12.19

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  39. Ramos, Colgan, Nou, Ovadia, Wilson, Arnsten (2005). The beta-1 adrenergic antagonist, betaxolol, improves working memory performance in rats and monkeys. Biol. Psychiatry 58, 894–900.

  40. ähnlich: Arnsten (2000): Stress impairs prefrontal cortical function in rats and monkeys: role of dopamine D1 and norepinephrine alpha-1 receptor mechanisms. Prog Brain Res. 2000;126:183-92.

  41. Für starke Stimulation des D1-Dopaminrezeptors: Zahrt, Taylor, Mathew, Arnsten (1997): Supranormal stimulation of D1 dopamine receptors in the rodent prefrontal cortex impairs spatial working memory performance. J Neurosci. 1997 Nov 1;17(21):8528-35.