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Guanfacine for ADHD


Guanfacine for ADHD

Guanfacine has been approved in the USA since 2009, including for adult ADHD.
In Germany, guanfacine was approved in retarded form in 2015 and came onto the market in 2016 with the indication for ADHD in children and adolescents.1
Guafacine is a selective postsynaptic α-2A adrenoreceptor agonist in frontal pyramidal neurons.2
Guanfacine is also an imidazoline receptor agonist.
Guanfacine inhibited ionic currents elicited by NaV1.7 channels encoded by SCN9A and other NaV channel subtypes to varying degrees.3
It is not subject to the Narcotics Ordinance.

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

ADHD efficacy likely due to increased α-2A-adrenergic signaling, postsynaptically in the PFC.4

A selective α-2A-adrenoreceptor-Antagonist significantly increased noradrenaline, serotonin and dopamine levels in rats, which correlated with reduced monoamine turnover.5

Alpha-2 adrenoreceptors (also known as adrenoceptors) are activated by the neurotransmitters adrenaline and noradrenaline. They are therefore responsible for the effects mediated by adrenaline and noradrenaline.
Agonists strengthen the effect of the receptors, antagonists weaken it.
Guanfacine has a noradrenergic effect.

Maximum blood plasma values after 5 hours.
Elimination half-life 18 hours, therefore suitable for single daily intake.
Increased absorption of active ingredients when taken with a high-fat meal; should therefore be taken on an empty stomach
Guanfacine should not be taken with grapefruit juice.6
The tablets must not be chewed or crushed.
Metabolism also via CYP3A4 and CYP3A5, therefore potential for interactions with drugs such as ketoconazole and rifampicin.6
Inhibitor of these CYP subtypes.

1. Effectiveness, application

Numerous studies have confirmed the effectiveness of guanfacine for ADHD.678910
Guanfacine is effective in children and adolescents who do not respond optimally to stimulants.1112 Guanfacine is also approved for this purpose in Europe.13
According to one study, an alpha agonist (such as guanfacine) was primarily used in an academic medical treatment center (probably in the US) for children with ADHD, behavioral disorders (DBD) or autism spectrum disorder between the ages of 2 and 5. In children without autism spectrum disorder, stimulants were primarily used.14
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 placebo compared to previous medication.15

1.1. Effect of guanfacine on symptoms

It is argued that guanfacine has a more selective effect on the PFC and the inattention and organization problems it harbors, while stimulants have a broader effect and, in addition to the PFC, also influence the striatum, which is primarily responsible for hyperactivity and impulsivity.16

  • Improved working memory4
  • Attention improved417
  • Reduction of the ADHD-RS-IV total score by 8.9 with guanfacine, atomoxetine only by 3.8.18
  • Rejection sensitivity and/or dysphoria in ADHD: A combination of clonidine and guanfacine is said to be helpful.19
  • Hyperactivity202117
  • Impulsiveness20417
  • Comorbid disorders in children and adolescents with ADHD2223
    • Autism symptoms
    • Oppositional defiant behavior21
    • Emotional and behavioral dysregulation due to traumatic stress experiences.23
    • Possibly for tics
    • No effect on anxiety symptoms
    • Effects on depression are open
    • The side effects of guanfacine are similar in comorbid conditions and in pure ADHD
  • Effect comparable in ADHD-I and ADHD-C.17
  • Guanfacine has long been used as a treatment for high blood pressure. In ADHD, it has particular benefits in the treatment of comorbid tic disorders.24
  • While stimulants primarily increase the dopamine effect level and secondarily the noradrenaline level, guanfacine, as an alpha2 receptor agonist, improves signal transmission in the frontal lobe by making the signal clearer and more distinct.24

1.2. Effect size of guanfacine

  • The mean effect size of guanfacine is said to be 0.76. Stimulants, on the other hand, are between 0.9 and 1.1 (in responders).1 Other studies come to comparable results.25
  • Reduction of the ADHD-RS-IV total score by 8.9 with guanfacine, atomoxetine only by 3.818
  • A combination medication of methylphenidate and guanfacine achieves a higher response rate than guanfacine or methylphenidate alone. In one study, guanfacine alone proved to be inferior to methylphenidate alone in 68% of those affected with a symptom reduction of at least 50% (81% of those affected with a symptom reduction of at least 50%). However, a combination medication of MPH and guanfacine was the most successful (91% of those affected showed a symptom reduction of at least 50%).26
  • The effect on ADHD symptoms is slightly worse than that of stimulants if the latter respond well. The effect is better in children than in adolescents.23

1.3. Mechanisms of action of guanfacine

  • As an alpha-2-adrenoceptor agonist, guanfacine (like clonidine) significantly reduces the release of dopamine in the nucleus accumbens in the laboratory.27
  • Methylphenidate and amphetamine drugs increase the power of alpha (in rats), while atomoxetine and guanfacine do not.28
  • Guanfacine appears to have several modes of action:
    • Reduces direct noradrenergic transmission between locus coeruleus and orbitofrontal cortex (OFC) in the resting state2
    • Reduces the release of noradrenaline in the locus coeruleus, orbitofrontal cortex and reticular nucleus of the thalamus2
    • Improves direct catecholaminergic transmission from the locus coeruleus to the orbitofrontal cortex (OFC)2
    • Improved catecholamine release by inhibiting GABA in the intermediate pathway locus coeruleus - reticular nucleus of the thalamus - mediodorsal nucleus of the thalamus - orbitofrontal cortex (OFC)2
    • Reduced GABA release in the mediodorsal thalamic nucleus2
    • Increased AMPA-induced release of L-glutamate, noradrenaline and dopamine in the orbitofrontal cortex (OFC) through subchronic administration2
    • Guanfacine administration directly into the OFC did not alter the release of catecholamines in the OFC2
  • Acute local administration in locus coeruleus in therapeutic dosage causes29
    • Reduced noradrenaline release in OFC, VTA and nucleus reticularis (of the thalamus)
    • Unchanged dopamine release in the OFC
  • Chronic administration (14 days) in therapeutic dosage causes29
    • Downregulation of the α2A adrenoceptor in locus coeruleus, OFC and VTA, thereby
      • Increased basal noradrenaline release in OFC, VTA, nucleus reticularis (of the thalamus)
      • Increased dopamine release in the OFC
    • Unaltered GABAergic transmission within the thalamus
    • Phase-wise increased glutamatergic transmission between thalamus and cortex.
  • Alpha-2A receptor agonists such as guanfacine and clonidine are thought to improve phasic noradrenaline release in the nucleus coeruleus, which improves attention as well as working memory and visuomotor-associated learning (as opposed to long-term tonic NE release, which impairs performance).30

1.4. Responding from Guanfacin

One study looked at characteristics that predicted good responding to guanfacine or MPH monotherapy and MPH/guanfacine combination medication:

  • Higher hyperactivity-impulsivity and oppositional symptoms before treatment31
    • Predictor for good results with MPH monotherapy, guanfacine monotherapy and MPH/guanfacine combination medication
  • Less anxiety before the treatment31
    • Predictor for good results with MPH monotherapy, guanfacine monotherapy and MPH/guanfacine combination medication
  • High event-related mid-frontal beta power before treatment31
    • EEG activity from cortical sources localized in the regions of the middle frontal bone and middle occipital bone
    • Stronger modulations during encoding and retrieval predictor for good results with MPH monotherapy and guanfacine monotherapy
  • Weak event-related mid-frontal beta power before treatment31
    • EEG activity from cortical sources localized in the regions of the middle frontal bone and middle occipital bone
    • Predictor for good results with MPH/guanfacine combination medication

In preschool ADHD, low externalizing or internalizing symptom severity correlated with a high likelihood of response to stimulants. At high externalizing or internalizing symptom levels, the response rate of stimulants approached that of alpha-2 agonists:32

Responder Symptom severity: weak medium strong
Stimulants Externalizing 96.4 % 74.3 % 66.6 %
Alpha-2 agonists Externalizing 40 % 50 % 67 %
Stimulants Internalizing 80.6 % 77.5 % 50 %
Alpha-2 agonists Internalizing 57.7 % 70 % 57.7 %

2. Side effects

  • Higher side effects than methylphenidate and atomoxetine4
  • The side effects of guanfacine are similar in comorbid conditions and in pure ADHD22
  • Fewer side effects than clonidine (less antihypertensive and less sedative)33
  • Guanfacine should not be discontinued abruptly due to its antihypertensive effect.6

No liver damage or increased enzyme levels in the blood serum due to guanfacine are known.34

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

3. Degradation of guanfacine

Guanfacine is broken down via cytochrome P450 3A4, CYP3A4 for short.

This cytochrome is more active in women than in men,35 so women may need a higher dose than men.
There are also 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.36

4. Interactions of guanfacine

4.1. CYP3A4 inducer

  • Phenobarbital (strong)3738
  • Rifampin / Rifampicin (strong)3738
  • Quinolones37
  • Anticonvulsants
    • Phenytoin (strong)3738
    • Carbamazepine (strong)3738
    • Oxcarbazepine (weak)3738
  • Modafinil (weak)3738
  • Armodafnil (weak)38
  • Topiramate (weak)38
  • Dexamethasone37
    • Not: Prednisone37
  • St. John’s wort (weak)3738
  • Ginger37
  • Garlic37
  • Licorice37

4.1.1. CYP3A4 inducer and guanfacine

Strong CYP3A4 inducers reduce the blood level of guanfacine within 2 to 3 weeks after the start of administration, while weak and moderate CYP3A4 inducers can cause this.38 Conversely, the guanfacine level rises again 2 to 3 weeks after discontinuation of CYP3A4 inducers.

While the package leaflet recommends doubling the dose of guanfacine with concomitant administration of CYP3A4 inducers, augmenting administration of phenobarbital required a 5-fold dose in a single case.38 Avoiding strong CYP3A4 inducers appears to be advisable when taking guanfacine at the same time.

4.2. CYP3A4 inhibitors

  • Antibiotics.
    • Macrolides
      • Erythromycin (strong)3837
      • Clarithromycin (strong)3837
      • Telithromycin37
    • Chloramphenicol37
  • Antifungals:
    • Fluconazole37
    • Ketoconazole (strong)3837
    • Itraconazole37
  • Diltiazem (strong)38
  • Grapefruit juice (strong)3837
  • Fluoxetine (weak to moderate)38
  • Fluvoxamine (weak to moderate)38
  • Protease inhibitors:
    • Ritonavir37
    • Indinavir37
    • Nelfinavir37
  • Verapamil37
  • Aprepitant37
  • Nefazodon37
  • Amiodarone37
  • Cimetidine37
  • Valerian37
  • Turmeric37
  • Ginseng37

4.2.1. CYP3A4 inhibitors and guanfacine

Strong CYP3A4 inhibitors increase the blood level of guanfacine after the start of administration, weak and moderate CYP3A4 inhibitors may do so.38

While the package leaflet recommends halving the dose of guanfacine with concomitant administration of CYP3A4 inhibitors, halving the dose does not appear to be sufficient when taking augmenting antipsychotics.38 Avoiding CYP3A4 inhibitors appears to be advisable when taking guanfacine at the same time.

Grapefruit juice should always be avoided when taking psychiatric medication.38

4.3. Other interactions of guanfacine

Valproate is said to show increased plasma levels when taken in parallel with guanfacine.39

Guanfacine and clonidine should be antagonized by tricyclic antidepressants and phenothiazines.40

Simultaneous use of beta-blockers or sudden discontinuation of guanfacine can lead to a hypertensive reaction.40

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

A meta-analysis of 87 randomized placebo-controlled double-blind studies found no evidence of a decrease in the effect of methylphenidate, amphetamine drugs, atomoxetine or α2 antagonists with prolonged use.41

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

A strong increase in noradrenaline / dopamine shuts down the PFC. This deactivation of the PFC occurs via alpha-1 adrenoceptors, which have a lower noradrenaline and cortisol affinity than alpha-2 adrenoceptors and are therefore only addressed at very high noradrenaline and cortisol levels. 4243444546

A particularly strong increase in DA and NE during severe stress could therefore lead to a (frequent) underactivation of the PFC, as is typical in ADHD-I.
This could explain Raynaud’s and high blood pressure problems in some ADHD-I sufferers, which are also mediated by alpha-1 adrenoceptors.

The question is whether alpha-1-adrenoceptor antagonists, which are successfully used against Raynaud’s and high blood pressure, might not also be helpful against PFC blockades in ADHD-I.

The agonization of the more affine alpha-2 receptors has the opposite effect to the antagonization of the alpha-1 receptors. As with the cortisol receptors, the less affine receptor (there: glucocorticoid receptor, here: alpha-1 adrenoceptor) is responsible for switching off the system and is only addressed at very high levels of messenger substances. If the more affine receptors (there: mineralocorticoid receptor, here: alpha-2 receptor) are too pronounced, the less affine switch-off receptors are not reached. Alpha-2 agonists occupy the free capacities of the more affine receptors, leaving more messenger substance free, which can now address the alpha-1 adrenoceptors. In ADHD-I, guanfacine and yohimbine should therefore enhance PFC deactivation.

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

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

7. Report of the person concerned

An ADHD sufferer reports on guanfacine:

“I take 1 mg of guanfacine about 5 to 6 hours before going to bed.
If I take it in the morning, I get a bit tired and don’t feel like it helps that much. If 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? The first time I took it, after 5-6 hours I felt a funny crackling sensation in my neck/under my ears, then a kind of wet-feeling pressure wave came through my head, which made me dizzy for a short time, but went away immediately 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 my head, not just in my neck.

It also helps me against an extremely strong stress response that sometimes paralyzes my brain.
When I started university, I kept having blackouts during exams. It feels like a kind of “stress squeeze” in my stomach, which is squeezed out and causes a “stress wave” in the abdomen, which then crawls up and tries to tense the chest, and the brain above the eyes and “on top” feels like it “switches off”. I can then no longer think clearly. This is extremely attenuated with guanfacine.“

This is the most vivid description of the deactivation 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!


  2. Okada, Fukuyama, Kawano, Shiroyama, Suzuki, Ueda (2019): Effects of acute and sub-chronic administrations of guanfacine on catecholaminergic transmissions in the orbitofrontal cortex. Neuropharmacology. 2019 Feb 22. pii: S0028-3908(19)30062-0. doi: 10.1016/j.neuropharm.2019.02.029.

  3. de Cássia Collaço R, Lammens M, Blevins C, Rodgers K, Gurau A, Yamauchi S, Kim C, Forrester J, Liu E, Ha J, Mei Y, Boehm C, Wohler E, Sobreira N, Rowe PC, Valle D, Brock MV, Bosmans F (2023): Anxiety and dysautonomia symptoms in patients with a NaV1.7 mutation and the potential benefits of low-dose short-acting guanfacine. Clin Auton Res. 2023 Dec 8. doi: 10.1007/s10286-023-01004-1. PMID: 38064009.

  4. Guanfacin, Wirkstoff Aktuell, Ausgabe 2/2016, Stand 11.04.2015, Information der KBV

  5. Harvey, Uys, Viljoen, Shahid, Sonntag, Meyer (2021): Hippocampal monoamine changes in the Flinders sensitive line rat: A case for the possible use of selective α2C-AR-antagonists in stress and anxiety disorders in companion animals. Res Vet Sci. 2021 Mar;135:175-183. doi: 10.1016/j.rvsc.2021.01.013. PMID: 33529845.

  6. NPS MedicineWise (2018): Guanfacine hydrochloride for attention deficit hyperactivity disorder; Aust Prescr. 2018 Aug; 41(4): 131–132. doi: 10.18773/austprescr.2018.042 PMCID: PMC6091781 PMID: 30116086

  7. Poitras, McCormack (2018): Guanfacine Hydrochloride Extended-Release for the Treatment of Attention Deficit Hyperactivity Disorder in Adults: A Review of Clinical Effectiveness, Cost-Effectiveness, and Guidelines; CADTH Rapid Response Report: Summary with Critical Appraisal; Ottawa (ON): Canadian Agency for Drugs and Technologies in Health; 2018 Sep 11.

  8. Yu S, Shen S, Tao M (2023): Guanfacine for the Treatment of Attention-Deficit Hyperactivity Disorder: An Updated Systematic Review and Meta-Analysis. J Child Adolesc Psychopharmacol. 2023 Mar;33(2):40-50. doi: 10.1089/cap.2022.0038. PMID: 36944092. METASTUDIE

  9. Neuchat EE, Bocklud BE, Kingsley K, Barham WT, Luther PM, Ahmadzadeh S, Shekoohi S, Cornett EM, Kaye AD (2023): The Role of Alpha-2 Agonists for Attention Deficit Hyperactivity Disorder in Children: A Review. Neurol Int. 2023 May 22;15(2):697-707. doi: 10.3390/neurolint15020043. PMID: 37218982; PMCID: PMC10204383. REVIEW

  10. Yu S, Shen S, Tao M (2023): Guanfacine for the Treatment of Attention-Deficit Hyperactivity Disorder: An Updated Systematic Review and Meta-Analysis. J Child Adolesc Psychopharmacol. 2023 Mar;33(2):40-50. doi: 10.1089/cap.2022.0038. PMID: 36944092. METASTUDY, k = 12, n = 2.653

  11. Childress (2012): Guanfacine extended release as adjunctive therapy to psychostimulants in children and adolescents with attention-deficit/hyperactivity disorder. Adv Ther. 2012 May;29(5):385-400. doi: 10.1007/s12325-012-0020-1.

  12. Bukstein, Head (2012): Guanfacine ER for the treatment of adolescent attention-deficit/hyperactivity disorder; Expert Opin Pharmacother. 2012 Oct;13(15):2207-13. doi: 10.1517/14656566.2012.721778.

  13. Huss, Chen, Ludolph (2016): Guanfacine Extended Release: A New Pharmacological Treatment Option in Europe.Clin Drug Investig. 2016 Jan;36(1):1-25. doi: 10.1007/s40261-015-0336-0

  14. Mittal, Boan, Kral, Lally, van Bakergem, Macias, LaRosa (2019): Young Children with Attention-Deficit/Hyperactivity Disorder and/or Disruptive Behavior Disorders Are More Frequently Prescribed Alpha Agonists Than Stimulants. J Child Adolesc Psychopharmacol. 2019 Oct 17. doi: 10.1089/cap.2019.0105.

  15. Butterfield, Saal, Young, Young (2016): Supplementary guanfacine hydrochloride as a treatment of attention deficit hyperactivity disorder in adults: A double blind, placebo-controlled study. Psychiatry Res. 2016 Feb 28;236:136-41. doi: 10.1016/j.psychres.2015.12.017. n = 26

  16. Levy (2008): Pharmacological and therapeutic directions in ADHD: Specificity in the PFC. Behav Brain Funct. 2008 Feb 28;4:12. doi: 10.1186/1744-9081-4-12. PMID: 18304369; PMCID: PMC2289834.

  17. Sallee, Kollins, Wigal (2012): Efficacy of guanfacine extended release in the treatment of combined and inattentive only subtypes of attention-deficit/hyperactivity disorder. J Child Adolesc Psychopharmacol. 2012 Jun;22(3):206-14. doi: 10.1089/cap.2010.0135. PMID: 22612526; PMCID: PMC3373219. n = 631

  18. Guanfacin, Wirkstoff Aktuell, Ausgabe 2/2016, Stand 11.04.2015, Information der KBV, randomisierte placebokontrollierte Doppelblindstudie mit n = 337

  19. Dodson: How ADHD Ignites Rejection Sensitive Dysphoria; The extreme emotional pain of perceived rejection is a feeling unique to people with ADHD, and it can be debilitating. Learn how RSD may be impacting your patients; in: ADDitude. Strategies and Support für ADD & LD

  20. Lukkes, Drozd, Fitz, Molosh, Clapp, Shekhar (2020): Guanfacine treatment improves ADHD phenotypes of impulsivity and hyperactivity in a neurofibromatosis type 1 mouse model. J Neurodev Disord. 2020 Jan 15;12(1):2. doi: 10.1186/s11689-019-9304-y. PMID: 31941438; PMCID: PMC6961243.

  21. Muir, Perry (2010): Guanfacine extended-release: in attention deficit hyperactivity disorder; Drugs. 2010 Sep 10;70(13):1693-702. doi: 10.2165/11205940-000000000-00000

  22. de Groof, De La Marche, Danckaerts (2019): [Effectiveness of guanfacin on comorbid disorders in children and adolescents with adhd: a systematic literature review]. [Article in Dutch] Tijdschr Psychiatr. 2019;61(12):845-853.

  23. Connor, Arnsten, Pearson, Greco (2014): Guanfacine extended release for the treatment of attention-deficit/hyperactivity disorder in children and adolescents.Expert Opin Pharmacother. 2014 Aug;15(11):1601-10. doi: 10.1517/14656566.2014.930437.

  24. Barkley (2014): Dr Russell Barkley on ADHD Meds and how they all work differently from each other; Youtube

  25. Childress, Hoo-Cardiel, Lang, (2020): Evaluation of the current data on guanfacine extended release for the treatment of ADHD in children and adolescents. Expert opinion on pharmacotherapy, 1–10. Advance online publication. doi:10.1080/14656566.2019.1706480

  26. McCracken, McGough, Loo, Levitt, Del’Homme, Cowen, Sturm, Whelan, Hellemann, Sugar, Bilder (2018): Combined Stimulant and Guanfacine Administration in Attention-Deficit/Hyperactivity Disorder: A Controlled, Comparative Study. Am Acad Child Adolesc Psychiatry. 2016 Aug; 55(8): 657–666.e1. doi: 10.1016/j.jaac.2016.05.015; PMCID: PMC4976782; NIHMSID: NIHMS800851; PMID: 27453079

  27. Nurse, Russell, Taljaard (1985): Effect of chronic desipramine treatment on adrenoceptor modulation of [3H]dopamine release from rat nucleus accumbens slices. Brain Res. 1985 May 20;334(2):235-42

  28. Takahashi, Ohmiya, Honda, Ni (2018): The KCNH3 inhibitor ASP2905 shows potential in the treatment of attention deficit/hyperactivity disorder. PLoS One. 2018 Nov 21;13(11):e0207750. doi: 10.1371/journal.pone.0207750. eCollection 2018.

  29. Fukuyama, Nakano, Shiroyama, Okada (2021): Chronic Administrations of Guanfacine on Mesocortical Catecholaminergic and Thalamocortical Glutamatergic Transmissions. Int J Mol Sci. 2021 Apr 16;22(8):4122. doi: 10.3390/ijms22084122. PMID: 33923533.

  30. Steinhausen, Rothenberger, Döpfner (2010): Handbuch ADHS, Seiten 84, 85

  31. Michelini, Lenartowicz, Vera, Bilder, McGough, McCracken, Loo SK (2022): Electrophysiological and Clinical Predictors of Methylphenidate, Guanfacine, and Combined Treatment Outcomes in Children With Attention-Deficit/Hyperactivity Disorder. J Am Acad Child Adolesc Psychiatry. 2022 Aug 8:S0890-8567(22)01229-1. doi: 10.1016/j.jaac.2022.08.001. PMID: 35963559. n = 181

  32. Blum NJ, Shults J, Barbaresi W, Bax A, Cacia J, Deavenport-Saman A, Friedman S, Loe IM, Mittal S, Vanderbilt D, LaRosa A, Harstad E. Do Externalizing and Internalizing Symptoms Moderate Medication Response in Preschool Attention-Deficit/Hyperactivity Disorder? A DBPNet Study. J Dev Behav Pediatr. 2023 Sep 1;44(7):e447-e454. doi: 10.1097/DBP.0000000000001209. PMID: 37696030

  33. Sorkin, Heel (1986): Guanfacine. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in the treatment of hypertension.Drugs. 1986 Apr;31(4):301-36. Betrifft vermutlich Guanfacin-IR, nicht GXR, also nicht Intuniv

  34. Guanfacine. Source LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-2019

  35. Keiner (2015): Gendermedizin – Dosisanpassung selten erforderlich. Pharmazeutische Zeitung.

  36. Law R, Lewis D, Hain D, Daut R, DelBello MP, Frazier JA, Newcorn JH, Nurmi E, Cogan ES, Wagner S, Johnson H, Lanchbury J (2022): Characterisation of seven medications approved for attention-deficit/hyperactivity disorder using in vitro models of hepatic metabolism. Xenobiotica. 2022 Nov 1:1-32. doi: 10.1080/00498254.2022.2141151. PMID: 36317558.

  37. CYP3A4 bei DocCheck Flexikon, abgerufen am 23.12.19

  38. Schoretsanitis, de Leon, Eap, Kane, Paulzen (2019): Clinically Significant Drug-Drug Interactions with Agents for Attention-Deficit/Hyperactivity Disorder. CNS Drugs. 2019 Dec;33(12):1201-1222. doi: 10.1007/s40263-019-00683-7.

  39. Ambrosini, Sheikh (1998): Increased plasma valproate concentrations when coadministered with guanfacine. J Child Adolesc Psychopharmacol. 1998;8(2):143-7. doi: 10.1089/cap.1998.8.143. PMID: 9730080.

  40. Markowitz, Patrick (2001): Pharmacokinetic and pharmacodynamic drug interactions in the treatment of attention-deficit hyperactivity disorder. Clin Pharmacokinet. 2001;40(10):753-72. doi: 10.2165/00003088-200140100-00004. PMID: 11707061. REVIEW

  41. Castells, Ramon, Cunill, Olivé, Serrano (2020): Relationship Between Treatment Duration and Efficacy of Pharmacological Treatment for ADHD: A Meta-Analysis and Meta-Regression of 87 Randomized Controlled Clinical Trials. J Atten Disord. 2020 Feb 20:1087054720903372. doi: 10.1177/1087054720903372. PMID: 32075485.

  42. Ramos, Arnsten (2007): Adrenergic pharmacology and cognition: focus on the prefrontal cortex. Pharmacol Ther. 2007 Mar; 113(3):523-36., Kapitel 6

  43. Birnbaum, Gobeske, Auerbach, Taylor, Arnsten (1999): A role for norepinephrine in stress-induced cognitive deficits: α-1-adrenoceptor mediation in prefrontal cortex. Biol. Psychiatry 46, 1266–1274.

  44. 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.

  45. 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.

  46. 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.