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Clinical data
Pronunciation /mɒkˈsɒnɪdn/
Trade names Physiotens
AHFS/ International Drug Names
Routes of
Oral (tablets)
ATC code
Legal status
Legal status
  • UK: POM (Prescription only)
  • In general: ℞ (Prescription only)
Pharmacokinetic data
Bioavailability 88% (Tmax = 1 hour)
Protein binding 7.2–10%[2][1]
Metabolism Liver (10–20%)[1]
Metabolites Dehydrogenated moxonidine (major), hydroxymethyl-moxonidine, hydroxy-moxonidine, dihydroxy-moxonidine[3]
Elimination half-life ~2.2–2.8 hours
Excretion Renal (90%),[4] feces (~1%)[1]
CAS Number
PubChem CID
ECHA InfoCard 100.158.061 Edit this at Wikidata
Chemical and physical data
Formula C9H12ClN5O
Molar mass 241.677 g/mol
3D model (JSmol)
 ☒N☑Y (what is this?)  (verify)

Moxonidine (INN) is a new-generation alpha-2/imidazoline receptor agonist antihypertensive drug licensed for the treatment of mild to moderate essential hypertension.[5][6] It may have a role when thiazides, beta-blockers, ACE inhibitors, and calcium channel blockers are not appropriate or have failed to control blood pressure. In addition, it demonstrates favourable effects on parameters of the insulin resistance syndrome, apparently independent of blood pressure reduction. It is manufactured by Solvay Pharmaceuticals under the brand name Physiotens.

Mechanism of action[edit]

Moxonidine is a selective agonist at the imidazoline receptor subtype 1 (I1).[5] This receptor subtype is found in both the rostral ventro-lateral pressor and ventromedial depressor areas of the medulla oblongata. Moxonidine therefore causes a decrease in sympathetic nervous system activity and, therefore, a decrease in blood pressure.

Compared to the older central-acting antihypertensives, moxonidine binds with much greater affinity to the imidazoline I1-receptor than to the α2-receptor. In contrast, clonidine binds to both receptors with equal affinity.

In addition, moxonidine may also promote sodium excretion, improve insulin resistance and glucose tolerance and protect against hypertensive target organ damage, such as kidney disease and cardiac hypertrophy.

Pharmacodynamic properties[edit]

Effects on insulin resistance

In all animal models of insulin resistance, moxonidine had striking effects on the development of insulin resistance, hyperinsulinaemia and impaired glucose homeostasis. Given the importance of insulin resistance as a risk factor for cardiovascular disease, it is of considerable relevance that it has been shown to improve insulin sensitivity.

Safety pharmacology[edit]

Routine toxicology studies have provided no evidence that moxonidine has any teratogenic, mutagenic or carcinogenic potential. No evidence has been found of serious adverse effects on organs or organ systems, and the drug has not been shown to have deleterious effects on perinatal or postnatal growth and development.


Moxonidine should be avoided in patients with moderate to severe renal impairment. Abrupt discontinuation of the drug should also be avoided. If concomitant treatment with a beta blocker has to be stopped, the beta blocker should be discontinued first, then moxonidine after a few days. Alcohol may potentiate the hypotensive effects of Moxonidine.

Drug interactions[edit]

Concomitant administration of moxonidine and a thiazide diuretic such as hydrochlorothiazide is not indicated, as both drugs' hypotensive effects may be enhanced.


It is contraindicated if there has been a past history of angioedema; heart conduction disorders (e.g. sick sinus syndrome, second- or third-degree heart block); bradycardia; severe heart failure or coronary artery disease. Also: Raynaud's syndrome, intermittent claudication, epilepsy, depression, Parkinson's disease, glaucoma. Use in pregnancy is discouraged. Moxonidine passes into breast milk.

Excess mortality has been seen in patients with symptomatic heart failure in the MOXCON study.[7] However, the MOXCON trial prescribed very high dose of 3.0 mg daily which is above the normal dose of 0.2–0.6 mg daily.


Noteworthy side effects include dry mouth, headache, fatigue, dizziness, intermittent facial oedema, nausea, sleep disturbances (rarely sedation), asthenia, vasodilatation, and rarely, skin reactions.


  1. ^ a b c "Physiotens Tablets (moxonidine) Product Information" (PDF). Abbott Australasia Pty Ltd, 32-34 Lord Street, Botany NSW 2019, Australia. Retrieved 1 September 2016. 
  2. ^ Weimann, HJ; Rudolph, M (1992). "Clinical Pharmacokinetics of Moxonidine". Journal of Cardiovascular Pharmacology. 20 (Suppl. 4): S37–S41. doi:10.1097/00005344-199220004-00008. 
  3. ^ He, MM; Abraham, TL; Lindsay, TJ; Schaefer, HC; Pouliquen, IJ; Payne, C; Czeskis, B; Shipley, LA; Oliver, SD; Mitchell, MI (March 2003). "Metabolism and Disposition of the Antihypertensive Agent Moxonidine in Humans" (PDF). Drug Metabolism and Disposition. 31 (3): 334–42. doi:10.1124/dmd.31.3.334. PMID 12584161. Retrieved 1 September 2016. 
  4. ^ Farsang, C (2001). "Moxonidine: Clinical Profile" (PDF). Journal of Clinical and Basic Cariology. an Independent International Scientific Journal. 4 (3): 197–299. Retrieved 1 September 2016. 
  5. ^ a b Fenton, Caroline; Keating, Gillian M.; Lyseng-Williamson, Katherine A. (2006). "Moxonidine: a review of its use in essential hypertension". Drugs. 66: 477–496. 
  6. ^ Fairbanks, C. A; Wilcox, G. L (1999). "Moxonidine, a selective alpha2-adrenergic and imidazoline receptor agonist, produces spinal antinociception in mice". The Journal of Pharmacology and Experimental Therapeutics. 290 (1): 403–12. PMID 10381806. 
  7. ^ Cohn J, et al. (2003). "Adverse mortality effect of central sympathetic inhibition with sustained-release moxonidine in patients with heart failure (MOXCON)". Eur J Heart Fail. 5 (5): 659–67. doi:10.1016/S1388-9842(03)00163-6. PMID 14607206.