Moxonidine: Difference between revisions

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			{{Short description\|Antihypertensive medication}}
	{{Drugbox		{{Drugbox
	\| Verifiedfields = changed		\| Verifiedfields = changed
			\| Watchedfields = changed
	\| verifiedrevid = ~~408765028~~		\| verifiedrevid = 462255851
	\| IUPAC_name = 4-~~chloro~~-''N''-(4,5-dihydro-1''H''-imidazol-2-yl)-<br>6-methoxy-2-methylpyrimidin-5-amine		\| IUPAC_name = 4-Chloro-''N''-(4,5-dihydro-1''H''-imidazol-2-yl)-<br />6-methoxy-2-methylpyrimidin-5-amine
	\| image = Moxonidine.svg		\| image = Moxonidine.svg
	\| width = 180		\| width = 180

	<!--Clinical data-->		<!--Clinical data-->
			\| pronounce = {{IPAc-en\|m\|ɒ\|k\|ˈ\|s\|ɒ\|n\|ɪ\|d\|iː\|n}}
⚫	\| tradename =
	\| Drugs.com = {{drugs.com\|international\|moxonidine}}		\| Drugs.com = {{drugs.com\|international\|moxonidine}}
	\| pregnancy_AU = B3		\| pregnancy_AU = B3
	\| legal_UK = POM		\| legal_UK = POM
			\| legal_status = Rx-only
	\| routes_of_administration = Oral		\| routes_of_administration = Oral (])

	<!--Pharmacokinetic data-->		<!--Pharmacokinetic data-->
	\| bioavailability = 88%		\| bioavailability = 88% (])
			\| protein_bound = 7.2–10%<ref>{{cite journal\| vauthors = Weimann HJ, Rudolph M \|title=Clinical Pharmacokinetics of Moxonidine\|journal=Journal of Cardiovascular Pharmacology\|date=1992\|volume=20\|issue=Suppl. 4\|pages=S37–S41\|doi=10.1097/00005344-199220004-00008\|doi-access=free}}</ref><ref name="Physiotens PI">{{cite web\|title=Physiotens Tablets (moxonidine) Product Information\|url=https://gp2u.com.au/static/pdf/P/PHYSIOTENS-PI.pdf\|publisher=Abbott Australasia Pty Ltd, 32-34 Lord Street, Botany NSW 2019, Australia\|access-date=1 September 2016}}</ref>
	\| protein_bound =
	\| metabolism =		\| metabolism = ] (10–20%)<ref name="Physiotens PI" />
			\| metabolites = Dehydrogenated moxonidine (major), hydroxymethyl-moxonidine, hydroxy-moxonidine, dihydroxy-moxonidine<ref>{{cite journal \| vauthors = He MM, Abraham TL, Lindsay TJ, Schaefer HC, Pouliquen IJ, Payne C, Czeskis B, Shipley LA, Oliver SD, Mitchell MI \| display-authors = 6 \| title = Metabolism and disposition of the antihypertensive agent moxonidine in humans \| journal = Drug Metabolism and Disposition \| volume = 31 \| issue = 3 \| pages = 334–342 \| date = March 2003 \| pmid = 12584161 \| doi = 10.1124/dmd.31.3.334 }}</ref>
	\| elimination_half-life = 2.2 hours		\| elimination_half-life = ~2.2–2.8 hours
	\| excretion = ]
			\| excretion = ] (90%),<ref>{{cite journal\|last1=Farsang\|first1=C\|title=Moxonidine: Clinical Profile\|journal=Journal of Clinical and Basic Cardiology. An Independent International Scientific Journal\|date=2001\|volume=4\|issue=3\|pages=197–299\|url=http://www.kup.at/kup/pdf/897.pdf\|access-date=1 September 2016}}</ref> feces (~1%)<ref name="Physiotens PI" />

	<!--Identifiers-->		<!--Identifiers-->
	\| CAS_number_Ref = {{cascite\|~~correct~~\|??}}		\| CAS_number_Ref = {{cascite\|changed\|??}}
	\| CAS_number = 75438-57-2		\| CAS_number = 75438-57-2
	\| ATC_prefix = C02		\| ATC_prefix = C02
Line 30:		Line 34:
	\| ChemSpiderID_Ref = {{chemspidercite\|correct\|chemspider}}		\| ChemSpiderID_Ref = {{chemspidercite\|correct\|chemspider}}
	\| ChemSpiderID = 4645		\| ChemSpiderID = 4645
	\| UNII_Ref = {{fdacite\|~~changed~~\|FDA}}		\| UNII_Ref = {{fdacite\|correct\|FDA}}
	\| UNII = CC6X0L40GW		\| UNII = CC6X0L40GW
	\| KEGG_Ref = {{keggcite\|correct\|kegg}}		\| KEGG_Ref = {{keggcite\|correct\|kegg}}
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	\| ChEMBL_Ref = {{ebicite\|correct\|EBI}}		\| ChEMBL_Ref = {{ebicite\|correct\|EBI}}
	\| ChEMBL = 19236		\| ChEMBL = 19236
		⚫	\| tradename = Physiotens, Moxon

	<!--Chemical data-->		<!--Chemical data-->
	\| C=9 \| H=12 \| Cl=1 \| N=5 \| O=1		\| C=9 \| H=12 \| Cl=1 \| N=5 \| O=1
		⚫	\| smiles = Clc1nc(C)nc(OC)c1NC2=NCCN2
	\| molecular_weight = 241.677 g/mol
⚫	\| smiles = Clc1nc(nc(OC)~~c1N/C2~~=~~N/CCN2)C~~
	\| InChI = 1/C9H12ClN5O/c1-5-13-7(10)6(8(14-5)16-2)15-9-11-3-4-12-9/h3-4H2,1-2H3,(H2,11,12,15)
	\| InChIKey = WPNJAUFVNXKLIM-UHFFFAOYAJ
	\| StdInChI_Ref = {{stdinchicite\|correct\|chemspider}}		\| StdInChI_Ref = {{stdinchicite\|correct\|chemspider}}
	\| StdInChI = 1S/C9H12ClN5O/c1-5-13-7(10)6(8(14-5)16-2)15-9-11-3-4-12-9/h3-4H2,1-2H3,(H2,11,12,15)		\| StdInChI = 1S/C9H12ClN5O/c1-5-13-7(10)6(8(14-5)16-2)15-9-11-3-4-12-9/h3-4H2,1-2H3,(H2,11,12,15)
Line 48:		Line 50:
	\| StdInChIKey = WPNJAUFVNXKLIM-UHFFFAOYSA-N		\| StdInChIKey = WPNJAUFVNXKLIM-UHFFFAOYSA-N
	}}		}}
	'''Moxonidine''' (]) ({{IPAc-en\|icon\|m\|ɒ\|k\|ˈ\|s\|ɒ\|n\|ɪ\|d\|iː\|n}}) is a new generation centrally acting ] drug licensed for the treatment of mild to moderate essential ]. It may have a role when ], ]s, ]s and ]s are not appropriate or have failed to control blood pressure. In addition, it demonstrates favourable effects on parameters of the ] syndrome, apparently independent of blood pressure reduction. It is manufactured by ] Pharmaceuticals under the brand name '''Physiotens'''.

			'''Moxonidine''' (]) is a new-generation alpha-2/imidazoline receptor agonist ] drug licensed for the treatment of mild to moderate ].<ref name=Monox>{{cite journal \| vauthors = Fenton C, Keating GM, Lyseng-Williamson KA \| title = Moxonidine: a review of its use in essential hypertension \| journal = Drugs \| volume = 66 \| issue = 4 \| pages = 477–496 \| year = 2006 \| pmid = 16597164 \| doi = 10.2165/00003495-200666040-00006 \| s2cid = 195691757 }}</ref><ref name=pmid10381806>{{cite journal \| vauthors = Fairbanks CA, Wilcox GL \| title = Moxonidine, a selective alpha2-adrenergic and imidazoline receptor agonist, produces spinal antinociception in mice \| journal = The Journal of Pharmacology and Experimental Therapeutics \| volume = 290 \| issue = 1 \| pages = 403–412 \| date = July 1999 \| pmid = 10381806 \| url = http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=10381806 }}</ref> It may have a role when ], ]s, ]s, and ]s are not appropriate or have failed to control blood pressure. In addition, it demonstrates favourable effects on parameters of the ] syndrome, apparently independent of blood pressure reduction. It is also a ] releaser.<ref>{{cite journal \| vauthors = Bamberger CM, Mönig H, Mill G, Gödde E, Schulte HM \| title = Growth hormone secretion in response to the new centrally acting antihypertensive agent moxonidine in normal human subjects: comparison to clonidine and GHRH \| journal = Experimental and Clinical Endocrinology & Diabetes \| volume = 103 \| issue = 3 \| pages = 205–208 \| year = 1995 \| pmid = 7584524 \| doi = 10.1055/s-0029-1211351 }}</ref> It is manufactured by ] Pharmaceuticals (acquired by ] in 2009) under the brand name '''Physiotens''' and Moxon.
⚫	==Mechanism of ~~actions~~==
⚫	Moxonidine is a selective ] at the ] subtype 1 (I<sub>1</sub>). This receptor subtype is found in both the rostral ventro-lateral pressor and ventromedial depressor areas of the ]. Moxonidine therefore causes a decrease in ] activity and, therefore, a decrease in ].

		⚫	==Mechanism of action==
	Compared to the older central-acting antihypertensives, moxonidine binds with much greater affinity to the imidazoline I<sub>1</sub>-receptor than to the α<sub>2</sub>-receptor. In contrast, ] binds to both receptors with equal affinity.
		⚫	Moxonidine is a selective ] at the ] subtype 1 (I<sub>1</sub>).<ref name=Monox/> This receptor subtype is found in both the rostral ventro-lateral pressor and ventromedial depressor areas of the ]. Moxonidine therefore causes a decrease in ] activity and, therefore, a decrease in ].

			Compared to the older central-acting antihypertensives, moxonidine binds with much greater affinity to the imidazoline I<sub>1</sub>-receptor than to the α<sub>2</sub>-receptor. In contrast, ] binds to both receptors with near equal affinity. Moxonidine has an affinity for I<sub>1</sub> that is 33 times greater than α<sub>2</sub>, compared to clonidine which is only four times greater.<ref>{{cite journal \| vauthors = Prichard BN, Owens CW, Graham BR \| title = Pharmacology and clinical use of moxonidine, a new centrally acting sympatholytic antihypertensive agent \| journal = Journal of Human Hypertension \| volume = 11 \| issue = Suppl 1 \| pages = S29–S45 \| date = August 1997 \| pmid = 9321737 }}</ref>
⚫	In addition, moxonidine may also promote ] excretion, improve insulin resistance and ] tolerance and protect against hypertensive target organ damage, such as ] disease and ] ].

		⚫	In addition, moxonidine may also promote ] excretion, improve insulin resistance and ] tolerance and protect against hypertensive target organ damage, such as ] disease and ] ].

	==Pharmacodynamic properties==		==Pharmacodynamic properties==
			{{Unreferenced section\|date=April 2016}}

	~~'''~~Effects on insulin resistance~~'''~~		===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.		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.

			==Contraindications==
	Based on animal models, it has demonstrated that moxonidine is capable of:
		⚫	It is contraindicated if there has been a past history of ]; heart conduction disorders (e.g. ], second- or third-degree ]); ]; severe ] or ]. Also: ], ], ], depression, ], ]. Use in pregnancy is discouraged. Moxonidine passes into breast milk.
	* normalising plasma insulin levels
	* improving glucose uptake in peripheral cells
	* lowering lipid levels
	* decreasing food intake and reducing weight gain in obese animals.

		⚫	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.{{medcn\|date=November 2023}}
	'''Renal function'''

		⚫	Excess mortality has been seen in patients with symptomatic ] in the MOXCON study.<ref>{{cite journal \| vauthors = Cohn JN, Pfeffer MA, Rouleau J, Sharpe N, Swedberg K, Straub M, Wiltse C, Wright TJ \| display-authors = 6 \| title = Adverse mortality effect of central sympathetic inhibition with sustained-release moxonidine in patients with heart failure (MOXCON) \| journal = European Journal of Heart Failure \| volume = 5 \| issue = 5 \| pages = 659–667 \| date = October 2003 \| pmid = 14607206 \| doi = 10.1016/S1388-9842(03)00163-6 \| s2cid = 45883678 \| doi-access = free }}</ref> However, the MOXCON trial utilised a very high dose of 3.0 mg daily which is well above the normal dose of 0.2–0.6 mg daily.
	Evidence is accumulating to show that sympathetic overactivity is substantially involved in the development and progression of chronic renal failure, contributing to a poor overall cardiovascular prognosis. Moxonidine has been shown to reduce structural renal damage in various models of renal failure.

	'''Cardiac structure'''

	In spontaneously hypertensive rats, moxonidine significantly reduced total heart weight, left ventricular weight and the ratio of ventricular weight to body weight compared with an untreated control group.

⚫	==Safety ~~pharmacology~~==

		⚫	==Adverse effects==
			{{Unreferenced section\|date=April 2016}}
		⚫	Noteworthy ]s include dry mouth, headache, fatigue, dizziness, intermittent facial oedema, nausea, sleep disturbances (rarely sedation), ], vasodilatation, and rarely, skin reactions.
		⚫	===Safety===
			{{Unreferenced section\|date=April 2016}}
	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.		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.

	==Cautions==
⚫	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.

	==Drug interactions==		==Drug interactions==
	Concomitant administration of moxonidine and a thiazide diuretic such as ] is ~~not~~ ~~indicated,~~ as ~~both drugs' hypotensive effects may be enhanced~~.		Concomitant administration of moxonidine and a thiazide diuretic such as ] gave a synergistic antihypertensive effect.
			<ref>{{cite journal \| vauthors = Frei M, Küster L, Gardosch von Krosigk PP, Koch HF, Küppers H \| title = Moxonidine and hydrochlorothiazide in combination: a synergistic antihypertensive effect \| journal = Journal of Cardiovascular Pharmacology \| volume = 24 \| issue = Suppl 1 \| pages = S25–S28 \| year = 1994 \| pmid = 7533223 \| doi = 10.1097/00005344-199424001-00005 \| doi-access = free }}</ref>

			== See also ==
	==Contra-indications==
			* ]
⚫	It is contraindicated if there has been a past history of ]; heart conduction disorders (e.g. ], second- or third-degree ]); ]; severe ] or ]~~, severe liver or renal impairment~~. Also: ], ], ], depression, ], ]. Use in pregnancy is discouraged. Moxonidine passes into breast milk.

		⚫	== References ==
⚫	Excess mortality has been seen in patients with symptomatic ].<ref>{{cite journal \|~~author~~=Cohn J ~~''et~~ ~~al.''~~ \|title=Adverse mortality effect of central sympathetic inhibition with sustained-release moxonidine in patients with heart failure (MOXCON) \|journal=~~Eur~~ J Heart ~~Fail~~ \|volume=5 \|issue=5 \|pages=~~659–67~~ \|~~year~~=2003 \|pmid=14607206 \|doi=10.1016/S1388-9842(03)00163-6}}</ref>
		⚫	{{Reflist}}

			== External links ==
⚫	==~~Side-~~effects==
			*{{Commonscatinline}}
⚫	Noteworthy ]s include dry mouth, headache, fatigue, dizziness, nausea, sleep disturbances (rarely sedation), ], vasodilatation, and rarely, skin reactions.

⚫	==References==
⚫	{{Reflist}}

	{{Antihypertensives and diuretics}}		{{Antihypertensives and diuretics}}
			{{Adrenergic receptor modulators}}
			{{Imidazoline receptor modulators}}

			]
			]
	]		]
		⚫	]
		⚫	]
	]		]
			]
	]		]
⚫	]
⚫	]

	]
	]
	]
	]
	]

Latest revision as of 19:35, 10 December 2024

Antihypertensive medication Pharmaceutical compound

Moxonidine
Clinical data

Pronunciation	/mɒkˈsɒnɪdiːn/
Trade names	Physiotens, Moxon
AHFS/Drugs.com	International Drug Names
Pregnancy category	AU: B3
Routes of administration	Oral (tablets)
ATC code	C02AC05 (WHO)
Legal status
Legal status	UK: POM (Prescription only) In general: ℞ (Prescription only)
Pharmacokinetic data
Bioavailability	88% (T_max = 1 hour)
Protein binding	7.2–10%
Metabolism	Liver (10–20%)
Metabolites	Dehydrogenated moxonidine (major), hydroxymethyl-moxonidine, hydroxy-moxonidine, dihydroxy-moxonidine
Elimination half-life	~2.2–2.8 hours
Excretion	Renal (90%), feces (~1%)
Identifiers
IUPAC name 4-Chloro-N-(4,5-dihydro-1H-imidazol-2-yl)- 6-methoxy-2-methylpyrimidin-5-amine
CAS Number	75438-57-2
PubChem CID	4810
ChemSpider	4645
UNII	CC6X0L40GW
KEGG	D05087
ChEMBL	ChEMBL19236
CompTox Dashboard (EPA)	DTXSID5045170
ECHA InfoCard	100.158.061
Chemical and physical data
Formula	C₉H₁₂ClN₅O
Molar mass	241.68 g·mol
3D model (JSmol)	Interactive image
SMILES Clc1nc(C)nc(OC)c1NC2=NCCN2
InChI InChI=1S/C9H12ClN5O/c1-5-13-7(10)6(8(14-5)16-2)15-9-11-3-4-12-9/h3-4H2,1-2H3,(H2,11,12,15) Key:WPNJAUFVNXKLIM-UHFFFAOYSA-N
(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. 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 also a growth hormone releaser. It is manufactured by Solvay Pharmaceuticals (acquired by Abbott in 2009) under the brand name Physiotens and Moxon.

Mechanism of action

Moxonidine is a selective agonist at the imidazoline receptor subtype 1 (I₁). 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 near equal affinity. Moxonidine has an affinity for I₁ that is 33 times greater than α₂, compared to clonidine which is only four times greater.

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

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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.

Contraindications

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.

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.

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

Adverse effects

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

Safety

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.

Drug interactions

Concomitant administration of moxonidine and a thiazide diuretic such as hydrochlorothiazide gave a synergistic antihypertensive effect.

References

Weimann HJ, Rudolph M (1992). "Clinical Pharmacokinetics of Moxonidine". Journal of Cardiovascular Pharmacology. 20 (Suppl. 4): S37 – S41. doi:10.1097/00005344-199220004-00008.
^ "Physiotens Tablets (moxonidine) Product Information" (PDF). Abbott Australasia Pty Ltd, 32-34 Lord Street, Botany NSW 2019, Australia. Retrieved 1 September 2016.
He MM, Abraham TL, Lindsay TJ, Schaefer HC, Pouliquen IJ, Payne C, et al. (March 2003). "Metabolism and disposition of the antihypertensive agent moxonidine in humans". Drug Metabolism and Disposition. 31 (3): 334–342. doi:10.1124/dmd.31.3.334. PMID 12584161.
Farsang, C (2001). "Moxonidine: Clinical Profile" (PDF). Journal of Clinical and Basic Cardiology. An Independent International Scientific Journal. 4 (3): 197–299. Retrieved 1 September 2016.
^ Fenton C, Keating GM, Lyseng-Williamson KA (2006). "Moxonidine: a review of its use in essential hypertension". Drugs. 66 (4): 477–496. doi:10.2165/00003495-200666040-00006. PMID 16597164. S2CID 195691757.
Fairbanks CA, Wilcox GL (July 1999). "Moxonidine, a selective alpha2-adrenergic and imidazoline receptor agonist, produces spinal antinociception in mice". The Journal of Pharmacology and Experimental Therapeutics. 290 (1): 403–412. PMID 10381806.
Bamberger CM, Mönig H, Mill G, Gödde E, Schulte HM (1995). "Growth hormone secretion in response to the new centrally acting antihypertensive agent moxonidine in normal human subjects: comparison to clonidine and GHRH". Experimental and Clinical Endocrinology & Diabetes. 103 (3): 205–208. doi:10.1055/s-0029-1211351. PMID 7584524.
Prichard BN, Owens CW, Graham BR (August 1997). "Pharmacology and clinical use of moxonidine, a new centrally acting sympatholytic antihypertensive agent". Journal of Human Hypertension. 11 (Suppl 1): S29 – S45. PMID 9321737.
Cohn JN, Pfeffer MA, Rouleau J, Sharpe N, Swedberg K, Straub M, et al. (October 2003). "Adverse mortality effect of central sympathetic inhibition with sustained-release moxonidine in patients with heart failure (MOXCON)". European Journal of Heart Failure. 5 (5): 659–667. doi:10.1016/S1388-9842(03)00163-6. PMID 14607206. S2CID 45883678.
Frei M, Küster L, Gardosch von Krosigk PP, Koch HF, Küppers H (1994). "Moxonidine and hydrochlorothiazide in combination: a synergistic antihypertensive effect". Journal of Cardiovascular Pharmacology. 24 (Suppl 1): S25 – S28. doi:10.1097/00005344-199424001-00005. PMID 7533223.

External links

Media related to Moxonidine at Wikimedia Commons

Sympatholytic (and closely related) antihypertensives (C02)

Sympatholytics
(antagonize α-adrenergic
vasoconstriction)

Central

α₂-Adrenergic receptor agonists	Clonidine Guanabenz Guanfacine Guanoxabenz Methyldopa Tiamenidine
Adrenergic release inhibitors	Bethanidine Bretylium Debrisoquine Guanadrel Guanazodine Guancydine Guanethidine Guanoclor Guanoxan
Imidazoline receptor agonists	Moxonidine Rilmenidine Tolonidine
Ganglion-blocking/nicotinic antagonists	Hexamethonium Mecamylamine Pentolinium Trimethaphan

Peripheral

Indirect

Monoamine oxidase inhibitors	Pargyline
VMAT inhibitors	Bietaserpine Deserpidine Methoserpidine Reserpine Syrosingopine
Tyrosine hydroxylase inhibitors	Metirosine

Direct

α₁-Adrenergic receptor blockers	Doxazosin Ketanserin Indoramin Prazosin Trimazosin Urapidil
Non-selective α-adrenergic receptor blockers	Phentolamine

Other antagonists

Serotonin receptor antagonists	Ketanserin Lidanserin
Endothelin receptor antagonists (for PHTooltip Pulmonary hypertension)	dual (Aprocitentan, Bosentan, Macitentan (+tadalafil), Riociguat) selective (Ambrisentan (+tadalafil), Sitaxentan, Sotatercept)

WHO-EM
Withdrawn from market
Clinical trials:
- Phase III
- Never to phase III

Adrenergic receptor modulators

α₁

Agonists

Antagonists

Abanoquil
Ajmalicine
Alfuzosin
Anisodamine
Anisodine
Atiprosin
Atypical antipsychotics (e.g., brexpiprazole, clozapine, olanzapine, quetiapine, risperidone)
Benoxathian
Beta blockers (e.g., adimolol, amosulalol, arotinolol, carvedilol, eugenodilol, labetalol)
Buflomedil
Bunazosin
Corynanthine
Dapiprazole
Domesticine
Doxazosin
Ergolines (e.g., acetergamine, ergotamine, dihydroergotamine, lisuride, nicergoline, terguride)
Etoperidone
Fenspiride
Hydroxyzine
Indoramin
Ketanserin
L-765,314
mCPP
Mepiprazole
Metazosin
Monatepil
Moxisylyte
Naftopidil
Nantenine
Neldazosin
Niaprazine
Niguldipine
Pardoprunox
Pelanserin
Perlapine
Phendioxan
Phenoxybenzamine
Phentolamine
Phenylpiperazine antidepressants (e.g., hydroxynefazodone, nefazodone, trazodone, triazoledione)
Piperoxan
Prazosin
Quinazosin
Quinidine
Silodosin
Spegatrine
Spiperone
Talipexole
Tamsulosin
Terazosin
Tiodazosin
Tolazoline
Tetracyclic antidepressants (e.g., amoxapine, maprotiline, mianserin)
Tricyclic antidepressants (e.g., amitriptyline, clomipramine, doxepin, imipramine, trimipramine)
Trimazosin
Typical antipsychotics (e.g., chlorpromazine, fluphenazine, loxapine, thioridazine)
Urapidil
WB-4101
Zolertine

α₂

Agonists

Antagonists

1-PP
Adimolol
Amesergide
Aptazapine
Atipamezole
Atypical antipsychotics (e.g., asenapine, brexpiprazole, clozapine, lurasidone, olanzapine, paliperidone, quetiapine, risperidone, zotepine)
Azapirones (e.g., buspirone, gepirone, ipsapirone, tandospirone)
BRL-44408
Buflomedil
Cirazoline
Efaroxan
Esmirtazapine
Fenmetozole
Fluparoxan
Idazoxan
Ketanserin
Lisuride
mCPP
Mianserin
Mirtazapine
NAN-190
Pardoprunox
Phentolamine
Phenoxybenzamine
Piperoxan
Piribedil
Rauwolscine
Rotigotine
Setiptiline
Spegatrine
Spiroxatrine
Sunepitron
Terguride
Tolazoline
Typical antipsychotics (e.g., chlorpromazine, fluphenazine, loxapine, thioridazine)
Yohimbine

Agonists

Abediterol
Alifedrine
Amibegron
Arbutamine
Arformoterol
Arotinolol
BAAM
Bambuterol
Befunolol
Bitolterol
Broxaterol
Buphenine
Carbuterol
Carmoterol
Cimaterol
Clenbuterol
Colterol
Corbadrine
Denopamine
Deoxyepinephrine (epinine, N-methyldopamine)
Dipivefrine
Dobutamine
Dopamine
Dopexamine
Droxidopa (L-DOPS)
Epinephrine
Etafedrine
Etilefrine
Etilevodopa
Ethylnorepinephrine
Eugenodilol
Fenoterol
Formoterol
Hexoprenaline
Higenamine
Ibopamine
Indacaterol
Isoetarine
Isoprenaline
Isoxsuprine
L-DOPA (levodopa)
L-Phenylalanine
L-Tyrosine
Levosalbutamol
Lubabegron
Mabuterol
Melevodopa
Methoxyphenamine
Methyldopa
Mirabegron
Norepinephrine
Orciprenaline
Oxyfedrine
PF-610355
Phenylpropanolamine
Pirbuterol
Prenalterol
Ractopamine
Procaterol
Reproterol
Rimiterol
Ritodrine
Salbutamol
Salmeterol
Solabegron
Terbutaline
Tretoquinol
Tulobuterol
Vibegron
Vilanterol
Xamoterol
XP21279
Zilpaterol
Zinterol

Antagonists

See also: Receptor/signaling modulators
Dopaminergics
Serotonergics
Monoamine reuptake inhibitors
Monoamine releasing agents
Monoamine metabolism modulators
Monoamine neurotoxins

v t e Imidazoline receptor modulators
IRTooltip Imidazoline receptor	Agonists: 2-BFI 7-Me-Marsanidine Agmatine Apraclonidine BU224 Clonidine Clorgyline Harmalas LNP-509 LNP-911 mCPP Moxonidine Rilmenidine S-23515 S-23757 Antagonists: BU99006 Efaroxan Idazoxan Unsorted/unknown: CR-4056 Pargyline
See also: Receptor/signaling modulators

Imidazoline receptor modulators

IRTooltip Imidazoline receptor

Antagonists: BU99006
Efaroxan
Idazoxan

Unsorted/unknown: CR-4056
Pargyline

See also: Receptor/signaling modulators

Categories: