| Stereochemistry | ACHIRAL |
| Molecular Formula | C9H12ClN5O |
| Molecular Weight | 241.677 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
COC1=C(NC2=NCCN2)C(Cl)=NC(C)=N1
InChI
InChIKey=WPNJAUFVNXKLIM-UHFFFAOYSA-N
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)
| Molecular Formula | C9H12ClN5O |
| Molecular Weight | 241.677 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
Moxonidine is a second-generation, centrally acting antihypertensive drug with a distinctive mode of action. Moxonidine activates I1-imidazoline receptors (I1-receptors). Imidazoline I1-receptor agonism represents a new mode of antihypertensive action to inhibit peripheral alpha-adrenergic tone by a central mechanism. Adrenaline, noradrenaline and renin levels are reduced, a finding consistent with central inhibition of sympathetic tone. Moxonidine acts centrally to reduce peripheral sympathetic activity, thus decreasing peripheral vascular resistance. In patients with mild to moderate hypertension, moxonidine reduces blood pressure (BP) as effectively as most first-line antihypertensives when used as monotherapy and is also an effective adjunctive therapy in combination with other antihypertensive agents. It improves the metabolic profile in patients with hypertension and diabetes mellitus or impaired glucose tolerance, is well tolerated, has a low potential for drug interactions and may be administered once daily in most patients. Moxonidine is a good option in the treatment of patients with mild to moderate hypertension, particularly as adjunctive therapy in patients with the metabolic syndrome.
CNS Activity
Originator
Approval Year
Cmax
AUC
T1/2
Doses
AEs
Overview
| CYP3A4 | CYP2C9 | CYP2D6 | hERG |
|---|---|---|---|
OverviewOther
| Other Inhibitor | Other Substrate | Other Inducer |
|---|---|---|
Drug as perpetrator
Drug as victim
Tox targets
PubMed
Sample Use Guides
Treatment should be started with 0.2 mg Physiotens in the morning. The dose may be titrated after two weeks to 0.4 mg given as one dose or as divided doses (morning and evening) until a satisfactory response is achieved. If the response is still unsatisfactory after a further 2 weeks treatment, the dosage can be increased up to a maximum of 0.6 mg in divided doses (morning and evening). A single daily dose of 0.4 mg and a divided daily dose of 0.6 mg of Physiotens should not be exceeded. Physiotens may be taken with or without food.
Route of Administration:
Oral
It was investigate the effects of moxonidine on neurons in the rostral ventrolateral medulla (RVLM) with electrophysiological properties similar to premotor sympathetic neurons in vivo. Moxonidine (2-10 microM) was applied to the perfusate on 4 irregularly firing neurons, and 2 regularly firing neurons. Moxonidine (2 microM) produced only minor depolarization in 2 of these neurons. However, on 4 tested neurons, moxonidine (10 microM) elicited a profound inhibitory effect with hyperpolarization (near -20 mV); these neurons practically ceased firing. These changes were partially reversible. The results would indicate that neurons in the RVLM, recorded in vitro and with similar electrophysiological characteristics to a group of neurons previously identified in vivo in the same bulbar region as barosensitive premotor sympathetic neurons, can be modulated by imidazoline-derivative adrenergic agonists. These results could help to understand the hypotensive effects of moxonidine.
