Moxonidine - CAS 75438-57-2
Catalog number:
75438-57-2
Category:
Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C9H12ClN5O
Molecular Weight:
241.68
COA:
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Targets:
Imidazoline Receptor
Description:
Moxonidine is a selective agonist at the imidazoline receptor subtype (I1). It binds with much greater affinity to the imidazoline I1-receptor than to the α2-receptor while clonidine binds to both receptors with equal affinity.
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Purity:
>98%
MSDS:
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1.Centrally acting drug moxonidine decreases reactive oxygen species via inactivation of the phosphoinositide-3 kinase signaling in the rostral ventrolateral medulla in hypertensive rats.
Wang YK1, Yu Q, Tan X, Wu ZT, Zhang RW, Yang YH, Yuan WJ, Hu QK, Wang WZ. J Hypertens. 2016 May;34(5):993-1004. doi: 10.1097/HJH.0000000000000887.
OBJECTIVE: Centrally acting antihypertensive action of moxonidine is a result of activation of Imidazoline-1 receptor (I1R) in the rostral ventrolateral medulla (RVLM). Hypertension shows an increase in reactive oxygen species (ROS) in the RVLM. The present objective was to determine the phosphoinositide-3 kinase (PI3K) signaling pathway involved in the effect of moxonidine on ROS generation in the RVLM of spontaneously hypertensive rat (SHR).
2.Adherence to EBM guidelines in clinical practice.
Khafizianova RKh, Burykin IM. Int J Risk Saf Med. 2015;27 Suppl 1:S53-4. doi: 10.3233/JRS-150687.
BACKGROUND: Adequate and rational pharmacotherapy is an important element of rehabilitation of patients with myocardial infarction. Orders of the Ministry of Health of the Russian Federation, domestic and international guidelines, and scientific publications - all contain a complete algorithm for rational pharmacotherapy [1, 2]. These documents are based on the principles of evidence-based medicine (EBM) and help practicing physicians to carry out individualized and rational pharmacotherapy. However, clinical studies have shown low adherence of physicians to clinical guidelines. In the Russian Federation the death rate from cardiovascular diseases is higher than in developed countries. Thus, studies of the causes of high cardiovascular mortality are needed.
3."Hyperglutamatergic cortico-striato-thalamo-cortical circuit" breaker drugs alleviate tics in a transgenic circuit model of Tourette׳s syndrome.
Nordstrom EJ1, Bittner KC2, McGrath MJ2, Parks CR 3rd2, Burton FH3. Brain Res. 2015 Dec 10;1629:38-53. doi: 10.1016/j.brainres.2015.09.032. Epub 2015 Oct 8.
The brain circuits underlying tics in Tourette׳s syndrome (TS) are unknown but thought to involve cortico/amygdalo-striato-thalamo-cortical (CSTC) loop hyperactivity. We previously engineered a transgenic mouse "circuit model" of TS by expressing an artificial neuropotentiating transgene (encoding the cAMP-elevating, intracellular A1 subunit of cholera toxin) within a small population of dopamine D1 receptor-expressing somatosensory cortical and limbic neurons that hyperactivate cortico/amygdalostriatal glutamatergic output circuits thought to be hyperactive in TS and comorbid obsessive-compulsive (OC) disorders. As in TS, these D1CT-7 ("Ticcy") transgenic mice׳s tics were alleviated by the TS drugs clonidine and dopamine D2 receptor antagonists; and their chronic glutamate-excited striatal motor output was unbalanced toward hyperactivity of the motoric direct pathway and inactivity of the cataleptic indirect pathway. Here we have examined whether these mice׳s tics are countered by drugs that "break" sequential elements of their hyperactive cortical/amygdalar glutamatergic and efferent striatal circuit: anti-serotonoceptive and anti-noradrenoceptive corticostriatal glutamate output blockers (the serotonin 5-HT2a,c receptor antagonist ritanserin and the NE alpha-1 receptor antagonist prazosin); agmatinergic striatothalamic GABA output blockers (the presynaptic agmatine/imidazoline I1 receptor agonist moxonidine); and nigrostriatal dopamine output blockers (the presynaptic D2 receptor agonist bromocriptine).
4.Constructing the ecstasy of MDMA from its component mental organs: Proposing the primer/probe method.
Ray TS1. Med Hypotheses. 2016 Feb;87:48-60. doi: 10.1016/j.mehy.2015.12.018. Epub 2015 Dec 23.
The drug MDMA, commonly known as ecstasy, produces a specific and distinct open hearted mental state, which led to the creation of a new pharmacological class, "entactogens". Extensive literature on its mechanisms of action has come to characterize MDMA as a "messy" drug with multiple mechanisms, but the consensus is that the distinctive entactogenic effects arise from the release of neurotransmitters, primarily serotonin. I propose an alternative hypothesis: This hypothesis emerges from "mental organ" theory, which embodies many hypotheses, the most relevant of which are: I propose the "primer/probe" method to test these hypotheses. A "primer" is a drug that selectively activates 5-HT2 (e.g. DOB or MEM) or serotonin-1 (5-HT1) and 5-HT2 (e.g. DOET or 2C-B-fly). A "probe" is a drug that activates a receptor whose corresponding mental organ we wish to load into consciousness in order to understand its role in the mind. The mental organ is loaded into consciousness when the primer and probe are taken together, but not when taken separately.
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