Clonidine - CAS 4205-90-7
Catalog number: 4205-90-7
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
C9H9Cl2N3
Molecular Weight:
230.09
COA:
Inquire
Targets:
Others
Description:
Clonidine is an α2-Adrenergic agonist for neuropathic pain.
Purity:
≥98%
Appearance:
White to Off-White Solid
Synonyms:
CLONIDINE BASE;Clonidine (base and/or unspecified salts);CLONIDINE (200 MG);1H-Imidazol-2-amine, N-(2,6-dichlorophenyl)-4,5-dihydro-;2-((2,6-dichlorophenyl)amino)-2-imidazoline;2-(2,6-dichloroanilino)-1,3-diazacyclopentene-(2);2-(2,6-dichloroanilino)-2-i
Solubility:
Soluble in DMSO
Storage:
Store at -20 °C
MSDS:
Inquire
Application:
α2 adrenergic agonist
Quality Standard:
Enterprise standard
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly.
Quantity:
Milligrams-Grams
Melting Point:
141-144 ºC
Density:
1.5g/cm3
InChIKey:
GJSURZIOUXUGAL-UHFFFAOYSA-N
InChI:
1S/C9H9Cl2N3/c10-6-2-1-3-7(11)8(6)14-9-12-4-5-13-9/h1-3H,4-5H2,(H2,12,13,14)
Canonical SMILES:
c1(NC2=NCCN2)c(cccc1Cl)Cl
1.Imidazolines increase the levels of the autophagosomal marker LC3-II in macrophage-like RAW264.7 cells.
Nakagawa S;Ueno T;Manabe T;Kawasaki K Can J Physiol Pharmacol. 2018 Aug;96(8):845-849. doi: 10.1139/cjpp-2018-0021. Epub 2018 Apr 10.
This study evaluated whether imidazolines can induce autophagy in the murine macrophage-like cell line RAW264.7. Idazoxan increased the content of LC3-II, an autophagosomal marker, in RAW264.7 cells. To determine whether this effect was due to the induction of its synthesis or inhibition of its degradation, idazoxan treatment was performed in the presence of bafilomycin A;1;, which blocks autophagosome-lysosome fusion, as well as Pepstatin A and E-64d, both of which block protein degradation in autolysosomes. An increased content of LC3-II was observed in the presence of bafilomycin A;1; as well as the protease inhibitors. Furthermore, an increased number of autophagosomes was observed following idazoxan treatment using an autophagosome-specific dye. This indicated that idazoxan induced autophagy. Other imidazolines, such as efaroxan, clonidine, and 2-(2-benzofuranyl)-2-imidazoline, also increased the LC3-II content in RAW264.7 cells in the presence of bafilomycin A;1;. Taken together, these results indicate that some imidazolines, including idazoxan, can induce autophagy in RAW264.7 cells.
2.Clonidine and guanfacine attenuate phencyclidine-induced dopamine overflow in rat prefrontal cortex: mediating influence of the alpha-2A adrenoceptor subtype.
Jentsch JD;Sanchez D;Elsworth JD;Roth RH Brain Res. 2008 Dec 30;1246:41-6. doi: 10.1016/j.brainres.2008.10.006. Epub 2008 Oct 18.
N-methyl-D-aspartic acid/glutamate receptor antagonists induce psychotomimetic effects in humans and animals, and much research has focused on the neurochemical and network-level effects that mediate those behavioral changes. For example, a reduction in NMDA-dependent glutamatergic transmission triggers increased release of the monoamine transmitters, and some of these changes are implicated in the cognitive, behavioral and neuroanatomical effects of phencyclidine (PCP). Alpha-2 adrenoceptor agonists (e.g., clonidine) are effective at preventing many of the behavioral, neurochemical and anatomical effects of NMDA antagonists. Evidence has indicated that a key mechanism of the clonidine-induced reversal of the effects of NMDA antagonists is an attenuation of enhanced dopamine release. We have pursued these findings by investigating the effects of alpha-2 agonists on PCP-evoked dopamine efflux in the prefrontal cortex of freely moving rats. Clonidine (0.003-0.1 mg/kg, i.p.) dose-dependently attenuated the ability of PCP (2.5 mg/kg, i.p.) to increase cortical dopamine output. The effects of clonidine were prevented by the alpha-2A subtype selective antagonist BRL-44408 (1 mg/kg, i.p.).
3.Cardiovascular Effects Mediated by Imidazoline Drugs: an Update.
Cobos-Puc LE;Aguayo-Morales H Cardiovasc Hematol Disord Drug Targets. 2018 Jun 29. doi: 10.2174/1871529X18666180629170336. [Epub ahead of print]
Clonidine is a centrally acting antihypertensive drug. Hypotensive effect of clonidine is mediated mainly by central a2-adrenoceptors and/or imidazoline receptors located in a complex network of the brainstem. Unfortunately, clonidine produces side effects such as sedation, mouth dry, and depression. Moxonidine and rilmenidine, compounds of the second generation of imidazoline drugs, with fewer side effects, display a higher affinity for the imidazoline receptors compared with a2-adrenoceptors. The antihypertensive action of these drugs is due to inhibition of the sympathetic outflow primarily through central I1-imidazoline receptors in the RVLM, although others anatomical sites and mechanisms/receptors are involved. Agmatine is regarded as the endogenous ligand for imidazoline receptors. This amine modulates the cardiovascular function. Indeed, when is administered in the RVLM mimic the hypotension of clonidine. Recent findings have shown that imidazoline drugs also exerts biological response directly on the cardiovascular tissues, which can contribute to their antihypertensive response. Currently, new imidazoline receptors ligands are in development. In the present review, we provide a brief update on the cardiovascular effects of clonidine, moxonidine, rilmenidine, and the novel imidazoline agents since representing an important therapeutic target for some cardiovascular diseases.
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CAS 4205-90-7 Clonidine

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