| Name | Clonidine |
| Description | Clonidine (Kapvay) is a centrally active alpha-adrenergic agonist used predominantly as an antihypertensive agent, usually in combination with other agents. Despite wide-scale use for many years, clonidine has not been linked definitively to either serum aminotransferase elevations or clinically apparent liver injury. |
| In vitro | Clonidine (0.01, 0.1 or 1 μM) significantly induces CGRP (α and β) mRNA expression in a dose-dependent manner in endothelial cells. Clonidine treatment (1 μM) for 24 h significantly increases the NO level in endothelial cells. NO pathway modulates CGRP production induced by clonidine [2]. |
| In vivo | Clonidine (3-50 μg/kg, i.p.) potently suppresses dopamine efflux in the prefrontal cortex induced by PCP. Pretreatment with the alpha-2A receptor antagonist (BRL-44408) prevents clonidine from suppressing PCP-induced dopamine overflow in the prefrontal cortex [3]. Clonidine (50 μg/kg, i.p.) induces a significant decrease in body temperature of rat lasting 3 hr, with the maximum at 1 hr after administration. An intracerebroventricular pretreatment of rats with neutral doses of phentolamine 15 min before clonidine considerably antagonizes the clonidine-induced hypothermia[1]. In DMSO-pretreated SO rats, clonidine (0.6 μg i.c.) has no effect on blood pressure. However, after central adenosine A1R blockade (DPCPX) in SO rats, clonidine significantly (P < 0.05, one-way ANOVA) reduces blood pressure. In contrast, in DMSO-pretreated ABD rats, clonidine (0.6 μg i.c.) causes a significant reduction in blood pressure; importantly, central A1R blockade (DPCPX pretreatment) does not influence (P > 0.05, one-way ANOVA) clonidine-evoked reduction in blood pressure in ABD rats. In DPCPX-pretreated SO rats and along with the appearance of the hypotensive response, clonidine causes a significant (P < 0.05) increase in the RVLM pERK1/2 level compared with basal or clonidine treatment in DMSO-pretreated SO rats. In a vehicle (DMSO)-pretreated ABD rats, clonidine significantly (P < 0.05) enhances RVLM pERK1/2, and this response is not affected by DPCPX pretreatment [4]. |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
| Solubility Information | H2O : 2 mg/mL （8.69 mM), Sonication is recommended.
DMSO : 15 mg/mL (65.19 mM), Sonication is recommended.
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| Keywords | α2-adrenergic | Clonidine | inhibit | Inhibitor | anesthesia | Adrenergic Receptor | Beta Receptor |
| Inhibitors Related | Olanzapine | Mirtazapine | Octopamine hydrochloride | Gemfibrozil | Dexmedetomidine hydrochloride | Phenylephrine hydrochloride | Isoprenaline hydrochloride | Amitriptyline hydrochloride | Trazodone hydrochloride | Mianserin hydrochloride |
| Related Compound Libraries | Anti-Neurodegenerative Disease Compound Library | Bioactive Compound Library | Membrane Protein-targeted Compound Library | Anti-Cancer Clinical Compound Library | Drug Repurposing Compound Library | FDA-Approved Drug Library | Anti-Cancer Approved Drug Library | Bioactive Compounds Library Max | GPCR Compound Library | Anti-Cancer Drug Library |
United States
