Clonidine

SKU: orb1300116

Description

Clonidine (Kapvay) is a centrally acting alpha-2 adrenergic agonist primarily used to treat hypertension. It is a valuable research tool for studying sympathetic nervous system regulation in cardiovascular and neuropharmacology models, both in vivo and in vitro. Despite long-term clinical use, it has not been associated with significant liver injury.

Research Area

Neuroscience, Pharmacology & Drug Discovery

Key Properties

• CAS Number: 4205-90-7
• MW: 230.09
• Purity: 99.42% (May vary between batches)
• Formula: C₉H₉Cl₂N₃
• SMILES: N(C1=C(Cl)C=CC=C1Cl)C=2NCCN2
• Target: Adrenergic Receptor
• Solubility: 10% DMSO+40% PEG300+5% Tween 80+45% Saline:5 mg/mL (21.73 mM);H2O:2 mg/mL (8.69 mM);DMSO:262 mg/mL (1138.68 mM)

Bioactivity

• 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 . 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. 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 .
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• 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 .
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Storage & Handling

• Storage: -20°C
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

Kapvay, inhibit, Nexiclon, Inhibitor, Clonidine, Catapres, Beta Receptor, anesthesia, AdrenergicReceptor, Adrenergic Receptor, α2 adrenergic receptor, α2-adrenergic

Compound Identifiers

PubChem CID

2803