1. GPCR/G Protein
    Neuronal Signaling
  2. Adrenergic Receptor
  3. Clonidine hydrochloride

Clonidine hydrochloride 

Cat. No.: HY-B0409A Purity: 99.96%
Handling Instructions

Clonidine hydrochloride is an agonist of α2-adrenoceptor and potent antihypertensive agent.

For research use only. We do not sell to patients.

Clonidine hydrochloride Chemical Structure

Clonidine hydrochloride Chemical Structure

CAS No. : 4205-91-8

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10 mM * 1 mL in DMSO USD 66 In-stock
Estimated Time of Arrival: December 31
100 mg USD 60 In-stock
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500 mg USD 168 In-stock
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Based on 1 publication(s) in Google Scholar

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Clonidine hydrochloride is an agonist of α2-adrenoceptor and potent antihypertensive agent.

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 (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]. Clonidine (0.003-0.05 mg/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]. 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 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 vehicle (DMSO)-pretreated ABD rats, clonidine significantly (P < 0.05) enhances RVLM pERK1/2, and this response is not affected by DPCPX pretreatment[4].

Clinical Trial
Molecular Weight









Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month
Solvent & Solubility
In Vitro: 

H2O : 33.33 mg/mL (125.04 mM; Need ultrasonic)

DMSO : 7.6 mg/mL (28.51 mM; Need ultrasonic and warming)

Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 3.7516 mL 18.7582 mL 37.5164 mL
5 mM 0.7503 mL 3.7516 mL 7.5033 mL
10 mM 0.3752 mL 1.8758 mL 3.7516 mL
*Please refer to the solubility information to select the appropriate solvent.
Animal Administration

On the day of the experiment, the flow rate is increased to 2 μL/min approximately 2 h before beginning the collection of baseline samples. Dialysates are collected every 20 min; after 4 baseline samples are collected, animals are pretreated with an intra-peritoneal (i.p.) injection of either 0.9% saline (the vehicle), clonidine (0.0033, 0.01 or 0.05 mg/kg) or guanfacine (0.05 or 0.5 mg/kg), before receiving an injection of PCP (2.5 mg/kg, i.p.) 20 min later. In a separate study, BRL (1.0 mg/kg) is administered 20 min prior to clonidine. In addition, for some control experiments, the animals only receive one injection of saline, clonidine (0.01 or 0.05 mg/kg), guanfacine (0.5 mg/kg) or BRL (1.0 mg/kg).

MCE has not independently confirmed the accuracy of these methods. They are for reference only.


Purity: 99.96%

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