Clonidine hydrochloride

CAS No. 4205-91-8

Clonidine hydrochloride( Catapres | Kapvay | ST 155 )

Catalog No. M14433 CAS No. 4205-91-8

Clonidine Hydrochloride is a centrally acting alpha-agonist hypotensive agent.

Purity : >98% (HPLC)

COA Datasheet HNMR HPLC MSDS Handing Instructions
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50MG 34 In Stock
100MG 49 In Stock
200MG 60 In Stock
500MG 129 In Stock
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Biological Information

  • Product Name
    Clonidine hydrochloride
  • Note
    Research use only, not for human use.
  • Brief Description
    Clonidine Hydrochloride is a centrally acting alpha-agonist hypotensive agent.
  • Description
    Clonidine Hydrochloride is a centrally acting alpha-agonist hypotensive 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.(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. 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. 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.
  • 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.
  • 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. 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. 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.
  • Synonyms
    Catapres | Kapvay | ST 155
  • Pathway
    Endocrinology/Hormones
  • Target
    Adrenergic Receptor
  • Recptor
    α2-adrenergic receptor
  • Research Area
    Cardiovascular Disease
  • Indication
    ——

Chemical Information

  • CAS Number
    4205-91-8
  • Formula Weight
    266.55
  • Molecular Formula
    C9H10Cl3N3
  • Purity
    >98% (HPLC)
  • Solubility
    Ethanol: 53 mg/mL (198.87 mM); Water: 53 mg/mL (198.87 mM); DMSO: 53 mg/mL (198.87 mM)
  • SMILES
    Cl.ClC1=CC=CC(Cl)=C1NC1=NCCN1
  • Chemical Name
    ——

Shipping & Storage Information

  • Storage
    (-20℃)
  • Shipping
    With Ice Pack
  • Stability
    ≥ 2 years

Reference

1.Fairbanks CA, et al. J Pharmacol Exp Ther. 2002 Jan;300(1):282-90.
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