Home Neuronal Signaling Dopamine Receptor inhibitor Chlorpromazine HCl

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Chlorpromazine HCl Dopamine Receptor inhibitor

Cat.No.S2456

Chlorpromazine HCl is a dopamine and potassium channel inhibitor with IC50 of 6.1 and 16 μM for inward-rectifying K+ currents and time-independent outward currents.
Chlorpromazine HCl Dopamine Receptor inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 355.33

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Quality Control

Batch: Purity: 99.96%
99.96

Cell Culture, Treatment & Working Concentration

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
CHO cells Function assay Compound was evaluated for the binding affinity against [3H]8-OH-DPAT-labeled 5-hydroxytryptamine 1A receptor sites in cloned CHO cells, Ki=0.673 μM
CHO cells Function assay Compound was evaluated for the binding affinity against [3H]U-86,170-labeled D2 sites in cloned CHO cells, Ki=0.003 μM
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Solubility

In vitro
Batch:

DMSO : 71 mg/mL (199.81 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Water : 71 mg/mL

Ethanol : 71 mg/mL

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In vivo
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Chemical Information, Storage & Stability

Molecular Weight 355.33 Formula

C17H19ClN2S.HCl

 Storage (From the date of receipt)
CAS No. 69-09-0 Download SDF Storage of Stock Solutions

Mechanism of Action

Targets/IC50/Ki
Dopamine receptor
Potassium channel
In vitro
Chlorpromazine affects miniature IPSCs (mIPSCs) by decreasing the binding (kon) and by increasing the unbinding (koff) rates of GABAARs. Chlorpromazine modulates activated TRPA1 currents in a voltage-dependent way, leading to a block at positive potentials and an increased open probability at negative potentials.
In vivo
Chlorpromazine independently down-regulates the production of various T cell-derived lymphokines (IL-2, IFN-gamma, IL-4, TNF, and GM-CSF) and up-regulates the secretion of IL-10 in an in vivo model of acute superantigen-driven immune activation. Chlorpromazine -mediated amplification of the SEB-driven Chlorpromazine secretion is accompanied by an enhanced IL-10 mRNA accumulation. Chlorpromazine protects mice, normal or adrenalectomized, and guinea pigs against lethality of LPS, and inhibits TNF serum levels. Chlorpromazine protects against LPS lethality when administered 30 minutes (min) before, simultaneously, or up to 10 min after LPS and is ineffective when given 30 min after LPS, paralleling the inhibitory effect on TNF production. Chlorpromazine significantly inhibits LPS lethality and hepatotoxicity in mice sensitized to LPS toxicity by actinomycin D, whereas under these conditions DEX is inactive. Chlorpromazine protects brain tissue from hypoxia-induced irreversible loss of synaptic transmission in rats. Chlorpromazine also significantly delays the occurrence of the hypoxia-induced spreading depression (SD) in rats.
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/2033366/
  • [5] https://pubmed.ncbi.nlm.nih.gov/3022872/

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT06238089 Recruiting
Intellectual Disability
University of Plymouth|Peninsula Clinical Trials Unit
 December 19 2023 --
NCT05206747 Recruiting
Mania|Sleep|Bipolar Disorder
Ottawa Hospital Research Institute
 September 7 2022 Not Applicable
NCT03548714 Completed
Alcohol Dependence|Alcohol Interaction
Pop Test Oncology LLC|Pharmacotherapies for Alcohol and Substance Use Disorders Alliance|Congressionally Directed Medical Research Programs|Michael E. DeBakey VA Medical Center|Baylor College of Medicine|University of California San Diego
 September 1 2018 Phase 1

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