Home Transmembrane Transporters Potassium Channel activator Hydralazine HCl

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Hydralazine HCl Potassium Channel activator

Cat.No.S2562

Hydralazine HCl is a hydrochloride salt of hydralazine, which is a direct-acting smooth muscle relaxant used to treat hypertension by acting as a vasodilator primarily in arteries and arterioles.
Hydralazine HCl Potassium Channel activator Chemical Structure

Chemical Structure

Molecular Weight: 196.64

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Quality Control

Batch: Purity: 99.95%
99.95

Solubility

In vitro
Batch:

Water : 39 mg/mL

DMSO : Insoluble
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : Insoluble

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In vivo
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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
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Chemical Information, Storage & Stability

Molecular Weight 196.64 Formula

C8H8N4.HCl

 Storage (From the date of receipt)
CAS No. 304-20-1 Download SDF Storage of Stock Solutions

Synonyms N/A SMILES C1=CC=C2C(=C1)C=NN=C2NN.Cl

Read more about storage stability stock solution CAS number SMILES

Mechanism of Action

Targets/IC50/Ki
Potassium Channel
In vitro
Hydralazine impairs up-regulation of RAG-2 gene expression and reduces secondary Ig gene rearrangements. Hydralazine subverts B lymphocyte tolerance to self and contributes to generation of pathogenic autoreactivity by disrupting receptor editing. Hydralazine directly scavenges free acrolein, decreasing intracellular acrolein availability and thereby suppressing macromolecular adduction. Hydralazine inhibits cross-linking if adding 30 min after commencing acrolein exposure but is ineffective if added after a 90-min delay. Hydralazine (0.1-10 mM) inhibits both extracellular and intracellular ROS production by inflammatory macrophages, by a ROS-scavenging mechanism probably affecting superoxide radical (O(2)(*-))-generation by xanthine oxidase (XO) and nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide phosphate (NADH/NADPH) oxidase. Hydralazine (0.1-10 mM) significantly reduces NO(*) generation, and this effect is attributable to an inhibition of NOS-2 gene expression and protein synthesis. Hydralazine also effectively blocks COX-2 gene expression which perfectly correlated with a reduction of protein levels and PGE(2) synthesis. Hydralazine protects against not only acrolein-mediated injury, but also compression in guinea pig spinal cord ex vivo. Hydralazine can significantly alleviate acrolein-induced superoxide production, glutathione depletion, mitochondrial dysfunction, loss of membrane integrity, and reduces compound action potential conduction.
In vivo
Hydralazine affords strong, dose-dependent protection against the increases in plasma marker enzymes but not the hepatic glutathione depletion produced by allyl alcohol in mice.
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/17995940/
  • [5] https://pubmed.ncbi.nlm.nih.gov/15131244/

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2026-08-27)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT04842552 COMPLETED
Alzheimer Disease
Shahid Sadoughi University of Medical Sciences and Health Services
 2021-08-02 PHASE3
NCT06218199 RECRUITING
Heart Failure, Congestive
Heart Center Research, LLC
 2021-07-08 PHASE4
NCT03514108 COMPLETED
Heart Failure; Diabetes
Henrik Wiggers
 2018-03-01 PHASE4
NCT05230901 UNKNOWN
Aortic Stenosis, Severe
University Medical Center Goettingen
 2022-02-23 PHASE3
NCT06360601 UNKNOWN
Preeclampsia Severe
Tanta University
 2024-04-01 PHASE1; PHASE2
NCT07572656 COMPLETED
Preeclampsia
Muhammad Aamir Latif
 2024-05-01

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