For research use only.
CAS No. 304-20-1
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.
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|Description||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 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. |
-  Mazari L, et al. Proc Natl Acad Sci U S A,?007, 104(15), 6317-6322.
-  Burcham PC, et al. Mol Pharmacol,?006, 69(3), 1056-1065.
-  Leiro JM, et al. Int Immunopharmacol,?004, 4(2), 163-177.
|In vitro||Water||1 mg/mL (5.08 mM)|
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Clinical Trial Information
|NCT Number||Recruitment||interventions||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT04164004||Not yet recruiting||Other: Kansas City Cardiomyopathy Questionnaire-12||Heart Failure||Stanford University||May 1 2020||Not Applicable|
|NCT03619317||Unknown status||--||Cancer of Esophagus||Aarhus University Hospital Skejby|Danish Cancer Society||June 25 2018||--|
|NCT01587313||Completed||Drug: Isosorbide dinitrate / hydralazine capsules||Healthy||Arbor Pharmaceuticals Inc.||April 2012||Phase 1|
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