Haloperidol hydrochloride - CAS 1511-16-6
Catalog number: 1511-16-6
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
Dopamine Receptor | Nitric oxide synthase (NOS)
Haloperidol hydrochloride is a dopamine antagonist that specifically targets D2-like receptors, with effect to treat schizophrenia, acute psychosis, and delirium. And it is also a non-competitive inhibitor of NOS1 (nNOS). Ki: D2 receptors=1.2, D3 receptor
Solid powder
4-[4-(4-chlorophenyl)-4-hydroxypiperidin-1-yl]-1-(4-fluorophenyl)butan-1-one;hydrochloride haloperidol hydrochloride UNII-UM06W2ADRY UM06W2ADRY Haloperidol (hydrochloride) CHEMBL545608 1511-16-6
Soluble to 25 mM in DMSO with gentle warming
Store in a cool and dry place and at 0 - 4℃ for short term (days to weeks) or -47℃ for long term (months to years).
Shelf Life:
2 years
Melting Point:
226-227.5 °C
Canonical SMILES:
1.N-4-tert-butyl benzyl haloperidol chloride suppresses Ca2+-dependent Egr-1 expression and subsequently inhibits vascular smooth muscle cell proliferation induced by angiotensin II.
Chen Y;Zheng J;Zhang Y;Wang J;Liu Q;Huang Z;Gao F;Zhou Y;Shi G Cell Physiol Biochem. 2009;23(4-6):295-304. doi: 10.1159/000218176. Epub 2009 May 6.
BACKGROUND: ;N-4-Tert-Butyl benzyl haloperidol chloride (C(3)) was a novel calcium antagonist synthesized in our laboratory. The present study is to explore the effect of C(3) on vascular smooth muscle cell proliferation and the mechanism involved.;METHODS: ;The effects of C(3) on Ang II-induced cytosolic free Ca(2+) concentration change, VSMC proliferation, the key early growth response factor 1 (Egr-1) were evaluated by laser scanning confocal microscopy, microtiter tetrazolium (MTT) proliferation assay, flow cytometry analysis, Western blot and RT-PCR analysis, respectively. An extracellular Ca(2+) chelator EGTA and antisense Egr-1 oligodeoxyribonucleotides (ODNs) were used to establish the relation between Ca(2+)-dependent Egr-1 expression induced by Ang II and VSMC proliferation.;RESULTS: ;C(3) attenuated the Ang II-induced extracellular Ca(2+) influx, inhibited VSMCs proliferation and arrested VSMCs in G(1)-phase. C(3) also triggered a significant reduction in PDGF-A and cyclin D1, Cdk2 along with an overexpression of p21Cip1. Antisense Egr-1 ODNs inhibited VSMCs proliferation, which was related to G(1)-phase arrest, due to inhibiting the expression of Egr-1 and C(3) inhibited the overexpression of Egr-1.
2.Antidepressants in 'depressed' schizophrenic inpatients. A controlled trial.
Kramer MS;Vogel WH;DiJohnson C;Dewey DA;Sheves P;Cavicchia S;Little P;Schmidt R;Kimes I Arch Gen Psychiatry. 1989 Oct;46(10):922-8.
Fifty-eight actively psychotic inpatients who initially met criteria for long-standing schizophrenia and subsequently met Research Diagnostic Criteria for a current episode of schizoaffective disorder (mainly schizophrenic) with a depressive syndrome, and who scored at least 30 (mean = 55, SEM = 1.6) on the Brief Psychiatric Rating Scale and 17 (mean = 23, SEM = 0.7) on the Hamilton Rating Scale for Depression, were treated for 5 weeks with haloperidol hydrochloride and benztropine. Haloperidol and benztropine treatment was continued, while those patients who consistently scored greater than 17 on the Hamilton Rating Scale for Depression were randomly assigned to the following double-blind treatment groups for 4 weeks: adjunctive amitriptyline hydrochloride, desipramine hydrochloride, or placebo. Adjunctive desipramine or amitriptyline showed no significant therapeutic advantage, when compared with haloperidol and placebo, on the Brief Psychiatric Rating Scale or the Hamilton Rating Scale for Depression. After 4 weeks of combine therapy, patients receiving adjunctive amitriptyline or desipramine, as compared with those receiving adjunctive placebo, tended to score higher on the Brief Psychiatric Rating Scale hallucinatory behavior item and on the thinking disturbance factor than patients receiving placebo.
3.Solution-mediated phase transformation of salts during dissolution: investigation using haloperidol as a model drug.
Greco K;Mcnamara DP;Bogner R J Pharm Sci. 2011 Jul;100(7):2755-68. doi: 10.1002/jps.22507. Epub 2011 Feb 16.
Soluble salts can undergo solution-mediated phase transformation to a lower solubility form due to pH gradients in the gastrointestinal tract. Therefore, dissolution rate rather than solubility may be the best predictor of bioavailability for such compounds. The purpose of this project was to examine the kinetics of the conversion of a basic compound, haloperidol, and its salt forms using a flow-through dissolution apparatus and rotating disk method in neutral conditions. The effects of buffer concentration, salt form, dissolution apparatus, and hydrodynamics were examined. Raman microscopy was used to characterize solids after dissolution. Haloperidol mesylate and haloperidol chloride showed a decrease in dissolution rate with time in the dissolution media. Haloperidol mesylate and haloperidol chloride dissolution rates also decreased with increasing buffer capacity. Raman microscopy confirmed phase conversion from the salt forms to the free base form in phosphate buffer. Hydrodynamics did not affect the time course of the solution-mediated phase transformation of salt forms. Dissolution and precipitation appear to be a function of pH close to the surface of the dissolving solid. In situations where equilibrium solubility of salts cannot be assessed experimentally, dissolution experiments are useful for examining the extent and duration of the dissolution rate enhancement.
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