Catalog number: 51-12-7
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Monoamine Oxidase
Nialamide is used as an antidepressant for it is a monoamine oxidase inhibitor (MAOI) of the hydrazine class. It might be efficient under the combination action with 5-hydroxytryptophan in antidepressant.
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≥ 99%
White solid
10 mM in DMSO
-20°C Freezer
Nialamide is a a monoamine oxidase inhibitor (MAOI) of the hydrazine class that is useful as an antidepressant agent.
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Melting Point:
152-154 °C
Canonical SMILES:
1.Development and validation of a hydrophilic interaction liquid chromatography-tandem mass spectrometry method for determination of isoniazid in human plasma.
Huang L1, Marzan F, Jayewardene AL, Lizak PS, Li X, Aweeka FT. J Chromatogr B Analyt Technol Biomed Life Sci. 2009 Jan 15;877(3):285-90. doi: 10.1016/j.jchromb.2008.12.024. Epub 2008 Dec 24.
An LC-MS/MS method for the determination of isoniazid in human plasma was developed and validated. Human plasma aliquots of 100 microL were used for analysis. The assay used nialamide as the internal standard. The calibration curve concentration range was 50-10,000 ng/mL. Sample preparation utilized protein precipitation, and the supernatant was directly injected onto silica column without reconstitution. The recovery was over 90% and matrix effect was negligible. The method is simple and fast, which is advantageous in respect to instability of isoniazid in human plasma and loss on reconstitution due to its low molecular weight.
2.Preproenkephalin knockout mice show no depression-related phenotype.
Bilkei-Gorzo A1, Michel K, Noble F, Roques BP, Zimmer A. Neuropsychopharmacology. 2007 Nov;32(11):2330-7. Epub 2007 Mar 21.
Clinical, preclinical, and pharmacological studies have suggested that decreased enkephalin tone is associated with depression-like symptoms and increase in enkephalin signaling could have a therapeutic value in the treatment of depression. In this study we demonstrate that, surprisingly, animals lacking enkephalin (preproenkephalin, Penk1(-/-)) showed no depression-related phenotype in the Porsolt forced swimming or tail suspension tests. Moreover, Penk1(-/-) mice had a lower frequency of depression-related behavior in stress-induced hypoactivity and ultrasonic vocalization models of depression, similar to animals treated with antidepressant drugs, although this effect was specific to the genetic background. In addition, there was no significant difference in the efficacy of antidepressant reference compounds in wild-type and knockout animals. Nialamide and amitriptyline were even slightly more effective in animals with genetic deletion of Penk1, whereas the minimal effective dose of imipramine and fluoxetine was the same in the two genotypes.
3.Parallel nociceptive reflex pathways with negative and positive feedback functions to foot extensors in the cat.
Schomburg ED1, Steffens H, Wada N. J Physiol. 2001 Oct 15;536(Pt 2):605-13.
1. Nociceptive reflex pathways to foot extensors were investigated with particular attention given to those not following a flexor reflex (FRA) or withdrawal pattern. 2. In anaemically decapitated, high spinal paralysed cats nociceptive afferents of the foot pad were activated by noxious radiant heat (48-60 degrees C), while for comparison non-nociceptive afferents were activated by weak mechanical stimulation of the skin or graded electrical nerve stimulation. The reflex action of the afferents on hindlimb motoneurones, innervating plantaris and intrinsic foot extensors (tibial nerve), was investigated by intracellular recording, by monosynaptic reflex testing and by recording of neurograms during fictive locomotion. A possible descending control of the nociceptive and non-nociceptive pathways was tested by application of opioidergic and monoaminergic compounds. 3. Beside the typical FRA pattern evoked in the majority of hindlimb motoneurone pools by nociceptive afferents from different skin areas of the foot, the results revealed parallel excitatory and inhibitory nociceptive reflex pathways from the central pad and partly from the toe pads to foot extensors.
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