32176-53-7

Upstream product

• 28657-55-8 6-(o-Chlorophenyl)-4-methyl-3(2H)-pyridazinone 
• 29242-26-0 4-(2-Chloro-phenyl)-2-hydroxy-2-methyl-4-oxo-butyric acid 
• 2142-68-9 1-(2-chlorophenyl)ethanone 

Downstream Products

• 118269-87-7 [6-(2-Chloro-phenyl)-4-methyl-pyridazin-3-yl]-(2-morpholin-4-yl-ethyl)-amine; hydrochloride 
• 105538-24-7 6-Amino-3-(2-chloro-phenyl)-1-(3-ethoxycarbonyl-propyl)-5-methyl-pyridazin-1-ium; bromide 
• 105538-04-3 6-(2-Chloro-phenyl)-4-methyl-pyridazin-3-ylamine 

Relevant academic research and scientific papers

3-Aminopyridazine derivatives with atypical antidepressant, serotonergic, and dopaminergic activities

Minaprine [3[(β-morpholinoethyl)amino]4-methyl-6-phenylpyridazine dihydrochloride] is active in most animal models of depression and exhibits in vivo a dual dopaminomimetic and serotoninomimetic activity profile. In an attempt to dissociate these two effe

Synthesis and Structure-Activity Relationships of Series of Aminopyridazine Derivatives of γ-Aminobutyric Acid Acting as Selective GABA-A Antagonists

We have recently shown that an aryloaminopyridazine derivarive of GABA, SR 95103 , is a selective and competitive GABA-A receptor antagonist.In order to further explore the structural requirements for GABA receptor affinity, we synthesized a series of 38 compounds by attaching various pyridazinic structures to GABA or GABA-like side chains.Most of the compounds displaced GABA from rat brain membranes.All the active compounds antagonized the GABA-elicited enhancement of diazepam binding, strongly suggesting that all these compounds are GABA-A receptor antagonists.None of the compounds that displaced GABA from rat brain membranes interacted with other GABA recognition sites (GABA-B receptor, GABA uptake binding site, glutamate decarboxylase, GABA-transaminase).They did not interact with the Cl- ionophore associated with the GABA-A receptor and did not interact with the benzodiazepine, strychnine, and glutamate binding sites.Thus these compounds appear to be specific GABA-A receptor antagonists.In terms of structure-activity, it can be concluded that a GABA moiety bearing a positive charge is necessary for optimal GABA-A receptor recognition.Additional binding sites are tolerated only if they are part of a charge-delocalized amidinic or guanidinic system.If this delocalization is achieved by linking a butyric acid moiety to the N(2) nitrogen of a 3-aminopyridazine, GABA-antagonistic character is produced.The highest potency (ca.250 times bicuculline) was observed when an aromatic ? system, bearing electron-donating substituents, was present on the 6-position of the pyridazine ring.