105537-91-5

Upstream product

• 5469-69-2 6-chloro-pyridazin-3-ylamine 
• 24067-17-2 4-nitrophenylboronic acid 
• 100-19-6 (4-nitrophenyl)ethanone 
• 105537-49-3 3-(p-Nitrophenyl)-6-oxo-1,6-dihydropyridazine 
• 99708-47-1 3-(p-Nitrophenyl)-6-chloropyridazine 
• 105537-48-2 ethyl β-(p-nitrobenzoyl)lactate 

Downstream Products

• 105537-81-3 6-Amino-1-(3-carboxy-propyl)-3-(4-nitro-phenyl)-pyridazin-1-ium; bromide 
• 105538-29-2 6-Amino-1-(3-ethoxycarbonyl-propyl)-3-(4-nitro-phenyl)-pyridazin-1-ium; bromide 

Relevant academic research and scientific papers

Discovery of 2-(Imidazo[1,2- b]pyridazin-2-yl)acetic Acid as a New Class of Ligands Selective for the γ-Hydroxybutyric Acid (GHB) High-Affinity Binding Sites

Gabazine, a γ-aminobutyric acid type A (GABAA) receptor antagonist, has previously been reported to inhibit the binding of [3H]NCS-382, a representative ligand of the high-affinity binding site for the neuroactive substance γ-hydroxy

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.