Addiction Research

According to the World Health Organization (WHO), addiction is 'a chronic disease of the central nervous system that is characterized by a loss of control over impulsive behavior that leads to compulsive drug seeking and taking, and to relapses even after months of abstinence'. Addiction is a complex neuroadaptive process, where drugs of abuse alter cellular and molecular aspects of neural function. The brain circuits mediating the various behavioral effects of these drugs are rendered more, or less, responsive to those effects.

Addiction Research Products Targets

Products for Addiction Research - Page 25

Cat.No. Product Name Information/Activity
BCC6555 (-)-Bicuculline methobromide (-)-Bicuculline methobromide (l-Bicuculline methobromide) is a potent GABAA receptor antagonist. (-)-Bicuculline methobromide blocks afterhyperpolarizations (AHPs) mediated by Ca2+-activated K+ channels in various types of neurons.
BCN3763 (-)-Bicuculline methochloride (-)-Bicuculline methochloride (l-Bicuculline methochloride) is a potent GABAA receptor antagonist. (-)-Bicuculline methochloride blocks afterhyperpolarizations (AHPs) mediated by Ca2+-activated K+ channels in various types of neurons.
BCN1238 (+)-Bicuculline (+)-Bicuculline is a light-sensitive competitive antagonist of GABA-A receptor.
BCC3782 Furosemide Furosemide is a loop diuretic inhibitor of Na+/2Cl-/K+ (NKCC) cotransporter of which used in the treatment of congestive heart failure and edema.
BCC6193 PHP 501 trifluoroacetate 1236105-75-1
BCC5705 Picrotoxin Picrotoxin (Cocculin) is a natural noncompetitive antagonist of GABAA receptor, binds to the interface pocket on the GABAR. Picrotoxin (Cocculin) causes overstimulation and induces convulsions.
BCC7266 SCS 3232-36-8
BCC6997 SR 95531 hydrobromide Gabazine is a selective and competitive antagonist of GABAA receptor, with an IC50 of ~0.2 μM for GABA receptor.
BCC7510 TB 21007 207306-50-1
BCC7471 U 93631 U93631 is a GABAA receptor ligand of novel chemical structure with IC50 of 100 nM,and has been shown to induce a rapid, time-dependent decay of GABA-induced whole-cell Cl-currents in recombinant GABAA receptors.