SCH58261

SCH 58261 causes the inhibition of rabbit platelet aggregation and porcine coronary artery relaxation by antagonizing competitively the effects induced by CGS 21680. ^[1]

In mice with Spinal cord injury, SCH58261 (0.01 mg/kg, i.p.) reduces demyelination and levels of TNF-α, Fas-L, PAR, Bax expression and activation of JNK MAPK. Chronic SCH58261 administration improves the neurological deficit up. ^[2]

In rats with 6-OHDA-induced Parkinson's disease, SCH58261 (2 mg/kg, i.p.) improves the 6-OHDA-induced bradykinesia and motor disturbance. ^[3]

• Receptor binding assay

  Rat brain tissues (cortex and striatum) are obtained from male Sprague-Dawley rats weighing 250 to 300 g. Bovine brain tissues (frontal cortex and striatum) are obtained from a local abattoir within 10 mm from animal sacrifice. A1 and A2a ADO receptor binding assays are performed using [³H]CHA and [³H]CGS 21680 [³H]2-[4-(2-carboxyethyl)-phenethylamino]- 5’-N-ethylcarboxamidoadenosinel as radioligands, respectively. Binding assay to CHO cells stably transfected with the rat brain A3 ADO receptor is performed using [¹²⁵I]AB-MECA as radioligand. In order to determine the type of inhibition (competitive or noncompetitive), saturation experiments at A1 ADO ([³H]CHA, 0.125-64 nM) and A2a ADO receptors ([³HJCGS 21680, 1-128 aM) are carried out on rat brain tissues in the absence or in the presence of different concentrations of SCH 58261 (7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4- triazolo[1,5-c]pyrimidine}. The affinity of SCH 58261 for several neurotransmitter binding sites, such as alpha-1, alpha-2 and beta-1 adrenoceptors, D1 and D2 dopamine receptors, 5-HT1 and 5-HT2 receptors, M1 and M2 muscarinic receptors, mu-opioid, benzodiazepine and N-methyl-D-aspartate receptors, is measured according to standard methods.

• Animal Models

  Mice with Spinal cord injury

• Dosages

  0.01 mg/kg

• Administration

  i.p.