Disease relevance of CV 1808

• Adenosine-induced hyperalgesia is mimicked by the A2-agonists, 5'-(N-ethyl)-carboxamido-adenosine and 2-phenylaminoadenosine but not by the A1-agonist, N6-cyclopentyladenosine and antagonized by the adenosine A2-receptor antagonist, PD 081360-0002 but not by the A1-antagonist, 1,3-dipropyl-8-(2-amino-4-chlorophenyl)xanthine [1].
• CV-1808 (0.25 microgram/kg/min i.v. infusion throughout the experimental period, starting 10 min before coronary occlusion) inhibited coronary circulatory failure and TXA2 release [2].
• The effect of 2-phenylaminoadenosine (CV-1808) against myocardial ischemia was studied in anesthetized dogs [3].
• Myocardial infarct size determined 60 min after reperfusion was significantly reduced by CV-1808 [2].
• The administration of CPA (165 micrograms) resulted only in a reduction in IOP, while the administration of CV-1808 produced only an initial ocular hypertension [4].

High impact information on CV 1808

• At times corresponding to the rise in IOP, the administration of high doses of CV-1808 (165 micrograms) produced a significant increase in aqueous humor flow and protein concentration [5].
• Adenosine and 2-phenylaminoadenosine (CV-1808) inhibit human neutrophil bactericidal function [6].
• The order of potency of antagonists and most agonists was the same in both cell types, but 2-phenylaminoadenosine and 2-chloroadenosine were relatively less potent in PC12 cells than in CHO cells [7].
• 5. Affinity values and rank order of potency of both receptor agonists and antagonists were similar to those previously obtained in human platelet and rat striatal membranes, except for CV 1808 which was more potent than CGS 21680 [8].
• Competition with various other adenosine receptor agonists results in a potency order of (IC50, microM): 2-phenylaminoadenosine (CV 1808, 0.34) > APE (0.96) > CGS 22988 (5.2) > 2-chloroadenosine (30) > CGS 21680 and NECA (> 100) [9].

Biological context of CV 1808

• Using 5 nM [3H]CV 1808, unlabeled CV 1808 produced shallow inhibition curves in all three brain areas, with 61 to 75% of the binding displaying IC50 values of 16 to 24 nM, whereas the remaining 28 to 37% of binding had lower affinity (IC50 595-1130 nM) [10].
• 3. The rank order of agonist potency to reduce the rate of peristalsis was: N6-cyclopentyladenosine (CPA) > NECA > R(-)-N6-(2-phenylisopropyl)adenosine (R-PIA) > chloroadenosine (2-CADO) > S-PIA > 2-phenylaminoadenosine (CV-1808) [11].
• If [3H]CGS 21680 is used for ice-cold assays, or if either [3H]CV 1808 or [3H]CGS 21680 are used for assays at 21 degrees C, the potency order of competing compounds changes markedly and becomes characteristic of A2a adenosine receptor binding sites; CGS 15943 > or = CGS 21680 congruent to NECA > CGS 22988 > or = CV 1808 [12].
• The ED50 values for pulmonary vasodilation were 1.9 x 10(-8) mol/L for 5'-N-ethylcarboxamidoadenosine (NECA), 4.5 x 10(-8) mol/L for 2-phenylaminoadenosine (CV-1808), 2.6 x 10(-6) mol/L for R(-)-N6-(2-phenylisopropyl) adenosine (R-PIA), and 6.5 x 10(-6) mol/L for cyclopentyladenosine, results consistent with an adenosine A2 receptor [13].

Anatomical context of CV 1808

• Neither the reduction in IOP induced by R-PIA nor the rise in IOP induced by CV-1808 was affected by surgical removal of the superior cervical ganglion [14].
• The A2 selective agonist CV 1808 was a 4-5 times more potent displacer in cortex and hippocampus than in the striatum [15].
• The two A2a selective agonists CGS 21680 and CV-1808 were essentially inactive in transfected COS-7 cells, but were very active in PC-12 cells known to possess functional A2a receptors [16].
• CV 1808 was 10 times more active than dipyridamole in enhancing the response of the vas deferens to exogenous adenosine [17].
• Thus, CV-1808 appeared to be effective for salvaging ischemic myocardium [2].

Associations of CV 1808 with other chemical compounds

• The rank order of potencies of the analogs as inhibitors of the responses to cholecystokinin octapeptide was N6-cyclopentyladenosine greater than 5'-N-ethylcarboxamidoadenosine much greater than 2-phenylaminoadenosine (CV 1808) [18].
• Like dopamine antagonists, NECA and CV-1808 also decreased hyperactivity caused by d--amphetamine at doses that did not cause ataxia whereas A1-selective adenosine agonists reduced amphetamine's effects only at ataxic doses [19].

Gene context of CV 1808

• 2-Chloroadenosine (2-CADO) and 2-phenylaminoadenosine (CV 1808) were compared in a CNS purinergic receptor binding assay and the inhibition of neurogenic contractions of the vas deferens [17].

Analytical, diagnostic and therapeutic context of CV 1808

• The topical administration of CV-1808 produced a rapid rise in IOP, with a maximum increase of 15.6 +/- 1.6 mm Hg [5].
• In the present study, the antinociceptive effects after intrathecal injection of each of 6 N6-substituted adenosine analogs and of 2-phenylaminoadenosine were compared with the affinity for the A1- and A2-adenosine receptors [20].
• Quantitation of 6-amino-2-phenylamino-9-beta-D-ribofuranosyl-9-H-purine (CV-1808) and its metabolite, 2-(2-hydroxyphenyl)aminoadenosine, in human serum and urine by high performance liquid chromatography using a fluorimetric detector [21].
• During intravenous infusion of CV-1808 (0.25 and 0.5 microgram/kg/min for 10 min) the ST-segment elevation in the epicardial ECG induced by a 5-min occlusion of a coronary arterial branch was occasionally enhanced in association with cardiac acceleration [3].

References