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Document Figure 1 Structures of the positive inotropes digoxin [3,4], DPI 201-106 [15], and BDF 9148 [15–17]. In digoxin the R group is (O-2,6-dideoxy-β-D-ribo-hexopyranosyl-(1 rarrow.gif 4)-O-2, 6-dideoxy-β-D-ribo-hexopyranosyl-(1 rarrow.gif 4)-2, 6-dideoxy-β-D-ribo-hexopyranosyl)oxy. In DPI 201-106 the configuration at the hydroxyl-bearing carbon influences cardiac activity. Page 296 fatigue, visual disturbances, and anorexia, and in cardiac side-effects that depend on the nature and extent of the underlying heart disease [3]. Careful monitoring of digoxin serum levels and bioavailability have reduced the incidence of digitalis toxicity [3] and the recent introduction of digoxin-binding antibodies or antibody fragments has provided an effective means of treating severe digitalis toxicity [3,7]. Nevertheless the quest continues for a substitute for the cardiac glycosides in the treatment of chronic CHF. Positive inotropic compounds can be classified into three groups: cAMP generators, intracellular calcium regulators, and modulators of ion channels or pumps [11]. The cAMP generators such as dopamine, dobutamine, and milrinone (a phosphodiesterase inhibitor) may worsen ischemia, cause arrhythmias, and increase mortality [2,6]. Intracellular calcium modulators have not reached clinical use, possibly because of additional effects such as vasoconstriction, http://legacy.netlibrary.com/nlreader/nlReader.dll?bookid=12640&filename=Page_296.html (1 of 2) [4/5/2004 5:18:07 PM]
Document Page 297 whereas, calcium sensitizers such as EMD 57033 may be useful positive inotropic compounds, even in the diseased myocardium [12]. Ion channel modulation represents another approach to positive inotropy [13]. Sodium channel modulators increase Na + influx and prolong the plateau phase of the action potential; sodium/calcium exchange then leads to an increase in the level of calcium available to the contractile elements, thus increasing the force of cardiac contraction [13,14]. Synthetic compounds such as DPI 201-106 and BDF 9148 (Figure 1) increase the mean open time of the sodium channel by inhibiting channel inactivation [15]. Importantly, BDF 9148 remains an effective positive inotropic compound even in severely failing human myocardium [16] and in rat models of cardiovascular disease [17]. Modulators of calcium and potassium channel activities also function as positive inotropes [13], but in the remainder of this article we shall focus on sodium channel modulators. II. The Anthopleurins Two decades ago “drugs from the sea” were the subject of high expectations and a good deal of effort in various centers around the world. The number of therapeutically useful compounds to have emerged from that effort has been rather limited, but with the advent of high-throughput screening it is likely that useful new leads will be found, even from species investigated previously. Notwithstanding, some valuable leads did emerge from work carried out in the 1970s, amongst which were the polypeptide cardiac stimulants known as the anthopleurins. These were isolated from sea anemones, where they are components of the animal's venom and are believed to have a function in defense and the capture of prey. The work that led to the isolation and characterization of these and related polypeptides from sea anemones is covered in earlier reviews [18,19] and will not be reiterated here. The best characterized of the anthopleurins is anthopleurin-A (AP-A), which was isolated from the northern Pacific sea anemone Anthopleura xan- thogrammica and consists of 49 residues cross-linked by three disulfide bonds [18,20]. It is active as a cardiac stimulant at nanomolar concentrations in vitro, making it some 200 fold more potent on a molar basis that digoxin. Its positive inotropic activity is not associated with any significant effects on heart rate or blood pressure [21], and in conscious dogs its therapeutic index is 7.5, which is about three-fold higher than that of digoxin [8]. Anthopleurin-A is active under conditions of stress and hypocalcaemia [18,22], as well as in ischemic myocardium where many other positive inotropes give equivocal results [23]. The profile of activity for AP-A suggests that it is a potentially valuable lead in the development of an alternative positive inotrope to digoxin http://legacy.netlibrary.com/nlreader/nlReader.dll?bookid=12640&filename=Page_297.html [4/5/2004 5:18:14 PM]
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Document Page 108 mulate during tre
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Document We determined the structur
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Document Figure 3 Previously known
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Document 17 Structure and Functiona
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Document Table 1 Approval Indicatio
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Document Page 438 proteins. One pot
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Document II. Type IFNs A great deal
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Document Page 441 sequence of the m
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Document Figure 5 Velcro-key model
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Document Page 476 nM, respectively.
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Document Page 488 against most of t
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Document A. The Canyon Page 491 The
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Document Subsequent studies have sh
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Document Page 495 of the RNA and pr
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Document Figure 4 A ribbon diagram
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Document Figure 5 Some compounds wh
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Document D ddI, 152 tumour necrosis
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Document antistasin peptides, 281 c
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