Drug Name Allopurinol

Therapeutic effects. ?-Blockers protect the heart from the oxygenwasting effect of sympathetic inotropism (p. 306) by blocking cardiac ?-receptors; thus, cardiac work can no longer be augmented above basal levels (the heart is “coasting”). This effect is utilized prophylactically in angina pectoris to prevent myocardial stress that could trigger an ischemic attack.
Apropos nomenclature: antibiotics are produced by microorganisms (fungi, bacteria) and are directed “against life” at any phylogenetic level (prokaryotes, eukaryotes). Chemotherapeutic agents originate from chemical synthesis. This distinction has been lost in current usage.

 

Acyclovir triphosphate is a preferred substrate of viral DNA polymerase; it inhibits enzyme activity and, following its incorporation into viral DNA, induces strand breakage because it lacks the 3’-OH group of deoxyribose that is required for the attachment of additional nucleotides.
Compared with full antibodies, fragments have superior tissue penetrability, more rapid renal elimination, and lower antigenicity. The pharmacokinetics of cardiac glycosides (A) are dictated by their polarity, i.e., the number of hydroxyl groups. Membrane penetrability is virtually nil in ouabain, high in digoxin, and very high in digitoxin.