Abstract
The order of acute intravenous toxicity of caronamide, as represented by the LD50, was quite comparable for mice, rabbits and dogs; being 1405 mg./kg., 1320 mg./kg. and 1575 mg./kg., respectively. The magnitude of the toxicity in mice was intermediate between that for crystalline potassium penicillin and sodium penicillin. The principal manifestation of toxicity was the sedation that the compound seemed to produce in all three species of animals at high dosages.
The oral administration to rats of 0.5 gm. of caronamide/day seemed to produce no evidence of hematologic or histologic damage as compared to control animals. Similarly, dogs were given dosages of from 0.4 to 1.5 gm./kg./day for a period of four weeks, and a monkey was given 1.0 gm./kg./day for four weeks. Of the studies involving blood and urine chemistry, hematology and histology, a non-fermentable reducing substance which appeared in the urine of dogs receiving the higher drug dosages was the only definite manifestation of a systemic effect attributable to the drug.
Footnotes
- Received August 1, 1947.
- 1946 by The American Society for Pharmacology and Experimental Therapeutics
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