{'fraction_non_alphanumeric': 0.032, 'fraction_numerical': 0.029333333333333333, 'mean_word_length': 4.774358974358974, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Toxicity studies with fluindarol, 2-(p-(trifluoromethyl)phenyl)-1,3-indandione, an agent with anticoagulant properties (BS 7616 D).

The phenylindandione derivative fluindarol was subjected to a toxicological investigation in view of its possible use as an anticoagulant in man. The acute oral LD50 in rats and rabbits was 198 and 123 mg/kg, respectively. The acute intraperitoneal LD50 in the rat was 125 mg/kg. Dogs survived single oral doses of up to 2810 mg/kg; if the drug was given for four consecutive days, an oral LD50 of 118 mg/kg was obtained. In a four-week experiment in the rat, doses ranging from 108 to 7 mg/kg caused mortality which occurred sooner and more frequently in the females than the males; the organs showed haemorrhages and at the higher dose levels the liver showed parenchymal necrosis. Similar results were obtained with chlorindione, which tended to be somewhat less toxic. It was confirmed that a distinction should be made between the “toxicity” of an anticoagulant which is due to its pharmacological properties and true organ toxicity. Fluindarol was considered too toxic for clinical use.