1. The antagonistic relationship between OMP and vitamin B₆ was studied using the running fit as an index. Pyridoxine (PIN) was found to have a suppressive effect when less than 1500μg/g of OMP was used. When the dose of OMP is raised to this limit, an almost equal quantity of vitamin B₆ is required for suppression.
2. Two additional compounds, similar in structure to OMP, were also found to induce running fits.
3. The toxicity of these compounds is lower than that of OMP but the running fit appears earlier.
4. Of the two compounds, the running fit induced by 2, 5-dimethyl-4-aminopyrimidine (I) can be suppressed by PIN, but PIN has no effect on the seizure induced by 2, 6-dimethyl-4-aminopyrimidine (II).
5. Both I and II are shown to intensify the toxicity of OMP. 2-Methyl-4-aminopyrimidine (III) which singly possesses no toxicity, also intensifies the toxicity of OMP.
6. OMP, I, II and III should be called “toxopyrimidine group substances” considering its properties.

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The cell-free extract prepared from staphylococci under low temperature in vacuo hydrolyzes thiamine and the action coincides with that of thiaminase II. This enzyme is thermolabile and nondialyzable. The optimum pH is about 7.0 and the optimum temperature is 40°. It is strongly inhibited by copper, mercury and silver ions. It does not break down the disulfide forms of thiamine but degrades many thiamine derivatives. These results suggest that thiaminase II is present in bacteria other than B. aneurinolyticus, though minor in activity.

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The author examined the biological activity of dichloroflavin, i.e., 6, 7-dichlorc-9-(D-1′-ribityl) isoalloxazine by the use of rats. A large amount of dichloro-flavin was shown to have a toxic action; it impaired the ability of the liver for retaining riboflavin, and disturbed severely the kidney function.
The growth was retarded after the appearence of toxic symptoms.

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1. The pharmacological actions of DPN and ADS on the blood vessels of a surviving ear, on the cardiac systole of a living rabbit's heart's heart and of a surviving guinea pig's heart and on the rabbit's blood pressure were tested.
2. Both DPN and ADS had a contracting effect on the blood vessels of a rabbit's ear, an inhibitory effect on the cardiac systole of living rabbits and of a surviving guinea pig's heart, and the hypotensive effect on rabbits.
3. The inhibitory effect of both DPN and ADS on the cardiac systole of living rabbits and the hypotensive effect of DPN on rabbits were not influenced by atropine. No difference was seen in their effects with or without bilateral vagotomy at the neck.
4. DPN acted hypotensively even in the state of hypotension caused by a hypodermic injection of chloral hydrate.

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1. The actions of ADS and DPN on the uteri of rabbits, the guts of guinea pigs and rabbits, and the bladders of guniea pigs were examined pharmacologically. Various organs of the animals which had been administered a large dose of DPN intravenously were also examined histologically.
2. Both ADS and DPN showed contracting effects on the uteri of rabbits and on the bladders of guinea pigs, and relaxing effects on the guts of guinea pigs and rabbits.
3. The contracting effect of ADS or DPN on the uteri of rabbits was not inhibited by atropine or PBM, but was decreased by PPV.
4. The relaxing effect of ADS or DPN on the guts of guinea pigs and rabbits was not influenced either by atropine or PBM. ADS and DPN did not inhibit the gut-contracting effect of histamine, ACH or BaCl₂. The increase of the tonus of a rabbit's gut by PCP was easily relaxed by DPN.
5. Intravenous administration of a large dose of DPN to an animal produced vasodilatation and congestion in the lungs, spleen, liver, kidneys, suprarenal glands, ileum, caecum, stomach, testis and epididymis, and marked hemorrhages in some of the organs.

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