Bidrin (3-Hydroxy-N,N-dimethylcrotonamide dimethylphosphate) 
Azodrin (3-Hydroxy-N-methylcrotonamide dimethylphosphate) (N-methyl bidrin, 
SD 9129). 
Using pee -labeled bidrin and rats, 83% of the recovered activity 
after injection was in the form of dimethylphosphate after 20 hours. 
Metabolites were excreted rapidly. Within 24 hours, 83% of the injected 
dose had been excreted. Extensive oxidation occurred with the formation 
of hydroxymethyl bidrin and N-methyl bidrin (azodrin). Subsequent 
hydrolysis gave rise to dimethyl phosphate, bidrin acid, desmethyl bidrin 
acid, monomethylphosphate, and finally inorganic phosphate. Hydrolysis 
of bidrin itself gave rise to desmethyl bidrin (199). 
When administered orally to rats, 63-/1% of the pre was excreted in 
48 hours. No marked sex or compound differences were noted. Most of the 
radioactivity was excreted in urine within 6 hours. An additional 5-62 
appeared in the feces within 48 hours following treatment. Residual P 
in the tissues did not vary with sex. An additional 12% was recovered as 
GPO. within 48 hours after treatment of male rats with bidrin-N-methyl- 
c!* (984, 983). 
Urinalyses on dogs, mice, and rabbits, as well as on rats and goats, 
indicated that species variation existed in the rate at which bidrin-P32 
was metabolized and the extent of metabolite excretion in the urine (984). 
Significant amounts of N-hydroxymethylamide analog of azodrin 
appeared following administration to rats of either bidrin or azodrin 
while the N-methyl-N-hydroxymethylamide compound was present only 
following bidrin treatment, and the unsubstituted amide only following 
azodrin treatment (984). 
In rats administered azodrin only trace amounts of azodrin acid 
were detected in extracts, indicating minimal hydrolytic degradation by 
amidase action. Dimethyl phosphate and O-demethyl azodrin were the major 
degradation products of azodrin. It was felt that degradation followed 
formation of hydroxymethyl azodrin rather than loss of HCHO. The finding 
of only trace amounts of N-demethyl azodrin and the stability of the pure 
compound seemed to indicate that demethylation was a minor reaction (200). 
Goats treated orally with bidrin or azodrin excreted in the urine 
a high proportion of the administered P32 or N-methyl-C!"* labels. Trace 
amounts of bidrin, azodrin, the N-hydroxymethylamide analog of azodrin, 
and the unsubstituted amide were present in the urine (984). Labeled 
compounds appeared in the goat milk after treatment with either P32 or 
55 
